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msmarco_passage_01_289420511 | Tabs3 | Time and Billing Software | 2021 Reviews, Pricing, Demos | Tabs3 | Time and Billing Software | 2021 Reviews, Pricing, Demos
Tabs3
About Tabs3
Tabs3 provides both Tabs3 Billing and Tabs3 Financials depending on your needs. The billing software helps you get bills out quickly and easily and provides management reports. The Financials product meets the accounting requirements of law firms via financial statements, invoicing, bank reconciiation, and client trust accounts.
Video Overview
Tabs3 Billing
Tabs3 Financial Software
Video Overview
Tabs3 Billing
Tabs3 Billing is reliable, award winning software designed for law firms. It makes it easy to get your bills out quickly, and manage the business side of your firm. Automatically e-mail PDF statements to clients one at a time, or in batches. Bill your standard rate or set up custom rates and billing options per client or attorney.
Add Tabs3 Taskbill software for electronic billing formats such as LEDES. Choose from the many statement layouts. Use your firm’s logo to make your own unique statement design. Easily review billed and unbilled time, accounts receivable (what clients owe you), attorney productivity, receipt allocation (rules that determine what each attorney has earned), your top clients, and more.
Tracking Your Time Is Easy
Timers help you track time as you go, and then turn billable hours into fees that will appear on the client’s next statement. See a recap of your worked hours to make sure all of your time is entered. Simple forms make it easy to enter your time. You can track hours worked and hours to bill, and create task-based statements such as LEDES (Tabs3 Taskbill required). You can even enter your time and costs from your phone or tablet using Tabs3 Connect – a Platinum feature.
Bill Exactly the Way You Want To
Tabs3 gives you virtually unlimited billing rate flexibility. Use one of the standard billing rates for an attorney, bill by timekeeper level (partner, associate, etc.), or create custom rates for any timekeeper for any client. You can also use contingency, split fee, flat fee, and retainer, progress, and electronic task based billing. Then customize your statement to show exactly what you want.
Get Your Bills Out Faster
You can print or e-mail your statements as PDFs. You can automatically generate all of the e-mails and PDFs at once and automatically insert last payment date, outstanding balance, statement notes, and other client information into the e-mail. E-mail statements one at a time or in batches, and password protect statements for high-profile clients. Print draft statements and track which ones are still under internal review. Use Tabs3 reports to review unbilled time and expenses for any timekeeper or client. Click on any transaction on a bill to edit or update it.
Useful Reports to Stay on Top of the Business of Law
Dozens of reports give you insight into your firm. Run a Recap of Hours Report to find time that has not been turned in. The Top Client Report ranks clients by work-in-process, billed amounts, write offs and more. The Timekeeper Productivity Reports show you what each timekeeper has billed, written off and their effective billing rates. The Client Inactivity Report identifies clients with no activity. The Collections Report makes follow-up easy by showing you the clients with outstanding balances, and their contact information, billing, and payment history. Export any report to Microsoft Excel ®.
Secure Your Information
Make sure that people in your firm only see the information they are supposed to see by restricting access to certain timekeepers, clients, or matters. You decide who can add, view, and delete information.
Advanced Compensation Formulas
Set up compensation rules for originating, primary and secondary timekeepers. Here are some examples of how compensation rules can be used:
Kathy gets 2% of receipts from all working timekeepers.
Bruce gets 5% of receipts from work done by Amber, Deb and Phil.
Dan gets 5% of receipts for ACME Insurance until June 2007.
Brad gets 10% of receipts for Widgets International until he receives a total of $10,000.
Free Practice Management Software.
Every Tabs3 license includes a one-user license of PracticeMaster practice management software to try before you buy.
Tabs3 Financial Software
Tabs3 Financial software is the best accounting solution for your law firm because it is specifically designed to meet the accounting requirements of law firms. With minimal setup and zero workarounds to satisfy most bar associations, you can print financial statements, write checks, reconcile bank statements, and manage client trust accounts in one easy-to-use and fully integrated system.
Because Tabs3 Financial software was designed to work with Tabs3 Billing software, you can call one technical support team for assistance if you ever have questions.
Video Overview
Customizable Chart of Accounts.
Because every firm’s chart of accounts is unique, you may add, change or delete any of the provided accounts. Individual accounts optionally integrate with Tabs3 to help you allocate payments to specific timekeepers.
Easy Bank Statement Reconciliation
Reconcile bank statements to your cash accounts.
Detailed and Summary Financial Statements
Income statements, trial balances and journal reports are just a few clicks away!
Write Checks
Print checks then post them to Tabs3 General Ledger. Makes bill paying easier.
Stay Organized
Track invoices and keep a list of all vendors in one place.
Create 1099 Forms.
Print 1099 forms or create a 1099 Disk File for electronic submission.
Integrates With Tabs3 Billing Software.
Assign your existing Tabs3 clients to a trust account in one easy step and easily make payments to your firm out of a client’s trust account. Optionally process deposits via credit card. Trust account balances optionally print on Tabs3 statements.
Print Checks
Write checks out of your client’s trust account, then print check registers and easily reconcile your trust accounts to bank statements.
Product Overview
Developer Software Technology, Inc.
Type Time and Billing, Legal Accounting, and Legal
Client OS Windows
Deployment On-Premises
Starting Price $72/month
Market Focus
Ratio of reviewers by organization size.
Enterprise 0%
Mid-Market 8%
Small Business 82%
Freelancers 10%
Industry Focus
Ratio of reviewers by sector.
98%
98%
Professional Services
2%
2%
Consulting
Other Software by Software Technology, Inc.
PracticeMaster |
msmarco_passage_01_290051180 | What does ploy mean - Definition of ploy - Word finder | What does ploy mean - Definition of ploy - Word finder
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Word finder
Word definitions
ploy
What is "ploy"
Crossword clues for ploy
ploy
Devious tactic
Tricky move
Sneaky stratagem
Sly stratagem
Cunning tactic
Cunning scheme
Cunning move
Clever strategy
Artful stratagem
Wily maneuver
Tricky action
Strategic maneuver
One-up tactic
Underhanded tactic
Strategic gimmick
Shrewd move
Red herring, e.g
Queen sacrifice in chess, e.g
Piece of strategy
Outwitting maneuver
One-up trick
One-up maneuver
One-up job
Muhammad Ali's rope-a-dope tactic, e.g
Karpov gambit, e.g
Gamer's maneuver
Game maneuver
Disconcerting trick
Disconcerting action
Cunning maneuver
Crafty maneuver
Bit of gamesmanship
Artful maneuver
Tactical maneuver
Stratagem
Ruse
Feint
Sneaky maneuver
Maneuver used to gain an advantage
Sneaky tactic
Sly maneuver
Clever tactic
Something from one's bag of tricks
Tricky maneuver
Subterfuge
Scheme
Devious maneuver
An opening remark intended to secure an advantage for the speaker
A maneuver in a game or conversation
Fast one
Gambit
Karpov gambit, e.g.
Device
Game tactic
Manoeuvre in old technical college with internal switch
Cunning plan
Former college having a change of heart in scheme
Artful dodge
Bit of subterfuge
Red herring, sometimes
Bit of trickery
Clever maneuver
Bit of strategy
Sly tactic
Deceptive maneuver
Tricky tactic
Longman Dictionary of Contemporary English
ploy
noun
COLLOCATIONS FROM OTHER ENTRIES
tactical move/decision/ploy
▪ a tactical decision to send in troops
COLLOCATIONS FROM CORPUS
■ ADJECTIVE
political
▪ Critics say the program is unrealistic and a political ploy.
■ NOUN
marketing
▪ A neat marketing ploy, and a good way of interesting children in aviation.
▪ But this year an even more offensive marketing ploy is keeping me away from my Christmas shopping.
▪ A promo video stressing the artist's style is a shrewd marketing ploy which exploits the music industry's visual obsession.
▪ New York drug dealers seem to go in for sophisticated marketing ploys.
▪ This kind of collection, though usually available individually, is increasingly and intelligently proving to be a marketing ploy.
EXAMPLES FROM OTHER ENTRIES
▪ He's not really ill, it's just a ploy to make us feel sorry for him.
▪ The ploy didn't work.
▪ The religious element of their election campaign was a cynical ploy.
EXAMPLES FROM CORPUS
▪ A neat marketing ploy, and a good way of interesting children in aviation.
▪ But his main ploy was to portray Weld as a friend of the rich eager to reduce educational opportunities for ordinary citizens.
▪ Certainly Mosley's constant harping on the theme of left-wing intimidation was a fairly effective recruiting ploy throughout the 1930s.
▪ It is a ploy, but he had good reason to believe it would be an effective one.
▪ This ploy should give the stockmarket a boost.
▪ Using government subsidies to increase local authority rents is not a new ploy.
▪ Why give her the satisfaction of knowing her ploy had succeeded?
The Collaborative International Dictionary
Ploy
Ploy \Ploy\, n. Sport; frolic. [Prov. Eng. & Scot.]
Ploy
Ploy \Ploy\, v. i. [Prob. abbrev. fr. deploy.] (Mil.) To form a column from a line of troops on some designated subdivision; -- the opposite of deploy.
--Wilhelm.
Douglas Harper's Etymology Dictionary
ploy
1722, "anything with which one amuses oneself," Scottish and northern England dialect, possibly a shortened form of employ or deploy. Popularized in the sense "move or gambit made to gain advantage" by British humorist Stephen Potter (1900-1969).
Wiktionary
ploy
Etymology 1 n. A tactic, strategy, or gimmick. Etymology 2
vb. (context military English) To form a column from a line of troops on some designated subdivision.
WordNet
ploy
n. an opening remark intended to secure an advantage for the speaker [syn: gambit]
a maneuver in a game or conversation [syn: gambit, stratagem]
Wikipedia
Ploy
Ploy is a 2007 Thai film written and directed by Pen-Ek Ratanaruang. The film premiered during the Directors' Fortnight at the 2007 Cannes Film Festival.
The drama film stars Thai actress Lalita Panyopas in a story of a middle-aged married couple who question their relationship after seven years. Ananda Everingham is featured in a supporting role as a bartender.
The film contained sex scenes that were shown at Cannes, but due to censorship concerns had to be re-edited by the director so the film could be shown in cinemas in Thailand when it opened there on June 7, 2007. The uncensored version of the film was shown in Thailand at the 2007 Bangkok International Film Festival.
Ploy (board game)
Ploy is an abstract strategy board game for two or four players, commercially released by 3M Company in 1970, as part of the 3M bookshelf game series. The game is said to have a "chess-like feel". As in chess, the game features several types of pieces, each with their own moving capabilities. The 3M game set includes a board and fifty pieces of various colors and shapes. The game is marketed as a "space-age strategy game". It is also considered to be one of the “better” chess variations.
Usage examples of "ploy".
One facet of their ploy was to claim that all Kings since the Abdication of Chivalry were pretenders, that the bastardy of FitzChivalry Farseer was wrongly construed as an obstacle to his inheriting the throne.
He became fully aware of the political ploys, the secret deals and dirty tricks, Brount employed to solidify his control over the territory.
There were book tapes and musicassettes enough to make sure she would not be bored, even if she had not had ploys of her own to occupy the time.
I was less a partaker of their ploys and banquets, either at birth, bridal, or burial.
For a few dizzy seconds I considered the possibility of a conspiracy, an elaborate ploy by Nina and Willi to confuse me into thinking that only one threat remained.
Or was it a legitimate ploy to give Eugene the same advantage that Crush Bonbon hadaccesss to public opinion?
Lucas scrambled to get to Dels, picked him up, and filled him in on the Spooner ploy.
If not for her ploy, Felicity knew her chances of visiting Randwulf Manor or, more farfetched, being invited to join aristocrats at their leisure would have been nil.
Sticking the ice wagon in the leadoff slot had been another quixotic front office ploy.
She still did not know what ploy her littermate was engaged in, but that he held some touch with Lormt, with the Lady Mereth, there was no denial.
As a political ploy to gain the support of the Roman Army, the early Christians took the entire series of rituals from a religion called the Mithraists and turned it into their Mass.
He had terrified Madam Shing into calling on me and telling his lie for him -- he knew the ploy had worked, because it got both me and the police there -- and he wanted to make further use of me.
The officers tried a number of psychological ploys, carefully crafted to trick Raimunda into a confession, but the spindly 12-year-old stuck resolutely to his story of the smoking globes and the floating shadow.
One facet of their ploy was to claim that all Kings since the Abdication of Chivalry were pretenders, that the bastardy of FitzChivalry Farseer was wrongly construed as an obstacle to his inheriting the throne.
This could be yet another ploy, or a test, or whatever peace mediators did to their victims. |
msmarco_passage_01_295231936 | How Many Calories are in Green Juice? | How Many Calories are in Green Juice?
How Many Calories are in Green Juice?
February 1, 2014 By Mike Cernovich
How many calories are in green juice? This is a hard question to answer, since green juices you make at home do not contain labels stating the number of calories that the juice contains. The short answer: A typical 16 ounce green juice is will contain anywhere from 140 to 220 calories. The exact amount of calories in your juice will vary based on how much juice you get from apples, leafy greens like spinach and kale, and water-rich vegetables like cucumber.
How to you calculate how many calories are in green juice?
It’s hard to say with exact certainty many calories are in juice because juice recipes vary. Some juices contain more leafy greens like spinach and kale (which are low in calories) and some contain more fruits like apples, oranges, and pears (which are higher in calories).
Even though it’s nearly impossible to say exactly how many calories are in green juice, we can make a close approximation. Simply measure out how many ounces (there are 8 ounces in a cup) of each ingredient is contained in a juice. Then add it up to get the final number.
(Some juices come with nutritional information.)
Apple juice and orange juice contain 110 calories per 8 ounces.
Most of us drink between 16-and-36 ounces of green juice. 16 ounces of apple juice or orange juice contains 220 calories. Apple juice and orange juice are the most calorically dense juice. That is, it has more calories per ounce than any other juice.
Thus, the most calories any green juice could have would be less than 220 calories, since the apple juice would be diluted with kale, spinach, beets, carrots, cucumbers, and other veggies.
Carrot juice contains 94 calories per 8 ounces.
Carrot juice is another calorically dense juice. (It’s also extremely potent and healthy and contains no fat. Don’t be put off by the term “calorically dense.” That simply means that an ounce of carrot juice has more calories than an ounce of cucumber juice.)
If you drank a 16 ounce carrot juice, your juice would contain approximately 190 calories.
Kale juice contains approximately 70 calories per 8 ounces.
Although it’s easy to determine how many calories are in apple juice, orange juice, and carrot juice, it’s trickier to figure out how many calories of juice are in kale juice.
Consider this: 8 ounces of whole kale contains approximately 112 calories. But approximately 1/3 of those calories come form insoluble fiber, which is removed during juice.
With an Omega juicer, you can get 8 ounces of kale juice from 16 ounces of kale. 16 ounces of kale would contain 220 calories. Since 1/3 of those calories come from fiber that is removed during juice, then 16 ounces of kale juice would contain 145 calories.
Cucumber juice contains approximately 70 calories per 8 ounces.
Cucumber is water rich vegetable. When you juice cucumbers, you separate the juice from the pulp. After juicing one to two large cucumbers, you will have approximately 8 ounces of juice, which equates to about 70 calories.
V8 juice contains 50 calories per 8 ounces.
V8 Juice, which contains tomatoes primarily and includes spinach and carrots and beets contains 50 calories per 8 ounce serving. (Low Sodium V8 Juice is great for when you’re traveling or too busy to juice. Here’s the best price on V8 Juice.)
A typical 16 ounce juice has 140 to 220 calories.
As you can see, a typical 16 ounce green juice has 140 to 220 calories. The exact amount of calories in your juice will vary based on how much juice you get from apples, beets, oranges, pears, grapefruit, kale, spinach, lettuce, celery, and cucumber.
That said, I don’t know anyone who got fat from drinking too many green juices. People gain weight from eating too much junk food. People actually lose weight when juicing because cravings for sugar and other junk food decrease.
Many people lose an amazing amount of fat drinking nothing but juice. Check out our Juice Fast page for more details.
Read next: Best Juice for Fat Loss. |
msmarco_passage_01_295769711 | Cost of a Rowing Machine - Consumer Information and Prices Paid - CostHelper | Cost of a Rowing Machine - Consumer Information and Prices Paid - CostHelper
CostHelper > Sports & Fitness > Rowing Machine
Rowing Machine Cost
How Much Does a Rowing Machine Cost?
Typically: $134-$1,000
High: $1,000-$2,000+
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Using varying resistance levels, rowing machines build and tone muscles of the upper arms, legs and back while providing a cardiovascular workout.
Rowers come in four types-- piston, magnetic, air and water. Piston, air and magnetic rowers accommodate between 250 and 300 pounds. Water machines can often hold 500 pounds.
Typical costs:
Most rowers cost between $134 and $1,000 based on the type of resistance and construction material. Rowers are most often made of metal, but some top-of-the-line models, which cost $2,500, are made partially of high-quality wood.
Piston rowers usually cost the least because they are smaller and do not simulate real rowing. The Rowing Machine Superstore sells the piston-based Stamina GlideMaster 1210 Conversion Rower [ 1] with a built-in abdominal exerciser for $149.
Magnetic rowers and air rowers are often mid-range in price. Although both employ long strokes, magnetic rowers are usually smoother, larger and quieter. The air-based Integrity 3000 [ 2] tracks time, speed and distance of a ride for $174, but lacks the durability, strength settings and PC interface technology for training offered by the magnetic Kettler Ergo Coach [ 3] for $1,259.
Water rowers are usually the most expensive ( $1,095 to $2,500) because they use a tank of water to simulate the tough resistance posed by a lake or river. With its patented WaterFlywheel design, WaterRower offers a range of top-quality rowers [ 4] , like its Classic model made of Danish-oil embossed black walnut for $1,495.
Related articles: Elliptical Machine, Exercise Bike, Treadmill
What should be included:
All rowers should have adjustable resistance to control the intensity of a workout. Most models include a console that tracks the speed, distance and time of a row. Costlier models have ergonomic tracks, wireless control features and adjustable, contoured seats.
Machines come with limited warranties for at least one year, though better brands offer longer warranties. Concept2 offers a 2-year warranty for its Model E and other machines that cost $850 to $1,200, depending on their advanced console features.
Shopping for a rowing machine:
The Rowing Machine Superstore [ 5] often sells low- and mid-range rowers at discounts to 15 percent for online orders and offers free shipping for some sale models.
Mega Fitness sells a wide variety of rowers, including several Water Rower models.
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10 Quick and Inexpensive Home Makeover Projects To Do While At Home
You may not be able to host the large family gathering for the holidays, but there are still many ways to pick up items curbside to spruce up your indoor space for your everyday enjoyment and to bring a more festive spirit. || Posted December 30 2020
7 Lesser-Known Discounts for the 50+ Crowd
As they age, members of the Baby Boomer generation don't like to admit that they're senior citizens, but they love getting discounts. It's kind of a quandary, because some of the best deals available are reduced prices for older folks. || Posted October 21 2013
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msmarco_passage_01_296805525 | 6 Best Auto Dialer Software for Small Business | 6 Best Auto Dialer Software for Small Business
Sales > Sales Tools | Buyer's Guide
6 Best Auto Dialer Software for Small Business
WRITTEN BY: Lisa McGreevy
Published August 8, 2019
Lisa has over 20 years of experience in business and consumer technology. She uses her expertise to answer your questions about CRM software and other valuable sales tools.
This article is part of a larger series on VoIP.
Auto dialer software dials lists of phone numbers automatically and is typically used in cold calling sales. We looked at a range of auto dialer software and narrowed it down to the top six based on price, features like call analytics and call routing, and customer support to determine the best auto dialer overall.
Top 6 Small Business Auto Dialer Software
Auto Dialer Software
Best for
ChaseData
(Best overall) Small businesses that need a comprehensive auto dialer at a competitive price
Five9
Small businesses that want a cloud-based auto dialer that doesn’t require expensive equipment
Velocify Dial-IQ
Businesses that need an auto dialer with built-in lead management designed for sales teams
Voicent
Businesses that want an auto dialer offering a menu of a la carte features and options
PhoneBurner
Businesses that want an auto dialer that rely heavily on CRM tools for cold calling leads and sales pipeline movement
CallHub
Advocacy, volunteer, and nonprofit groups that use temporary phone banks
How We Evaluated the Best Auto Dialer Software
The best auto dialer app software saves time and money by automating the dialing procedure. Auto dialers play pre-programmed messages to answering machines, route live calls to agents, and skip non-serviceable or busy numbers. Auto dialers can increase the call connect ratio, leading to higher agent productivity and increased sales.
We evaluated auto dialer software based on:
Price: The companies we evaluated offer plans based on a tiered pricing structure, number of users, or features selected. To evaluate each company fairly, we attempted to compare packages costs on a per-user basis with similar features.
Ease of use: Auto dialer customers typically manage their accounts through software installed on their computer or via web browser. We evaluated how easy the software is to install and set up or use in a browser.
Call automation: Some of the companies we considered offered features like automatic call routing to the next available agent, but we also considered other features like preview dialing, automatic lead scoring, or other call-based workflow automation.
Customer relationship management (CRM) integration: We looked at each auto dialer’s relationship management integration because it saves you money and time by tracking call data automatically and promoting efficient team collaboration.
Voice-over-internet-protocol (VoIP) integration: Auto dialers work with a user’s existing phone service to dial calls. We evaluated auto dialer software based on its ability to integrate easily with VoIP business phone systems.
Call analytics: This feature provides detailed reports on agent performance, call volume, campaign success, caller demographics, and myriad other reports.
Training and coaching tools: Monitor, whisper, and barge tools help refine agent performance, enhance the onboarding experience, and improve quality assurance. Therefore, we evaluated software based on the business phone features they offer.
Customer support: Auto dialer companies should offer easily accessible online documentation and customer support. The companies we reviewed offer a combination of phone, email and chat support, online knowledge bases, and community forums.
Based on our research, we recommend ChaseData as the best overall auto dialer for small businesses that need a reliable auto dialer with great customer support at a competitive price. Here’s how the six services we evaluated stack up for price, features, and customer support.
Best Overall Auto Dialer for Small Businesses: ChaseData
ChaseData is a leading auto dialer software platform that offers auto dialing as part of its call center package. It’s known as one of the best cloud-based auto dialer solutions on the market with features like inbound call capability, and CRM integration. With pricing from $89 per user, per month, ChaseData is great for businesses that need inbound call center features with outbound auto dialing at a price that’s on par with other auto dialers on the market.
ChaseData Pricing
ChaseData’s Small Business Edition is a moderately-priced $89 per user, per month, and includes one voice channel per agent. The Professional Edition is $139 per user, per month, and includes four voice channels per agent. The Enterprise Edition is $169 per user, per month, and includes six voice channels per agent.
ChaseData Pricing Tiered Features
Small Business Edition
Professional Edition
Enterprise Edition
Pricing
$89/user, per month
$139/user, per month
$169/user, per month
Voice Channels Per Agent
1
4
6
Preview Dialing
✔
✔
✔
Progressive Dialing
✔
✔
✔
Inbound Capability Included
✔
✔
✔
Auto Attendant & IVR
✔
✔
✔
Automatic Call Distribution
✔
✔
✔
Skill-based Routing
✔
✔
✔
Remote Agent Capability
✔
✔
✔
Standard Reporting Package
✔
✔
✔
Predictive Dialing
✔
✔
Trainee Mode
✔
✔
Zapier Integrations
✔
✔
SOAP-based Salesforce API
✔
Small Business Edition
ChaseData’s Small Business package includes one voice channel per agent, preview and progressive dialing, inbound calling and call routing, auto attendant, remote agent capability, and a reporting package. This tier lacks predictive dialing, trainee mode, and Zapier integration included in the Professional Edition and the SOAP-based Salesforce API [application programming interface] included in the Enterprise Edition.
You won’t find the lead building and management tools offered by Velocify Dial-IQ or email campaign management tools Voicent has to offer. However, at $89 per user, per month, this tier is the least expensive ChaseData option and more affordable than Velocify Dial-IQ’s or Voicent’s plans, making it a good choice for small teams and startups with low call volume.
Professional Edition
ChaseData’s Professional Edition adds predictive dialing and a trainee mode for onboarding new agents and Zapier integrations for more than 500 apps. This tier lacks the SOAP-based Salesforce API included in the Enterprise Edition, making Velocify Dial-IQ a better choice if that’s an issue for auto dialer software.
You won’t find integration the fundraising CRM integration CallHub has to offer or the turnkey auto dialer and contact center solution of Five9 here. But at $139 per user, per month, this tier is about even with plans from Velocify Dial-IQ and Voicent. It’s right for medium-sized businesses and companies with high-volume outbound call centers.
Enterprise Edition
ChaseData’s Enterprise Edition adds a SOAP-based Salesforce API for the integration government, financial, healthcare, and other high-profile sectors need. Six voice channels per agent keep customers connected quickly and efficiently. This tier is an excellent choice for medium to large companies with complex calling needs.
At $169 per user, per month, this tier is pricier than Voicent or Velocify Dial-IQ, but it’s still a good value for the bundle of features. ChaseData’s customer support is solid across each tier, with an extensive online knowledge base, support specialist ticketing system, email and fax support, and phone support.
What ChaseData Is Missing
Unlike Five9 and Voicent, predictive dialing is only available in the higher-priced tiers. PhoneBurner offers CRM integration at every plan level and Velocify Dial-IQ has a built-in lead management tool. If those are features that you can’t do without, ChaseData may not be the right fit for your company.
What Users Think About ChaseData
ChaseData customer reviews online have positive things to say about the company overall. They report that the auto dialer service is a good value for the money, and the technology is easy to use. However, some ChaseData customers report the agents’ screens tend to freeze sometimes.
Best Auto Dialer Software That Doesn’t Need Additional Equipment: Five9
Five9 is a cloud-based contact center solution that doesn’t require expensive equipment to use. Its technology is cloud-based so agents can log in from anywhere with only a high-speed internet connection, computer, and headset. With plans starting at around $185 per user, per month, Five9 isn’t the cheapest option on the market, but it’s great for businesses wanting to avoid complex auto dialer setups or solutions that require workers to be at a single location.
Five9 Pricing
Five9’s pricing is only available by consultation but is based on usage, features, number of seats, and month-to-month vs. annual plan. While Five9 does not advertise their pricing, our research indicates Five9’s plans start around $185 per month, per user. However, as this is only an estimate, businesses should request a quote directly from Five9.
Five9 Features
Five9’s feature set is appealing to businesses that don’t want to invest time or money in expensive software downloads or equipment. It lacks Velocify Dial-IQ’s lead management tools and PhoneBurner’s business app integration, but agents can plug in a headset, turn on a monitor, log on to the system, and get to work.
Call Automation
Five9 bundles power, progressive, and preview auto dialers into its outbound call center technology. It also includes predictive dialing that learns historical call patterns and adjusts outbound calls automatically, unlike ChaseData, which charges extra for predictive dialing. PhoneBurner doesn’t offer predictive, progressive, or preview dialers as part of its service.
Inbound Call Center Package
Five9’s inbound call center package includes speech recognition, automatic call distribution, interactive voice response tools, and on-screen caller information. Like ChaseData, these features are included in the software package. An inbound center call package with similar features is available at Voicent for an additional $15 per month.
Coaching & Management Tools
Each agent has access to a desktop interface that provides visual cues to guide agent actions, chat with customers, engage with customers via email and other omnichannel activities. The intuitive interface reduces training time and reduces agent onboarding costs. ChaseData offers similar built-in tools, but CallHub requires a Zapier integration to activate LiveChat.
System Integrations
Five9 integrates with Salesforce, Microsoft, Zendesk, Oracle, Microsoft, NetSuite CRM products and includes a toolkit for building solutions for other web-based CRMs. ChaseData also offers limited CRM integration, but only at the Professional and Enterprise tier levels.
Customer Support
Five9’s offers an extensive online knowledge base and 24/7 online and phone support. Direct access to the senior support team and a dedicated technical account manager is also available for an additional cost.
What Five9 Is Missing
This auto dialer company has a lot to offer, but it comes with a hefty price tag. Five9 also lacks the strong lead generation features and CRM integration of competitors like Velocify Dial-IQ, ChaseData, and PhoneBurner.
What Five9 Users Are Saying
Five9 online customer reviews are positive, and customers appear happy with the company. Clients say the service integrates cleanly with Salesforce and the interface is user-friendly. On the downside, some customers say the dialer freezes up occasionally on outgoing calls.
Best Auto Dialer Software for Lead Management: Velocify Dial-IQ
Velocify Dial-IQ is an auto dialer with built-in lead management software designed to boost the productivity of sales teams, with plans from around $100 per user, per month. The outbound sales dialer integrates into existing phone systems to manage thousands of calls simultaneously. This sales dialer helps sales teams work more efficiently, making it the best choice for lead management.
Velocify Dial-IQ Pricing
Velocify Dial-IQ’s pricing is only available by consultation. Our research indicates Dial-IQ costs approximately $100 per user, per month, plus 1.5 cents per minute. Per user, Velocify Dial-IQ’s pricing is approximately the market average. Per-minute calling rates are higher than Voicent’s and about the same as CallHub’s.
Velocify Dial-IQ Features
Velocify Dial-IQ is tailor-made with sales teams in mind. Auto dialer products like Five9 or ChaseData may work in a wide range of offices and industries, but Velocify Dial-IQ is designed to deliver the features sales teams need most from an auto dialing software solution like tailored call routing, call prioritization, and live coaching.
Call Automation
Call automation is a common feature of contact center software, but Velocify Dial-IQ takes it a step further by notifying all available agents of a high-potential inbound lead and connects the first agent who responds. Admins have complete control over which leads are distributed by this program and what agents receive the calls.
Inbound Call Center Package
Velocify Dial-IQ is an outbound-only dialer only and does not offer inbound calling capabilities. Businesses that want an auto dialer with an inbound call center package should check out ChaseData, Five9, or Voicent.
Coaching & Management Tools
Velocify Dial-IQ’s coaching and training tools help refine agent performance, enhance the onboarding experience, and improve quality assurance. This feature is also available at ChaseData in the Professional and Enterprise tier levels and Voicent for an additional charge above the base plan.
Coaching and training modes include:
Listen mode: Managers cannot speak to either party
Whisper mode: Manager can speak to the agent, but the prospect can’t hear
Barge mode: Manager can speak to both parties on the call
System Integrations
Velocify Dial-IQ integrates with Salesforce and offers Salesforce mobile compatibility as an advanced feature. The system’s integration is much more limited than what you’ll find at Five9 and PhoneBurner.
Customer Support
Like ChaseData, Five9, Voicent, and PhoneBurner, Velocify Dial-IQ has an online knowledge base available for customer reference. The company also offers email assistance and phone support.
What Velocify Dial-IQ Is Missing
Since Velocify is designed for lead building and management, it’s not packed with features that address the auto dialing needs of companies across a range of industries from fundraising organizations that need integration with constituent management software to live chat tools for order processing. Businesses looking for features like progressive and predictive dialing or a variety of agent management tools may want to stick with options like CallHub or ChaseData.
What Users Think About Velocify Dial-IQ
Velocify Dial-IQ customer reviews online have generally positive things to say about the company. Customers say it’s easy to set up and use and organizes leads very well. However, some customers report customer service can be slow to respond at times.
Best Auto Dialer Software With a la Carte Features: Voicent
Voicent is a full-featured auto dialer software platform with a menu of a la carte choices for growing companies. Optional add-ons to the base package include an inbound call center package, call center manager software, workflow automation, and more. With a monthly plan for $29 per agent, per month, Voicent is a good choice for companies that want a solution that can grow with them.
Voicent Pricing
Voicent prices are $29 per agent, per month, for monthly plans or $19 per agent, per month, with yearly agreements. The base plan includes automatic dialer technology and an agent dashboard. Voicent pricing is initially lower than industry averages but can add up quickly once options like email campaign tools workflow automation tools are added.
More features are available for an additional cost, including:
Inbound call center package with phone number: $15 per number
Call center management: $10 per user
Interactive text messaging with phone number: $15 per number
Caller ID: $2 per ID
Workflow automation: $99 per account
After choosing a base plan and option features, customers choose a calling plan:
Calling Plan
Included Credit*
Pay as you go: 4 cents per minute
0
$75
2,500 (3 cents per minute)
$130
6,500 (2 cents per minute)
$375
25,000 (1.5 cents per minute)
*One credit = a one-minute phone call or one text message
Voicent Features
Voicent customers can select a variety of options like call automation or inbound calling tools to add to their base platform and calling plan. That could save a company hundreds of dollars per month over plans from PhoneBurner and Five9 that come bundled with features like CRM integration or lead filtering tools customers may not use.
Call Automation
Voicent’s base package includes predictive, progressive, power, and auto dialers at no additional cost, making this solution a good choice for companies that need call automation. ChaseData charges extra for predictive dialing, and PhoneBurner doesn’t offer predictive, progressive, or preview dialers at all.
Inbound Call Center Package
This package includes interactive voice response tools, a business phone system, and a virtual receptionist for an additional $15 per month. ChaseData also includes inbound calling tools at each tier level, but ChaseData’s packages are more expensive than Voicent’s.
Coaching and Management Tools
Voicent offers agent monitoring and recording tools, whisper coaching, agent reporting and tracking, and advanced call pacing algorithms for an additional $10 per user above the base plan price. Coaching and management tools are included in Velocify Dial-IQ’s package and ChaseData’s Professional and Enterprise tier levels.
System Integrations
Unlike ChaseData and PhoneBurner, Voicent does not offer systems integrations tools with its base plan. However, customers are allowed 50,000 CRM records per user. For more records per user, customers are required to upgrade to a custom or enterprise-level plan.
Customer Support
Voicent has an extensive online knowledge base, in-product walkthroughs, video resources, and an online customer support ticketing system. The company also offers four tiers of paid training and setup support ranging from a one-time purchase fee of $149 to $499, depending on the level of service.
What Voicent Is Missing
Voicent doesn’t offer reporting and analytics or lead management tools found in similar products on the market. Businesses that need those features are better served by one of the other options on this list.
What Users Think About Voicent
Voicent online customer reviews have positive things to say about the company, particularly about the company’s customer service. They also believe the service is a good value for the money. We didn’t see any negative reports or reviews of the company during our search.
Best Auto Dialer Software for CRM Integration: PhoneBurner
PhoneBurner is an auto dialer that integrates seamlessly with Salesforce, HubSpot, and Zapier. It also has an open API that companies can use to design their own software connections and is priced at $149 per user, per month. We believe PhoneBurner is an excellent choice for businesses that rely heavily on CRM tools for cold calling leads and moving interested prospects seamlessly through the sales pipeline.
PhoneBurner Pricing
PhoneBurner pricing is $149 per user, per month with discounts available based on term length and team size. Features include unlimited power dialing, call and email tracking, and call recording. PhoneBurner pricing is on par with the higher-end service plans of similar products.
PhoneBurner Features
PhoneBurner includes call automation but lacks Velocify Dial-IQ’s inbound lead call routing feature. It offers systems integration with Zapier and Salesforce, much like the upper tiers of ChaseData. PhoneBurner also includes call tracking, analytics, and recording but, unlike Voicent, doesn’t charge extra.
Call Automation
PhoneBurner automates calling tasks like manual dialing, personalized follow-up emails, and post-call notes so that agents can move through calls quickly. PhoneBurner also drops prerecorded messages into voicemail boxes with one click to eliminate time wasted waiting for the beep.
Inbound Call Center Package
PhoneBurner is an outbound-only auto dialer and does not offer inbound calling capabilities. Businesses that want a solution with an inbound call center package should check out ChaseData, Five9, or Voicent.
Coaching & Management Tools
PhoneBurner’s dedicated admin portal lets you add, remove and edit seats, pull real-time reports, and manage leads directly inside. Admins can also build self-updating real-time motivational leaderboards to broadcast directly to teams.
System Integrations
For companies that already have a CRM system, PhoneBurner integrates with Zapier and the Classic and Lightning editions of Salesforce. A flexible developer API allows customers to connect other existing software to PhoneBurner to launch dial sessions. This is helpful for companies that want lead management but don’t already have a system in place.
Customer Support
PhoneBurner has an online knowledge base, live support chat, email support, an online support ticketing system, and phone support from 5 a.m. to 5 p.m. Pacific time, Monday through Friday. Real-time status alerts also let customers know if PhoneBurner is experiencing slowdowns or downtime.
What PhoneBurner Is Missing
Although this solution automates the process of manual dialing, PhoneBurner doesn’t offer predictive, progressive, or preview dialers as part of its service. That could be a deal-breaker for some sales teams, so ChaseData or Five9 would serve businesses that need that particular functionality better.
What Users Think About PhoneBurner
Online reviews of PhoneBurner are overall positive. Customers say there are no hidden charges or fees, and that it works as advertised. However, some customers say setup was a bit tricky.
Best Auto Dialer Software for Temporary Phone Banking: CallHub
CallHub is an auto dialer service designed to connect nonprofits and advocacy groups. Integration with virtual phone banking a pay-as-you-go price structure keeps organizations within budget. With pricing from 1.2 cents per 30-second increments, rather than based on a monthly subscription, CallHub is the right choice for businesses that use temporary phone banking for fundraising or other short-term campaigns.
CallHub Pricing
CallHub’s pay-as-you-go pricing is based on 30-second billing increments. Outbound United States calls are 1.4 cents and inbound are 1.2 cents. There are no setup or subscription fees. CallHub’s pricing is low compared to similar services. However, it also lacks features like call routing and training tools those services offer.
Pricing for call automation are also pay-as-you-go, and depend on usage and mode of connection:
Browser: 0.7 cents
Phone: 1.4 cents
Dial in: 1.2 cents
Softphone: 0.8 cents
CallHub Features
Nonprofits, advocacy groups, and fundraising organizations often work with volunteers, short-term staff, and use temporary phone-banks. CallHub’s pay-as-you-go pricing structure and free, unlimited agent accounts, and integration with CiviCRM make CallHub a great choice. PhoneBurner, ChaseData, or Five9 are better choices for companies with permanent staffing needs and sales outreach strategies.
Inbound Call Center Package
CallHub offers inbound calling for short message service (SMS) text message response but doesn’t offer inbound call center tools or features. Businesses that want a solution with an inbound call center package should check out ChaseData, Five9, or Voicent.
Coaching and Management Tools
CallHub’s agent management tools allow admins to assemble agents and volunteers into an unlimited configuration of teams and assign teams into calling campaigns as needed. Unlike many other auto dialer services, agents and volunteers can be grouped under a single team name or organized into discrete groups to work on different tasks.
Call Automation
CallHub’s offers a predictive dialer that speeds up or slows down the dialing rate according to real-time agent activity. It also includes power and preview dialers. Voicent offers the same dialers as part of its base package, but it costs more than CallHub. PhoneBurner doesn’t offer the three dialers at all, and ChaseData charges extra for predictive dialing.
System Integration
Like, ChaseData and Five9, CallHub integrates with several business applications, including Salesforce, Zapier. However, CallHub is the only auto dialer on this list to also integrate with popular fundraising CRM platform CiviCRM.
Customer Support
CallHub offers 24-hour email support on weekdays with a guaranteed 99% response time. The company also has an online how-to and FAQs section, although not as robust as support options at auto dialer services like ChaseData or Voicent.
What CallHub Is Missing
CallHub falls short in its customer support and online documentation. That could be a deal-breaker for advocacy groups, nonprofits, and volunteer organizations that often lack the resources for internal tech support of their own.
What Users Think About CallHub
Online reviews of CallHub are generally positive. Customers say it’s a good value for the money, and it’s easy to set up calling campaigns. However, some customers report an occasional drop in call quality.
Bottom Line
Auto dialer software does more than dial a list of phone numbers. It also plays recorded messages, connects calls to sales agents, provides analytics, integrates with CRM platforms, and collects call data to help train sales agents. A good auto dialer software solution should also provide excellent customer support.
The best auto dialer software depends on what you need it to do for your business. Small businesses that want a comprehensive auto dialer at a competitive price can’t miss with ChaseData. Visit ChaseData’s website to check out a product demo and get a free trial of its auto dialer.
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Pilkington Optiwhite™ low iron extra clear glass product comparison. Available in thicknesses between 2 mm and 19 mm, the widest range on the market, Pilkington Optiwhite™ provides increased design flexibility. When combined with other Pilkington products, it can offer additional benefits such as thermal insulation or self-cleaning. We have been producing the Pilkington Optiwhite™ range for over twenty-five years with high consistency and quality, making this low iron, extra clear glass highly valued by our customers whether as exterior or interior glazing, furniture or a wide range of other applications
Self Cleaning Glass
Long described as an impossible dream, self-cleaning glass is now a reality. After years of research and development leading glass manufacturer Pilkington has introduced the Pilkington Activ™ range of products. The range has products which combine both self-cleaning and solar control properties, making them highly desirable amongst homeowners looking for the ultimate in glass solutions.
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msmarco_passage_01_304384073 | Hobe Sound, FL Profile: Facts & Data | Hobe Sound, FL Profile: Facts & Data
Hobe Sound, FL Profile: Facts & Data
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COVID-19 Data: Martin County | US
The Hobe Sound Census Designated Place had a population of 13,538 as of July 1, 2020.
The primary coordinate point for Hobe Sound is located at latitude 27.0595 and longitude -80.1364 in Martin County . The formal boundaries for the Hobe Sound Census Designated Place encompass a land area of 7.05 sq. miles and a water area of 0.68 sq. miles. Martin County is in the Eastern time zone (GMT -5). The elevation is 23 feet.
The Hobe Sound Census Designated Place ( GNIS ID: 2402592) has a U1 Census Class Code which indicates a census designated place with an official federally recognized name. It also has a Functional Status Code of "S" which identifies a statistical entity .
Florida is one of 20 states where Census County Divisions (CCDs) are used for statistical tracking of subdivisions within each county. The Hobe Sound Census Designated Place is located within Port Salerno-Hobe Sound CCD of Martin County.
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Hobe Sound, FL Data & Demographics (As of July 1, 2020)
POPULATION
Total Population
13,538 (100%)
Population in Households
13,283 (98.1%)
Population in Families
9,865 (72.9%)
Population in Group Quarters1
255 ( 1.9%)
Population Density
1,905
Diversity Index2
33
INCOME
Median Household Income
$50,739
Average Household Income
$85,749
% of Income for Mortgage4
20%
Per Capita Income
$40,925
Wealth Index5
131
HOUSING
Total HU (Housing Units)
7,660 (100%)
Owner Occupied HU
4,967 (64.8%)
Renter Occupied HU
1,424 (18.6%)
Vacant Housing Units
1,269 (16.6%)
Median Home Value
$242,375
Average Home Value
$391,155
Housing Affordability Index3
118
HOUSEHOLDS
Total Households
6,391
Average Household Size
2.08
Family Households
3,709
Average Family Size
3
NOTES
Group Quarters - a place where people live or stay in a group living arrangement. Includes college residents halls, nursing facilities, military barracks, and correctional facilities.
The Diversity Index is a scale of 0 to 100 that represents the likelihood that two persons, chosen at random from the same area, belong to different races or ethnic groups. If an area's entire population belongs to one race AND one ethnic group, then the area has zero diversity. An area's diversity index increases to 100 when the population is evenly divided into two or more race/ethnic groups.
The Housing Affordability Index base is 100 and represents a balance point where a resident with a median household income can normally qualify to purchase a median price home. Values above 100 indicate increased affordability, while values below 100 indicate decreased affordability.
The % of Income for Mortgage quantifies the percentage of median household income dedicated to mortgage payments on a home priced at the median value (assuming a 30-year mortgage and a 20% down payment).
The Wealth Index is based on a number of indicators of affluence including average household income and average net worth, but it also includes the value of material possessions and resources. It represents the wealth of the area relative to the national level. Values above or below 100 represent above-average wealth or below-average wealth compared to the national level.
GROWTH RATE / YEAR
2010-2020
2020-2025
Population
0.54%
0.67%
Households
0.59%
0.72%
Families
0.38%
0.59%
Median Household Income
0.94%
Per Capita Income
2.1%
Owner Occupied HU
0.7%
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Hobe Sound, FL - Peer Comparisons by Rank and Percentile
The table below compares Hobe Sound to the other 919 incorporated cities, towns and CDPs in Florida by rank and percentile using July 1, 2020 data. The location Ranked # 1 has the highest value. A location that ranks higher than 75% of its peers would be in the 75th percentile of the peer group.
Variable Description
Rank
Percentile
Total Population
# 271
71st
Population Density
# 419
55th
Median Household Income
# 524
43rd
Housing Affordability Index
# 207
23rd
Per Capita Income
# 208
77th
Diversity Index
# 635
31st
Additional comparisons and rankings can be made with a VERY EASY TO USE Florida Census Data Comparison Tool.
City Profile Count
Hobe Sound, FL - Most Popular Things to Do
Top 20 Most Popular Places Near Hobe Sound
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msmarco_passage_01_306949466 | Who owns the beer | FlowingData | Who owns the beer | FlowingData
Who owns the beer
August 25, 2011
Topic
Network Visualization / beer, breweries
When you walk the beer aisle at the grocery store, there are lots of different brands and types, so it can be easy to think that all of those beverages come from different companies. Maybe you felt like supporting the little guy by buying that beer that looks like it came from a smaller brewery; however, you just might be buying from one of the big guys. In a follow-up to the soda structure map, Phil Howard and Ginger Ogilvie map the structure of the top 13 beer companies.
AB InBev owns, co-owns or distributes more than 36 brands, for example, while MillerCoors controls at least 24 more. MillerCoors also brews Metropoulos & Company’s products under contract (thus the company that controls Pabst and 21 other brands is a “virtual” beer company).
Stella Artois, Beck’s, and St. Pauli Girl: owned by AB InBev. Or how about Dos Equis, New Castle, and Amstel? Those are owned by Heineken, which is partially owned by Tiger Beer, which in turn distributed by AB InBev. Yep.
Check out the high-resolution version and other breakdowns here. Any surprises?
[ Who Owns Brew | Thanks, Phil] |
msmarco_passage_01_307148267 | Fair Labor Standards Act (FLSA) Coverage (Exempt vs. Non-Exempt -- The Online Wages, Hours and Overtime Pay Resource | Fair Labor Standards Act (FLSA) Coverage (Exempt vs. Non-Exempt -- The Online Wages, Hours and Overtime Pay Resource
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Coverage under the FLSA
Most jobs are governed by the FLSA. Some are not. Some jobs are excluded from FLSA coverage by statute. Other jobs, while governed by the FLSA, are considered "exempt" from the FLSA overtime rules.
Exclusions from FLSA coverage.
Particular jobs may be completely excluded from coverage under the FLSA overtime rules. There are two general types of complete exclusion. Some jobs are specifically excluded in the statute itself. For example, employees of movie theaters and many agricultural workers are not governed by the FLSA overtime rules. Another type of exclusion is for jobs which are governed by some other specific federal labor law. As a general rule, if a job is governed by some other federal labor law, the FLSA does not apply. For example, most railroad workers are governed by the Railway Labor Act, and many truck drivers are governed by the Motor Carriers Act, and not the FLSA. Many of FLSA exclusions are found in §213 of the FLSA.
Exempt or Nonexempt.
Employees whose jobs are governed by the FLSA are either "exempt" or "nonexempt." Nonexempt employees are entitled to overtime pay. Exempt employees are not. Most employees covered by the FLSA are nonexempt. Some are not.
Some jobs are classified as exempt by definition. For example, "outside sales" employees are exempt ("inside sales" employeesare nonexempt). For most employees, however, whether they are exempt or nonexempt depends on (a) how much they are paid, (b) how they are paid, and (c) what kind of work they do.
With few exceptions, to be exempt an employee must (a) be paid at least $23,600 per year ($455 per week), and (b) be paid on a salary basis, and also (c) perform exempt job duties. These requirements are outlined in the FLSA Regulations (promulgated by the U.S. Department of Labor). Most employees must meet all three "tests" to be exempt.
Salary level test.
Employees who are paid less than $23,600 per year ($455 per week) are nonexempt. (Employees who earn more than $100,000 per year are almost certainly exempt.)
Salary basis test.
Generally, an employee is paid on a salary basis if s/he has a "guaranteed minimum" amount of money s/he can count on receiving for any work week in which s/he performs "any" work. This amount need not be the entire compensation received, but there must be some amount of pay the employee can count on receiving in any work week in which s/he performs any work. Some "rules of thumb" indicating that an employee is paid on a salary basis include whether an employee's base pay is computed from an annual figure divided by the number of paydays in a year, or whether an employee's actual pay is lower in work periods when s/he works fewer than the normal number of hours. However, whether an employee is paid on a salary basis is a "fact," and thus specific evaluation of particular circumstances is necessary. Whether an employee is paid on a salary basis is not affected by whether pay is expressed in hourly terms (as this is a fairly common requirement of many payroll computer programs), but whether the employee in fact has a "guaranteed minimum" amount of pay s/he can count on.
The FLSA salary basis test applies only to reductions in monetary amounts. Requiring an employee to charge absences from work to leave accruals is not a reduction in "pay," because the monetary amount of the employee's paycheck remains the same. Similarly, paying an employee more than the guaranteed salary amount is not normally inconsistent with salary basis status, because this does not result in any reduction in the base pay.
With some exceptions, the base pay of a salary basis employee may not be reduced based on the "quality or quantity" of work performed (provided that the employee does "some" work in the work period). This usually means that the base pay of a salary basis employee may not be reduced if s/he performs less work than normal, if the reason for that is determined by the employer. For example, a salary basis pay employee's base pay may not be reduced if there is "no work" to be performed (such as for a plant closing or slow period), and a salary basis employee's base pay may not be reduced for partial day absences. However, employers may "dock" the base pay of salary basis employees in full day increments, for disciplinary suspensions, or for personal leave, or for sickness under a bona fide sick leave plan (as for example if the employee has run out of accrued sick leave).
Thus, there can be "permissible" and "impermissible" reductions in salary basis pay. Permissible reductions have no effect on the employee's exempt status. Impermissible reductions may, in that the general rule is that an employee who is subjected to impermissible reductions in salary is no longer paid on a salary basis, and is therefore nonexempt. However, employers have several avenues by which they can "cure" impermissible reductions in salary basis pay, and as a practical matter these make it unlikely that an otherwise exempt employee would become nonexempt because of salary basis pay problems.The salary basis pay requirement for exempt status does not
apply to some jobs (for example, doctors, lawyers and schoolteachers are exempt even if the employees are paid hourly).
The duties tests.
An employee who meets the salary level tests and also the salary basis tests is exempt only if s/he also performs exempt job duties. These FLSA exemptions are limited to employees who perform relatively high-level work. Whether the duties of a particular job qualify as exempt depends on what they are. Job titles or position descriptions are of limited usefulness in this determination. (A secretary is still a secretary even if s/he is called an "administrative assistant," and the chief executive officer is still the CEO even if s/he is called a janitor.) It is the actual job tasks that must be evaluated, along with how the particular job tasks "fit" into the employer's overall operations.
There are three typical categories of exempt job duties, called "executive," "professional," and "administrative."
Exempt executive job duties.
Job duties are exempt executive job duties if the employee
regularly supervises two or more other employees, and also
has management as the primary duty of the position, and also,
has some genuine input into the job status of other employees (such as hiring, firing, promotions, or assignments).
Supervision means what it implies. The supervision must be a regular part of the employee's job, and must be of other employees. Supervision of non-employees does not meet the standard. The "two employees" requirement may be met by supervising two full-time employees or the equivalent number of part-time employees. (Two half-time employees equal one full-time employee.)
"Mere supervision" is not sufficient. In addition, the supervisory employee must have "management" as the "primary duty" of the job. The FLSA Regulations contain a list of typical management duties. These include (in addition to supervision):
interviewing, selecting, and training employees;
setting rates of pay and hours of work;
maintaining production or sales records (beyond the merely clerical);
appraising productivity; handling employee grievances or complaints, or disciplining employees;
determining work techniques;
planning the work;
apportioning work among employees;
determining the types of equipment to be used in performing work, or materials needed;
planning budgets for work;
monitoring work for legal or regulatory compliance;
providing for safety and security of the workplace.
Determining whether an employee has management as the primary duty of the position requires case-by-case evaluation. A "rule of thumb" is to determine if the employee is "in charge" of a department or subdivision of the enterprise (such as a shift). One handy clue might be to ask who a telephone inquiry would be directed to if the called asked for "the boss." Typically, only one employee is "in charge" at any particular time. Thus, for example, if a "sergeant" and a "lieutenant" are each at work at the same time (in the same unit or subunit of the organization), only the lieutenant is "in charge" during that time.
An employee may qualify as performing executive job duties even if s/he performs a variety of "regular" job duties as well. For example, the night manager at a fast food restaurant may in reality spend most of the shift preparing food and serving customers. S/he is, however, still "the boss" even when not actually engaged in "active" bossing duties. In the event that some "executive" decisions are required, s/he is there to make them, and this is sufficient.
The final requirement for the executive exemption is that the employee have genuine input into personnel matters. This does not require that the employee be the final decision maker on such matters, but rather that the employee's input is given "particular weight." Usually, it will mean that making personnel recommendations is part of the employee's normal job duties, that the employee makes these kinds of recommendations frequently enough to be a "real" part of the job, and that higher management takes the employee's personnel suggestions or recommendations
seriously.
Exempt professional job duties.
The job duties of the traditional "learned professions" are exempt. These include lawyers, doctors, dentists, teachers, architects, clergy. Also included are registered nurses (but not LPNs), accountants (but not bookkeepers), engineers (who have engineering degrees or the equivalent and perform work of the sort usually performed by licensed professional engineers), actuaries, scientists (but not technicians), pharmacists, and other employees who perform work requiring "advanced knowledge" similar to that historically associated with the traditional learned professions.
Professionally exempt work means work which is predominantly intellectual, requires specialized education, and involves the exercise of discretion and judgment. Professionally exempt workers must have education beyond high school, and usually beyond college, in fields that are distinguished from (more "academic" than) the mechanical arts or skilled trades. Advanced degrees are the most common measure of this, but are not absolutely necessary if an employee has attained a similar level of advanced education through other means (and perform essentially the same kind of work as similar employees who do have advanced degrees).
Some employees may also perform "creative professional" job duties which are exempt. This classification applies to jobs such as actors, musicians, composers, writers, cartoonists, and some journalists. It is meant to cover employees in these kinds of jobs whose work requires invention, imagination, originality or talent; who contribute a unique interpretation or analysis.
Identifying most professionally exempt employees is usually pretty straightforward and uncontroversial, but this is not always the case. Whether a journalist is professionally exempt, for example, or a commercial artist, will likely require careful analysis of just what the employee actually does.
Exempt Administrative job duties.
The most elusive and imprecise of the definitions of exempt job duties is for exempt "administrative" job duties.
The Regulatory definition provides that exempt administrative job duties are
(a) office or nonmanual work, which is
(b) directly related to management or general business operations of the employer or the employer's customers, and
(c) a primary component of which involves the exercise of independent judgment and discretion about
(d) matters of significance.
The administrative exemption is designed for relatively high-level employees whose main job is to "keep the business running." A useful rule of thumb is to distinguish administrative employees from "operational" or "production" employees. Employees who make what the business sells are not administrative employees. Administrative employees provide "support" to the operational or production employees. They are "staff" rather than "line" employees. Examples of administrative functions include labor relations and personnel (human resources employees), payroll and finance (including budgeting and benefits management), records maintenance, accounting and tax, marketing and advertising (as differentiated from direct sales), quality control, public relations (including shareholder or investment relations, and government relations), legal and regulatory compliance, and some computer-related jobs (such as network, internet and database administration). (See Computer employees .)
To be exempt under the administrative exemption, the "staff" or "support" work must be office or nonmanual, and must be for matters of significance. Clerical employees perform office or nonmanual support work but are not administratively exempt. Nor is administrative work exempt just because it is financially important, in the sense that the employer would experience financial losses if the employee fails to perform competently. Administratively exempt work typically involves the exercise of discretion and judgment, with the authority to make independent decisions on matters which affect the business as a whole or a significant part of it.
Questions to ask might include whether the employee has the authority to formulate or interpret company policies; how major the employee's assignments are in relation to the overall business operations of the enterprise (buying paper clips versus buying a fleet of delivery vehicles, for example); whether the employee has the authority to commit the employer in matters which have significant financial impact; whether the employee has the authority to deviate from company policy without prior approval.
An example of administratively exempt work could be the buyer for a department store. S/he performs office or nonmanual work and is not engaged in production or sales. The job involves work which is necessary to the overall operation of the store -- selecting merchandize to be ordered as inventory. It is important work, since having the right inventory (and the right amount of inventory) is crucial to the overall well-being of the store's business. It involves the exercise of a good deal of important judgment and discretion, since it is up to the buyer to select items which will sell in sufficient quantity and at sufficient margins to be profitable. Other examples of administratively exempt employees might be planners and true administrative assistants (as differentiated from secretaries with fancy titles). Bookkeepers, "gal Fridays," and most employees who operate machines are not administratively exempt.
Merely clerical work may be administrative, but it is not exempt. Most secretaries, for example, may accurately be said to be performing administrative work, but their jobs are not usually exempt. Similarly, filing, filling out forms and preparing routine reports, answering telephones, making travel arrangements, working on customer "help desks," and similar jobs are not likely to be high-level enough to be administratively exempt. Many clerical workers do in fact exercise some discretion and judgment in their jobs. However, to "count" the exercise of judgment and discretion must be about matters of considerable importance to the operation of the enterprise as a whole.
Routinely ordering supplies (and even selecting which vendor to buy supplies from) is not likely to be considered high- enough to qualify the employee for administratively exempt status. There is no "bright line." Some secretaries may indeed be high-level, administratively exempt employees (for example, the secretary to the CEO who really does "run his life"), while some employees with fancy titles (e.g., "administrative assistant") may really be performing nonexempt clerical duties.
Rights of exempt employees.
An exempt employee has virtually "no rights at all" under the FLSA overtime rules. About all an exempt employee is entitled to under the FLSA is to receive the full amount of the base salary in any work period during which s/he performs any work (less any permissible deductions). Nothing in the FLSA prohibits an employer from requiring exempt employees to "punch a clock," or work a particular schedule, or "make up" time lost due to absences. Nor does the FLSA limit the amount of work time anemployer may require or expect from any employee, on any
schedule. ("Mandatory overtime" is not restricted by the FLSA.)
Keep in mind that this discussion is limited to rights underthe FLSA. Exempt employees may have rights under other laws or by way of employment policies or contracts.
Rights of nonexempt employees.
Nonexempt employees are entitled under the FLSA to time and one-half their "regular rate" of pay for each hour they actually work over the applicable FLSA overtime threshold in the applicable FLSA work period. (See, " FLSA Overtime ")
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msmarco_passage_01_310242514 | Dare Font | Dare Typeface | Free Fonts and Web Fonts | Dare Font | Dare Typeface | Free Fonts and Web Fonts
Dare font
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license
Free for personal use
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decorative, brush, dare
author note
Font I made that is similar to the old DARE program. If you wanna use it for personal use be my guest, if you want to use it for commercial use contact me. b0bafett77@yahoo.com CJ Cook
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DARE font is one of Dare font variant which has Regular style. This font come in ttf format and support 108 glyphs. Based on font metric, DARE Regular has usweight 400, width 5, and italic angle 0. This font is labeled as .
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msmarco_passage_01_316764847 | Stinchcombe Surname Origin, Meaning & Last Name History | Stinchcombe Surname Origin, Meaning & Last Name History
Stinchcombe Surname
369,492 nd
Most Common
surname in the World
Approximately 973 people bear this surname
Most prevalent in:
England
Highest density in:
Wales
Stinchcombe Surname Definition:
A parish in Gloucestershire.
Stinchcombe Surname Distribution Map
+ −
Leaflet | Population data © Forebears
Continents Nations
1880 1881 1901 2014
By incidence
By incidence By frequency By rank
Fullscreen
Select a nation to see the distribution at regional and subregional levels
2014
1901
1881
1880
Sort results
Incidence (high to low) Incidence (low to high) Alphabetic A-Z Alphabetic Z-A Rank (high to low) Rank (low to high)
Place
Incidence
Frequency
Rank in Area
England
564
1:98,791
10,454
Canada
143
1:257,661
24,352
Wales
96
1:32,235
3,244
Australia
79
1:341,718
28,950
United States
67
1:5,409,835
270,257
New Zealand
9
1:503,147
33,029
Scotland
6
1:892,303
28,047
Malaysia
2
1:14,747,112
316,340
Norway
1
1:5,142,286
129,201
Sweden
1
1:9,846,757
347,448
Japan
1
1:127,844,293
73,547
France
1
1:66,422,722
504,397
Brazil
1
1:214,074,332
1,693,628
Bahamas
1
1:391,751
2,737
Ireland
1
1:4,708,939
29,543
Show All Nations
Place
Incidence
Frequency
Rank in Area
Ireland
3
1:1,476,622
29,385
Sort results
Incidence (high to low) Incidence (low to high) Alphabetic A-Z Alphabetic Z-A Rank (high to low) Rank (low to high)
Place
Incidence
Frequency
Rank in Area
England
304
1:80,182
8,629
Wales
33
1:47,528
2,451
Place
Incidence
Frequency
Rank in Area
United States
15
1:3,347,912
150,340
Stinchcombe Surname Meaning
From Where Does The Surname Originate? meaning and history
A parish in Gloucestershire.
— Patronymica Britannica (1860) by Mark Antony Lower
Stinchcombe is an ancient Gloucestershire surname evidently derived in the first place from the parish of that name in the county. There was a yeoman thus called in Hawkesbury 200 years ago; and last century the name occurred in Acton and Cromhall (Bigl.). There are still Stinchcombes in Cromhall and Hawkesbury.
— Homes of Family Names in Great Britain (1890) by Henry Brougham Guppy
Submit Information on This Surname for a Chance to Win a $79 Genealogy DNA Test
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Name Variants Description
B
I
•
“ ”
HTML
Display Statistics on:
Average Salary in:
United States
Canada England United States Wales
Religious Adherence in:
Ireland
Ireland
Political Affiliation in:
United States
United States
Stinchcombe Demographics
Average Stinchcombe Salary in
United States
$55,959 USD
Per year
Rank:
267,694 of 1,180,305
Percentage of all salaries earned by bearers:
0.0000282141
Rank: 204,423 of 1,181,369
Percentage of national average salary:
129.68%
Sample size: 43 (2014)
Average Salary in
United States
$43,149 USD
Per year
Per month:
$3,596 USD
Per week:
$799 USD
Per day:
$118 USD
View the highest/lowest earning families in The United States
Stinchcombe Last Name Facts
Where Does The Last Name Stinchcombe Come From? nationality or country of origin
Stinchcombe has its highest incidence in England. It may be rendered as a variant:. For other potential spellings of this name click here.
How Common Is The Last Name Stinchcombe? popularity and diffusion
This surname is the 369,492 nd most common surname at a global level It is held by approximately 1 in 7,489,770 people. This last name occurs predominantly in Europe, where 69 percent of Stinchcombe are found; 69 percent are found in Northern Europe and 69 percent are found in British Isles.
The surname is most frequent in England, where it is borne by 564 people, or 1 in 98,791. In England it is mostly concentrated in: Gloucestershire, where 30 percent are found, Somerset, where 9 percent are found and Nottinghamshire, where 6 percent are found. Excluding England this last name is found in 14 countries. It is also found in Canada, where 15 percent are found and Wales, where 10 percent are found.
Stinchcombe Family Population Trend historical fluctuation
The prevalency of Stinchcombe has changed through the years. In England the number of people bearing the Stinchcombe last name increased 186 percent between 1881 and 2014; in Wales it increased 291 percent between 1881 and 2014; in The United States it increased 447 percent between 1880 and 2014 and in Ireland it declined 67 percent between 1901 and 2014.
Stinchcombe Last Name Statistics demography
The religious devotion of those carrying the Stinchcombe last name is principally Anglican (67%) in Ireland.
In The United States those bearing the Stinchcombe last name are 1.23% more likely to be registered Democrats than the national average, with 52% registered to vote for the political party.
The amount Stinchcombe earn in different countries varies notably. In United States they earn 29.69% more than the national average, earning $55,959 USD per year and in Canada they earn 6.16% more than the national average, earning $52,741 CAD per year.
Phonetically Similar Names
Sort results
Incidence (high to low) Incidence (low to high) Alphabetic A-Z Alphabetic Z-A Similarity (high to low) Similarity (low to high) Prevalent jurisdiction A-Z Prevalent jurisdiction Z-A
Surname
Similarity
Worldwide Incidence
Prevalency
Stinchc Ombe
96
1
/
Stinchecombe
96
1
/
Stinchcomb
95
1,992
/
Stynchcombe
91
4
/
Stinchicomb
91
0
/
Stenchcombe
91
0
/
Stynchcomb
86
12
/
Stinchcamb
86
1
/
Stunchcomb
86
1
/
Stenchcomb
86
0
/
Stenchicomb
82
0
/
Show All Similar Surnames
Search for Another Surname
Stinchcombe Reference & Research
Stinchcombe FamilyTree DNA Project - A description of a group researching the paternal lines of men who bear the surname with the help of DNA analysis.
The name statistics are still in development, sign up for information on more maps and data
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Footnotes
Surnames are taken as the first part of an person's inherited family name, caste, clan name or in some cases patronymic
Descriptions may contain details on the name's etymology, origin, ethnicity and history. They are largely reproduced from 3rd party sources; diligence is advised on accepting their validity - more information
Name distribution statistics are generated from a global database of over 4 billion people - more information
Heatmap: Dark red means there is a higher occurrence of the name, transitioning to light yellow signifies a progressively lower occurrence. Clicking on selected countries will show mapping at a regional level
Rank: Name are ranked by incidence using the ordinal ranking method; the name that occurs the most is assigned a rank of 1; name that occur less frequently receive an incremented rank; if two or more name occur the same number of times they are assigned the same rank and successive rank is incremented by the total preceeding names
Ethnic group cannot necessarily be determined by geographic occurrence
Similar: Names listed in the "Similar" section are phonetically similar and may not have any relation to Stinchcombe
To find out more about this surname's family history, lookup records on FamilySearch, MyHeritage, FindMyPast and Ancestry. Further information may be obtained by DNA analysis |
msmarco_passage_01_320686942 | Forensic Science Salary - Forensic Science Careers | Forensic Science Salary - Forensic Science Careers
Forensic Science Salary
After graduation, generally forensic scientists find work within federal or state crime laboratories. Working for the government can provide a person with additional pay in the form of benefits, however most entry-level positions in forensic science crime labs pay minimum at first, usually averaging around $1500 per month. Over time, a forensic scientist can build experience which increases ones pay. Some forensic scientists who have been in the business for 5 years see their salaries double from $1500 to $3000 per month just because of the experience factor. Other forensic scientists eventually earn salaries that are between $35,000 and $50,000 per year.
Determining ones pay usually involves several different factors. Location, type of facility, experience and certification all play parts in ones annual income. Another factor is what type of forensic scientist you are. Toxicologists can earn starting salaries up to $55,000 while a Forensic Quality Manager can earn up to $93,000. As mentioned, salaries can be determined by location. For those living in rural, secluded areas crime may not occur as often as someone living in a large city where crime occurs daily. If you work for the government, you have to be willing to get paid what they are willing to pay you. If crime is not occurring, they may not have many hours to provide you, which can decrease your pay. Getting yourself certified by the American Board of Criminalists or the American Board of Forensic Toxicology can help your pay increase too. Certification lets employers know that you are experienced, skilled, educated and trained for the task at hand.
Annual Salaries by State
Below is a list of the average median salary, according to the BLS, for each State as of 2009.
Alabama
$54,340
Alaska
$74,690
Arizona
$57,230
Arkansas
$51,400
California
$80,140
Colorado
$72,650
Connecticut
$72,750
Delaware
$77,960
D.C.
$94,620
Florida
$63,960
Georgia
$53,530
Hawaii
$76,640
Idaho
$57,260
Illinois
$76,360
Indiana
$53,350
Iowa
$62,890
Kansas
$54,780
Kentucky
$56,660
Louisiana
$51,890
Maine
$55,040
Maryland
$77,910
Massachusetts
$69,980
Michigan
$69,970
Minnesota
$65,450
Mississippi
$47,080
Missouri
$54,210
Montana
$61,430
Nebraska
$58,980
Nevada
$70,310
New Hampshire
$63,980
New Jersey
$85,930
New Mexico
$54,650
New York
$68,530
North Carolina
$48,250
North Dakota
$59,160
Ohio
$64,220
Oklahoma
$51,890
Oregon
$68,400
Pennsylvania
$68,890
Rhode Island
$68,000
South Carolina
$51,400
South Dakota
$57,280
Tennessee
$54,180
Texas
$58,720
Utah
$62,410
Vermont
$62,130
Virginia
$77,460
Washington
$76,330
West Virginia
$49,220
Wisconsin
$65,540
Wyoming
$61,470 |
msmarco_passage_01_322254858 | When Do Babies Start Babbling - For Kids and Moms - The Modern Parents Guide to Life Blog
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BabyBaby Development
When Do Babies Start Babbling
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Melanie Bielski—February 18, 2016
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When do babies start babblingand other answers to questions on your child’s language development.
There is something so magical about those first sweet sounds your baby makes. Oh, how those little coos and soft sounds can make your heart flutter! Soon those soft coos turn into a variety of vowels and before you know it your little love is babbling consonants. And sure enough, you are babbling too! So just when do babies start babbling?
Babble, babble! Just when do babies start babbling?
Typically by 3 months of age, your baby will begin to explore her voice by cooing and making soft pleasurable sounds. Coos are soft sounds, typically vowels. Tender vocalizations that gently shape “ahh”, “ohh”, and “mmm”.
Between 3 and 6 months of age, those soft vocalizations become more distinct and a few consonants emerge. Typically those first sounds include m, b, p, and g. These sounds are most often combined with the vowel ‘ah’. You may hear your little one produce “ma”, “ba”, “pa”, or “ga”. Once your babe starts to produce these early consonants, he is officially babbling! Yes, that quickly cooing becomes babbling! Now the fun begins and the stage is set for her first words to develop!
Between 6 months and 9 months of age, your baby’s babbling becomes more complex. She will add more consonants and vowels to her sound repertoire. You will hear longer sequences of sounds such as repeating the same sound “ba-ba-ba-ba” and sequences that change the consonant only “ba-ba-ga-ga”.
Between 9 months and 12 months of age, she will begin to babble varied syllable strings which means changing consonants and vowel patterns. For example, she may look at you, smile, and babble “mama-be-be-be-go” with a natural rhythm to her sound sequence that sounds like she is trying words. In ways she is trying words! Often this is called jabbering. She is experimenting with the power of sound combinations and the effect they have on you. Perhaps you respond with an interpretation, “mama and baby go? You want mama and baby go outside?” Perhaps you imitate her and wait for her to vocalize again. She is learning from your response that sounds can make words and words have meaning.
Typically between 12 months and 15 months, those babbling jabbering sequences really start to sound like words! The sequences contain sound variation and are paired with changes in intonation and rhythm. Often you will stop yourself and wonder if your baby just said “ball”, “dog”, “cookie”, or another familiar word. Perhaps you are hearing words or word approximations. During this time frame a parent typically hears their baby’s first true words! First words typically include “mama” and “dada” and one to two other words for familiar objects.
Between 15 months and 18 months of age, words continue to develop with many children having 5-10 words, some will use 10-25 words. Often children continue to babble and jabber during this time frame. Babbling is by now quite complex and often referred to as jargon. Jargon sounds like a real language, perhaps a foreign language though, because typically you can not understand it! Jargon contains real words paired with other babbled sequences that create a sentence type structure, but you are only able to interpret a word or two of what your child said.
By 24 months of age, typically all form of jargon and babbling have disappeared from your child’s language. Now words are rapidly developing and your baby…gasp, toddler, is creating a variety of word combinations to express her wants, needs, and thoughts. Typically a child of 24 months of age will use 50-200 words daily to communicate.
The development of speech and languageis certainly magical! From the first sweet coo to babbling games. From that first joyous word to your child wrapping their arms around you and exclaiming, “I love you, momma!” Coo, babble, and jabber along with your baby on this wonderful sound adventure!
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msmarco_passage_01_338070973 | MCP vs Circuit Breaker | Mike Holt's Forum | MCP vs Circuit Breaker | Mike Holt's Forum
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MCP vs Circuit Breaker
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kody916
Start date
Nov 17, 2015
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kody916
Member
Location
Illinois
Nov 17, 2015
#1
Based on what I know, MCP is only used for short circuit protection and Circuit breaker is used for overload as well as short circuit protection.
what factor actually determines if we have to use an MCP or Circuit Breaker?
I recently saw a drawing where an MCP was protecting a motor. How would that MCP protect the cable/motor incase there is an overload condition.
Thanks
B
big john
Senior Member
Location
Portland, ME
Nov 17, 2015
#2
Check out 430.40 and 430.52.
If you want the protection afforded by a good overload relay, then you don't need to have a thermal-magnetic breaker in the circuit and you are allowed to protect the conductors with a MCP. They share protection ability with the relay covering the "thermal" functions, and the MCP covering the "magnetic" trip functions.
Jraef
Moderator
Staff member
Location
San Francisco Bay Area, CA, USA
Occupation
Electrical Engineer
Nov 17, 2015
#3
"MCP" is actually a trade name (from Westinghouse, now Eaton) for what is officially called an Instantaneous Trip (IT) Circuit Breaker. Another common term is "Magnetic Only" or "Mag-Only" circuit breaker. All it means is that the circuit breaker has no thermal trip sensing elements. They can ONLY be used as part of a FACTORY assembled tested and listed assembly, specifically a "Combination Motor Starter". The reason is, as per those NEC sections, it can ONLY be used when the motor starter circuit contains a separate Thermal Over Load Relay (TOL). So the TOL protects the entire circuit against an overload, the MCP protects everything only from a short circuit. And MCP (IT) breaker is NOT UL listed, it is only UL Recognized as a component, because it can ONLY be used as part of a larger assembly and needs another device (ie. the TOL) to make it function correctly in a circuit protection scheme.
YOU can never "decide" whether or not to use an MCP/IT CB, other than indirectly by buying a factory built, tested and listed combo starter that uses one.
Historically, Thermal-Magnetic (TM) Cicuit Breakers used to come with a fixed and sealed Magnetic Trip based on the thermal rating. So if you had a motor starter, it was sometimes a problem to get a magnetic trip that could be set to correctly protect the motor windings. This was especially true of small motors, because the smallest CB you could buy was 15A, but if you had a 1/2HP 480V motor with a FLC of 1.1A, and the mag trip of the 15A CB was 150A (10x the rating), it was too high to protect that motor from a short circuit. So Westinghouse came out with that MCP because it had ADJUSTABLE magnetic trips that could be turned down (or up) to closely match the motor needs.
Since then, many, if not most, TM breaker mfrs have gone to making the mag trips adjustable now, so the real NEED for an IT breaker has actually gone away. Starter mfrs still use them however because for them, it saves money not having to include the thermal trips.
If you saw a motor connected to an IT/MCP breaker with no motor starter and TOL, that would be illegal. But... when the Europeans came on the scene here in North America, they use a breaker that has adjustable THERMAL trips. Technically, that was not something that could be used as a "Circuit Breaker" as defined by UL489 here in North America until relatively recently, but you could use it as a "Manual Motor Starter" under UL508, as long as there was a circuit breaker or fuses somewhere ahead of it. Sometime recently (when I wasn't looking), UL changed to allow adjustable thermal trips and still call it a "Circuit Breaker", as long as it is ONLY used on a motor circuit. Officially, that is now called a Motor Protection Circuit Breaker (MPCB). But in Europe, they call them "Motor Circuit Protectors" because the copyright laws that Westinghouse and Eaton had did not apply there. So you sometimes see MPCBs called out as "MCP"s in EU equipment.
Got that?
T
templdl
Senior Member
Location
Wisconsin
Nov 17, 2015
#4
kody916 said:
Based on what I know, MCP is only used for short circuit protection and Circuit breaker is used for overload as well as short circuit protection.
what factor actually determines if we have to use an MCP or Circuit Breaker?
I recently saw a drawing where an MCP was protecting a motor. How would that MCP protect the cable/motor incase there is an overload condition.
Thanks
Click to expand...
Have you reviewed NEC art 430-52? It covers both.
don_resqcapt19
Moderator
Staff member
Location
Illinois
Occupation
retired electrician
Nov 18, 2015
#5
Jraef said:
... But in Europe, they call them "Motor Circuit Protectors" because the copyright laws that Westinghouse and Eaton had did not apply there. So you sometimes see MPCBs called out as "MCP"s in EU equipment.
Got that?
Click to expand...
And to add a bit more to any possible confusion there is also a fuse device called a "motor short-circuit protector". 430.53 (C) (7).
Informational Note: A motor short-circuit protector, as used in this section, is a fused device and is not an instantaneous trip circuit breaker.
Click to expand...
H
Haji
Banned
Location
India
Nov 18, 2015
#6
kody916 said:
Circuit breaker is used for overload as well as short circuit protection.
Click to expand...
A thermal magnetic circuit breaker actually senses over current and not over load, strictly speaking, because there is a definite operation of circuit breaker over 135% of current setting only.
don_resqcapt19
Moderator
Staff member
Location
Illinois
Occupation
retired electrician
Nov 18, 2015
#7
Haji said:
A thermal magnetic circuit breaker actually senses over current and not over load, strictly speaking, because there is a definite operation of circuit breaker over 135% of current setting only.
Click to expand...
By definition, in the NEC, an over current protective device provides overload protection.
Overcurrent. Any current in excess of the rated current of equipment or the ampacity of a conductor. It may result from overload, short circuit, or ground fault.
Overcurrent Protective Device, Branch-Circuit. A device capable of providing protection for service, feeder, and branch circuits and equipment over the full range of overcurrents between its rated current and its interrupting rating. Such devices are provided with interrupting ratings appropriate for the intended use but no less than 5000 amperes.
Click to expand...
A
adamscb
Senior Member
Location
USA
Occupation
EE
Nov 18, 2015
#8
There are two main types of rises in current: short-circuits, and overloads. Overloads arise when electrical equipment draw only slightly more than rated current, which can increase over time. At first, overloads do not harm your system. However, if left unchecked, damage can be caused. On the other hand, short-circuits happen very quickly, and produce currents that are several magnitudes larger than full load. Short-circuits must be eliminated very quickly.
MCP-style breakers only offer protection from short-circuits. These are very common in MCC buckets. Inside MCC buckets, you have your breaker and then your overloads beneath the starter. Why do you need both? The answer is to provide protection for both short-circuits and overloads. The MCP circuit breaker provides short-circuit protection, while the overloads provide the overload protection.
So then this question arises: why aren't overloads used, let's say in 480v switchgear breakers? The breakers commonly found in low-voltage switchgear sections are called thermal-magnetic breakers, because they provide both overload (thermal) and short-circuit (magnetic) protection. You don't need to install overloads in this case because the circuit breaker already provides overload protection.
When you try to differentiate between an MCP and a "circuit breaker", in reality an MCP is a special type of circuit breaker (MCP stands for Motor Circuit Protector). MCPs are used almost exclusively in branch circuits, while thermal-mags are used in feeder circuits.
Hope this helps.
G
GoldDigger
Moderator
Staff member
Location
Placerville, CA, USA
Occupation
Retired PV System Designer
Nov 18, 2015
#9
There are several reasons for using separate overload instead of relying on the thermal trip of a breaker:
1. The overload current needs to be set precisely to allow full load operation but trip just above that point. A fixed value breaker usually will not allow you to get close enough.
2. A good motor overload will have a time characteristic that fits the motor temperature rise and damage curves better than the breaker. Especially over the time scale involved with too frequent restarts of the motor.
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msmarco_passage_01_342902888 | Bridal Shower before Wedding Invitations are sent out? — The Knot Community | Bridal Shower before Wedding Invitations are sent out? — The Knot Community
Pre-wedding Parties
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Bridal Shower before Wedding Invitations are sent out?
athlete010688 member
July 2011
in Pre-wedding Parties
Is it bad etiquette to send out bridal shower invitations before I send out the wedding invitations? If my sister waits to send out until I send out the wedding invitations, it's only about 1 1/2-2 weeks before the bridal shower. DIdn't know the etiquette on this! Thanks!
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Re: Bridal Shower before Wedding Invitations are sent out?
ShakeUpTampa member
July 2011 edited December 2011
I guess it varies by social circle but in my social circle it's a bit presumptuous to send out a gift party invite before announcing the date of the wedding. Did you send save the dates to these people? My MOH aligned everything already so her invites for the party will go out about 1.5-2 weeks after the invites and the girls will have a couple weeks to rsvp.
Nichole Tampa, FL
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MairePoppy Connecticut mod
July 2011 edited December 2011
In my social circle, showers are held 1 to 3 months before the wedding. The shower invitations would be sent out about a month before the shower. Wedding invitations are usually sent out 8 to 10 weeks before the wedding. So it is typical for the shower invitations to go out before the wedding invitations.
If it makes more sense to send the shower invitations before the wedding invitations, then that's what she should do.
Have fun at your shower : )
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samnathaw member
July 2011 edited December 2011
My shower will occur before our invitations are sent out. We did send save the dates however, so the women invited to the shower have already had indication of an invitation!
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hschieferstein
July 2011 edited December 2011
I think most of the time shower invites go out prior to wedding invites.
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kmmssg mod
July 2011 edited December 2011
My DD had to fly home to attend her shower and it was 3 months before her wedding. That is when she could get time off so that is when we did it. Everyone received a wedding invitation and no one seemed bent out of shape about it.
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MAMA41206 member
July 2011 edited December 2011
My shower is on Saturday and I'm not sending out my wedding invitations until next week (8 weeks before Wedding).
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peanutty2 member
July 2011 edited December 2011
I think it's okay as long as everyone is invited to the wedding too and hopefully at least knows about the wedding. Did you send STDs?
Typically, where I am anyway, the shower is 2-3 months before the wedding. So it'd be too early for invites to go out.
I sent STDs. So only those people definately invited to the wedding are invited to the shower. My shower is about 2 weeks before I'll be sending out wedding invites. Just worked out that way.
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LoveMuffins member
July 2011 edited December 2011
My shower happend about 2 weeks before my invites went out, so it would've been hard not to send the shower invites before the wedding ones! I definitely wasn't going to send my wedding invites out 4 months in advance!
I think the shower invites should be sent about 3 weeks - a month before the shower.
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Hellokatie0517 member
July 2011 edited December 2011
Sending out STDs, helps curb any etiquette issues as far as people being invited to a shower prior to receiving a wedding invite. Just make sure that whoever is throwing your shower knows to only invite people that are invited to the wedding!
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athlete010688 member
July 2011 edited December 2011
Thanks everyone! I didn't think it would be that big of a deal. And yes, everyone that is invited to the shower, is invited to the wedding.
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MelanieReese13
February 2013
II was just wondering the same thing! Since i am sending out my save-the-dates i think it is fine to send out bridal shower invitations before wedding invites. Thanks everyone!
n Response to <a href="http://forums.theknot.com/Sites/theknot/Pages/Main.aspx/special-topic-wedding-boards_pre-wedding-parties_bridal-shower-before-wedding-invitations-sent-out?plckFindPostKey=Cat:Special Topic Wedding BoardsForum:32Discussion:25990b4b-76ba-4c59-8dbb-e910c399d3e1Post:8f0e1287-d9bc-4393-89fe-883ee93a182c">Re: Bridal Shower before Wedding Invitations are sent out?</a>:
[QUOTE]My shower happend about 2 weeks before my invites went out, so it would've been hard not to send the shower invites before the wedding ones! I definitely wasn't going to send my wedding invites out 4 months in advance! I think the shower invites should be sent about 3 weeks - a month before the shower.
Posted by LoveMuffins [/QUOTE]
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pearnjeff member
September 2014
My niece gets married at the end of march '15. She had her shower last weekend. Her save the dates went out last weekend. I get married in 6 weeks. What is the etiquette? My sister says having a shower 6 months in advance before the save the dates are mailed is ok. My shower was over labor day weekend because my sister didn't want my shower the same weekend as her daughters.. she said it was "her Daughters weekend". There are people who were sent save the dates who did not go to the shower. Is this bad etiquette?
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Maggie0829 Ravens & Bohs & Crabs & O's member
September 2014
pearnjeff said:
My niece gets married at the end of march '15. She had her shower last weekend. Her save the dates went out last weekend. I get married in 6 weeks. What is the etiquette? My sister says having a shower 6 months in advance before the save the dates are mailed is ok. My shower was over labor day weekend because my sister didn't want my shower the same weekend as her daughters.. she said it was "her Daughters weekend". There are people who were sent save the dates who did not go to the shower. Is this bad etiquette?
@pearnjeff - I think having a shower 6 months before your wedding and before STDs even go out is kind of crazy. Now I had my shower before invites went out but only a month before invites went out (invites went out 8 weeks before wedding date).
As far as your shower and not including everyone who got a STD, that is fine. Typically showers are for the nearest and dearest to the bride and not meant for the entire wedding guest list.
As for your sister and her wanting her daughter to have "her weekend," I think she needs to lay off the crazy MOB juice.
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photokitty where I want to be mod
September 2014
I'm closing this Zombie. Thanks for answering @pearnjeff 's question @maggie0829.
@pearnjeff please refrain from bumping super old threads, if you have a question you can feel free to start a new discussion if your search does not answer your question.
Thanks!
~xoxo~
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Someone having minimal experience with keyboards can, with some practice, reach a typing speed of about 20 words per minute through practice using online typing tests, keyboarding games, typing speed tests and typing tutorials. An average typist can achieve about 30 to 45 WPM (usually the minimum required for dispatch positions and other typing data entry jobs). Advanced typists generally are expected to operate at typing speeds above 60 WPM.
As of 2005, Barbara Blackburn is the fastest typist in the world, according to The Guinness Book of World Records. Using the Dvorak Simplified Keyboard, she has maintained 150 words per minute for 50 minutes, 170 words per minute for shorter periods of time, and has been clocked at a peak typing speed of 212 words per minute. It is noteworthy that Blackburn failed her typing class in high school. She first encountered the Dvorak keyboard in 1938, quickly learned to achieve very high average typing speeds, and occasionally toured giving speed-typing demonstrations during her secretarial career.
Can you compete with Ms. Blackburn on speed typing? There is only one way to find out... Take our free typing test to assess your words per minute typing speed. |
msmarco_passage_01_365081777 | The Penn FTD Center | Power Of Attorney, Guardianship, and Legally Authorized Representative | The Penn FTD Center | Power Of Attorney, Guardianship, and Legally Authorized Representative
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Power Of Attorney, Guardianship, and Legally Authorized Representative
Power Of Attorney, Guardianship, and Legally Authorized Representative
Power of Attorney
Frontotemporal degenerative (FTD) disorders can affect an individual’s ability to communicate verbally, limit thought processes and impair judgment. As FTD disorders progress, it will become more challenging for the affected individual to make sound decisions for his/herself regarding personal health care, financial and legal matters. It is important that discussions about who will make decisions on behalf of an individual with FTD. Ideally these discussions should begin early in the course of the condition, when a loved one with FTD is most fully able to participate and determine who is in the best position to look after personal interests when he/she is no longer able to do so.
What is Power of Attorney?
Power of Attorney (POA) is a written authorization granting another person the power to act on behalf of an individual in private affairs, business or other legal matters. A power of attorney specifically defines which aspects of the individual’s life will be managed by another. The individual authorizing another to act on his/her behalf is called the principal or grantor of the POA. The individual authorized to act on the principal’s behalf is referred to as the agent or attorney .
How do I choose a Power of Attorney?
An individual initiating the POA must have capacity for such decisions at the time the POA is written. Capacity is defined in most states as the ability of an individual to understand the nature and consequences of granting power of attorney to another.
Some states and jurisdictions are able to grant a Springing Power of Attorney that only becomes effective when a specified event occurs, such as the principal becoming incapacitated. Under common law, a traditional power of attorney becomes ineffective if the principal dies or becomes incapacited. This can be avoided if the principal specifies that the POA is to remain valid even in the event of their incapacity. This type of durable power of attorney becomes effective when it is signed by both parties and stays in effect throughout the period the principal is unable to make decisions for him/herself due to physical or mental illness.
The principal granting the power of attorney may revoke it at any time as long as they are still determined to have capacity.
What is a Health Care Power of Attorney or Health Care Proxy?
In some areas of the country, a durable power of attorney can also serve as a health care power of attorney or health care proxy . A health care POA or health care proxy designates the person who can make health care decisions for the principal if they are unable to communicate their wishes. A health care proxy is able to make decisions on the principal’s behalf regarding routine as well as end-of-life care. A loved one may chose a single person to serve as durable power of attorney for all decisions or may opt to designate one individual to handle health care decisions and a different individual to handle financial and legal decisions.
Guardianship
What is Guardianship?
If a loved one does not designate a power of attorney, it may become necessary to ask the court to appoint a guardian to manage their affairs. Guardians are given the legal authority to care for the personal and property interests of another person, who is referred to as a ward .
The following criteria generally must be met for a court to appoint a guardian:
The individual is not able to make decisions regarding his/her own affairs
The individual has not executed, or does not have the mental capacity to currently execute, a power of attorney
Serious harm may come to the person if a guardian is not appointed
Types of Guardianship
Courts can grant guardianship of the person, guardianship of the person’s estate or property or combined guardianship for both. A guardian who has been given responsibility by the court for both the personal well-being and financial interests of the ward is known as a general guardian . The court can choose to appoint one individual as guardian of the person and a different individual as the guardian of the person’s estate.
How do I obtain Guardianship?
If you believe that your loved one needs a guardian to prevent serious harm to their person or their estate, you will need to hire an experienced attorney and petition the court for guardianship. Guardianship takes significant control away from an individual and in the court’s eyes should only be pursued when other strategies have been seriously considered.
Legally Authorized Representative
What is a Legally Authorized Representative?
The U.S. Department of Health and Human Services defines a legally authorized representative as “any individual person, judicial body or other body of individuals who are legally authorized under state and federal law to consent to research participation on behalf of a designated person.”
A legally authorized representative can be appointed when an adult is unable to make or communicate an informed decision due to mental or physical impairment.
Who is Eligible to serve as a Legally Authorized Representative?
In the state of Pennsylvania, the following individuals may be considered legally authorized representatives of a potential research subject and capable of providing surrogate consent:
A court-appointed guardian authorized in a current court order to consent to the subject's participation in the research.
A health care agent appointed by the subject in a power of attorney.
A "health care representative" when the individual cannot speak for his/herself and where there has been no guardian appointed by the court and no health care power of attorney designated. (PA Act 169).
Any of the following relatives, in descending order of priority, who is reasonably available, may also act as the subject’s health care representative:
The spouse (unless an action for divorce is pending)
Adult children (18 years of age or older)
A parent.
An adult sibling
An adult grandchild
An adult who has knowledge of the potential research subject’s preferences and values, including but not limited to religious and moral beliefs, who is able to assess how the patient would make decisions
Getting Started
It is always best if you and your loved one consult with a lawyer who has experience in drafting powers of attorney.
Resources for finding a lawyer in your area:
Pennsylvania Bar Association
http://www.pabar.org/public/Membership/lrsblurb.asp
National Academy of Elder Law Attorneys, Inc.
http://www.naela.org/
Read more about Powers of Attorney in the PA Bar Association’s publication A Guide to Legal Issues for Pennsylvania Senior Citizens |
msmarco_passage_01_370196734 | Purchasing Power Parity
Pacific Exchange Rate Service: Current Exchange Rates; Database of Historical Exchange Rates; Canadian Dollar Services; Exchange Rate Economics; daily updated exchange rate data; exchange rate charts, plots, and diagrams
Purchasing Power Parity
What is Purchasing Power Parity?
Purchasing power parity (PPP) is a theory which states that
exchange rates between currencies are in equilibrium when their
purchasing power is the same in each of the two countries. This
means that the exchange rate between two countries should equal
the ratio of the two countries' price level of a fixed basket of
goods and services. When a country's domestic price level is
increasing (i.e., a country experiences inflation), that country's
exchange rate must depreciated in order to return to PPP.
The basis for PPP is the "law of one price". In the absence of
transportation and other transaction costs, competitive markets
will equalize the price of an identical good in two countries when
the prices are expressed in the same currency. For example, a
particular TV set that sells for 750 Canadian Dollars [CAD] in
Vancouver should cost 500 US Dollars [USD] in Seattle when the
exchange rate between Canada and the US is 1.50 CAD/USD. If the
price of the TV in Vancouver was only 700 CAD, consumers in
Seattle would prefer buying the TV set in Vancouver. If this
process (called "arbitrage") is carried out at a large scale, the
US consumers buying Canadian goods will bid up the value of the
Canadian Dollar, thus making Canadian goods more costly to
them. This process continues until the goods have again the same
price. There are three caveats with this law of one price. (1) As
mentioned above, transportation costs, barriers to trade, and
other transaction costs, can be significant. (2) There must be
competitive markets for the goods and services in both
countries. (3) The law of one price only applies to tradeable
goods; immobile goods such as houses, and many services that are
local, are of course not traded between countries.
Economists use two versions of Purchasing Power Parity: absolute
PPP and relative PPP. Absolute PPP was described in the previous
paragraph; it refers to the equalization of price levels across
countries. Put formally, the exchange rate between Canada and the
United States ECAD/USDis equal to the price level in
Canada PCANdivided by the price level in the United
States PUSA. Assume that the price level ratio
PCAD/PUSDimplies a PPP exchange rate of 1.3
CAD per 1 USD. If today's exchange rate ECAD/USDis 1.5
CAD per 1 USD, PPP theory implies that the CAD will appreciate
(get stronger) against the USD, and the USD will in turn
depreciate (get weaker) against the CAD.
Relative PPP refers to rates of changes of price levels,
that is, inflation rates. This proposition states that the rate of
appreciation of a currency is equal to the difference in inflation
rates between the foreign and the home country. For example, if Canada
has an inflation rate of 1% and the US has an inflation rate of 3%,
the US Dollar will depreciate against the Canadian Dollar by 2% per
year. This proposition holds well empirically especially when the
inflation differences are large.
Does PPP determine exchange rates in the short term?
No. Exchange rate movements in the short term are news-driven. Announcements about interest rate changes, changes in perception
of the growth path of economies and the like are all factors that
drive exchange rates in the short run. PPP, by comparison,
describes the long run behaviour of exchange rates. The economic
forces behind PPP will eventually equalize the purchasing power of
currencies. This can take many years, however. A time horizon of
4-10 years would be typical.
How is PPP calculated?
The simplest way to calculate purchasing power parity between two
countries is to compare the price of a "standard" good that is in
fact identical across countries. Every year The Economistmagazine publishes a light-hearted version of PPP: its "Hamburger
Index" that compares the price of a McDonald's hamburger around
the world. More sophisticated versions of PPP look at a large
number of goods and services. One of the key problems is that
people in different countries consumer very different sets of
goods and services, making it difficult to compare the purchasing
power between countries.
According to PPP, by how much are currencies overvalued or undervalued?
The following two charts compare the PPP of a currency
with its actual exchange rate relative to the US Dollar and relative
to the Canadian Dollar, respectively. The charts are updated periodically to
reflect the current exchange rate. It is also updated once
a year to reflect new estimates of PPP. The PPP estimates are
taken from studies carried out by the Organization
of Economic Cooperation and Development (OECD) and others; however,
they should not be taken as "definitive". Different methods of
calculation will arrive at different PPP rates.
The currencies listed below are compared to the US
Dollar. A green bar indicated that the local currency is overvalued by
the percentage figure shown on the axis; the currency is thus expected
to depreciate against the US Dollar in the long run. A red bar
indicates undervaluation of the local currency; the currency is thus
expected to appreciate against the US Dollar in the long run.
The currencies listed below are compared to the Canadian
Dollar. A green bar indicated that the local currency is overvalued by
the percentage figure shown on the axis; the currency is thus expected
to depreciate against the Canadian Dollar in the long run. A red bar
indicates undervaluation of the local currency; the currency is thus
expected to appreciate against the Canadian Dollar in the long run.
The currencies listed below are compared to the European Euro. A green bar indicated that the local currency is overvalued by
the percentage figure shown on the axis; the currency is thus expected
to depreciate against the Euro in the long run. A red bar
indicates undervaluation of the local currency; the currency is thus
expected to appreciate against the Euro in the long run.
Where can I get more information?
• OECD
National Accounts: The OECD publishes PPPs for all OECD
countries. You can retrieve a table with the OECD's 1950-2015 PPP rates. This is a comma-seprated file that can be easily
imported into a spreadsheet program.
• From The Economistmagazine: The Big Mac Index- as they put it "The world's most accurate financial indicator (to be based on a fast food item), with a ten-year retrospective on burgernomics"
• Wilfred J. Ethier: Modern International Economics, 3rd edition. W. W. Norton & Comp., New York/London: 1995. Chapter 18, section 2 on "Price Linkages" contains
an excellent non-technical overview of PPP
• Kenneth Rogoff: The Purchasing Power Parity Puzzle,
Journal of Economic Literature, 34(2), June 1996, pages 647-668.
This recent survey provides an overview of developments
with respect to research on PPP, including the
emerging consensus that deviations from PPP do damp out but only
very slowly, at roughly fifteen percent per year. It remains
difficult to explain why the estimated speed of convergence
to PPP is so slow.
• For the more technically minded, I recommend searching the
EconLitdatabase for recent research papers on PPP. This is a very active
branch of economic research, both theoretically and empirically.
© 2019 by Werner Antweiler, University
of British Columbia. All rights reserved.
The Pacific Exchange Rate Service is located in Vancouver,
Canada.
Pacific Home Page|
About this service|
Contact Pacific |
|
msmarco_passage_01_380673600 | Pictures of the Types of Honeysuckle | LoveToKnow | Pictures of the Types of Honeysuckle | LoveToKnow
Pictures of the Types of Honeysuckle
Copied!
Attractive to Wildlife
Source
There are 180 types of honeysuckle plants worldwide, but only about 20 in North America.
Known for fragrant, trumpet-shaped flowers, many honeysuckles are grown to attract both butterflies and hummingbirds.
They may be lovely, but some can become invasive. Read on to select a honeysuckle that will attract wildlife without becoming a problem.
Honeysuckle Vines
Source
Vine honeysuckles, such as this Lonicera periclymenum, grow beautifully over doorways, arbors or fences and can reach heights of up to 30 feet (about 10 meters.)
When choosing a vine honeysuckle, avoid L. Japonica, also known as Japanese honeysuckle, which may take over your garden as well as the surrounding landscape.
Never plant any vine honeysuckles close to a valued tree or shrub. These vines climb so tightly that they may strangle the supporting plant, a habit that gives honeysuckle its other common name: woodbine.
Honeysuckle Bushes
Source
There are five types of honeysuckle bush common to North America: Tartarian, Standish, Amur, Pretty and Morrow's. Each of these varieties is considered invasive, and prohibited in many regions.
Bush honeysuckles grow six to ten feet tall and form a dense thicket of vegetation that chokes out other species.
Replace these bushes with red chokecherry, serviceberry, or viburnum to enjoy a flowering shrub that will not harm the rest of your garden.
The Problem with Berries
Source
The bright red berries that grow on many types of honeysuckle brighten your garden and are an attractive food source for birds, but even these cheery red fruits can prove problematic.
Berry-eating birds require fat from the fruit and seeds they eat. Honeysuckle berries are higher in sugar than many native berries, and may come to make up much of the birds' diet.
The seeds, dispersed in the bird's droppings, will germinate elsewhere and out-compete the more nutritious natural vegetation.
Winter Honeysuckle
Source
Winter honeysuckle can extend the growing season well into the colder months. Its fragrant, early spring blossoms and persistent autumn foliage add a burst of color to an otherwise drab off-season garden.
Not as aggressive as its bushier cousins, winter honeysuckle can still become a problem in some regions, particularly the Middle Atlantic states.
Check with your State Department of Natural Resources or local university extension office to see if this honeysuckle is a safe choice for your area.
Box Honeysuckle
Source
Box honeysuckle is distinctly different from other members of the family.
Its blooms are inconspicuous and only mildly scented, and its growth pattern is considerably more restrained than that of other honeysuckles.
Landscapers use this honeysuckle bush as a hardy and quick-growing alternative to boxwood, shown here, for creating elaborate hedges and topiary designs.
Honeyberries
Source
Recently, a Siberian species of honeysuckle has gained popularity for its edible berries.
L. caerulea has not shown invasive tendencies and can be a pleasant and nonthreatening addition to your flowerbed or kitchen garden.
Often marketed as honeyberries, these honeysuckles are hardy to zone two and bear an abundance of fruit in early June, even in northern latitudes.
Native Types of Honeysuckle
Source
As an alternative to potentially invasive exotic honeysuckles, consider planting a native species like this L. Hispidula or an L. flava.
Somewhat less showy than imported honeysuckles, many native species are equally fragrant and are friendly to the natural landscape.
They require a minimum of care and will produce blooms reliably over the course of the summer.
Choosing Your Honeysuckle
Source
Whether you want a plant to produce berries, brighten your garden in the winter or attract wildlife, a honeysuckle might be a good choice.
Just choose a variety that is harmless as well as beautiful, and you can enjoy this perfumed showpiece worry-free.
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msmarco_passage_01_383930491 | When to Hiera (Aka: How Do I Module?) - Shit Gary Says | When to Hiera (Aka: How Do I Module?) - Shit Gary Says
When to Hiera (Aka: How Do I Module?)
Dec 8th, 2013
I’m convinced that writing Puppet modules is the ultimate exercise in bikeshedding: if it works, someone’s probably going to tell you that you could have done it better, if you’re using the methods suggested today, they’re probably going to be out-of-date in about 6 months, and good luck writing something that someone else can use cleanly without needing to change it.
I can help you with the last two.
Data and Code Separation == bliss?
I wrote a blog post about 2 years ago detailing why separating your data from your Puppet code was a good idea. The idea is still valid, which means it’s probably one of the better ideas I’ve ever stolen (Does anyone want any HD-DVDs?). Hunter Haugen and I put together a quick blog post on using Hiera to solve the data/code problem because there wasn’t a great bit of documentation on Hiera at that point in time. Since then, Hiera’s been widely accepted as “a good idea” and is in use in production Puppet environments around the world. In most every environment, usage of Hiera by more than just one person eventually gives birth to the question that inspired this post:
“What the hell does and does NOT belong in Hiera?”
Puppet data models
The params class pattern
Many Puppet modules out there since Puppet 2.6 have begun using this pattern:
puppetlabs-mysql/manifests/server.pp
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23
class mysql::server ( $config_file = $mysql::params::config_file, $manage_config_file = $mysql::params::manage_config_file, $old_root_password = $mysql::params::old_root_password, $override_options = {}, $package_ensure = $mysql::params::server_package_ensure, $package_name = $mysql::params::server_package_name, $purge_conf_dir = $mysql::params::purge_conf_dir, $remove_default_accounts = false, $restart = $mysql::params::restart, $root_group = $mysql::params::root_group, $root_password = $mysql::params::root_password, $service_enabled = $mysql::params::server_service_enabled, $service_manage = $mysql::params::server_service_manage, $service_name = $mysql::params::server_service_name, $service_provider = $mysql::params::server_service_provider, # Deprecated parameters $enabled = undef, $manage_service = undef ) inherits mysql::params { ## Puppet goodness goes here }
If you’re not familiar, this is a Puppet class definition for mysql::server that has several parameters defined and defaulted to values that come out of the mysql::params class. The mysql::params class looks a bit like this:
puppetlabs-mysql/manifests/params.pp
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23
class mysql::params { case $::osfamily { 'RedHat': { if $::operatingsystem == 'Fedora' and (is_integer($::operatingsystemrelease) and $::operatingsystemrelease >= 19 or $::operatingsystemrelease == "Rawhide") { $client_package_name = 'mariadb' $server_package_name = 'mariadb-server' } else { $client_package_name = 'mysql' $server_package_name = 'mysql-server' } $basedir = '/usr' $config_file = '/etc/my.cnf' $datadir = '/var/lib/mysql' $log_error = '/var/log/mysqld.log' $pidfile = '/var/run/mysqld/mysqld.pid' $root_group = 'root' } 'Debian': { ## More parameters defined here } } }
This pattern puts all conditional logic for all the variables/parameters used in the module inside one class – the mysql::params class. It’s called the ‘params class pattern’ because we suck at naming things.
Pros:
All conditional logic is in a single class
You always know which class to seek out if you need to change any of the logic used to determine a variable’s value
You can use the include function because parameters for each class will be defaulted to the values that came out of the params class
If you need to override the value of a particular parameter, you can still use the parameterized class declaration syntax to do so
Anyone using Puppet version 2.6 or higher can use it (i.e. anyone who’s been using Puppet since about 2010).
Cons:
Conditional logic is repeated in every module
You will need to use inheritance to inherit parameter values in each subclass
It’s another place to look if you ALSO use Hiera inside the module
Data is inside the manifest, so business logic is also inside params.pp
Hiera defaults pattern
When Hiera hit the scene, one of the first things people tried to do was to incorporate it into existing modules. The logic at that time was that you could keep all parameter defaults inside Hiera, rid yourself of the params class, and then just make Hiera calls out for your data. This pattern looks like this:
puppetlabs-mysql/manifests/server.pp
1 2 3 4 5 6 7 8 9
class mysql::server ( $config_file = hiera('mysql::params::config_file', 'default value'), $manage_config_file = hiera('mysql::params::manage_config_file', 'default value'), $old_root_password = hiera('mysql::params::old_root_password', 'default value'), ## Repeat the above pattern ) { ## Puppet goodness goes here }
Pros:
All data is locked up in Hiera (and its multiple backends)
Default values can be provided if a Hiera lookup fails
Cons:
You need to have Hiera installed, enabled, and configured to use this pattern
All data, including non-business logic, is in Hiera
If you use the default value, data could either come from Hiera OR the default (multiple places to look when debugging)
Hybrid data model
This pattern is for those people who want the portability of the params.pp class combined with the power of Hiera. Because it’s a hybrid, there are multiple ways that people have set it up. Here’s a general example:
puppetlabs-mysql/manifests/server.pp
1 2 3 4 5 6
class mysql::server ( $config_file = hiera('mysql::params::config_file', $mysql::params::config_file), $manage_config_file = hiera('mysql::params::manage_config_file', $mysql::params::manage_config_file), $old_root_password = hiera('mysql::params::old_root_password', $mysql::params::old_root_password), ## Repeat the above pattern ) inherits mysql::params {
Pros:
Data is sought from Hiera first and then defaulted back to the params class parameter
Keep non-business logic (i.e. OS specific data) in the params class and business logic in Hiera
Added benefits of both models
Cons:
Where did the variable get set – Hiera or the params class? Debugging can be hard
Requires Hiera to be setup to use the module
If you fudge a variable name in Hiera, you get the params class default – see Con #1
Hiera data bindings in Puppet 3.x.x
In Puppet 3.0.0, there was a concept introduced called Data Bindings. This created a federated data model automatically incorporating a Hiera lookup. Previously, the order that Puppet would use to determine the value of a parameter was to first use a value passed with the parameterized class declaration syntax (i.e. the below:).
parameterized class declaration
1 2 3
class { 'apache': package_name => 'httpd', }
If a parameter was not passed with the parameterized class syntax (like the ‘package_name’ parameter above’), Puppet would then look for a default value inside the class definition (i.e. the below:).
parameter default in a class definition
1 2 3 4 5
class ntp ( $ntpserver = 'default.ntpserver.org' ) { # Use $ntpserver in a file declaration... }
If the value of ‘ntpserver’ wasn’t passed with a parameterized class declaration, then the value would be set to ‘default.ntpserver.org’, since that’s the default set in the above class definition.
Failing both of these conditions, Puppet would throw a parse error and say that it couldn’t determine a value for a class parameter.
As of Puppet 3.0.0, Puppet will now do a Hiera lookup for the fully namespaced value of a class parameter
Roles and Profiles
The roles and profiles pattern has been written about a number of times and is ALSO considered to be ‘a best practice’ when setting up your Puppet environment. What roles and profiles gets you is a ‘wrapper class’ that allows you to declare classes within this wrapper class:
profiles/manifests/wordpress.pp
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35
class profiles::wordpress { # Data Lookups $site_name = hiera('profiles::wordpress::site_name') $wordpress_user_password = hiera('profiles::wordpress::wordpress_user_password') $mysql_root_password = hiera('profiles::wordpress::mysql_root_password') $wordpress_db_host = hiera('profiles::wordpress::wordpress_db_host') $wordpress_db_name = hiera('profiles::wordpress::wordpress_db_name') $wordpress_db_password = hiera('profiles::wordpress::wordpress_db_password') ## Create user group { 'wordpress': ensure => present, } user { 'wordpress': ensure => present, gid => 'wordpress', password => $wordpress_user_password, home => '/var/www/wordpress', } ## Configure mysql class { 'mysql::server': root_password => $wordpress_root_password, } class { 'mysql::bindings': php_enable => true, } ## Configure apache include apache include apache::mod::php } ## Continue with declarations...
Notice that any variables that might have business specific logic are set with Hiera lookups. These Hiera lookups do NOT have default values, which means the hiera () function will throw a parse error if a value is not returned. This is IDEAL because we WANT TO KNOW if a Hiera lookup fails – this means we failed to put the data in Hiera and should be corrected BEFORE a state that might contain invalid data is enforced with Puppet.
You then have a ‘Role’ wrapper class that simply includes many of the ‘Profile’ wrapper classes:
roles/manifests/frontend.pp
1 2 3 4 5 6 7
class roles::frontend { include profiles::mysql include profiles::apache include profiles::java include profiles::jboss # include more profiles... }
The idea being that Profiles abstract all the technical bits that need to declared to setup a piece of technology, and Roles will abstract all the business logic for what pieces of technology should be installed on a certain ‘class’ of machine. Basically, you can say that “all our frontend infrastructure should have mysql, apache, java, jboss…”. In this statement, the Role is ‘frontend infrastructure’ and the Profiles are ‘mysql, apache, java, jboss…’.
Pros:
Hiera data lookups are confined to a wrapper class OUTSIDE of the component modules (like mysql, apache, java, etc…)
Data lookups for parameters containing business logic are done with Hiera
Non-business specific data is pulled from the module (i.e. the params class)
Wrapper modules can be ‘included’ with the include function, helping to eliminate multiple class declarations using the parameterized class declaration syntax
Component modules are backward-compatible to Puppet 2.6 while wrapper modules still get to use a modern data lookup mechanism (Hiera)
Component modules do NOT contain any business specific logic, which means they’re portable
Cons:
Hiera must be setup to use the wrapper modules
Wrapper modules add another debug path for variable data
Wrapper modules add another layer of abstraction
Data in Puppet Modules
R.I. Pienaar (the original author of MCollective, Hiera, and much more) published a blog post recently on implementing a folder for Puppet modules that Hiera can traverse when it does data lookups. This construct isn’t new, there was a feature request for this behavior filed in October of 2012 with a subsequent pull request that implemented this functionality (they’re both worth reads for further information). The pull request didn’t get merged, and so R.I. implemented the functionality inside a module on the Puppet Forge . In a nutshell, it’s a hiera.yaml configuration file INSIDE THE MODULE that implements a module-specific hierarchy, and a ‘data’ folder (also inside the module) that allows for individual YAML files that Hiera could read. This hierarchy is consulted AFTER the site-specific hiera.yaml file is read (i.e. /etc/puppet/hiera.yaml or /etc/puppetlabs/puppet/hiera.yaml ), and the in-module data files are consulted AFTER the site-specific Hiera data files are read (normally found in either /etc/puppet/hieradata or /etc/puppetlabs/puppet/hieradata ).
The argument here is that there’s a data store for SITE-SPECIFIC Hiera data that should be kept outside of modules, but there’s not a MODULE-SPECIFIC data store that Hiera can use. The argument isn’t whether data that should be shared with other people belongs inside a site-specific Hiera datastore (protip: it doesn’t. Data that’s not business-specific should be shared with others and kept inside the module), the argument is that it shouldn’t be locked up inside the DSL where the barrier-to-entry is learning Puppet’s DSL syntax. Whereas /etc/puppet/hiera.yaml or /etc/puppetlabs/puppet/hiera.yaml sets up the hierarchy for all your site-specific data, there’s no per-module hiera.yaml file for all module-specific data, and there’s no place to put module-specific Hiera data.
But module-specific data goes inside the params class and business-specific data goes inside Hiera, right?
Sure, but for some people the Puppet DSL is a barrier. The argument is that there should be a lower barrier to entry to contribute parameter data to Puppet that doesn’t require you to learn the syntax of if/case/selector statements in the Puppet DSL. There’s also the argument that if you want to add support for an operatingsystem to your module, you have to modify the params class file and add another entry to the if/case/selector statement – wouldn’t it be easier to just add another YAML file into a data folder that doesn’t affect existing datafiles?
Great, ANOTHER hierarchy to traverse for data – that’s going to get confusing
Well, think about it right now – most EVERY params class of EVERY module (if it supports multiple operatingsystems) does some sort of conditional logic to determine values for parameters on a per-OS basis. That’s something that you need to traverse. And many modules use different conditional data to determine what paramters to use. Look at the mysql params class example above – it not only splits on $osfamily, but it also checks specific operatingsystems. That’s a conditional inside a conditional. You’re TRAVERSING conditional data right now to find a value – the only difference is that this method doesn’t use the DSL, it uses Hiera and YAML.
Sure, but this is outside of Puppet and you’re losing visibility inside Puppet with your data
You’re already doing that if you’re using the params class. In this case, visibility is moved to YAML files instead of separate Puppet classes.
Setting it up
You will first need to install R.I.’s module from the Puppet Forge. As of this writing, it’s version 0.0.1, so ensure you have the most recent version using the puppet module tool:
[root@linux modules]# puppet module install ripienaar/module_data Notice: Preparing to install into /etc/puppetlabs/puppet/modules ... Notice: Downloading from https://forge.puppetlabs.com ... Notice: Installing -- do not interrupt ... /etc/puppetlabs/puppet/modules └── ripienaar-module_data (v0.0.1)
Next, you’ll need to setup a module to use the data-in-modules pattern. Take a look at the tree of a sample module:
[root@linux modules]# tree mysql/ mysql/ ├── data │ ├── hiera.yaml │ └── RedHat.yaml └── manifests └── init.pp
I created a sample mysql module based on the examples above. All of the module’s Hiera data (including the module-specific hiera.yaml file) goes in the data folder. This module should be placed in Puppet’s modulepath – and if you don’t know where Puppet’s modulepath is set, run the puppet config face to determine that:
[root@linux modules]# puppet config print modulepath /etc/puppetlabs/puppet/modules:/opt/puppet/share/puppet/modules
In my case, I’m putting the module in /etc/puppetlabs/puppet/modules (since I’m running Puppet Enterprise). Here’s the hiera.yaml file from the sample mysql module:
mysql/data/hiera.yaml
1 2
:hierarchy: - "% {::osfamily}"
I’ve also included a YAML file for the $osfamily of RedHat:
mysql/data/RedHat.yaml
1 2 3 4
--- mysql::config_file: '/path/from/data_in_modules' mysql::manage_config_file: true mysql::old_root_password: 'password_from_data_in_modules'
Finally, here’s what the mysql class definition looks like from manifests/init.pp:
mysql/manifests/init.pp
1 2 3 4 5 6 7 8 9
class mysql ( $config_file = 'module_default', $manage_config_file = 'module_default', $old_root_password = 'module_default' ) { notify { "The value of config_file: $ {config_file}": } notify { "The value of manage_config_file: $ {manage_config_file}": } notify { "The value of old_root_password: $ {old_root_password}": } }
Everything should be setup to notify the value of a couple of parameters. Now, to test it out…
Testing data-in-modules
Let’s include the mysql class with puppet apply to see where it’s looking for data:
[root@linux modules]# puppet apply -e 'include mysql' Notice: The value of config_file: /path/from/data_in_modules Notice: /Stage [main]/Mysql/Notify [The value of config_file: /path/from/data_in_modules]/message: defined 'message' as 'The value of config_file: /path/from/data_in_modules' Notice: The value of manage_config_file: true Notice: /Stage [main]/Mysql/Notify [The value of manage_config_file: true]/message: defined 'message' as 'The value of manage_config_file: true' Notice: The value of old_root_password: password_from_data_in_modules Notice: /Stage [main]/Mysql/Notify [The value of old_root_password: password_from_data_in_modules]/message: defined 'message' as 'The value of old_root_password: password_from_data_in_modules' Notice: Finished catalog run in 0.62 seconds
Since I’m running on an operatingsystem whose family is ‘RedHat’ (i.e. CentOS), you can see that the values of all the parameters were pulled from the Hiera data files inside the module. Let’s temporarily change the $osfamily fact value and see what happens:
[root@linux modules]# FACTER_osfamily=Debian puppet apply -e 'include mysql' Notice: The value of config_file: module_default Notice: /Stage [main]/Mysql/Notify [The value of config_file: module_default]/message: defined 'message' as 'The value of config_file: module_default' Notice: The value of old_root_password: module_default Notice: /Stage [main]/Mysql/Notify [The value of old_root_password: module_default]/message: defined 'message' as 'The value of old_root_password: module_default' Notice: The value of manage_config_file: module_default Notice: /Stage [main]/Mysql/Notify [The value of manage_config_file: module_default]/message: defined 'message' as 'The value of manage_config_file: module_default' Notice: Finished catalog run in 0.51 seconds
This time, when I specified a value of Debian for $osfamily, the parameter values were pulled from the declaration in the mysql class definition (i.e. from inside mysql/manifests/init.pp ).
Testing outside of Puppet
One of the big pros of Hiera is that it comes with the hiera binary that can be run from the command line to test values. This works just fine for site-specific module data that’s defined in the central hiera.yaml file that’s usually defined in /etc/puppet or /etc/puppetlabs/puppet, but the data-in-modules pattern relies on a Puppet indirector to point to the current module’s data folder, and thus (as of right now) there’s not a simple way to run the hiera binary to pull data out of modules WITHOUT running Puppet. This is not a dealbreaker, and doesn’t stop anybody from hacking up something that WILL look inside modules for data, but as of right now it doesn’t yet exist. It also makes debugging for values that come out of modules a bit more difficult.
The scorecard for data-in-modules
Pros:
Parameters are defined in YAML and not Puppet DSL (i.e. you only need to know YAML and not the Puppet DSL)
Adding parameters is as simple as adding another YAML file to the module
Module authors provide module data that can be read by Puppet 3.x.x Hiera data bindings
Cons:
Must be using Puppet 3.0.0 or higher
Additional hierarchy and additional Hiera data file to consult when debugging
Not (currently) an easy/straightforward way to use the hiera binary to test values
Currently depends on a Puppet Forge module being installed on your system
What are you trying to say?
I am ALL ABOUT code portability, re-usability, and not building 500 apache modules. Ever since people have been building modules, they’ve been putting too much data inside modules (to the point where they can’t share them with anyone else). I can’t tell you how many times I’ve heard “We have a module for that, but I can’t share it because it has all our company-specific data in it.”
Conversely, I’ve also seen organizations put EVERYTHING in their site-specific Hiera datastore because “that’s the place for Puppet data.” They usually end up with 15+ levels in their Hiera hierarchies because they’re doing things like this:
hiera.yaml
1 2 3 4 5 6 7 8 9 10 11 12
--- :backends: - yaml :hierarchy: - "% {clientcert}" - "% {environment}" - "% {osfamily}" - "% {osfamily}/% {operatingsystem}" - "% {osfamily}/% {operatingsystem}/% {os_version_major}" - "% {osfamily}/% {operatingsystem}/% {os_version_minor}" # Repeat until you have 15 levels of WTF
This leads us back again to “What does and DOESN’T go in Hiera?” I usually say the following:
Data in site-specific Hiera datastore
Business-specific data (i.e. internal NTP server, VIP address, per-environment java application versions, etc…)
Sensitive data
Data that you don’t want to share with anyone else
Data that does NOT go in the site-specific Hiera datastore
OS-specific data
Data that EVERYONE ELSE who uses this module will need to know (paths to config files, package names, etc…)
Basically, if I ask you if I can publish your module to the Puppet Forge , and you object because it has business-specific or sensitive data in it, then you probably need to pull that data out of the module and put it in Hiera.
The recommendations that I give when I go on-site with Puppet users is the following:
Use Roles/Profiles to create wrapper-classes for class declaration
Do ALL Hiera lookups for site-specific data inside your ‘Profile’ wrapper classes
All module-specific data (like paths to config files, names of packages to install, etc…) should be kept in the module in the params class
All ‘Role’ wrapper classes should just include ‘Profile’ wrapper classes – nothing else
But what about Data in Modules?
I went through all the trouble of writing up the Data in Modules pattern, but I didn’t recommend or even MENTION it in the previous section. The reason is NOT because I don’t believe in it (I actually think the future will be data outside of the DSL inside a Puppet module), the reason is because it’s not YET in Puppet’s core and because it’s not YET been widely tested. If you’re an existing Puppet user that’s been looking for a way to split data outside of the DSL, here is your opportunity. Use the pattern and PLEASE report back on what you like and don’t like about it. The functionality is in a module, so it’s easy to tweak. If you’re new to Puppet and are comfortable with the DSL, then the params class exists and is available to you.
To voice your opinion or to follow the progress of data in modules, follow or comment on this Puppet ticket.
Update
R.I. posted another article on the problem with params.pp that is worth reading. He gives compelling reasons on why he built Hiera, why params.pp WORKS, but also why he believes it’s not the future of Puppet. R.I. goes even further to explain that it’s not necessarily the Puppet DSL that is the barrier to entry, it’s that this sort of data belongs in a file for config data and not INSIDE THE CODE itself (i.e. inside the Puppet DSL). Providing data inside modules gives module authors a way to provide this configuration data in files that AREN’T the Puppet DSL (i.e. not inside the code).
Comments |
msmarco_passage_01_386602609 | What Happened to Sean Kingston - 2018 Update - Gazette Review | What Happened to Sean Kingston - 2018 Update - Gazette Review
Entertainment
What Happened to Sean Kingston – 2018 Update
By
Jake Briscoe
-
March 14th, 2017
Sean Kingston is known for being one of the more popular hip-hop artists in the mainstream industry. During the late 2000’s and early 2010’s, he was regularly cranking out tracks that charted well and that people greatly enjoyed. Over the course of his career, Sean Kingston has been able to collaborate with well-known musical artists like T-Pain, Dr. Dre, Kanye West, and Nicki Minaj. I think it’s safe to say that most people who are closely familiar with pop music have at least heard of this guy. However, Sean Kingston has gone kind of quiet in recent years. If you just listen to pop music that plays on the radio, you may have gone a while without hearing from him. What happened to him? Is Sean Kingston still making music? In this article, I plan on answering both of those questions, among others. I’m going to be briefly summarizing Sean’s rise to fame while also providing his fans with an update regarding his more recent work. Without further ado, let’s see what we can find out about this hip-hop star.
Sean Kingston’s Early Life and Career
Sean Kingston, also known by his birth name of Kisean Anderson, was born in February of 1990 in Miami, Florida. Miami is obviously a place with a very prominent musical scene, but Kisean didn’t end up staying there very long. He and his family moved to Jamaica when he was just six years old, and his time in the country would inform a lot of his later work. Anderson would attend high school in Ocho Rios, a town on the northern coast of Jamaica. Believe it or not, Kingston was influenced by music at a very young age due to his familial ties to the industry. His grandfather is Lawrence Lindo, a Jamaican producer who is perhaps better known under his stage name Jack Ruby. Jack Ruby is best known for his work with artists like Burning Spear, Foundation, and Link and Chain. With this kind of connection to music, it’s no surprise that he was drawn to the craft at such a young age.
Sean Kingston was first discovered through his Myspace page. (Although no one really uses Myspace anymore, it used to be very similar to YouTube in that it was a place that aspiring artists went in order to be discovered.) Sean was found by Tommy Rotem, who worked for Beluga Heights Records at the time. Beluga Heights is also known for being the label to have discovered Jason Derulo. In 2007, Kingston recorded the single “Beautiful Girls”. It was released in May of 2007, and it was an international success. It became a massive hit in the United States, but it was also highly popular in Australia, Canada, Ireland, Hungary, and several other countries. Due to this sudden success, Kingston was given the opportunity to tour with a few other popular mainstream artists, like Kelly Clarkson, Gwen Stefani, and Beyoncé.
Sean didn’t seem all too interested in being a one hit wonder, and so he went right to work on his album. He released Tomorrow in September of 2009, and it featured a couple of successful singles. The album’s lead single “Fire Burning” was hugely popular, and it has been a two time platinum hit in the United States. Needless to say, with the release of this single, Kingston had become a serious commercial hit. In August, the album was also preceded by the release of the single “Face Drop”, which admittedly wasn’t quite as popular as “Fire Burning”. Outside of those songs, not many people know this but Sean Kingston also co-wrote the song “Whatcha Say”, which is considered to be the breakout hit of the musical artist Jason Derulo.
Sean Kingston and Back 2 Life
Following Kingston’s success in Tomorrow, he got right back to making music. The album’s first single was “Eenie Meenie”, a collaboration with Justin Bieber. Although Justin Bieber has a decent relationship with the hip-hop community today, back in 2010 he had yet to shed his “pretty boy” image. As a result, this collaboration was met with controversy in the overall industry. A lot of people looked down on Sean for being willing to collaborate with such an artist. In August of 2010, he released the song “Letting Go (Dutty Love)”, which featured Nicki Minaj. This song kind of coincided with Nicki Minaj’s meteoric rise to fame, and it was commercially and critically successful. Sean was showing a real talent at creating hit singles. Later that year, Sean Kingston would go on to release a couple of other songs, including “Dumb Love” and “Party All Night (Sleep All Day)”.
Despite the controversy that he faced for collaborating with Justin Bieber in “Eenie Meenie”, he indicated an interest in collaborating even further with the artist. The pair planned on creating a mixtape entitled Our World, which was going to feature new versions of songs like “Pretty Boy Swag” and “Billionaire”. Our World was finished, and it had around 12-14 songs when it was. Sean even previewed the mixtape to some of his fans on uStream. However, it was never actually released. Although this mixtape was never released, Kingston still released his first official mixtape in early 2011 as King of Kingz. The tape features collaborations with artists like Justin Bieber, Akon, and Flo Rida. His second studio album, called Back 2 Life, was released in September of 2013.
Beginning in 2014, Sean Kingston was working on his third studio album. He announced in 2014 that he was recording a song with Zendaya on a song called “Heart on Empty”. For whatever reason, this song was never actually released. In early 2015, he was promoting his album through Instagram and his Twitter account. Finally, in September of 2015 he released the album’s lead single “Wait Up”, which was his first song to be released in close to two years. There was a fairly long break following the release of this single, however. Is Sean Kingston still intending on releasing this fourth album? Or has he been discouraged by some of his recent hardship? Let’s check up on this Jamaican artist and see what he has been up to.
What’s Sean Kingston Doing Now in 2018 – Recent Updates
A recent picture of Sean Kingston in 2017, on the cover of his upcoming EP Made in Jamaica.
As of now, Sean Kingston is still intending on releasing a fourth studio album. In 2016, he released music videos for two more songs to come from the album: “One Way” and “All I Got”. The video for “One Way” was released in January and the video for “All I Got” was released in March. As of this writing, the album was yet to receive an official release date or even a title of any kind. Very recently, Sean Kingston was begun work on his Made in Jamaica EP. Just a short while ago, he released the first track off of this EP: “CHANCE”. This track features Vybz Kartel, and it currently has tens of thousands of listens on Sean Kingston’s Soundcloud account. Although he may not get the same mainstream media coverage that he used to get, Sean Kingston is still definitely working hard to create music. |
msmarco_passage_01_387690323 | Realm of Graphic Design History: #6: Heroic Realism | Realm of Graphic Design History: #6: Heroic Realism
Realm of Graphic Design History
Wednesday, November 7, 2012
#6: Heroic Realism
In Chapter 14 the material begins to delve more into the aspects of pictorial modernism. The event of the World War II greatly affected the usage of posters as vital tools of graphic communication. Using simplified visual language that could send out a clear, convincing message to a largely unintelligent, fickle public was key. There are many forms of poster designs, but the one that caught my attention was the usage of "Heroic Realism". The style wasn't really expanded in the text (compared to stuff like the Plakatsil) so I thought it'd be a relatively interesting topic to research outside of the reading material.
"Heroic Realism" is an art motif that is generally used as a propaganda strategy. It is popularly and efficiently used by communist/socialist governments in order to control and sway the mentality of their people through emotional visual cues. During the Nazi regimen, Hitler delved away from the abstract poster work of the war and decided to imitate the more literal design style of The Allies' poster work. Hitler strived to appeal to a unintelligent mass of people, and succeeded in controlling their beliefs and mindsets largely through his speeches and manifestos, but also equally as important as through his commissioning of posters that contained elements of "heroic realism". He often portrayed the glorious, Aryan figure as an idol for all the German people to admire and remind them about the goal of the Nazi ideology. Heroic figures, such as celebrities or war heroes, are often idolized and can easily control people's actions. The Nazis purposely created posters that demonstrated strength and honor in a perfect "hero" who's bravery could be best acknowledged through service for his government and self-sacrifice. "Classic" figures that promoted strength and honor united a nationalistic morale amongst the German people.
Similarly to the Nazis, the Americans, British, and other Ally members also used heroic realism to inspire people to join the war. The most popular historical piece could be considered to be the Uncle Sam poster that points at the viewer and convinces them that joining the army is the dignified and right choice to take.
The poster is bursting with nationalistic pride and was extremely successful in convincing many young American men into being recruited into the U.S. Army. It boosted the national morale of the people and inspired them to be more involved in the war. This poster especially reminds me of the Captain America Movie, where Captain America as a young lad sees this exact poster and is immediately motivated to join the army even though he is weak and frail. His desire to be "heroic" is the poster's successful goal for its viewer. Heroic realism tricks people into feeling that glamorous sense of heroism and adrenaline to do something awe-inspiring for the country.
Heroic Realism is timeless; in this present age, aspects of it are still heavily used. For example, U.S. army commercials that showcase the galvanizing and benevolent acts of those in the army as "cool, proud, and adventurous" inspire many young people to join because they want to be respected, admired, and be apart of protecting the country as a "hero". It makes me wonder how easily we can be continued to be swayed by propaganda, and if it's morally ethical to use heroic realism to manipulate our minds, especially since in this era we are less ignorant and more educated about matters.
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(Attached is an advertisement to join the Navy. It's really cool)
< http://webartacademy.com/fine-art-heroic-realism >
< http://www.eyemagazine.com/feature/article/designing-heroes >
< http://www.howarddavidjohnson.com/visionary/mystic.htm >
< http://www.nytimes.com/2008/11/11/business/media/11adco.html >
< http://www.loc.gov/exhibits/treasures/trm015.html >
Posted by gdhistory at 3:17 AM
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#10: Legend of Pop - Peter Max
Doyle Dane Bernbach Advertising Agency
#7: Ben Shahn
#6: Heroic Realism
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msmarco_passage_01_39666636 | Enterocutaneous Fistula: Background, Etiology, Prognosis | Enterocutaneous Fistula: Background, Etiology, Prognosis
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Drugs & Diseases > General Surgery
Enterocutaneous Fistula
Updated: Mar 18, 2020
Author: Vikram Kate, FRCS, MS, MBBS, PhD, FACS, FACG, FRCS (Edin), FRCS (Glasg), FIMSA, MAMS, MASCRS, FFST (Ed); Chief Editor: John Geibel, MD, MSc, DSc, AGAF more...
Sections
Enterocutaneous Fistula
Sections Enterocutaneous Fistula
Overview
Background
Etiology
Prognosis
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Presentation
History and Physical Examination
Complications
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Workup
Laboratory Studies
Imaging Studies
Other Tests
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Treatment
Approach Considerations
Conservative Therapy
Surgical Therapy
Postoperative Care
Other Interventions
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Media Gallery
References
Overview
Background
A fistula is an abnormal communication between two epithelialized surfaces; an enterocutaneous fistula (ECF), as the name indicates, is an abnormal communication between the small or large bowel and the skin. An ECF can arise from the duodenum, jejunum, ileum, colon, or rectum. (See the image below.)
Almost healed wound around an enterocutaneous fistula.
View Media Gallery
Although fistulas arising from other regions of the gastrointestinal (GI) tract (eg, stomach and esophagus) may sometimes be included in the definition of ECF, the discussion in this article is limited to the conventional definition of this condition. A fistula-in-ano, though anatomically an ECF, conventionally is not referred to as such, because its presentation and management are different.
An ECF, which is classified as an external fistula (as opposed to an internal fistula, which is an abnormal communication between two hollow viscera), is a complication that is usually seen after surgery on the small or large bowel. In one study, about 95% of ECFs were postoperative, and the ileum was the most common site of ECF [ 1] ; 49% of fistulas were high-output, and 51% were low-output.
ECFs are a common presentation in general surgical wards, and despite advances in the management of these lesions, they are still responsible for a significant mortality (5-20%), attributable to associated sepsis, nutritional abnormalities, and electrolyte imbalances.
Understanding the pathophysiology of, as well as the risk factors for, ECFs should help to reduce their occurrence. Moreover, the well-established treatment guidelines for these lesions, along with some newer treatment options, should help clinicians achieve better outcomes in patients with an ECF.
Treatment of ECFs continues to be a difficult task. The problems associated with an intestinal wound breakdown were mentioned as early as 53 BCE, by Celsus, who stated that “the large intestine can be sutured, not with any certain assurance, but because this doubtful hope is preferable to certain despair; for occasionally it heals up."
In the mid-19th century, John Hunter also described the difficulties in treating ECFs, insisting that "in such cases nothing is to be done but dressing the wound superficially, and when the contents of the wounded viscus become less, we may hope for a cure."
In a landmark article, Edmunds et al provided a comprehensive discussion of ECF. Of 157 patients in the study, 67 developed ECF following surgery. Important complications of ECF included fluid and electrolyte imbalance, malnutrition, and generalized peritonitis. Mortality was 62% in patients with gastric and duodenal fistulas, 54% in patients with small-bowel fistulas, and 16% with colonic fistulas. [ 2]
Zhou et al described a novel technique of using the orchid Bletilla striata in the closure of ECF. [ 3] In a case of ECF following colonic neoplasm resection managed conservatively, application of B striata led to spontaneous closure of the fistula. This plant was found to suppress inflammation and promote wound healing.
Next: Etiology
Etiology
An ECF can occur as a complication following any type of surgery on the GI tract. Indeed, more than 75% of all ECFs arise as a postoperative complication, whereas about 15-25% result from abdominal trauma or occur spontaneously in relation to cancer, irradiation, inflammatory bowel disease (IBD), or ischemic or infective conditions. The etiology of ECFs can thus be characterized as postoperative, traumatic, or spontaneous.
Postoperative
Postoperative causes of ECFs include the following:
Disruption of anastomosis
Inadvertent enterotomy - Occurs especially in patients with adhesions, when dissection can cause multiple serosal tears and an occasional full-thickness tear
Inadvertent small-bowel injury - Occurs during abdominal closure, especially after ventral hernia repair
Disruption of anastomosis can result from inadequate blood flow due to an improper vascular supply, especially when extensive mesenteric vessels have to be ligated. Tension on anastomotic lines following colonic resection, restoration of continuity without adequate mobilization, or a minimal leak or infection can lead to perianastomotic abscess formation, resulting in disruption, as seen in patients with anterior resection for rectal carcinoma. In addition, if anastomosis is performed in an unhealthy bowel (eg, diseased, ischemic), it can lead to disruption and cause an ECF.
Inadvertent picking up of the bowel during abdominal closure can result in a small-bowel fistula; this especially can occur with the use of open inlay mesh or intraperitoneal onlay mesh repair by the laparoscopic method, when the viscera comes in contact with the mesh, leading to adhesions and sometimes to disruption.
Gastroduodenal fistulas are seen most often after surgery for perforated peptic ulcer, especially in developing countries, where perforated peptic ulcer is more common. In patients with a perforated duodenal ulcer, when the perforation is large, extensive contamination is present. When the duration between perforation and surgery is long, there is a high possibility of a postoperative leak, leading to a lateral duodenal fistula. This problem is difficult to treat, and mortality is high. Other causes of gastroduodenal leak include surgery for stomach and the biliary tract mcancers.
A colocutaneous fistula can develop after colonic surgery, especially when the blood supply to a low colorectal/anal anastomosis is compromised or when there is tension at the anastomotic suture line. This type of fistula can also result from diseases of the colon, such as IBD or malignancy leading to perforation, pericolic abscess formation, and ECF.
Surgery for appendicitis, appendicular perforation at the base, or drainage of an appendicular abscess can also lead to a colocutaneous fistula. Radiation therapy is also another major cause of colonic fistula. [ 4] In rare cases, migration of a polypropylene or composite mesh from a hernia repair can lead to ECF formation [ 5, 6]
Traumatic
Traumatic ECF results from iatrogenic surgical trauma to the bowel that may or may not be recognized. Road traffic accidents with injury to the gut can also lead to an ECF. [ 7]
Spontaneous
Spontaneous causes of ECF, seen in about 15-25% of cases, include the following:
Malignancy
Radiation enteritis with perforation
Intra-abdominal sepsis
IBD (eg, Crohn disease [ 4] )
Ulcerative colitis (UC) can also lead to spontaneous ECF, but most cases of ECF associated with this IBD occur as a postoperative complication of restorative proctocolectomy. [ 8] Rarely, inadvertent incision of a malignant tumor can lead to an ECF (see the image below). In this patient, a urachal tumor was inadvertently incised when the patient underwent an appendectomy by midline incision. The patient presented with ECF (colocutaneous fistula) as the urachal tumor that ulcerated on the abdominal wall postoperatively had also infiltrated the sigmoid colon.
Postoperative malignant enterocutaneous fistula.
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A duodenal fistula can occur in association with a perforated duodenal ulcer, but again, it most often arises postoperatively, resulting from a leak.
Previous
Next: Etiology
Prognosis
ECF is a common condition in most general surgical wards. Mortality has fallen significantly since the late 1980s, from as high as 40-65% to as low as 5-20%, largely as a result of advances in intensive care, nutritional support, antimicrobial therapy, wound care, and operative techniques. [ 9, 10] Even so, the mortality is still high, in the range of 30-35%, in patients with high-output ECFs.
Once a patient develops an ECF, the morbidity associated with the surgical procedure or the primary disease increases, affecting the patient's quality of life, lengthening the hospital stay, and raising the overall treatment cost. Malnutrition, sepsis, and fluid electrolyte imbalance are the primary causes of mortality in patients with an ECF.
Another factor that may be a predictor for poor healing outcomes is psoas muscle density, which can reflect sarcopenia. [ 11] Assessment of psoas muscle density can identify patients with ECF who will have poorer outcomes, and these patients may benefit from additional interventions and recovery time before operative repair.
If sepsis is not controlled, progressive deterioration occurs and patients succumb to septicemia. Other sepsis-related complications include intra-abdominal abscess, soft-tissue infection, and generalized peritonitis. [ 12]
However, patients with an ECF with favorable factors for spontaneous closure have a good prognosis and a lower mortality.
Favorable factors for spontaneous closure
Spontaneous closure of an ECF is determined by certain anatomic factors. Fistulas that have a good chance of healing include the following:
End fistulas (eg, those arising from leakage through a duodenal stump after Pólya gastrectomy)
Jejunal fistulas
Colonic fistulas
Continuity-maintained fistulas - These allow the patient to pass stool
Small-defect fistulas
Long-tract fistulas
In addition, a fistulous tract of more than 2 cm has a higher possibility of spontaneous closure. Spontaneous closure is also possible if the bowel-wall disruption is partial and other factors are favorable. If the disruption is complete, surgical intervention is necessary to restore intestinal continuity.
Unfavorable factors for spontaneous closure
When an ECF is associated with adverse factors, then spontaneous closure does not commonly occur, and surgical intervention, despite its associated risks, is frequently required. In these patients, the outcome is less likely to be good. [ 13]
Factors preventing the spontaneous closure of an ECF can be remembered by using the acronym FRIEND, which represents the following [ 14] :
F oreign body
R adiation
I nflammation/infection/IBD
E pithelialization of the fistula tract
N eoplasm
D istal obstruction - A distal obstruction prevents the spontaneous closure of an ECF, even in the presence of other favorable factors; if present, surgical intervention is needed to relieve the obstruction
In addition, lateral duodenal, ligament of Treitz, and ileal fistulas have less tendency to spontaneously close. [ 12]
Excoriation
Skin excoriation (see the image below) is one of the complications that can lead to significant morbidity in patients with ECF. When the enteric contents are more fluid than solid, this becomes a difficult problem; the skin excoriation makes it difficult to put a collecting bag or dressings over the fistula, and more leakage leads to an increase in the excoriation.
Enterocutaneous fistula with severe skin excoriation.
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Previous
Clinical Presentation
References
Kumar P, Maroju NK, Kate V. Enterocutaneous fistulae: etiology, treatment, and outcome - a study from South India. Saudi J Gastroenterol. 2011 Nov-Dec. 17 (6):391-5. [Medline]. [Full Text].
EDMUNDS LH Jr, WILLIAMS GM, WELCH CE. External fistulas arising from the gastro-intestinal tract. Ann Surg. 1960 Sep. 152:445-71. [Medline]. [Full Text].
Zhou H, Jin Y, Gu C, Chen Y, Xia J. Bletilla striata promotes the healing of enterocutaneous fistula: A case report. Medicine (Baltimore). 2019 Jul. 98 (27):e16288. [Medline]. [Full Text].
Berry SM, Fischer JE. Classification and pathophysiology of enterocutaneous fistulas. Surg Clin North Am. 1996 Oct. 76 (5):1009-18. [Medline].
Bostanci O, Idiz UO, Yazar M, Mihmanli M. A Rare Complication of Composite Dual Mesh: Migration and Enterocutaneous Fistula Formation. Case Rep Surg. 2015. 2015:293659. [Medline].
Al-Subaie S, Al-Haddad M, Al-Yaqout W, Al-Hajeri M, Claus C. A case of a colocutaneous fistula: A rare complication of mesh migration into the sigmoid colon after open tension-free hernia repair. Int J Surg Case Rep. 2015. 14:26-9. [Medline].
Fischer PE, Fabian TC, Magnotti LJ, Schroeppel TJ, Bee TK, Maish GO 3rd, et al. A ten-year review of enterocutaneous fistulas after laparotomy for trauma. J Trauma. 2009 Nov. 67 (5):924-8. [Medline].
Regadas FS, Pinto RA, Murad-Regadas SM, Canedo JA, Leal M, Nogueras JJ, et al. Short-term outcome of infliximab and other medications on patients with inflammatory bowel disease undergoing ileostomy reversal. Colorectal Dis. 2011 May. 13 (5):555-60. [Medline].
Falconi M, Sartori N, Caldiron E, Salvia R, Bassi C, Pederzoli P. Management of digestive tract fistulas. A review. Digestion. 1999. 60 Suppl 3:51-8. [Medline].
Dudrick SJ, Maharaj AR, McKelvey AA. Artificial nutritional support in patients with gastrointestinal fistulas. World J Surg. 1999 Jun. 23 (6):570-6. [Medline].
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Rahbour G, Siddiqui MR, Ullah MR, Gabe SM, Warusavitarne J, Vaizey CJ. A meta-analysis of outcomes following use of somatostatin and its analogues for the management of enterocutaneous fistulas. Ann Surg. 2012 Dec. 256 (6):946-54. [Medline].
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Schecter WP. Management of enterocutaneous fistulas. Surg Clin North Am. 2011 Jun. 91 (3):481-91. [Medline].
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Media Gallery
Almost healed wound around an enterocutaneous fistula.
Fistulogram showing enterocutaneous fistula.
Fistulogram showing a colocutaneous fistula following anastomotic leak after colostomy closure.
Intubation of fistulous tract with drain.
Zinc oxide cream for skin protection.
Zinc oxide cream barrier around enterocutaneous fistula, with the fistula opening seen.
Eversion of mucosa in an enterocutaneous fistula, an unfavorable condition for spontaneous closure.
Enterocutaneous fistula with severe skin excoriation.
Postoperative malignant enterocutaneous fistula.
Fistula tract being excised.
Wound manager.
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Contributor Information and Disclosures
Author
Vikram Kate, FRCS, MS, MBBS, PhD, FACS, FACG, FRCS (Edin), FRCS (Glasg), FIMSA, MAMS, MASCRS, FFST (Ed) Professor of General and Gastrointestinal Surgery and Senior Consultant Surgeon, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), India
Vikram Kate, FRCS, MS, MBBS, PhD, FACS, FACG, FRCS (Edin), FRCS (Glasg), FIMSA, MAMS, MASCRS, FFST (Ed) is a member of the following medical societies: American College of Gastroenterology, American College of Surgeons, American Society of Colon and Rectal Surgeons, Fellow of the Faculty of Surgical Trainers (RCSEd), Royal College of Physicians and Surgeons of Glasgow, Royal College of Surgeons of Edinburgh, Royal College of Surgeons of England, Society for Surgery of the Alimentary Tract, Fellow of the Faculty of Surgical Trainers (RCSEd)
Disclosure: Nothing to disclose.
Coauthor (s)
Mohsina Subair, MBBS, MS (GenSurg), MRCS (Edin) Senior Resident, Department of Plastic and Reconstructive Surgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Mohsina Subair, MBBS, MS (GenSurg), MRCS (Edin) is a member of the following medical societies: Association of Surgeons of India, Royal College of Surgeons of Edinburgh, Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.
Gurushankari Balakrishnan, MBBS Junior Resident Physician, Department of Surgery, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), India
Gurushankari Balakrishnan, MBBS is a member of the following medical societies: Association of Minimal Access Surgeons of India, Association of Surgeons of India, Medical Council of India, Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.
Chief Editor
John Geibel, MD, MSc, DSc, AGAF Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow; Fellow of the Royal Society of Medicine
John Geibel, MD, MSc, DSc, AGAF is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.
Acknowledgements
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Reference Salary Employment
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msmarco_passage_01_398055015 | Netherlands - Geography, Government and History | Netherlands - Geography, Government and History
Humanities › Geography
Geography of the Netherlands
Learn All about the Kingdom of the Netherlands
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Geography
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Population
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By
Amanda Briney
Geography Expert
M.A., Geography, California State University - East Bay
B.A., English and Geography, California State University - Sacramento
Amanda Briney, M.A., is a professional geographer. She holds a Certificate of Advanced Study in Geographic Information Systems (GIS) from California State University.
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Amanda Briney
Updated October 03, 2019
The Netherlands, officially called the Kingdom of the Netherlands, is located in northwest Europe. The Netherlands borders the North Sea to its north and west, Belgium to the south, and Germany to the east. The capital and largest city in the Netherlands is Amsterdam, while the seat of government and therefore most government activity is in the Hague. In its entirety, the Netherlands is often called Holland, while its people are referred to as Dutch. The Netherlands is known for its low-lying topography and dikes, along with its liberal government.
Fast Facts: Netherlands
Official Name: Kingdom of the Netherlands
Capital: Amsterdam
Population: 17,151,228 (2018)
Official Language: Dutch
Currency: Euro (EUR)
Form of Government: Parliamentary constitutional monarchy
Climate: Temperate; marine; cool summers and mild winters
Total Area: 16,040 square miles (41,543 square kilometers)
Highest Point: Vaalserberg at 1,056 feet (322 meters)
Lowest Point: Zuidplaspolder at –23 feet (–7 meters)
History of the Netherlands
In the first century BCE, Julius Caesar entered the Netherlands and found that it was inhabited by various Germanic tribes. The region was then divided into a western portion that was inhabited mainly by Batavians while the east was inhabited by the Frisians. The western part of the Netherlands became a part of the Roman Empire.
Between the fourth and eighth centuries, the Franks conquered what is today the Netherlands and the area was later given to the House of Burgundy and the Austrian Habsburgs. In the 16th century, the Netherlands were controlled by Spain but in 1558, the Dutch people revolted and in 1579, the Union of Utrecht joined the seven northern Dutch provinces into the Republic of the United Netherlands.
During the 17th century, the Netherlands grew in power with its colonies and navy. However, the Netherlands eventually lost some of its importance after several wars with Spain, France, and England in the 17th and 18th centuries. In addition, the Dutch also lost their technological superiority over these nations.
In 1815, Napoleon was defeated and the Netherlands, along with Belgium, became a part of the Kingdom of the United Netherlands. In 1830, Belgium formed its own kingdom and 1848, King Willem II revised the Netherlands' constitution to make it more liberal. From 1849–1890, King Willem III ruled over the Netherlands and the country grew significantly. When he died, his daughter Wilhelmina became queen.
During World War II, the Netherlands was continuously occupied by Germany beginning in 1940. As a result, Wilhelmina fled to London and established a "government in exile." During WWII, over 75% of the Netherlands' Jewish population was killed. In May 1945, the Netherlands was liberated and Wilhelmina returned the country. In 1948, she abdicated the throne and her daughter Juliana was queen until 1980 when her daughter Queen Beatrix took the throne.
Following WWII, the Netherlands grew in strength politically and economically. Today, the country is a large tourist destination and most of its former colonies have gained independence and two (Aruba and the Netherlands Antilles) are still dependent areas.
The Government of the Netherlands
The Kingdom of the Netherlands is considered a constitutional monarchy ( list of monarchs) with a chief of state (Queen Beatrix) and a head of government filling the executive branch. The legislative branch is the bicameral States General with the First Chamber and the Second Chamber. The judicial branch is made up of the Supreme Court.
Economics and Land Use in the Netherlands
The economy of the Netherlands is stable with strong industrial relations and a moderate unemployment rate. The Netherlands is also a European transportation hub and tourism is also increasing there. The largest industries in the Netherlands are agroindustries, metal and engineering products, electrical machinery and equipment, chemicals, petroleum, construction, microelectronics, and fishing. Agricultural products of the Netherlands include grains, potatoes, sugar beets, fruits, vegetables, and livestock.
Geography and Climate of the Netherlands
The Netherlands is known for its very low lying topography and reclaimed land called polders. About half of the land in the Netherlands is below sea level, but polders and dikes make more land available and less prone to flooding for the growing country. There are also some low hills in the southeast but none of them rise above 2,000 feet.
The climate of the Netherlands is temperate and is highly affected by its marine location. As a result, it has cool summers and mild winters. Amsterdam has a January average low of 33 degrees (0.5˚C) and an August high of just 71 degrees (21˚C).
More Facts About the Netherlands
The official languages of the Netherlands are Dutch and Frisian.
The Netherlands has large minority communities of Moroccans, Turks, and Surinamese.
The largest cities in the Netherlands are Amsterdam, Rotterdam, The Hague, Utrecht, and Eindhoven.
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Briney, Amanda. "Geography of the Netherlands." ThoughtCo, Feb. 16, 2021, thoughtco.com/geography-of-the-netherlands-1435240. Briney, Amanda. (2021, February 16). Geography of the Netherlands. Retrieved from https://www.thoughtco.com/geography-of-the-netherlands-1435240 Briney, Amanda. "Geography of the Netherlands." ThoughtCo. https://www.thoughtco.com/geography-of-the-netherlands-1435240 (accessed May 31, 2021).
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msmarco_passage_01_401137071 | Convergent Plate Boundaries - Convergent Boundary | Convergent Plate Boundaries - Convergent Boundary
Home » Teaching Plate Tectonics » Convergent Boundaries
Convergent Plate Boundaries
Teaching
Plate
Tectonics
Teaching Plate Tectonics
Earth's Internal Structure
Divergent Boundary
Convergent Boundary
Transform Boundary
Tectonic Features Map
Convergent plate boundaries are locations where lithospheric plates are moving towards one another. The plate collisions that occur in these areas can produce earthquakes, volcanic activity, and crustal deformation.
Teaching Plate Tectonics
Earth's Internal Structure
Convergent Boundary
Divergent Boundary
Transform Boundary
Tectonic Features Map
Convergent Plate Boundary - Oceanic and Continental Plates
When continental and oceanic plates collide, the thinner and more dense oceanic plate is overridden by the thicker and less dense continental plate. The oceanic plate is forced down into the mantle in a process known as "subduction." As the oceanic plate descends, it is forced into higher temperature environments. At a depth of about 100 miles (160 km), materials in the subducting plate begin to approach their melting temperatures and a process of partial melting begins.
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This partial melting produces magma chambers above the subducting oceanic plate. These magma chambers are less dense than the surrounding mantle materials and are buoyant. The buoyant magma chambers begin a slow ascent through the overlying materials, melting and fracturing their way upwards. The size and depth of these magma chambers can be determined by mapping the earthquake activity around them. If a magma chamber rises to the surface without solidifying, the magma will break through in the form of a volcanic eruption.
The Washington-Oregon coastline of the United States is an example of this type of convergent plate boundary. Here the Juan de Fuca oceanic plate is subducting beneath the westward-moving North American continental plate. The Cascade Mountain Range is a line of volcanoes above the melting oceanic plate. The Andes Mountain Range of western South America is another example of a convergent boundary between an oceanic and continental plate. Here the Nazca Plate is subducting beneath the South American plate.
Visit the Interactive Plate Boundary Map to explore satellite images of convergent boundaries between oceanic and continental plates. Two locations are marked to show this type of plate boundary - the Cascade volcanoes along the Washington-Oregon coast of North America and the Andes mountain range on the western margin of South America.
Effects of a convergent boundary between an oceanic and continental plate include: a zone of earthquake activity that is shallow along the continent margin but deepens beneath the continent; sometimes an ocean trench immediately off shore of the continent; a line of volcanic eruptions a few hundred miles inland from the shoreline; destruction of oceanic lithosphere.
Convergent Plate Boundary - Oceanic
When a convergent boundary occurs between two oceanic plates, one of those plates will subduct beneath the other. Normally the older plate will subduct because of its higher density. The subducting plate is heated as it is forced deeper into the mantle, and at a depth of about 100 miles (150 km) the plate begins to melt. Magma chambers are produced as a result of this melting, and the magma is lower in density than the surrounding rock material. It begins ascending by melting and fracturing its way through the overlying rock material. Magma chambers that reach the surface break through to form a volcanic eruption cone. In the early stages of this type of boundary, the cones will be deep beneath the ocean surface but later grow to be higher than sea level. This produces an island chain. With continued development the islands grow larger, merge, and an elongate landmass is created.
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Japan, the Aleutian Islands, and the Eastern Caribbean islands of Martinique, St. Lucia, and St. Vincent and the Grenadines are examples of islands formed through this type of plate boundary. Visit the Interactive Plate Boundary Map to explore satellite images of these three areas.
Effects that are found at this type of plate boundary include: a zone of progressively deeper earthquakes; an oceanic trench; a chain of volcanic islands; the destruction of oceanic lithosphere.
Convergent Plate Boundary - Continental
This is a difficult boundary to draw. First it is complex and second, it is poorly understood when compared to the other types of plate boundaries. In this type of convergent boundary, a powerful collision occurs. The two thick continental plates collide, and both of them have a density that is much lower than the mantle, which prevents subduction (there may be a small amount of subduction, or the heavier lithosphere below the continental crust might break free from the crust and subduct).
Fragments of crust or continent margin sediments might be caught in the collision zone between the continents, forming a highly deformed melange of rock. The intense compression can also cause extensive folding and faulting of rocks within the two colliding plates. This deformation can extend hundreds of miles into the plate interior.
The Himalaya Mountain Range is the best active example of this type of plate boundary. Visit the Interactive Plate Boundary Map to explore satellite images of the Himalaya Range where the Indian and Eurasian plates are currently in collision. The Appalachian Mountain Range is an ancient example of this collision type and is also marked on the map.
Effects found at a convergent boundary between continental plates include: intense folding and faulting; a broad folded mountain range; shallow earthquake activity; shortening and thickening of the plates within the collision zone.
Contributor: Hobart King
Publisher, Geology.com
Teaching
Plate
Tectonics
Teaching Plate Tectonics
Earth's Internal Structure
Divergent Boundary
Convergent Boundary
Transform Boundary
Tectonic Features Map
Teaching Plate Tectonics
Earth's Internal Structure
Convergent Boundary
Divergent Boundary
Transform Boundary
Tectonic Features Map
More Plate Tectonics
Plate Tectonics Map
Teaching Plate Tectonics
What is the San Andreas Fault?
What Is The Moho?
The East Africa Rift System
What Causes a Tsunami?
How did the Hawaiian Islands Form?
Types of Volcanic Eruptions
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msmarco_passage_01_401209770 | Largest Desert in the World - Desert Map | Largest Desert in the World - Desert Map
Home » Records » Largest Desert
The World's Largest Deserts
A map showing the generalized location of Earth's ten largest deserts and a table of over 20 major deserts.
World desert map: This map shows the generalized location of Earth's ten largest deserts on the basis of surface area. The table at the bottom of this page provides the names, generalized locations, and surface areas of over twenty major deserts. Base map by NOAA.
Sand dunes in the Sahara Desert of Libya: Most people think of deserts as "sandy" landscapes. That is true part of the time. This is a view of sand dunes in the Sahara Desert of Libya - an area known as the Ubari (or Awbari) Sand Sea. Photo copyright iStockphoto / PatrickPoendl.
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What is a Desert?
A desert is a landscape or region that receives very little precipitation - less than 250 mm per year (about ten inches). Approximately 1/3 of Earth's land surface is a desert. There are four different types of deserts based upon their geographic situation: 1) polar deserts, 2) subtropical deserts, 3) cold winter deserts, and 4) cool coastal deserts. As shown on the map above, deserts occur on all of Earth's continents.
The Largest Desert
The two largest deserts on Earth are in the polar areas. The Antarctic Polar Desert covers the continent of Antarctica and has a size of about 5.5 million square miles. The second-largest desert is the Arctic Polar Desert. It extends over parts of Alaska, Canada, Greenland, Iceland, Norway, Sweden, Finland, and Russia. It has a surface area of about 5.4 million square miles.
McMurdo Dry Valleys: The largest deserts on Earth are in the polar regions. This is one of the McMurdo "dry valleys" near Lake Hoare, Antarctica. The Canada Glacier is in the background. Photograph by Peter West, National Science Foundation.
Non-Polar Deserts
The rest of Earth's deserts are outside of the polar areas. The largest is the Sahara Desert, a subtropical desert in northern Africa. It covers a surface area of about 3.5 million square miles. A list of more than twenty of the largest non-polar deserts can be found below.
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Vegetation of the Sonoran Desert in Arizona: Cacti and grasses in Arizona's Sonoran Desert. Photo copyright iStockphoto / vlynder.
The Desert Environment
When most people think of a desert, they imagine a landscape covered with sand and sand dunes. Although many deserts are sand-covered, most are not. Many desert landscapes are rocky surfaces. They are rocky because any sand-size or smaller particles on the surface are quickly blown away. Rocky deserts are barren wind-swept landscapes.
Most deserts receive so little precipitation that surface streams usually only flow immediately after rainfall - unless the stream has a source of water outside of the desert. Streams that enter a desert usually suffer major water losses before they exit. Some of the water is lost to evaporation. Some is lost to transpiration (taken up by plants and then released to the atmosphere from the plants). And, some is lost to infiltration (water soaking into the ground through the bottom of the stream channel).
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Desert Fauna and Flora
The plants and animals that live in a desert must be adapted to the environment. Plants must be very tolerant to intense sun, prolonged periods without precipitation, and have an ability to prevent moisture loss to conditions of severe temperature ranges, dry winds, and low humidity.
Animals must be able to tolerate temperature extremes, temperature ranges, and have an ability to survive with very little water. Many animals adapt to desert conditions by living underground and being active at night.
Major Deserts of the World
Name
Type of Desert
Surface Area
Location
Antarctic
Polar
5.5 million mi²
Antarctica
Arctic
Polar
5.4 million mi²
Alaska, Canada, Greenland, Iceland, Norway, Sweden, Finland, Russia
Sahara
Subtropical
3.5 million mi²
Northern Africa
Arabian
Subtropical
1 million mi²
Arabian Peninsula
Gobi
Cold Winter
500,000 mi²
China and Mongolia
Patagonian
Cold Winter
260,000 mi²
Argentina
Great Victoria
Subtropical
250,000 mi²
Australia
Kalahari
Subtropical
220,000 mi²
South Africa, Botswana, Namibia
Great Basin
Cold Winter
190,000 mi²
United States
Syrian
Subtropical
190,000 mi²
Syria, Iraq, Jordan, Saudi Arabia
Chihuahuan
Subtropical
175,000 mi²
Mexico
Great Sandy
Subtropical
150,000 mi²
Australia
Kara-Kum
Cold Winter
135,000 mi²
Uzbekistan, Turkmenistan
Colorado Plateau
Cold Winter
130,000 mi²
United States
Gibson
Subtropical
120,000 mi²
Australia
Sonoran
Subtropical
120,000 mi²
United States, Mexico
Kyzyl-Kum
Cold Winter
115,000 mi²
Uzbekistan, Turkmenistan, Kazakhstan
Taklamakan
Cold Winter
105,000 mi²
China
Iranian
Cold Winter
100,000 mi²
Iran
Thar
Subtropical
75,000 mi²
India, Pakistan
Simpson
Subtropical
56,000 mi²
Australia
Mojave
Subtropical
54,000 mi²
United States
Atacama
Cool Coastal
54,000 mi²
Chile
Namib
Cool Coastal
13,000 mi²
Angola, Namibia, South Africa
More Earth Extremes
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msmarco_passage_01_401360726 | Igneous Rocks | Pictures of Intrusive and Extrusive Rock Types | Igneous Rocks | Pictures of Intrusive and Extrusive Rock Types
Home » Rocks » Igneous Rocks
Pictures of Igneous Rocks
Photos and Descriptions of Common Intrusive and Extrusive Igneous Rock Types
Article by: Hobart M. King, PhD, RPG
Andesite is a fine-grained, extrusive igneous rock composed mainly of plagioclase with other minerals such as hornblende, pyroxene, and biotite. The specimen shown is about two inches (five centimeters) across.
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What are Igneous Rocks?
Igneous rocks are formed from the solidification of molten rock material. Some form below Earth's surface. Some form on or above Earth's surface. We describe these two basic types:
Intrusive igneous rocks crystallize below Earth's surface, and the slow cooling that occurs there allows large crystals to form. Examples of intrusive igneous rocks are: diabase, diorite, gabbro, granite, pegmatite, and peridotite.
Extrusive igneous rocks erupt onto the surface, where they cool quickly to form small crystals. Some cool so quickly that they form an amorphous glass. These rocks include: andesite, basalt, dacite, obsidian, pumice, rhyolite, scoria, and tuff.
Pictures and brief descriptions of some common igneous rock types are shown on this page.
Dacite is a fine-grained, extrusive igneous rock that is usually light in color. It has a composition that is intermediate between rhyolite and andesite. The specimen shown is about four inches (ten centimeters) across.
Basalt is a fine-grained, dark-colored extrusive igneous rock composed mainly of plagioclase and pyroxene. The specimen shown is about two inches (five centimeters) across.
Diabase is an intrusive igneous rock composed mostly of plagioclase feldspar and pyroxene minerals. The grains in diabase are larger than those in basalt but smaller than those in gabbro. Diabase is used in the construction industry as trap rock or dimension stone. When the diabase contains colorful labradorite crystals, it makes an especially nice architectural stone.
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Gabbro is a coarse-grained, dark-colored, intrusive igneous rock that contains feldspar, pyroxene, and sometimes olivine. The specimen shown above is about two inches (five centimeters) across.
Diorite is a coarse-grained, intrusive igneous rock that contains a mixture of feldspar, pyroxene, hornblende, and sometimes quartz. The specimen shown above is about two inches (five centimeters) across.
Obsidian is a dark-colored volcanic glass that forms from the very rapid cooling of molten rock material. It cools so rapidly that crystals do not form. The specimen shown above is about two inches (five centimeters) across.
Granite is a coarse-grained, light-colored, intrusive igneous rock that contains mainly quartz, feldspar, and mica minerals. The specimen above is about two inches (five centimeters) across.
Peridotite is a coarse-grained intrusive igneous rock that is composed almost entirely of olivine. It may contain small amounts of amphibole, feldspar, quartz, or pyroxene. The specimen shown above is about two inches (five centimeters) across.
Pegmatite is a light-colored, extremely coarse-grained intrusive igneous rock. It forms near the margins of a magma chamber during the final phases of magma chamber crystallization. It often contains rare minerals that are not found in other parts of the magma chamber. The specimen shown above is about two inches (five centimeters) across.
Rhyolite is a light-colored, fine-grained, extrusive igneous rock that typically contains quartz and feldspar minerals. The specimen shown above is about two inches (five centimeters) across.
Pumice is a light-colored vesicular igneous rock. It forms through very rapid solidification of a melt. The vesicular texture is a result of gas trapped in the melt at the time of solidification. The specimen shown above is about two inches (five centimeters) across.
Scoria is a dark-colored, vesicular, extrusive igneous rock. The vesicles are a result of trapped gas within the melt at the time of solidification. It often forms as a frothy crust on the top of a lava flow or as material ejected from a volcanic vent and solidifying while airborne. The specimen shown above is about two inches (five centimeters) across.
Fire Opal is sometimes found filling cavities in rhyolite. Long after the rhyolite has cooled, silica-rich ground water moves through the rock, sometimes depositing gems like opal, red beryl, topaz, jasper, or agate in the cavities of the rock. This is one of many excellent geological photographs generously shared through a Creative Commons License by Didier Descouens.
Unakite is a colorful rock composed of green epidote and pink orthoclase. It is formed when granite, an igneous rock, is metamorphosed by hydrothermal activity. Attractive pieces of unakite are often used to make cabochons, tumbled stones, small sculptures, and other lapidary items. It is named after the Unaka Mountains of eastern Tennessee.
" Trap Rock " is a layman's term for any dark-colored igneous rock that is used to make crushed stone. This crushed stone can be used as road base material, or as an aggregate in concrete or asphalt. The most common types of trap rock are basalt, diabase, gabbro, and peridotite. Image copyright iStockphoto / Brilt.
The best way to learn about rocks is to have a collection of specimens to examine while you study. Seeing and handling the rocks will help you understand their composition and texture much better than reading about them on a website or in a book. The Geology.com store offers inexpensive rock collections that can be mailed anywhere in the United States or U.S. Territories. Mineral collections and instructive books are also available.
Welded Tuff is a rock that is composed of materials that were ejected from a volcano, fell to Earth, and then lithified into a rock. It is usually composed mainly of volcanic ash and sometimes contains larger size particles such as cinders. The specimen shown above is about two inches (five centimeters) across.
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msmarco_passage_01_401365648 | Iron Ore: Sedimentary Rock - Pictures, Definition & More | Iron Ore: Sedimentary Rock - Pictures, Definition & More
Home » Rocks » Sedimentary Rocks » Iron Ore
Iron Ore
What Is Iron Ore, How Does It Form, and What Is It Used For?
Article by: Hobart M. King, PhD, RPG
Iron Ore: A specimen of oolitic hematite iron ore. The specimen shown is about two inches (five centimeters) across.
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What is Iron Ore?
Earth's most important iron ore deposits are found in sedimentary rocks. They formed from chemical reactions that combined iron and oxygen in marine and fresh waters. The two most important minerals in these deposits are iron oxides: hematite (Fe 2 O 3) and magnetite (Fe 3 O 4 ). These iron ores have been mined to produce almost every iron and steel object that we use today - from paper clips to automobiles to the steel beams in skyscrapers.
Banded Iron Formation: Close-up view of a banded iron formation. In this specimen bands of hematite (silver) alternate with bands of jasper (red). This photo spans an area of rock about one foot wide. Photo taken by André Karwath, GNU Free Documentation License.
How Does Iron Ore Form?
Nearly all of Earth's major iron ore deposits are in rocks that formed over 1.8 billion years ago. At that time Earth's oceans contained abundant dissolved iron and almost no dissolved oxygen.
The iron ore deposits began forming when the first organisms capable of photosynthesis began releasing oxygen into the waters. This oxygen immediately combined with the abundant dissolved iron to produce hematite or magnetite.
These minerals deposited on the sea floor in great abundance, forming what are now known as the "banded iron formations." The rocks are "banded" because the iron minerals deposited in alternating bands with silica and sometimes shale. The banding might have resulted from seasonal changes in organism activity.
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Steel Mill: Most iron ore is used to make steel. Here a steel slab is being cut to length in a steel mill. Image copyright iStockphoto / Alfredo Tisi.
What is Iron Ore Used For?
The primary use of iron ore is in the production of iron. Most of the iron produced is then used to make steel. Steel is used to make automobiles, locomotives, ships, beams used in buildings, furniture, paper clips, tools, reinforcing rods for concrete, bicycles, and thousands of other items. It is the most-used metal by both tonnage and purpose.
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msmarco_passage_01_401496154 | Shale: Sedimentary Rock - Pictures, Definition & More | Shale: Sedimentary Rock - Pictures, Definition & More
Home » Rocks » Sedimentary Rocks » Shale
Shale
Shale is the most abundant sedimentary rock and is in sedimentary basins worldwide.
Article by: Hobart M. King, PhD, RPG
Shale: Shale breaks into thin pieces with sharp edges. It occurs in a wide range of colors that include red, brown, green, gray, and black. It is the most common sedimentary rock and is found in sedimentary basins worldwide.
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What is Shale?
Shale is a fine-grained sedimentary rock that forms from the compaction of silt and clay-size mineral particles that we commonly call "mud." This composition places shale in a category of sedimentary rocks known as "mudstones." Shale is distinguished from other mudstones because it is fissile and laminated. "Laminated" means that the rock is made up of many thin layers. "Fissile" means that the rock readily splits into thin pieces along the laminations.
Uses of Shale
Some shales have special properties that make them important resources. Black shales contain organic material that sometimes breaks down to form natural gas or oil. Other shales can be crushed and mixed with water to produce clays that can be made into a variety of useful objects.
Conventional Oil and Natural Gas Reservoir: This drawing illustrates an "anticlinal trap" that contains oil and natural gas. The gray rock units are impermeable shale. Oil and natural gas forms within these shale units and then migrates upwards. Some of the oil and gas becomes trapped in the yellow sandstone to form an oil and gas reservoir. This is a "conventional" reservoir - meaning that the oil and gas can flow through the pore space of the sandstone and be produced from the well.
Conventional Oil and Natural Gas
Black organic shales are the source rock for many of the world's most important oil and natural gas deposits. These shales obtain their black color from tiny particles of organic matter that were deposited with the mud from which the shale formed. As the mud was buried and warmed within the earth, some of the organic material was transformed into oil and natural gas.
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The oil and natural gas migrated out of the shale and upwards through the sediment mass because of their low density. The oil and gas were often trapped within the pore spaces of an overlying rock unit such as a sandstone (see illustration). These types of oil and gas deposits are known as "conventional reservoirs" because the fluids can easily flow through the pores of the rock and into the extraction well.
Although drilling can extract large amounts of oil and natural gas from the reservoir rock, much of it remains trapped within the shale. This oil and gas is very difficult to remove because it is trapped within tiny pore spaces or adsorbed onto clay mineral particles that make up the shale.
Unconventional Oil and Gas Reservoir: This drawing illustrates the new technologies that enable the development of unconventional oil and natural gas fields. In these gas fields, the oil and gas are held in shales or another rock unit that is impermeable. To produce that oil or gas, special technologies are needed. One is horizontal drilling, in which a vertical well is deviated to horizontal so that it will penetrate a long distance of reservoir rock. The second is hydraulic fracturing. With this technique, a portion of the well is sealed off and water is pumped in to produce a pressure that is high enough to fracture the surrounding rock. The result is a highly fractured reservoir penetrated by a long length of well bore.
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Unconventional Oil and Natural Gas
In the late 1990s, natural gas drilling companies developed new methods for liberating oil and natural gas that is trapped within the tiny pore spaces of shale. This discovery was significant because it unlocked some of the largest natural gas deposits in the world.
The Barnett Shale of Texas was the first major natural gas field developed in a shale reservoir rock. Producing gas from the Barnett Shale was a challenge. The pore spaces in shale are so tiny that the gas has difficulty moving through the shale and into the well. Drillers discovered that they could increase the permeability of the shale by pumping water down the well under pressure that was high enough to fracture the shale. These fractures liberated some of the gas from the pore spaces and allowed that gas to flow to the well. This technique is known as " hydraulic fracturing " or "hydrofracing."
Drillers also learned how to drill down to the level of the shale and turn the well 90 degrees to drill horizontally through the shale rock unit. This produced a well with a very long "pay zone" through the reservoir rock (see illustration). This method is known as " horizontal drilling ."
Horizontal drilling and hydraulic fracturing revolutionized drilling technology and paved the way for developing several giant natural gas fields. These include the Marcellus Shale in the Appalachians, the Haynesville Shale in Louisiana and the Fayetteville Shale in Arkansas. These enormous shale reservoirs hold enough natural gas to serve all of the United States' needs for twenty years or more.
Shale in brick and tile: Shale is used as a raw material for making many types of brick, tile, pipe, pottery, and other manufactured products. Brick and tile are some of the most extensively used and highly desired materials for building homes, walls, streets, and commercial structures. Image copyright iStockphoto / Guy Elliott.
Shale Used to Produce Clay
Everyone has contact with products made from shale. If you live in a brick house, drive on a brick road, live in a house with a tile roof, or keep plants in "terra cotta" pots, you have daily contact with items that were probably made from shale.
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Many years ago these same items were made from natural clay. However, heavy use depleted most of the small clay deposits. Needing a new source of raw materials, manufacturers soon discovered that mixing finely ground shale with water would produce a clay that often had similar or superior properties. Today, most items that were once produced from natural clay have been replaced by almost identical items made from clay manufactured by mixing finely ground shale with water.
Rock & Mineral Kits: Get a rock, mineral, or fossil kit to learn more about Earth materials. The best way to learn about rocks is to have specimens available for testing and examination.
Shale Used to Produce Cement
Cement is another common material that is often made with shale. To make cement, crushed limestone and shale are heated to a temperature that is high enough to evaporate off all water and break down the limestone into calcium oxide and carbon dioxide. The carbon dioxide is lost as an emission, but the calcium oxide combined with the heated shale makes a powder that will harden if mixed with water and allowed to dry. Cement is used to make concrete and many other products for the construction industry.
Oil shale: A rock that contains a significant amount of organic material in the form of solid kerogen. Up to 1/3 of the rock can be solid organic material. This specimen is approximately four inches (ten centimeters) across.
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Oil Shale
Oil shale is a rock that contains significant amounts of organic material in the form of kerogen. Up to 1/3 of the rock can be solid kerogen. Liquid and gaseous hydrocarbons can be extracted from oil shale, but the rock must be heated and/or treated with solvents. This is usually much less efficient than drilling rocks that will yield oil or gas directly into a well. Extracting the hydrocarbons from oil shale produces emissions and waste products that cause significant environmental concerns. This is one reason why the world's extensive oil shale deposits have not been aggressively utilized.
Oil shale usually meets the definition of "shale" in that it is "a laminated rock consisting of at least 67% clay minerals." However, it sometimes contains enough organic material and carbonate minerals that clay minerals account for less than 67% of the rock.
Shale core samples: When shale is drilled for oil, natural gas, or mineral resource evaluation, a core is often recovered from the well. The rock in the core can then be tested to learn about its potential and how the resource might be best developed.
Composition of Shale
Shale is a rock composed mainly of clay-size mineral grains. These tiny grains are usually clay minerals such as illite, kaolinite, and smectite. Shale usually contains other clay-size mineral particles such as quartz, chert, and feldspar. Other constituents might include organic particles, carbonate minerals, iron oxide minerals, sulfide minerals, and heavy mineral grains. These "other constituents" in the rock are often determined by the shale's environment of deposition, and they often determine the color of the rock.
Black shale: Organic-rich black shale. Natural gas and oil are sometimes trapped in the tiny pore spaces of this type of shale.
Colors of Shale
Like most rocks, the color of shale is often determined by the presence of specific materials in minor amounts. Just a few percent of organic materials or iron can significantly alter the color of a rock.
Shale gas plays: Since the late 1990s, dozens of previously unproductive black organic shales have been successfully developed into valuable gas fields. See the article: " What is Shale Gas? "
Black and Gray Shale
A black color in sedimentary rocks almost always indicates the presence of organic materials. Just one or two percent organic materials can impart a dark gray or black color to the rock. In addition, this black color almost always implies that the shale formed from sediment deposited in an oxygen-deficient environment. Any oxygen that entered the environment quickly reacted with the decaying organic debris. If a large amount of oxygen was present, the organic debris would all have decayed. An oxygen-poor environment also provides the proper conditions for the formation of sulfide minerals such as pyrite, another important mineral found in most black shales.
The presence of organic debris in black shales makes them the candidates for oil and gas generation. If the organic material is preserved and properly heated after burial, oil and natural gas might be produced. The Barnett Shale, Marcellus Shale, Haynesville Shale, Fayetteville Shale, and other gas-producing rocks are all dark gray or black shales that yield natural gas. The Bakken Shale of North Dakota and the Eagle Ford Shale of Texas are examples of shales that yield oil.
Gray shales sometimes contain a small amount of organic matter. However, gray shales can also be rocks that contain calcareous materials or simply clay minerals that result in a gray color.
Utica and Marcellus Shale: Two black organic shales in the Appalachian Basin are thought to contain enough natural gas to supply the United States for several years. These are the Marcellus Shale and Utica Shale.
Red, Brown, and Yellow Shale
Shales that are deposited in oxygen-rich environments often contain tiny particles of iron oxide or iron hydroxide minerals such as hematite, goethite, or limonite. Just a few percent of these minerals distributed through the rock can produce the red, brown, or yellow colors exhibited by many types of shale. The presence of hematite can produce a red shale. The presence of limonite or goethite can produce a yellow or brown shale.
Green Shale
Green shales are occasionally found. This should not be surprising because some of the clay minerals and micas that make up much of the volume of these rocks are typically a greenish color.
Natural gas shale well: In less than ten years, shale has skyrocketed to prominence in the energy sector. New drilling and well development methods such as hydraulic fracturing and horizontal drilling can tap the oil and natural gas trapped within the tight matrix of organic shales. Image copyright iStockphoto / Edward Todd.
Hydraulic Properties of Shale
Hydraulic properties are characteristics of a rock such as permeability and porosity that reflect its ability to hold and transmit fluids such as water, oil, or natural gas.
Shale has a very small particle size, so the interstitial spaces are very small. In fact they are so small that oil, natural gas, and water have difficulty moving through the rock. Shale can therefore serve as a cap rock for oil and natural gas traps, and it also is an aquiclude that blocks or limits the flow of groundwater.
Although the interstitial spaces in a shale are very small, they can take up a significant volume of the rock. This allows the shale to hold significant amounts of water, gas, or oil but not be able to effectively transmit them because of the low permeability. The oil and gas industry overcomes these limitations of shale by using horizontal drilling and hydraulic fracturing to create artificial porosity and permeability within the rock.
Some of the clay minerals that occur in shale have the ability to absorb or adsorb large amounts of water, natural gas, ions, or other substances. This property of shale can enable it to selectively and tenaciously hold or freely release fluids or ions.
Expansive soils map: The United States Geological Survey has prepared a generalized expansive soils map for the lower 48 states.
Engineering Properties of Shale Soils
Shales and the soils derived from them are some of the most troublesome materials to build upon. They are subject to changes in volume and competence that generally make them unreliable construction substrates.
Landslide: Shale is a landslide-prone rock.
Expansive Soils
The clay minerals in some shale-derived soils have the ability to absorb and release large amounts of water. This change in moisture content is usually accompanied by a change in volume which can be as much as several percent. These materials are called " expansive soils ." When these soils become wet they swell, and when they dry out they shrink. Buildings, roads, utility lines, or other structures placed upon or within these materials can be weakened or damaged by the forces and motion of volume change. Expansive soils are one of the most common causes of foundation damage to buildings in the United States.
Shale delta: A delta is a sediment deposit that forms when a stream enters a standing body of water. The water velocity of the stream suddenly decreases and the sediments being carried settle to the bottom. Deltas are where the largest volume of Earth's mud is deposited. The image above is a satellite view of the Mississippi delta, showing its distributary channels and interdistributary deposits. The bright blue water surrounding the delta is laden with sediment.
Slope Stability
Shale is the rock most often associated with landslides. Weathering transforms the shale into a clay-rich soil which normally has a very low shear strength - especially when wet. When these low-strength materials are wet and on a steep hillside, they can slowly or rapidly move down slope. Overloading or excavation by humans will often trigger failure.
Shale on Mars: Shale is also a very common rock on Mars. This photo was taken by the mast camera of the Mars Curiosity Rover. It shows thinly bedded fissile shales outcropping in the Gale Crater. Curiosity drilled holes into the rocks of Gale Crater and identified clay minerals in the cuttings. NASA image.
Environments of Shale Deposition
An accumulation of mud begins with the chemical weathering of rocks. This weathering breaks the rocks down into clay minerals and other small particles which often become part of the local soil. A rainstorm might wash tiny particles of soil from the land and into streams, giving the streams a "muddy" appearance. When the stream slows down or enters a standing body of water such as a lake, swamp, or ocean, the mud particles settle to the bottom. If undisturbed and buried, this accumulation of mud might be transformed into a sedimentary rock known as "mudstone." This is how most shales are formed.
The shale-forming process is not confined to Earth. The Mars rovers have found lots of outcrops on Mars with sedimentary rock units that look just like the shales found on Earth (see photo).
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msmarco_passage_01_40273851 | Open Inguinal Hernia Repair: Practice Essentials, Background, Indications | Open Inguinal Hernia Repair: Practice Essentials, Background, Indications
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Drugs & Diseases > Clinical Procedures
Open Inguinal Hernia Repair
Updated: May 21, 2021
Author: Vinay Kumar Kapoor, MBBS, MS, FRCS, FAMS; Chief Editor: Kurt E Roberts, MD more...
Sections
Open Inguinal Hernia Repair
Sections Open Inguinal Hernia Repair
Overview
Practice Essentials
Background
Indications
Contraindications
Technical Considerations
Outcomes
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Periprocedural Care
Preprocedural Planning
Equipment
Patient Preparation
Monitoring & Follow-up
Show All
Technique
Approach Considerations
Lichtenstein Tension-Free Mesh Repair
Other Approaches
Postoperative Care
Complications
Show All
Medication
Medication Summary
Local Anesthetics
Local Anesthetic/NSAID Combination
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Analgesics
Show All
Questions & Answers
Media Gallery
References
Overview
Practice Essentials
Inguinal hernia repair is one of the most commonly performed surgical procedures in the world. Most surgeons now prefer to perform a tension-free mesh repair. The Lichtenstein tension-free hernioplasty is currently one of the most popular techniques for repair of inguinal hernias.
The image below depicts the anatomy of the inguinal canal.
Anatomy of inguinal canal.
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Indications and contraindications
The existence of an inguinal hernia has traditionally been considered sufficient reason for operative intervention. However, the following considerations should be taken into account:
Some studies have shown that the presence of a reducible hernia is not, in itself, an indication for surgery and that the risk of incarceration is less than 1%
Symptomatic patients should undergo repair
Even asymptomatic patients who are medically fit should be offered surgical repair
Because of the higher frequency of femoral hernias in women, procedures that provide coverage of the femoral space (eg, laparoscopic repair) at the time of initial operation may be better suited for women as primary repairs
Inguinal hernia repair has no absolute contraindications. However, the following considerations should be taken into account:
Any medical issues should be fully addressed beforehand and the operation delayed accordingly
Patients with elevated American Society of Anesthesiologists (ASA) scores and high operative risk should undergo a full preoperative workup and determination of the risk-to-benefit ratio
Recurrences after a primary posterior technique may be treated with Lichtenstein hernioplasty; recurrences after a primary anterior technique should be treated with TEP, TAPP, or open posterior repair
Asymptomatic reducible direct inguinal hernia in an elderly patient with multiple uncontrollable comorbidities and an elevated ASA score does not require repair and may be left alone for close observation and follow-up
See Overview for more detail.
Preparation
No special equipment is required for inguinal hernia repair. Instruments and materials on hand may include the following:
Syringe
25-Gauge needle
Surgical knife with blade
Mosquito forceps
Dissecting scissors
Polypropylene or polyester mesh
Langenbeck retractors
Adson thumb forceps
Needle holder
Sutures (absorbable or nonabsorbable)
Penrose drain or umbilical tape
Inguinal hernia repair can be performed with the following types of anesthesia:
General
Regional (spinal epidural)
Local (infiltration field block)
For Lichtenstein hernioplasty, local anesthesia is safe and generally preferable. Antibiotic prophylaxis is not routinely indicated in low-risk cases but may be considered when risk factors are present.
See Periprocedural Care for more detail.
Procedure
Inguinal hernia repairs are of the following three general types:
Herniotomy (removal of the hernial sac only)
Herniorrhaphy (herniotomy plus repair of the posterior wall of the inguinal canal)
Hernioplasty (herniotomy plus reinforcement of the posterior wall of the inguinal canal with a synthetic mesh)
The Lichtenstein tension-free mesh repair, which is an example of hernioplasty and is currently one of the most popular open inguinal hernia repair techniques, includes the following components:
Opening of the subcutaneous fat along the line of the incision
Opening of the Scarpa fascia down to the external oblique aponeurosis and visualization of the external inguinal ring and the lower border of the inguinal ligament
Opening of the deep fascia of the thigh and exposure of the femoral canal to check for a femoral hernia
Division of the external oblique aponeurosis from the external ring laterally for up to 5 cm, safeguarding the ilioinguinal nerve
Mobilization of the superior (safeguarding the iliohypogastric nerve) and inferior flaps of the external oblique aponeurosis to expose the underlying structures
Mobilization of the spermatic cord, along with the cremaster, including the ilioinguinal nerve, the genitofemoral nerve, and the spermatic vessels; all of these structures may then be encircled in a Penrose drain or tape
Opening of the coverings of the spermatic cord and identification and isolation of the hernia sac
Inversion, division, resection, or ligation of the sac, as indicated
Placement and fixation of mesh to the edges of the defect or weakness in the posterior wall of the inguinal canal to create a new artificial internal ring, with care taken to allow some laxity to compensate for increased intra-abdominal pressure when the patient stands
Resection of any nerves that are injured or of doubtful integrity
In males, gentle pulling of the testes back down to their normal scrotal position
Closure of spermatic cord layers, the external oblique aponeurosis, subcutaneous tissue, and the skin
Other approaches to open inguinal hernia repair include the following:
Plug-and-patch repair - This adds a polypropylene plug shaped as a cone, which can be deployed into the internal ring after reduction of an indirect sac
Prolene Hernia System (PHS) - This consists of an anterior oval polypropylene mesh connected to a posterior circular component
McVay repair - In this approach, the conjoined (transversus abdominis and internal oblique) tendon is sutured to the Cooper ligament with interrupted nonabsorbable sutures
Bassini repair - This approach involves suturing the transversalis fascia and the conjoined tendon to the inguinal ligament behind the spermatic cord, as well as placing a vertical relaxing incision in the anterior rectus sheath
Shouldice repair - This is a four-layer procedure in which transversalis fascia is incised from the internal ring laterally to the pubic tubercle medially, upper and lower flaps are created and then overlapped with two layers of sutures, and the conjoined tendon is sutured to the inguinal ligament (again in two overlapping layers)
Darn repair - This is a pure-tissue tensionless technique that is performed by placing a continuous suture between the conjoined tendon and the inguinal ligament without approximating the two structures
See Technique for more detail.
Next: Background
Background
Hernias are abnormal protrusions of a viscus (or part of it) through a normal or abnormal opening in a cavity (usually the abdomen). They are most commonly seen in the groin; a minority are paraumbilical or incisional. In the groin, inguinal hernias are more common than femoral hernias.
Inguinal hernias occur in about 15% of the adult population, and inguinal hernia repair is one of the most commonly performed surgical procedures in the world. [ 1] Approximately 800,000 mesh hernioplasties are performed each year in the United States, [ 2] 100,000 in France, and 80,000 in the United Kingdom.
There is morphologic and biochemical evidence that adult male inguinal hernias are associated with an altered ratio of type I to type III collagen. [ 3] These changes lead to weakening of the fibroconnective tissue of the groin and development of inguinal hernias. Recognition of this process led to acknowledgment of the need for prosthetic reinforcement of weakened abdominal wall tissue.
Given the evidence that the use of mesh lowers the recurrence rate, [ 4, 5] as well as the availability of various prosthetic meshes for the reinforcement of the posterior wall of the inguinal canal, most surgeons now prefer to perform a tension-free mesh repair. Accordingly, this article focuses primarily on the Lichtenstein tension-free hernioplasty, which is one of the most popular techniques used for inguinal hernia repair. [ 6, 7]
Types of hernia
An indirect hernia is defined as a defect protruding through the internal or deep inguinal ring, whereas a direct hernia is a defect protruding through the posterior wall of the inguinal canal. To put it in a more anatomic way, an indirect hernia is lateral to the inferior epigastric artery and vein, whereas a direct hernia is medial to these vessels. The Hesselbach triangle is the zone of the inguinal floor through which direct hernias protrude, and its boundaries are the epigastric vessels laterally, the rectus sheath medially, and the inguinal ligament inferiorly. [ 8]
An incomplete hernia is confined to the inguinal canal, whereas a complete hernia comes out of the inguinal canal through the external or superficial ring into the scrotum. Direct hernias are always incomplete, whereas indirect hernias can also be complete.
A sliding inguinal hernia is one in which a portion of the wall of the hernia sac is made up of an intra-abdominal organ. As the peritoneum is stretched and pushed through the hernia defect and becomes the hernia sac, retroperitoneal structures such as the colon or bladder are dragged along with it and thus come to make up one of its walls.
Bilateral pediatric hernias are most commonly indirect hernias and arise because of the patency of the processus vaginalis. Simple ligation of the hernia sac (herniotomy) alone is enough. Surgical treatment of indirect hernias in adults, unlike that in children, requires more than simple ligation of the hernia sac. This is because the patent processus is only part of the story. With time, the internal ring dilates, leaving an adult with what can be a sizable defect in the floor of the inguinal canal; this must be closed in addition to division or reduction of the indirect hernia sac.
A hydrocele is a commonly encountered pathology related to hernias. A communicating hydrocele is, by definition, a form of indirect hernia, albeit with an extremely small defect through which only peritoneal fluid enters the sac but no viscus (eg, omentum or bowel) comes out.
Types of hernia repair
Inguinal hernia repairs may be divided into the following three general types:
Herniotomy (removal of the hernial sac only) - This, by itself, is adequate for an indirect inguinal hernia in children in whom the abdominal wall muscles are normal; formal repair of the posterior wall of the inguinal canal is not required
Herniorrhaphy (herniotomy plus repair of the posterior wall of the inguinal canal) - This may be suitable for a small hernia in a young adult with good abdominal wall musculature; the Bassini and Shouldice repairs are examples of herniorrhaphy
Hernioplasty (herniotomy plus reinforcement of the posterior wall of the inguinal canal with a synthetic mesh) - This is required for large hernias and hernias in middle-aged and elderly patients with poor abdominal wall musculature; the Lichtenstein tension-free mesh repair is an example of hernioplasty
Open vs laparoscopic repair
Although numerous surgical approaches have been developed to treat inguinal hernias, the Lichtenstein tension-free mesh-based repair remains the criterion standard. [ 1] In a Cochrane review comparing mesh with nonmesh open repair, the evidence was sufficient to conclude that the use of mesh was associated with a reduced rate of recurrence. [ 2]
Laparoscopic approaches are feasible in expert hands, but the learning curve for laparoscopic hernia repair is long (200-250 cases), the severity of complications is greater, detailed analyses of cost-effectiveness are lacking, and long-term recurrence rates have not been determined. [ 9] The role of laparoscopic inguinal hernia repair in the treatment of an uncomplicated, unilateral hernia is yet to be resolved.
Nevertheless, transabdominal preperitoneal (TAPP) or totally extraperitoneal (TEP) laparoscopic inguinal hernioplasty may offer specific benefits for some patients, such as those with recurrent hernia after conventional anterior open hernioplasty, those with bilateral hernias, and those undergoing laparoscopy for other clean operative procedures.
A 2014 meta-analysis of seven studies comparing laparoscopic repair with the Lichtenstein technique for treatment of recurrent inguinal hernia concluded that despite the advantages to be expected with the former (eg, reduced pain and earlier return to normal activities), operating time was significantly longer with the minimally invasive technique, and the choice between the two approaches depended largely on the availability of local expertise. [ 10]
For further details on the debate over laparoscopic versus open repair, see Laparoscopic Inguinal Hernia Repair. For information on manual reduction of hernias, see Hernia Reduction.
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Next: Background
Indications
Classically, the existence of an inguinal hernia, in and of itself, has been considered reason enough for operative intervention. However, some studies have shown that the presence of a reducible hernia is not, in itself, an indication for surgery and that the risk of incarceration is less than 1%. [ 11]
Patients experiencing symptoms (eg, pain or discomfort) should undergo repair; however, as many as one third of patients with inguinal hernias are asymptomatic. [ 11] The question of observation versus surgical intervention in this asymptomatic or minimally symptomatic population was addressed in two randomized clinical trials. [ 6, 7] The two trials yielded similar results: After long-term follow-up, no significant difference in hernia-related symptoms was noted, and watchful waiting did not increase the complication rate.
In one study, the substantial patient crossover from the observation group to the surgery arm led the authors to conclude that observation may delay but not prevent surgery. [ 11] This reasoning holds particularly true in the younger patient population. Thus, even an asymptomatic patient, if medically fit, should be offered surgical repair. A long-term follow-up study determined that most patients with a painless inguinal hernia will develop symptoms over time and concluded that surgery is recommended for medically fit patients. [ 12]
Koch et al found that recurrence rates were higher in women and that recurrence was 10 times more likely to be of the femoral variety in women than it was in men. [ 13] Such findings have led some to the conclusion that procedures providing coverage of the femoral space (eg, laparoscopic repair) at the time of initial operation are better suited for women as primary repairs. [ 14]
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Next: Background
Contraindications
Inguinal hernia repair has no absolute contraindications. Just as in any other elective surgical procedure, the patient's medical status must be optimized. Any medical issues (eg, upper respiratory tract or skin infection, poorly controlled diabetes mellitus, chronic constipation, urinary obstruction, persisting cough, obstruction or strangulation, or allergy to local anesthesia or prosthetic devices) should be fully addressed and the operation delayed accordingly.
Patients with elevated American Society of Anesthesiologists (ASA) scores and high operative risk should undergo a full preoperative workup and determination of the risk-to-benefit ratio.
Recurrences after a primary posterior technique (eg, TEP, TAPP, or open posterior repair) may be treated with Lichtenstein hernioplasty. [ 5] Recurrence after a primary anterior technique should preferably be dealt with by means of TEP, TAPP, or open posterior repair.
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Next: Background
Technical Considerations
Anatomy
A useful learning tool for gaining a working knowledge of the inguinal region is to visualize the region as it is surgically approached in the open technique of hernia repair. The inguinal region is part of the anterolateral abdominal wall, which is made up of the following nine layers, from superficial to deep:
Skin
Camper fascia
Scarpa fascia
External oblique aponeurosis
Internal oblique muscle
Transversus abdominis
Transversalis fascia
Preperitoneal fat
Peritoneum
The first layers encountered upon dissection through the subcutaneous tissues are the Camper and Scarpa fasciae. Contained in this space are the superficial branches of the femoral vessels—namely, the superficial circumflex and the epigastric and external pudendal arteries, which can be safely ligated and divided when encountered.
The inguinal canal can be visualized as a tunnel traveling from lateral to medial in an oblique fashion (see the image below). It has a roof facing anteriorly, a floor facing posteriorly, a superior (cranial) wall, and an inferior (caudal) wall. The canal contents (in men, cord structures; in women, the round ligament) are the traffic that traverses the tunnel.
Anatomy of inguinal canal.
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The external oblique aponeurosis serves as the roof of the inguinal canal and opens just lateral to and above the pubic tubercle. This is the external or superficial inguinal ring, which allows the cord structures egress from the inguinal canal to the scrotum. [ 15]
The floor of the canal is composed of the transversus abdominis and the transversalis fascia. The entrance to the inguinal canal is through these layers, and this entrance constitutes the internal or deep inguinal ring.
The inferior wall is the inguinal (Poupart) ligament. This ligament is formed by the lower edge of the external oblique aponeurosis and extends from the anterior superior iliac spine to its attachments at the pubic tubercle and fans out to form the lacunar (Gimbernat) ligament. [ 16, 17] The inguinal ligament folds over itself to form the shelving edge. This folded-over sling of external oblique aponeurosis is the true lower wall of the inguinal canal.
The superior wall consists of a union of the internal oblique muscle and the transversus abdominis aponeurosis, which arches from its attachment at the lateral segment of the inguinal ligament over the internal inguinal ring, ending medially at the rectus sheath and coming together inferomedially to insert on the pubic tubercle, thus forming the conjoined tendon. [ 17, 8]
In males, the contents of the inguinal canal include the obliterated processus vaginalis (which, when patent, forms the sac of the indirect inguinal hernia), the spermatic cord, and the ilioinguinal nerve (which comes out of the superficial inguinal ring along with the spermatic cord). In females, the inguinal canal contains the ilioinguinal nerve and the round ligament of the uterus.
The coverings of the spermatic cord include the following:
Internal spermatic fascia, derived from the transversalis fascia at the deep inguinal ring
Cremaster muscle, derived from the internal oblique muscle at the deep inguinal ring
External spermatic fascia, derived from the external oblique aponeurosis at the superficial inguinal ring (present only in the scrotum and not in the inguinal canal)
The contents of the spermatic cord include the following:
Vas deferens
Testicular artery
Artery of the ductus deferens
Cremasteric artery
Pampiniform plexus
Genital branch of the genitofemoral nerve
Parasympathetic and sympathetic nerves
Lymphatic vessels
The key nerves in the inguinal region are as follows (see the image below):
Iliohypogastric nerve
Ilioinguinal nerve
Genital branch of the genitofemoral nerve
Anatomy of nerves of groin.
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The ilioinguinal nerve runs medially through the inguinal canal along with the cord structures traveling from the internal ring to the external ring. It innervates the upper and medial parts of the thigh, the anterior scrotum, and the base of the penis.
The iliohypogastric nerve runs below the external oblique aponeurosis but cranial to the spermatic cord, then perforates the external oblique aponeurosis cranial to the superficial ring. It innervates the skin above the pubis.
The genital branch of the genitofemoral nerve lies within the spermatic cord and travels with the cremasteric vessels through the inguinal canal. It innervates the cremaster muscle and provides sensory innervation to the scrotum.
Some variations in the anatomic distribution of these nerves may be observed—for instance, the occasional absence of an ilioinguinal nerve. [ 18]
The Hesselbach triangle is bounded by the inguinal ligament below, the lateral border of the rectus abdominis medially, and the inferior epigastric vessels laterally (see the image below). The sac of a direct hernia lies in this triangle, whereas the neck of an indirect hernia sac lies outside the triangle (lateral to the inferior epigastric vessels).
Hesselbach triangle. Image courtesy of Wikimedia Commons.
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Best practices
Lichtenstein open tension-free mesh hernioplasty is suitable for all adult patients, irrespective of age, weight, general health, and the presence of concomitant medical problems. For patients with large scrotal (irreducible) inguinal hernias, those who have undergone major lower abdominal surgery, and those in whom no general anesthesia is possible, the Lichtenstein repair is the preferred surgical technique.
This operation, performed under local anesthesia, is not difficult to learn (learning curve, 5 cases), and trained surgical residents are able to perform it without compromising the patient’s care and long-term outcome. [ 19, 20] The procedure is time-tested, safe, and economical, and it does not involve the long operating time characteristic of laparoscopic repairs. [ 5] In addition, it has a low complication rate and has become the gold standard in open tension-free hernioplasties. [ 21, 22]
Lichtenstein hernioplasty is well suited for smaller community-based, regional, and teaching hospitals, and it offers good immediate and long-term results. Moreover, the excellent results achieved with this repair appear to be unrelated to the surgeons’ level of experience. The technique has been evaluated in large series and has become popular among surgeons all around the world.
In a comparative study of open mesh techniques for inguinal hernia repair, Lichtenstein’s operation was similar to mesh-plug or Prolene Hernia System (PHS; Ethicon, West Somerville, NJ) repair in terms of time to return to work, complications, chronic pain, and hernia recurrence in the short-to-middle term. [ 23] Indeed, postoperative pain after a Lichtenstein hernioplasty is minimal; according to a meta-analysis of all reported randomized studies, the pain is comparable to that occurring after laparoscopic repair. [ 24]
Use of mesh for repair
Emphasizing the Halsted principle of no tension, the Lichtenstein group advocated routine use of mesh in 1984. The prosthesis used to reinforce the weakened posterior wall of the inguinal canal is placed between the transversalis fascia and the external oblique aponeurosis and extends well beyond the Hesselbach triangle. Mesh implants do not actively shrink, but they are passively compressed by the natural process of wound healing. Mesh shrinkage occurs only to the extent to which the tissue contracts.
A mesh with a small pore size is likely to shrink more. Shrinkage of the different types of mesh in vivo is in the range of 20-40%; thus, it is important for the surgeon to ensure that the mesh adequately overlaps the defect on all sides. It is advisable to use a large (eg, 7.5 × 15 cm) sheet of mesh extending approximately 2 cm medial to the pubic tubercle, 3-4 cm above the Hesselbach triangle, and 5-6 cm lateral to the internal ring so as to allow for mesh shrinkage.
Although the use of traditional microporous or heavyweight polypropylene meshes over the past two decades has reduced the recurrence rate after hernia surgery to less than 1%, a major concern has been the formation of a rigid scar plate that causes patient discomfort and chronic pain, impairing quality of life. More than 50% of patients with a large mesh prosthesis in the abdominal wall complain of paresthesia, palpable stiff edges of the mesh, or physical restriction of abdominal wall mobility. [ 4]
It was assumed that the flexibility of the abdominal wall is restricted by implantation of excessive foreign material and by excessive scar tissue formation. A better knowledge of the biomechanics of the abdominal wall and the influence of mesh on those mechanics has led to the current understanding that “less is more.”
In other words, a less-dense, lighter-weight mesh with larger pores, though still stronger than the abdominal wall and thus usable for the purposes of repair, will result in less inflammation, better incorporation, better abdominal wall compliance, greater abdominal wall flexibility, less pain, and possibly less scar contraction; therefore, its use will lead to a better clinical outcome. [ 5, 25]
Lightweight composite mesh was developed in the conviction that the ideal mesh should be just strong enough to handle the pressure of the abdominal wall while remaining as low in mass and as thin as possible. The advantage of increasing the mesh pore size is that it makes it easier for tissue to grow through the pores and thereby create a thinner, better-integrated scar.
The newer lightweight composite meshes offer a combination of thinner filament size, larger pore size, reduced mass, and increased percentage of absorbable material. Thus, less foreign material is implanted, the scar tissue has greater flexibility (with almost physiologic abdominal wall mobility), there are fewer patient complaints, and the patient’s quality of life is better.
The use of lightweight mesh for Lichtenstein hernia repair has not been shown to affect recurrence rates, but it has been found to improve some aspects of pain and discomfort 3 years after surgery. [ 26] According to data from randomized, controlled trials and retrospective studies, light meshes seem to have some advantages with respect to postoperative pain and foreign body sensation. [ 5, 27]
Complication prevention
Since the widespread acceptance of mesh-based repairs and the significant reduction of inguinal hernia recurrence, the most vexing complication of herniorrhaphy has been chronic groin pain. Causalgia syndromes of each of the three nerves of the groin (ilioinguinal, iliohypogastric, and genitofemoral) are well described. [ 17, 8] There remains some controversy as to whether the nerves should be sectioned or preserved. [ 28, 29] Current recommendations favor nerve identification and preservation. [ 14, 30, 31]
The ilioinguinal nerve, which runs anterior to the spermatic cord, can be protected by employing gentle dissection and by isolating the nerve behind a leaf of the incised external oblique aponeurosis with a straight hemostat clamp.
The iliohypogastric nerve can be injured when creating the superior flap of the external oblique aponeurosis and by a bite taken when fixing the mesh to the conjoint tendon.
Another cause of significant postherniorrhaphy pain is the placement of a stitch into the periosteum. This is often the point of maximal postoperative tenderness; accordingly, the surgeon must maneuver with care when anchoring the pubic tubercle bite. [ 32, 33]
Toward the deep inguinal ring, the hernia sac becomes thin and fragile and adheres more closely to the spermatic cord. Caution should be exercised in dissecting the hernia sac to avoid injury to the cord structures and splitting of the neck of the sac. In adults, the rate of vas deferens injury is estimated at 0.3%. To protect against such injury, the surgeon must always remain aware of the posterior location of the vas deferens when dissecting the hernia sac.
If reduction of the hernial sac proves difficult at operation, a sliding hernia should be suspected. The cecum (on the right side), the sigmoid colon (on the left side), and the urinary bladder (on either side) form the wall of the sac of a sliding hernia; they are not the contents of the hernial sac and are not inside the sac. In a sliding hernia, it is difficult to separate the hernial sac from the structures that form its wall; thus, the hernial sac should be reduced en masse along with these structures, without any attempt to separate them from the hernial sac.
In a complete indirect inguinal hernia, which descends into the scrotum, it is not necessary to remove the entire hernial sac; the sac may be transected in the distal inguinal canal, and the distal part of the sac in the scrotum can be left behind. Hemostasis, however, should be ensured at the cut edge of the distal part of the hernial sac to prevent bleeding and scrotal hematoma. In addition, to prevent the formation of a hydrocele, the distal sac should not be closed.
If it is not possible to return the contents of the hernial sac to the peritoneal cavity even after the sac has been opened, a sliding hernia is likely. Because the viscus is not inside the sac but makes up part of the wall of the sac, any attempt to excise the complete sac is likely to injure the viscus. Only that part of the sac that is distal to the sliding viscus should be excised; the sac is then closed, and the remaining sac, along with the viscus, is reduced into the extraperitoneal space.
Inguinal hernia in a child (even a neonate) should be repaired as early as possible; because the neck of the hernia sac is very narrow, the risk of complications is very high. In children, the superficial and deep inguinal rings almost overlap each other, with the result that that the inguinal canal is very short. A very small incision is made over the superficial inguinal ring; there is no need to open the inguinal canal. Herniotomy alone is performed, with the hernia sac divided at the superficial ring.
Vascular injury is a less common but reported and potentially disastrous pitfall. It can be avoided by respecting the proximity of the femoral vessels, particularly when the mesh is being sutured to the inguinal ligament. [ 33] Hematoma formation can be due either to injury of the inferior epigastric vessels or to failure to ligate the superficial subcutaneous veins.
Any aggravating factors (eg, chronic cough, chronic constipation, or urinary straining) should be looked into and controlled, if possible, before any hernia is repaired so as to prevent or reduce postoperative stress on the hernia repair, which may increase the risk of recurrence.
The use of an amply sized (eg, 7.5 × 15 cm) piece of mesh is crucial for minimizing recurrence. It must be large enough to extend 2 cm medial to the pubic tubercle, 3-4 cm above the Hesselbach triangle, and 5-6 cm lateral to the internal ring. It should not be laid under tension, so that its center can achieve a slightly domed configuration, which compensates for the forward protrusion of the transversalis fascia upon standing and for the shrinkage of the mesh over time.
In male patients, a testis may be pulled out of the scrotum while the spermatic cord is being manipulated; accordingly, it is important always to remember to pull the testes gently back down to their normal scrotal position after the procedure is completed.
As in all operations, infection is a concern, but in clinical settings where the rate of wound infection is low (< 5%), there is no indication for the routine use of antibiotic prophylaxis in low-risk patients. However, if any risk factors for wound infection (eg, recurrent hernia, advanced age, diabetes mellitus, immunosuppressive conditions, or expected prolonged operating times) are present, antibiotic prophylaxis should be considered. Such prophylaxis should also be used at centers where high wound infection rates are observed in elective settings. [ 34, 35]
Anticoagulation prophylaxis is generally unnecessary; the duration of the operation is not long, and the patient can be mobilized the same evening.
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Next: Background
Outcomes
Since the widespread acceptance of mesh-based repair, the rate of hernia recurrence has fallen substantially, to 1% or less. Consequently, more attention is being paid to other complications, such as postherniorrhaphy chronic pain. [ 36]
Large studies examining mortality risk from various groin operations found that elective inguinal herniorrhaphy was safe and had a low mortality risk that was similar to or even lower than the standardized mortality in the studied population. [ 1, 37]
Although pain is more common in the acute postoperative period, it remains chronically severe in 3% of patients, having significant effects on their work and social activities. [ 38] A large Swedish study found that 30% of postherniorrhaphy patients reported long-term pain or discomfort, 6% of whom experienced pain intense enough to alter their activities of daily living. [ 39]
Another phenomenon that can be experienced after hernia repair is groin numbness. In a large Scottish study that included more than 5500 patients, this was reported to various degrees in as many as 9%. [ 39]
Other complications include seroma formation, bruising and hematoma (7% of cases), and wound infection (1-7% of cases). [ 1, 40]
Ischemic orchitis leading to testicular atrophy or even necrosis is a catastrophic but well-known complication of inguinal hernia repair. Symptoms include painful testicular swelling and fever commencing 2-3 days after surgery. [ 41] The exact cause of this rare complication is unclear, but it is thought to be secondary to venous thrombosis rather than arterial injury. A high index of suspicion for postoperative ischemic orchitis, in conjunction with emergency testicular ultrasonography, may help avoid orchiectomy.
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Periprocedure
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Akyol C, Kocaay F, Orozakunov E, Genc V, Kepenekci Bayram I, Cakmak A, et al. Outcome of the patients with chronic mesh infection following open inguinal hernia repair. J Korean Surg Soc. 2013 May. 84 (5):287-91. [Medline]. [Full Text].
van Veen RN, Mahabier C, Dawson I, Hop WC, Kok NF, Lange JF, et al. Spinal or local anesthesia in lichtenstein hernia repair: a randomized controlled trial. Ann Surg. 2008 Mar. 247 (3):428-33. [Medline].
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New implant combined with bupivacaine hydrochloride approved for pain after hernia repair. Anesthesiology News. September 4, 2020. Available at https://www.anesthesiologynews.com/Online-First/Article/03-20/New-Implant-Combined-with-Bupivacaine-Hydrochloride-Approved-for-Pain-After-Hernia-Repair/59475.
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Media Gallery
Anatomy of inguinal canal.
Anatomy of nerves of groin.
Open inguinal hernia repair. Skin incision.
Open inguinal hernia repair. Division of external oblique aponeurosis.
Open inguinal hernia repair. Cord structures and hernia sac encircled by Penrose drain.
Open inguinal hernia repair. Hernia sac separated from cord structures.
Open inguinal hernia repair. Development of preperitoneal space.
Open inguinal hernia repair. Deployment of Prolene Hernia System (PHS).
Open inguinal hernia repair. Final position of Prolene Hernia System (PHS) mesh.
Open inguinal hernia repair. Closure of external oblique aponeurosis.
Open inguinal hernia repair. Skin closure.
Open inguinal hernia repair. Draping and incision.
Open inguinal hernia repair. External oblique aponeurosis with external inguinal ring.
Open inguinal hernia repair. External oblique aponeurosis with external inguinal ring.
Open inguinal hernia repair. Reflected part of inguinal ligament exposed for fixing inferior edge of mesh.
Open inguinal hernia repair. Inferior flap of external oblique aponeurosis developed to expose inguinal ligament from pubic tubercle to midinguinal point.
Open inguinal hernia repair. Superior flap of external oblique aponeurosis is developed as high as possible to provide ample space for mesh placement.
Open inguinal hernia repair. Lifting up cord with hernia sac medial to external inguinal ring.
Open inguinal hernia repair. Avascular plane between posterior inguinal wall and cord structures.
Open inguinal hernia repair. Cord structures and hernia sac looped along with ilioinguinal and genitofemoral nerves.
Open inguinal hernia repair. Cremaster muscle picked up to be incised longitudinally between hemostats.
Open inguinal hernia repair. Indirect hernia sac dissected and being separated from lipoma of cord and cord structures.
Open inguinal hernia repair. Lipoma of cord dissected free and excised.
Open inguinal hernia repair. Indirect hernia sac separated from cord structures in midinguinal region toward neck of sac.
Open inguinal hernia repair. Voluminous indirect hernia sac separated from cord structures in midinguinal region up to neck of sac.
Open inguinal hernia repair. Hernia sac being divided near neck.
Open inguinal hernia repair. Contents of hernia sac reduced and proximal end to be sutured closed.
Open inguinal hernia repair. Anterior wall of distal sac incised to prevent hydrocele formation.
Open inguinal hernia repair. Fixation of lower edge of mesh.
Open inguinal hernia repair. First medialmost stitch in mesh, fixed about 2 cm medial to pubic tubercle, where anterior rectus sheath inserts into pubis.
Open inguinal hernia repair. Same suture is utilized as continuous suture to fix lower edge of mesh to reflected part of inguinal ligament up to internal ring.
Open inguinal hernia repair. Lower edge of mesh sutured to inguinal ligament up to internal inguinal ring. To accommodate cord structures, lateral end of mesh is divided into wider upper (two thirds) tail and narrower lower (one third) tail.
Open inguinal hernia repair. Wider upper tail of mesh is passed underneath cord, and mesh is placed posteriorly in inguinal canal behind spermatic cord.
Open inguinal hernia repair. Fixation of upper edge of mesh.
Open inguinal hernia repair. Slit made in mesh to accommodate iliohypogastric nerve. Two interrupted sutures are taken under vision to fix upper edge of mesh while safeguarding iliohypogastric nerve.
Open inguinal hernia repair. Upper tail is crossed over lower tail around spermatic cord, thus creating internal ring. Lower edges of two tails are tucked together to inguinal ligament just lateral to internal ring.
Open inguinal hernia repair. Tails are then passed underneath external oblique aponeurosis to give overlap of about 5 cm beyond internal ring.
Open inguinal hernia repair. External oblique aponeurosis sutured with 2-0 polypropylene.
Open inguinal hernia repair. Subcutaneous tissue approximated with 3-0 plain catgut.
Open inguinal hernia repair. Skin approximated with 2-0 polypropylene subcuticular suture.
Hesselbach triangle. Image courtesy of Wikimedia Commons.
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Contributor Information and Disclosures
Author
Vinay Kumar Kapoor, MBBS, MS, FRCS, FAMS Professor of Surgical Gastroenterology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India
Vinay Kumar Kapoor, MBBS, MS, FRCS, FAMS is a member of the following medical societies: Association of Surgeons of India, Indian Association of Surgical Gastroenterology, Indian Society of Gastroenterology, Medical Council of India, National Academy of Medical Sciences (India), Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.
Specialty Editor Board
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Chief Editor
Kurt E Roberts, MD Assistant Professor, Section of Surgical Gastroenterology, Department of Surgery, Director, Surgical Endoscopy, Associate Director, Surgical Skills and Simulation Center and Surgical Clerkship, Yale University School of Medicine
Kurt E Roberts, MD is a member of the following medical societies: American College of Surgeons, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.
Acknowledgements
Harry L Adler, MD Assistant Clinical Professor of Surgery, Mount Sinai Hospital; Assistant Director and Consulting Physician, Maimonides Medical Center
Harry L Adler, MD is a member of the following medical societies: American College of Physician Executives, American College of Surgeons, and Association for Academic Surgery
Disclosure: Nothing to disclose.
Simon Lavotshkin, MD Staff Physician, Department of Surgery, Maimonides Medical Center; Surgical Research Fellow, Departments of Pediatrics, Cell and Developmental Biology, Weill Medical College of Cornell University
Simon Lavotshkin, MD is a member of the following medical societies: American College of Surgeons and Association for Academic Surgery
Disclosure: Nothing to disclose.
Jerzy M Macura, MD Chief of Advanced Laparoscopic Surgery, Director of Bariatric Surgery, Maimonides Medical Center
Jerzy M Macura, MD is a member of the following medical societies: American Society for Metabolic and Bariatric Surgery, American Society of Abdominal Surgeons, and Society of American Gastrointestinal and Endoscopic Surgeons
Disclosure: Nothing to disclose.
Pradeep Saxena, MBBS, MS Associate Professor, Department of Surgery, Gandhi Medical College, India
Pradeep Saxena, MBBS, MS is a member of the following medical societies: Association of Colon and Rectal Surgeons of India and Association of Surgeons of India
Disclosure: Nothing to disclose.
Danny A Sherwinter, MD Attending Surgeon, Department of Mimially Invasive Surgery and Bariatrics, Associate Program Director, Department of Surgery, Maimonides Medical Center; Director of Minimally Invasive and Bariatric Surgery, American Society for Metabolic and Bariatric Surgery (ASMBS) Center of Excellence
Danny A Sherwinter, MD is a member of the following medical societies: American College of Surgeons, American Society for Metabolic and Bariatric Surgery, Society of American Gastrointestinal and Endoscopic Surgeons, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Acknowledgments
The authors and editors of Medscape Reference thank Karen Medin for her illustrations.
Dr Saxena gratefully acknowledges the contributions of Dr Deepak Krishna, Resident Surgical Officer, and Dr Dinesh Khatri, Resident Surgical Officer, Department of Surgery, Gandhi Medical College and Hamidia Hospital, to the development and writing of this article.
Dr Kapoor would like to express his gratitude to his teachers and trainers, (the late) Prof Atm Prakash and Prof L K Sharma, who taught him the techniques and principles of hernia repair when he was a surgical trainee at the All India Institute of Medical Sciences, New Delhi, India, in the early 1980s.
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Drugs & Diseases > Cardiology
Coronary Artery Atherosclerosis
Updated: Apr 09, 2021
Author: Sandy N Shah, DO, MBA, FACC, FACP, FACOI; Chief Editor: Yasmine S Ali, MD, FACC, FACP, MSCI more...
Sections
Coronary Artery Atherosclerosis
Sections Coronary Artery Atherosclerosis
Overview
Practice Essentials
Background
Anatomy
Pathophysiology
Etiology
Epidemiology
Prognosis
Patient Education
Show All
Presentation
History
Physical Examination
Show All
DDx
Workup
Approach Considerations
Fractional Flow Reserve
Lipid Studies
C-Reactive Protein
Serum Markers
Echocardiography
Nuclear Imaging Studies
Computed Tomography
Electron Beam Computed Tomography
Optical Coherence Tomography Imaging
Magnetic Resonance Imaging
Positron Emission Tomography
Coronary Angiography
Doppler Velocity Probes
Ultrasonography
Histology
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Treatment
Approach Considerations
Preventive Strategies
Treatment of Low HDL levels and High Triglyceride levels in Patients With Diabetes
ACE Inhibitors to Reduce Blood Pressure
Antiplatelet Agents for Acute Coronary Events
Pharmacologic Treatment of Angina
Hormone Therapy Concerns
Antibiotic Therapy in Coronary Artery Atherosclerosis
Revascularization Procedures
European Society of Cardiology Guidelines
Lifestyle Changes
Additional Therapies for Atherosclerosis
Stable Coronary Artery Disease after Intervention
Consultations
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Guidelines
Guidelines Summary
2020 ACC Guidelines on CV Disease Risk Reduction in T2D
2018 ACC Expert Consensus Decision Pathway on Novel Therapies for CV Risk Reduction in TD2 and ASCVD
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Medication
Medication Summary
HMG-CoA Reductase Inhibitors
PCSK9 Inhibitors
Calcium Channel Blocker
ACE Inhibitors
Platelet Aggregation Inhibitors
Polyunsaturated Fatty Acids
Fibric Acid Derivatives
Bile Acid Sequestrants
Antioxidants
Antianginal Agent
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Questions & Answers
Media Gallery
Tables
References
Overview
Practice Essentials
Atherosclerotic coronary heart disease is the single leading cause of death of men and women in the United States and, in fact, around the world. Atherosclerosis is the principal cause of coronary artery disease (CAD), in which atherosclerotic changes are present within the walls of the coronary arteries. See the image below.
Coronary Artery Atherosclerosis. Cardiac catheterization and coronary angiography in the left panel shows severe left anterior descending coronary artery stenosis. This lesion was treated with stent placement in the left anterior descending coronary artery, as observed in the right panel.
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Signs and symptoms
The signs and symptoms of coronary artery atherosclerosis include the following:
Chest pain or pressure
Jaw pain
Shortness of breath
Weakness, fatigue, reduced exertional capacity
Dizziness, palpitations
Leg swelling (when left ventricular dysfunction is present)
Weight gain (when left ventricular dysfunction is present)
Diaphoresis
Stable angina pectoris
Intermittent claudication
Tachycardia: Common in persons with acute coronary syndrome (ACS) and acute myocardial infarction (AMI)
Atrial fibrillation
Ventricular tachycardia or ventricular fibrillation
High or low blood pressure
S 4 gallop: A common early finding of diastolic dysfunction
S 3 gallop: An indication of reduced left ventricular function and a poor prognostic sign
Heart murmurs
Tachypnea
Syncope
Pulmonary edema (in acute cases of myocardial infarction or congestive heart failure)
See Presentation for more detail.
Diagnosis
Laboratory tests:
Complete blood count (CBC)
Chemistry panel
Lipid profile
Thyroid function tests: To exclude thyroid disorders
Blood glucose and hemoglobin A 1C (HbA 1C) measurement
Myocardial fractional flow reserve (FFR)
Coronary flow reserve (CFR)
C-reactive protein level
Cardiac Troponin (in cases of suspected acute coronary syndrome)
Imaging studies:
Echocardiography
Nuclear imaging
Cardiac computed tomography with CT angiography
Electron beam CT scanning (for calculation of coronary artery calcium score)
Optical coherence tomography imaging
Magnetic resonance imaging
Positron emission tomography
Coronary angiography
See Workup for more detail.
Management
The following are used in the management of angina [ 1] :
Nitrates
Beta blockers
Calcium channel blockers
Ranolazine
Other agents used in the treatment of coronary artery stenosis or to aid in the management of coronary artery disease after intervention, or for the presentation of acute coronary syndromes, include the following:
Angiotensin-converting enzyme inhibitors to reduce blood pressure
Antiplatelet agents for acute coronary events
Intravenous glycoprotein IIb/IIIa inhibitors
Aspirin
Thienopyridine antiplatelet agents (e.g., clopidogrel, prasugrel)
Ticagrelor
HMG-CoA reductase inhibitors, or statins, to lower LDL cholesterol levels and stabilize atherosclerotic plaque
PCSK-9 inhibitors in select high-risk patients with known CAD and need for additional LDL lowering
Treatment procedures for coronary artery atherosclerosis include the following:
Coronary artery bypass grafting (CABG)
Percutaneous coronary intervention (PCI)
Percutaneous transluminal coronary angioplasty (PTCA)
In high- and intermediate-risk patients with 3-vessel disease, PCI was associated with significantly higher rates of revascularization and of major adverse cardiac and cerebrovascular events than CABG [ 2, 3] ; the two procedures were equally effective in the treatment of low-risk patients with 3-vessel disease and in low- and intermediate-risk patients with left main CAD.
See Treatment and Medication for more detail.
Next: Background
Background
Coronary artery atherosclerosis is the single most common cause of death in men and women in the United States. It is the principal cause of coronary artery disease (CAD), in which atherosclerotic changes are present within the walls of the coronary arteries. CAD is a progressive disease process that generally begins in childhood and manifests clinically in middle to late adulthood.
The word "atherosclerosis" is of Greek origin and literally means focal accumulation of lipid (ie, athere [gruel]) and thickening of arterial intima (ie, sclerosis [hardening]). Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by the following:
Endothelial dysfunction
Vascular inflammation
Buildup of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall
Atherosclerotic buildup results in the following:
Plaque formation
Vascular remodeling
Acute and chronic luminal obstruction
Abnormalities of blood flow
Diminished oxygen supply to target organs
By impairing or obstructing normal blood flow, atherosclerotic buildup causes myocardial ischemia. (See Pathophysiology .)
Approximately 14 million Americans have CAD. Each year, 1.5 million individuals develop acute myocardial infarction (AMI), the most deadly presentation of CAD, and more than 500,000 of these individuals die. (See Epidemiology .)
Nonetheless, there has been a 30% reduction in mortality from CAD since the late 20th century. Many factors have contributed to this, including the introduction of coronary care units, coronary artery bypass grafting (CABG), thrombolytic therapy, percutaneous coronary intervention (PCI), and a renewed emphasis on lifestyle modification. (See Treatment and Management .)
A major advance in the treatment of coronary artery atherosclerosis has been the development of a refined understanding of the nature of atherosclerotic plaque and the phenomenon of plaque rupture, which is the predominant cause of acute coronary syndrome (ACS) and AMI. Cardiologists now know that in many cases (perhaps more than half), the plaque that ruptures and results in the clinical syndromes of ACS and AMI is less than 50% occlusive. These so-called vulnerable plaques, as compared with stable plaques, consist of a large lipid core, inflammatory cells, and thin, fibrous caps that are subjected to greater biomechanical stress, thus leading to rupture that perpetuates thrombosis and ACS. The process of plaque rupture is illustrated in the diagram below.
Coronary Artery Atherosclerosis. A vulnerable plaque and the mechanism of plaque rupture.
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The treatment of such ruptured plaques has taken a leap forward with the widespread use of newer antiplatelet and antithrombotic agents. Nonetheless, the greatest impact on the CAD epidemic can only be achieved through therapies tailored to prevent the rupture of these vulnerable plaques. Such plaques are likely more prevalent than occlusive plaques are. Currently, it is not possible to clinically identify most vulnerable plaques, and no data support the local treatment of them. On the other hand, strong evidence from many randomized trials supports the efficacy of statin-class drugs in lipid lowering and of angiotensin-converting enzyme (ACE) inhibitors in improving endothelial function, with the use of both types of agents likely leading to plaque stabilization. (See Medication .)
Previous
Next: Background
Anatomy
The healthy epicardial coronary artery consists of the following 3 layers:
Intima
Media
Adventitia
The intima is an inner monolayer of endothelial cells lining the lumen; it is bound on the outside by internal elastic lamina, a fenestrated sheet of elastin fibers. The thin subendothelial space in between contains thin elastin and collagen fibers along with a few smooth muscle cells (SMCs).
The media are bound on the outside by an external elastic lamina that separates them from the adventitia, which consists mainly of fibroblasts, SMCs, and a matrix containing collagen and proteoglycans.
The endothelium is the monolayered inner lining of the vascular system. It covers almost 700 m 2 and weighs 1.5 kg.
The endothelium has various functions. It provides a nonthrombogenic surface via a surface covering of heparan sulfate and through the production of prostaglandin derivatives such as prostacyclin, which is a potent vasodilator and an inhibitor of platelet aggregation.
The endothelium secretes the most potent vasodilator, endothelium-derived relaxing factor (EDRF), a thiolated form of nitric oxide. EDRF formation by endothelium is critical in maintaining a balance between vasoconstriction and vasodilation in the process of arterial homeostasis. The endothelium also secretes agents that are effective in lysing fibrin clots. These agents include plasminogen and procoagulant materials, such as von Willebrand factor and type 1 plasminogen activator inhibitor. In addition, the endothelium secretes various cytokines and adhesion molecules, such as vascular cell adhesion molecule-1 and intercellular adhesion molecule-1, and numerous vasoactive agents, such as endothelin, A-II, serotonin, and platelet-derived growth factor, which may be important in vasoconstriction.
Endothelium, through the above mechanisms, regulates the following:
Vascular tone
Platelet activation
Monocyte adhesion and inflammation
Thrombus generation
Lipid metabolism
Cellular growth and vascular remodeling
Previous
Next: Background
Pathophysiology
Initially thought to be a chronic, slowly progressive, degenerative disease, atherosclerosis is a disorder with periods of activity and quiescence. Although a systemic disease, atherosclerosis manifests in a focal manner and affects different organ systems in different patients for reasons that remain unclear.
Pooled whole-exome sequencing (WES) appears to have potential for providing insights into the pathogenesis of coronary artery atherosclerosis (CAD). In a study that used this technology on 17 Israeli patients with multiple cardiovascular risk factors but normal coronary arteries and 17 control subjects with multivessel CAD, investigators found 19 genetic variants that may provide protection from CAD, but whose mechanism remains unclear. [ 4]
Plaque growth and vascular remodeling
The lesions of atherosclerosis do not occur in a random fashion. Hemodynamic factors interact with the activated vascular endothelium. Fluid shear stresses generated by blood flow influence the phenotype of the endothelial cells by modulation of gene expression and regulation of the activity of flow-sensitive proteins.
Atherosclerotic plaques (or atheromas), which may require 10-15 years for full development, characteristically occur in regions of branching and marked curvature at areas of geometric irregularity and where blood undergoes sudden changes in velocity and direction of flow. Decreased shear stress and turbulence may promote atherogenesis at these important sites within the coronary arteries, the major branches of the thoracic and abdominal aorta, and the large conduit vessels of the lower extremities.
A study by Samady et al suggests low shear segments in the coronary arteries develop greater plaque and necrotic core progression and constrictive remodeling, whereas high shear segments develop greater necrotic core and calcium progression, regression of fibrous and fibrofatty tissue, and excessive expansive remodeling. [ 5] This suggests a transformation to a more vulnerable phenotype.
The earliest pathologic lesion of atherosclerosis is the fatty streak, which is observed in the aorta and coronary arteries of most individuals by age 20 years. The fatty streak is the result of focal accumulation of serum lipoproteins within the intima of the vessel wall. Microscopy reveals lipid-laden macrophages, T lymphocytes, and smooth muscle cells in varying proportions. The fatty streak may progress to form a fibrous plaque, the result of progressive lipid accumulation and the migration and proliferation of SMCs.
Platelet-derived growth factor, insulinlike growth factor, transforming growth factors alpha and beta, thrombin, and angiotensin II (A-II) are potent mitogens that are produced by activated platelets, macrophages, and dysfunctional endothelial cells that characterize early atherogenesis, vascular inflammation, and platelet-rich thrombosis at sites of endothelial disruption. The relative deficiency of endothelium-derived nitric oxide further potentiates this proliferative stage of plaque maturation.
The SMCs are responsible for the deposition of extracellular connective tissue matrix and form a fibrous cap that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris. Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ. Human coronary arteries enlarge in response to plaque formation, and luminal stenosis may occur only when the plaque occupies more than 40% of the area bounded by the internal elastic lamina. Developing atherosclerotic plaques acquire their own microvascular network, the vasa vasorum, which are prone to hemorrhage and contribute to progression of atherosclerosis. [ 6]
As endothelial injury and inflammation progress, fibroatheromas grow and form the plaque. As the plaque grows, two types of remodeling, positive remodeling and negative remodeling, occur, as illustrated in the image below.
Coronary Artery Atherosclerosis. Positive and negative arterial remodeling are illustrated.
View Media Gallery
Positive remodeling is an outward compensatory remodeling (the Glagov phenomenon) in which the arterial wall bulges outward and the lumen remains uncompromised. Such plaques grow further; however, they usually do not cause angina, because they do not become hemodynamically significant for a long time. In fact, the plaque does not begin to encroach on the lumen until it occupies 40% of the cross-sectional area. The encroachment must be at least 50-70% to cause flow limitation. Such positively remodeled lesions thus form the bulk of the vulnerable plaques, grow for years, and are more prone to result in plaque rupture and ACS than stable angina, as documented by intravascular ultrasonography (IVUS) studies.
Many fewer lesions exhibit almost no compensatory vascular dilation, and the atheroma steadily grows inward, causing gradual luminal narrowing. Many of the plaques with initial positive remodeling eventually progress to the negative remodeling stage, causing narrowing of the vascular lumen. Such plaques usually lead to the development of stable angina. They are also vulnerable to plaque rupture and thrombosis.
Plaque rupture
Denudation of the overlying endothelium or rupture of the protective fibrous cap may result in exposure of the thrombogenic contents of the core of the plaque to the circulating blood. This exposure constitutes an advanced or complicated lesion. The plaque rupture occurs due to weakening of the fibrous cap. Inflammatory cells localize to the shoulder region of the vulnerable plaque. T lymphocytes elaborate interferon gamma, an important cytokine that impairs vascular smooth muscle cell proliferation and collagen synthesis. Furthermore, activated macrophages produce matrix metalloproteinases that degrade collagen.
These mechanisms explain the predisposition to plaque rupture and highlight the role of inflammation in the genesis of the complications of the fibrous atheromatous plaque. A plaque rupture may result in thrombus formation, partial or complete occlusion of the blood vessel, and progression of the atherosclerotic lesion due to organization of the thrombus and incorporation within the plaque.
Plaque rupture is the main event that causes acute presentations. However, severely obstructive coronary atheromas do not usually cause ACS and MI. In fact, most of the atheromas that cause ACS are less than 50% occlusive, as demonstrated by coronary arteriography. Atheromas with smaller obstruction experience greater wall tension, which changes in direct proportion to their radii.
Most plaque ruptures occur because of disruption of the fibrous cap, which allows contact between the highly thrombogenic lipid core and the blood. These modestly obstructive plaques, which have a greater burden of soft lipid core and thinner fibrous caps with chemoactive cellular infiltration near the shoulder region, are called vulnerable plaques. The amount of collagen in the fibrous cap depends on the balance between synthesis and destruction of intercellular matrix and inflammatory cell activation.
T cells that accumulate at sites of plaque rupture and thrombosis produce the cytokine interferon gamma, which inhibits collagen synthesis. Already-formed collagen is degraded by macrophages that produce proteolytic enzymes and by matrix metalloproteinases (MMPs), particularly MMP-1, MMP-13, MMP-3, and MMP-9. The MMPs are induced by macrophage- and SMC-derived cytokines such as IL-1, tumor necrosis factor (TNF), and CD154 or TNF-alpha. Authorities postulate that lipid lowering stabilizes the vulnerable plaques by modulating the activity of the macrophage-derived MMPs.
Histologic composition and structure
A system devised by Stary et al classifies atherosclerotic lesions according to their histologic composition and structure. [ 7]
In a type I lesion, the endothelium expresses surface adhesion molecules E selectin and P selectin, attracting more polymorphonuclear cells and monocytes in the subendothelial space.
In a type II lesion, macrophages begin to take up large amounts of LDL (fatty streak).
In a type III lesion, as the process continues, macrophages become foam cells.
In a type IV lesion, lipid exudes into the extracellular space and begins to coalesce to form the lipid core.
In a type V lesion, SMCs and fibroblasts move in, forming fibroatheromas with soft inner lipid cores and outer fibrous caps.
In a type VI lesion, rupture of the fibrous cap with resultant thrombosis causes ACS.
As lesions stabilize, they become fibrocalcific (type VII lesion) and, ultimately, fibrotic with extensive collagen content (type VIII lesion).
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Next: Background
Etiology
A complex and incompletely understood interaction is observed between the critical cellular elements of the atherosclerotic lesion. These cellular elements include endothelial cells, smooth muscle cells, platelets, and leukocytes. Interrelated biologic processes that contribute to atherogenesis and the clinical manifestations of atherosclerosis are as follows:
Vasomotor function
Thrombogenicity of the blood vessel wall
State of activation of the coagulation cascade
The fibrinolytic system
SMC migration and proliferation
Cellular inflammation
The encrustation theory, proposed by Rokitansky in 1851, suggested that atherosclerosis begins in the intima with deposition of thrombus and its subsequent organization by the infiltration of fibroblasts and secondary lipid deposition.
In 1856, Virchow proposed that atherosclerosis starts with lipid transudation into the arterial wall and its interaction with cellular and extracellular elements, causing "intimal proliferation."
Endothelial injury as the mechanism of atherosclerosis
In his response-to-injury hypothesis, Ross postulated that atherosclerosis begins with endothelial injury, making the endothelium susceptible to the accumulation of lipids and the deposition of thrombus. The mechanisms of atherogenesis remain uncertain, but the response-to-injury hypothesis is the most widely accepted proposal.
In the 1990s, Ross and Fuster proposed that vascular injury starts the atherosclerotic process. [ 8] Such injuries can be classified as follows:
Type I - Vascular injury involving functional changes in the endothelium, with minimal structural changes, (ie, increased lipoprotein permeability and white blood cell adhesion)
Type II - Vascular injury involving endothelial disruption, with minimal thrombosis
Type III - Vascular injury involving damage to media, which may stimulate severe thrombosis, resulting in unstable coronary syndromes
According to the response-to–vascular injury theory, injury to the endothelium by local disturbances of blood flow at angulated or branch points, along with systemic risk factors, perpetuates a series of events that culminate in the development of atherosclerotic plaque.
As discussed in greater detail below, endothelial damage occurs in many clinical settings and can be demonstrated in individuals with dyslipidemia, hypertension, diabetes, advanced age, nicotine exposure, and products of infective organisms (ie, Chlamydia pneumoniae ). Damage to the endothelium may cause changes that are localized or generalized and that are transient or persistent, as follows:
Increased permeability to lipoproteins
Decreased nitric oxide production
Increased leukocyte migration and adhesion
Prothrombotic dominance
Vascular growth stimulation
Vasoactive substance release
Endothelial dysfunction is the initial step that allows diffusion of lipids and inflammatory cells (ie, monocytes, T lymphocytes) into the endothelial and subendothelial spaces. Secretion of cytokines and growth factors promotes intimal migration, SMC proliferation, and accumulation of collagen matrix and of monocytes and other white blood cells, forming an atheroma. More advanced atheromas, even though nonocclusive, may rupture, thus leading to thrombosis and the development of ACS and MI.
Role of low-density lipoprotein-oxidative stress
The most atherogenic type of lipid is the low-density lipoprotein (LDL) component of total serum cholesterol. The endothelium's ability to modify lipoproteins may be particularly important in atherogenesis. LDLs appear to be modified by a process of low-level oxidation when bound to the LDL receptor, internalized, and transported through the endothelium. LDLs initially accrue in the subendothelial space and stimulate vascular cells to produce cytokines for recruiting monocytes, which causes further LDL oxidation. Extensively oxidized LDL (oxLDL), which is exceedingly atherogenic, is picked up by the scavenger receptors on macrophages, which absorb the LDL.
Cholesterol accumulation in macrophages is promoted by oxLDL; the macrophages then become foam cells. In addition, oxLDL enhances endothelial production of leukocyte adhesion molecules (ie, cytokines and growth factors that regulate SMC proliferation, collagen degradation, and thrombosis [eg, vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1]).
Oxidized LDL inhibits nitric oxide synthase activity and increasing reactive oxygen species generation (eg, superoxide, hydrogen peroxide), thus reducing endothelium-dependent vasodilation. Moreover, oxLDL alters the SMC response to A-II stimulation and increasing vascular A-II concentrations. The SMCs that proliferate in the intima to form advanced atheromas are originally derived from the media. The theory that accumulation of SMCs in the intima represents the sine qua non of the lesions of advanced atherosclerosis is now widely accepted.
Substantial evidence suggests that oxLDL is the prominent component of atheromas. Antibodies against oxLDL react with atherosclerotic plaques, and plasma levels of immunoreactive altered LDL are greater in persons with AMI than in controls. Oxidative stress has therefore been recognized as the most significant contributor to atherosclerosis by causing LDL oxidation and increasing nitric oxide breakdown.
Risk factors for coronary artery atherosclerosis
A number of large epidemiologic studies in North America and Europe have identified numerous risk factors for the development and progression of atherosclerosis. These factors, which can be classified as either modifiable or nonmodifiable, include the following:
Hyperlipidemia and dyslipidemia
Hypertension
Cigarette and tobacco use
Air pollution
Diabetes mellitus
Age
Sex
Family history
Obesity
Sedentary lifestyle
Sleep disorders, such as obstructive sleep apnea
Chronic kidney disease
Auto-immune inflammatory diseases such as rheumatoid arhtritis and systemic lupus
The American College of Cardiology Foundation/American Heart Association 2010 report on cardiovascular risk assessment in asymptomatic adults recommends global risk scoring (eg, Framingham Risk Score [ 9] ) and a family history of cardiovascular disease be obtained in all adult women and men. [ 10]
Numerous novel risk factors have been identified that add to the predictive value of the established risk factors and may prove to be a target for future medical interventions.
Risk factors specific to women include pregnancy and complications of pregnancy such as gestational diabetes, preeclampsia, third trimester bleeding, preterm birth, and birth of an infant small for gestational age. The 2011 update to the American Heart Association guideline for the prevention of cardiovascular disease (CVD) in women recommends that risk assessment at any stage of life include a detailed history of pregnancy complications. It also states that postpartum, obstetricians should refer women who experience these complications to a primary care physician or cardiologist. [ 11]
The presence of risk factors accelerates the rate of development of atherosclerosis. Diabetes causes endothelial dysfunction, decreases endothelial thromboresistance, and increases platelet activity, thus accelerating atherosclerosis.
Established risk factors successfully predict future cardiac events in about 50-60% of patients. A concerted effort to identify is also being made to validate new markers of future risk of the clinical consequences of atherosclerosis has been made.
Other risk factors for coronary artery atherosclerosis include the following:
Family history of premature CAD
Hypoalphalipoproteinemia
Syndromes of accelerated atherosclerosis - Graft atherosclerosis, CAD after cardiac transplantation
Chronic kidney disease [ 12]
Systemic lupus erythematosus [ 13]
Rheumatoid arthritis [ 14]
Metabolic syndrome [ 15]
Chronic inflammation
Infectious agents
Increased fibrinogen levels
Increased lipoprotein (a) levels
Familial hypercholesterolemia
Depression
According to the 2011 update to the American Heart Association guideline for CVD prevention in women, risk factors that are more common or may be more significant in women include psychosocial factors such as depression and autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. The Heart and Estrogen/progestin Replacement Study evaluated the effects of hormone replacement therapy on cardiovascular events among postmenopausal women with CAD and found that sudden cardiac death comprised most cardiac deaths among this group of women. [ 16] Women with these conditions should be evaluated for CVD and for other risk factors. Women with clinically evident CVD should also be screened for these conditions, which can affect adherence or otherwise complicate secondary CVD prevention efforts. [ 11]
A study by Semba et al, however, suggests that high concentrations of plasma klotho, a recently discovered hormone that has been implicated in atherosclerosis, are independently associated with a lower likelihood of having CVD. [ 17]
For more information, see Risk Factors for Coronary Artery Disease.
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Next: Background
Epidemiology
The true frequency of atherosclerosis is difficult, if not impossible, to accurately determine because it is a predominantly asymptomatic condition. The process of atherosclerosis begins in childhood with the development of fatty streaks. These lesions can be found in the aorta shortly after birth and appear in increasing numbers in those aged 8-18 years. More advanced lesions begin to develop when individuals are aged approximately 25 years. Subsequently, an increasing prevalence of the advanced complicated lesions of atherosclerosis is noted, and the organ-specific clinical manifestations of the disease increase with age through the fifth and sixth decades of life.
United States statistics
In the United States, approximately 14 million persons experience CAD and its various complications. Congestive heart failure (CHF) that develops because of ischemic cardiomyopathy in hypertensive MI survivors has become the most common discharge diagnosis for patients in American hospitals. Approximately 80 million people, or 36.3% of the population, have cardiovascular disease.
Annually, approximately 1.5 million Americans have an AMI, a third of whom die. In 2009, 785,000 Americans were estimated to have suffered a first MI, and about 470,000 Americans were estimated to have had a recurrent event. An additional 195,000 "silent" heart attacks are estimated to occur each year. About every 34 seconds, an American will have an MI. CAD remains the number 1 cause of death for men and women in the United States and is responsible for approximately 20% of all US deaths. From 1995–2005, the death rate from CAD declined 34.3%, but the actual number of deaths declined only 19.4%.
International statistics
The international incidence of ACS and AMI, especially in developed countries, is similar to that observed in the United States. Despite consumption of rich foods, inhabitants of France and the Mediterranean region appear to have a lower incidence of CAD. This phenomenon (sometimes called the French paradox) is partly explained by greater use of alcohol, with its possible HDL-raising benefit, and by consumption of the Mediterranean diet, which includes predominant use of monounsaturated fatty acids, such as olive oil or canola oil, as well as omega-3 fatty acids, which are less atherogenic. Eskimos have been found to have a lower prevalence of CAD as a result of consuming fish oils containing omega-3 fatty acids.
The Spanish cohort of the European Prospective Investigation into Cancer and Nutrition assessed the association between consumption of fried foods and risk of coronary heart disease. They found that among people living in Spain, where olive or sunflower oil is commonly used for frying, the consumption of fried foods was not associated with coronary heart disease or with all-cause mortality. This further suggests that the Mediterranean diet may help lower the risk of CAD. [ 18]
Findings from the World Health Organization's Monitor Trends in Cardiovascular Diseases (MONICA) project involving 21 countries showed a 4% fall in CAD death rates. Improvement in the case fatality rate accounted for only one third of the decline. However, two thirds of the decline resulted from a reduction in the number of events. These findings strongly suggest that the largest impact on decreasing the global burden of atherosclerosis will come from prevention of events.
The frequency of clinical manifestations of atherosclerosis in Great Britain, west of Scotland in particular, is especially high. The same is true of Scandinavia in general and of Finland in particular. Russia and many of the former states of the Soviet Union have recently experienced an exponential increase in the frequency of coronary heart disease that likely is the result of widespread economic hardship and social upheaval, a high prevalence of cigarette habituation, and a diet high in saturated fats.
Westernization and the rise of coronary heart disease
The frequency of coronary heart disease in the Far East is significantly lower than that documented in the West. Ill-defined genetic reasons for this phenomenon may exist, but significant interest surrounds the role of diet and other environmental factors in the absence of clinical atherosclerotic vascular disease in these populations. Atherosclerotic cardiovascular disease is also rare on the African continent, although growing evidence indicates that this too is changing, as a result of rapid westernization and urbanization of the traditionally rural and agrarian African populations. The prevalence of coronary heart disease is also increasing in the Middle East, India, and Central and South America. [ 6] The rate of CAD in ethnic immigrant populations in the United States approaches that of the disease in whites, supporting the role of these putative environmental factors.
Race-associated prevalences of coronary artery disease
The incidence, prevalence, and manifestations of CAD vary significantly with race, as does the response to therapy.
African Americans appear to have higher morbidity and mortality rates of CAD, even when the statistics are corrected for educational and socioeconomic status. The risk-factor burden experienced by African Americans differs from that of Caucasian Americans. The prevalence of hypertension, obesity, dysmetabolic syndrome, and lack of physical activity are much higher in African Americans, whereas the prevalence of hypercholesterolemia is lower. African Americans with AMI present for treatment later than patients do on average, are less often subjected to invasive strategies, and experience greater overall mortality. (Similar statistics can also be cited for presentation and treatment of patients with stable CAD.)
Asian Indians exhibit a 2- to 3-fold higher prevalence of CAD than do whites in the United States. They also have greater prevalences of hypoalphalipoproteinemia, high lipoprotein (a) levels, and diabetes.
Sex-associated prevalences of coronary artery disease
Men traditionally have a higher prevalence of CAD. Women, however, follow men by 10 years, especially after menopause. (The value of estrogen supplementation for prevention of CAD has been discredited by the Heart and Estrogen/Progestin Replacement Study [HERS]). [ 19, 20]
The presence of diabetes, as well as tobacco use, eliminates the protection from heart disease associated with female sex. In women, as in men, the most common cause of death is CAD, which accounts for more deaths in women than those related to breast and uterine diseases combined. Women with AMI present later than average, are less often subjected to invasive strategies, and experience greater overall mortality. (Similar statistics can also be cited for the presentation and treatment of patients with stable CAD.)
The 2011 update to the American Heart Association guideline for the prevention of cardiovascular disease in women recommends changes in prevention and treatment practices [ 11] :
Women should be considered as high risk, and as candidates for aggressive treatment, if their risk of dying from any cardiovascular event in the next 10 years is 10% or greater.
Research studies should publish efficacy and adverse drug reactions (ADRs) by gender, as both can differ in women.
Evidence from clinical trials tends to overestimate the real-world efficacy of therapies in female patients, who are generally older and have more comorbidities than test subjects. The guideline is now “effectiveness-based” rather than “evidence-based.”
Effectiveness-based considerations have reduced the strength of previous recommendations for use of aspirin, statins (in women with elevated C-reactive protein but normal cholesterol), and aggressive glycemic control in diabetes.
The elderly and coronary artery disease
Age is the strongest risk factor for the development of CAD. Most cases of CAD become clinically apparent in patients aged 40 years or older, but elderly persons experience higher mortality and morbidity rates from it. Approximately 82% of people who die of CAD are 65 years or older. Complication rates of multiple therapeutic interventions tend to be higher in the elderly; however, the magnitude of benefit from the same interventions is greater in this population, because these patients form a high-risk subgroup.
Calculating risk of coronary artery atherosclerosis
In 2013 ACC/AHA published the Pooled Cohort ASCVD Risk Equation is the new cardiovascular risk equation. It was developed due to limitations of the Framingham risk score. This 10 year Pooled Cohort ASCVD Risk Equation is available as online calculator at the ACC website. It incorporates following end points: fatal stroke, nonfatal stroke, fatal coronary heart disease, and nonfatal myocardial infarction. The parameters utilized in calculating ASCVD risk are white or black race, age, sex, diabetes, smoking, systolic blood pressure, hypertension treatment, total cholestrol, and high density lipoprotein cholestrol. [ 21]
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Next: Background
Prognosis
As previously mentioned, approximately 1.5 million Americans per year have an AMI, with a third of these events proving fatal. The survivors of MI have a poor prognosis, carrying a 1.5- to 15-fold higher risk of mortality and morbidity than the rest of the population.
Historically, for example, 25% of men and 38% of women die within 1 year after having an MI, although these rates may overstate the 1-year mortality today, given advances in the treatment of CHF and sudden cardiac death. Among survivors, 18% of men and 34% of women have a second MI within 6 years, 7% of men and 6% of women die suddenly, 22% of men and 46% of women are disabled with CHF, and 8% of men and 11% of women have a stroke.
According to a prospective study using data from the Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter (CONFIRM) Registry, incident mortality and MI rates do not differ significantly between men and women among patients matched for age, risk factors, symptoms, and extent of CAD. [ 22] These findings conflict with those from the Women’s Health Initiative, which found that in women with nonspecific or atypical chest pain, the risk of nonfatal MI is twice as great as that in men.
The prognosis in patients with atherosclerosis depends on the following factors:
Presence of inducible ischemia
Left ventricular function
Presence of arrhythmias
Revascularization potential (complete vs incomplete)
Aggressiveness of risk alteration
Compliance with medical therapy
The prognosis of atherosclerosis also depends on systemic burden of disease, the vascular bed (s) involved, and the degree of flow limitation. Wide variability is noted, and clinicians appreciate that many patients with critical limitation of flow to vital organs may survive many years, despite a heavy burden of disease. Conversely, MI or sudden cardiac death may be the first clinical manifestation of atherosclerotic cardiovascular disease in a patient who is otherwise asymptomatic with minimal luminal stenosis and a light burden of disease.
Much of this phenotypic variability is likely to be determined by the relative stability of the vascular plaque burden. Plaque rupture and exposure of the thrombogenic lipid core are critical events in the expression of this disease process and determine the prognosis. The ability to determine and quantify risk and prognosis in patients with atherosclerosis is limited by the inability to objectively measure plaque stability and other predictors of clinical events.
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Patient Education
Education regarding CAD is extremely important. Publications and articles available from the American Heart Association provide a wealth of information.
The most effective and probably the most cost-efficient means of reducing the burden of disease secondary to atherosclerosis in the general population is primary prevention. The role of diet and exercise in the prevention of atherosclerotic cardiovascular disease has been well established. Education of the general population regarding healthy dietary habits and regular exercise will reduce the prevalence of multiple coronary heart disease risk factors. (See Treatment and Management) For patients with risk factors refractory to lifestyle interventions, education can enhance compliance with prescribed therapy.
For patient education resources, see the Heart Health Center and Cholesterol Center, as well as High Cholesterol, Lifestyle Cholesterol Management, Chest Pain, Coronary Heart Disease, Heart Attack, Angina Pectoris, and Statins (Cholesterol Drugs).
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Clinical Presentation
References
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Media Gallery
Coronary Artery Atherosclerosis. Stress test, part 1. Resting electrocardiogram showing normal baseline ST segments. (See the image below for part 2.)
Coronary Artery Atherosclerosis. Stress test, part 2. Stress electrocardiogram showing significant ST-segment depression. (See the image above for part 1.)
Coronary Artery Atherosclerosis. Stress nuclear imaging showing anterior, apical, and septal wall perfusion defects during stress, which are reversible as observed on the rest images. These defects strongly suggest the presence of significant stenosis in the left anterior descending coronary artery.
Coronary Artery Atherosclerosis. Cardiac catheterization and coronary angiography in the left panel shows severe left anterior descending coronary artery stenosis. This lesion was treated with stent placement in the left anterior descending coronary artery, as observed in the right panel.
Coronary Artery Atherosclerosis. A vulnerable plaque and the mechanism of plaque rupture.
Coronary Artery Atherosclerosis. Positive and negative arterial remodeling are illustrated.
Coronary Artery Atherosclerosis. Low power, hematoxylin and eosin (H&E) stain of an atheromatous plaque of the coronary artery. The wall is thickened, and no internal or external elastic lamina is seen. There is a thick fibrous cap containing some neovascularization in the lower left of the image.
Coronary Artery Atherosclerosis. Low power, hematoxylin and eosin (H&E) stain of an atheromatous plaque of the coronary artery. There is marked luminal narrowing. The fibrous cap on the left contains a central lipid core containing macrophages and cholesterol clefts (lower center). Calcification (dark purple) is seen on the right.
Coronary Artery Atherosclerosis. Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the left anterior descending coronary artery, which was dilated by percutaneous transluminal coronary angioplasty.
of 9
Tables
Table. Four Statin Benefit Groups and Major Recommendations
Table. Four Statin Benefit Groups and Major Recommendations
Group
Recommendation
1.
Age ≥21 years with clinical ASCVD (including history of or current acute coronary syndrome, myocardial infarction, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, PAD presurmed to be of atherosclerotic origin)
1.For patients age >75 years, high-intenstiy statin (or moderate-intensity statinif not candidate for high-intensity due to safety concerns)
2. For patients age >75 years, moderate-intensity statin
2.
Adults aged ≥21 years with LDL-C ≥190 mg/dl (not due to modifiable
1. High-intensity statin therapy to achieve ≥50% reduction in LDL-C statin (or moderate-intenstiy if not a candidate for high-intensity statin due to safety concerns)
2. May consider combining statin and non-statin therapy to further reduce LDL-C
3. Cascade screeing of close biologic relatives should be performed to identify others with the disease who would benefit from treatment.
3.
Adults aged 40-75 years without ASCVD but with diabetes and with LDL-C 70-189 mg/dL
1. Moderate-intensity statin
2. If 10-year ASCVD risk ≥7.5%, consider high-intensity statin.
4.
Adults aged 40-75 years without ASCVD or diabetes, and with LDL-C 70-189 mg/dL and an estimated 10 year risk for ASCVD of ≥7.5%
1. Estimate 10-year ASCVD risk using Pooled Cohort Equations
a. if ≥7.5%, moderate- or high-intensity statin;
b. If ≥to < 7.5%, consider moderate-intensity statin.
2. If selected individuals with 10-year ASCVD risk < 5%, or age < 40 or > 75 years, individualize decisions based on presence of other high-risk features.
3. Before initiation of statin therapy for primary prevention, it is reasonable for clinicians and patients to engage in a discussion that considers the potential for ASCVD risk-reduction benefits and for adverse effects and drug-drug interactions, as well as patient preferences for treatment.
ASCVD = atherosclerotic cardiovascular disease; LDL-C = low-density lipoprotein cholesterol; PAD = peripheral artery disease; TIA = transient ischemic attack.
Back to List
Contributor Information and Disclosures
Author
Sandy N Shah, DO, MBA, FACC, FACP, FACOI Cardiologist
Sandy N Shah, DO, MBA, FACC, FACP, FACOI is a member of the following medical societies: American College of Cardiology, American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Osteopathic Association, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions
Disclosure: Nothing to disclose.
Specialty Editor Board
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Chief Editor
Yasmine S Ali, MD, FACC, FACP, MSCI Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine; President, LastSky Writing, LLC
Yasmine S Ali, MD, FACC, FACP, MSCI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Medical Writers Association, National Lipid Association, Tennessee Medical Association
Disclosure: Serve (d) as a director, officer, partner, employee, advisor, consultant or trustee for: MCG Health, LLC; LastSky Writing, LLC; Philips Healthcare; Cardiac Profiles, Inc.; Corvidane; M Health; GE Healthcare; Athena Health; PeerView Institute; Verywell Health; HealthCentral.
Additional Contributors
F Brian Boudi, MD, FACP Clinical Associate Professor, University of Arizona College of Medicine (Phoenix Campus); Fellow, Sarver Heart Center, University of Arizona College of Medicine; Regional Faculty, American Heart Association; Adjunct Assistant Professor of Medicine, Mid-Western University; Staff Physician, Site Director for Clinical Rotations Emergency Medicine, Phoenix Veterans Administration Health Care System
F Brian Boudi, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Society of Echocardiography, Arizona Medical Association, Association of Program Directors in Internal Medicine, American College of Healthcare Executives, American Society of Nuclear Cardiology
Disclosure: Nothing to disclose.
Chowdhury H Ahsan, MD, PhD, MRCP, FSCAI Clinical Professor of Medicine, Director of Cardiac Catheterization and Intervention, Marlon Cardiac Catheterization Laboratory, Director of Cardiovascular Research, University Medical Center, University of Nevada School of Medicine
Chowdhury H Ahsan, MD, PhD, MRCP, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions, American Stroke Association
Disclosure: Received consulting fee from sanofi for consulting; Received honoraria from astra zeneca for speaking and teaching; Received honoraria from BI for speaking and teaching.
Acknowledgements
Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society
Disclosure: Nothing to disclose.
John A McPherson, MD, FACC, FAHA, FSCAI Associate Professor of Medicine, Division of Cardiovascular Medicine, Director of Cardiovascular Intensive Care Unit, Vanderbilt Heart and Vascular Institute
John A McPherson, MD, FACC, FAHA, FSCAI is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, Society of Critical Care Medicine, and Tennessee Medical Association
Disclosure: CardioDx Consulting fee Consulting; Gilead Consulting fee Consulting; Abbott Vascular Corp. Consulting fee Consulting
James L Orford, MBChB
Disclosure: Nothing to disclose.
Andrew P Selwyn, MD, MA, FACC, FRCP
Disclosure: Nothing to disclose.
George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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msmarco_passage_01_404147789 | License FAQs | Department Of Natural Resources Division | License FAQs | Department Of Natural Resources Division
License FAQs
Questions
How do I get help with my license purchase?
How do I purchase a license online?
How do I get the free 65+ resident senior license?
Who qualifies as a resident?
I can’t log into my DNR account using my lifetime license number. Why?
What licenses do I need?
How do I get a Waterfowl and Migratory Bird Stamp, Deer or Turkey Harvest Record or SIP permit?
How do I reprint my hunter education card/sign up for a class?
What is the "new" license and boat registration system?
Can a Georgia license agent charge more than a $3.00 transaction fee?
Does Georgia have a disability hunting and fishing license?
My name changed. How do I update my current license?
How do I reprint (replace) a lost/ruined license?
How do I update my mailing address or email?
I’m not a U.S. resident. How do I purchase a Georgia hunting or fishing license?
I’m just going along on the hunting or fishing trip. Do I need a license?
Why does DNR require your Social Security Number for licenses?
Transaction fees for licenses are $2.50 if purchasing online, $3.00 if purchasing through agent, or $5.00 if purchasing over phone.
Service fees for boat registrations are $10 by mail, online and phone. The service fee for boat registration renewal is $8.00 when renewing online.
How do I get help with my license purchase?
The Call Center can be reached at 1-800-366-2661. The Call Center is open Monday–Friday from 8:00 a.m.–6:00 p.m., and Saturday–Sunday from 9:00 a.m.–5:00 p.m. The Service Desk is closed Christmas Day, and may operate under reduced hours on major holidays.
How do I purchase a license online?
Buy and print licenses online. You will need a MasterCard® or Visa® or Discover® credit card to purchase licenses.
Lifetime licenses with fees cannot be purchased online because of strict age and residency documentation requirements. Disability licenses may not be obtained online because of strict disability documentation requirements.
You must have a printer attached to your computer that is capable of printing graphics (either black and white or in color). You will be instructed to print your license document and you will need to carry it with you while participating in that activity. The license you print is the only license you will receive.
Adobe Acrobat Reader is necessary to view and print your license from our online site. The most recent version of Adobe Acrobat Reader for Windows or Macintosh can be downloaded for free at the following site: http://get.adobe.com/reader/.
Also, be sure that pop-up blocker or similar settings are turned off in your web browser. The license will appear as a pop up screen.
Step One
You will be asked to provide information that will assist us in locating, updating or creating your customer account.
Step Two
Select the licenses you want to buy and add them to your shopping cart.
Step Three
You may use Visa or MasterCard or Discover card to pay for your license. A convenience fee of $2.50 will be added to your total.
Step Four
Print your license and carry this printed document when hunting or fishing.
How do I get the free 65+ resident senior license?
Georgia residents 65 and older born before July 1, 1952 can obtain a free Senior Lifetime Sportsman’s hunting and fishing license. There are no transaction fees for this free license. This license does not have to be renewed, and is valid for your lifetime. Persons 65 and older born on July 1, 1952 or after may purchase low cost lifetime or annual licenses. There are three ways to obtain the free resident Senior Lifetime Sportsman’s License.
Online
Find a License Agent Near You
Telephone: 1-800-366-2661
An optional durable plastic lifetime license card is available for $10, and can be obtained using any of the three methods above when obtaining the free license, or by using the Lifetime License Application. If you use the Lifetime License Application, select the “ (S) Senior Lifetime Commemorative Card (65+ Senior Lifetime Holders) ------- $10.00” and return it to the address on the form.
Detailed procedures for logging into your online account for obtaining or replacing any license .
Who qualifies as a resident?
For all recreational hunting and fishing licenses except lifetime licenses, resident means any person who has been domiciled within the State of Georgia for a period of at least three months.
Full-time military personnel on active duty, and the dependents of such military personnel and out-of-state college students living in Georgia may purchase resident annual or short term licenses. Students may use a current Georgia student ID as documentation.
Domiciled means a person's fixed, permanent, and principal home for legal purposes. A person may own land or dwellings and may stay for a time in several states, but may only have one domicile, and therefore may not be a resident of two states at the same time.
For purposes of purchasing a lifetime license, "Resident" is defined as any person with a continuous domicile within Georgia for a minimum of 3 consecutive months immediately prior to procuring the license. Proof of such residency is a valid Georgia driver’s license or Georgia ID card dated three months previous.
Nonresident landowners owning land in Georgia must obtain a nonresident license to hunt or fish. Nonresident family members of a resident landowner must obtain a nonresident license to hunt or fish, except that nonresidents under age 16 may fish or hunt small game without a Georgia license. When hunting big game, nonresidents less than 16 must possess a valid nonresident hunting license, but are exempt from the big game license requirement.
Any person who is a resident of Georgia for 30 days must obtain a Georgia driver's license before operating a motor vehicle in Georgia. Except for certain noncitizens with foreign licenses, residents must surrender all valid licenses from other states—no person can have more than one valid driver's license at any time. (O.C.G.A. §40-5-20)
I can’t log into my DNR account. Why?
If you get any error message when logging into your customer account, even if the error message appears unrelated to the criteria used, try using one of the other log in choices (driver’s license number, last four of SSN number, or DNR customer number). If you continue to have problems logging in, contact the Call Center at 1-800-366-2661 during the Call Center business hours listed at the top of this page.
What licenses do I need?
A full description of hunting and fishing licenses and requirements appears in the hunting regulations guide and the fishing regulations guide, available online and in booklet form at most license agents and at WRD offices.
When purchasing licenses online, a description of each license appears when the mouse pointer hovers over the ”i” symbol.
How do I get a Waterfowl and Migratory Bird Stamp, Deer or Turkey Harvest Record or SIP permit?
Online
Find a License Agent in Your County
Telephone (1.800.366.2661)
Adults can obtain the Resident or Nonresident Deer or Turkey Harvest Record, Waterfowl and Migratory Bird Permit online or SIP permit for free.
Choose the link license link "Online."
You will use your driver's license number or DNR customer number or last four of SSN, your last name, and your date of birth to access your DNR license account.
You may update any personal information in your account on the appropriate screen, including current address, etc. Be sure to add your email address to your account so that you will receive email notification before your license expires - if you renew your license before it expires you will receive a discount of $2.50 on your total license purchase.
Select Purchase A License. Select Harvest Record (Deer & Turkey), Waterfowl and Migratory Bird Stamp, or SIP Permit to add them to your cart, if you require them.
Once you've added the necessary items, click to complete the transaction and/or continue to checkout. From there just follow the prompts to complete the entire transaction. At the end of the transaction, you'll be able to click the button to "Print License". That will generate a pdf image of your license which can be printed. There will be no transaction fee or other charge for these free permits.
The Harvest Record (Deer & Turkey), Waterfowl and Migratory Bird Stamp, or SIP Permit (fishing) are a requirement for residents or non-residents hunting deer, turkey, migratory birds or fishing.
If you don't see the free Harvest Record (Deer & Turkey), Waterfowl and Migratory Bird Stamp, or SIP Permit available in the list of licenses, you may already have obtained the privileges and these privileges are already on your account. In that case print a free copy of your license following the instructions. The free Harvest Record (Deer & Turkey), Waterfowl and Migratory Bird Stamp, or SIP Permit should appear on your license.
Adobe Acrobat Reader is necessary to view and print your license. The newest versions of Reader for all platforms can be downloaded for free at http://get.adobe.com/reader/.
Also, be sure that pop-up blocker or similar settings are turned off in your web browser. The license/receipt will appear as a pop up screen. If you’ve given us your email address, you will also receive your license/receipt by email.
Alternatively, you may obtain a license at any Georgia license agent location. You can ask the agent to update any personal information in your account.
What is the "new" license and boat registration system?
In December 2007, DNR first entered into a contract with an outside vendor to design and manage an automated hunting and fishing license and boat registration system. This system was required to replace a failing automated licensing system that was not going to be licensed and available to DNR after December 2008. Absent a significant funding source to develop and manage a new system “in-house”, DNR explored contractual options for obtaining a “no cost to state” contract like those adopted in many other states. Funding for this type of system would be recovered by the addition of a service charge paid by the buyer at the time of the purchase. The hunting and fishing license and boat registration system was put out for competitive bid, and a bid was awarded that lasted from 2009 until 2014.
A new contract award effective July 1, 2014 to another outside vendor brings builds on previous improvements and adds additional customer service options. A Service Desk located in Georgia brought new jobs to our state, and new license purchase and vessel registration options were added.
The system provides online, mobile and telephone sales, as well as walk-in license sales at approximately 800 Georgia retail license agents. Boat registration is available online, by telephone and by mail. Service fees apply to all hunting and fishing license transactions, boat registrations and boat registration renewals.
Hunting and fishing license buyers receive a license discount of $2.50 on a transaction if they renew their annual hunting or fishing license before it expires, in effect negating the service fee. Customers providing their email address receive reminders about the discount before hunting and fishing license expiration, and at purchase receive an immediate email copy of their license/receipt. Licenses renewed early "stack" at the end of the expiring license so the renewed license is good for the full 365 day period, and sportsman can build multiple year licenses of any duration by combining annual licenses.
Boaters receive a renewal notification by mail about 60 days before their registration expires. Mailing of registration decals and boat registration cards occurs quickly for boat owners that have completed the registration process.
The Georgia Service Desk operated by the vendor will field about 200,000 calls per year to answer questions about Georgia boat registration and recreational hunting and fishing licenses at no charge to the caller, and to process license sales and boat registrations.
Can a Georgia license agent charge more than a $3.00 transaction fee?
Georgia Hunting and Fishing License Retail Agents (Sub-Agents) may not charge more than the state cost of each individual license plus a $3.00 Sub-Agent issuance fee. For example, a Georgia resident fishing license will cost a customer a total of $12.00 ($9.00 for the state cost of the license and a $3.00 Sub-Agent issuance fee). The $3.00 fee is charged one time for each license transaction, and a customer may purchase multiple licenses in a single transaction.
Extra fees are not allowed under the Georgia License Sub-Agent Agreement. Sub-Agents will only issue licenses over the counter, and only by using the secure, authorized Sub-Agent site provided by our outside contractor. Sub-Agents may charge fees for additional services such as license lamination, but these extra services must be optional.
Some locations sell hunting and fishing licenses using the same generally available online connection to the DNR license sales system that a customer would use from their own home computer. These locations are not Georgia Hunting and Fishing License Dealers (Sub-Agents), and can charge any transaction fee they choose. These locations have no agreement with DNR, have not received training on the license system, do not have Agent phone support, and cannot reverse customer payment transactions if the wrong license is issued.
Does Georgia have a disability hunting and fishing license?
Georgia offers discounted Disability Hunting and Fishing Licenses for permanently and totally disabled Georgia residents. There are full privilege Sportsman’s licenses and hunting or fishing only options, and there are 3-year and annual options. The 3-year option saves persons $6 over the life of the license compared to annual licenses, and does not require recertification of disability status each year.
The Disability Hunting and Fishing License cannot be obtained or renewed online - you will need to complete the Disability License Application form and mail it and supporting documents to the address on the form. Additional information and instruction for completing the form are on the back of the application. Strict document requirements document requirements are on the back of the form, and should be carefully reviewed and followed. Disability Hunting and Fishing License Application.
You will need to send the following with your completed application:
1. Either:
If veteran's affairs certified your disability—a copy of the Veterans Affair’s letter stating that you are 100% disabled, or one of the other documents listed in the application. The letter or document needs to be dated within the last year, and rather than being date stamped have a date included in the letter. If you are using the Veterans Affairs letter, the application describes a procedure near the bottom of the front page after “Veterans Office:” that we have worked out with the Veterans Office to request an acceptable Hunting and Fishing License Authorization Letter with an included date—please show them this section of the application if they are unfamiliar with the procedure.
OR
If the Social Security Administration certified your disability, you may send us a copy of the BPQY form (SSA-2459) AND the BPQY cover letter (SSAL634) dated within the past year. You may obtain these from the Social Security Office by calling 1-800-772-1213, and ask for a BPQY (SSA-2459) form and cover letter (SSA-L634).
2. AND
Proof of Georgia residency which may be a copy of a state issued identification card or driver’s license.
More information about document requirements is available on the Disability Hunting and Fishing License Application.
My name changed. How do I update my current license?
Regular Paper License and Updating Your Customer Account
It is important that the name on your license match photo identification (such as a driver's license). First, change your driver’s license to your new name. The,n coordinate the name change through our Service Desk at 1-800-366-2661. They will ask that you mail, fax or email a copy of your new driver's license or other legal documentation of name change. Or you may mail three pieces of information (1. old and new name plus birth date, 2. driver’s license, and 3. legal document) to the address below with a request to change your name. There is no charge for this service.
Georgia Department of Natural Resources
P.O. Box 934943
Atlanta, GA 31193-4943
Once your customer account is updated, you can replace (reprint) your current Georgia hunting and fishing license with your new name online for free through the online web site, by telephone or at a Georgia license agent.
How do I reprint (replace) a lost/ruined license?
Regular paper licenses can be replaced using the procedures below.
You can only replace your hunting or fishing license if it has not expired.
You can replace (reprint) all current Georgia hunting and fishing licenses online for FREE at www.GoOutdoorsGeorgia.com.
You will use your driver's license number or DNR customer number or SSN and your date of birth to access your DNR license account.
You will update personal information, address, and residency if changes are needed, and confirm by checking the appropriate box, Be sure to add your email address to your account so that you will receive email notification before your license expires—if you renew your license before it expires you will receive a discount of $2.75 on your total license purchase.
After you confirm your information is correct. Select the “Replace all Current Licenses” button.
You may then print your license at no charge.
Be sure that pop-up blocker or similar settings are turned off in your web browser. The license will appear as a pop-up screen.
Alternatively, any Georgia license agent can print a free replacement. You can ask the dealer to update any personal information in your account.
How do I replace a durable plastic lifetime license card?
A replacement durable plastic lifetime license card can be ordered online, ordered at retail license agents, ordered using the Lifetime Sportsman's License application form by mailing it to the address on the form, or by calling 1-800-366-2661. Customers may hand-deliver the completed application to selected Wildlife Resources Division office. Credit card transactions may not be available at every WRD office if hand delivered—please call the local office to verify. Replacement cards cost $10 plus the appropriate transaction fee ($2.50 online, $3.00 at WRD offices and retail agents, and $5.00 by telephone).
Resident Senior Lifetime License holders with this free license that have never obtained an optional plastic lifetime license card can order the card Online for a fee of $10 plus a $2.50 service fee, or they may use the options above to order a card.
Online Procedures:
Choose the link to "Purchase/Reprint Hunting & Fishing Licenses and Recreational Passes."
You will use your driver's license number or DNR customer number or SSN and date of birth to access your DNR license account.
You will update personal information, address, and residency, and confirm by checking the appropriate box, After you confirm your information is correct, select the “Purchase Licenses” button. Choose Lifetime Replacement to replace your lifetime license card. The cost for a replacement plastic card is $10 plus a $2.50 service fee if done online.
You may use your receipt as a temporary hunting and fishing license until your new plastic card arrives. It will take approximately 14 days to receive the replacement card.
Alternatively, you may order a replacement card at any Georgia license agent location. You can ask the agent to update any personal information in your account.
How do I update my mailing address or email?
Information in your WRD hunting/fishing/ boating customer online account such as mailing address or email can be edited by logging into your account. Use your driver's license number or DNR customer number or last four of SSN, last name, and date of birth to log into your account. Your customer information comes up and is editable.
If you wish to print a copy of your license with the new information, log into your account, check and certify your information is correct, and select "Reprint All Current Licenses." Your license document will appear as a popup that can be saved or printed.
Alternatively, you can call 1-800-366-2661 and request that your information be changed. You will need your driver's license number or DNR customer number and date of birth to verify your identity.
Also, you can stop in at any Georgia license dealer and they will go online, edit your information, and print a free replacement. List of agents by county.
I’m not a U.S. resident. How do I purchase a Georgia hunting or fishing license?
Non-residents may purchase a Georgia hunting and/or fishing license or GORP through any of the three available outlets. If you choose to purchase a license online, once you are on the purchase site, choose "Non-Resident", and check that are not a U.S. citizen. You will be able to identify a wide variety of documents to use for identification, and be able to enter the identification number on the document you decide to use. You'll need to carry this identification document with you in addition to your printed license while engaging in the activity requiring the license. Non-residents including non-resident children are covered under the same rules basic for residents. For example, non-resident children under 16 are not required to have a fishing license.
I am just going along on the hunting or fishing trip. Do I need a license?
Any person who is hunting or fishing, or providing any type of assistance to a hunter or angler must be licensed. Spotting game, carrying hunting gear, dragging out the deer, assisting in field dressing the deer, bringing over the ATV, handing up the gun to a person on a stand, netting a fish, baiting a hook, and similar activities would be a few examples of providing assistance to a hunter or angler. There are many other examples. You do not need a license if you provide no assistance to the hunter or angler. Simply taking pictures of the activity or taking pictures of the harvest would not require a license.
Why does DNR require your Social Security Number for licenses?
The 2002 session of the Georgia General Assembly amended Title 19, which deals with domestic relations and child support, to require that all persons buying any license or permit under Title 27 (Game and Fish Code) must furnish their Social Security number prior to the purchase of any such license or permit. This was done so as to bring Georgia into compliance with federal law (Title 42), which compels all states to adopt procedures for collecting Social Security numbers from persons procuring commercial, professional or recreational licenses and permits. The purpose of both laws is to enhance and improve the enforcement of child support laws. No dissemination of the Social Security number to any entity other than the Department of Human Resources is permitted, unless by court order.
What License Do I Need?
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msmarco_passage_01_404855942 | Prilosec and Weight Gain | Prilosec and Weight Gain
Prilosec and Weight Gain
Prilosec and Weight Gain: An Overview
There are a number of possible side effects with Prilosec ® ( omeprazole ). Weight gain does appear to be one of them. This data comes from clinical trials where Prilosec was extensively studied and its side effects were documented.
Understanding Clinical Trials
Before medicines are approved, they must go through several clinical studies where thousands of people are given a particular medicine and are then compared to a group of people not given the medicine. In these studies, the side effects are always documented. As a result, it is possible to see what side effects occur, how often they appear, and how they compare to the group not taking the medicine. Side effects are then usually separated into those side effects that occur in more than 1 percent of people and those that occur in less than 1 percent of people.
For people taking Prilosec, weight gain was reported as a rare side effect of the medication, occurring in less than 1 percent of people.
Prilosec and Weight Gain: Suggestions
If you are noticing unexplained weight gain while taking Prilosec, there are some things that you can do. Some suggestions include:
Eating a heart-healthy diet. This diet should include:
o Lots of fruits, vegetables, grains, and fat-free or low-fat milk and milk products
o Lean meats, poultry, fish, beans, eggs, and nuts
o Limited foods with saturated fats, trans fats, cholesterol, magnesium (salt), and added sugars.
Getting regular physical activity for at least 30 minutes a day on most days of the week.
Limiting your intake of alcohol.
Also, if you are noticing a weight gain with Prilosec, talk to your healthcare provider. He or she can give you other suggestions for dealing with any weight gain. He or she may also look for other causes of weight gain, such as certain types of medical conditions. If the weight gain continues, he or she may also recommend other lifestyle changes or possibly switching to another medicine.
(Click BMI Calculator to see if your weight is within a healthy range.)
eMedTV's free HealthSavvy service can help you stay up-to-date on this topic. Sign up for HealthSavvy now.
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msmarco_passage_01_425707650 | Coffee withdrawal symptoms? | Go Ask Alice! | Coffee withdrawal symptoms? | Go Ask Alice!
Coffee withdrawal symptoms?
Hi Alice,
Been reading your site for a while and wanted to first thank you for an excellent site! So anyway, here's the question:
I've been having headaches off and on for the past year and noticed that it seems to coincide with days that I don't drink coffee in the morning. I've heard of becoming "addicted" to caffeine, so I decided I should just go ahead and quit for a while. This past week, I cut out coffee and all caffeine-related products from my diet, and have been suffering from pounding headaches every day. Today (six days from my last cup of coffee) is the first day that I don't seem to have a headache. Is this common? And also, any ideas on what will happen if I do have some coffee? Will my system require coffee every day again (at the sake of a pounding headache)? I'm completely clueless on this, and I love coffee, so any advice would be helpful.
— de-caffeinated and hating it
Dear de-caffeinated and hating it,
Headaches are a normal response to an abrupt and drastic cut in the supply of caffeine to the system. If you drink lots of coffee, or somehow provide your body with a steady, high supply of caffeine, with time, your body will develop a tolerance to caffeine. When you deprive your body of the caffeine it has grown accustomed to, it struggles to cope with this sudden change. In the coping process, you end up with a pounding headache. Headaches, irritability, lethargy, nervousness, and mild depression are all fairly common withdrawal symptoms associated with caffeine intake. As you have experienced, withdrawal symptoms from cutting caffeine from your routine typically go away after several days.
Withdrawal symptoms from a caffeine "detox" are nowhere near as severe as symptoms of withdrawal from other drugs. Although it does produce physical dependence, most of us would not identify caffeine as a dependency-producing drug. For more information on caffeine specifically, you can check out Long-term effects of caffeine-based drugs in the Go Ask Alice! Alcohol & Other Drugs archives.
As for your other issue, it's not a question of "if I do have some coffee...?" — rather, it's one of "can I have some coffee without having some more, and then maybe one more cup for the road?" It's possible to drink a cup of coffee every now and then, or even one a day, without developing such a strong tolerance that your headaches come back to haunt you on your first coffeeless morning. The key here is moderation. It's also good to be aware of the caffeine content of other beverages you drink, primarily teas and sodas. Make sure you're not substituting one form of caffeine for another. For more information, see Caffeine content.
If you really can't live without coffee, drink one cup of full strength and then switch to decaf for the rest of the day. Or, make your pots half-decaf and half-caff, and use premium coffee roasts, such as French Roast, Viennese, and Yukon Gold... get the aroma?
Bottoms up!
Alice! |
msmarco_passage_01_425887312 | How do birth control pills work? | Go Ask Alice! | How do birth control pills work? | Go Ask Alice!
Sexual & Reproductive Health
Contraception
Birth Control Pills
How do birth control pills work?
Alice,
How do birth control pills work?
— Woman
Dear Woman,
Despite being small in size, birth control pills pack a punch in preventing pregnancy! This occurs through several mechanisms, mainly by stopping ovulation; when ovaries don't release eggs, sperm can't find and fertilize them to result in a pregnancy. Most birth control pills contain synthetic forms of one or more hormones: estrogen and progestin. These hormones stabilize natural hormone levels and prevent estrogen from peaking in the middle of the menstrual cycle. Without the estrogen bump, the pituitary gland doesn't release other hormones that normally cause the ovaries to release mature eggs. Specifically, synthetic estrogen works to stop the pituitary gland from producing follicle stimulating hormone (FSH) and luteinizing hormone (LH) in order to prevent ovulation. It also supports the uterine lining (endometrium) to prevent breakthrough bleeding mid-cycle. Meanwhile, synthetic progestin works to stop the pituitary gland from producing LH in order to prevent an egg from being released, make the uterine lining inhospitable to a fertilized egg, partially limit the sperm's ability to fertilize the egg, and thicken the cervical mucus to hinder sperm movement (although this effect may not be key to preventing pregnancy). Want to know more? Keep on reading!
There are two kinds of hormonal birth control pills. Different types of pills contain different amounts of progestin and estrogen. The first is called a combination pill, which contains both estrogen and progestin. One added benefit of combination pills is that users experience less breakthrough bleeding. Combination pills can be broken down into two categories, which differ in how frequently users have withdrawal bleeding (which mimics a menstrual period). Conventional pills generally have 21 or 24 active pills and seven or four inactive pills, respectively, creating packs of 28 pills. For continuous dosing or extended cycles pills, the packs can have 84 active pills with seven inactive pills or contain only active pills. With either form of pill, the inactive pills can trigger the withdrawal bleeding, and if the active pills were taken correctly and consistently, pregnancy protection will still exist during this time. If using a formulation with only active pills, the bleeding may stop completely. On top of being separated into conventional and continuous, combination pills are also categorized by hormone dosage. The monophasic active pills contain the same amount of estrogen and progestin during the cycle. However, in multiphasic active pills, the amounts of estrogen and progestin change during the cycle. Of the multiphasic pills, biphasic pills have two different progesterone doses, one of which is increased halfway through the cycle, while triphasic pills gradually increase the dose of estrogen (and in some cases, progesterone) two times during the cycle.
The second kind of hormonal birth control pill is the progestin-only pill (also known as the minipill). The amount of progestin in the minipill is less than in the combined pill. It works by thickening the cervical mucus and thinning the endometrium. Sometimes it will suppress ovulation. The progestin-only pills come in 28 day pill packs. Each day is an active pill and doesn't contain any inactive pills. The progestin-only pills may cause some people to experiencing breakthrough bleeding between periods.
Both combination and progestin-only pills are available in several brands, and each has a slightly different blend of hormones. All birth control pills work most effectively when daily, but the consequences of not taking the pill at the same time every day differ based on pill type. Combination pills need to be taken every day but not necessarily at the same exact time every day. Minipills must be taken at the same time every day within a three hour window. Regardless of the kind, when you forget your pill (or take it three to four hours late or more), this causes a dip in your body's levels of the birth control hormones. To maximize pregnancy prevention potential and to minimize side effects, consider picking a time you're likely to remember – maybe first thing in the morning or right before bed – to take your pills every day. If you're concerned that you have missed a dose, it's wise to consult with a health care provider, as the correct course of action depends on the type and brand of birth control.
As if there aren’t already enough options to consider, hormonal birth control is also available in more than just pill form! The combination formula is available as a patch and a vaginal ring, while the progestin-only formula is available in intramuscular shots, an implant, and in intrauterine devices. Some may prefer these other forms of hormonal birth control because they can be taken less often (and consequently are easier to remember). However, for some people, hormonal birth control may not be an option due to various medical conditions or undesirable side effects. Figuring out what works best for a person may take some trial and error to determine what side effects are manageable and which aren't. Some folks need to try several out over time to find one that is agreeable to them, beyond just being effective.
For more information on how birth control pills work, check out the Go Ask Alice! Sexual and Reproductive Health archives. You can also read more in the Contraception section to learn more about different types of contraceptives. Your health care provider can also offer more information about different kinds of birth control, including which method might be best for your lifestyle and needs.
Take care,
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msmarco_passage_01_425994531 | Marijuana: Does it cause cancer? | Go Ask Alice! | Marijuana: Does it cause cancer? | Go Ask Alice!
Alcohol & Other Drugs
Marijuana, Hash, & Other Cannabis
General Health
Cancer
Marijuana: Does it cause cancer?
Dear Alice,
I have been reading some of your info about marijuana. My question is: If it is so much stronger than smoking cigarettes and has some of the same ingredients, why don't we hear reports of people who have some form of cancer?
Dear Reader,
Despite the fact that humans have been growing marijuana for thousands of years, and using it recreationally in the United States since the early 20th century, its effects have not been as thoroughly studied as those of tobacco and cigarette smoking. Most studies exploring the relationship between marijuana smoking and cancer are retrospective case-control studies (a type of observational study in which participants are selected based on their health status, such as having cancer or not having cancer). Many of these studies have shown that the individuals who have smoked marijuana have also smoked cigarettes. Because there is a clear correlation between cigarettes and cancer, the use of them among marijuana smokers in these studies makes it difficult to tease apart a connection between cancer and marijuana specifically. And despite the knowledge that carcinogens in smoked marijuana have the potential to cause cancer, more research is needed to see if there is any relationship between marijuana and cancer (as well as some other health consequences, including lung function, bronchial irritation, and/or chronic obstructive pulmonary disease).
Frequent marijuana users tend to consume less of the drug than heavy cigarette smokers; however, marijuana smokers usually inhale more deeply and keep the smoke in their lungs for a longer period than tobacco smokers. It is possible that these behaviors increase the lung's exposure to chemical by-products associated with smoking. Burning marijuana for smoking releases many substances, some of which are carcinogens, including tar, carbon monoxide, and cyanide. One known carcinogen, benzopyrene seems to be greater in pot smoke than cigarette smoke.
Determining whether there’s a link between marijuana and cancer isn’t exactly clear cut. Besides the use of cigarettes and marijuana overlapping in many studies, retrospective case-control studies are limited to what people remember and choose to report — both of which are potential sources of bias. Also, observational studies can show correlation (or lack thereof) but not cause and effect. So, in this case, two things that seem to be related to one another may not indicate a cause, but instead are influenced by other factors. Identifying a cause and effect can be tricky, too, because the ability to control for those other factors in research presents ethical concerns (i.e., instructing some study participants to smoke marijuana and others not to, then monitor all participants for cancer growth). However, prospective observational studies (such as recruiting participants who either do or do not smoke marijuana already and are willing to be followed for changes in health status) may be helpful in understanding the relationship between smoking marijuana and cancer (and/or other health issues).
On the flip side, researchers are also looking for possible health benefits associated with marijuana use — especially among individuals with cancer. Some preclinical (meaning very early stage) studies suggest marijuana may have some antitumor properties. In terms of clinical (later stage) studies, research has shown that marijuana can help manage symptoms of cancer and side effects of some cancer treatments, including:
Pain relief
Anxiety
Sleep
Appetite stimulation
Nausea and vomiting
The bottom line is that more research is needed to better understand the connection between marijuana use and potential health risks and/or benefits. For now, keep your eyes peeled for what information future studies might reveal. To learn more about what factors are associated with cancer, check out the American Cancer Society (ACS) and the National Cancer Institute (NCI).
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msmarco_passage_01_42749333 | Intracranial Pressure Monitoring: Background, Indications, Contraindications | Intracranial Pressure Monitoring: Background, Indications, Contraindications
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Drugs & Diseases > Clinical Procedures
Intracranial Pressure Monitoring
Updated: Apr 01, 2018
Author: Gaurav Gupta, MD, FAANS, FACS; Chief Editor: Jonathan P Miller, MD more...
Sections
Intracranial Pressure Monitoring
Sections Intracranial Pressure Monitoring
Overview
Background
Indications
Contraindications
Complications
Show All
Periprocedural Care
Patient Education & Consent
Equipment
Patient Preparation
Anesthesia
Show All
Technique
Approach Considerations
Intraparenchymal Fiberoptic Catheter Placement
Interpretation of Waveforms
Show All
References
Overview
Background
Elevated intracranial pressure (ICP) is seen in head trauma, [ 1] hydrocephalus, [ 2] intracranial hemorrhage, sub-arachnoid hemorrhage from ruptured brain aneurysm, intracranial tumors, [ 3] hepatic encephalopathy, [ 4] and cerebral edema. [ 5] Intractable elevated ICP can lead to death or devastating neurological damage either by reducing cerebral perfusion pressure (CPP) [ 6] and causing cerebral ischemia or by compressing and causing herniation of the brainstem or other vital structures. Prompt recognition is crucial in order to intervene appropriately.
Intractable high ICP is the most common "terminal event" leading to death in neurosurgical patients. [ 7] The association between the severity of intracranial hypertension and poor outcome after severe head injury is well recognized. [ 6] Outcomes tend to be good in patients with normal ICP, whereas those with elevated ICP are much more likely to have an unfavorable outcome. [ 8] Elevated ICP carries a mortality rate of around 20%. [ 9]
The rapid recognition of elevated ICP is therefore of obvious and paramount importance so that it can be monitored and so that therapies directed at lowering ICP can be initiated. A raised ICP is measurable both clinically and quantitatively. Continuous ICP monitoring is important both for assessing the efficacy of therapeutic measures and for evaluating the evolution of brain injury. [ 10]
Although some investigators have questioned invasive ICP monitoring in improving patient outcomes, [ 11, 12] numerous retrospective series and data bank studies have favored the technique. [ 13, 14, 15, 16]
The goal of ICP monitoring is to ensure maintenance of optimal CPP. The ICP also forms a basis for medical or surgical intervention in cases of increased ICP with agents such as 3% sodium chloride (NaCl), mannitol, or diuretics (Lasix), ventriculostomy, cerebrospinal fluid (CSF) diversion, and pentobarbital coma or surgical decompression in cases of intractable ICP elevation that do not respond to conservative management.
ICP monitoring may be discontinued when the ICP remains in the normal range within 48-72 hours of withdrawal of ICP therapy or if the patient’s neurological condition improves to the point where he or she is following commands.
History
The concept of ICP (normal or abnormal) being a function of the volume and compliance of each component of the intracranial compartment was proposed by the Scottish anatomist and surgeon Alexander Monro (1733-1817) and his student George Kellie (1758-1829) during the late 18th century. [ 17, 18] The interrelationship came to be known as the Monro-Kellie hypothesis. This doctrine states that the cranial compartment is encased in a nonexpandable case of bone, and, thus, the volume inside the cranium is fixed.
The doctrine further states that, in an incompressible cranium, the blood, CSF, and brain tissue exist in a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another. For example, the arterial blood entering the brain requires a continuous outflow of venous blood to make room. If something does not exit the cranial compartment to make room, the ICP increases, resulting in pathology.
The confirmatory exsanguination experiments of Abercrombie, also a student of Monro, demonstrated graphically the extent to which the body placed physiological priority on maintaining the perfusion of the brain. [ 19] He drained dogs of their blood and was able to observe that the brain remained comparatively well perfused until shortly before death regardless of the dog’s position in space (hanging upside down or right side up, to control for the effects of gravity), unless the blood was drained from an intracranial vessel directly, in which case death resulted almost immediately.
The reciprocal relationship between venous and arterial blood was considered the main variable in ICP and perfusion until 1848, when George Burrows, an English physician, repeated many of the exsanguination and gravitational experiments of Abercrombie and Kellie and found a reciprocal relationship between the volume of CSF and the volume of blood in the intracranial compartment. [ 20]
Leyden, working in Germany in 1866, demonstrated that elevated ICP leads to a slowed pulse and difficulty breathing, with eventual arrest of breathing entirely. [ 21] This work was built on in 1890 by Spencer and Horsley [ 22] , who found that, in the case of intracerebral tumors, death was brought about by the arrest of breathing due to increased ICP. Increased ICP was thus taken to represent a common endpoint for several insults to the brain.
In 1891, Quinke published the first studies on the technique of lumbar puncture (LP) and insisted that a glass pipette be affixed to the needle so that the CSF pressure could be measured. [ 23] This technique for repeated measurement of CSF fluid pressure as an assessment of ICP became widely used and was the earliest clinical method of ICP measurement.
In 1903, Cushing described what is now widely known as the "Cushing Triad" as a clinical tool for recognizing the presence of elevated ICP. The triad consists of a widening pulse pressure (rising systolic, declining diastolic), irregular respirations, and bradycardia. [ 24] In 1922, Jackson noted that the pulse, respiration, and blood pressure are affected only once the medulla is compressed, and some patients with clinical signs of brain compression had normal lumbar CSF pressures. [ 25] Cushing quantified the Monro-Kelly doctrine, writing that the sum of the volume of the brain plus the CSF volume plus the intracranial blood volume is constant. Therefore, an increase in one should reduce one or both of the others. [ 26]
In 1964, Langfitt demonstrated that LP could induce brainstem compression through transtentorial herniation or herniation of the tonsils through the foramen magnum and that, further, when the ventricular system does not communicate, spinal pressure is not an accurate reflection of ICP. [ 27] LP fell into disuse for ICP monitoring, and researchers began to directly cannulate the ventricular system. [ 28]
In 1965, Nils Lundberg revolutionized ICP monitoring with his work using bedside strain gauge manometers to record ICP continuously via ventriculostomy. [ 29] In his technique, a ventricular catheter was connected to an external strain gauge. This method has proven to be accurate and reliable and also permits therapeutic CSF drainage. Catheter-based ventricular monitoring systems were not applied systematically until the mid-1970s, when monitoring via a strain gauge became widespread after Becker and Miller reported good results in 160 patients with traumatic brain injury. They demonstrated clear evidence of good outcomes among patients in whom elevated ICP could be quickly recognized and subsequently lowered. [ 13]
Physiology
The most important role of the circulatory system, aside from transporting blood into all parts of the body, is to maintain optimal CPP. [ 30] The formula for calculating CPP is below.
CPP = mean arterial blood pressure (MAP) - mean intracranial pressure (MIC)
CPP is the pressure gradient acting across the cerebrovascular bed and, therefore, a major factor in determining cerebral blood flow (CBF). [ 31] CBF is kept constant in spite of wide variation in CPP and MAP by autoregulation.
Autoregulation is a process of adjustment on the part of the brain’s arterioles that keeps cerebrovascular resistance constant over a range of CPP. Increased CPP causes stretching of the walls of the arterioles, which compensate by dilating and relieving this pressure. Likewise, in the setting of decreased pressure, the arterioles constrict to maintain CPP. This autoregulation prevents transient pressure increases from being transmitted to smaller distal vessels. When the MAP is less than 65 mm Hg or greater than 150 mm Hg, the arterioles are unable to autoregulate, and blood flow becomes entirely dependent on the blood pressure, a situation defined as "pressure-passive flow." The CBF is no longer constant but is dependent on and proportional to the CPP.
Thus, when the MAP falls below 65 mm Hg, the cerebral arterioles are maximally dilated and the brain is at risk for ischemia because of insufficient blood flow to meet its needs. Likewise, at a MAP greater than 150 mm Hg, the cerebral arterioles are maximally constricted and any further increases in pressure cause excess CBF that may result in increased ICP.
Note that, while autoregulation works well in the normal brain, it is impaired in the injured brain. As a result, pressure-passive flow occurs within and around injured areas and, perhaps, globally in the injured brain. Ideally, the goal is to maintain the CPP more than 60 mm Hg, and this can be done by either decreasing the ICP or increasing the systolic blood pressure using vasopressors. Caution should be used to use only vasopressors that do not increase ICP.
The volume of the skull contains approximately 85% brain tissue and extracellular fluid, 10% blood, and 5% CSF. If brain volume increases, for example in the setting of cancer, there is a compensatory displacement of CSF into the thecal sac of the spine followed by a reduction in intracranial blood volume by vasoconstriction and extracranial drainage. If these mechanisms are successful, ICP remains unchanged. Once these mechanisms are exhausted, further changes in intracranial volume can lead to dramatic increases in ICP.
The time course of a change in the brain has significance for how ICP responds. A slow-growing tumor, for example, is often present with normal or minimally elevated ICP, as the brain has had time to accommodate. On the other hand, a sudden small intracranial bleed can produce a dramatic rise in ICP. Eventually, whether acute or insidious in progression, compensatory mechanisms are exhausted, and elevated ICP follows.
The relationship between ICP and intracranial volume is described by a sigmoidal pressure-volume curve. Volume expansion of up to 30 cm 3 usually results in insignificant changes in ICP because it can be compensated by extrusion of CSF from the intracranial cavity into the thecal sac of the spine and, to a lesser extent, by extrusion of venous blood from the cranium. When these compensatory mechanisms have been exhausted, ICP rises rapidly with further increases in volume until it reaches the level comparable with the pressure inside of cerebral arterioles (which depends on MAP and cerebrovascular resistance but normally measures between 50 and 60 mm Hg). At this point, the rise of ICP is halted as cerebral arterioles begin to collapse and the blood flow completely ceases.
The relationship between ICP and CBF and functional effects was described thoroughly by Symon and colleagues, as follows: [ 32]
CBF of 50 mL/100 g/min: Normal
CBF of 25 mL/100 g/min: Electroencephalogram slowing
CBF of 15 mL/100 g/min: Isoelectric electroencephalogram
CBF of 6 to 15 mL/100 g/min: Ischemic penumbra
CBF of less than 6 mL/100 g/min: Neuronal death
Normal intracranial pressure
ICP is generally measured in mm Hg to allow for comparison with MAP and to enable quick calculation of CPP. It is normally 7-15 mm Hg in adults who are supine, with pressures over 20 mm Hg considered pathological and pressures over 15 mm Hg considered abnormal. [ 33]
Note that ICP is positional, with elevation of the head resulting in lower values. A standing adult generally has an ICP of -10 mm Hg but never less than -15 mm Hg. [ 34] In supine children, ICP is normally lower, in the range of 15 mm Hg, with infants having ICP from 5-10 mm Hg and newborns have subatmospheric pressures regardless of position. [ 35]
In adults, the choroid plexus and other locations in the CNS produce CSF at a rate of 20 mL/hour, for a total of 500 mL/day. It is reabsorbed by the arachnoid granulations into the venous circulation. CSF volume is most commonly increased by a blockage of absorption due to ventricular obstruction, occlusion of venous sinuses, or clogging of the arachnoid granulations.
Causes of increased intracranial pressure
Increased ICP may result from the following:
Space-occupying lesions: Tumor, abscess, intracranial hemorrhage (epidural hematoma, subdural hematoma, intraparenchymal hematoma)
CSF flow obstruction (hydrocephalus): Space-occupying lesion that obstructs normal CSF flow, aqueductal stenosis, Chiari malformation
Cerebral edema: Due to head injury, ischemic stroke with vasogenic edema, hypoxic or ischemic encephalopathy, postoperative edema
Increase in venous pressure: Due to cerebral venous sinus thrombosis, heart failure, superior vena cava or jugular vein thrombosis/obstruction
Metabolic disorders: Hypo-osmolality, hyponatremia, uremic encephalopathy, hepatic encephalopathy
Increased CSF flow production: Choroid plexus tumors (papilloma or carcinoma)
Idiopathic intracranial hypertension
Pseudo tumor cerebri
Indications
The most common indication for invasive ICP monitoring is closed head injury. [ 33] Per the Guidelines for the Management of Severe Traumatic Brain Injury, [ 36] an ICP monitor should be placed in patients with a Glasgow coma score less than 8T (after resuscitation) and after reversal of paralytics or sedatives that may have been used during intubation. (See the Glasgow Coma Scale calculator.)
Other candidates for ICP monitoring are as follows:
A patient who is awake yet at risk for increased ICP under general anesthesia for a necessary nonneurosurgical procedure (eg, orthopedic limb-saving procedure), rendering clinical observation impossible
Patients who have nonsurgical intracranial hemorrhage but are intubated for nonneurosurgical reasons, preventing clinical examination
Patients with moderate head injury who have contusions to the brain parenchyma that are at risk of evolving (Extreme caution and clinical judgment must be exercised for lesions in the temporal fossa, since their proximity to the brainstem can lead to catastrophic herniation and brainstem compression with little change in the global ICP.)
Perioperative ICP monitoring is indicated in patients who have just undergone tumor or arteriovenous malformation resection and are at risk for cerebral edema with an inability to follow a clinical neurological examination.
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Contraindications
Placement of an ICP monitor has no absolute contraindications, because it is a relatively low-risk procedure. However, clinical judgment should be exercised, especially in patients with a known bleeding disorder. Patients with thrombocytopenia (platelets count of < 10,000/µL), known platelet dysfunction (inhibition due to antiplatelet agents such as aspirin/clopidogrel or uremic encephalopathy), prothrombin time greater than 13 seconds, or an international normalized ratio (INR) greater than 1.3 are at elevated risk for hemorrhage secondary to placement of an ICP monitor.
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Complications
EVD placement
Potential complications include intraparenchymal, intraventricular, or subdural hemorrhage. Recent studies have shown that catheter-related hemorrhages occur in 1%-33% of patients. [ 37]
Infection occurs in 1%-12% of patients. Symptoms suggestive of infection should prompt CSF analysis for cell count and culture along with antibiotic therapy, as appropriate. Staphylococci are the most common pathogens. Higher rates of bacterial ventriculitis/meningitis occur with longer duration of EVD placement. [ 38] Risks may be minimized with careful placement of the catheter and maintenance of the system under strict sterile conditions, use of antibiotic prophylaxis (eg, cefuroxime 750 mg every 8 hours from the time of catheter insertion until 24-48 hours after removal). [ 39] Exchange of the catheter every 5 days, although a common practice, does not appear to decrease the risk of infection; in fact, repeated catheter insertions have been found to be associated with higher risk of ventriculitis. [ 40]
Catheter occlusion due to clotted blood at the EVD orifice may be relieved by irrigation with sterile saline or catheter replacement.
System malfunction is possible. For example, damping of the waveform may be caused by apposition of the catheter tip against the ventricular wall or obstruction of the catheter by a blood clot or an air bubble.
Intraparenchymal fiberoptic catheter placement
Potential complications of intraparenchymal fiberoptic catheter placement include intraparenchymal, cortical, or subdural hemorrhage. Infection can occur, although it is rare.
The catheter can be kinked or bent, leading to errors in measurement. If the monitor is damaged, the fiberoptic probe should be replaced. Usually, the bolt itself (which secures the probe to the skull) does not need to be replaced.
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Periprocedure
References
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Contributor Information and Disclosures
Author
Gaurav Gupta, MD, FAANS, FACS Associate Professor of Neurosurgery, System Co-Director, Cerebrovascular and Endovascular Neurosurgery, Fellowship Director, Endovascular Neurosurgery Fellowship (Site), Department of Surgery, Division of Neurosurgery, Rutgers RWJ Barnabas Healthcare, Rutgers Robert Wood Johnson Medical School
Gaurav Gupta, MD, FAANS, FACS is a member of the following medical societies: American Academy of Neurology, American Association for the Advancement of Science, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, Congress of Neurological Surgeons, Facial Pain Association, Society for Neuroscience, Society of NeuroInterventional Surgery
Disclosure: Nothing to disclose.
Coauthor (s)
Sudipta Roychowdhury, MD Clinical Associate Professor of Radiology, Department of Radiology, Rutgers Robert Wood Johnson Medical School; Attending Radiologist/Neuroradiologist, University Radiology Group, PC
Sudipta Roychowdhury, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Neuroradiology, Medical Society of New Jersey, Radiological Society of New Jersey, Radiological Society of North America, Society of NeuroInterventional Surgery
Disclosure: Nothing to disclose.
Chief Editor
Jonathan P Miller, MD Director, Functional and Restorative Neurosurgery, Director of Epilepsy Surgery, Attending Neurosurgeon, University Hospitals Cleveland Medical Center; Director, Functional and Restorative Neurosurgery Center, UH Cleveland Medical Center Neurological Institute; Associate Professor of Neurosurgery, Fellowship Director, Functional and Stereotactic Neurosurgery, Associate Residency Program Director, Department of Neurosurgery, Surgical Director, Neuromodulation Center, Case Western Reserve University School of Medicine
Jonathan P Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, American Epilepsy Society, American Society for Stereotactic and Functional Neurosurgery, Congress of Neurological Surgeons, International Neuromodulation Society, North American Neuromodulation Society, Ohio State Neurosurgical Society, Society of Neurological Surgeons
Disclosure: Nothing to disclose.
Additional Contributors
Michael G Nosko, MD, PhD Associate Professor of Surgery, Chief, Division of Neurosurgery, Medical Director, Neuroscience Unit, Medical Director, Neurosurgical Intensive Care Unit, Director, Neurovascular Surgery, Rutgers Robert Wood Johnson Medical School
Michael G Nosko, MD, PhD is a member of the following medical societies: Academy of Medicine of New Jersey, Congress of Neurological Surgeons, Canadian Neurological Sciences Federation, Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, New York Academy of Sciences, Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Thomas J Cusack, MS University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Thomas J Cusack, MS is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Medical Society of New Jersey
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msmarco_passage_01_431078343 | Pulling Back the Curtain on Making Partner in a Big 4 Firm - Going Concern | Pulling Back the Curtain on Making Partner in a Big 4 Firm - Going Concern
Big 4 January 23, 2014
Pulling Back the Curtain on Making Partner in a Big 4 Firm
by Adrienne Gonzalez
Ed. note: Sam Flynn is a Big 4 Senior Manager lingering around waiting to decide if he wants to be a partner. This is his story.
Recently, I watched a new firm video discussing the partner admission process. The presentation included perspectives from several parties including the CEO and newly minted partners. This was a new development for our firm. I’m not sure if they read accounting tabloids and wanted to dispel some “myths” (highly unlikely) or if they just realized that experienced folks are running for the hills more often because they don’t know anything about the process, or when it will apply to them, and they wanted to plug that flow a bit (much more likely). Whatever the reason, it provided me with a chance to convey what my firm is describing as the “process” and the key attributes required to make partner. After watching it, I was pleased to see that many of the aspects of making partner I've seen discussed on Going Concern, while not exactly “written” in this presentation, were at least addressed and confirmed.
Gimme the Stats
The presentation started with some stats. The first was to levelset how few partners are actually made each year. There are less than 10,000 partners in the Big 4 combined (all practices) with roughly 75% of those being audit partners. Our firm is in the neighborhood of 2,000 partners with 50-70 new partners each year with the audit numbers being consistent around 75%. This means roughly 4% turnover in the partner class assuming a consistent level of partners leaving for retirement or other pastures. On average let’s say about 40 new audit partners are made in a year. Given the size of a Big 4 firm, you’re not talking about a lot of partner opportunity each year since the senior manager pool is pretty large.
The Sweet Sixteen
The second stat thrown out there was the number of years to partner, which is on average 16. This marks a bit of an increase from when I first joined the firm. In those days (a scant 12 years ago) the mantra was that the path to partnership was a 12-15 year road on average. Certainly a lot has changed since then (the biggest of course being audit fees not continuing to skyrocket) and this is the first time I had heard the number of years formalized. They also made the point that all of the partners they directly hire from outside the firm don’t impact the number of spaces for the homegrown partners. There was a lot of talk about how these partners actually make more opportunities for the firm because they bring with them a book of business, etc etc but at that point it sounded mostly like lip service to defend why it takes so long to make partner. This was especially true when coupled with talk about how it’s not the length of time it takes to make partner, but the time you get to be in that role that’s more important.
The other major item covered in terms of “pulling the curtain” back was the process. While I knew most of the steps, I did actually learn a little more about the depth of the interview cycle as well as the specific timeline for making these decisions (it’s basically a year-long cycle). The major steps look like this:
1) Decide the pipeline. The firm leadership figures out which of the senior managers are in the pipeline to become partner. The big point here was to make sure as a senior manager you had a “sponsor”. This might be your “mentor” or just someone you know will speak up for you when other partners get together. The best way to be in the pipeline is to have another partner talk enough about you so that there is no choice for you but to be in the pipeline. Score a point for “it’s not what you know but who you know.”
2) Functional panel interviews. You get a chance to be grilled by people within your function (e.g., audit) to make sure you are partner worthy. Here they are interviewing more people than they have partner slots for and it’s quite possible that you don’t make the cut. If you miss it, then you work on a development plan so you can try again the next year. It didn’t sound like there was much of a chance for you though if you miss year 2.
3) Cross functional panel interviews. Similar to the functional panel interviews but done with individuals outside of your practice and generally with folks you’ve never met before. This allows you to demonstrate your knowledge of the firm and gives strangers a chance to see how well you carry yourself as a potential partner. Concurrently, the firm does their background checks on you (perhaps looking for friends who need a few bucks and are willing to make illegal insider trades).
4) Board of Directors interview. This is the one on one interview that makes or breaks your partner candidacy. It will be with a Board member you don’t know, in a service line that you are not primarily in. The interviews become tailored to your own experience and are the final determination of whether you have what it takes to hold yourself as a partner in the firm. It’s billed as a “two-way” interview so the firm is also looking for you to come to the table with insightful questions that demonstrate you know about (and care about) the operations of the firm. In the end, this becomes the determination of whether you belong in the “club.”
5) If you make it through the above the firm announces you as a partner and you get showered in the financial gains that come along with it (after you take out a loan to cover the initial capital contribution of course). The partners made it very clear that some aspects about being a partner aren’t the hottest like paying full amount of health care costs, subject to dealing with liability, having to keep a capital account. However, they were also quick to point out that other aspects are pretty sweet, such as large financial gain, multiple partner retirement plans and tax services to keep the IRS happy, and that these more than trump the potential cons of partnership.
Your Part of the Deal
The rest of the presentation covered all of the “skills and behaviors” needed to become a partner. There was nothing overly surprising in this portion. They focused a lot on ethics and integrity, which wasn’t surprising considering the events of the past year. This included the need to make sure you were on top of all of the little compliance things thrown your way during the year. They also mentioned it helps to bring with you a portfolio of which companies you are thinking about pursuing, which you are already pursuing and which you have helped to previously win. Finally, they reiterated that it wouldn’t be bad if you were willing to take on new industries and new geographies to help fill the gaps at the firm.
The unintentional highlight of the presentation was the topic of diversity. Three times diversity was mentioned by one individual including a discussion of the diversity advisory board, which I wasn’t aware existed, without ever saying what exactly was considered “diverse”. Then someone else jumped in and stated that it didn’t mean you had to be diverse, it could also cover what you did to make sure your teams were diverse. It was so generic and felt so different than the rest of the presentation that it was clear it was just a check the box activity to make sure they covered that the partnership wasn’t entirely a white man’s club.
Overall, I don’t think there was much that was groundbreaking in this presentation but it was nice to see a somewhat open discussion of the process for us potentially in the pipeline.
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msmarco_passage_01_432017229 | Phil Jayhan: The "4" Flights of 9/11 – What Happened to the Passengers? | Phil Jayhan: The "4" Flights of 9/11 – What Happened to the Passengers?
/ Home / News / Accountability / 9/11 / Phil Jayhan: The "4" Flights of 9/11 – What Happened to the Passengers?
Phil Jayhan: The "4" Flights of 9/11 – What Happened to the Passengers?
August 8, 2010 by Steve Beckow
We discussed the passengers on the 9/11 planes the other day. Phil Jayhan, a well-known 9/11 researcher, has done some work on the question.
The “4” Flights of 9/11 – What about the Passengers? What happened to them?
by Phil Jayhan
Let’s Roll Forum
March 7, 2010
https://tinyurl.com/2ak3xmh
Most people are not aware that there are issues with the 4 groups of people who flew on the 4 flights of 9/11 from 3 locations. There are so many issues it would take a newsroom full of dedicated reporters a long time to sift through it all.
There are problems with the boarding of passengers on 3 flights. And on the 4th flight we find 2 boardings, an unusual event to say the least. Two of the aircraft, we are to believe didn’t even take off on 9/11, as this is what registers in the BTS database for flights 11 & 77 on 911. Two of the aircraft that allegedly struck the towers, can be plausibly shown to be drones, calling into question both passenger and crew from those respective flights. (11 & 175) While flight 77 obviously didn’t crash at the Pentagon from all evidence shown, and flight 77 is one of the 2 flight which BTS shows no departure time for.
While flight 93 wasn’t even a regular flight on 9/11, it was created in the last 2 hours before it flew. And as you will see are good reasons to believe Flight 93 was boarded twice at Newark. If this sounds confusing, it is because it was meant to be so. But I believe this article shows it is possible to make some simple sense out of the days events and tie them all together.
What was alleged to have been Flight 11, crashing into the North Tower on 9/11/2001 at 8:46 AM. Notice the bright flash at the towers face just prior to impact.
This was taken by the Naudet brothers, filming a documentary of 911. Below is a screen-shot of the BTS database, Bureau of Traffic Statistics. Oddly it shows that Flight 11, with no wheels off time, or departure time, showing that it never took off on 9/11.
This exact same oddity is duplicated regarding the Flight 77, the other American Airlines flight on 9/11 which allegedly took off from Dulles. The BTS database shows that the 2 American airlines planes, flights 11 & 77, as having no wheels off time or departure times. This is actually a key to understanding 9/11 as well as the mystery of the planes & passengers.
One mystery compounds into another creating a chain or sequence of events that become confusion. The largest blunder that 911 investigators have made is to be aware of this BTS discrepancy and then act as though it wasn’t there. Nearly everyone who becomes aware of this BTS discrepancy, then go on to assume that these passengers somehow still ended up on flight 11.
The passengers did disappear after all, did they not? And we were all told that they boarded and were on flight 11, right? We have Air Traffic controllers as eye witnesses saying that flight 11 was seen on radar, and followed all the way to the North Tower of the World Trade Center complex. We also then have the cell phone calls from the passengers themselves, to bolster this story, do we not?
Thus the path of least resistance to the investigator of 911 is to assume that the BTS discrepancies regarding flight 11 & 77 is just a snafu or a glitch. Or perhaps, facing all of the obstacles above, the 911 investigator thinks it less difficult to shift focus into other areas of investigation, of which, thanks to the planners of 911, there is an abundance. Please see the rest of story below the chart below;
BTS – Bureau of Traffic Statistics showing Flight 11 never departed from Boston Logan international Airport on 9/11/2001.
The problem with nearly all 911 research regarding this issue of the BTS discrepancies of flights 11 & 77 is it all ends here, and no more questions are asked. If you ask the right question, you usually get the right answer. If you ask the wrong question, you usually get the wrong answer. If you ask no more questions at all, you will get no more answers. And thus, it is left there, with no more questions. So lets start asking some of the questions which have never been asked or pursued.
Question # 1. Do we have any evidence that shows the passengers at the airport, boarding terminals or boarding the planes?
Answer: No – Not on any of the “4 flights” of 911 [Is this not a huge red flag already? If such footage existed, and by all means if the governments story is true, there is indeed footage of all the passengers at the airports and boarding terminals. Yet not an inch of footage of this video has ever once been produced.] **The answer why there is no video of any of the passengers at any of the terminals or airports is because it simply does not exist and never did exist.
Question # 2. How does a passenger purchase a ticket for a Flight which will not fly on 9/11?
This is conceivably possible. Flights are canceled all the time and combined with other flights according to the dictates of the airlines and passenger loads any given day. Yet there are no records of any such occurrences on 9/11. The official story is set in stone. The people boarded Flight 11. They boarded AT Flight 11’s gate.
Question #3. How does a passenger fly on a flight which never takes off on 911?
Now this is impossible. This is where the tougher questions are needed. The passengers all disappeared and that, seamlessly, on 911. This is beyond dispute. And yet they never could have boarded a flight that did not take off. They might have conceivably purchased tickets for these flights, but they could have never actually gotten onto flight 11, boarded and then taken off. Why? Because the BTS database is accurate and also definite. Flight 11 did not depart on 911. Unfortunately this presents a conundrum and a wall of confusion that none stepped over till now.
Question # 4. Where did the passengers go, if not onto flight 11?
Were they herded into rooms at the airports as some theorists have assumed? Were they tricked onto boarding another flight, which they thought was flight 11, a sort of ‘patsy plane’ if you will? These are all legitimate questions because we do after all have the collective disappearance of of 92 souls. They had to have gone somewhere, because they couldn’t have gone nowhere. They didn’t board or fly on flight 11.
We have no reports of any disturbances at any of the airports, much less Boston Logan, which would likely happen if airport officials tried to sequester 92 people trying to board a flight inside an International airport with hundreds of witnesses all around, and yet they collectively disappeared. Not onto flight 11. And not sequestered at the airports. Then where?
At this point we are running out of ground to walk on unless we pass over the most difficult bridge of all and ask the most unpleasant of all questions;
Question # 5. Were any of the passengers on flight 11 or any of the 4 planes part of the conspiracy of 9/11?
As an investigator, all things need to be considered. Regardless of peoples emotions, and all lines need to be investigated. The fact that there were no disruptions at any of the airports, indicates that the passengers disappeared seamlessly. Without struggle. Without commotion. Without notice. And without video surveillance.
The fact the government has not produced a single video showing any of the passengers is likely because if they did so, it would prove upon analysis that the passengers were in a part of the airport they never should have been on 9/11. This is why the government cannot produce the video of any of the passengers on 911 at the airports, with the possible exception of Flight 93 which we will touch on later.
The fact that the passengers disappeared seamlessly would indicate that they were willing participants by and large. It is plausible to believe that some passengers were just regular people, and randomly chosen for death & disappearance on 9/11. The planners after all were doing as much for 3000 people at the World trade Center. A few more is nothing to them. But it is not plausible to believe this is the case for all of the passengers.
This item is what I believe is an issue which cannot be answered without more data. Whether or not regular passengers were chosen and incorporated into these flights, or whether or not they were all in one way or another part of the conspiracy.
Perhaps it is a mixture of real passengers and conspirators. It is beyond the scope of this article to deal with all of the passengers and possible connections to 911 planning, although there is a mountain of supporting evidence, when there should be none. And for at least 3 of the planes passengers in question, their disappearance at the airports deserve further investigation, for we know that the 3 groups of people from flights 11, 175 and 77 were not passengers on their respective flights.
The fact that the passengers from these 3 groups, at 2 airports disappeared so seamlessly is indicative that they were possibly willing participants. Combined with the lack of video the government has released showing any of the passengers at any of the 3 airports, it surely isn’t implausible to believe that they are in a position where they cannot produce the video without incriminating themselves.
My belief is that they do have video of the 3 groups of people at the 2 airports (93 is not included here) but cannot release it because it will show the passengers in a part of the airport they were never supposed to have been. Which would of curse help citizen investigators come closer to determining how 911 was operationally pulled off regarding the passengers and 4 planes. Why else would they withhold it?
It should be noted that all of the above, regarding Flight 11 was also repeated at Dulles International Airport. Done twice at 2 airports. The 2 flights which the BTS shows as never having taken off, flight 11 & 77, the two American airlines planes. One from Boston, one from Dulles. The passengers for the other ghost flight, 77, the flight which the BTS shows as never having taken off, by and large mirror what is described above with flight 11.
All of the passengers of flight 77 disappeared, seamlessly, yet they didn’t get onto or take off on flight 77, because the BTS shows it as never having taken off on 9/11. And likewise, no reports of commotion or disruptions at Dulles, as one would expect if an entire plane-load of passengers were being redirected against their wills, in a public International airport. I emphasize, that they disappeared seamlessly. Without notice. Without commotion, & as the passengers on the other ghost flight of 911, flight 11 at Boston Logan, without video surveillance.
This constitutes our 2nd conundrum regarding the passengers and the 4 flights on 9/11. 2 groups of people, one from flight 11 at Boston and one from flight 77 at Dulles would both seamlessly disappear under similar circumstances. And both groups of people would never board either of the flights, 11 or 77. Because the BTS database tells us this flight never departed. Let the conundrum remain for now, and don’t ignore it, because in it lies part of the solution to understanding how they operationally pulled off at least one layer of 911.
We encounter our third conundrum with the photographic evidence of flight 175. Even from a casual observance of all the evidence of pictures and video we have of flight 175, it is quite obvious it was not a commercial airliner, much less flight 175 which had passengers on board.
Thus if commercial flight 175 did not hit the South Tower as we were all told, our third conundrum now becomes what happened to those passengers on flight 175? A third group of missing people. If they were not aboard that plane, and all evidence tells us they weren’t, then where did the passengers from flight 175 go to? Were the planes switched in mid-air? Taken over by remote control and flown into the towers? Where o where did this third group of people, the passengers from flight 175 disappear to? Is anyone starting to see a pattern here? One group after another of the 4 groups of people on 911 have all sorts of difficulties with their stories and the story of their disappearance.
As we move along to Flight 93 we will find even more issues. Though not quite the same, and as a matter of fact, we will get a glimpse of the key to understanding this mysteries outlined above. Something nobody was ever intended to read or see. It is simply an unintended consequence of 9/11 and something the planners of 911 couldn’t ever plan for or forsee.
Flight 93 was boarded twice. By two groups of people at two separate locations at Newark Airport. We know this because of two credible eye-witnesses. This is also more then likely the reason why flight 93 was 41 minutes late in taking off on 9/11. We were never supposed to know or learn of this 2nd boarding for flight 93, this was one of those things they couldn’t forsee. After closing it’s door at the terminal, Flight 93 reopened the door to the plane, to allow Mark Bingham aboard. Mark Bingham has for all intents and purposes totally messed up and missed his plane. They literally re-opened the door to the airplane at the terminal jet-bridge and allowed him onto the plane.
Quote:
Mark Bingham: Flight 93
One passenger was late. Mark Bingham had overslept and his friend, Matthew Hall, drove madly from Manhattan to Newark. They screeched to a halt outside Terminal A at 7:40. Bingham leapt from the car, lugging the old, blue-and-gold canvas bag he’d used as a rugby player at the University of California at Berkeley a decade earlier. United attendants reopened the door to the boarding ramp and let him on the plane. Lucky he was that Flight 93 was 41 minutes late or he might have missed his flight.
After pulling away from the gate, flight 93 goes around the corner to pick up another ‘charter’ for the days flight, a second group of people. This was never reported on. Nor were you ever intended to so much as get a glimpse of this 2nd boarding. It happened as the result of a planning snafu.
Quote:
Triton’s Clayton White on other side of recruiting
“You might say Clayton White’s life has come full circle since February 1996.
White’s career didn’t end there, however. He eventually made the NFL’s New York Giants as a free agent and spent three seasons in the league, the last one in 2002 with the Tampa Bay Buccaneers.
But the most lasting memory of White’s time in New York had nothing to do with football. “We had played a Monday night game in Denver, and flew back home the next morning,” White said. “We landed in Newark, N.J., about 6:45 in the morning. We usually get off the plane on the tarmac and board a bus to get to our cars.
“ I noticed another plane sitting next to ours because the people were walking to the plane across the tarmac instead of through the jetway.
“Two weeks later, as we’re taking another plane to a game, one of the stewardesses informed us the plane that had been boarding next to us was Flight 93 that crashed in Pennsylvania on 9/11. That was a very eerie feeling .” – Fayetteville Observer (01/31/06)
Triton Clayton White saw something he wasn’t supposed to see, because the planners of 911 did not take into consideration the possibility of charter flights offloading on the same tarmac they were to pick up this 2nd group of people with Flight 93. Triton Clayton White (New York Giant Football player) saw FLIGHT 93 being boarded on the Tarmac at Newark, which is another separate boarding then when they picked people up at the terminal using a jet-bridge.
That self same terminal at Newark, to this day, has a flag at it, where the hero’s of 9/11 boarded their fateful flight. Make no mistake about it, the first group of people boarded at the terminal, and a 2nd group of people boarded on the Tarmac. All onto flight 93, and all of this at Newark on 9/11.
But who is this 2nd group of people being boarded onto flight 93, and why the cloak and dagger boarding of a 2nd group of passengers onto Flight 93 on the tarmac, AFTER the boarding at the terminal?
This presents us with our 4th conundrum. There appears to be incredibly serious issues with each of the flights, their boardings, their departures, identities, destinations, and now this?
STATUS: NO DEPARTURE: NO BOARDING: On flight 11, we have passengers which boarded and disappeared onto a plane which never took off and which video evidence plausibly shows to be a military drone.
STATUS: DEPARTURE & BOARDING: On flight 175, we have a different issue, as the plane which struck the towers was not commercial flight 175, with those passengers aboard, and also all sorts of plausible evidence that shows this plane to be a military drone as well.
STATUS: NO DEPARTURE: NO BOARDING: On flight 77, we have passengers which allegedly board and depart on a flight which never departed that day, according to BTS.
STATUS: DEPARTURE & TWO BOARDINGS: On flight 93, we have an unusual late passenger being let on the plane after missing it, as well as a second boarding on the tarmac after its first initial boarding at the terminal using a jet-bridge.
This is as far as my research has gone, sorry I cannot supply any answers or solutions beyond this, but feel free to chime in with your own research and ideas. Psyche. Just kidding. Actually, if your still with me, we are nearly done with wrapping up all the loose ends and tying it all together and seeing what happened on 911 as well as the most plausible explanation to all of the mysteries regarding the passengers and flights.
From here out, it is actually very simple. At Boston they did a variation of the disappearing coin trick, with an additional coin thrown in, Delta flight 1989, as we will see, and at Dulles, they used the disappearing deck trick. Simply put, the passengers of flight 77 at Dulles are the same group of people who we see on the SECOND BOARDING AT NEWARK AIRPORT. The passengers at Dulles caught an earlier flight which took them to Newark where they were to rendevouz with Flight 93, and did so successfully. Howbeit, there is a witness to this deception, Triton Clayton White, the New york Giant who saw Flight 93 boarding ON THE TARMAC. After its FIRST BOARDING AT THE TERMINAL.
At Boston Logan International Airport, they used a similar deception. Here, the passengers from both flights 11 & 175 are combined into one flight. It would eventually become delta flight 1989 and land at Cleveland International Airport … While flight 93, now having also the passengers from flight 77 from the 2nd boarding at Newark, will head to the same destination; Cleveland International Airport.
Stuart Air Force Base Mystery – Explained
Above Stuart air force base we are told that flight 11 and 175 nearly collided they got so close. We were also given snippets of this through air traffic control tapes. The explanation for this is as plausible as it is logical. This is where the 2 military drones which were to strike to world trade centers took off from. They would replace the flight path of Flight 175 as well as the path of flight 11, which up to this point was provided for by an electronic warfare plane which was one of “4” such aircraft in the air for the War games which were taking place on 9/11/2001.
Sometime shortly after this, Flight 175 NOW HAVING BEEN REPLACED BY A MILITARY DRONE ON RADAR will change its transponder to Delta 1989, and make an emergency landing at Cleveland, with reports of a bomb aboard. This plane would contain roughly 200 people, and not only is it plausible that these people were the people from flights 11 & 175, it is highly probable and likely. Another plane, Flight 93, would also land at Cleveland airport.
This was confirmed by both the Mayor of Cleveland, and United Airlines who publicly acknowledged on 911 and confirmed flight 93 landed in Cleveland. Flight 93 would end up being sequestered at one end of the airport, at the NASA Glenn hangar, while the other flight containing the other passengers from 11 & 175, now designated as Delta 1989, would be sequestered at the other end of the airport, at the I-X Exposition center. The two flights, Delta 1989 and United flight 93 had roughly 260 some people between them, the same number as the “4” flights, 11, 175, 77 & 93.
The Cleveland Airport Mystery – Explained
The following is from Woodybox, a diligent 911 researcher. In a nutshell he explains why it was 2 separate aircraft which landed at Cleveland. In my above article, the reason why is obvious.
Quote:
We can conclude that Delta 1989 landed at 10:10, and at 12:30 the 69 passengers were taken into the FAA headquarter. Flight X landed at 10:45, and at 11:15 the 200 passengers were taken into the evacuated NASA Center.
Cleveland Hopkins Airport – note that the blue runways were in planning yet on 9/11. The big black rectangle in the South is the I-X Center
5) The exact location of the plane
This is the final proof that we have to do with two different planes. Both planes were sitting on a runway, but miles away from each other. One plane was at the west end of runway 28/10 near the NASA center (point 10 in the map). This is confirmed by Associated Press and an eyewitness (5A). The other plane was sitting at the south end of runway 18/36 near the I-X-Center (point 36), also confirmed by two eyewitnesses (5B). The geographic conditions on the airport suggest that the passengers at the West end were taken to the NASA Center and the passengers at the South end to the FAA headquarter.
We summarise our findings:
………………………………………….. ……..Delta 1989……………….Flight X
Moment of landing…………………………..10:10…… …………………10:45
Begin of evacuation………………………….12:30…. …………………..11:15
Number of passengers……………………….69………. ………………….200
Passengers brought to…………. ……….FAA/Airport……………….NASA
Exact location……………………………Runway 18/36 …………Runway 28/10
………………………………………….. …near I-X Center……….near NASA Center
___________________________________________________________
Steve:
End of first article
Readers can stop here if they wish. Or they may join WoodyBox below, whose article forms a separate piece but which Phil drew on for his own article.
Phil picks up his narrative on the words “Not only does this show….”
___________________________________________________________
For the full complete story that this was taken from by Woody see here below.
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msmarco_passage_01_437922099 | Money and Currency in Peru | Money and Currency in Peru
Central & South America Peru
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Money and Currency in Peru
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Tony Dunnell is a travel writer specializing in Peruvian tourism and the founder of the How to Peru blog.
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When you first arrive in Peru, you’ll need to adapt to the financial side of things: The currency, the shopping culture, and money-related customs. If you’re not familiar with Peruvian currency or handling money in Peru, read on for some frequently asked questions.
01 of 08
Currency
The currency of Peru is the nuevo sol (symbol: S/.). Nuevo sol banknotes come in denominations of 10, 20, 50, 100 and 200. One nuevo sol (S/.1) is subdivided into 100 céntimos. Coins are available in denominations of 1, 5, 10, 20 and 50 céntimos, as well as larger denominations of 1, 2 and 5 nuevos soles.
02 of 08
Exchange Rate
During the last decade, the nuevo sol has been one of the most stable currencies in the Latin American region. As of October 2018, the Peruvian nuevo sol was trading at 3.33 per US dollar.
03 of 08
The Best Way to Carry Money
How you decide to carry your money in Peru depends on factors such as the duration of your trip and your style of travel. It’s not a great idea to carry large amounts of cash in Peru (dollars or nuevos soles), but it’s certainly a viable option for short visits (up to a week). Otherwise, you can simply withdraw money when needed from ATMs all over Peru. Visa is the most widely accepted debit or credit card in Peru; there will be fees associated with each withdrawal. Traveler’s checks are also an option (ideally in US dollars or Euros) but may be hard to cash in small towns and villages, and the exchange rate can be poor.
04 of 08
Where to Exchange
There are four options for exchanging money in Peru: Banks, street moneychangers, casas de cambio (“exchange houses”), and hotels. Banks often have incredibly long queues, making any exchange a protracted process. Street changers are handy and offer comparatively fair exchange rates, but changing money in the street comes with its own problems. You need to guard against potentially shady deals and the risk of street theft following the exchange. Overall, casas de cambio tend to be the best option, with good exchange rates, short queues, and a secure environment.
Continue to 5 of 8 below.
05 of 08
Change Shortage
Many South American nations have a change shortage. In Peru, for example, a storekeeper may not accept a S/.100 note as payment for an item priced at S/.2, due to the fact that he doesn’t have enough small change (or he’d be handing over all the small change in the till creating problems for future customers). It’s a good idea to create change when possible so that you have a healthy supply of S/.10 and S/.20 notes.
06 of 08
Fake Money
Fake money is a problem in Peru -- both nuevos soles and dollars. The problem tends to be worse in certain parts of the country, especially in Peru’s major cities. Spotting a counterfeit banknote can be difficult, so the sooner you become familiar with the local currency, the sooner you’ll be able to spot a fake. You also need to watch out for money scams, such as deliberate short-changing and swindles involving sleight of hand.
07 of 08
Tipping
Tipping isn’t particularly common in Peru, but there are certain situations in which a tip is appropriate. Waiters in higher-end restaurants, tour guides and staff in top-end hotels often expect a tip, whereas taxi drivers and staff in small family-run restaurants do not.
08 of 08
Haggling
Haggling is common in Peru, especially in situations where a price is not clearly labeled. This includes items for sale in traditional markets and taxi fares. Always bear in mind that prices quoted to foreign tourists tend to be inflated (often jokingly referred to as “gringo prices” or the “gringo tax”), so don’t be afraid to negotiate for what you believe to be a reasonable price. At the same time, don’t haggle to the extent that you strip a poor artisan of all her profits.
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msmarco_passage_01_441936761 | How to Get from Las Vegas to the Grand Canyon | How to Get from Las Vegas to the Grand Canyon
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How to Travel from Las Vegas to the Grand Canyon by Car, Bus, Helicopter, or Plane
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If you're in Las Vegas with some time to spare, the Grand Canyon is a worthwhile respite from the slot machines and card tables of the neon-lit Strip. Located less than 300 miles from the North Rim, South Rim, and Grand Canyon East, and less than 150 miles from Grand Canyon West, Sin City offers many an excursion by helicopter and bus. A side trip will take you about 4.5 hours one way if you'd prefer to drive yourself.
The Grand Canyon is one of the many national parks you can visit from Las Vegas. You can get there by plane, train, bus, car, or helicopter. Renting a vehicle from Las Vegas will give you the freedom to explore fun roadside attractions along the way and is much less complicated than taking a plane. Bus tours and train transport are both much slower, but relatively straightforward. Keep in mind that the North and South Rims of the Grand Canyon are about a 300-mile drive apart. The North Rim is extremely remote compared to the heavily trafficked and tourist-centric South Rim, so many choose the latter.
How to Get From Las Vegas to Grand Canyon National Park
Time
Cost
Best For
Car/Motorcycle
2 hours to Grand Canyon West
4.5 hours to North Rim and South Rim
5 hours to Grand Canyon East
From $30 per day for rental car, plus $25 each way for gas
Traveling at your own pace
Bus
10 to 12 hours
$59 to $85; tours starting at $75
Maintaining a budget
Train
10 to 12 hours
$250
A unique experience
Flight
4 to 10 hours
$350 to $700
Quick trips
By Flight
The Grand Canyon does have an airport in Tusayan, Arizona, but the closest hub for commercial air travel is in Flagstaff, nearly 2 hours away. A flight from either the McCarran International Airport in Las Vegas or the Boulder City Municipal Airport to Flagstaff Pulliam will take about an hour and a half and cost anywhere between $50 and $250 depending on the day and season. Arriving by commercial flight is not ideal when you factor in transportation from the airport to the park, so those who prefer to fly usually opt for a "flightseeing" tour instead.
The one offered by Pappillion, in particular, starts at $372 and offers bird's-eye views of the Hoover Dam, Lake Mead, and the Colorado River in addition to the Grand Canyon. Upon arrival, a motorcoach transfers passengers from the airport to the Bright Angel Lodge and Mather Point on the South Rim. The tour takes about 9.5 hours from hotel to hotel, including a lunch break, time for hiking, and more. Similar tours are offered via helicopter by Maverick .
By Train
Travel the old-fashioned way on the Grand Canyon Railway, a 64-mile heritage railroad that runs between Williams, Arizona, and the South Rim. First, getting to the station requires guests to take an Amtrak bus from the Gray Line Tour Center in Las Vegas to Kingman, where they then transfer onto a two-hour train to Williams. The final leg—from Williams to the South Rim—is only an hour long, but it runs through a stretch of untouched forest on the outskirts of the canyon.
The train usually departs once a day from Williams (at 9:30 a.m. from July through October and 8:30 a.m. from November to January) and departs from the Grand Canyon at 2:30 or 3:30 p.m. every afternoon. Altogether, the trip from Las Vegas to the South Rim can take between 10 and 12 hours and cost a total of $250 for the bus ticket and two train tickets, but it is an unforgettable experience.
By Bus
Traveling by bus to the Grand Canyon will also take you about 10 to 12 hours. FlixBus runs regular routes from downtown Las Vegas to the Phoenix Sky Harbor International Airport (5 hours, 30 minutes), then to Flagstaff Station (2 hours, 30 minutes). Buses depart from the city at 11 a.m. daily and tickets cost $15 to $22 for the first leg and $9 to $13 for the second. When you get to Flagstaff Station, you can catch the Arizona Shuttle to Maswik Lodge on the South Rim (2 hours) for $35 to $50.
Because the last departure is at 3:45 p.m., you may have to stay overnight in Flagstaff, inevitably driving up the cost and prolonging the journey. Because of the inconvenient transfers, most people will opt for a group bus tour instead of taking public buses.
A typical tour includes stops at the National Geographic Visitors Center in Tusayan and two spectacular lookouts, Mather Point and Bright Angel Lodge. There is usually time for short hikes and self-exploring on these excursions. Popular tours include full-day outings by Canyon Tours and Grand Canyon Destinations, starting at $75.
By Car
The easiest and perhaps most versatile way to travel from Las Vegas to the Grand Canyon is by car. There are about 10 rental car companies on offer at the McCarran International Airport's Rent-A-Car Center, but you can also rent from various places on the Strip. You may be able to secure a rental car through your hotel, too.
The North Rim is located 264 miles from downtown Las Vegas. The easiest way to get there is to take I-15 North to Utah 59 South, then follow Arizona 389 East to 89A and Arizona 67 South. The last stretch will lead you through the stunning Kaibab National Forest.
The South Rim is a more popular destination and arguably a more entertaining route. It's about 280 miles from Las Vegas and you can get there by following U.S. 93 South to I-40 East, then Arizona 64 North, which leads into Grand Canyon National Park by way of Tusayan, the closest town. Popular stops along the way include the Hoover Dam and the small towns of Seligman and Williams, Arizona. Views of the desert landscape are fabulous along this route, making it popular among avid motorcyclists.
Grand Canyon West, where the famous SkyWalk is, is only 130 miles from Las Vegas and best for a day trip. Grand Canyon East is the farthest from Las Vegas, about 336 miles away. It can be accessed from Arizona 64 West, a short trip on U.S. 89 North from Flagstaff.
If you decide to drive, you should allocate at least two days to the journey—especially if you're going further than Grand Canyon West. Carry plenty of water in the summer and make sure to bring warm clothing in the winter as the desert can be frigid. For a standard rental car, expect to pay about $30 per day.
What to See in the Grand Canyon
There are countless things to see and do at the Grand Canyon. On the South Rim—the canyon's top tourist destination—you can take in the spectacular views from Mather Point, Yavapai Point, Hopi Point, and Bright Angel Lodge, all accessible by a free shuttle provided by the National Park Service. You can walk along the canyon's edge on the Rim Trail or descend into it on the popular Bright Angel Trail. Then, dine at one of the lodges and shop for souvenirs.
On the North Rim, the view from Bright Angel Point should not be missed. Though it does have a visitor center and lodge, this is a more remote part of the park, offering less tourist attractions and more backcountry adventures. Popular hikes include the paved Bright Angel Point Trail, Cape Royal Trail, and Cape Final Trail.
The main attraction at Grand Canyon West is the Skywalk, a horseshoe-shaped glass platform that extends 70 feet from the canyon's edge. Here, you can also zip line, take a helicopter or boat tour, or go white-water rafting. Grand Canyon East is home to the Little Colorado River Tribal Park, the 5,000-foot-tall Tower Butte, Horseshoe Bend, Antelope Canyon, and Lake Powell.
What are Other Good Day Trips From Las Vegas?
Las Vegas is surrounded by a vast desert boasting extraordinary natural sights in every direction. The Valley of Fire State Park is a popular side trip only 45 minutes from the city. It contains countless sandstone formations with that wave-like pattern characteristic of the region, all spread over 46,000 acres. A 2-hour, 15-minute drive from the Strip, Death Valley National Park in California offers sand dunes as far as the eye can see. Just don't go during the peak of summer as it can get up to 120 degrees Fahrenheit.
Hoover Dam, a concrete dam in the Black Canyon of the Colorado River, is a quick jaunt (about 40 minutes) from Sin City. Red Rock Canyon —packed with sandstone peaks, as its name suggests—is only 20 minutes away. For something spooky, take the Extraterrestrial Highway to Alamo, home of Area 51 and the Little A’le’inn (2 hours, 20 minutes).
When is the Best Time to Visit Las Vegas?
The best time to visit Las Vegas is during spring and fall, from March to May (with the exception of spring break) and September to November. Folks flock to the pools and air-conditioned casinos of Las Vegas during the summer months, but the shoulder seasons are cooler, less crowded, cheaper, and provide an all-around less chaotic experience. Plus, if you're keen to get out into the desert for a day or two, you'll want to avoid the hottest months, as three-digit temps are the summer standard.
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msmarco_passage_01_444035811 | Solar 101: Watts, Amps, Volts | Learning Center | Go Power! | Solar 101: Watts, Amps, Volts | Learning Center | Go Power!
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msmarco_passage_01_45002266 | Noncoronary Atherosclerosis: Practice Essentials, Overview of Atherosclerosis, Etiology of Atherosclerosis | Noncoronary Atherosclerosis: Practice Essentials, Overview of Atherosclerosis, Etiology of Atherosclerosis
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Drugs & Diseases > Cardiology
Noncoronary Atherosclerosis Overview of Atherosclerosis
Updated: Dec 23, 2019
Author: F Brian Boudi, MD, FACP; Chief Editor: Yasmine S Ali, MD, FACC, FACP, MSCI more...
Sections
Noncoronary Atherosclerosis
Sections Noncoronary Atherosclerosis
Practice Essentials
Overview of Atherosclerosis
Etiology of Atherosclerosis
Risk Factors for Atherosclerosis
Epidemiology of Atherosclerosis
Patient History
Physical Examination
Lipid Profile
Blood Glucose and Hemoglobin A1C
Ultrasonographic Examination
MRI and Scintigraphy
Treatment of Atherosclerosis
Drug Agents
Guidelines
Questions & Answers
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Tables
References
Overview of Atherosclerosis
Practice Essentials
Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by endothelial dysfunction, vascular inflammation, and the buildup of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. This buildup results in plaque formation, vascular remodeling, acute and chronic luminal obstruction, abnormalities of blood flow, and diminished oxygen supply to target organs.
Noncoronary atherosclerosis refers to atherosclerotic disease affecting large and medium-sized noncoronary arteries (eg, extracranial cerebrovascular disease, lower extremity occlusive disease, aneurysmal disease).
Signs and symptoms
The signs and symptoms of noncoronary atherosclerosis are highly variable. Patients with mild atherosclerosis may present with clinically important symptoms and signs of disease. However, many patients with anatomically advanced disease may have no symptoms and experience no functional impairment.
Signs and symptoms of noncoronary atherosclerosis that affect different organ systems include the following:
Central nervous system: Stroke, reversible ischemic neurologic deficit, transient ischemic attack
Peripheral vascular system: Intermittent claudication, impotence, nonhealing ulceration and infection of the extremities
Gastrointestinal (GI) vascular system: Mesenteric angina characterized by epigastric or periumbilical postprandial pain—may be associated with hematemesis, hematochezia, melena, diarrhea, nutritional deficiencies, and weight loss; abdominal aortic aneurysm that is typically asymptomatic (sometimes pulsatile) until the dramatic, and often fatal, signs and symptoms of rupture
Target organ failure: Occult or symptomatic visceral ischemia
Diagnosis
Examination findings of noncoronary atherosclerosis are highly variable but may provide objective evidence of extracellular lipid deposition, stenosis or dilatation of large muscular arteries, or target organ ischemia or infarction, such as the following:
Hyperlipidemia: Xanthelasma and tendon xanthomata
Cerebrovascular disease: Diminished carotid pulses, carotid artery bruits, and focal neurologic deficits
Peripheral vascular disease: Decreased peripheral pulses, peripheral arterial bruits, pallor, peripheral cyanosis, gangrene, and ulceration
Abdominal aortic aneurysm: Pulsatile abdominal mass, peripheral embolism, and circulatory collapse
Atheroembolism: Livedo reticularis, gangrene, cyanosis, ulceration, digital necrosis, GI bleeding, retinal ischemia, cerebral infarction, and renal failure
Laboratory testing
Lipid profile
Blood glucose and hemoglobin A1c
Imaging studies
Ultrasonography: For evaluating brachial artery reactivity and carotid artery intima-media thickness (measures of vessel wall function and anatomy, respectively) [ 1]
Intravascular ultrasonography: Generally considered the criterion standard for the anatomic study of the vessel wall (provides images of the thickness and the acoustic density of the vessel wall)
Magnetic resonance imaging: For noninvasive assessment of blood vessel wall structure and characterization of plaque composition
Nuclear perfusion imaging with single-photon emission computed tomography (SPECT) scanning or positron emission tomography (PET) scanning
Management
The prevention and treatment of atherosclerosis require risk factor control, including the medical management of hypertension, hyperlipidemia and dyslipidemia, diabetes mellitus, and cigarette habituation.
Pharmacotherapy
The following medications may be used in the management of noncoronary atherosclerosis:
HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme) reductase inhibitors (eg, pravastatin, simvastatin, lovastatin, fluvastatin, atorvastatin, rosuvastatin, pitavastatin)
Fibric acid derivatives (eg, fenofibrate, gemfibrozil)
Bile acid sequestrants (eg, cholestyramine, colestipol
Omega-3 polyunsaturated fatty acid
Next: Overview of Atherosclerosis
Overview of Atherosclerosis
Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by endothelial dysfunction, vascular inflammation, and the buildup of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. This buildup results in plaque formation, vascular remodeling, acute and chronic luminal obstruction, abnormalities of blood flow, and diminished oxygen supply to target organs.
For patient education information, see Cholesterol Center and Brain & Nervous System Center, as well as High Cholesterol , Cholesterol Charts (What the Numbers Mean), How to Lower Cholesterol, and Stroke.
See Coronary Artery Atherosclerosis for more information on this topic.
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Next: Overview of Atherosclerosis
Etiology of Atherosclerosis
The mechanisms of atherogenesis remain uncertain. An incompletely understood interaction exists between the critical cellular elements—endothelial cells, smooth muscle cells, platelets, and leucocytes—of the atherosclerotic lesion. Vasomotor function, the thrombogenicity of the blood vessel wall, the state of activation of the coagulation cascade, the fibrinolytic system, smooth muscle cell migration and proliferation, and cellular inflammation are complex and interrelated biologic processes that contribute to atherogenesis and the clinical manifestations of atherosclerosis.
The "response-to-injury" theory is most widely accepted explanation for atherogenesis. Endothelial injury causes vascular inflammation and a fibroproliferative response ensues. Probable causes of endothelial injury include oxidized low-density lipoprotein (LDL) cholesterol; infectious agents; toxins, including the byproducts of cigarette smoking; hyperglycemia; and hyperhomocystinemia.
Circulating monocytes infiltrate the intima of the vessel wall, and these tissue macrophages act as scavenger cells, taking up LDL cholesterol and forming the characteristic foam cell of early atherosclerosis. These activated macrophages produce numerous factors that are injurious to the endothelium.
Elevated serum levels of LDL cholesterol overwhelm the antioxidant properties of the healthy endothelium and result in abnormal endothelial metabolism of this lipid moiety. Oxidized LDL is capable of a wide range of toxic effects and cell/vessel wall dysfunctions that are characteristically and consistently associated with the development of atherosclerosis. These dysfunctions include impaired endothelium-dependent dilation and paradoxical vasoconstriction. These dysfunctions are the result of direct inactivation of nitric oxide by the excess production of free radicals, reduced transcription of nitric oxide synthase messenger ribonucleic acid (mRNA), and posttranscriptional destabilization of mRNA.
The decrease in the availability of nitric oxide also is associated with increased platelet adhesion, increased plasminogen activator inhibitor, decreased plasminogen activator, increased tissue factor, decreased thrombomodulin, and alterations in heparin sulfate proteoglycans. The consequences include a procoagulant milieu and enhanced platelet thrombus formation. Furthermore, oxidized LDL activates inflammatory processes at the level of gene transcription by up-regulation of nuclear factor kappa-B, expression of adhesion molecules, and recruitment of monocytes/macrophages.
The lesions of atherosclerosis do not occur in a random fashion. Hemodynamic factors interact with the activated vascular endothelium. Fluid shear stresses generated by blood flow influence the phenotype of the endothelial cells by modulation of gene expression and regulation of the activity of flow-sensitive proteins. Atherosclerotic plaques characteristically occur in regions of branching and marked curvature at areas of geometric irregularity and where blood undergoes sudden changes in velocity and direction of flow. Decreased shear stress and turbulence may promote atherogenesis at these important sites within the coronary arteries, the major branches of the thoracic and abdominal aorta, and the large conduit vessels of the lower extremities. (This article will focus on noncoronary sites of atherogenesis.)
One study suggested that hypercholesterolemia-induced neutrophilia develops in arteries primarily during early stages of atherosclerotic lesion formation. [ 2]
The earliest pathologic lesion of atherosclerosis is the fatty streak, which is the result of focal accumulation of serum lipoproteins within the intima of the vessel wall. Microscopy reveals lipid-laden macrophages, T lymphocytes, and smooth muscle cells in varying proportions.
The fatty streak may progress to form a fibrous plaque, the result of progressive lipid accumulation and the migration and proliferation of smooth muscle cells.
Platelet-derived growth factor, insulinlike growth factor, transforming growth factors alpha and beta, thrombin, and angiotensin II are potent mitogens that are produced by the activated platelets, macrophages, and dysfunctional endothelial cells that characterize early atherogenesis, vascular inflammation, and platelet-rich thrombosis at sites of endothelial disruption. The relative deficiency of endothelium-derived nitric oxide further potentiates this proliferative stage of plaque maturation.
The proliferating smooth muscle cells are responsible for the deposition of extracellular connective tissue matrix and form a fibrous cap that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris. Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ.
Progressive luminal narrowing of an artery due to expansion of a fibrous plaque results in impairment of flow once more than 50-70% of the lumen diameter is obstructed. Flow impairment causes symptoms of inadequate blood supply to the target organ in the event of increased metabolic activity and oxygen demand.
Developing atherosclerotic plaques acquire their own microvascular network, which consists of a collection of vessels known as the vasa vasorum. These vessels are prone to hemorrhage and contribute to the progression of atherosclerosis. [ 3]
Denudation of the overlying endothelium or rupture of the protective fibrous cap may result in exposure of the thrombogenic contents of the core of the plaque to the circulating blood. This exposure constitutes an advanced or complicated lesion.
The plaque rupture occurs due to weakening of the fibrous cap. Inflammatory cells localize to the shoulder region of the vulnerable plaque. T lymphocytes elaborate interferon gamma, an important cytokine that impairs vascular smooth muscle cell proliferation and collagen synthesis. In addition, activated macrophages produce matrix metalloproteinases that degrade collagen. These mechanisms explain the predisposition to plaque rupture and highlight the role of inflammation in the genesis of the complications of the fibrous atheromatous plaque.
A plaque rupture may result in thrombus formation, partial or complete occlusion of the blood vessel, and progression of the atherosclerotic lesion due to organization of the thrombus and incorporation within the plaque.
Development of atherosclerosis from childhood through adulthood
The process of atherosclerosis begins in childhood with the development of fatty streaks. These lesions can be found in the aorta shortly after birth and appear in increasing numbers in persons aged 8-18 years. More advanced lesions begin to develop when individuals are aged approximately 25 years. Subsequently, an increasing prevalence of the advanced complicated lesions of atherosclerosis exists, and the organ-specific clinical manifestations of the disease increase with age through the fifth and sixth decades of life.
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Next: Overview of Atherosclerosis
Risk Factors for Atherosclerosis
A number of large epidemiologic studies in North America and Europe have identified numerous risk factors for the development and progression of atherosclerosis.
The risk factors can be divided into modifiable and nonmodifiable types and include hyperlipidemia, hypertension, cigarette habituation, diabetes mellitus, age, sex, physical inactivity, and obesity. In addition, a number of novel risk factors have been identified that add to the predictive value of the established risk factors and may prove to be a target for future medical interventions.
Hypertension
Hypertension has been shown, in epidemiologic and experimental studies, to accelerate atherosclerotic vascular disease and increase the incidence of clinical complications.
The mechanism by which hypertension causes these effects is not known, and some uncertainty exists as to what the primary and secondary factors are in a typically multifactorial syndrome. These factors may include the above-mentioned hyperlipidemia, hypertension, diabetes mellitus, obesity, and physical inactivity.
Hypertension is associated with morphologic alterations of the arterial intima and functional alterations of the endothelium that are similar to the changes observed in hypercholesterolemia and established atherosclerosis. Endothelial dysfunction is a feature of hypertension, hyperlipidemia, and atherosclerosis and is known to represent and contribute to the procoagulant, proinflammatory, and proliferative components of atherogenesis.
Diabetes mellitus
This is an important risk factor for hyperlipidemia and atherosclerosis and is commonly associated with hypertension, abnormalities of coagulation, platelet adhesion and aggregation, increased oxidative stress, and functional and anatomic abnormalities of the endothelium, and endothelial vasomotion.
Cigarette smoking
Cigarette smokers have double the risk for stroke compared with nonsmokers. [ 4]
C-reactive protein
In a cohort of healthy men, baseline C-reactive protein (CRP) levels were found to be predictive of symptomatic peripheral vascular disease. CRP reflects systemic inflammation, and these results support the hypothesis that chronic inflammation may play a role in the pathogenesis and progression of atherosclerosis.
Standardization of the CRP assay is required before this test may be clinically useful, and whether CRP levels are a truly modifiable risk factor remains unclear.
Metabolic syndrome
Metabolic syndrome is more common and elevated in association with risk factors for atherosclerosis, including elevated body mass index, lack of exercise, smoking, age, and diet.
Familial hypercholesterolemia
Familial hypercholesterolemia is an autosomal dominant disorder caused by a defect in the gene for the hepatic LDL receptor. In the United States, heterozygous familial hypercholesterolemia occurs in approximately 1 in 500 individuals. Homozygous familial hypercholesterolemia occurs in approximately 1 in 1 million individuals in the United States, and total cholesterol may exceed 1000 mg/dL.
Also see Risk Factors for Coronary Artery Disease.
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Next: Overview of Atherosclerosis
Epidemiology of Atherosclerosis
Rate of occurrence
The true frequency of atherosclerosis is difficult, if not impossible, to accurately determine, because it is a predominantly asymptomatic condition.
A study by Semba et al suggests that high concentrations of plasma klotho, a hormone that has been implicated in atherosclerosis, are independently associated with a lower likelihood of having CVD. [ 5]
Sex predilection
Atherosclerosis is more common in men than in women. The higher prevalence of atherosclerosis in men is thought to be due to the protective effects of female sex hormones. This effect is absent after menopause in women.
Age predilection
Most cases of atherosclerotic vascular disease become clinically apparent in patients aged 40 years or older.
Prognosis
The prognosis of atherosclerosis depends on a number of factors, including systemic burden of disease, the vascular bed (s) involved, and the degree of flow limitation. Wide variability exists, and clinicians appreciate that many patients with critical limitation of flow to vital organs may survive many years, despite a heavy burden of disease. (Conversely, myocardial infarction or sudden cardiac death may be the first clinical manifestation of atherosclerotic cardiovascular disease in a patient who is otherwise asymptomatic with minimal luminal stenosis and a light burden of disease.)
Much of this phenotypic variability is likely to be determined by the relative stability of the vascular plaque burden. Plaque rupture and exposure of the thrombogenic lipid core are critical events in the expression of the atherosclerotic disease process and determine the prognosis of atherosclerosis.
The ability to determine and quantify risk and prognosis in patients with atherosclerosis is limited by the inability to objectively measure plaque stability and other predictors of clinical events.
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Next: Overview of Atherosclerosis
Patient History
The symptoms of noncoronary atherosclerosis are highly variable. Patients with mild atherosclerosis may present with clinically important symptoms and signs of disease. However, many patients with anatomically advanced disease may have no symptoms and experience no functional impairment.
Although atherosclerosis was initially thought to be a chronic, slowly progressive, degenerative disease, it is now apparent that the disorder has periods of activity and quiescence. Although a systemic disease, atherosclerosis manifests in a focal manner and affects different organ systems in different patients for reasons that remain unclear.
Stroke, reversible ischemic neurologic deficit, and transient ischemic attack are manifestations of the impairment of the patient’s vascular supply to his or her central nervous system and are characterized by the sudden onset of a focal neurologic deficit of variable duration.
Peripheral vascular disease typically manifests as intermittent claudication, impotence, and nonhealing ulceration and infection of the extremities. Intermittent claudication describes calf, thigh, or buttock pain that is exacerbated by exercise and relieved by rest. Intermittent claudication may be accompanied by pallor of the extremity and paresthesias. (A patient with limb claudication can be assumed to have a significant atherosclerotic plaque burden in multiple vascular beds, including the coronary and cerebral vessels. In evaluating preoperative risk in such a patient, pay particular attention to careful risk stratification and medical or interventional efforts to reduce this risk.)
Visceral ischemia may be occult or symptomatic prior to the signs and symptoms of target organ failure.
Mesenteric angina is characterized by epigastric or periumbilical postprandial pain and may be associated with hematemesis, hematochezia, melena, diarrhea, nutritional deficiencies, and weight loss.
Abdominal aortic aneurysm typically is asymptomatic prior to the dramatic, and often fatal, symptoms and signs of rupture, although patients may describe a pulsatile abdominal mass.
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Physical Examination
As previously mentioned, the symptoms of noncoronary atherosclerosis are highly variable. Patients with mild atherosclerosis may present with clinically important disease signs and symptoms, while many patients with anatomically advanced disease display no symptoms and have no associated functional impairment.
The physical signs of noncoronary atherosclerosis provide objective evidence of extracellular lipid deposition, stenosis or dilatation of large muscular arteries, or target organ ischemia or infarction. These symptoms include the following:
Hyperlipidemia – Xanthelasma and tendon xanthomata
Cerebrovascular disease - Diminished carotid pulses, carotid artery bruits, and focal neurologic deficits
Peripheral vascular disease - Decreased peripheral pulses, peripheral arterial bruits, pallor, peripheral cyanosis, gangrene, and ulceration
Abdominal aortic aneurysm - Pulsatile abdominal mass, peripheral embolism, and circulatory collapse
Atheroembolism - Livedo reticularis, gangrene, cyanosis, ulceration, digital necrosis, gastrointestinal bleeding, retinal ischemia, cerebral infarction, and renal failure
The Copenhagen City Heart Study found that xanthelasmata (raised yellow patches around the eyelids) but not arcus corneae (white or grey rings around the cornea) constitutes an independent risk factor for cardiovascular disease. Presence of xanthelasmata indicated increased risk for myocardial infarction, ischemic heart disease, and severe atherosclerosis. [ 6]
With regard to atheroembolism, the presence of pedal pulses in the setting of peripheral ischemia suggests microvascular disease and includes cholesterol embolization.
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Lipid Profile
Elevated LDL cholesterol is a risk factor for atherosclerotic vascular disease. High triglycerides associated with low high-density lipoprotein (HDL) cholesterol—a pattern categorized as atherogenic dyslipidemia and often found in insulin resistance—are also a risk factor for vascular disease.
The dal-PLAQUE trial tested the safety and efficacy of dalcetrapib, using novel noninvasive multimodality imaging to assess structural and inflammatory indices of atherosclerosis as primary endpoints. The results suggest that dalcetrapib showed no evidence of a pathological effect related to the arterial wall over 24 months; however, dalcetrapib may have potential beneficial vascular effects, including the reduction in total vessel enlargement over 24 months. The long-term safety and efficacy needs to be further investigated. [ 7]
Nicholls et al studied the efficacy and safety of cholesteryl ester transfer protein (CETP) inhibitors in combination with commonly used statins. They found that, compared with placebo or statin monotherapy, evacetrapib raised HDL-C and lowered LDL-C levels, with or without a statin drug. [ 8]
In an industry-supported study, patients with atherosclerotic cardiovascular disease and LDL-C levels of < 70 mg/dl (1.81 mol/L) experienced no incremental clinical benefit from the addition of niacin to statin therapy during a 36-month follow-up period, despite significant improvements in HDL-C and triglyceride levels. [ 9]
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Blood Glucose and Hemoglobin A1C
Routine measurement of blood glucose and hemoglobin A 1c is appropriate in patients with diabetes mellitus. Measuring any number of parameters that may reflect inflammation, coagulation, fibrinolytic status, and platelet aggregability is possible. These measurements may prove to be valuable, but at this time, how these measurements affect clinical decision-making is unclear, and including them in routine clinical practice is premature.
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Ultrasonographic Examination
Ultrasonography aids in evaluating brachial artery reactivity and carotid artery intima-media thickness, which are measures of vessel wall function and anatomy, respectively. These evaluations remain research techniques at this time but hold promise as reliable, noninvasive (and therefore repeatable) measures of disease and surrogate end points for the evaluation of therapeutic interventions.
Brachial artery reactivity
The loss of endothelium-dependent vasodilation is a feature of even the early stages of atherosclerosis.
Flow-mediated dilation of the brachial artery has been pioneered as a means of evaluating the health and integrity of the endothelium. The healthy endothelium dilates in response to an increase in blood flow, whereas vessels affected by atherosclerosis do not dilate and may paradoxically constrict.
The availability of high-resolution ultrasonographic systems makes the visualization and measurement of small, peripheral conduit vessels, such as the human brachial artery, possible.
Carotid artery intima-media thickness
B-mode ultrasonography of the common and internal carotid arteries is a noninvasive measure of arterial wall anatomy that may be performed repeatedly and reliably in asymptomatic individuals. The combined thickness of the intima and media of the carotid artery is associated with the prevalence of cardiovascular risk factors and disease and an increased risk of myocardial infarction and stroke. This association is at least as strong as the associations observed with traditional risk factors.
Intravascular ultrasonography
Intravascular ultrasound (IVUS) is a catheter-based examination that provides images of the thickness and the acoustic density of the vessel wall. It has long been considered the criterion standard for the study of the anatomy of the vessel wall.
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MRI and Scintigraphy
Magnetic resonance imaging (MRI) may be used to gain information noninvasively about blood vessel wall structure and to characterize plaque composition. MRI of carotid plaque allows for the visualization of plaque composition and plaque components that have been associated with a higher risk of subsequent embolic events. Blood suppressed T1- and T2-weighted and proton density-weighted fast spin echo, gradient echo, and time-of-flight sequences are used to quantify plaque components. [ 10]
Nuclear perfusion imaging is performed with the use of single-photon emission computed tomography (SPECT) scanning or positron emission tomography (PET) scanning, which relies on the administration of radionuclide isotope that is accumulated by the targeted tissue.
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Treatment of Atherosclerosis
The prevention and treatment of atherosclerosis require risk factor control, including the medical treatment of hypertension, hyperlipidemia, diabetes mellitus, and cigarette habituation.
Some studies have claimed reversal of atherosclerosis with pharmacologic agents such as statins and cilostazol, but these need to be further tested before it can be determined whether they offer any significant benefit in reducing clinical events. [ 11]
Advances in the understanding of the vascular biology of atherosclerosis have raised the possibility of using novel therapies to address more directly the various aspects of endothelial dysfunction and the role of endothelial dysfunction in atherogenesis. Potential cellular targets include vascular smooth muscle cells, monocyte/macrophage cell lines, platelets, and endothelial cells. Evidence exists that antiplatelet agents, antioxidant therapies, amino acid supplementation, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers may prove to prevent or slow the progression of the disease.
Screening
Cardiovascular disease (CVD) risk factors associated with lifestyle include smoking, alcohol intake, diet, and exercise. Screening guidelines for modifiable lifestyle CVD risks in adults have been issued by the following organizations:
US Preventive Services Task Force (USPSTF)
American Heart Association (AHA)/American College of Cardiology (ACC)
European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS)
A comparison of the recommendations for diet, physical activity, and tobacco use screening and interventions are listed in Table 1, below.
Table. Screening and Intervention Recommendations for Diet, Physical Activity, and Tobacco Use (Open Table in a new window)
Adult Guidelines
Year
Risk Factor
Screening Populations
Recommended Interventions
US Preventive Services Task Force (USPSTF) [ 12]
2014
Diet and physical activity
Overweight or obese adults with additional cardiovascular risk
Intensive behavioral counseling interventions to promote a healthful diet and physical activity
USPSTF [ 13]
2012
Diet and physical activity
Adult without obesity who do not have known CVD risk factors
Primary care professionals should individualize the decision to offer or refer adults without obesity who do not have hypertension, dyslipidemia, abnormal blood glucose levels, or diabetes to behavioral counseling to promote a healthful diet and physical activity.
American Heart Association [ 14]
2010
Diet and physical activity
All adults
Clinicians should provide individual or group-based interventions to promote and maintain healthy diet and physical activity that include a combination of two or more of the following strategies:
Setting specific, proximal goals
Providing feedback on progress
Providing strategies for self-monitoring
Establishing a plan for frequency and duration of follow-up
Using motivational interviews
Building self-efficacy
European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) [ 15]
2012
Diet, physical activity, and tobacco use
All adults
Risk estimation for CVD using the Systematic COronary Risk Evaluation (SCORE)
All smokers offered assistance to quit
All patients encouraged to adopt healthy diet and increase physical activity
Multimodal behavioral interventions, integrating health education, physical exercise, and psychological therapy for psychosocial risk factors and coping with illness, should be prescribed for all patients with CVD
USPSTF [ 16]
2015
Tobacco Use
All adults
Ask all adults, including pregnant women, about tobacco use; advise those who use tobacco to stop using it, and provide behavioral interventions and US Food and Drug Administration-approved pharmacotherapy for smoking cessation.
Treatment of hypertension
The dietary and pharmacologic treatment of hypertension is associated with a decreased incidence of stroke.
See the Guidelines section for the classification and treatment of hypertension.
Management of hyperlipidemia and dyslipidemia
The 3-hydroxy-3-methyl Co-A (HMG-CoA) reductase inhibitors inhibit the rate-limiting step of cholesterol synthesis in the liver. They are effective in lowering the serum total cholesterol, LDL cholesterol, and triglyceride levels and in raising the serum HDL cholesterol level. HMG-CoA reductase inhibitors also have a low incidence of adverse effects, the most common being hepatotoxicity and myopathy.
The success of the HMG-CoA reductase inhibitors in reducing circulating lipid levels and improving the clinical and anatomic course of atherosclerosis has focused attention on the management of hyperlipidemia.
In addition, an important role remains for other hypolipidemic agents that may be of particular benefit for patients with refractory LDL hypercholesterolemia, hypertriglyceridemia, low HDL cholesterol, and elevated lipoprotein (a).
See the Guidelines section for management of cholesterol and dyslipidemia.
Management of diabetes mellitus
For patients with diabetes mellitus, strict control of comorbid risk factors is especially important. Ample evidence exists that such control reduces the incidence of the clinical complications of microvascular and macrovascular disease.
The benefit of strict glycemic control in the prevention of macrovascular disease has been difficult to confirm, although this intuitively is beneficial and is known to retard the progression of microvascular disease.
See the Guidelines section for CV risk reduction therapies in type 2 diabetes mellitus and CVD.
Treatment of familial hypercholesterolemia
Treatment options for familial hypercholesterolemia include combination drug therapy, although drug therapy alone often is inadequate because of the relative or absolute deficiency of hepatic LDL receptors.
Lipid apheresis is an effective means of reducing circulating lipid levels. Liver transplantation has been performed on young patients with severe disease.
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Drug Agents
HMG-CoA reductase inhibitors
These agents are competitive inhibitors of 3-hydroxy-3-methyl Co-A reductase, an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis, resulting in up-regulation of LDL receptors in response to the decrease in intracellular cholesterol. The HMG-CoA reductase inhibitors are indicated for the secondary prevention of cardiovascular events and for the treatment of hypercholesterolemia and mixed dyslipidemia.
A number of HMG-CoA reductase inhibitors are indicated for patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments. One study suggests that the maximal doses of rosuvastatin and atorvastatin resulted in significant regression of coronary atherosclerosis. Although rosuvastatin resulted in lower LDL cholesterol levels and higher HDL cholesterol levels, a similar degree of regression of percent atheroma value (PAV) was observed in the two groups. [ 17] However, these agents may be less effective in patients with rare homozygous familial hypercholesterolemia, possibly because these patients are lacking functional LDL receptors, making it more likely to raise serum transaminases.
HMG-CoA reductase inhibitors include the following:
Pravastatin (Pravachol)
Simvastatin (Zocor)
Lovastatin (Mevacor, Altocor)
Fluvastatin (Lescol)
Atorvastatin (Lipitor)
Rosuvastatin (Crestor)
Pitavastatin (Livalo)
Fibric acid derivatives
The precise mechanism of action of this class of drugs is complex and incompletely understood. These agents increase the activity of lipoprotein lipase and enhance the catabolism of triglyceride-rich lipoproteins, which is responsible for an increase in the HDL cholesterol fraction.
A decrease in hepatic very low-density lipoprotein (VLDL) synthesis and an increase in cholesterol excretion into bile also appear to occur. The fibrates typically reduce triglyceride levels by 20-50% and increase HDL cholesterol levels by 10-15%. The decrease in VLDL and triglyceride levels results from the ability of fibric acid derivatives to enhance the synthesis of lipoprotein lipase.
The effect of fibric acid derivatives on LDL cholesterol is variable. Levels may be expected to decrease by 10-15%. In patients with marked hypertriglyceridemia, LDL cholesterol levels may increase, which likely reflects the ability of the LDL receptor to clear the increased LDL generated by increased VLDL catabolism.
Fibrate therapy may also be responsible for a decrease in the clotting ability of platelets and fibrinogen levels, which may account for some of the reported clinical benefits.
Fibric acid derivatives include fenofibrate (Tricor) and gemfibrozil (Lopid).
Bile acid sequestrants
The bile acid sequestrants block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol. This results in a decrease in intrahepatic levels of cholesterol. The liver compensates by up-regulating hepatocyte LDL-receptor activity. The net effect is a 10-25% reduction in LDL cholesterol, but no consistent effect on triglycerides or HDL cholesterol exists.
Bile acid sequestrants include cholestyramine (Questran, LoCholest, Prevalite) and colestipol (Colestid).
Vitamin E (Vita-Plus E, Softgels, Aquasol E)
This antioxidant protects polyunsaturated fatty acids in membranes from attack by free radicals but is not seen to have a central role.
Omega-3 polyunsaturated fatty acid
The possible benefits of omega-3 polyunsaturated fatty acid in the treatment of atherosclerosis include effects on lipoprotein metabolism, hemostatic function, platelet/vessel wall interactions, antiarrhythmic actions, and the inhibition of proliferation of smooth muscle cells and therefore growth of the atherosclerotic plaque.
Fish oil feeding has also been found to result in moderate reductions in blood pressure and to modify vascular neuroeffector mechanisms.
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Guidelines
2019 ACC/AHA Prevention of CVD Guidelines
In September 2019, the American College of Cardiology (ACC) and the American Heart Association (AHA) published joint guidelines on the primary prevention of cardiovascular disease. [ 18]
It is recommended that atherosclerotic cardiovascular disease (ASCVD)–related risk factors be controlled via a team-based approach.
For adults, health-care visits should routinely include counseling on optimization of a physically active lifestyle.
At least 150 minutes per week of accumulated moderate-intensity or 75 minutes per week of vigorous-intensity aerobic physical activity (or an equivalent combination of moderate and vigorous activity) is recommended for ASCVD risk reduction in adults.
Improvement of the ASCVD risk factor profile through weight loss is recommended for patients with overweight or obesity.
It is recommended that adults with overweight or obesity achieve and maintain weight loss with the aid of counseling and comprehensive lifestyle interventions (including calorie restriction).
Improvement of glycemic control, achievement of weight loss (if necessary), and improvement of other ASCVD risk factors, via a tailored nutrition plan aimed at providing a heart-healthy dietary pattern, is recommended for all adults with type 2 diabetes mellitus (T2DM).
Improvement of glycemic control, achievement of weight loss (if necessary), and improvement of other ASCVD risk factors, via at least 150 minutes per week of moderate-intensity physical activity or 75 minutes of vigorous-intensity physical activity, is recommended for adults with T2DM.
If, as a result of a risk discussion, a decision is made to employ statin therapy, adults with high blood cholesterol with an intermediate ASCVD risk (≥7.5% to < 20% 10-year ASCVD risk) should be treated with a moderate-intensity statin.
In patients with high blood cholesterol who have an intermediate ASCVD risk (≥7.5% to < 20% 10-year ASCVD risk), reduction of low-density lipoprotein cholesterol (LDL-C) levels by at least 30% is recommended, while optimal ASCVD risk reduction can be targeted, particularly in high-risk patients (≥20% 10-year ASCVD risk), by reducing LDL-C levels by at least 50%.
Maximally tolerated statin therapy is recommended in patients aged 20-75 years with an LDL-C level of at least 190 mg/dL (≥4.9 mmol/L).
Among the nonpharmacologic interventions recommended for adults with elevated blood pressure (BP) or hypertension, including patients who need antihypertensive agents, are the following:
Weight loss
A heart-healthy dietary pattern
Sodium reduction
Dietary potassium supplementation
Increased physical activity with a structured exercise program
Limited alcohol
Primary prevention of cardiovascular disease (CVD) with BP-lowering medications is recommended for adults with an estimated 10-year ASCVD risk of at least 10% and an average systolic BP (SBP) of 130 mm Hg or higher or an average diastolic BP (DBP) of at least 80 mm Hg.
A BP target of below 130/80 mm Hg is recommended for adults with confirmed hypertension and a 10-year ASCVD event risk of at least 10%.
Treatment to a BP goal of below 130/80 mm Hg is recommended for adults with hypertension and chronic kidney disease.
Antihypertensive drug treatment should be administered to adults with T2DM and hypertension who have a BP of 130/80 mm Hg or higher, the aim being to reduce BP to below 130/80 mm Hg.
For adults, cessation of tobacco use should be facilitated by evaluation of such use at every health-care visit, with the status of a patient’s tobacco use recorded as a vital sign.
All adult tobacco users should be advised to quit.
In adult tobacco users, quit rates should be maximized by combining behavioral interventions with pharmacotherapy.
For more information, please go to Cardiovascular Disease Primary Prevention/Lifestyle Guidelines.
2019 ESC/EAS Dyslipidemia Guidelines
In August 2019, the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) released updates to their 2016 guidelines for the management of dyslipidemia. [ 19, 20] Among the changes are new and more aggressive proposed goals for low-density lipoprotein cholesterol (LDL-C) levels, revised cardiovascular (CV) risk stratification, particularly for patients at high to very high risk, as well as new patient management recommendations. [ 19, 20]
New LDL targets across CV risk categories
For very-high-risk patients (10-year risk of CV death ≥10%): Use an LDL-C reduction of at least 50% from baseline and an LDL-C goal of below 1.4 mmol/L (< 55 mg/dL).
For very high-risk patients who experience a second vascular event within 2 years (not necessarily of the same type as the first event) while taking maximally tolerated statin therapy: An LDL-C goal of below 1.0 mmol/L (< 40 mg/dL) may be considered.
For patients at high risk (10-year risk for CV death of 5% to < 10%): Use an LDL-C reduction of at least 50% from baseline and an LDL-C goal of below 1.8 mmol/L (< 70 mg/dL).
For individuals at moderate risk (10-year risk for CV death of 1% to < 5%): Consider an LDL-C goal of below 2.6 mmol/L (< 100 mg/dL).
For individuals at low risk (10-year risk for CV death < 1%): Consider an LDL-C goal of below 3.0 mmol/L (< 116 mg/dL).
New recommendations
Cardiovascular imaging for assessment of ASCVD risk (should be considered)
Consider assessment of carotid and/or femoral arterial plaque burden on arterial ultrasonography as a risk modifier in individuals at low or moderate risk.
Consider coronary artery calcium (CAC) score assessment with computed tomography (CT) as a risk modifier in the CV risk assessment of asymptomatic individuals at low or moderate risk.
Lipid analyses for CVD risk estimation (should be considered)
Consider measurement of lipoprotein (a) (Lp (a)) at least once in each adult’s lifetime to identify those with very high inherited Lp (a) levels above 180 mg/dL (>430 nmol/L) who may have a lifetime risk of atherosclerotic CV disease (ASCVD) that is equivalent to the risk associated with heterozygous familial hypercholesterolemia (FH).
Pharmacotherapy of patients with hypertriglyceridemia (should be considered)
In high-risk (or above) patients with triglyceride (TG) levels between 1.5 and 5.6 mmol/L (135-499 mg/dL) despite statin treatment, consider the combination of n-3 polyunsaturated fatty acids (PUFAs) (icosapent ethyl 2 × 2g/day) with statins.
Treatment of patients with heterozygous FH (should be considered)
For primary prevention in individuals with FH at very-high risk, consider an LDL-C reduction of over 50% from baseline and an LDL-C goal below 1.4 mmol/L (< 55 mg/dL).
Dyslipidemia therapy in older patients
For primary prevention in older people aged up to 75 years, statin therapy is recommended based on the level of risk.
For primary prevention in older people older than 75 years, initiation of statin treatment may be considered if they are at high risk or above.
Dyslipidemia therapy in the setting of diabetes mellitus
For patients with type 2 diabetes mellitus (T2DM) at very-high risk, an LDL-C reduction of at least 50% from baseline and an LDL-C goal of below 1.4 mmol/L (< 55mg/dL) is recommended.
For those with T2DM at high risk, an LDL-C reduction of at least 50% from baseline and an LDL-C goal of below 1.8 mmol/L (< 70 mg/dL) is recommended.
For individuals with T1DM who are at high or very-high risk, statins are recommended.
Consider intensification of statin therapy before introducing combination therapy. If the goal is not reached, consider a statin combined with ezetimibe. (Each should be considered.)
Statin therapy is not recommended in premenopausal diabetic patients who are considering pregnancy or who are not using adequate contraception.
Lipid-lowering therapy in patients with ACS (should be considered)
For patients who present with an acute coronary syndrome (ACS), and whose LDL-C levels are not at goal despite already taking a maximally tolerated statin dose and ezetimibe, consider adding a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor early after the event (if possible, during hospitalization for the ACS event).
For more information, please go to Primary and Secondary Prevention of Coronary Artery Disease , Familial Hypercholesterolemia , Hypertriglyceridemia, and LDL Cholesterol Genetics.
2019 ACC Novel CV Risk Reduction Therapies in Type 2 Diabetes and CVD: Consensus Decision Pathways
The expert consensus decision pathways on the use of two major new classes of diabetes drugs—sodium-glucose cotransporter type 2 (SGLT2) inhibitors and glucagon-like peptide 1 receptor agonists (GLP-1RAs)—for cardiovascular (CV) risk reduction in patients with type 2 diabetes (TD2) and atherosclerotic CV disease (ASCVD) were released in November 2018 by the American College of Cardiology. [ 21, 22] The main focus of management is in the outpatient ambulatory setting.
The SGLT2 inhibitors appear to reduce major adverse CV events (MACE) and the risk of heart failure (HF) but increase the risk for genital mycotic infections, whereas GLP-1RAs offer reductions in MACE but are associated with transient nausea and vomiting. Both classes of agents have benefits in reducing blood pressure and weight, and they have a low risk for hypoglycemia.
For CV risk reduction, initiate agents with demonstrated CV benefit from either drug class at the lowest doses; no uptitration is necessary for SGLT2 inhibitors, whereas the GLP-1RAs should be slowly uptitrated (to avoid nausea) to the maximal tolerated dose.
At the initiation of an SGLT2 inhibitor or a GLP-1RA agent, clinicians should avoid hypoglycemia in patients by monitoring those with A1C levels near or below target, particularly when patients' existing diabetes therapies include sulfonylureas, glinides, or insulin.
In addition to reducing MACE and CV death, SGLT2 inhibitors are also suitable for preventing hospitalization for HF.
Empagliflozin is the preferred SGLT2 inhibitor based on the available evidence and overall benefit-risk balance.
Liraglutide should be the preferred agent among the GLP-1RAs for CV event risk reduction.
Two SGLT2 inhibitors (ie, canagliflozin, ertugliflozin) appear to be associated with an increased risk of amputation. It is unclear whether or not this is a class effect; therefore, clinicians should closely monitor patients on these agents who have a history of amputation, peripheral arterial disease, neuropathy, or diabetic foot ulcers.
Patients with T2D and clinical ASCVD on metformin therapy (or in whom metformin is contraindicated or not tolerated) should have an SGLT2 inhibitor or GLP-1RA with proven CV benefit added to their treatment regimen. For patients not on background metformin therapy, practitioners may use their clinical judgment to prescribe an SGLT2 inhibitor or GLP-1RA for CV risk reduction.
It appears reasonable to concomitantly use an SGLT2 inhibitor and a GLP-1RA with demonstrated CV benefit if clinically indicated, although such combination therapy has not been studied for CVD risk reduction.
For more information, please go to Coronary Artery Atherosclerosis.
2018 ACC/AHA Cholesterol Management Guidelines
The recommendations on management of blood cholesterol were released in November 2018 by the ACC, AHA, and multiple other medical societies. [ 23, 24]
The guideline's top 10 key recommendations for reducing the risk of atherosclerotic cardiovascular disease through cholesterol management are summarized below.
Emphasize a heart-healthy lifestyle across the life course of all individuals.
In patients with clinical atherosclerotic cardiovascular disease (ASCVD), reduce low-density lipoprotein cholesterol (LDL-C) levels with high-intensity statin therapy or the maximally tolerated statin therapy.
In individuals with very high-risk ASCVD, use an LDL-C threshold of 70 mg/dL (1.8 mmol/L) to consider the addition of nonstatins to statin therapy.
In patients with severe primary hypercholesterolemia (LDL-C level ≥190 mg/dL [≥4.9 mmol/L]), without calculating the 10-year ASCVD risk, begin high-intensity statin therapy.
In patients 40 to 75 years of age with diabetes mellitus and an LDL-C level of ≥70 mg/dL: Start moderate-intensity statin therapy without calculating their 10-year ASCVD risk.
In patients aged 40 to 75 years evaluated for primary ASCVD prevention: Have a clinician–patient risk discussion before starting statin therapy.
In nondiabetic patients aged 40 to 75 years and with the following characteristics:
LDL-C levels ≥70 mg/dL (≥1.8 mmol/L), at a 10-year ASCVD risk of ≥7.5%: Start a moderate-intensity statin if a discussion of treatment options favors statin therapy.
A 10-year risk of 7.5-19.9% (intermediate risk): Risk-enhancing factors favor initiation of statin therapy.
LDL-C levels ≥70-189 mg/dL (≥1.8-4.9 mmol/L), at a 10-year ASCVD risk of ≥7.5-19.9%: If a decision about statin therapy is uncertain, consider measuring coronary artery calcium (CAC) levels.
Assess patient adherence and the percentage response to LDL-C–lowering medications and lifestyle changes with a repeat lipid measurement 4-12 weeks after initiation of statin therapy or dose adjustment; repeat every 3-12 months as needed.
2018 USDHHS Physical Activity Guidelines
The guidelines on physical activity were released in November 2018 by the Physical Activity Guidelines Advisory Committee of the USDHHS. [ 25, 26]
Age- and condition-related recommendations
Children aged 3-5 years: Should be physically active throughout the day to enhance growth and development.
Children aged 6-17 years: Sixty minutes or more of moderate-to-vigorous physical activity per day.
Adults: At least 150-300 minutes per week of moderate-intensity aerobic physical activity, OR 75-150 minutes per week of vigorous-intensity aerobic physical activity, OR an equivalent combination of moderate- and vigorous-intensity aerobic activity; muscle-strengthening activities should be performed on two or more days per week.
Older adults: Multicomponent physical activity to include balance training, aerobic activity, and muscle-strengthening activity.
Pregnant and postpartum women: At least 150 minutes of moderate-intensity aerobic activity weekly.
Adults with chronic conditions or disabilities who are able: Follow key guidelines and perform both aerobic and muscle-strengthening activities.
Sleep, daily functioning, and mental health
Strong evidence demonstrates that moderate-to-vigorous physical activity improves sleep quality by decreasing the time it takes to fall asleep; it can also increase deep-sleep time and decrease daytime sleepiness.
Single episodes of physical activity promote improvements in executive function, to include organization of daily activities and future planning. Cognition (ie, memory, processing speed, attention, academic performance) also can be improved with physical exercise.
Regular physical activity reduces the risk of clinical depression, as well as reducing depressive symptoms and symptoms of anxiety.
Strong evidence demonstrates regular physical activity improves perceived quality of life.
Risk of diseases and conditions
Regular physical activity minimizes excessive weight gain, helps maintain weight within a healthy range, improves bone health, and prevents obesity, even in children as young as 3-5 years.
In pregnant women, physical activity helps reduce excessive weight gain in pregnancy and helps reduce the risk of developing gestational diabetes and postpartum depression.
Regular physical activity has been shown to improve cognitive function and to reduce the risk of dementia; falls and fall-related injuries; and cancers of the breast, esophagus, colon, bladder, lung, endometrium, kidney, and stomach. It also helps retard the progression of osteoarthritis, type 2 diabetes, and hypertension.
Promotion of physical activity
School- and community-based programs can be effective.
Environmental and policy changes should improve access to physical activity and support of physical activity behavior.
Information and technology should be used to promote physical activity, to include activity monitors (eg, wearable devices), smartphone apps, computer-tailored printed material, and Internet-based programs for self-monitoring, message delivery, and support.
For more information, please go to Therapeutic Exercise.
2017 ACC/AHA Classification and Treatment of Hypertension
The ACC/AHA guidelines eliminate the classification of prehypertension and divides it into two levels [ 27, 28] : (1) elevated blood pressure (BP), with a systolic pressure between 120 and 129 mm Hg and diastolic pressure less than 80 mm Hg, and (2) stage 1 hypertension, with a systolic pressure of 130 to 139 mm Hg or a diastolic pressure of 80 to 89 mm Hg.
In adults at increased risk of heart failure (HF), the optimal BP in those with hypertension should be less than 130/80 mm Hg.
Adults with HF r EF (HF with reduced ejection fraction) and hypertension should be prescribed GDMT (guideline-directed management and therapy) titrated to attain a BP of less than 130/80 mm Hg.
Nondihydropyridine calcium channel blockers (CCBs) are not recommended in the treatment of hypertension in adults with HF r EF.
Adults with hypertension and chronic kidney disease (CKD) should be treated to a BP goal of less than 130/80 mm Hg.
After kidney transplantation, it is reasonable to treat patients with hypertension to a BP goal of less than 130/80 mm Hg.
After kidney transplantation, it is reasonable to treat patients with hypertension with a calcium antagonist on the basis of improved glomerular filtration rate (GFR) and kidney survival.
Immediate lowering of SBP to less than 140 mm Hg in adults with spontaneous intracerebral hemorrhage (ICH) who present within 6 hours of the acute event and have an SBP between 150 mm Hg and 220 mm Hg is not of benefit to reduce death or severe disability and can be potentially harmful.
Adults with acute ischemic stroke and elevated BP who are eligible for treatment with intravenous tissue plasminogen activator should have their BP slowly lowered to less than 185/110 mm Hg before thrombolytic therapy is initiated.
In adults with an acute ischemic stroke, BP should be less than 185/110 mm Hg before administration of intravenous tissue plasminogen activator and should be maintained below 180/105 mm Hg for at least the first 24 hours after initiating drug therapy.
For adults who experience a stroke or transient ischemic attack (TIA), treatment with a thiazide diuretic, ACE inhibitor, or ARB, or combination treatment consisting of a thiazide diuretic plus ACE inhibitor, is useful.
In adults with an untreated SBP greater than 130 mm Hg but less than 160 mm Hg or DBP greater than 80 mm Hg but less than 100 mm Hg, it is reasonable to screen for the presence of white coat hypertension by using either daytime ABPM (ambulatory BP monitoring) or HBPM (home BPM) before diagnosis of hypertension.
In adults with untreated office BPs that are consistently between 120 mm Hg and 129 mm Hg for SBP or between 75 mm Hg and 79 mm Hg for DBP, screening for masked hypertension with home BP monitoring (or ABPM) is reasonable.
In adults with hypertension, screening for primary aldosteronism is recommended in the presence of any of the following concurrent conditions: resistant hypertension, hypokalemia (spontaneous or substantial, if diuretic induced), incidentally discovered adrenal mass, family history of early-onset hypertension, or stroke at a young age (< 40 years).
Adult men and women with elevated BP or hypertension who currently consume alcohol should be advised to drink no more than 2 and 1 standard drinks per day, respectively.
Two or more antihypertensive medications are recommended to achieve a BP target of less than 130/80 mm Hg in most adults with hypertension, especially in black adults with hypertension.
Women with hypertension who become pregnant should not be treated with ACE inhibitors, ARBs, or direct renin inhibitors.
Use of BP-lowering medications is recommended for secondary prevention of recurrent CVD events in patients with clinical CVD and an average SBP of 130 mm Hg or higher or an average DBP of 80 mm Hg or higher, and for primary prevention in adults with an estimated 10-year atherosclerotic cardiovascular disease (ASCVD) risk of 10% or higher and an average SBP of 130 mm Hg or higher or an average DBP of 80 mm Hg or higher.
Use of BP-lowering medication is recommended for primary prevention of CVD in adults with no history of CVD and with an estimated 10-year ASCVD risk < 10% and an SBP of 140 mm Hg or higher or a DBP of 90 mm Hg or higher.
Adults with an elevated BP or stage 1 hypertension who have an estimated 10-year ASCVD risk less than 10% should be managed with nonpharmacological therapy and have a repeat BP evaluation within 3 to 6 months.
Adults with stage 1 hypertension who have an estimated 10-year ASCVD risk of 10% or higher should be managed initially with a combination of nonpharmacological and antihypertensive drug therapy and have a repeat BP evaluation in 1 month.
For adults with a very high average BP (eg, SBP ≥180 mm Hg or DBP ≥110 mm Hg), evaluation followed by prompt antihypertensive drug treatment is recommended.
Simultaneous use of an ACE inhibitor, ARB, and/or renin inhibitor is potentially harmful and is not recommended to treat adults with hypertension.
For more information, please go to Hypertension.
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Next: Overview of Atherosclerosis
Questions & Answers
Overview
What is noncoronary atherosclerosis?
What are the signs and symptoms of noncoronary atherosclerosis?
How is noncoronary atherosclerosis diagnosed?
How is noncoronary atherosclerosis prevented?
Which medications are used in the treatment of noncoronary atherosclerosis?
What causes noncoronary atherosclerosis?
How does noncoronary atherosclerosis develop?
What is the role of familial hypercholesterolemia in the etiology of noncoronary atherosclerosis?
What are the risk factors for noncoronary atherosclerosis?
What is the role of hypertension in the etiology of noncoronary atherosclerosis?
What is the role of diabetes mellitus in the etiology of noncoronary atherosclerosis?
What is the role of cigarette smoking in the etiology of noncoronary atherosclerosis?
What is the role of C-reactive protein (CRP in the etiology of noncoronary atherosclerosis?
What is the role of metabolic syndrome in the etiology of noncoronary atherosclerosis?
What is the prevalence of noncoronary atherosclerosis?
What are the sexual predilections of noncoronary atherosclerosis?
At what age is noncoronary atherosclerosis typically diagnosed?
What is the prognosis of noncoronary atherosclerosis?
Which clinical history findings are characteristic of noncoronary atherosclerosis?
Which physical findings are characteristic of noncoronary atherosclerosis?
What is the role of a lipid profile in the workup of noncoronary atherosclerosis?
What is the role of blood glucose and HA1c in the workup of noncoronary atherosclerosis?
What is the role of ultrasonography in the workup of noncoronary atherosclerosis?
Which brachial artery findings on ultrasonography are characteristic of noncoronary atherosclerosis?
Which carotid artery findings on ultrasonography are characteristic of noncoronary atherosclerosis?
What is the role of intravascular ultrasonography (IVUS) in the workup of noncoronary atherosclerosis?
What is the role of MRI in the workup of noncoronary atherosclerosis?
What is the role of scintigraphy in the workup of noncoronary atherosclerosis?
What is included in risk factor control for the prevention of noncoronary atherosclerosis?
What are the screening recommendations for the noncoronary atherosclerosis?
How is hypertension treated in patients with noncoronary atherosclerosis?
How are hyperlipidemia and dyslipidemia treated in patients with noncoronary atherosclerosis?
How is diabetes mellitus treated in patients with noncoronary atherosclerosis?
How is familial hypercholesterolemia treated in patients with noncoronary atherosclerosis?
What is the role of HMG-CoA reductase inhibitors in the treatment of noncoronary atherosclerosis?
What is the role of fibric acid derivatives in the treatment of noncoronary atherosclerosis?
What is the role of bile acid sequestrants in the treatment of noncoronary atherosclerosis?
What is the role of vitamin E in the treatment of noncoronary atherosclerosis?
What is the role of omega-3 polyunsaturated fatty acid in the treatment of noncoronary atherosclerosis?
What are the ACC/AHA guidelines on the primary prevention of cardiovascular disease?
What are the ESC/EAS treatment guidelines for dyslipidemia?
What are the ACC guidelines on cardiovascular risk reduction in patients with type 2 diabetes?
What are the ACC/AHA guidelines on cholesterol management?
What are the USDHHS physical activity guidelines?
What are the ACC/AHA guidelines on the classification and treatment of hypertension?
Previous
References
Weissgerber A, Scholz M, Teren A, et al. The value of noncoronary atherosclerosis for identifying coronary artery disease: results of the Leipzig LIFE Heart Study. Clin Res Cardiol. 2016 Feb. 105 (2):172-81. [Medline].
Drechsler M, Megens RT, van Zandvoort M, Weber C, Soehnlein O. Hyperlipidemia-triggered neutrophilia promotes early atherosclerosis. Circulation. 2010 Nov 2. 122 (18):1837-45. [Medline].
Kolodgie FD, Gold HK, Burke AP, Fowler DR, Kruth HS, Weber DK, et al. Intraplaque hemorrhage and progression of coronary atheroma. N Engl J Med. 2003 Dec 11. 349 (24):2316-25. [Medline].
Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K, et al. Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009 Jan 27. 119 (3):e21-181. [Medline].
Semba RD, Cappola AR, Sun K, et al. Plasma Klotho and Cardiovascular Disease in Adults. J Am Geriatr Soc. 2011 Aug 24. [Medline].
Christoffersen M, Frikke-Schmidt R, Schnohr P, et al. Xanthelasmata, arcus corneae, and ischaemic vascular disease and death in general population: prospective cohort study. BMJ. 2011 Sep 15. 343:d5497. [Medline]. [Full Text].
Fayad ZA, Mani V, Woodward M, et al. Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging (dal-PLAQUE): a randomised clinical trial. Lancet. 2011 Oct 29. 378 (9802):1547-59. [Medline].
Nicholls SJ, Brewer HB, Kastelein JJ, et al. Effects of the CETP inhibitor evacetrapib administered as monotherapy or in combination with statins on HDL and LDL cholesterol: a randomized controlled trial. JAMA. 2011 Nov 16. 306 (19):2099-109. [Medline].
Boden WE, Probstfield JL, Anderson T, Chaitman BR, Desvignes-Nickens P, Koprowicz K, et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011 Dec 15. 365 (24):2255-67. [Medline].
Makris GC, Teng Z, Patterson AJ, et al. Advances in MRI for the evaluation of carotid atherosclerosis. Br J Radiol. 2015 Aug. 88 (1052):20140282. [Medline].
Katakami N, Kim YS, Kawamori R, Yamasaki Y. The phosphodiesterase inhibitor cilostazol induces regression of carotid atherosclerosis in subjects with type 2 diabetes mellitus: principal results of the Diabetic Atherosclerosis Prevention by Cilostazol (DAPC) study: a randomized trial. Circulation. 2010 Jun 15. 121 (23):2584-91. [Medline].
[Guideline] LeFevre ML, US Preventive Services Task Force. USPSTF Recommendation summary: Healthful diet and physical activity for Cardiovascular Disease Prevention in adults with cardiovascular risk factors: behavioral counseling. Available at http://www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/healthy-diet-and-physical-activity-counseling-adults-with-high-risk-of-cvd. August 2014; Accessed: December 2, 2015.
[Guideline] US Preventive Services Task Force. USPSTF. Final recommendation statement: Healthful diet and physical activity for cardiovascular disease prevention in adults without known risk factors: behavioral counseling. Available at http://www.uspreventiveservicestaskforce.org/Page/Document/RecommendationStatementFinal/healthful-diet-and-physical-activity-for-cardiovascular-disease-prevention-in-adults-behavioral-counseling. July 2017; Accessed: December 23, 2019.
[Guideline] Artinian NT, Fletcher GF, Mozaffarian D, et al, for the American Heart Association Prevention Committee of the Council on Cardiovascular Nursing. Interventions to promote physical activity and dietary lifestyle changes for cardiovascular risk factor reduction in adults: a scientific statement from the American Heart Association. Circulation. 2010 Jul 27. 122 (4):406-41. [Medline]. [Full Text].
[Guideline] Perk J, De Backer G, Gohlke H, et al, for the European Association for Cardiovascular Prevention & Rehabilitation (EACPR), ESC Committee for Practice Guidelines (CPG). European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts). Eur Heart J. 2012 Jul. 33 (13):1635-701. [Medline]. [Full Text].
[Guideline] US Preventive Services Task Force. Tobacco smoking cessation in adults, including pregnant women: behavioral and pharmacotherapy interventions. Available at http://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/tobacco-use-in-adults-and-pregnant-women-counseling-and-interventions1.. September 2015; Accessed: December 23, 2019.
Nicholls SJ, Ballantyne CM, Barter PJ, et al. Effect of two intensive statin regimens on progression of coronary disease. N Engl J Med. 2011 Dec 1. 365 (22):2078-87. [Medline].
[Guideline] Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the primary prevention of cardiovascular disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019 Sep 10. 74 (10):1376-414. [Medline]. [Full Text].
[Guideline] Mach F, Baigent C, Catapano AL, et al, for the ESC Scientific Document Group . 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2019 Aug 31. [Medline]. [Full Text].
Hughes S. New European lipid guidelines take aggressive approach. Medscape Medical News. Available at https://www.medscape.com/viewarticle/917551.. September 1, 2019; Accessed: October 3, 2019.
[Guideline] Das SR, Everett BM, Birtcher KK, et al. 2018 ACC expert consensus decision pathway on novel therapies for cardiovascular risk reduction in patients with type 2 diabetes and atherosclerotic cardiovascular disease: a report of the American College of Cardiology Task Force on Expert Consensus Decision Pathways. J Am Coll Cardiol. 2018 Dec 18. 72 (24):3200-23. [Medline]. [Full Text].
Hughes S. ACC consensus on new diabetes drugs to reduce CV outcomes. Medscape Medical News. Available at https://www.medscape.com/viewarticle/905580.. November 27, 2018.; Accessed: January 30, 2019.
[Guideline] Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the management of blood cholesterol: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019 Jun 25. 73 (24):e285-e350. [Medline]. [Full Text].
Stiles S. New AHA/ACC cholesterol treatment guideline expands role of LDL targets. Medscape Medical News. Available at https://www.medscape.com/viewarticle/904736.. November 10, 2018; Accessed: December 5, 2018.
[Guideline] 2018 Physical Activity Guidelines Advisory Committee. 2018 Physical Activity Guidelines Advisory Committee Scientific Report.Washington, DC: US Department of Health and Human Services, 2018. Available at https://health.gov/paguidelines/second-edition/report/pdf/PAG_Advisory_Committee_Report.pdf.. Accessed: November 28, 2018.
[Guideline] Piercy KL, Troiano RP, Ballard RM, et al. The physical activity guidelines for Americans. JAMA. 2018 Nov 20. 320 (19):2020-8. [Medline].
[Guideline] Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018 Jun. 71 (6):e13-e115. [Medline]. [Full Text].
Jeffrey S. New ACC/AHA hypertension guidelines make 130 the new 140. Medscape Medical News. Available at https://www.medscape.com/viewarticle/888560. November 13, 2017; Accessed: January 12, 2018.
Grundy SM, Cleeman JI, Merz CN, Brewer HB Jr, Clark LT, Hunninghake DB, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. J Am Coll Cardiol. 2004 Aug 4. 44 (3):720-32. [Medline].
Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002 Dec 17. 106 (25):3143-421. [Medline].
Stone NJ, Bilek S, Rosenbaum S. Recent National Cholesterol Education Program Adult Treatment Panel III update: adjustments and options. Am J Cardiol. 2005 Aug 22. 96 (4A):53E-59E. [Medline].
[Guideline] Goff DC Jr, Lloyd-Jones DM, Bennett G, Coady S, D'Agostino RB Sr, Gibbons R, et al. 2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Nov 12. [Medline]. [Full Text].
[Guideline] Stone NJ, Robinson J, Lichtenstein AH, Merz CN, Blum CB, Eckel RH, et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Nov 12. [Medline]. [Full Text].
Maroules CD, Rosero E, Ayers C, Peshock RM, Khera A. Abdominal Aortic Atherosclerosis at MR Imaging Is Associated with Cardiovascular Events: The Dallas Heart Study. Radiology. 2013 Oct. 269 (1):84-91. [Medline].
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Tables
Table. Screening and Intervention Recommendations for Diet, Physical Activity, and Tobacco Use
Table. Screening and Intervention Recommendations for Diet, Physical Activity, and Tobacco Use
Adult Guidelines
Year
Risk Factor
Screening Populations
Recommended Interventions
US Preventive Services Task Force (USPSTF) [ 12]
2014
Diet and physical activity
Overweight or obese adults with additional cardiovascular risk
Intensive behavioral counseling interventions to promote a healthful diet and physical activity
USPSTF [ 13]
2012
Diet and physical activity
Adult without obesity who do not have known CVD risk factors
Primary care professionals should individualize the decision to offer or refer adults without obesity who do not have hypertension, dyslipidemia, abnormal blood glucose levels, or diabetes to behavioral counseling to promote a healthful diet and physical activity.
American Heart Association [ 14]
2010
Diet and physical activity
All adults
Clinicians should provide individual or group-based interventions to promote and maintain healthy diet and physical activity that include a combination of two or more of the following strategies:
Setting specific, proximal goals
Providing feedback on progress
Providing strategies for self-monitoring
Establishing a plan for frequency and duration of follow-up
Using motivational interviews
Building self-efficacy
European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) [ 15]
2012
Diet, physical activity, and tobacco use
All adults
Risk estimation for CVD using the Systematic COronary Risk Evaluation (SCORE)
All smokers offered assistance to quit
All patients encouraged to adopt healthy diet and increase physical activity
Multimodal behavioral interventions, integrating health education, physical exercise, and psychological therapy for psychosocial risk factors and coping with illness, should be prescribed for all patients with CVD
USPSTF [ 16]
2015
Tobacco Use
All adults
Ask all adults, including pregnant women, about tobacco use; advise those who use tobacco to stop using it, and provide behavioral interventions and US Food and Drug Administration-approved pharmacotherapy for smoking cessation.
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Contributor Information and Disclosures
Author
F Brian Boudi, MD, FACP Clinical Associate Professor, University of Arizona College of Medicine (Phoenix Campus); Fellow, Sarver Heart Center, University of Arizona College of Medicine; Regional Faculty, American Heart Association; Adjunct Assistant Professor of Medicine, Mid-Western University; Staff Physician, Site Director for Clinical Rotations Emergency Medicine, Phoenix Veterans Administration Health Care System
F Brian Boudi, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Society of Echocardiography, Arizona Medical Association, Association of Program Directors in Internal Medicine, American College of Healthcare Executives, American Society of Nuclear Cardiology
Disclosure: Nothing to disclose.
Coauthor (s)
Chowdhury H Ahsan, MD, PhD, MRCP, FSCAI Clinical Professor of Medicine, Director of Cardiac Catheterization and Intervention, Marlon Cardiac Catheterization Laboratory, Director of Cardiovascular Research, University Medical Center, University of Nevada School of Medicine
Chowdhury H Ahsan, MD, PhD, MRCP, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions, American Stroke Association
Disclosure: Received consulting fee from sanofi for consulting; Received honoraria from astra zeneca for speaking and teaching; Received honoraria from BI for speaking and teaching.
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology
Disclosure: Nothing to disclose.
Chief Editor
Yasmine S Ali, MD, FACC, FACP, MSCI Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine; President, LastSky Writing, LLC
Yasmine S Ali, MD, FACC, FACP, MSCI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Medical Writers Association, National Lipid Association, Tennessee Medical Association
Disclosure: Serve (d) as a director, officer, partner, employee, advisor, consultant or trustee for: MCG Health, LLC; LastSky Writing, LLC; Philips Healthcare; Cardiac Profiles, Inc.; Corvidane; M Health; GE Healthcare; Athena Health; PeerView Institute; Verywell Health; HealthCentral.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors James L Orford, MBChB and Andrew P Selwyn, MD, MA, FACC, FRCP, to the development and writing of the source article.
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msmarco_passage_01_454610203 | Benefits | Benefits
Is Graviola a Cancer Cure?
Since it is a natural product not patentable, cannot say this with certainty. Graviola Extract is only a dietary supplement, 100% natural and pure. It might be used as a complement as a dietary supplement in medical treatment because the benefits found in the leaf of Graviola named acetogenins.
There is no incompatibility and unlike, it complements very well with any traditional treatment that the patient is going through. They have absolutely no secondary effects, intolerance reactions or allergies.
The acetogenins derived from long chain fatty acids have direct action on the mitochondria, is uses to protect and improve the immune system.
How should Graviola be consumed?
Because the Graviola is a product of a plant that also cleanses the stomach, we recommend taking Graviola extract in a phased manner, from less to more, in order to make the body adjusts to this product.
Other Benefits of Taking Graviola
Graviola, besides being a dietary supplement that might helps in traditional treatment for lung, liver, colon, pancreas, kidney and stomach. It is also traditionally used to combat anxiety states, depression and nervousness.
Graviola is a small tree, vertical, grows 5 to 6 meters in height with large leaves, dark green and shiny. It is native to the rainforest of Peru, Brazil and Puerto Rico. The fruit is sold in local markets in the tropics where it is called soursop, guanabana or Brazilian Cherimoya and is excellent for making drinks and sherbets and, though slightly sour-acid, can be eaten out of hand.
Medicine and Graviola go hand in hand.
All parts of the Graviola tree are used in natural medicine as a dietary supplement in the tropics, including bark, roots, fruit, and fruit seeds. The various features and applications are attributed to various parts of the tree. Generally, in many countries said that is being use as fruit and fruit juice, to the treatment of worms and parasites, and can be used as a complement for diarrhea and dysentery. Some countries use the crushed graviola seeds against internal and external parasites, head lice, and worms .
Active ingredient: Acetogenins
Important information about Cancer:
Perhaps one of the most important discoveries related to cancer is that of the parasites. Some Naturalist or Health Professionals said that Cancer patients are infected with parasites. As reference, Dr. Hulda Clark book "The Cure for All Cancers" (The Cure For all cancers), sold in many countries, said in her book that she discovered that cancer and parasite are related. She concluded in her book that many cancer patients are infected with parasites. Parasites (the same present in our dogs and cats) both create toxic within the body, with their dropping and urine, which the body is not able to defense against cancer and succumbed to the attack of the cancer cells, as she established in her book.
There are hundreds of people who have given testimonies of the herbal treatment success as mentioned in Dr. Clark book.
Is Graviola a Cancer Cure? (2)
Since it is a natural product not patentable, cannot say this with certainty. Graviola Extract is only a dietary supplement, 100% natural and pure. It might be used as a complement as a dietary supplement in medical treatment because the benefits found in the leaf of Graviola named acetogenins.
There is no incompatibility and unlike, it complements very well with any traditional treatment that the patient is going through. They have absolutely no secondary effects, intolerance reactions or allergies.
The acetogenins derived from long chain fatty acids have direct action on the mitochondria, is uses to protect and improve the immune system.
How should Graviola be consumed?
Because the Graviola is a product of a plant that also cleanses the stomach, we recommend taking Graviola extract in a phased manner, from less to more, in order to make the body adjusts to this product.
Other Benefits of Taking Graviola
Graviola, besides being a dietary supplement that might helps in traditional treatment for lung, liver, colon, pancreas, kidney and stomach. It is also traditionally used to combat anxiety states, depression and nervousness.
Graviola is a small tree, vertical, grows 5 to 6 meters in height with large leaves, dark green and shiny. It is native to the rainforest of Peru, Brazil and Puerto Rico. The fruit is sold in local markets in the tropics where it is called soursop, guanabana or Brazilian Cherimoya and is excellent for making drinks and sherbets and, though slightly sour-acid, can be eaten out of hand.
Medicine and Graviola go hand in hand.
All parts of the Graviola tree are used in natural medicine as a dietary supplement in the tropics, including bark, roots, fruit, and fruit seeds. The various features and applications are attributed to various parts of the tree. Generally, in many countries said that is being use as fruit and fruit juice, to the treatment of worms and parasites, and can be used as a complement for diarrhea and dysentery. Some countries use the crushed graviola seeds against internal and external parasites, head lice, and worms .
Active ingredient: Acetogenins
Important information about Cancer:
Perhaps one of the most important discoveries related to cancer is that of the parasites. Some Naturalist or Health Professionals said that Cancer patients are infected with parasites. As reference, Dr. Hulda Clark book "The Cure for All Cancers" (The Cure For all cancers), sold in many countries, said in her book that she discovered that cancer and parasite are related. She concluded in her book that many cancer patients are infected with parasites. Parasites (the same present in our dogs and cats) both create toxic within the body, with their dropping and urine, which the body is not able to defense against cancer and succumbed to the attack of the cancer cells, as she established in her book.
There are hundreds of people who have given testimonies of the herbal treatment success as mentioned in Dr. Clark book.
Cancer and Chemotherapy
One of the most common treatments is chemotherapy. Patients receiving chemotherapy are deteriorating rapidly because of side effects, besides the poor quality of life and suffering which are subjected, and which is causing nausea, anorexia, hair loss, fatigue and vomiting among others. The latest research cast doubt on the supposed effectiveness of chemotherapy.
The cancer patient enters an exorbitant cost between chemotherapy, radiation, surgery, x-rays, specialized studies and anaesthesia. The action of chemotherapy is not specific, since it affects both cancer cells and healthy cells and also normal tissues of the body.
The Graviola extract can be used as a natural supplement in combination with the chemotherapy or any other traditional treatment, since it is a 100% natural and no harm to the good cells and might help with the cellular regeneration. Additionally it is well known that chemotherapy can affect the digestive system and Graviola extract is easily digestible. In the past our ancestors use Graviola for many stomach disorders.
One of the most common treatments is chemotherapy. Patients receiving chemotherapy are deteriorating rapidly because of side effects, besides the poor quality of life and suffering which are subjected, and which is causing nausea, anorexia, hair loss, fatigue and vomiting among others. The latest research cast doubt on the supposed effectiveness of chemotherapy.
The cancer patient enters an exorbitant cost between chemotherapy, radiation, surgery, x-rays, specialized studies and anesthesia. The action of chemotherapy is not specific, since it affects both cancer cells and healthy cells and also normal tissues of the body.
The Graviola extract can be used as a natural supplement in combination with the chemotherapy or any other traditional treatment, since it is a 100% natural and no harm to the good cells and might help with the cellular regeneration. Additionally it is well known that chemotherapy can affect the digestive system and Graviola extract is easily digestible
Cancer and Chemotherapy (2)
One of the most common treatments is chemotherapy. Patients receiving chemotherapy are deteriorating rapidly because of side effects, besides the poor quality of life and suffering which are subjected, and which is causing nausea, anorexia, hair loss, fatigue and vomiting among others. The latest research cast doubt on the supposed effectiveness of chemotherapy.
The cancer patient enters an exorbitant cost between chemotherapy, radiation, surgery, x-rays, specialized studies and anaesthesia. The action of chemotherapy is not specific, since it affects both cancer cells and healthy cells and also normal tissues of the body.
The Graviola extract can be used as a natural supplement in combination with the chemotherapy or any other traditional treatment, since it is a 100% natural and no harm to the good cells and might help with the cellular regeneration. Additionally it is well known that chemotherapy can affect the digestive system and Graviola extract is easily digestible. In the past our ancestors use Graviola for many stomach disorders.
One of the most common treatments is chemotherapy. Patients receiving chemotherapy are deteriorating rapidly because of side effects, besides the poor quality of life and suffering which are subjected, and which is causing nausea, anorexia, hair loss, fatigue and vomiting among others. The latest research cast doubt on the supposed effectiveness of chemotherapy.
The cancer patient enters an exorbitant cost between chemotherapy, radiation, surgery, x-rays, specialized studies and anesthesia. The action of chemotherapy is not specific, since it affects both cancer cells and healthy cells and also normal tissues of the body.
The Graviola extract can be used as a natural supplement in combination with the chemotherapy or any other traditional treatment, since it is a 100% natural and no harm to the good cells and might help with the cellular regeneration. Additionally it is well known that chemotherapy can affect the digestive system and Graviola extract is easily digestible
FAQ's
What is Graviola (Soursop, Annona muricata, soursop)?
Graviola, also known as soursop, (Annona muricata or guanabana) is a natural supplement extracted from graviola leaves, ("Annona muricata" or soursop).
How do you remove the extract of the Graviola?
It is extracted from the leaves of the tree "Annona muricata", "soursop" or soursop. The extract is superior to other herbal preparations, such as capsules, theses and infusions because many of the medicinal properties contained in the leaves, roots and bark are not soluble in water. The extract is more potent than other formulations because is as a tinture made of the leaves, it is also easier to digest the body and is 100% natural.
What are the bioactive ingredients of the extract of the Graviola?
The ingredients are bioactive acetogenins from the leaves of the tree. There are 350 discovered to date.
FAQ's (2)
What is Graviola (Soursop, Annona muricata, soursop)?
Graviola, also known as soursop, (Annona muricata or guanabana) is a 100% natural supplement of the Puerto Rican forest, extracted from graviola leaves, ("Annona muricata" or soursop).
Studies at several universities in the United States discovered acetogenins extremely powerful component. Many of the chemicals in the leaves of the graviola, contribute to improve the inmume system, as a complement in the preparation of patients with degenerative diseases. Graviola extract improves the digestive system to help the assimilation of nutrients and can be uses as cell protective.
How do you remove the extract of the Graviola?
It is extracted from the leaves of the tree "Annona muricata", "soursop" or soursop. The extract is superior to other herbal preparations, such as capsules, theses and infusions because many of the medicinal properties contained in the leaves, roots and bark are not soluble in water. The extract is more potent than other formulations because is as a tinture made of the leaves, it is also easier to digest the body and is 100% natural.
What are the bioactive ingredients of the extract of the Graviola?
The ingredients are bioactive acetogenins from the leaves of the tree. There are 350 discovered to date. The acetogenins are extremely potent, with an ED 50 (lethal dose 50) up 10-9 microgram per millilitre.
Who might needs to take the original Graviola extract?
1. Anyone who has a weak or compromised immune system.
2. As an adjunct or complement to traditional medical treatment
3. To improve the digestive system.
What is the difference between the Original Extract Graviola from other Graviola products?
The product is dietary supplement 100% natural, retaining all the medicinal properties contained in the leaves. There are no preservatives added, no glycerine. It's packaged in dark bottle light does not affect the bioactive components. Product from the Puerto Rico forest and has all the regulations stipulated by law of Puerto Rico, such as the Health Department of Puerto Rico.
Is there any incompatibility with other therapies?
No incompatibility with other therapies, on the contrary, complements very well with any therapy because it working potentializing results.
What are the properties of the Graviola?
Strengthens Immune System
Help Digestive System
As a complement in Medical treatment.
Recommended Dosage:
Preventive: 15 drops 3 times a day in 1 ounce of water.
Severe Conditions: 25 drops 3 times a day in 1 ounce of water.
Recommendations to use the product
1. Take ½ hour before eating or 1 hour after eating.
2. Do not use in pregnant women or patients using MAO inhibitors (monoamine oxidase).
3. The use of coenzyme Q10 should be avoided with the use of Graviola.
Cancer and the Mood
Like others diseases there is a close relationship between psychological stress, cancer and some illness. We all have cancer cells or genes in our body and are exposed to poor nutrition, modern chemicals and radiation.
These factors cause harmful mutations in cells. The important thing is to recognize the emotional part that leads to illness and cancer. Emotional stress, grief, anger and hatred are destructive and very harmful to our body. The continuity of these emotional burdens creates a mental toxin that affects all levels, both physical and spiritual, triggering self-destruct mechanisms.
To improve the cancer, the patient must harmonize the mind, body and spirit. The fear that produces the knowledge that has this disease will hasten death sooner than they would have lasted if they had never known.
Cancer and the Mood (2)
Like others diseases there is a close relationship between psychological stress, cancer and some illness. We all have cancer cells or genes in our body and are exposed to poor nutrition, modern chemicals and radiation.
These factors cause harmful mutations in cells. The important thing is to recognize the emotional part that leads to illness and cancer. Emotional stress, grief, anger and hatred are destructive and very harmful to our body. The continuity of these emotional burdens creates a mental toxin that affects all levels, both physical and spiritual, triggering self-destruct mechanisms.
To improve the cancer, the patient must harmonize the mind, body and spirit. The fear that produces the knowledge that has this disease will hasten death sooner than they would have lasted if they had never known.
Graviola Extract Benefits
Contains an bioactive ingredient knows as acetogenins.
Is more concentrate than teas and other product of Graviola.
Strengthens the healthy cells.
A good diet promotes good health and prevent the onset of a disease.
Graviola Extract Benefits (2)
Amazing for your Health as a dietary Supplement 100 % natural and pure.
Contains an bioactive ingredient knows as acetogenins.
Is more concentrate than teas and other product of Graviola.
Strengthens the healthy cells.
A good diet promotes good heath and prevent the onset of a disease.
Can be used to provide nutritional support to the immune system.
Acetogeninas
The Annonaceae acetogenins are waxy substances resulting from the combination of acids fatty long chain (C33 or C34) with a 2-unit propanol carbon-2 to form a prolactin.
Graviola is a plant which can be used not only the fruit that contains abundant nutrients and vitamins, but also the medicinal properties of its different parts, especially the leaves for their properties.
COUNTRIES IN WHICH THE ACTION WAS MEDICAL VALIDATED
The study of biological activity (multiple medicinal effects) of Annona muricata by laboratory tests has been conducted in various Uiversities around the world. Below are the countries that has conducted laboratory studies about this matter:
United States
Republic of Guyana
Indonesia
China
Philippines
Surinam
Trinidad and Tobago
Dominican Republic
Puerto Rico
Colombia
Brazil
Acetogeninas (2)
The Annonaceae acetogenins are waxy substances resulting from the combination of acids fatty long chain (C33 or C34) with a 2-unit propanol carbon-2 to form a prolactin.
Graviola is a plant which can be used not only the fruit that contains abundant nutrients and vitamins, but also the medicinal properties of its different parts, especially the leaves for their properties.
COUNTRIES IN WHICH THE ACTION WAS MEDICAL VALIDATED
The study of biological activity (multiple medicinal effects) of Annona muricata by laboratory tests has been conducted in various Uiversities around the world. Below are the countries that has conducted laboratory studies about this matter:
United States
Republic of Guyana
Indonesia
China
Philippines
Surinam
Trinidad and Tobago
Dominican Republic
Puerto Rico
Colombia
Brazil
Vocabulary:
CANCER
Hyperplasia of tissue as a result of abnormal increase in the number of cells (clonal expansion
of an altered cell) as a result of an oncogene.
ONCOGENE:
Gene that is present in the nucleus of cells in genetically predisposed individuals. Oncogene is transmitted in a hereditary and is found in cells in an inactive form. Not are always actives as they are repressed by normal genes which act as inhibitors of contact.
Oncogenes:
(Cancer-related term)
Cancer cell resistance to chemotherapy Drugs: Mechanism of Action
Some cancer cells develop multidrug resistance (MDR). Dr. Mc Laughlin, researcher at Purdue University California, explains it by saying that this resistance has a small percentage of cells because these develops a mediated-pump of a P-glycoprotein, which is capable of expelling anticancer agents (chemotherapy drugs) out of the cell, before it can kill the cell which the focus is still active oncogenic cell. The process of expelling anticancer agents Cell, by that bomb, requires large amounts of Adenosine Tri-Phosfato, ATP (energy). This pump is not present in the cells normal.
Bibliography:
In accordance with some studies we can found information of the properties of the acetogenins:
http://www.jsscon.org/ejournal/pdf/cancer-cure.pdf
http://www.peruvillage.com/health-nutrition-news/graviola-help-you-fight-the-cancer/
http://www.cancer-fighting-foods.org/graviola-cancer/
http://www.ncbi.nlm.nih.gov/pubmed/18598079
http://www.cancerletters.info/article/0304-3835 (95)92759-7/abstract?cc=y
http://www.answers.com/Q/What_fruits_have_annonaceous_acetogenins
http://www.reference.md/files/D054/mD054378.html
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047049
Aticancerous & Antitumor Actions: Kojima, N. "Systematic synthesis of antitumor Annonaceus acetogenins" Yakugaku Zasshi. 2004; 124 (10): 673-81.
Tormo, J. R., et al. "In vitro antitumor structure-activity relationships of threo/trans/threo mono-tetrahydro-furanic acetogenins: Correlations with their inhibition of mitochondrial complex I." Oncol. Res. 2003; 14 (3): 147-54.
Yuan, S. S., et at "Annonacin, a mono-tetrahydrofuran acetogenin, arrests cancer.cells at the Gl phase and causes cytotoxicity in a Bax- and caspase-3-related pathway." Life Sci. 2003 May: 72 (25): 2853-61.
Liaw, C. C., et al. "New cytotoxic monotetrahydrofuran Annonaceus acetogenins from Annona Muricata: J. Nat. Prod. 2002; 65 (4): 470-75
Gonzalez-Coloma, A, et al. "Selective action of acetogenin mitochondrial complex I inhibitors." Z. Naturforsch. 2002; 57 (11-12): 1028-34.
Chang, F. R., et al. "Novel cytotoxic Annonaceus acetogenins from Annona Muricata: J. Nat. Prod. 2001; 64 (7): 925-31.
Jaramillo, M. C., et al. "Cytotoxicity and antileishmanial activity of Annona Muricata pericarp." Fitoterapia. 2000; 71 (2): 183-6.
Betancur-Galvis, L, et al, "Antitumor and antiviral activity of Colombian medicinal plant extracts." Mem. Inst. Oswaldo Cruz. 1999; 94 (4): 531-35.
Kim, G. S., et al. "Muricoreacin and Murihexocin C, mono-tetrahydrofuran acetogenins, from the leaves of Annona Muricata.' Photochemistry. 1998; 49 (2): 565-71.
Kim, G. S., et al. "Two new mono-tetrahydrofuran ring acetogenins, Annomuricin E and Muricapentocin, from the leaves of Annona Muricata: J. Nat. Prod. 1998; 61 (4): 432-36.
Nicolas, H., et at, "Structure-activity relationships of diVerse Annonaceus acetogenins against multidrug resistant human mammary adenocarcinoma (MCF-7/Adr) cells." J. Med. Chem. 1997; 40 (13): 2102-6.
Zeng, L., et al. "Five new monotetrahydrofuran ring acetogenins from the leaves of Annona Muricata: J. Nat. Prod. 1996; 59 (11): 1035-42.
Graviola Extract
Why should be used as an extract as opposed to capsules or teas?
There are several reasons why the graviola extract, (Soursop) is used:
1. The extract eliminates the need for the body to process plant cellulose when digested in any other form.
2. The extract maintains all the medicinal properties contained within the leaves known as acetogenins.
3. The formulation of our Graviola extract is free of preservatives, glycerine oil, and water.
4. The use Graviola extract is superior to other forms, such as capsules, teas and infusions, because many of the medicinal properties contained in the leaves, (roots and bark are not soluble in water).
5. The Graviola extract is easier to digest and it absorbs the bioactive components (acetogenins) of the leaves.
6. With capsules; the body would have the need to digest the components used in the capsule, in the case of the Graviola extract this digestive step it is not necessary.
7. As for the teas, when compared with the extract, we found a marked difference, teas require heat and water.
8. Another benefit of Graviola extract is that it is easily digestible.
Graviola Extract (2)
Why should be used as an extract as opposed to capsules or teas?
There are several reasons why the graviola extract, (Soursop) is used:
1. The extract eliminates the need for the body to process plant cellulose when digested in any other form.
2. The extract maintains all the medicinal properties contained within the leaves known as acetogenins.
3. The formulation of our Graviola extract is free of preservatives, glycerine oil, and water.
4. The use Graviola extract is superior to other forms, such as capsules, teas and infusions, because many of the medicinal properties contained in the leaves, (roots and bark are not soluble in water).
5. The Graviola extract is easier to digest and it absorbs the bioactive components (acetogenins) of the leaves.
6. With capsules; the body would have the need to digest the components used in the capsule, in the case of the Graviola extract this digestive step it is not necessary.
7. As for the teas, when compared with the extract, we found a marked difference, teas require heat and water. Water and heat are not used during the formulation of our Graviola Extract as some of the bioactive components of the leaves are not soluble in water.
8. Another benefit of Graviola extract is that it is easily digestible.
Graviola extract is a 100% natural dietary supplement which might help with some health conditions. |
msmarco_passage_01_457854713 | The Great Rat Race: FindBugs Warning - Exception is caught when exception is not thrown | The Great Rat Race: FindBugs Warning - Exception is caught when exception is not thrown
The Great Rat Race
Wednesday, September 8, 2010
FindBugs Warning - Exception is caught when exception is not thrown
Performing static analysis of a Java code-base on a regular basis is an extremely useful exercise, and I have found FindBugs to be an extremely useful and worthy tool. One particular warning raised by FindBugs - exception is caught, when exception is not thrown - may appear to be a false positive at first, however, the tool basically recommends catching specific exception types, instead of having a "catch all" exception clause that catches the base Exception class.
The reason for this is pretty simple - catching the base Exception class will also catch the RuntimeException, which is a child class of Exception. This will mask potential programming mistakes. As a result of having a catch clause with the base Exception class, I have seen instances of NullPointerException - a child of RuntimeException - being caught and logged on numerous occasions. This potentially masks problems in the code, when an object instance was null, although it wasn't supposed to be so. If the object is null in only certain circumstances, then there is a distinct possibility that catching the base Exception will cause this problem to slip by in the development environment and fail in a production set-up at a customer site.
Catching specific exceptions and handling them appropriately - and perhaps differently - also makes for a better error-handling approach. Overall, it improves the readability of the code, where others are able to better understand and extend the exception handling mechanism.
Not long ago there was a trend among Java programmers to use the "*" notation while importing packages - e.g. java.util.*, instead of explicitly importing the classes required. This trend seems to have disappeared, and I hope that the trend of catching the base Exception class also cedes to the approach of explicitly catching the specific exceptions.
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msmarco_passage_01_46504458 | Substernal Goiter Surgery: Background, Indications, Contraindications | Substernal Goiter Surgery: Background, Indications, Contraindications
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Drugs & Diseases > Clinical Procedures
Substernal Goiter Surgery
Updated: Oct 01, 2019
Author: William R Ryan, MD; Chief Editor: Arlen D Meyers, MD, MBA more...
Sections
Substernal Goiter Surgery
Sections Substernal Goiter Surgery
Overview
Background
Indications
Contraindications
Technical Considerations
Outcomes
Show All
Periprocedural Care
Patient Education & Consent
Pre-Procedure Planning
Equipment
Patient Preparation
Monitoring & Follow-up
Show All
Technique
Approach Considerations
Transcervical Excision of Substernal Goiter
Midline Sternotomy
Show All
Medication
Medication Summary
Thyroid Products
Calcium Salts
Fat-Soluble Vitamins
Beta-adrenergic Receptor Blockers
Antithyroid Medications
Show All
Media Gallery
References
Overview
Background
Enlarged thyroid glands (ie, goiters) often extend in the mediastinum posterior to the sternum, making the gland, by definition, a substernal (or retrosternal) goiter. [ 1, 2, 3, 4, 5, 6, 7, 8, 9] When this occurs, thyroidectomy surgery (excision of part or all of the thyroid gland) has unique considerations that are important to understand for the surgeon and patient.
This article reviews substernal goiter and focuses on substernal thyroidectomy.
Most substernal goiters are composed of nontoxic multinodular thyroid glands, but can also represent a generalized enlargement of the thyroid gland, an enlargement of one particular nodule, or the inferior extension of thyroid carcinoma. Most (approximately 90%) substernal thyroid masses are benign goiters. [ 10, 11, 12, 6, 13, 14, 15]
Goiters are often idiopathic in etiology but may be caused by the following:
Iodine deficiency (although increases in dietary iodine, particularly with iodinated salt, have dramatically reduced the frequency of goiters in the United States) [ 16]
Goitrogens (foods such as cabbage, turnips, peanuts, and soybeans and drugs such as lithium, propylthiouracil, and amiodarone) [ 17, 18]
Heredity [ 19, 20]
Malignancy (with risk factors including radiation exposure, family history, multiple endocrine neoplasia type 2a [MEN 2a], and MEN 2b, among others) [ 21]
The incidence of sporadic nontoxic goiter in the United States has been estimated to be approximately 5%. In some developing countries in which iodine deficiency is severe, up to one third of a population can be affected by goiters. Studies of chest radiographic screenings in Australia and the United States suggest substernal goiter may occur in approximately 0.02% of the population. [ 22, 23] In one study, mean age at diagnosis was 55.3 +/- 3.58 years, and most cases were found in women (83.3%). [ 70] Substernal thyroidectomy patients have been found more likely to be older, Hispanic or Black, and have Medicare insurance. [ 78] Reportedly, of patients undergoing thyroidectomy, up to 20% can have substernal goiters. [ 5, 24, 25, 26, 11, 27] The definition of a substernal goiter is currently not standardized, with great variability at which depth of thyroid extension beyond the thoracic inlet fulfills criteria. [ 71]
Substernal goiters can often remain asymptomatic for many years. [ 28, 29] Goiters are sometimes discovered incidentally during neck and chest radiography. [ 12, 7] However, the natural expectation of goiters is continued progressive growth, which may result in lower-neck discomfort, a noticeable neck mass, and progressive compression of the trachea, esophagus, and great vessels, thereby causing dyspnea, dysphagia/globus, and neck venous congestion/superior vena cava syndrome, respectively. [ 3, 26, 6, 30, 12, 70]
Substernal goiters are often more prominent on one side of the trachea and are thus highly correlated with tracheoesophageal deviation to the opposite side (see image below). [ 31, 3]
Chest radiograph of substernal goiter with tracheal deviation to the right.
View Media Gallery
Independent of laterality, substernal goiters usually extend into the anterosuperior mediastinum. Unilateral extension is the most common finding with equal frequency between right and left-sided extensions. [ 77] With this type of extension, the recurrent laryngeal nerve is not usually displaced from the tracheoesophageal groove. Occasionally, substernal goiters may extend into the posterior mediastinum behind the trachea. Posterior mediastinal thyroid extension may displace the recurrent laryngeal nerve unexpectedly, further complicating surgical excision of the goiter. [ 14, 31]
Indications
The identification of substernal extension of an enlarged thyroid gland itself is generally an indication for surgery. [ 1, 2, 32, 33, 9, 3, 34] Many authors advocate surgical removal of substernal goiters, even when asymptomatic, for the reasons discussed below.
First, substernal goiters are highly likely to continually grow, leading to the development of compressive symptoms (rarely, but possibly, emergent). In addition, such goiters become increasingly difficult to excise with further growth over time.
Second, the risk of a substernal goiter harboring malignancy is 3%-21%. [ 10, 11, 12, 6, 13, 14, 15] The risk of postoperative diagnosis of thyroid cancer is increased in patients with substernal multinodular goiters compared to cervical mutinodular goiters. [ 73] Fine-needle aspiration (FNA) biopsy of nodules in larger substernal goiters suffers from the following factors:
Riskier in the setting of the large-caliber blood vessels of the mediastinum
Subject to increased sampling error
Not possible given the barrier of the chest bones
Unnecessary given the already present indication for removal
Substernal goiters in individuals who are not medically fit to undergo surgery or who decline excision should be evaluated for malignancy. [ 6] Radiologic evaluation (ultrasonography, CT scanning, or MRI) of the lateral and central neck and mediastinal lymph nodes helps to determine the likelihood of metastatic disease (see image below). [ 35, 36, 37]
CT scan of substernal goiter with tracheal compression.
View Media Gallery
If lymph nodes appear suspicious on preoperative imaging, FNA biopsy or intraoperative biopsy of the lymph nodes is warranted.
The presence of symptoms is another indication for substernal thyroidectomy. Negative thoracic pressure, swallowing, and gravity help direct the growing goiter into the mediastinum. [ 76] Compressive symptoms, as described above, are often enough to motivate a patient to seek attention and possibly request surgery. Although approximately 85% of goiters are euthyroid, a minority cause symptoms related to hyperthyroidism (eg, palpitations, irregular or rapid heart rates, weight loss, increased heat sensitivity, insomnia, nervousness, tremulousness, diarrhea) or even hypothyroidism (eg, fatigue, weight gain, increased cold sensitivity, depression, constipation, brittle hair).
Thyrotoxicity (hyperthyroidism) in goiters may result from an autonomously functioning nodule or may be precipitated by intake of iodides found in certain expectorants or in radiographic contrast media. Hyperthyroidism requires preoperative medical management to avoid thyroid storm perioperatively.
The appearance of a mass in the low anterior neck may motivate a patient enough to request surgical excision for cosmetic reasons (see image below). [ 38]
Photograph showing a goiter as a noticeable bilateral anterior inferior neck mass.
View Media Gallery
Rarely, the Pemberton sign (raising hands induces facial flushing, dilated neck veins, and even stridor from compressive effects of goiter) is an indication for a substernal thyroidectomy.
Surgical intervention is most often the appropriate treatment for substernal goiter. In cases of apparently benign thyroid disease, the surgery should include the removal of the substernal component and other thyroid tissue responsible for obstructive symptoms. Thus, when possible, surgery can be limited to the removal of a single lobe and the isthmus. [ 14]
Recurrence and extension beyond the carina were found to be main risk factors associated with postoperative complications. [ 80] The risk of complications is reduced when injury of the contralateral recurrent laryngeal nerve and parathyroid glands is avoided. In cases of bilateral compression or malignant disease, total thyroidectomy should be performed, particularly in tumors larger than 2 cm in which postoperative radioactive iodine treatment may be used. [ 21]
Previous
Next: Indications
Contraindications
Close observation may be appropriate for substernal goiters that are small, without symptoms, without radiographic evidence of visceral or vascular compromise, and/or when found in a patient of advanced age or at high surgical risk. Surgeons and medical physicians, in cooperation with the patient, must weigh the risks of surgery and general anesthesia with the presence of symptoms or the possible impending dangers of mass effect of a substernal goiter.
Suppressive therapy (using exogenous thyroid hormone to suppress the pituitary secretion of thyroid-stimulating hormone and its stimulatory effects on thyroid gland growth) is generally ineffective in the management of substernal goiters. Suppressive therapy can be considered when surgical excision is contraindicated but likely would not be very effective. [ 2, 1, 39, 34, 40]
Radioactive iodine therapy may be useful in the treatment of hyperthyroidism associated with goiters, but not in the reduction of compressive symptoms. [ 41]
Previous
Next: Indications
Technical Considerations
Procedure Planning
Physical examination
Along with a full neck examination, the physical examination (see image below) should include an assessment for the Chvostek sign (found in 10% of cases at baseline when eucalcemic) to determine if this reflex may be used to assess possible postoperative hypocalcemia.
Photograph showing a goiter as an extensive neck mass suggestive of malignancy.
View Media Gallery
A preoperative vocal cord examination can help determine the baseline condition and laryngeal function (see image below). [ 14] Patients with substernal goiters have been found to exhibit signs of laryngopharyngeal reflux at preoperative laryngoscopy. [ 81]
Blood tests
The following blood tests can be helpful preoperatively:
Thyroid-stimulating hormone (TSH)
Free thyroxine (FT4)
Calcium
Albumin
Parathyroid hormone (PTH)
TSH and FT4 are used to assess thyroid hormone production and the need for preoperative treatment of hyperthyroidism or thyroid hormone replacement in cases of hypothyroidism. Calcium, with albumin correction, and PTH can help predict the need for calcium (and vitamin D) replacement after thyroidectomy.
Imaging studies
When the presence and degree to which a goiter has substernal extension is unknown, CT scanning or MRI of the neck and chest can help assess both the need for surgery and preoperative planning. [ 42, 12] For example, one study shows that a CT-determined thyroid volume of ≥162 cm3 extending below the thoracic outlet was indicative for an extra-cervical approach. [ 79]
If CT scanning is performed, a scan without contrast is recommended by many. The iodine contained in contrast agents can reduce the uptake and efficacy of postoperative radioactive iodine used in addition to thyroidectomy for the treatment of thyroid malignancy. Iodinated contrast can reduce the efficacy of radioactive iodine for up to 6 months.
Ultrasonography is often an integral and recommended component of thyroid evaluation because of its detailed imagery, potential for directed biopsies, minimal risk profile, and lower cost. However, ultrasonography is not capable of visualizing substernal components of the thyroid gland because the bones of the chest (clavicles, ribs, manubrium, sternum) block the transmission of acoustic information.
Chest radiography and iodine-123 (I123) nuclear medicine scans can show a substernal goiter, but without much anatomic detail of the gland or the surrounding structures.
Barium esophagraphy may show indentation and deviation of the esophagus, suggesting a certain length of substernal goiter causing mass effect. However, the usefulness of esophagraphy is limited given its inability to accurately confirm a thyroid mass because of poor anatomic detail.
Complication Prevention
Overall, complications of substernal thyroidectomy are rare (< 5%). [ 1, 29, 26, 43] Effective, safe, and sterile surgical technique is important for minimizing the possible complications of substernal thyroidectomy (bleeding, hematoma, infection, hypoparathyroidism/hypocalcemia, injury to the external branch of the superior laryngeal nerve, and/or recurrent laryngeal nerve injury) and midline sternotomy (hematoma, seroma, mediastinitis/abscess/osteomyelitis, chest bone fracture, sternum shift/disfigurement or dehiscence, pneumothorax/pneumomediastinum). [ 5] Appropriate use of a midline sternotomy by a surgeon trained to do so is important. Indications for a midline sternotomy include ectopic thyroid tissue in the mediastinum, extension of goiter below the aortic arch, and large thyroid tissue extending towards the tracheal bifurcation. [ 72]
Prediction, identification, and treatment of postoperative hypoparathyroidism and hypocalcemia are important for the safety of the patient.
Physicians should educate patients concerning the need (or possible need in the case of thyroid lobectomy surgery) for daily thyroid hormone supplementation and possible future necessary dose adjustments.
To reduce the risks of continued hyperthyroidism, including the development of perioperative thyroid storm (acute, life-threatening elevations of thyroid hormone levels), surgeons, primary care physicians, internists, endocrinologists, and anesthesiologists should work to identify hyperthyroidism preoperatively, to reduce the hormone effects and production with medications such as beta-blockers and possibly antithyroid thioamides (propylthiouracil and methimazole), and to have medications (beta-blockers, propylthiouracil, sodium iodine, corticosteroids) available during and after the operation to reduce acute effects.
If signs of thyroid storm develop during substernal thyroidectomy, the surgical team should halt the surgical procedure.
Previous
Next: Indications
Outcomes
The goals of substernal thyroidectomy are as follows:
Complete excision without surgical complications
An incision and resulting scar as small and as safe as possible
Resolution of symptoms and/or hyperthyroidism
Cosmetic improvement with removal of low anterior neck mass
Determination of the presence of malignancy
Potential complications of substernal thyroidectomy
Injury to the recurrent laryngeal nerve due to thyroidectomy has a reported incidence in the literature of 1%-5% for temporary paralysis and 2% or lower for permanent paralysis. [ 44, 45, 46, 47, 48, 49] In some studies, risk of injury to the recurrent laryngeal nerve was not increased in operations with sternotomy. [ 74]
Injury to the external branch of the superior laryngeal nerve due to thyroidectomy has a reported incidence in the literature of 0%-20% (mostly 5%-10%) for temporary paralysis and 5% or lower for permanent paralysis. [ 50, 49, 51, 52]
Postoperative hypoparathyroidism due to total thyroidectomy (not in cases of lobectomy) has a reported incidence in the literature of 0.3%-17.5% for temporary dysfunction and 0%-3.4% for permanent dysfunction. [ 53, 54, 55, 48, 49] It is often possible to identify and preserve the parathyroid glands during surgery. [ 75] Risk of hypoparathyroidism in operations with sternotomy have been shown to be the same in operations without sternotomy. [ 74]
Hematoma and infection due to thyroidectomy each has a reported incidence of less than 2%. [ 54, 45]
Seroma formation due to thyroidectomy has a reported incidence of 1%-6%. [ 54, 45]
Hypothyroidism is an expected outcome of total thyroidectomy. Thyroid lobectomy also has a reported incidence of 18%-50%. [ 56, 57, 58, 59] Patients with Hashimoto thyroiditis and/or elevated anti-TPO antibody levels appear to be at an increased risk of hypothyroidism after thyroid lobectomy. [ 60] If lymphocytic infiltration and germinal center formation are found in the lobectomy pathologic specimen, thyroid replacement may become increasingly necessary. [ 61]
Randolph et al (2011) found that bilateral goiters larger than 9 cm in diameter and/or heavier than 40 g (including some substernal goiters) are a risk factor for difficult intubation, recurrent laryngeal nerve injury, and postoperative hypocalcemia. [ 62] The degree of goiter extension was found to be directly related to risk of postoperative dysphonia. [ 82] Others studies corroborate the findings of increased risks of vocal cord dysfunction and hypocalcemia with substernal goiter surgery. [ 63, 4] However, Raffaelli et al (2011) found no increased rate of complications with substernal thyroidectomy compared to non–substernal thyroidectomy. [ 5]
With total thyroidectomy for bilateral goiter, the risk of recurrence is virtually zero. [ 64] Thyroid lobectomy and cases in which a thyroid cancer is excised carry the risk of recurrent disease depending on the extent and stage of each disease.
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Periprocedure
References
Abboud B, Sleilaty G, Mallak N, Abou Zeid H, Tabchy B. Morbidity and mortality of thyroidectomy for substernal goiter. Head Neck. 2010 Jun. 32 (6):744-9. [Medline].
Katlic MR, Wang CA, Grillo HC. Substernal goiter. Ann Thorac Surg. 1985 Apr. 39 (4):391-9. [Medline].
Shin JJ, Grillo HC, Mathisen D, et al. The surgical management of goiter: Part I. Preoperative evaluation. Laryngoscope. 2011 Jan. 121 (1):60-7. [Medline].
White ML, Doherty GM, Gauger PG. Evidence-based surgical management of substernal goiter. World J Surg. 2008 Jul. 32 (7):1285-300. [Medline].
Raffaelli M, De Crea C, Ronti S, Bellantone R, Lombardi CP. Substernal goiters: incidence, surgical approach, and complications in a tertiary care referral center. Head Neck. 2011 Oct. 33 (10):1420-5. [Medline].
Netterville JL, Coleman SC, Smith JC, Smith MM, Day TA, Burkey BB. Management of substernal goiter. Laryngoscope. 1998 Nov. 108 (11 Pt 1):1611-7. [Medline].
Page C, Strunski V. Cervicothoracic goitre: an anatomical or radiological definition? Report of 223 surgical cases. J Laryngol Otol. 2007 Nov. 121 (11):1083-7. [Medline].
Singh B, Lucente FE, Shaha AR. Substernal goiter: a clinical review. Am J Otolaryngol. 1994 Nov-Dec. 15 (6):409-16. [Medline].
Rios A, Rodriguez JM, Balsalobre MD, Tebar FJ, Parrilla P. The value of various definitions of intrathoracic goiter for predicting intra-operative and postoperative complications. Surgery. 2010 Feb. 147 (2):233-8. [Medline].
Sanders LE, Rossi RL, Shahian DM, Williamson WA. Mediastinal goiters. The need for an aggressive approach. Arch Surg. 1992 May. 127 (5):609-13. [Medline].
Shaha AR, Alfonso AE, Jaffe BM. Operative treatment of substernal goiters. Head Neck. 1989 Jul-Aug. 11 (4):325-30. [Medline].
Mercante G, Gabrielli E, Pedroni C, et al. CT cross-sectional imaging classification system for substernal goiter based on risk factors for an extracervical surgical approach. Head Neck. 2011 Jun. 33 (6):792-9. [Medline].
Casella C, Pata G, Cappelli C, Salerni B. Preoperative predictors of sternotomy need in mediastinal goiter management. Head Neck. 2010 Sep. 32 (9):1131-5. [Medline].
Randolph GW. The importance of pre- and postoperative laryngeal examination for thyroid surgery. Thyroid. 2010 May. 20 (5):453-8. [Medline].
Prades JM, Dumollard JM, Timoshenko A, et al. Multinodular goiter: surgical management and histopathological findings. Eur Arch Otorhinolaryngol. 2002 Apr. 259 (4):217-21. [Medline].
Derwahl M, Studer H. Nodular goiter and goiter nodules: Where iodine deficiency falls short of explaining the facts. Exp Clin Endocrinol Diabetes. 2001. 109 (5):250-60. [Medline].
Gaitan E. Goitrogens in food and water. Annu Rev Nutr. 1990. 10:21-39. [Medline].
Derwahl M, Studer H. Multinodular goitre: 'much more to it than simply iodine deficiency'. Baillieres Best Pract Res Clin Endocrinol Metab. 2000 Dec. 14 (4):577-600. [Medline].
Wychulis AR, Payne WS, Clagett OT, Woolner LB. Surgical treatment of mediastinal tumors: a 40 year experience. J Thorac Cardiovasc Surg. 1971 Sep. 62 (3):379-92. [Medline].
Brix TH, Hegedüs L. Genetic and environmental factors in the aetiology of simple goitre. Ann Med. 2000 Apr. 32 (3):153-6. [Medline].
NCCN (National Comprehensive Cancer Network) Guidelines. Thyroid Carcinoma. 2011.
Reeve TS, Rubinstein C, Rundle FF. Intrathoracic goitre: its prevalence in Sydney metropolitan mass radiography surveys. Med J Aust. 1957 Aug 3. 44 (5):149-56. [Medline].
Rundle FF, De Lambert RM, Epps RG. Cervicothoracic tumors: a technical aid to their roentgenologic localization. Am J Roentgenol Radium Ther Nucl Med. 1959 Feb. 81 (2):316-21. [Medline].
Sand ME, Laws HL, McElvein RB. Substernal and intrathoracic goiter. Reconsideration of surgical approach. Am Surg. 1983 Apr. 49 (4):196-202. [Medline].
Vadasz P, Kotsis L. Surgical aspects of 175 mediastinal goiters. Eur J Cardiothorac Surg. 1998 Oct. 14 (4):393-7. [Medline].
Torre G, Borgonovo G, Amato A, et al. Surgical management of substernal goiter: analysis of 237 patients. Am Surg. 1995 Sep. 61 (9):826-31. [Medline].
Huins CT, Georgalas C, Mehrzad H, Tolley NS. A new classification system for retrosternal goitre based on a systematic review of its complications and management. Int J Surg. 2008 Feb. 6 (1):71-6. [Medline].
Rodriguez JM, Hernandez Q, Piñero A, Ortiz S, Soria T, Ramirez P, et al. Substernal goiter: clinical experience of 72 cases. Ann Otol Rhinol Laryngol. 1999 May. 108 (5):501-4. [Medline].
Erbil Y, Bozbora A, Barbaros U, Ozarmagan S, Azezli A, Molvalilar S. Surgical management of substernal goiters: clinical experience of 170 cases. Surg Today. 2004. 34 (9):732-6. [Medline].
Gittoes NJ, Miller MR, Daykin J, Sheppard MC, Franklyn JA. Upper airways obstruction in 153 consecutive patients presenting with thyroid enlargement. BMJ. 1996 Feb 24. 312 (7029):484. [Medline]. [Full Text].
Mackle T, Meaney J, Timon C. Tracheoesophageal compression associated with substernal goitre. Correlation of symptoms with cross-sectional imaging findings. J Laryngol Otol. 2007 Apr. 121 (4):358-61. [Medline].
Hedayati N, McHenry CR. The clinical presentation and operative management of nodular and diffuse substernal thyroid disease. Am Surg. 2002 Mar. 68 (3):245-51; discussion 251-2. [Medline].
Agarwal G, Aggarwal V. Is total thyroidectomy the surgical procedure of choice for benign multinodular goiter? An evidence-based review. World J Surg. 2008 Jul. 32 (7):1313-24. [Medline].
Newman E, Shaha AR. Substernal goiter. J Surg Oncol. 1995 Nov. 60 (3):207-12. [Medline].
Hegedüs L. Thyroid ultrasound. Endocrinol Metab Clin North Am. 2001 Jun. 30 (2):339-60, viii-ix. [Medline].
Belardinelli L, Gualdi G, Ceroni L, Guadalaxara A, Polettini E, Pappalardo G. Comparison between computed tomography and magnetic resonance data and pathologic findings in substernal goiters. Int Surg. 1995 Jan-Mar. 80 (1):65-9. [Medline].
Weber AL, Randolph G, Aksoy FG. The thyroid and parathyroid glands. CT and MR imaging and correlation with pathology and clinical findings. Radiol Clin North Am. 2000 Sep. 38 (5):1105-29. [Medline].
Tsang FH, Wan IY, Lee TW, Ng SK, Yim AP. Management of retrosternal goitre with superior vena cava obstruction. Heart Lung Circ. 2007 Aug. 16 (4):312-4. [Medline].
McHenry CR, Piotrowski JJ. Thyroidectomy in patients with marked thyroid enlargement: airway management, morbidity, and outcome. Am Surg. 1994 Aug. 60 (8):586-91. [Medline].
Monchik JM, Materazzi G. The necessity for a thoracic approach in thyroid surgery. Arch Surg. 2000 Apr. 135 (4):467-71; discussion 471-2. [Medline].
Manders JM, Corstens FH. Radioiodine therapy of euthyroid multinodular goitres. Eur J Nucl Med Mol Imaging. 2002 Aug. 29 Suppl 2:S466-70. [Medline].
Farling PA. Thyroid disease. Br J Anaesth. 2000 Jul. 85 (1):15-28. [Medline].
Testini M, Nacchiero M, Miniello S, et al. Management of retrosternal goiters: experience of a surgical unit. Int Surg. 2005 Apr-Jun. 90 (2):61-5. [Medline].
Chiang FY, Lee KW, Huang YF, Wang LF, Kuo WR. Risk of vocal palsy after thyroidecitomy with identification of the recurrent laryngeal nerve. Kaohsiung J Med Sci. 2004 Sep. 20 (9):431-6. [Medline].
Filho JG, Kowalski LP. Postoperative complications of thyroidectomy for differentiated thyroid carcinoma. Am J Otolaryngol. 2004 Jul-Aug. 25 (4):225-30. [Medline].
Hermann M, Alk G, Roka R, Glaser K, Freissmuth M. Laryngeal recurrent nerve injury in surgery for benign thyroid diseases: effect of nerve dissection and impact of individual surgeon in more than 27,000 nerves at risk. Ann Surg. 2002 Feb. 235 (2):261-8. [Medline].
Lo CY, Kwok KF, Yuen PW. A prospective evaluation of recurrent laryngeal nerve paralysis during thyroidectomy. Arch Surg. 2000 Feb. 135 (2):204-7. [Medline].
Prim MP, de Diego JI, Hardisson D, Madero R, Gavilan J. Factors related to nerve injury and hypocalcemia in thyroid gland surgery. Otolaryngol Head Neck Surg. 2001 Jan. 124 (1):111-4. [Medline].
Rosato L, Avenia N, Bernante P, De Palma M, Gulino G, Nasi PG, et al. Complications of thyroid surgery: analysis of a multicentric study on 14,934 patients operated on in Italy over 5 years. World J Surg. 2004 Mar. 28 (3):271-6. [Medline].
McIvor NP, Flint DJ, Gillibrand J, Morton RP. Thyroid surgery and voice-related outcomes. Aust N Z J Surg. 2000 Mar. 70 (3):179-83. [Medline].
Karlan MS, Catz B, Dunkelman D, Uyeda RY, Gleischman S. A safe technique for thyroidectomy with complete nerve dissection and parathyroid preservation. Head Neck Surg. 1984 Jul-Aug. 6 (6):1014-9. [Medline].
Loré JM Jr, Kokocharov SI, Kaufman S, Richmond A, Sundquist N. Thirty-eight-year evaluation of a surgical technique to protect the external branch of the superior laryngeal nerve during thyroidectomy. Ann Otol Rhinol Laryngol. 1998 Dec. 107 (12):1015-22. [Medline].
Shaha AR, Jaffe BM. Parathyroid preservation during thyroid surgery. Am J Otolaryngol. 1998 Mar-Apr. 19 (2):113-7. [Medline].
Ozbas S, Kocak S, Aydintug S, Cakmak A, Demirkiran MA, Wishart GC. Comparison of the complications of subtotal, near total and total thyroidectomy in the surgical management of multinodular goitre. Endocr J. 2005 Apr. 52 (2):199-205. [Medline].
Pattou F, Combemale F, Fabre S, et al. Hypocalcemia following thyroid surgery: incidence and prediction of outcome. World J Surg. 1998 Jul. 22 (7):718-24. [Medline].
McHenry CR, Slusarczyk SJ. Hypothyroidisim following hemithyroidectomy: incidence, risk factors, and management. Surgery. 2000 Dec. 128 (6):994-8. [Medline].
Miller FR, Paulson D, Prihoda TJ, Otto RA. Risk factors for the development of hypothyroidism after hemithyroidectomy. Arch Otolaryngol Head Neck Surg. 2006 Jan. 132 (1):36-8. [Medline].
Piper HG, Bugis SP, Wilkins GE, Walker BA, Wiseman S, Baliski CR. Detecting and defining hypothyroidism after hemithyroidectomy. Am J Surg. 2005 May. 189 (5):587-91; discussion 591. [Medline].
Farkas EA, King TA, Bolton JS, Fuhrman GM. A comparison of total thyroidectomy and lobectomy in the treatment of dominant thyroid nodules. Am Surg. 2002 Aug. 68 (8):678-82; discussion 682-3. [Medline].
Stoll SJ, Pitt SC, Liu J, Schaefer S, Sippel RS, Chen H. Thyroid hormone replacement after thyroid lobectomy. Surgery. 2009 Oct. 146 (4):554-8; discussion 558-60. [Medline]. [Full Text].
Johner A, Griffith OL, Walker B, et al. Detection and management of hypothyroidism following thyroid lobectomy: evaluation of a clinical algorithm. Ann Surg Oncol. 2011 Sep. 18 (9):2548-54. [Medline].
Randolph GW, Shin JJ, Grillo HC, et al. The surgical management of goiter: Part II. Surgical treatment and results. Laryngoscope. 2011 Jan. 121 (1):68-76. [Medline].
Sancho JJ, Kraimps JL, Sanchez-Blanco JM, et al. Increased mortality and morbidity associated with thyroidectomy for intrathoracic goiters reaching the carina tracheae. Arch Surg. 2006 Jan. 141 (1):82-5. [Medline].
Vasica G, O'Neill CJ, Sidhu SB, Sywak MS, Reeve TS, Delbridge LW. Reoperative surgery for bilateral multinodular goitre in the era of total thyroidectomy. Br J Surg. 2012 May. 99 (5):688-92. [Medline].
Belmont MJ, Wax MK, DeSouza FN. The difficult airway: cardiopulmonary bypass--the ultimate solution. Head Neck. 1998 May. 20 (3):266-9. [Medline].
Saha SP, Rogers AG, Earle GF, Nachbauer C, Baker M. Surgical management of intrathoracic goiter. J Ky Med Assoc. 1997 Oct. 95 (10):421-3. [Medline].
Wright CD, Mathisen DJ. Mediastinal tumors: diagnosis and treatment. World J Surg. 2001 Feb. 25 (2):204-9. [Medline].
Allo MD, Thompson NW. Rationale for the operative management of substernal goiters. Surgery. 1983 Dec. 94 (6):969-77. [Medline].
Mellière D, Saada F, Etienne G, Becquemin JP, Bonnet F. Goiter with severe respiratory compromise: evaluation and treatment. Surgery. 1988 Mar. 103 (3):367-73. [Medline].
Târcoveanu E, Vasilescu A, Vlad N, et al. Retrosternal Goiters. Rev Med Chir Soc Med Nat Iasi. 2012. 116 (2):523-531. [Medline].
Testini M, Gurrado A, Bellantone R, Brazzarola P, Cortese R, De Toma G, et al. Recurrent laryngeal nerve palsy and substernal goiter. An Italian multicenter study. J Visc Surg. 2014 Jun. 151 (3):183-9. [Medline].
Coskun A, Yildirim M, Erkan N. Substernal goiter: when is a sternotomy required?. Int Surg. 2014 Jul-Aug. 99 (4):419-25. [Medline].
Campbell MJ, Candell L, Seib CD, Gosnell JE, Duh QY, Clark OH, et al. Unanticipated thyroid cancer in patients with substernal goiters: are we underestimating the risk?. Ann Surg Oncol. 2015 Apr. 22 (4):1214-8. [Medline].
Rolighed L, Rønning H, Christiansen P. Sternotomy for substernal goiter: retrospective study of 52 operations. Langenbecks Arch Surg. 2015 Apr. 400 (3):301-6. [Medline].
Heineman TE, Kadkade P, Kutler DI, Cohen MA, Kuhel WI. Parathyroid Localization and Preservation during Transcervical Resection of Substernal Thyroid Glands. Otolaryngol Head Neck Surg. 2015 Jun. 152 (6):1024-8. [Medline].
Di Crescenzo V, Vitale M, Valvano L, Napolitano F, Vatrella A, Zeppa P, et al. Surgical management of cervico-mediastinal goiters: Our experience and review of the literature. Int J Surg. 2016 Apr. 28 Suppl 1:S47-53. [Medline].
Lin YS, Wu HY, Lee CW, Hsu CC, Chao TC, Yu MC. Surgical management of substernal goitres at a tertiary referral centre: A retrospective cohort study of 2,104 patients. Int J Surg. 2016 Mar. 27:46-52. [Medline].
Moten AS, Thibault DP, Willis AW, Willis AI. Demographics, disparities, and outcomes in substernal goiters in the United States. Am J Surg. 2016 Apr. 211 (4):703-9. [Medline].
Sormaz İC, Uymaz DS, İşcan AY, Özgür İ, Salmaslıoğlu A, Tunca F, et al. The Value of Preoperative Volumetric Analysis by Computerised Tomography of Retrosternal Goiter to Predict the Need for an Extra-Cervical Approach. Balkan Med J. 2018 Jan 20. 35 (1):36-42. [Medline].
Bove A, Di Renzo RM, D'Urbano G, Bellobono M, D'Addetta V, Lapergola A, et al. Preoperative risk factors in total thyroidectomy of substernal goiter. Ther Clin Risk Manag. 2016. 12:1805-1809. [Medline].
Rodrigues MG, Araujo VJF Filho, Matos LL, Hojaij FC, Simões CA, Araujo VJF Neto, et al. Substernal goiter and laryngopharyngeal reflux. Arch Endocrinol Metab. 2017 Jul-Aug. 61 (4):348-353. [Medline].
Chávez Tostado KV, Velázquez-Fernandez D, Chapa M, Pantoja Millán JP, Salazar MS, Herrera MF. Substernal Goiter: Correlation between Grade and Surgical Approach. Am Surg. 2018 Feb 1. 84 (2):262-266. [Medline].
Media Gallery
Chest radiograph of substernal goiter with tracheal deviation to the right.
CT scan of substernal goiter with tracheal compression.
Photograph showing a goiter as a noticeable bilateral anterior inferior neck mass.
Photograph showing a goiter as an extensive neck mass suggestive of malignancy.
A vocal cord examination via flexible fiberoptic laryngoscopy.
The left thyroid lobe being retracted anteromedially beyond the region of the left recurrent laryngeal nerve (pointed out by metal rod) with Berry ligament still connecting the lobe to the trachea.
Midline sternotomy with a self-retaining retractor exposing the mediastinal component of a substernal thyroidectomy. Photograph taken after dissection of gland from surrounding attachments.
Thyroid specimens from substernal thyroidectomy.
Closure of neck wound with sutures and active drains.
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Contributor Information and Disclosures
Author
William R Ryan, MD Associate Professor, Head and Neck Oncologic/Endocrine Surgery, Department of Otolaryngology-Head and Neck Surgery, University of California, San Francisco, School of Medicine
William R Ryan, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society, The Triological Society
Disclosure: Receive consulting fees from Medtronic, Olympus, and Ziteo.
Chief Editor
Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society
Disclosure: Serve (d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;Cliexa, eMedevents, Neosoma, MI10<br/>Received income in an amount equal to or greater than $250 from: , Cliexa;;Neosoma<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; for: Neosoma, eMedevents, MI10.
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Type
VEHICLE
Vacca
A Vacca in Grand Theft Auto V.
( Rear quarter view)
Vehicle class
(GTA V/GTA Online)
Super
Vehicle type
Civilian car
Body style
2-door sports car
Capacity
2 (driver and passenger)
Appears in
Grand Theft Auto V
Grand Theft Auto Online
Manufacturer
Pegassi
Price
$ 240,000 ( GTA V)
( Legendary Motorsport and Southern San Andreas Super Autos)
$240,000 ( GTA Online)
( Legendary Motorsport)
Similar vehicle (s)
Tempesta
Reaper
Zentorno
Infernus
Miscellaneous Information
Dashboard Type
( GTA V / GTA Online)
Banshee (needle)
Vacca (dial texture)
Interior Type
Vacca
Traffic-default Color (s)
No.
P
S
Prl
W
1
4
3
111
156
2
5
3
111
156
3
6
3
111
156
4
38
3
89
156
5
80
3
68
156
6
89
3
89
156
7
92
3
90
156
8
111
3
0
156
9
13
3
0
156
10
39
3
0
156
11
31
3
28
156
12
41
3
0
156
13
37
0
106
156
14
0
3
0
156
Model Name (s)
vacca
Handling Name (s)
VACCA
Text Label Name (s)
VACCA
Population Information
Spawns Naturally?
No
"It's hard to measure success, but when you're on a car website and several thousand dollars is the "affordable option", we think it's fair to say you're doing ok for yourself. Perfect for the middle-aged man trying to get back in the dating game after a divorce. No room for kids. Just enough room for a 90-pound blonde in her early 20's who, thanks to growing up in the Internet age, thinks anal on the first date makes sense."
— Legendary Motorsport description.
The Pegassi Vacca is a two-door supercar in Grand Theft Auto V and Grand Theft Auto Online .
Contents
1
Design
1.1
Grand Theft Auto V and Grand Theft Auto Online
1.2
Current Design Gallery
2
Performance
2.1
Grand Theft Auto V and Grand Theft Auto Online
2.1.1
GTA V/GTA Online Overview
3
Modifications
3.1
Grand Theft Auto V and Grand Theft Auto Online
4
Image Gallery
5
Notable Owners
6
Locations
6.1
Grand Theft Auto V
6.2
Grand Theft Auto Online
7
Trivia
8
References
9
See Also
10
Navigation
Design
Grand Theft Auto V and Grand Theft Auto Online
"Not ready to commit to the Infernus? Why not take the little brother out for a spin? Almost as fast and just as many heads will turn when you toss the keys to a valet that makes $10 an hour and hope he doesn't wreck it. It's the car that says "I'm not that rich, but I am that vain. Blow me."
— Southern San Andreas Super Autos description.
The Vacca's design is a mix between the Lamborghini Gallardo for the greenhouse area and the front fascia and the Lamborghini Aventador. The front headlights are based mostly on the Lamborghini Gallardo, while the rear louvers are based on the Lamborghini Aventador. The rear hood vent and exhausts have some elements from the rear and sides of the McLaren MP4-12C .
The Vacca is considered as the little brother of the Infernus, sharing a similar body shape and layout, but with a slightly shorter lenght and standard doors. The front of the car features three meshed intakes, with the central one being smaller than the outer ones and having the license plate just above it. The upper area has headlamp housings that are finished in carbon-fibre, each one containing large circular units with smaller ones almost above them, while the front boot bears a slightly impressed area around the outer edges and opens to reveal a spacious luggage compartment. The manufacturer logo can be seen on the front of the boot compartment.
The sides of the car have large inset formations that lead to a set of dual vertical vents, intended to let air to flow through the engine bay and rear brakes, while the doors have mirror shells finished in carbon fibre. The greenhouse area follows a similar shape to its big brother and has blach trim around the windows and a rear engine compartment with carbon-fibre louvres on it, which opens to reveal the engine bay and inner sections also finished in carbon fibre.
The rear of the car features carbon-fibre slatted tail lamps on the outer edges, having two turning light strips on the upper side and two main/brake strips on the lower side, while the centre bears the manufacturer logo. On the middle section, the car has a vented panel that is also finished in carbon fibre, with a narrow shape around the centre and housing two trapezium-shaped exhaust tips. The lower area is occupied by the rear bumper that is fitted with a carbon-fibre diffuser, which holds the license plate on the centre and six blades at the bottom. The area behind the plate is also open for aerodynamic purposes.
The interior of the car is a derivative of the Banshee, sharing the same dials and gauges, central panel finished in carbon fibre and sports seats. However, the dials themselves have a yellow colour, and the horn cap bears the corresponding manufacturer emblem.
The Vacca can only be painted with a single colour, which is applied on the bodywork and the stitches of the dashboard, steering wheel and seats. The car uses five-spoke split rims with low-profile tyres.
Current Design Gallery
Front Quarter View
Top View
Rear Quarter View
Front View
Side View
Rear View
Engine View
Underside View
Inside View
Detail
Other modelling
Dashboard View
Performance
Grand Theft Auto V and Grand Theft Auto Online
The car is capable of high top speeds, owing to its high horse-power. Bearing a powerful engine, the Vacca is very easy to throw around on roads at high speeds. It can curve around bends with ease and weave in and out of traffic without much effort or body roll, though some oversteer is noticeable. Shifts are rather quick but sometimes it takes a while for the Vacca to gain traction after powerful take off, resulting in the transmission hesitating to upshift. This is a result of the vehicle using rear wheel drive instead of its sister car, the Obey 9F 's four wheel drive system. Crash deformation is good overall, with the vehicle being able to sustain multiple frontal hits without damaging its engine, which is located in the rear.
According to the website, the Vacca a 5.1L engine that can push 540hp. Its engine model, however, is not very detailed and cannot fully reveal the engine cylinder configuration, aside from the fact that it is set in a "V" configuration, as with its brother, the Infernus. It is coupled to a 6-speed gearbox in a rear-mid engine, rear wheel drive layout. Its engine sound is the same one from the Cheetah .
GTA V/GTA Online Overview
Vehicle Statistics - Grand Theft Auto V and Grand Theft Auto Online
Acceleration
(0-60 mph in Seconds)
Top Speed
(mph / kmh)
Gears
Engine
Drivetrain
(FWD / RWD / AWD)
Mass
(kg / lbs)
Fuel Tank
Size (litres)
Handling.meta [?]
N/A
94 / 152
6
N/A
RWD
1200 / 2646
65
Website Statements [?] / Badges
3.9 Seconds
190 / 306
6
5.1L 540hp (Website)
RWD
N/A
N/A
Observed
5.1 Seconds
120 / 193
6
RMR
RWD
Cannot be observed
Cannot be observed
Rockstar Games Social Club
Speed
81.555809%
Acceleration
75%
Braking
33.333336%
Traction
78.787872%
Modifications
Grand Theft Auto V and Grand Theft Auto Online
Category
Modification
Cost ( GTA V )
Cost ( GTA Online )
Image
Armor
No Armor
$500
$1,000
Armor Upgrade 20%
$2,500
$7,500
Armor Upgrade 40%
$6,250
$12,000
Armor Upgrade 60%
$10,000
$20,000
Armor Upgrade 80%
$17,500
$35,000
Armor Upgrade 100%
$25,000
$50,000
Bodywork
None
$350
$700
Roll Cage & Chassis Upgrade
$550
$1,100
Brakes
Stock Brakes
$500
$1,000
Street Brakes
$10,000
$20,000
Sport Brakes
$13,500
$27,000
Race Brakes
$17,500
$35,000
Engine
EMS Upgrade, Level 1
$4,500
$9,000
EMS Upgrade, Level 2
$6,250
$12,500
EMS Upgrade, Level 3
$9,000
$18,000
EMS Upgrade, Level 4
$16,750
$33,500
Exhausts
Stock Exhaust
$130
$260
Dual Shotgun Exhaust
$375
$750
Explosives
Ignition Bomb
N/A
$5,000
Remote Bomb
N/A
$7,500
Hoods
Stock Hood
$800
$1,600
Carbon Hood
$1,500
$3,000
Horns
Main article: Los Santos Customs/Horns
-
-
Lights
Headlights
Stock Lights
$300
$600
Xenon Lights
$1,450
$7,500
Neon Kits
Main article: Los Santos Customs/Lights
-
-
Loss/Theft Prevention
Tracker
N/A
Too Hot
Full Coverage
N/A
Too Hot
Plates
Blue on White 1
$50
$200
Blue on White 2
$50
$200
Blue on White 3
$50
$200
Yellow on Blue
$75
$300
Yellow on Black
$150
$600
Respray
Main article: Los Santos Customs/Respray Colors
-
-
Sell
Sell Vehicle
N/A
Too Hot
Spoilers
None
$3,000
$6,000
Low Level Spoiler
$3,750
$7,050
Carbon Wing
$5,000
$10,000
Suspension
Stock Suspension
$100
$200
Lowered Suspension
$500
$1,000
Street Suspension
$1,000
$2,000
Sport Suspension
$1,700
$3,400
Competition Suspension
$2,200
$4,400
Transmission
Stock Transmission
$500
$1,000
Street Transmission
$14,750
$29,500
Sports Transmission
$16,250
$32,500
Race Transmission
$20,000
$40,000
Turbo
None
$2,500
$5,000
Turbo Tuning
$12,500
$50,000
Wheels
Main article: Los Santos Customs/Wheels
-
-
Windows
None
$100
$500
Light Smoke
$200
$1,500
Dark Smoke
$450
$3,500
Limo
$700
$5,000
Image Gallery
Front quarter view. ( Rear quarter view)
The Vacca in the enhanced version.
The Vacca on the Rockstar Games Social Club.
The Vacca on Southern San Andreas Super Autos.
The Vacca on Legendary Motorsport.
The Vacca on the updated Rockstar Games Social Club.
The Vacca in a Cinematic preview on Rockstar Games Social Club.
Notable Owners
Devin Weston (possibly)
Locations
Grand Theft Auto V
Can be bought for $ 240,000 from Legendary Motorsport and Southern San Andreas Super Autos.
During the Epsilon mission Assuming the Truth, one spawns in the driveway at 3659 Wild Oats Drive in Vinewood Hills, just down the street from Franklin 's second safehouse, and thus will only spawn while playing as Michael. It may also spawn outside of this mission by driving the same car in this area.
During the mission The Wrap Up, one can be found parked just outside the front entrance to the Kortz Center as Michael flees the scene, near the car he originally arrived in. If used to escape, the player must be careful, as an enemy Buzzard Attack Chopper will be in the area.
During the mission Meltdown, a Vacca (believed to be Devin Weston 's) is parked in front of the Oriental Theater on Vinewood Boulevard after the cutscene. If used to drive back to Michael's mansion, it can be saved simply by parking it inside the garage before entering the house.
Grand Theft Auto Online
Can be bought for $240,000 from Legendary Motorsport.
Occasionally driven by the NPC Online Joyrider (Original version only).
Trivia
Vacca means cow in Italian. Vaca (Romanian: Vacă) also means cow in Spanish, Portuguese and Romanian. The term is also an Italian and Portuguese slang for "easy" women.
Its name is likely a play on Lamborghini's tendency to give their cars names that reference bulls and bullfighting.
The default radio stations for the Vacca are Los Santos Rock Radio, Vinewood Boulevard Radio and Radio Mirror Park.
According to Southern San Andreas Super Autos, the Vacca is the little brother of the Infernus (much like how the Gallardo is the little brother of the Murciélago).
This also hinted by the fact that the Vacca costs $240,000 while the Infernus costs $440,000. Strangely, despite the price of the Infernus being significantly more expensive than the Vacca, the Infernus spawns commonly on the streets of Los Santos, while the Vacca does not spawn on the streets at all.
The Vacca, like other vehicles, has no reverse lights.
When viewing the Online garage on the Rockstar Games Social Club, the Vacca design is used as the diagram model for all super cars.
According to the ambient files, the Vacca is one of several named vehicles in-game that make up distant car sounds. Other vehicles include the Entity XF, Cheetah, Comet, Daemon, Carbonizzare, Banshee and Feltzer.
References
↑ File: x64\audio\sfx\ONESHOT_AMBIENCE.rpf, under name "vacca".
See Also
Infernus - The Vacca's elder brother.
Reaper - Another Pegassi sports car with a similar design.
Navigation
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v • d • e
Vehicles in Grand Theft Auto V
Super
Adder | Bullet | Cheetah | Entity XF | Infernus | Osiris | T20 | Turismo R | Vacca | Voltic | Zentorno
Sports
9F ( Cabrio) | Alpha | Banshee | Blista Compact (Go Go Monkey Blista) | Buffalo ( S (Sprunk)) | Carbonizzare | Comet | Coquette | Elegy RH8 | Feltzer | Furore GT | Fusilade | Futo | Jester (Racecar) | Massacro (Racecar) | Penumbra | Rapid GT ( Convertible) | Schwartzer | Sultan | Surano
Muscle
Blade | Buccaneer | Chino | Coquette BlackFin | Dominator (Pisswasser) | Dukes (Duke O'Death) | Gauntlet (Redwood) | Hotknife | Phoenix | Picador | Rat-Loader (Rat-Truck) | Ruiner | Sabre Turbo | Slamvan | Stallion (Burger Shot) | Vigero | Virgo | Voodoo
Sports Classics
Coquette Classic | JB 700 | Manana | Monroe | Peyote | Pigalle | Roosevelt | Stinger | Stirling GT | Tornado ( Beater | Mariachi) | Z-Type
Sedans
Asea ( North Yankton) | Asterope | Emperor ( Beater | North Yankton) | Fugitive | Glendale | Ingot | Intruder | Premier | Primo | Regina | Schafter | Stanier | Stratum | Super Diamond | Surge | Tailgater | Warrener | Washington ( Romero Hearse | Stretch)
Compacts
Blista | Dilettante ( Security) | Issi | Panto | Prairie | Rhapsody
Coupés
Cognoscenti Cabrio | Exemplar | F620 | Felon ( GT) | Jackal | Oracle ( XS) | Sentinel ( XS) | Windsor | Zion ( Cabrio)
SUVs
Baller | BeeJay XL | Cavalcade | Dubsta | FQ 2 | Granger | Gresley | Habanero | Huntley S | Landstalker | Mesa ( North Yankton) | Patriot | Radius | Rocoto | Seminole | Serrano
Vans
Bison ( The Mighty Bush | McGill-Olsen) | Bobcat XL | Boxville ( GoPostal | Humane Labs | Taco Van) | Burrito ( Bugstars | Civilian | McGill Olsen | North Yankton | Gang) | Camper | Journey | Minivan | Pony ( SOTW) | Rumpo ( Deludamol | Paradise) | Speedo ( Clown Van) | Surfer ( Beater) | Youga
Utility
Vehicles
Airtug | Caddy (Golfer | Civilian) | Docktug | Fieldmaster ( North Yankton) | Forklift | Lawn Mower | Ripley | Sadler ( North Yankton) | Scrap Truck | Towtruck ( Large variant) | Tractor | Utility Truck ( Small variant)
Trailers
Army Trailer (Civilian | Extended) | Boat Trailer ( Large) | Proptrailer | Trailer ( Rake | Small (Utility | Generator) | Flatbed | Logs | Articulated (Container | Commercial | Big Goods | Fame or Shame) | Dock | Car carrier (Pack Man)| Tanker (RON | Army))
Commercial
Benson | Biff | Hauler | Mule | Packer | Phantom | Pounder | Stockade ( Bobcat Security)
Industrial
Cutter | Dock Handler | Dozer | Dump | Flatbed | Mixer | Rubble | Tipper
Service
Bus ( Airport) | Dashound | Rental Shuttle Bus ( Tourbus) | Taxi | Trashmaster
Emergency
Ambulance | FIB ( Buffalo) | Fire Truck | Lifeguard | Park Ranger | Police Bike | Police Cruiser ( Interceptor | Buffalo) | Police Rancher | Police Riot | Police Roadcruiser | Police Prison Bus | Police Transporter | Sheriff Cruiser | Sheriff SUV | Unmarked Cruiser
Military
Barracks ( Semi) | Crusader | Rhino Tank
Motorcycles
Akuma | Bagger | Bati 801 ( RR) | Carbon RS | Daemon | Double T | Faggio | Hakuchou | Hexer | Innovation | Nemesis | PCJ-600 | Ruffian | Sanchez ( Livery) | Sovereign | Thrust | Vader | Vindicator
Helicopters
Buzzard ( Attack Chopper) | Cargobob ( Jetsam | TPI) | Frogger ( FIB/TPI) | Maverick | Police Maverick ( Air Ambulance) | Skylift | Swift (Deluxe)
Planes
Atomic Blimp | Besra | Cargo Plane | Cuban 800 | Dodo | Duster | Jet | Luxor (Deluxe) | Mallard | Mammatus | Miljet | P-996 LAZER | Shamal | Titan | Velum | Vestra | Xero Blimp
Boats
Dinghy ( 4-seater) | Jetmax | Kraken | Marquis | Police Predator | Seashark ( Lifeguard) | Speeder | Squalo | Submersible | Suntrap | Toro | Tropic
Off-Road
Bifta | Blazer ( Hot Rod | Lifeguard) | Bodhi | Brawler | Dubsta 6x6 | Dune Buggy ( Space Docker) | Duneloader | Injection | Kalahari | Liberator | Marshall | Mesa | Rancher XL ( North Yankton) | Rebel ( Rusty) | Sandking XL ( SWB)
Cycles
BMX | Cruiser | Endurex Race Bike | Fixter | Scorcher | Tri-Cycles Race Bike | Whippet Race Bike
Trains
Aerial Tramway | Freight Train | Metropolitan
Static (Non-Controllable)
Daisy Lee | Dignity | Octopus | Olifantus | Ocean Motion | SS Bulker | The Sea Urchin | UFOs
Beta Vehicles
Admiral | APC | Autogyro | Baletrailer | Bobcat | Casco | Cavalcade FXT | Chavos | Cognoscenti | Combine Harvester | CS2000 | Digger | Enduro | Esperanto | Feroci | FIB ("Old" variant) | Frogger (with FIB livery) | Freeway | Furzen | Graintrailer | Hakumai | Hellfury | Hunter | Lokus | Marbelle | Mule (Ramp-door) | Napalm | Police Fugitive | RC Bandito | Sabre | Scamp | Seinove | Skimmer | Skivvy | Squaddie | Speedo variants | Unknown Stockade variant | Unknown high-wing plane | Unknown private jet | Uranus | Vulkan | Willard | Winky
Vehicles in GTA V ( Category) | Vehicle Brands | Vehicle Types | Special Vehicles | Beta Vehicles | Manufacturers | Vehicle Classes | Vehicle Features
DLC Content Vehicles
Added as part of the following GTA Online content updates:
Ill-Gotten Gains Part 2 | Ill-Gotten Gains Part 1 | Heists Update | Festive Surprise | Last Team Standing Update | San Andreas Flight School Update | Independence Day Special | I'm Not a Hipster Update | High Life Update | The Business Update | Valentine's Day Massacre Special | Beach Bum Update
Other Vehicles
Enhanced Version Release | Special/Collector's Edition and Pre-Order Bonus | Social Club
v • d • e
Vehicles in Grand Theft Auto Online
Super
811 | Adder | Autarch | Banshee 900R | Bullet | Cheetah | Cyclone | Deveste Eight | Emerus | Entity XF ( XXR) | ETR1 | FMJ | Furia | GP1 | Infernus | Itali GTB (Custom) | Krieger | Nero (Custom) | Osiris | Penetrator | RE-7B | Reaper | S80RR | SC1 | Scramjet | Sultan RS | T20 | Taipan | Tigon | Tempesta | Tezeract | Thrax | Turismo R | Tyrant | Tyrus | Vacca | Vagner | Vigilante | Visione | Voltic (Rocket) | X80 Proto | XA-21 | Zentorno | Zorrusso
Sports
8F Drafter | 9F ( Cabrio) | Alpha | Banshee | Bestia GTS | Blista Compact (Go Go Monkey) | Buffalo (S (Sprunk)) | Carbonizzare | Comet (Retro Custom (Safari) | SR) | Coquette (D10) | Drift Tampa | Elegy RH8 (Retro Custom) | Feltzer | Flash GT | Furore GT | Fusilade | Futo | GB200 | Hotring Sabre | Imorgon | Issi Sport | Itali GTO | Itali RSX | Jester ( Classic | Racecar) | Jugular | Khamelion | Komoda | Kuruma (Armored) | Locust | Lynx | Massacro (Racecar) | Neo | Neon | Omnis | Paragon R (Armored) | Pariah | Penumbra (FF) | Raiden | Rapid GT ( Convertible) | Raptor | Revolter | Ruston | Seven-70 | Schafter LWB | Schafter V12 | Schlagen GT | Schwartzer | Sentinel Classic | Specter (Custom) | Streiter | Sugoi | Sultan (Classic) | Surano | Tropos Rallye | V-STR | Verlierer | Veto ( Classic) | ZR380 ( Apocalypse | Future Shock | Nightmare)
Muscle
Blade | Buccaneer (Custom | Lurcher) | Chino (Custom) | Clique | Coquette BlackFin | Deviant | Dominator ( Apocalypse | Future Shock | GTX | Nightmare | Pisswasser) | Dukes (Beater | Duke O'Death) | Ellie | Faction (Custom (Donk)) | Gauntlet (Classic (Custom)) | Hellfire | Redwood) | Hermes | Hotknife | Hustler | Impaler ( Apocalypse | Future Shock | Nightmare) | Imperator ( Apocalypse | Future Shock | Nightmare) | Manana Custom | Moonbeam (Custom) | Nightshade | Peyote Gasser | Phoenix | Picador | Rat-Loader (Rat-Truck) | Ruiner (2000 (Wreck)) | Sabre Turbo (Custom) | Slamvan ( Apocalypse | Custom | Future Shock | Lost | Nightmare) | Stallion (Burger Shot) | Tampa ( Weaponized) | Tulip | Vamos | Vigero | Virgo | Virgo Classic (Custom) | Voodoo (Custom) | Yosemite (Drift)
Sports Classics
190z | Ardent | Casco | Cheburek | Cheetah Classic | Coquette Classic | Deluxo | Dynasty | Fagaloa | GT500 | Infernus Classic | JB 700 (W) | Mamba | Manana | Michelli GT | Monroe | Nebula Turbo | Peyote (Custom) | Pigalle | Rapid GT Classic | Retinue (Mk II) | Roosevelt (Fränken Stange | Valor) | Savestra | Stinger ( GT) | Stirling GT | Stromberg | Swinger | Toreador | Torero | Tornado ( Beater | Mariachi | Custom | Rat Rod) | Turismo Classic | Viseris | Z-Type | Zion Classic
Sedans
Asea | Asterope | Cognoscenti (Armored | 55 (Armored)) | Emperor ( Beater) | Fugitive | Glendale (Custom) | Ingot | Intruder | Premier | Primo (Custom) | Regina | Schafter | Schafter LWB (Armored) | Schafter V12 (Armored) | Stafford | Stanier | Stratum | Super Diamond | Surge | Tailgater | Turreted Limo | Warrener | Washington ( Romero Hearse | Stretch)
Compacts
Asbo | Blista (Kanjo) | Brioso R/A (300) | Club | Dilettante ( Security) | Issi ( Classic ( Apocalypse | Future Shock | Nightmare)) | Panto | Prairie | Rhapsody | Weevil
Coupés
Cognoscenti Cabrio | Exemplar | F620 | Felon ( GT) | Jackal | Oracle ( XS) | Sentinel ( XS) | Windsor (Drop) | Zion ( Cabrio)
SUVs
Baller (LE (Armored) | LE LWB (Armored)) | BeeJay XL | Cavalcade | Contender | Dubsta | FQ 2 | Granger | Gresley | Habanero | Huntley S | Landstalker (XL) | Mesa | Novak | Patriot ( Stretch) | Radius | Rebla GTS | Rocoto | Seminole (Frontier) | Serrano | Squaddie | Toros | XLS (Armored)
Vans
Bison ( The Mighty Bush | McGill-Olsen) | Bobcat XL | Boxville (Armored | GoPostal | Humane Labs | PostOP | Taco Van) | Burrito (Bugstars | Civilian | McGill Olsen | Gang (Gang-less)) | Camper | Journey | Minivan (Custom) | Pony | Rumpo (Custom | Paradise) | Speedo (Clown Van | Custom) | Surfer ( Beater) | Youga (Classic (4x4))
Utility
Vehicles
Airtug | Caddy (Golfer | Civilian | Bunker) | Docktug | Fieldmaster | Forklift | Lawn Mower | Ripley | Sadler | Scrap Truck | Slamtruck | Tractor | Utility Truck ( Small variant)
Trailers
Boat Trailer | Mobile Operations Center | Trailer ( Rake | Small (Utility | Generator) | Flatbed | Logs | Articulated (Container | Commercial | Big Goods) | Dock | Car carrier | Tanker (RON | Army | Heist))
Commercial
Benson | Biff | Cerberus ( Apocalypse | Future Shock | Nightmare) | Hauler ( Custom) | Mule (Ramp-door | Heist | Custom) | Packer | Phantom ( Custom | Wedge) | Pounder ( Custom) | Stockade | Terrorbyte
Industrial
Dock Handler | Dozer | Dump | Flatbed | Guardian | Mixer | Rubble | Tipper
Service
Brickade (Dune) | Bus ( Airport) | Dashound | Festival Bus | Rental Shuttle Bus ( Tourbus) | Taxi | Trashmaster (Rusty) | Wastelander
Emergency
Ambulance | FIB ( Buffalo) | Fire Truck | Lifeguard | Park Ranger | Police Bike | Police Cruiser ( Interceptor) | Police Riot | Police Prison Bus | Police Transporter | RCV | Sheriff Cruiser | Sheriff SUV | Unmarked Cruiser
Military
Anti-Aircraft Trailer | APC | Barracks ( Semi | Heist) | Barrage | Chernobog | Crusader | Half-track | Invade and Persuade Tank | Rhino Tank | Scarab ( Apocalypse | Future Shock | Nightmare) | Thruster | TM-02 Khanjali | Vetir
Motorcycles
Akuma | Avarus (Sanctus) | Bagger | Bati 801 ( RR) | BF400 | Carbon RS | Chimera | Cliffhanger | Daemon (Gang-less) | Defiler | Diabolus (Custom) | Double T | Enduro | Esskey | Faggio (Mod | Sport) | FCR 1000 (Custom) | Gargoyle ( Apocalypse Deathbike | Future Shock Deathbike | Nightmare Deathbike) | Hakuchou (Drag) | Hexer | Innovation | Lectro | Manchez (Scout) | Nemesis | Nightblade | Oppressor ( Mk II) | PCJ-600 | Rampant Rocket | Ruffian | Sanchez ( Livery) | Shotaro | Sovereign | Stryder | Thrust | Vader | Vindicator | Vortex | Wolfsbane (Rat Bike) | Zombie Chopper (Bobber)
Helicopters
Akula | Annihilator (Stealth) | Buzzard ( Attack Chopper) | Cargobob ( Jetsam | Drop Zone) | FH-1 Hunter | Frogger | Havok | Maverick | Police Maverick ( Air Ambulance) | Savage | Sparrow (Sea) | Skylift | SuperVolito (Carbon) | Swift (Deluxe) | Valkyrie (MOD.0) | Volatus
Planes
Alpha-Z1 | Avenger | B-11 Strikeforce | Besra | Blimp | Cuban 800 | Dodo | Duster | Howard NX-25 | Hydra | LF-22 Starling | Luxor (Deluxe) | Mallard | Mammatus | Miljet | Mogul | Nimbus | P-45 Nokota | P-996 LAZER | Pyro | RM-10 Bombushka | RO-86 Alkonost | Rogue | Seabreeze | Shamal | Titan | Tula | Ultralight | V-65 Molotok | Velum (5-Seater) | Vestra | Volatol
Boats
Avisa | Dinghy ( 4-seater | Heist | Yacht | Weaponized) | Jetmax | Kosatka | Kraken | Kurtz 31 Patrol Boat | Longfin | Marquis | Police Predator | Seashark ( Lifeguard | Yacht) | Speeder (Yacht) | Squalo | Submersible | Suntrap | Toro (Yacht) | Tropic (Yacht) | Tug
Off-Road
Bifta | Blazer (Aqua | Hot Rod | Lifeguard | Street) | Bodhi | Brawler | Bruiser ( Apocalypse | Future Shock | Nightmare) | Brutus ( Apocalypse Brutus | Future Shock | Nightmare) | Caracara (4x4) | Desert Raid | Dubsta 6x6 | Dune Buggy ( FAV | Ramp Buggy | Space Docker) | Duneloader | Everon | Freecrawler | Hellion | Injection | Insurgent (Pick-Up ( Custom)) | Kalahari | Kamacho | Liberator | Marshall | Menacer | Mesa | Nightshark | Outlaw | Rancher XL | RC Bandito | Rebel ( Rusty | Technical (Aqua | Custom)) | Riata | Sandking XL ( SWB) | Sasquatch ( Apocalypse | Future Shock | Nightmare) | Trophy Truck | Vagrant | Verus | Winky | Yosemite Rancher | Zhaba
Cycles
BMX | Cruiser | Endurex Race Bike | Scorcher | Tri-Cycles Race Bike | Whippet Race Bike
Trains
Freight Train | Tram
Open Wheel
BR8 | DR1 | PR4 | R88
Static (Non-Controllable)
Cargo Plane | Cutter | Daisy Lee | Dignity | Galaxy Super Yacht (Aquarius, Pisces, Orion) | Octopus | Olifantus | Ocean Motion | Ramius | SS Bulker | The Sea Urchin | UFOs | USS Luxington ATT-16
Beta Vehicles
Baletrailer | Cargobob variant | Cognoscenti variant | Police Transporter variant | Police Buffalo | Police Buffalo variant | Surfer variant | Vamos variant | Verlierer variant
Vehicles in GTA Online ( Category) | Vehicle Brands | Vehicle Types | Special Vehicles | Beta Vehicles | Manufacturers | Vehicle Classes | Vehicle Features
DLC Content Vehicles
The Cayo Perico Heist | Los Santos Summer Special | The Diamond Casino Heist | The Diamond Casino & Resort | Arena War | After Hours | Southern San Andreas Super Sport Series | The Doomsday Heist | Smuggler's Run | Gunrunning | Cunning Stunts: Special Vehicle Circuit | Import/Export | Bikers | Cunning Stunts | Further Adventures in Finance and Felony | Lowriders: Custom Classics | Be My Valentine | January 2016 Update | Festive Surprise 2015 | Executives and Other Criminals | Halloween Surprise | Lowriders | Ill-Gotten Gains Part 2 | Ill-Gotten Gains Part 1 | Heists Update | Festive Surprise | Last Team Standing Update | San Andreas Flight School Update | Independence Day Special | I'm Not a Hipster Update | High Life Update | The Business Update | Valentine's Day Massacre Special | Beach Bum Update
Other Vehicles
Enhanced Version Release | Special/Collector's Edition and Pre-Order Bonus | Social Club
Italicized vehicles indicate vehicles also available in story mode, but include exclusive modifications only available in GTA Online
Retrieved from " https://gta.fandom.com/wiki/Vacca?oldid=1321804 "
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msmarco_passage_01_470065209 | Have Osteoporosis? Why Your Spine, Wrists & Hips Are at Risk | Guide2BoneHealth | Have Osteoporosis? Why Your Spine, Wrists & Hips Are at Risk | Guide2BoneHealth
Have Osteoporosis? Why Your Spine, Wrists & Hips Are at Risk
As someone with osteoporosis, you already know you’re at risk for a fracture. Yet here’s something else to keep in mind: It’s important to make sure your current treatments are really working. If not, just a cough or a sneeze could result in a broken bone.
The parts of your body most likely to fracture? Your spine, wrists and hips. Here’s what you need to know about these vulnerable sites and why you and your doctor should ensure you’re receiving the treatment that provides the best protection. By age 50, the lifetime risk of fracture is 50% in women and 25% in men, according to the National Osteoporosis Foundation.
Your spine
Why you’re at risk: The bones that form the spine are softer and spongier than other bones. Pressure can build up on the fragile bones in your back, making the spine so sensitive that simply moving the wrong way can cause a fracture. In fact, spinal, or vertebral, fractures are the most common bone breaks caused by osteoporosis.
The signs: You may experience back pain or poor posture or notice you are getting shorter. It’s also possible not to experience any symptoms.
Recovery: Spinal fractures can take several weeks of rest and exercise to heal.
Your wrist
Why you’re at risk: Around menopause, women with osteoporosis have lost a lot of bone density, making wrists special targets during a fall or other accident. Broken wrists are most common in people under the age of 75.
The signs: Most people know when they have broken a wrist because of the intense pain and swelling.
Recovery: It can take up to eight weeks or longer to heal a broken wrist. You will likely have to wear a cast or splint and may even need surgery, depending on the type of break. A physical therapist can teach you exercises that can help you regain strength and improve your range of movement.
Your hips
Why you’re at risk: Osteoporosis takes a special toll on the hips. A hip bone can become so weak that even a minor fall can cause a break.
The signs: Symptoms include pain and aches in the groin area. Your injured leg may also seem shorter. Many people with hip fractures are unable to bear any weight or walk.
Recovery: Unfortunately, hip fractures can involve serious complications requiring surgery. They may take months to heal and can force you to reduce your activity. During recovery from a hip injury, most people will need some kind of assistance and will likely need to use a wheelchair or walker. In the best case, it can take three months of exercise after surgery to regain your strength and the full use of your leg. Sadly, many people who experience a hip fracture require nursing home care.
Alert! Pain is the most obvious sign that you have broken a bone. If you suspect a problem, don’t wait to get treated. Your doctor or an orthopedic specialist can confirm the diagnosis with an X-ray. And while it may seem logical to dismiss a broken wrist or hip as being due to a fall, it’s important to tell your primary care physician about any broken or fractured bones. He or she may recommend a bone mineral density test to see if osteoporosis was really the underlying cause.
Find Out How Your Spine Changes As You Age
Basics
Bone Density Testing: What to Expect
Did Osteoporosis Cause Your Fracture?
Osteoporosis at a Glance
What You Need to Know
Why Your Spine, Wrists & Hips Are at Risk
Top 4 Bone-Health Myths—Set Straight!
Osteoporosis Fast Facts
Separating Myths From Facts
How Fragile Are Your Bones?
How Your Spine Changes as You Age
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msmarco_passage_01_47105393 | Serum Calcium: Reference Range, Interpretation, Collection and Panels | Serum Calcium: Reference Range, Interpretation, Collection and Panels
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Drugs & Diseases > Laboratory Medicine
Serum Calcium
Updated: Nov 27, 2019
Author: Alina G Sofronescu, PhD, NRCC-CC, FACB; Chief Editor: Eric B Staros, MD more...
Sections
Serum Calcium
Sections Serum Calcium
Reference Range
Interpretation
Collection and Panels
Background
Show All
References
Reference Range
Calcium concentration, both total and free, is characterized by a high physiological variation, depending on age, sex, physiological state (eg, pregnancy), and even season (owing to the seasonal variation of vitamin D, which is directly involved in the regulation of calcium concentration). Therefore, separate reference intervals have been established according to the age and sex of the individual being tested.
Total calcium reference ranges are as follows [ 1] :
< 10 days: 7.6-10.4 mg/dL; 1.9-2.6 mmol/L
Umbilical: 9-11.5 mg/dL; 2.25-2.88 mmol/L
10 days-2 years: 9-10.6 mg/dL; 2.3-2.65 mmol/L
Child: 8.8-10.8 mg/dL; 2.2-2.7 mmol/L
Adult: 9-10.5 mg/dL; 2.25-2.62 mmol/L (Values tend to be reduced in elderly persons.)
Possible critical values for total calcium are < 6 mg/dL or >13 mg/dL. [ 1]
Next: Interpretation
Interpretation
Measurement of the ionized calcium component is generally obtained in specialized laboratories and through a special procedure. In most laboratories, autoanalyzers are used to measure the total serum calcium level accurately and reproducibly, although atomic absorption spectrophotometers probably provide even greater accuracy.
Unless serum proteins contain abnormalities, total serum calcium concentration is normally between 8.5 and 10.2 mg/dL of serum. Because ionized calcium is the only component of the total serum calcium level that is regulated by calciotropic hormones, decisions on the total serum calcium concentration should not be made unless changes in concentrations of plasma proteins, particularly albumin, are considered.
Total serum calcium is less difficult to measure than the ionized calcium component is, and ionized calcium measurements are rarely needed if serum protein concentrations can be measured.
In patients multiple myeloma, the globulin concentration is often increased, leading to excessive binding of calcium to the monoclonal paraprotein and occasional elevation of the total serum calcium concentration, yet the ionized calcium level may be normal in these individuals. Assessment of ionized calcium would be useful in such patients. It should be emphasized that these patients frequently have bone lesions, which leads to release of calcium from the damaged bone tissue.
Although serum calcium levels above 11.5 mg/dL commonly cause symptoms, patients may be asymptomatic at this level. Critical levels are reached above 12 mg/dL, with levels above 15 mg/dL (severe hypercalcemia) being a medical emergency.
Previous
Next: Interpretation
Collection and Panels
Preferred specimens are as follows:
Plasma, serum, whole blood
Urine specimens (random collection or 24-h timed collection)
Acceptable containers/tubes are as follows:
Green-top tube (sodium heparin, ammonium heparin, lithium heparin)
Red-top tube (clot activator)
Serum separator tube
Plasma separator tube
Electrolyte–balanced heparinized syringes (for whole blood sample testing)
Urine containers (may contain 6 mol/L HCl, 20-23 mL in 24-h urine collection, to prevent precipitation of calcium salts)
Specimen volumes are as follows:
0.5 mL plasma or serum (0.25 mL minimum volume)
0.5 mL whole blood
Entire urine collection
Specimen stability
Whole blood specimens should be analyzed within 15-30 minutes of collection. If this is not possible, the specimen should be kept in ice. On ice, the specimen is stable for at least 2 hours; however, if concurrent potassium testing is requested on the same specimen, the low temperature leads to a spurious increase in potassium within 1 hour of collection.
If the specimen cannot be analyzed within 1 hour, the preferred specimen is serum. The specimen should be centrifuged, and the serum or plasma should be removed from the cells within 2 hours of collection.
Samples can be stored at room temperature for 8 hours or refrigerated at 2-8 o C for up to 48 hours. If assays are not completed within 48 hours or the separated sample is to be stored beyond 48 hours, samples should be frozen at -15°C to -20°C. Frozen samples should be thawed only once. Analyte deterioration may occur in samples that are repeatedly frozen and thawed.
If drawing for more than total calcium, send the first tube drawn.
Collection considerations and sources of preanalytical errors [ 2]
Fist-clenching or forearm exercise can lead to falsely elevated ionized (free) calcium levels.
The sample should be drawn with the patient in a sitting position. Standing increases the total calcium concentration.
Hemolysis and delayed plasma/serum separation lead to a decreased calcium concentration.
Samples collected in tubes containing citrate, oxalate, or ethylenediaminetetraacetic acid (EDTA) are not suitable for calcium testing.
Measurement of calcium
Ionized calcium can be measured in whole blood using the ion-specific electrode (ISE) potentiometric method. This was designated by the International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) as the reference method for ionized/free calcium evaluation.
Total calcium also can be measured using the ISE potentiometric method, but the sample must be preacidified to release all bound and complexed calcium to a free form. However, total calcium is commonly measured with spectrophotometric methods, such as the o-Cresolphthalein Complexone method, Arsenazo III method, atomic absorption spectrometry, or, rarely, isotope dilution mass spectrometry (ID-MS). The atomic absorption spectrometry method was designated by the IFCC as the reference method for total serum calcium evaluation, while the ID-MS is considered “the definitive method” for total calcium evaluation developed by the National Institute of Standards and Technology. [ 3]
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Background
Description
Calcium is the fifth most abundant element in the body. Adults have a calcium content of over 1 kg, or approximately 2% of body weight. All but 1% is contained in the bones, where it exists as calcium hydroxyapatite. The extraosseous intracellular space and extracellular space contain a portion of the remaining 1%. A dynamic equilibrium is maintained between the extracellular space and the rapidly exchangeable fraction of bone calcium. In blood, virtually all calcium is present in the plasma.
About 50% of the calcium present in circulation is free (also known as ionized calcium); 40% of serum calcium is bound to proteins, especially albumin (80%) and, secondary, to globulins (20%); and about 10% exists as various small diffusible inorganic and organic anions (eg, bicarbonate, lactate, citrate).
Heart and skeletal muscle contractility are affected by calcium ions; in addition, calcium ions are vital to nervous system function and are associated with blood clotting and bone mineralization.
The concentration of serum calcium is tightly regulated by parathyroid hormone (PTH) and 1,25-hydroxy vitamin D.
For further reading, please see the Medscape Drugs and Diseases topics Hypocalcemia and Hypercalcemia.
Indications/Applications
Hypocalcemia
Serum total calcium concentrations below the reference interval for the appropriate age and sex reflect a hypocalcemic status. Nevertheless, results of total serum calcium should be interpreted with caution, as they might not follow the same pattern (decreased concentration) of free (ionized) calcium. This is because total calcium is influenced by multiple factors, such as concentration of albumin, serum pH, and concentration of immunoglobulins.
As 80% of the bound calcium present in the circulation is carried by albumin (albumin has multiple binding sites for calcium), changes in serum albumin concentration trigger significance changes in the concentration of total calcium. Hypoalbuminemia is the most common cause of pseudohypocalcemia. Therefore, serum albumin changes are generally corrected with the addition of 0.8 mg/dL for every gram that the serum albumin level falls below 4 g/dL. In patients with suspected hypercalcemia or hypocalcemia, this principle can be expressed as the following equation:
Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 (4.0 - serum albumin [g/dL])
The corrected total serum calcium concentration is normally 8.5-10.2 mg/dL, but there is no sure means of predicting the serum calcium level, for either hypocalcemia or hypercalcemia, at which symptoms will occur. The rapidity of change, as well as the absolute serum calcium concentration, impacts symptom development. It has been found, however, that hypocalcemic symptoms rarely occur if the corrected serum calcium concentration is above 8 mg/dL, while hypercalcemic symptoms rarely develop in patients with a corrected serum calcium level under 11 mg/dL. [ 4, 5, 6]
Calcium binds to the negatively charged sites of proteins, especially albumin. Therefore, this binding is pH-dependent. Alkalosis (increased serum pH) leads to increased protein ionization, increased negative charge and calcium binding, and, consequently, increased bound calcium concentration and decreased in free calcium. Acidosis (decreased pH) has the opposite effects.
Serum calcium is decreased (hypocalcemia) in the following conditions:
Hypoparathyroidism
Vitamin D deficiency (either from intake deficiency or decreased conversion/activation) or resistance (osteomalacia and rickets)
Chronic renal diseases (eg, renal acidosis, Fanconi syndrome)
Pseudohypoparathyroidism
Magnesium deficiency (PTH glandular release is magnesium-dependent)
Hyperphosphatemia
Massive transfusion
Hypoalbuminemia
Chronic liver disease and biliary obstructive diseases (from impaired absorption and conversion of vitamin D)
Overexpression of fibroblast growth factor 23 (oncogenic osteomalacia)
Severe calcium dietary deficiency
Severe pancreatitis (calcium saponification)
Hungry bone syndrome
Hypocalcemia results when the parathyroid glands are either absent or impaired. Impaired vitamin D synthesis can also cause the condition. Owing to an associated decrease in vitamin D synthesis and the presence of hyperphosphatemia and skeletal resistance to PTH, chronic renal failure is a frequent source of hypocalcemia. Latent or manifest tetany and osteomalacia are characteristic signs of hypocalcemia. [ 3]
Hypercalcemia
Serum total calcium concentrations above the reference interval for the appropriate age and sex reflect a hypercalcemic status.
Serum calcium is increased in the following:
Hyperparathyroidism (primary, such as multiple endocrine neoplasia (MEN) type 1, hyperplasia, adenoma, or carcinoma; or secondary, from chronic kidney injury and hyperphosphatemia or after PTH administration during treatment for osteoporosis)
Malignancies (humoral hypercalcemia of malignancy) that secrete PTH–related protein (PTHrP), especially squamous cell carcinoma of lung and renal cell carcinoma
Vitamin D excess
Milk-alkali syndrome
Multiple myeloma, owing to bone lesions
Paget disease of bone with prolonged immobilization
Sarcoidosis
Other granulomatous disorders
Familial hypocalciuria hypercalcemia
Vitamin A intoxication
Thyrotoxicosis
Hypothyroidism, owing to prolongation of vitamin D action as its metabolism is slowed down
Addison disease
Drug exposure: Some drugs that can increase serum calcium are as follows antacids (some), calcium salts, long-term thiazide therapy, lithium
Hypercalcemia results from increased mobilization of calcium from the skeletal system or increased intestinal absorption. The condition is usually caused by primary hyperparathyroidism or bone metastasis of carcinoma of the breast, prostate, thyroid gland, or lung.
In 10% of patients with malignancies, coexistent hyperparathyroidism is the source of hypercalcemia; this indicates that evaluation of serum PTH levels should be performed at initial presentation in all hypercalcemic patients. Surgical removal of one or more parathyroid glands is a consideration in patients with primary hyperparathyroidism and bone disease, renal stones or nephrocalcinosis, or other signs or symptoms. Severe hypercalcemia may cause cardiac arrhythmia. [ 3, 7, 8]
Urinary calcium
Urinary calcium laboratory results should be always normalized to the glomerular filtrate (GF) and take into account the serum and urine concentration of creatinine, using the following formula:
UCa [mg/100 mL GF] = (UCa [mg/dL] X SCr [mg/dL]) / UCr [mg/dL]
UCa = Urinary calcium concentration
SCr = Serum creatinine concentration
UCr = Urine creatinine concentration
Reference intervals for urinary calcium were established taking into account an unrestricted diet, as well as in fasting conditions.
In diet-unrestricted conditions, men and women can excrete up to 300 mg calcium/24 h; while in fasting, less than 200 mg/24 h calcium will be excreted in the urine.
Under fasting conditions, intestinal and renal calcium absorption are fixed, and the urinary excretion of calcium reflects the skeletal matrix resorption/release of calcium. A urinary calcium concentration of greater than 0.16 mg/ 100 mL GF is usually associated with osteoclastic bone resorption.
Evaluation of urinary calcium is a useful tool for assessing renal stones diseases and high-turnover osteoporosis. [ 3]
Considerations
During pregnancy, the serum albumin concentration often can be decreased. However, an increase in serum free calcium is not observed. However, pregnancy-specific reference intervals should be used for correct patient evaluation.
Drugs (eg, phenytoin) and bilirubin are commonly competing with calcium for albumin binding. Therefore, laboratory results from icteric patients and patients undergoing treatments with highly albumin-bonded drugs should be interpreted with caution.
Since gadolinium can interfere with most metal tests, 48 hours must elapse between administration of gadolinium-containing contrast media and specimen collection.
Previous
References
Pagana KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic & Laboratory Test Reference. 14th ed. St. Louis, Mo: Elsevier; 2019.
[Guideline] Clinical and Laboratory Standards Institute. C31-A2 Ionized Calcium Determinations: Precollection Variables, Specimen Choice, Collection, and Handling; Approved Guideline - Second Edition. Vol.12, No.10:
Burtis CA, Ashwood ER, Bruns DE. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 4th. Philadelphia, Pa: Saunders; 2005.
Deng XR, Zhang YF, Wang TG, Xu BH, Sun JC, Zhao LB, et al. Serum calcium level is associated with brachial-ankle pulse wave velocity in middle-aged and elderly Chinese. Biomed Environ Sci. 2014 Aug. 27 (8):594-600. [Medline].
Sanchis-Gomar F, Salvagno GL, Lippi G. Inhibition of xanthine oxidase and exercise on serum uric acid, 25 (OH)D3, and calcium concentrations. Clin Lab. 2014. 60 (8):1409-11. [Medline].
Kanagal DV, Rajesh A, Rao K, Devi UH, Shetty H, Kumari S, et al. Levels of Serum Calcium and Magnesium in Pre-eclamptic and Normal Pregnancy: A Study from Coastal India. J Clin Diagn Res. 2014 Jul. 8 (7):OC01-4. [Medline]. [Full Text].
Jacobs TP, Bilezikian JP. Clinical review: Rare causes of hypercalcemia. J Clin Endocrinol Metab. 2005 Nov. 90 (11):6316-22. [Medline].
Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1. 67 (9):1959-66. [Medline].
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Contributor Information and Disclosures
Author
Alina G Sofronescu, PhD, NRCC-CC, FACB Associate Professor, Board Certified Clinical Chemist, Medical Director of Clinical Chemistry and Toxicology Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Center
Alina G Sofronescu, PhD, NRCC-CC, FACB is a member of the following medical societies: American Association for Clinical Chemistry, Canadian Society of Clinical Chemists
Disclosure: Nothing to disclose.
Chief Editor
Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital
Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, Association for Molecular Pathology, College of American Pathologists
Disclosure: Nothing to disclose.
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msmarco_passage_01_473883100 | Gunpla | The Gundam Wiki | Fandom | Gunpla | The Gundam Wiki | Fandom
This article uses Creative Commons licensed content from Wikipedia 's Gundam model article.
The list of authors can be seen in the page history there.
Gunpla Logo
Gunpla (ガンプラ Ganpura ), a portmanteau of " Gun dam pla stic model", is the common name for plastic model kits depicting the vehicles and characters of the fictional Gundam universe by Bandai. These kits have become popular among mecha anime fans and model enthusiasts in Japan and in other nearby Asian countries since the 1980s. Gundam modeling spread in the 1990s with North America and Europe being exposed to Gundam through television, video and manga.
Contents
1
History
2
High Grade (HG)
3
High Grade Universal Century (HGUC)
4
Real Grade (RG)
5
Master Grade (MG)
6
Reborn-One Hundred (RE/100)
7
Perfect Grade (PG)
8
Special Editions
9
Non Plastic Gunpla
10
Other series
10.1
Super-Deformed
10.2
EX Model
10.3
U.C. Hard Graph
10.4
Speed Grade Collection
10.5
Gundam Fix Figuration
10.6
Mega Size Model
10.7
Entry Grade (EG)
10.8
First Grade (FG)
10.9
Non Grade (NG)
10.10
Advanced Grade (AG)
10.11
Ecopla
11
Display models
12
Yokohama Walking Gundam Model Series
13
Comparison
14
Building Gunpla kits
15
Tools
16
Bootleg Gunpla (pirated Gundam model kits)
17
Video gallery
18
Trivia
19
See also
20
External links
History
Gunpla gallery showing various grades and scales. Courtesy of Dalong's Gunpla Review.
Gunpla are manufactured by Bandai in Japan, or China, which has an exclusive license in manufacturing and marketing the kits around the world. The first Gunpla kits were sold in 1980 in Japan.
Gunpla kits consist of several trays of parts or "runners" that either snap-fit (most post-1990 models) or require glue (older models prior to 1990) to put together. The cover image on the box, or box art, is usually done by an illustrator with a picture illustration of the subject mecha design in action. All Gunpla are supplied with stickers and sometimes decals to apply extra colors and markings as seen in the show, movies, manga or video games. Smaller or lower grade kits often require paint to give the model a finished appearance.
The kits range in different scales with the most popular scales being: 1:144 (approx 13 cm tall), 1:100 (approx 16–19 cm tall) and 1:60 (approx 30 cm tall). Other scales include 1:200, 1:48, and the SD series.
Since the first Gunpla release, there has been a constant improvement in quality design, material and manufacturing technique by Bandai. The basic kits of the late 1980s (routinely re-released by Bandai, with some exceptions) require cement and paint. These kits when completed, have very limited range of motion which renders them almost not poseable. These models were retrospectively called FG ( First Grade ).
High Grade (HG)
Later on, after FG, the quality of the moulding of plastic was improved and HG ( High Grade) level kits were introduced in 1990. These kits at either 1:144 or 1:100 scale, provide for better range of motion and greater posability. It is important to note that the SEED and SEED DESTINY 1:100 scale models do not have HG listed anywhere on the box or manual, but they are considered HG in terms of quality.
High Grade Universal Century (HGUC)
The highly anticipated HG Universal Century series, commonly called the HGUC series, was released in May 1999. Created in an easy to collect 1:144 scale, it represented a chance to release versions of many Mobile Suits for the first time in kit form using refined designs and modern injection moulding technology. The high quality of the HGUC series makes it the rightful heir of the HG series released in the 1990s. New designs, with new mechanical improvements, continue to be introduced in the series even today. Furthermore, all modern 1/144 HG models, such as the Gundam SEED line, are built to the same quality of early HGUC models. Starting in 2010 the HGUC line incorporated mobile suits from the alternate timelines that had not received an HG release. In 2013 Bandai launched the "All Gundam Project" in conjunction with the release of Gundam Build Fighters to release all lead Gundams with the universal joint technology in the High Grade line.
Real Grade (RG)
In July 2010, Bandai introduced the 1:144 Real Grade (RG) line as part of the "Gundam 30th Anniversary", which takes design elements from the Master Grade and Perfect Grade line such as an inner skeletal frame. This Gunpla line achieves the largest range of motion in each joint.
Master Grade (MG)
The next level is designated as Master Grade (MG), which was introduced in 1995, and are only offered in 1:100 scale. These kits are manufactured using higher quality plastic and the resulting molds are of a greater standard. However, the model is more expensive, complicated and takes longer to construct. The finished models offer a superior range of motion compared to the lower level kits to provide for an even wider range of poses, thanks to an inner frame. Some of them actually include specially designed stands for added display ability. Master Grade kits are very presentable assembled straight from the box, but adding paint and detailing can greatly improve the appearance of the finished model.
Reborn-One Hundred (RE/100)
In September 2014, Bandai introduced the Reborn-One Hundred (RE/100) line. This 1:100 scale line consists of models that are too large, too obscure, or too costly to produce into the MG line. As such, the kits lack the inner frame and detail level of MG, but offer articulation levels equal to or better than 1:144 scale HG kits.
Perfect Grade (PG)
The highest quality kits are known as Perfect Grade (PG), introduced in 1998. These 1:60 scale models are made of even higher quality plastic and metal components. These kits include parts that have to be secured with screws, and often require some minor wiring for small LEDs. The market for the Perfect Grade level of models is limited due to the higher cost, often costing between $100 to $300. Perfect Grade models are a true challenge and their construction can take days, or even weeks.
Special Editions
Over the years, Bandai released special limited editions of various kits, usually as competition (such as the yearly Bandai Action Kits Asia (now Universal) Cup held in Hong Kong) prizes, or as an event-limited (such as Japanese toy expos, movie launch premieres) item, although sometimes these kits are sold as limited web-shop items or discreetly sold by Bandai. These kits usually come in clear plastic, metal-plated (certain kits are in so-called 24K gold finish), "gloss-finish", "pearl-finish", "titanium-finish", or any combination of these. Their prices are usually higher than their regular-release counterparts.
Non Plastic Gunpla
Bandai has also released some Gundam garage kit under their branch, B-club. These models are composed of unpainted resin with no decals provided, often needing modification by the modeler due to the inherent properties of the manufacturing process. While comparably more expensive (some surpassing $400) compared to plastic kits, they offer an unparalleled level of detail for the dedicated and experienced model builder.
A few select kits have also appeared manufactured from metal. These kits are offered by several different manufacturers and most commonly will result in a finished model of about MG level.
These types of models (real detail) usually take several days to build.
Other series
Super-Deformed
Also offered is an expanding line of small plastic kits labelled SD Gundam ( Super-Deformed Gundam) which are not presented in a particular scale. "SD" Gundams are comedic renditions of the various Gundam mecha designs featuring a disproportionately large "head." These kits are often much easier to construct but offer very limited possibility and require paint and detailing to truly "finish" the kit. The most famous line is the BB Senshi (known as SD GUNDAM BB Warriors in Bandai's English page). Depending on popularity of series, SD units may also be sold in separate product line (e.g.: Superior Defender Gundam Force ).
Bandai also offers Real Detail model kits, which is exclusive to the Cosmic Era universe. While the scale is 1:60, they are basically scaled up HG kits with some added details. The level of details and possibility are not comparable to Master Grade and Perfect Grade kits, but some models feature gimmicks like light up LEDs and includes a stand.
Bandai often produce limited run kits for special events (JAFCON, C3 or locale specific events.) These kits are generally packaged differently from normal production kits, but usually differ only in that they are fabricated with metal plating or in translucent plastic.
EX Model
This line depicts vehicles in supporting roles, such as tanks and fighters. They are less expensive than garage kits, yet have higher detail than regular plastic models. Although they are usually in 1:44 scale, vessels such as the Argama and White Base are in 1:1700. Other series featured in this line include Patlabor, Sentō Yōsei Yukikaze, and Ace Combat .
U.C. Hard Graph
Released in 2006, it uses the 1:35 scale for armored fighting vehicles. Kits can be bundled with soldiers, firearms, vehicles and MS parts.
Speed Grade Collection
Launched in 2007, this series consists of pre-painted kits molded in the 1:200 scale.
Gundam Fix Figuration
The Gundam Fix Figuration (G.F.F.) series of collectible figures was started based on the Gundam mechanical designs of Hajime Katoki and his 'Gundam Fix' illustration artbook and are released by Bandai.
Mega Size Model
A large-sized Gunpla line in the 1:48 scale, it was introduced on March 6, 2010 as part of the Gundam 30th Anniversary. The Mega Size Model RX-78-2 Gundam is based on the Green Tokyo Gundam Project (Gundam Front) 1/1 full-size model.
Entry Grade (EG)
Entry Grade, or EG, is a line of 1/144 scale model kits, or Gunpla, of the Mobile Suits from the Gundam meta series. Introduced in 2011 and made in China, the line was marketed to emerging markets in Asia. EG kits are similar to First Grade or No Grade 1/144 series Gunpla kits, wherein they contain no polycaps and are molded in only three colors.
First Grade (FG)
The original First Grade line, or FG, was part of the Gundam 20th Anniversary Big Bang Project in 1999 as a modern remake of the original 1980 1/144 kits. As such, the kits were molded in one color and contained no polycaps, but featured the snap-fit assembly of current kits. The three Gunpla in this line used designs based on their Perfect Grade counterparts.
Non Grade (NG)
The very first kits have been running for 30 years (starting with RX-78-2 Gundam) and are routinely re-released by Bandai. As these kits are limited in articulation and require glue (for the early kits) and paint to assemble, these have retroactively been categorized as No Grade (NG), to differentiate them from First Grade (FG).
Advanced Grade (AG)
Released in 2011 with the Mobile Suit Gundam AGE series, it comes with a Gage-ing Chip for the Gage-ing Battle Base arcade game.
Ecopla
A special limited release sold at events such as the "Gundam Expo." With the exception of clear parts, the kits are made from recyclable materials; specifically, melted-down plastic left over from the manufacture of other models.
Display models
For trade shows and toy fairs, Bandai displays some extremely large models in 1:6 or 1:12 scale. True to the scaling, some of these models are well over 5 feet (1.50 m) tall. Although most of these are one off promotional models used for display purposes, Bandai has produced a few of these for commercial purposes under their HY2M line. Notably, these are MS-06S "Zaku II Commander Type" (Char Aznable custom), which is now out of production, and the " RX-78-2 Gundam ". These generally retail for approximately $2,000 and are intended to be sold primarily to store owners as display fronts.
Yokohama Walking Gundam Model Series
In 2020, Bandai Spirits announced a series of model kits based on the design of the 1:1 scale walking RX-78-2 Gundam, located in the Port of Yokohama, Japan. These models are not assigned any grade, are in varying scales and have the detail level of High Grade model kits.
Comparison
The following are all the equivalent sets of a MS-06 Zaku II each demonstrating a different series of Gunpla Model Kits.
1/144 High Grade Universal Century Zaku II.
1/144 Real Grade Zaku II.
1/100 Master Grade Zaku II.
1/60 Perfect Grade Zaku II.
1/48 Mega Size Model Zaku II.
Non-scale SD Gundam BB Senshi Zaku II.
Photo credit: Dalong.net
Building Gunpla kits
Upon buying a Gunpla model kit, the buyer will receive several "runners" that either snap-fit (most post-1990 models) or require glue (older models prior to 1990) to put together. The runners include all of the kit's parts inside of a tree-like mold. There is also manual used for building the kit, and possibly decals, which are sometimes not provided in lower-grade kits. Popular tools used to cut the molds out of the runners include side-cutters and a hobby knife.
The runners provide a code used to differentiate each part from another. By following the manual, cut out the according parts needed from the runner and proceed to snap the parts together. These steps will become a repetitive process as there are several parts needed to be cut and snapped together. Another step that many builders also do is to remove "nub-marks", which are leftover piece of plastic from the runners. Tools used to remove the excess plastic are sandpaper and a hobby knife. Overdoing this process could result in damaging the whole part. The provided decals and stickers are used to display extra details, colors and markings as seen in the show, movies, manga or video games. Smaller or lower grade kits often require paint to give the model a finished appearance.
Tools
A list of tools commonly used to build Gunpla kits:
Side Cutters/Nippers - The most essential tool. They are used to cut parts out from the runners without damaging the plastic. Some beginners use nail cutters as a cheap alternative to side cutters.
Hobby Knife - Used to carefully remove the nubs or shave off the mold lines of the kit's parts. Popular brands include Olfa and X-Acto.
Metal File - Like the hobby knife, this is used to remove nub marks, but is more widely used on flat surfaces.
Sandpaper - Used to sand away remaining nubs not removed by the knife or metal file.
Paint - Comes in acrylic (water-based), lacquer, or enamel. Mr. Color manufactures paint colors specifically matched for Gunpla. Other popular brands include Tamiya, Testors, and Citadel.
Gundam Markers - Alcohol-based paint markers that are a quick and easy substitute for paint to cover up any damage caused by removing nubs.
Panel Lining Markers - Used to highlight the plastic edges and creases in the Gunpla kit. Excess ink can be removed with a cotton swab or an eraser.
Oil Wash - A more professional alternative to panel lining markers, this is a mix of enamel paint diluted in thinner. The paint is then lightly dipped on a line before it spreads to other intersecting panel lines. Excess paint is then cleaned up with a cotton swab dipped in lighter fluid.
Top Coat - Gives the model a desired finish and protects the paint and decals applied.
Bootleg Gunpla (pirated Gundam model kits)
In April 2010, Bandai sued two Chinese toy manufacturers for manufacturing and selling counterfeit Gunpla kits. The lawsuit states that Bandai demands 3.69 million RMB (roughly US$540,000) compensation from the companies.
Bootleg Gunpla companies include Daban, TT Hongli, Model GD, Elyn Hobbie, and Dragon Momoko.
Video gallery
Before Painting 1 About different types of paint
Before Painting 1
Before Painting 2 Oil base color
Before Painting 2
Before Painting 3 Acrylic
Before Painting 3
Before Painting 4 Enamel
Before Painting 4
Trying out airbrushing 1 Good paints for airbrushing
Airbrushing 1
Trying out airbrushing 2 Thinning paint
Airbrushing 2
Trying out airbrushing 3 What happens if I don't thin properly?
Airbrushing 3
Trying out airbrushing 4 Basic painting
Airbrushing 4
Trying out airbrushing 5 Keeping paint off of shafts
Airbrushing 5
Add a photo to this gallery
Trivia
A modified version of the Gunpla logo is also used for Sprukits, Bandai's other model kit line marketed in the U.S.
See also
High Grade
High Grade Universal Century
Real Grade
Master Grade
Reborn-One Hundred
Perfect Grade
Gundam Fix Figuration
List of Gundam Models since 1980
External links
Gunpla on Wikipedia
Gunplapedia
Bandai Hobby Site ( English version)
CDJapan Japanese online Store with all Gunpla models.
Hobby Link Japan Huge Japanese online hobby store.
Dalong's Gunpla Review Avid Gunpla and Giant Robot model collector.
Retrieved from " https://gundam.fandom.com/wiki/Gunpla?oldid=475532 "
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Gunpla
Gundam model
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msmarco_passage_01_47438933 | Red Cell Distribution Width (RDW) Test: Reference Range of the Red Cell Distribution Width (RDW), Interpretation of the Red Cell Distribution Width (RDW) Test, Collection and Panels | Red Cell Distribution Width (RDW) Test: Reference Range of the Red Cell Distribution Width (RDW), Interpretation of the Red Cell Distribution Width (RDW) Test, Collection and Panels
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Drugs & Diseases > Laboratory Medicine
Red Cell Distribution Width (RDW) Test
Updated: Jan 12, 2015
Author: Choladda Vejabhuti Curry, MD; Chief Editor: Eric B Staros, MD more...
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Red Cell Distribution Width (RDW) Test
Sections Red Cell Distribution Width (RDW) Test
Reference Range of the Red Cell Distribution Width (RDW)
Interpretation of the Red Cell Distribution Width (RDW) Test
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References
Reference Range of the Red Cell Distribution Width (RDW)
The red cell distribution width (RDW) test measures variation in red blood cell size or red blood cell volume as a part of a complete blood count (CBC), and it is used along with other RBC indices, especially mean corpuscular volume (MCV), to help determine the causes of anemia.
RDW is elevated in accordance with variation in red cell size (anisocytosis), ie, when elevated RDW is reported on complete blood count, marked anisocytosis (increased variation in red cell size) is expected on peripheral blood smear review.
The reference range for RDW is as follows:
RDW-SD 39-46 fL [ 1]
RDW-CV 11.6-14.6% in adult [ 2]
Reference ranges may vary depending on the individual laboratory and patient's age.
Indications/Applications
Red cell distribution width (RDW) laboratory test is a part of a standard complete blood count (CBC), and it is used along with other RBC indices, especially mean corpuscular volume (MCV) to help determine the causes of anemia.
Considerations
Elevated RDW provides a clue for heterogenous red cell size (anisocytosis) and/or the presence of 2 red cell populations, since other RBC indices (MCV, MCH and MCHC) reflect average values and may not adequately reflect RBC changes where mixed RBC populations are present, such as dimorphic RBC populations in sideroblastic anemia or combined iron deficiency anemia (decreased MCV and MCH) and megaloblastic anemia (increased MCV). Peripheral blood smear review can help confirm the above findings in these circumstances. [ 3, 4, 5]
Next: Interpretation of the Red Cell Distribution Width (RDW) Test
Interpretation of the Red Cell Distribution Width (RDW) Test
Red cell distribution width (RDW) is a red blood cell parameter that measures variability of red cell volume/size (anisocytosis). Depending on the types of hematology analyzer instruments, RDW can be reported statistically as coefficient of variation (CV) and/or standard deviation (SD), RDW-CV and/or RDW-SD, respectively. [ 1, 6]
RDW-SD (express in fL) is an actual measurement of the width of the red blood cell (RBC) size distribution histogram (see the first image below) and is measured by calculating the width (in fL) at the 20% height level of the RBC size distribution histogram (see the second image below). This parameter is therefore not influenced by the average RBC size (mean corpuscular volume, MCV).
RDW-CV (express in %) is calculated from standard deviation and MCV as follows (see the third image below):
RDW-CV (%) = 1 standard deviation of RBC volume/MCV x 100%
Of note, since RDW-CV is mathematically derived from MCV, it is therefore affected by the average RBC size (MCV).
RDW blood test: RBC size distribution histogram from a Sysmex SE-2100 analyzer from a subject with an MCV of 81.4 fL, RDW-SD of 38.2 fL, and RDW-CV of 12.8%.
View Media Gallery
RDW blood test: Determination of RDW-SD measurement. In this example, RDW-SD is 38.2 fL.
View Media Gallery
RDW blood test: Calculation of RDW-CV measurement, which is derived from 1SD divided by MCV times 100%. In this example, RDW-CV is 12.8%.
View Media Gallery
RDW blood test is useful in the following conditions: [ 7, 3, 1]
A high RDW helps provide a clue for a diagnosis of early nutritional deficiency such as iron, folate, or vitamin B12 deficiency as it becomes elevated earlier than other red blood cell parameters.
It aids in distinguishing between uncomplicated iron deficiency anemia (elevated RDW, normal to low MCV) and uncomplicated heterozygous thalassemia (normal RDW, low MCV); however, definitive tests are required. [ 8, 9]
It can also help distinguish between megaloblastic anemia such as folate or vitamin B12 deficiency anemia (elevated RDW) and other causes of macrocytosis (often normal RDW).
RDW can be used as a guidance for flagging samples that may need manual peripheral blood smear examination, since elevated RDW may indicate red cell fragmentation, agglutination, or dimorphic red blood cell populations.
RDW along with mean corpuscular volume (MCV) is helpful in narrowing the cause of anemia: [ 4]
Normal RDW and low MCV are associated with the following conditions:
Anemia of chronic disease
Heterozygous thalassemia
Hemoglobin E trait
High RDW and low MCV are associated with the following conditions:
Iron deficiency
Sickle cell-β-thalassemia
Normal RDW and high MCV are associated with the following conditions:
Aplastic anemia
Chronic liver disease [ 10]
Chemotherapy/antivirals/alcohol
High RDW and high MCV are associated with the following conditions:
Folate or vitamin B12 deficiency
Immune hemolytic anemia
Cytoxic chemotherapy
Chronic liver disease
Myelodysplastic syndrome
Normal RDW and normal MCV is associated with the following conditions:
Anemia of chronic disease
Acute blood loss or hemolysis
Anemia of renal disease
High RDW and normal MCV is associated with the following conditions:
Early iron, vitamin B12, or folate deficiency
Dimorphic anemia (for example, iron and folate deficiency)
Sickle cell disease
Chronic liver disease
Myelodysplastic syndrome
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Next: Interpretation of the Red Cell Distribution Width (RDW) Test
Collection and Panels
Collection and panel details for the RDW blood test are as follows:
Specimen: Whole blood, usually collected by venipuncture
Collection: EDTA tube (purple/lavender top) containing EDTA potassium salt additive as an anticoagulant (see image below)
EDTA tubes, purple top.
View Media Gallery
Panels: Complete blood count (CBC)
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References
Briggs C, Bain BJ. Basic Haematological Techniques. Bain BJ, Bates I, Laffan M, Lewis SM. Dacie and Lewis Practical Haematology. 11th ed. Philadelphia, PA: Churchill Livingstone/Elsevier; 2012. chap 3.
Vajpayee N, Graham SS, Bem S. Basic Examination of Blood and Bone Marrow. McPherson RA, Pincus MR. Henry's Clinical Diagnosis and Management by Laboratory Methods. 22nd. Elsevier/Saunders: Philadelphia, PA; 2011. 30.
Perkins SL. Examination of the Blood and Bone Marrow. Greer JP, Foester J, Rodgers GM, et al, eds. Wintrobe’s Clinical Hematology. 12th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009. Chapter 1:1-20.
Marks PW, Glader B. Approach to Anemia in the Adult and Child. Hoffman F, Benz EJ, Shattil SJ, eds. Hematology Basic Principles and Practice. 5th. Philadelphia, PA: Churchill Livingstone/Elsevier; 2009. 34.
Elghetany MT, Banki K. Erythrocytic Disorders. McPherson RA, Pincus MR. Henry's Clinical Diagnosis and Management by laboratory Methods. 22nd. Elsevier/Saunders: Philadelphia, PA; 2011. 32.
Harmening DM, Black A, Culp NB, et al. Principles of Automated Differential Analysis. Harmening DM. Clinical Hematology and Fundamentals of Hemostasis. 5th ed. Philadelphia, PA: F.A. Davis Company; 2009. chap 32.
Ryan DH. Examination of blood cells. Lichtman MA, Kipps TJ, Seligsohn U, et al, eds. Williams Hematology. 8th ed. New York, NY: The McGraw-Hill Companies, Inc.; 2010. Chapter 2.
Sultana GS, Haque SA, Sultana T, Ahmed AN. Value of red cell distribution width (RDW) and RBC indices in the detection of iron deficiency anemia. Mymensingh Med J. 2013 Apr. 22 (2):370-6. [Medline].
Vaya A, Alis R, Suescun M, Rivera L, Murado J, Romagnoli M, et al. Association of erythrocyte deformability with red blood cell distribution width in metabolic diseases and thalassemia trait. Clin Hemorheol Microcirc. 2014 Jul 25. [Medline].
Tekce H, Kin Tekce B, Aktas G, Tanrisev M, Sit M. The evaluation of red cell distribution width in chronic hemodialysis patients. Int J Nephrol. 2014. 2014:754370. [Medline]. [Full Text].
Media Gallery
RDW blood test: RBC size distribution histogram from a Sysmex SE-2100 analyzer from a subject with an MCV of 81.4 fL, RDW-SD of 38.2 fL, and RDW-CV of 12.8%.
RDW blood test: Determination of RDW-SD measurement. In this example, RDW-SD is 38.2 fL.
RDW blood test: Calculation of RDW-CV measurement, which is derived from 1SD divided by MCV times 100%. In this example, RDW-CV is 12.8%.
EDTA tubes, purple top.
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Contributor Information and Disclosures
Author
Choladda Vejabhuti Curry, MD Assistant Professor of Pathology and Immunology, Baylor College of Medicine; Hematopathologist and Cytopathologist, Section of Hematopathology, Texas Children's Hospital
Choladda Vejabhuti Curry, MD is a member of the following medical societies: American Society for Clinical Pathology, American Society of Cytopathology, American Society of Hematology, College of American Pathologists, United States and Canadian Academy of Pathology, Society for Hematopathology, European Association for Haematopathology, International Clinical Cytometry Society
Disclosure: Nothing to disclose.
Chief Editor
Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital
Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, Association for Molecular Pathology, College of American Pathologists
Disclosure: Nothing to disclose.
Acknowledgements
The author wishes to thank Karen Prince for her assistance in RBC size distribution histogram illustrations.
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msmarco_passage_01_483315367 | Kusum Name Meaning - Kusum Meaning & Definition, Hindu Girl Name | Kusum Name Meaning - Kusum Meaning & Definition, Hindu Girl Name
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Kusum is a Hindu Girl name and it is Hindi originated name with multiple meanings. Kusum name meaning is A Flower. Kusum name popularity and rank stands at 3120 among 29430 Hindu names.
Kusum Name Meaning in English
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msmarco_passage_01_486049756 | Mr. Jinks | Hanna-Barbera Wiki | Fandom | Mr. Jinks | Hanna-Barbera Wiki | Fandom
Mr. Jinks
Mr. Jinks was a character on The Huckleberry Hound Show. He was the cat who constantly chased Pixie and Dixie, of whom he routinely said, "I hate meeces to pieces!"
Contents
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About Mr. Jinks
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Television
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About Mr. Jinks
Jinks is an orange cat sporting a blue-colored bow tie.
Though Jinks often chases Pixie and Dixie, he has a soft spot for them, evident in episodes such as "Strong Mouse", "The Pushy Cat" and "Mouse Nappers". In the episode "Jinks Jr.", Jinks doesn't fully understand why he chases them, only that "cats are supposed to hate meeces". Even so, Jinks doesn't usually mean them any real harm, such as in the episode "The Ghost with the Most" when Dixie pretends he is dead after Jinks clobbers him, and Jinks is very remorseful and guilty, even partially traumatized.
In return, Pixie and Dixie care about Jinks deep down as well. Pixie and Dixie mostly have a love-hate relationship with Jinks, where they can both be equally cruel to each other and will retaliate when provoked.
Filmography
Television
The Huckleberry Hound Show (1958-1962)
Yogi's Gang (1973)
Laff-A-Lympics (1977-1979)
Yogi's Treasure Hunt (1985-1988)
Yo Yogi! (1991)
Cartoon Network promos and advertisements (1990's)
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Yogi Bear's All-Star Comedy Christmas Caper (1982)
Hanna-Barbera's 50th: A Yabba Dabba Doo Celebration (1989)
Guest Appearances
The Yogi Bear Show - "Yogi's Birthday Party" (1962)
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John Stephenson - Yo Yogi! (1991)
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msmarco_passage_01_49999010 | Hypermagnesemia: Overview, Renal Failure, Other Causes | Hypermagnesemia: Overview, Renal Failure, Other Causes
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Drugs & Diseases > Nephrology
Hypermagnesemia
Updated: May 04, 2020
Author: Tibor Fulop, MD, PhD, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN more...
Sections
Hypermagnesemia
Sections Hypermagnesemia
Overview
Renal Failure
Other Causes
Effects of Hypermagnesemia
Diagnosis and Summary
Prevention and Treatment of Hypermagnesemia
Show All
References
Overview
Overview
Hypermagnesemia is an uncommon laboratory finding and symptomatic hypermagnesemia is even less common. This disorder has a low incidence of occurrence, because the kidney is able to eliminate excess magnesium by rapidly reducing its tubular reabsorption to almost negligible amounts.
In 2018, the American Association of Poison Control Centers (AAPCC) reported 1952 single exposures to magnesium and magnesium salts, the majority unintentional (1603). There were 261 cases treated in a health care facility with 43 moderate outcomes and no major outcomes or deaths. [ 1]
In healthy adults, plasma magnesium ranges from 1.7-2.3 mg/dL. Approximately 30% of total plasma magnesium is protein-bound and approximately 70% is filterable through artificial membranes (15% complexed, 55% free Mg 2+ ions). With a glomerular filtration rate (GFR) of approximately 150 L per day and an ultrafiltrable magnesium concentration of 14 mg/L, the filtered magnesium load is approximately 2,100 mg per day.
Normally, only 3% of filtered magnesium appears in urine; thus, 97% is reabsorbed by the renal tubules. In contrast to sodium and calcium, only approximately 25-30% of filtered magnesium is reabsorbed in the proximal tubule. Approximately 60-65% of filtered magnesium is reabsorbed in the thick ascending loop of Henle and 5% is reabsorbed in the distal nephron. [ 2] Relatively little is known about cellular magnesium transport mechanisms. [ 3]
The most common cause of hypermagnesemia is renal failure. Other causes include the following [ 4, 5] :
Excessive intake
Lithium therapy
Hypothyroidism
Addison disease
Familial hypocalciuric hypercalcemia
Milk alkali syndrome
Depression
Next: Renal Failure
Renal Failure
Decreasing renal function represents a risk factor for magnesium accumulation, in the setting of exogenous supplementation. [ 6] Patients with end-stage renal disease often have mild hypermagnesemia, and the ingestion of magnesium-containing medications (eg, antacids, cathartics) can exacerbate the condition. [ 7, 8, 9] In patients undergoing regular dialysis, the serum magnesium level directly relates to the dialysate magnesium concentration. [ 10]
In patients with acute kidney injury, hypermagnesemia usually presents during the oliguric phase; the serum magnesium level returns to normal during the polyuric phase. If a patient receives exogenous magnesium during the oliguric phase, severe hypermagnesemia can result, especially if the patient is acidotic.
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Next: Renal Failure
Other Causes
People often take magnesium-containing medications (eg, antacids, [ 11] laxatives, [ 12, 13, 6] enemas). An analysis of 320 hospitalized patients prescribed magnesium oxide (MgO) as an antacid/laxative who developed hypermagnesemia (serum Mg levels ≥2.5 mg/dL) identified four independent risk factors for hypermagnesemia [ 14] :
Estimated glomerular filtration rate ≤55.4 mL/min (odds ratio [OR]: 3.105, P = 0.001)
Blood urea nitrogen ≥22.4 mg/dL (OR: 3.490, P < 0.001),
MgO dose ≥1650 mg/day (OR: 1.914, P = 0.039)
Duration of MgO administration ≥36 days (OR: 2.198, P = 0.012).
Hypermagnesemia can develop after treatment of drug overdoses with magnesium-containing cathartics, [ 15] and it also occurs in patients taking magnesium-containing medications for therapeutic purposes [ 16, 17] ; however, most of these patients have normal renal function. [ 18]
With certain gastrointestinal disorders (eg, gastritis, colitis, gastric dilation), increased absorption of magnesium may lead to hypermagnesemia even if the patient does not ingest a large amount of magnesium. [ 19, 20, 21] In any case, monitoring serum magnesium levels in patients taking magnesium-containing medications is prudent. Suicide attempts using magnesium-containing salt can lead to life-threatening hypermagnesemia, as well. [ 22]
Excessive tissue breakdown (sepsis, shock, large burns), especially with concurrent renal failure, can deliver a large amount of magnesium from the intracellular space, along with a massive elevation of phosphorus and potassium. [ 5] During cancer chemotherapy, both hypomagnesemia and hypermagnesemia may occour, with the latter expected after induction of chemotherapy. [ 23]
In the treatment of eclampsia, hypermagnesemia is induced deliberately and sometimes can be symptomatic. [ 16, 24, 25, 26] Occasionally, hypermagnesemia also can occur in the newborn infant. [ 27, 28] Immediately after birth, reduced Apgar scores and perinatal death has been decribed in infants after maternal exposure to intravenous magnesium for treatment of pre-eclampsia. [ 29] Maternal magnesium therapy can increase the need for feeding and respiratory support [ 30] and may cause neurobehavioral disorders in the newborn. [ 31]
Although magnesium-containing phosphorus binders are rarely used in end-stage renal disease patients, [ 32, 33] those agents can lead to elevated magnesium levels.
Lithium therapy causes hypermagnesemia by decreasing urinary excretion, although the mechanism for this is not completely clear.
Familial hypocalciuric hypercalcemia may cause modest elevations in serum magnesium. [ 34] This autosomal dominant disorder is characterized by very low excretion of calcium and magnesium and by a normal parathyroid hormone level. The abnormalities of calcium and magnesium handling are due to mutations in the calcium-sensing receptor, [ 35] resulting in increased magnesium reabsorption in the loop of Henle. More recently, mutations of the codon Arg15 (p.R15) in the adaptor-related protein complex 2, σ-2 subunit that interacts with the calcium-sensing receptor have been described. [ 36]
Hypothyroidism, adrenal insufficiency, milk-alkali syndrome [ 4, 5] and theophylline intoxication occasionally produce mild elevations of serum magnesium.
There has been some interest in the use of magnesium in the treatment and prevention of cardiac arrhythmias and in the treatment of subarachnoid hemorrhage. [ 37, 38] However, significant hypermagnesemia has not been reported in these settings.
The role of mild elevation of serum magnesium levels in select patient populations is still being defined. In a study examining the prevalence of serum magnesium (Mg) alterations and outcomes in 65,974 hospitalized adult patients, Mg levels of 2.1 mg/dL or higher were found in 20,777 patients (31.5%). An elevated Mg level of 2.3 mg/dL or higher was a predictor of adverse outcomes and associated with worse hospital mortality. [ 39]
In a different study by the same authors, both hypomagnesemia (< 1.5 mg/dL) and hypermagnesemia (> 2.3 mg/dl) on hospital admission were associated with an increased risk of developing in-hospital acute respiratory failure. The odds ratio was 1.69 (95% confidence index [CI], 1.19-2.36) with hypomagnesemia and 1.40 (95% CI, 1.02-1.91) with hypermagnesemia. [ 40]
In a study of patients admitted to an intensive cardiac care unit, initial magnesium levels ≥2.4 mg/dL (reference level 2.0 to < 2.2 mg/dL) were independently associated with increased in mortality (adjusted OR, 1.80; 95% CI: 1.25-2.59. [ 41] In a large study of 5339 critically ill patients from Switzerland, hypermagnesemia was a strong independent risk factor for 28-day mortality (hazard ratio, 11.6, P< 0.001). [ 42]
Similarly, in patients with chronic heart failure, a meta-analysis of 7 prospective studies with a total of 5172 subjects demonstrated that those with baseline hypermagnesemia had a significantly higher risk of cardiovascular mortality (risk ratio [RR],, 1.38; 95% CI, 1.07-1.78) or all-cause mortality (RR 1.35; 95% CI, 1.18-1.54). [ 43] On the other hand, in end-stage renal disease patients on dialysis—a population characterized by a particularly high mortality rate—a mild elevation of serum magnesium appeared protective against cardiovascular mortality but not associated with better overall survival. [ 44] A higher magnesium level, however, is associated with a better nutritional status in end-stage renal disease, which may confound this relationship. [ 45]
Finally, in dialysis patients, accumulation of anions that bind with magnesium may often result in a disconnect between the measured magnesium concentration and the biologically active ionized magnesium fraction. The ionized magnesium concentration may be low or normal, even when the total magnesium concentration is elevated. [ 46]
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Next: Renal Failure
Effects of Hypermagnesemia
Symptoms of hypermagnesemia usually are not apparent unless the serum magnesium level is greater than 2 mmol/L. Concomitant hypocalcemia, hyperkalemia, or uremia exaggerate the symptoms of hypermagnesemia at any given level.
Neuromuscular symptoms
These are the most common presenting problems. Hypermagnesemia causes blockage of neuromuscular transmission by preventing presynaptic acetylcholine release and by competitively inhibiting calcium influx into the presynaptic nerve channels via the voltage-dependent calcium channel. [ 47]
One of the earliest symptoms of hypermagnesemia is deep-tendon reflex attenuation. Facial paresthesias also may occur at moderate serum levels.
Muscle weakness is a more severe manifestation, occurring at levels greater than 5 mmol/L. This manifestation can result in flaccid muscle paralysis and depressed respiration and can eventually progress to apnea.
Paralytic ileus develops from smooth-muscle paralysis. [ 19] Pregnant women treated with magnesium sulfate for suppression of preterm labor are at risk. [ 48]
Conduction system symptoms
Hypermagnesemia depresses the conduction system of the heart and sympathetic ganglia. [ 47] A moderate increase in serum magnesium can lead to a mild decrease in blood pressure, and a greater concentration may cause severe symptomatic hypotension. Magnesium is also cardiotoxic and, in high concentrations, can cause bradycardia. [ 49] Occasionally, complete heart block and cardiac arrest may occur at levels greater than 7 mmol/L.
Hypocalcemia
Normally, a decrease in the plasma concentration of calcium will stimulate the secretion of parathyroid hormone (PTH). In patients with end-stage renal disease, however, high magnesium levels may suppress PTH secretion, [ 50, 51] This may contribute to hypocalcemia in this population.
Nonspecific symptoms
These symptoms include the following:
Shortness of breath
Nausea
Vomiting
Cutaneous flushing
Hypermagnesemia may interfere with blood clotting through interference with platelet adhesiveness, thrombin generation time, and clotting time.
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Next: Renal Failure
Diagnosis and Summary
Hypermagnesemia usually results from a combination of excess magnesium intake and a coexisting impairment of renal function. Diagnosis is usually straightforward and involves measuring serum magnesium levels, as many cases are unsuspected. [ 52] If a magnesium level is not immediately available, a clue to the existence of hypermagnesemia would be the disease context (preeclampsia, renal failure), the presence of magnesium-containing preparations, or a decreased anion gap.
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Next: Renal Failure
Prevention and Treatment of Hypermagnesemia
Prevention of hypermagnesemia is usually possible. Anticipate hypermagnesemia in patients who are receiving magnesium treatment, especially those with reduced renal function. Initially, withdraw magnesium therapy, which often is enough to correct mild to moderate hypermagnesemia.
In patients with symptomatic hypermagnesemia that is causing cardiac effects or respiratory distress, antagonize the effects by infusing calcium gluconate. Calcium antagonizes the toxic effect of magnesium, and these ions electrically oppose each other at their sites of action. This treatment usually leads to immediate symptomatic improvement. In subjects with frankly impaired ability to excrete magnesium (eg, end-stage renal disease), renal replacement therapy may also be necessary.
Drug Category: Diuretics
Agents that promote magnesium excretion are effective in treating hypermagnesemia.
Furosemide (Lasix) may promote excretion of magnesium. It increases excretion of water by interfering with the chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.
Drug Category: Calcium salts
Calcium may moderate nerve and muscle performance in hypermagnesemia.
Calcium gluconate (Kalcinate) directly antagonizes neuromuscular and cardiovascular effects of magnesium. Use in patients with symptomatic hypermagnesemia that is causing cardiac effects or respiratory distress.
Drug Category: Antidiabetic agents
Agents that shift magnesium ions into cells are helpful in treating hypermagnesemia.
Glucose and insulin may help promote magnesium entry into cells. Glucose should be administered with insulin to prevent hypoglycemia. Monitor blood sugar levels frequently.
Previous
References
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Quamme GA. Control of magnesium transport in the thick ascending limb. Am J Physiol. 1989 Feb. 256 (2 Pt 2):F197-210. [Medline].
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Bringhurst FR, Demay MB, Krane SM, et al. Bone and mineral metabolism in health and disease/hypermagnesemia. Kasper DL, et al, eds. Harrison's Principles of Internal Medicine. 16th ed. New York, NY: McGraw-Hill; 2005. 2245.
Mori H, Suzuki H, Hirai Y, Okuzawa A, Kayashima A, Kubosawa Y, et al. Clinical features of hypermagnesemia in patients with functional constipation taking daily magnesium oxide. J Clin Biochem Nutr. 2019 Jul. 65 (1):76-81. [Medline].
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Sugiyama M, Kusumoto E, Ota M, Kimura Y, Tsutsumi N, Oki E, et al. Induction of potentially lethal hypermagnesemia, ischemic colitis, and toxic megacolon by a preoperative mechanical bowel preparation: report of a case. Surg Case Rep. 2016 Dec. 2 (1):18. [Medline]. [Full Text].
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Schmid-Elsaesser R, Kunz M, Zausinger S, et al. Intravenous magnesium versus nimodipine in the treatment of patients with aneurysmal subarachnoid hemorrhage: a randomized study. Neurosurgery. 2006 Jun. 58 (6):1054-65; discussion 1054-65. [Medline].
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Author
Tibor Fulop, MD, PhD, FACP, FASN Professor of Medicine, Department of Medicine, Division of Nephrology, Medical University of South Carolina College of Medicine; Attending Physician, Medical Services, Ralph H Johnson VA Medical Center
Tibor Fulop, MD, PhD, FACP, FASN is a member of the following medical societies: American Academy of Urgent Care Medicine, American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society for Apheresis, International Society for Hemodialysis, Magyar Orvosi Kamara (Hungarian Chamber of Medicine)
Disclosure: Nothing to disclose.
Coauthor (s)
Sohail Abdul Salim, MD, FASN, FACP Consultant Physician, Central Nephrology; Affiliate Faculty, Department of Internal Medicine, Division of Nephrology, University of Mississippi Medical Center
Sohail Abdul Salim, MD, FASN, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, Mississippi State Medical Association, Renal Physicians Association
Disclosure: Nothing to disclose.
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine
George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, National Kidney Foundation
Disclosure: Nothing to disclose.
Chief Editor
Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Interim Chair, Deming Department of Medicine, Tulane University School of Medicine
Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.
Additional Contributors
Mahendra Agraharkar, MD, MBBS, FACP, FASN Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology
Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation
Disclosure: Nothing to disclose.
Anil Kumar Mandal, MD Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida College of Medicine
Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, Central Society for Clinical and Translational Research
Disclosure: Nothing to disclose.
Mark T Fahlen, MD Private Practice, Mark T Fahlen, MD, Inc
Mark T Fahlen, MD is a member of the following medical societies: American College of Physicians, Renal Physicians Association
Disclosure: Nothing to disclose.
Biruh T Workeneh, MD, PhD, FASN Associate Professor of Medicine, University of Texas MD Anderson Cancer Center
Biruh T Workeneh, MD, PhD, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology
Disclosure: Nothing to disclose.
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Sections Hypermagnesemia
Overview
Renal Failure
Other Causes
Effects of Hypermagnesemia
Diagnosis and Summary
Prevention and Treatment of Hypermagnesemia
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msmarco_passage_01_502493987 | Cost of Blood Tests - 2021 Healthcare Costs - CostHelper | Cost of Blood Tests - 2021 Healthcare Costs - CostHelper
CostHelper > Health & Personal Care > Tests, X-Rays & Imaging > Blood Tests
Blood Tests Cost
How Much Do Blood Tests Cost?
With Health Insurance: Copays of $0-$30 or 10%-50+% Coinsurance
Total Costs: $100-$3,000+ Without Insurance
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Blood tests can measure cells, lipids, proteins, sugars, hormones, tumor markers and other blood components. They are used to diagnose and treat of many diseases including diabetes, high cholesterol, thyroid disease and cancer.
Typical costs:
CostHelper readers with insurance report out-of-pocket costs of $283-$675 for blood tests, with an average of $432; total billed costs were $312-$1,200 (averaging $755 ), with the insurance either paying or discounting the total cost by $29-$525.
For patients covered by health insurance, out-of-pocket costs for blood work typically consist of a copay ranging from nothing to $30 or more, or coinsurance of 10%-50% or more; deductibles and out-of-pocket maximums will apply.
Blood tests are often covered by health insurance for preventive, diagnostic or treatment purposes, but coverage depends on the individual case and the terms of the health insurance plan.
CostHelper readers without health insurance report total costs of $700-$2,589, averaging $1,543. For patients not covered by health insurance, total costs can be $100-$3,000 or more, depending on the number and type of tests ordered; the cost of any doctor visits to order and interpret the tests; and whether the tests are done on an emergency basis.
Routine blood work done as part of an annual physical or a new patient exam can cost $100-$1,000 or more. Often ordered in connection with an annual physical, a complete blood count (CBC) test alone can cost $10-$150 or more.
Depending on the patient's symptoms, doctors typically order multiple tests to check for a number of conditions; comprehensive panels of tests can cost $80-$1,500 or more, and combining several testing packages can bring total costs to $1,500-$2,700 or more.
Related articles: Antibody Test, PSA Test
What should be included:
Before any blood test, the patient typically will be given instructions to follow, such as fasting for a certain number of hours. The medical provider then draws blood and sends it to a laboratory for analysis. Results usually are provided to the patient and/or their doctor within a few days to a week.
The National Institutes of Health lists types of common blood tests [ 1] .
Additional costs:
Depending on the results, the doctor may recommend additional testing.
Discounts:
The U.S. Department of Health and Human Services offers a locator [ 2] for clinics providing services on an income-based sliding scale.
Many hospitals offer discounts of up to 50% for uninsured/self-paying patients. For example, St. Joseph Hospital [ 3] in Orange, CA discounts its billed charges by 45%.
Shopping for blood tests:
Patients with health insurance that requires them to use "in network" providers should check whether a specific lab is within the network; a doctor who works within an insurance plan might, without checking, refer patients to a lab that isn't covered under that plan. Always double-check for insurance coverage before any blood work is done.
Blood tests can be done at the office of a primary care provider or specialist, in a clinic or in a hospital.
For patients who want anonymity or do not wish to go through a doctor, companies such as LabCorp [ 4] , Quest Diagnostics [ 5] and Health Testing Centers [ 6] offer laboratory testing direct to patients. However, it is important to seek the advice of a doctor for any health concerns.
Material on this page is for informational purposes only and should not be construed as medical advice. Always consult your physician or pharmacist regarding medications or medical procedures.
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What People Are Paying - Recent Comments
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Whoa! Too much.
Amount: $812.02
Posted by: Heartfailure121 in Morris, IL.
Posted: May 3rd, 2021 11:05AM
Medical Center: Morris Hospital
Type of Blood Test: Full Panel
Ridiculous.
W.O. insurance : $2,822.06
With Insurance: $812.02
Sounds like double billing insurance fraud.
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Medicare didn\'t cover blood tests for annual wellness
Amount: $0.00
Posted by: TimR in Greenville, TX.
Posted: June 10th, 2019 05:06PM
Medical Center: Lab Corp
Type of Blood Test: Annual Wellness
I have learned for any Medicare work to be careful: The patient authorization/sign up sheet typically has a phrase that if Medicare doesn't cover a cost, I will pay for it. I scratch this out and write that I decline and do not authorize any tests, treatments or other expenditures not covered by Medicare. I cannot afford them. I do not understand what is and is not covered. That is the responsibility of those offering the service to determine in advance. I now do this on every Medicare service. So far, no one has turned me down. I also request a copy of the document. In 2017 I received a bill from Labcorp for about $500 in blood work not covered by Medicare. I referred to my written document showing this was an unauthorized service, that I did not have the means to pay for it, and I was refusing to. After a few phone calls they admitted it was their mistake and cancelled the charges. I would rather find someone willing to do this than get caught with bills I can't pay.
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Portneuf medical hospital ER
Amount: $210.00
Posted by: Gino Smile in Pocatello, ID.
Posted: May 16th, 2019 11:05AM
Medical Center: Portneuf Medical Center
Type of Blood Test: 6 blood tests
they told us that the bill for the ER visit was only $210. later on we receive a bill for $1000. i got around 4-6 blood tests. all im mad about is that they lied to us.
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MYRTLE BEACH SC
Amount: $1,276.00
Posted by: Guy Majewski in Conway, SC.
Posted: January 21st, 2019 01:01PM
Medical Center:
Type of Blood Test: ANNUAL
SUPRISED THAT IT COSTS $1276 WHEN USING INSURANCE. COPAY WAS $176. LOOKING AT OTHER POSTS, I GUESS I GOT A (DEAL?)
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Blood testing
Amount: $299.00
Posted by: a user in Paramus, NJ.
Posted: May 29th, 2018 12:05PM
Medical Center: Lab Corp
Type of Blood Test:
I have medicare and supplemental insurance. I am being charged $299 for 4 blood tests that medicare did not cover. I don't know if my doctor screwed up on requesting the tests. This is total BS. Pay for medicare insurance & supplemental insurance and still get a bill. Why $299 for 4 blood tests with insurance?
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outrageous mark ups
Amount: $80.00
Posted by: DMR in aurora, IL.
Posted: May 12th, 2018 10:05AM
Medical Center: labcorp
Type of Blood Test: PT
Patient went where he was directed to go and his out of pocket was marked up about 80 to 90% in my experience as a Phlebotomist working with various Labs
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Small town NE Missouri hospital ridiculously costly and tests are unknown
Amount: $0.00
Posted by: MissSweet in Kirksville, MO.
Posted: March 22nd, 2018 02:03AM
Medical Center: Northeast Regional Medical Center
Type of Blood Test: Have yet to disclose that information me
Got a bill with no information about tests or cost of each, how many, what kind, information at the hospital was withheld until I got my bill... $6,187.97
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Price Pressure, blood work, and pricing models
Amount: $180.00
Posted by: hlc in Houston, TX.
Posted: February 10th, 2018 09:02AM
Medical Center: Labcorp
Type of Blood Test: Various
My insurance carrier initially refused payment due to a clerical error on their part. The bill from labcorp rolled in at $980. Months later and weeks from going to collections, insurance company corrected error and reprocessed, and amount reduced to $180 per negotiated discount with carrier. I got curious and have researched this issue extensively and have learned that both Labcorp and Quest offer a 45% discount for uninsured, but that you have to work with your doctor and the lab to get the discount. I also checked with multiple online web labs and have uncovered that discounts for the same tests from retail range from as little as 25% to a high of 43%. The marketing is sleek, but the pricing model is straight forward. The labs themselves are milking the uninsured by greater than 230% from those who know how to negotiate this mine field and the on-line labs are simply marking up a few points over the lab providers' uninsured discount. As for those who don't know, the markup is 540%
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Two Separate labs panel from one visit
Amount: $5,818.00
Posted by: GodBless Us in Lebanon, NH.
Posted: January 17th, 2018 07:01PM
Medical Center: By Doc and Hospital
Type of Blood Test: CBC, Thyroid, Hormone
Why is blood lab work so freaking expensive?
During one visit with Doc, my EOB from Ins. Company showed Doc Blood full CBC @ 900., Hospital Lab @ 4,918. Really? Three viles with Doc at one visit. What does it mean, Doc looked at one and sent two to Hospital? Who controls these outrageous fees? Thank God we have Insurance; billed 333. How do they get away billing it? God Bless America!
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Veterans' Health Clinic
Amount: $0.00
Posted by: Gary Jacobsen in Woodbridge, VA.
Posted: December 6th, 2017 09:12AM
Medical Center: Ft Belvoir VA
Type of Blood Test: Full panel
The Dept of Veterans' Affairs has various clinics that provide comprehensive care and blood tests for veterans. Mine is at Ft Belvoir, VA, and they do all tests for me at no cost. I then take test results to my civilian doctor.
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RIP OFF largest ever!
Amount: $4,780.00
Posted by: JOHN R PIEDRA in Charlottesville, VA.
Posted: November 11th, 2017 09:11AM
Medical Center: UVA Kidney Center
Type of Blood Test: CBC, TAC
I have had well over 50 blood tests since Kidney Transplant, each costing around $125 or less., $40 out of pocket after Insurance. UVA charged me $4,780 for exact same testing, and my out of pocket is $820 ! OUTRAGEOUS, NOT paying, and contacting State Attorney General
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Outrageous!
Amount: $5,302.92
Posted by: Chris B. in Glendale, AZ.
Posted: November 6th, 2017 10:11PM
Medical Center: Abruzzo Arrowhead
Type of Blood Test: CMP, CBC,Lipase
Went to the ER for pelvic pain. I was billed:
$92.82 for a liter of normal saline (IVF)
$732.12 for a CMP
$101.20 for a urinalysis
$250.47 for a CBC
$169.20 for a PT
$616.31 for "IV HYD INT >31M"
$350.66 for a lipase
$866.52 for "ABD ACUTE COMP"
and a whopping $2123.62 "for ER visit level IV"
... I was only in the ER for 2 hours, the "doctor"
examined me THROUGH MY CLOTHES (!), and then separately billed me over $500.00 for that "exam".
Thoroughly criminal, in my opinion.
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Blood work
Amount: $2,342.67
Posted by: Jonathon in Meriden, CT.
Posted: August 2nd, 2017 06:08PM
Medical Center: Quest diagnostics
Type of Blood Test: Lupus full screen
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Blood test order for an ovavian cyst
Amount: $1,495.00
Posted by: Molly Brown in Frederick, MD.
Posted: June 23rd, 2017 10:06AM
Medical Center: Woman Health Specialists
Type of Blood Test: CA 125
How can one blood test cost that much money...horrible.
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Blood Panel Cost
Amount: $187.00
Posted by: Bur1yman in Chicago, IL.
Posted: February 22nd, 2017 01:02PM
Medical Center: Northwestern Memorial
Type of Blood Test: Basic
In October, a full workup cost me $30 out of pocket. I just got a basic workup in Jan. after being put on blood meds and it cost me $187. Why so much for a more basic test?
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Newman memorial hospital -rip off
Amount: $1,800.00
Posted by: Care in Not sure, OK.
Posted: February 7th, 2017 03:02PM
Medical Center: Newman memorial hospital
Type of Blood Test: Thyroid, urine
My dr started using the facility for lab work. I have never been charged this much before, and can't afford to pay it, haven't worked since October. The hospital told me they actually out source it to someone else in another state, I called them to get a explanation but nobody answers.
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Outrageous lab fees
Amount: $7,939.32
Posted by: Cindy Bonyata in Houston, TX.
Posted: January 26th, 2017 01:01PM
Medical Center: Southwest Laboratory
Type of Blood Test: CBC
Simple CBC was ordered for unknown reasons by my pain mgmt dr. Won't send to my in network Labcorp - and charged a whopping $7939.32. Insurance wouldn't pay bc out of network. Now sending me the bill for a reduced $329.87! Um NO. I have a zero copay and excellent insurance. This is such a ripoff and I'm shutting them down.
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CLL profile blood test
Amount: $0.00
Posted by: Joan G. in Garner,, NC.
Posted: November 26th, 2016 08:11AM
Medical Center: Wake Med Garner, NC
Type of Blood Test: CLL
My insurance company was billed $3,220 for this test. They paid $643.80. This was not for a group of tests. The amount charged is outrageous. I don't think the hospital or doctors see or are aware of these excessive amounts. I feel the patient must stand up for the insurance company in these circumstances. The testing company is NeoGenomics Labs in Orlando, FL
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No brainer
Amount: $400.00
Posted by: No-lateral Pulmonary Embolism in Ocala, FL.
Posted: October 12th, 2016 03:10PM
Medical Center: Ocala Regional
Type of Blood Test: ABG
$400 co-payment BC/BS at hospital
The facility that ordered the ABG test won't do it because of type of insurance, but will do it if I pay cash. For a whopping $108. Gees where should I go, just a word of advice to people call around for prices if you can't get a price google it to get an idea.
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They ran every test possible...
Amount: $9,800.00
Posted by: Chelley in Clarksvile, TN.
Posted: June 23rd, 2016 10:06AM
Medical Center: Dr. Standley True Health Diagnostics
Type of Blood Test: Every test they could do
It was supposed to be basic bloodwork for wbc, and then thyroid level . Turns out they sent out my blood for every possible test and I wasn't informed. I now have a bill for something I won't be able to pay off.
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Blood test
Amount: $179.00
Posted by: Z Ali in Memphis, TN.
Posted: May 20th, 2016 06:05AM
Medical Center: Prime urgent medical
Type of Blood Test: Comprehensive
I got my blood test through this location for $179.
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Insane
Amount: $860.00
Posted by: insane cost in Cartersville, GA.
Posted: May 13th, 2016 02:05PM
Medical Center: Cartersville medical center
Type of Blood Test: HCG Beta - pregnancy test
Got an itemized bill from a recent ER visit. On top of charging me for medications (and a seperate charge for administering those medications) that I NEVER received, they charged $860 for a pregnancy test!
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blood test
Amount: $900.00
Posted by: DNYANPAL KOKRE in CHANDRAPUR, MS.
Posted: December 10th, 2015 09:12PM
Medical Center: sachin pathology
Type of Blood Test: b +ve
i want to know charge of blood of kft lft cbc
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QUESTLAB
Amount: $417.00
Posted by: MARIA GABRIELA CICARELLI in miami, FL.
Posted: November 3rd, 2015 11:11AM
Medical Center:
Type of Blood Test: CHOLESTEROL
Is outrageous how much the above entity is charging me the lab fees are totally inflated please send someone to check this company
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NEVER AGAIN AT Arcadia,CA Methoist Hospital of Southern CA
Amount: $0.00
Posted by: R. Exasperated in Arcadia, CA.
Posted: September 2nd, 2015 07:09AM
Medical Center: Methodist Hospital of So CA 91007
Type of Blood Test:
On order of Internist, for fulltime employed / ambultory/fully cognitive 66 year- old male not yet on Medicare.but has PPO insurance and confirmed Dx of HCM. No personal or family history/symptoms of Autoimmune Disease,Arthritis, Thyroid or kidney disease. Went to Methodist Hospital of So Cal,Arcadia,CA 91007 for outpatient routine draw of lab tests. With our PPO insurance I have listed the tests ordered,indication for tests, and cost to us AFTER INSURANCE : Free T4 (thyroid panel) $218.00; Sed rate-E- (sed rate test can't pinpoint problem that's causing inflammation in your body)-Sterling labs online charges $26; Meth.Hospital in 91007, $145.00, RF (rhematoid arthritis)$135, TSH (thyroid) $364.00, Vit B12-CYA for kidney disease $250. AntiNuclear AB, for autoimmune disease $12, Venipuncture $36-just to draw the blood for above tests=lab invoice is for a whopping $1160 after insurance!!! Thinking this facility wants us to pay for all Illegals or unemployed living here. NOT FAIR.
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Blood Test
Amount: $615.95
Posted by: Cierah in Clarion, PA.
Posted: May 15th, 2015 10:05AM
I was having problems with my foot. My foot was cold all the time and everything so I had a very large variety of test done the original cost without insurance is $2,579 but how can these texts cost so much!!
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Doctors in Florida May Not Upcharge Lab Fees when Patients Pay Cash
Amount: $0.00
Posted by: Dr Neal Wieder in Lake Mary, FL.
Posted: February 24th, 2015 04:02AM
Medical Center: Dr Wieder
Type of Blood Test: Varied
In the state of Florida ALL doctors may not Upcharge the cost of lab tests for cash patients unless they have their own lab. ie- a urine test done in office can be upcharged
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rip off
Amount: $1,350.00
Posted by: george smith in branson, MO.
Posted: February 22nd, 2015 04:02PM
Medical Center: cox
Type of Blood Test: cmp lipids testo
1350.00 after insurance hold on to your ass never again
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blood test for MMA
Amount: $439.00
Posted by: internetsurfer in Prineville, OR.
Posted: February 11th, 2015 07:02AM
Medical Center: mosiac medical
Type of Blood Test: infectious diseases
my brother had some blood testing done for infectious diseases so he could fight in an mma match, because this was non medical he was charged full price and paid out of pocket, total costs coming to 495 at a sliding scale clinic.
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Brazelia Med Spa complete in depth testing 1-16=2015
Amount: $3,019.00
Posted by: Sagwa in BOCA RATON, FL.
Posted: February 6th, 2015 01:02AM
Medical Center: Brazelia Med Spa
Type of Blood Test: lipids thyroid, vitamins, full panel gen
I went to Dr Brazelia for a free consultation for hormone and weight issues. Dr Brazelia was very holistic and knowledgeable in regards to correct nutrition and treating the whole person. She told me that my insurance would pay for the Blood Tests and I had a VERY thorough result packet with clear information, in fact each section had a green yellow or red level number indicating problem severity to normal with explanations.It included not only the numbers/levels but also genetic markers. My issue is my insurance DIDN'T Pay even though she told me it would. When she prescribed a 1 week cleanse based on the outcome of the tests and to start a diet program, which was way overpriced, I was told that my insurance didn't cover office visits and the diet things. I do not think its fair that she did the blood tests without approval from my insurance when she said it was covered. I need to work this one out with them somehow. I also agree with others here who think pricing should be up front
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blood test
Amount: $1,350.00
Posted by: I'm so screwed in Omaha, NE.
Posted: January 20th, 2015 07:01PM
Medical Center: Frontier
Type of Blood Test: "full panel"
When I had "a full panel" done a few years ago, all I had was a $25 copay. Now, my psychiatrist wanted to figure out if some of my symptoms were caused by something else. He gave me a note and told me to take it "anywhere that does blood tests." I went to a local urgent care clinic, and after about an hour of stalling, they said they would do it, but they couldn't guarantee how it would come out on billing because none of THEIR doctors had ordered it. By then I just wanted it to be over, so I let them take my blood. A couple months later, I find out that before insurance it was $3300, so $1300 (after insurance) is such a steal, right? We're already on a fixed income. Is there actually a way to argue this down?
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22 tests
Amount: $0.00
Posted by: elyn in paso robles, CA.
Posted: January 7th, 2015 04:01PM
It takes up to a month to see if my insurance will pay anything on all my blood work. And I am not sure what tests were done.
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Blood test
Amount: $447.17
Posted by: K_rel in Lubbock, TX.
Posted: December 22nd, 2014 05:12PM
Medical Center: Texas Tech Physicians
Type of Blood Test: 1st blood check for pregnant women
On my first appointment with the OBGYN for my pregnancy, they told me to do a blood test on location. I went the lady said the amount due was $60 with my insurance. Then two weeks later I receive a statement asking me to pay $447.17, and it bill does not even explain in detail why it is so high. I am a college student how do they think I am gonna get all that. In my country I would only pay $100 max for that same test. I am pissed off!!
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Blood test cost ...
Amount: $2,700.00
Posted by: Trump01 in Huntsville, AL.
Posted: December 4th, 2014 01:12PM
Medical Center: Crestwood Medical Center
Type of Blood Test: Comb Metab, lipid, thyroid, cbc
Do you believe it $2700…. clearly when medical facilities have exorbitant pricing - prices should be posted. When I go to Walmart - I see what things cost, also at Belks. Medical consumers should have the right to see pricing as well. We must give our life to register - license, medical card, list any and all people we have ever known. But we get little to NO info. So we can say no thanks - going down the road! Im new to the region and feel totally taken. BTW - I have insurance and my portion was over $800
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msmarco_passage_01_502947046 | Cost of Dental Implants - 2021 Healthcare Costs | Cost of Dental Implants - 2021 Healthcare Costs
CostHelper > Health & Personal Care > Dentistry & Orthodontics > Dental Implants
Dental Implants Cost
How Much Do Dental Implants Cost?
Single Dental Implant Average Cost: $2,488
Abutment, Implant and Crown Average Cost: $4,263
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A dental implant functions as an artificial root to anchor a replacement tooth or teeth. A small titanium post is surgically implanted in the jawbone, and as part of the healing process it bonds with the bone. A metal abutment is connected to the implant, and then a crown, bridge or denture is attached to the abutment. The work is typically done in stages, often with separate prices for the implant surgery, the abutment placement and the replacement tooth or teeth. There may also be a charge for a temporary "flipper" tooth while the jaw heals after surgery.
Typical costs:
A single implant typically costs $2,400-$3,000, but can be $4,000-$10,000 or more if additional procedures like extractions, bone grafts, tissue grafts or a sinus lift are needed. CostHelper readers report paying $1,000-$5,000 for an implant with an average cost of $2,488.
Placing an abutment and a dental crown on a single implant typically adds $500-$3,000 to the cost of just the implant, for a total of $1,500-$13,000 or more. CostHelper readers report paying $1,750-$8,270 for an implant, flipper tooth, abutment, crown and all needed procedures, with an average cost of $4,263.
Two to six implants topped with a partial or full-mouth dental bridge can cost $3,500-$30,000 or more, depending on the number of implants, bridge size and materials, and any other needed procedures. CostHelper readers report paying $4,000-$16,000 for a three- or four-tooth bridge on two implants, with an average price of $8,486.
Two to six implants with a removable denture plate can cost $3,500-$30,000 or more depending on the number and type of implants (mini-implants are less expensive), denture materials (in some cases an existing denture plate can be adapted for use with implants) and any other procedures needed. A full set (upper and lower) of implants and dentures can cost $7,000-$90,000 or more. CostHelper readers report paying $3,800-$27,858 for implants with a single denture plate, at an average cost of $14,226; and $6,549-$80,000 for a full set of implant-supported dentures (upper and lower), for an average expense of $34,119.
Dental insurance typically does not cover implants, because most insurance companies categorize implants as cosmetic procedures. However, some surgical costs might be covered by health insurance.
Related articles: Dental Veneers, Root Canal, Dental Crown, Tooth Extraction, Dentures, Dental Bridge
What should be included:
Implant surgery is typically performed by a dental surgical specialist -- a periodontist, an oral surgeon or a dentist with advanced training in implant surgery. Abutments and implant-supported crowns, bridges or dentures are typically placed by a dentist or a prosthodontist (specializing in restorative procedures). The International Congress of Oral Implantology has an overview of dental implants [ 1] .
Typically the implant site is allowed to heal for three to six months after surgery and one to two weeks after the abutment is placed. A temporary "flipper" tooth may be worn during this period. Although there are "instant" mini-implants where a bridge or denture is installed immediately after implant surgery, the standard process (including bone and tissue grafts or other procedures, if needed) takes three months to a year or more to complete. The Mayo Clinic explains what to expect [ 2] after dental implant surgery.
Additional costs:
Ask detailed questions about what is included in a price quote. An estimate for an implant may not include the abutment and crown.
Discounts:
Dental school clinics [ 3] offer reduced rates for services by supervised students or faculty. A CostHelper reader in North Carolina reports paying $60 for an extraction, $75 for a bone graft, $1,200 for a single implant and $600 for a crown at the University of North Carolina. Another reader was quoted $75,000 by a private dentist but paid about $20,000 to have the work done at the University of Medicine and Dentistry in New Jersey.
The National Institute of Dental and Craniofacial Research provides tips for finding low-cost dental care [ 4] .
Shopping for dental implants:
A comprehensive dental exam (with X-rays and possibly a CT scan, plus models made of the patient's mouth) is used to create an individualized treatment plan. The Mayo Clinic explains what to expect before dental implant surgery [ 5] .
If insurance coverage is available for any portion of the process, the company will provide a list of approved dentists and specialists. Or search for local members of the American Academy of Implant Dentistry [ 6] , the American Academy of Periodontology [ 7] , the American Association of Oral and Maxillofacial Surgeons [ 8] , the American College of Prosthodontists [ 9] , the American Dental Association [ 10] or the International Congress of Implantologists [ 11] .
Material on this page is for informational purposes only and should not be construed as medical advice. Always consult your physician or pharmacist regarding medications or medical procedures.
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Why is dental insurance stuck in the 80\'s?
Amount: $55,000.00 not covered by insurance
Posted by: Frogsoup09 in St. Louis, MO.
Posted: December 2nd, 2020 01:12AM
Which Tooth: upper and lower implants needed
In 1986, I started my first full time Big Girl job, which came with options for medical insurance that ranged from "Volkswagon to Cadillac, and everything in between" which was up to me to choose based on my needs, what I could afford, etc. However, there was only 1 option for dental coverage, and it was the same as any you have ever heard of, 2 free annual cleanings, fillings at 80%, root canals and crowns covered at 50%, TO A MAX OF $1000 per year paid by the dental plan. Here it is 35 years later, and the dental plans are still EXACTLY THE SAME, STILL ONLY $1000 max insurance per year! EVERYTHING IN THE WORLD HAS GONE UP IN PRICE TREMENDOUSLY SINCE 1986, SO WHY IS DENTAL COVERAGE STILL ONLY A MAX OF $1000 PER YEAR???????????? And I hear, read, see, all the time, "dental problems can impact your entire body, from the heart, to organs, digestive, and nervous systems." If dental health is so important to well being, why won't insurance companies catch up with the times?
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One implant, 4 crowns
Amount: $4,800.00 not covered by insurance
Posted by: 5k less for retirement in Portland, ME.
Posted: November 11th, 2020 02:11PM
Which Tooth: 4 front
I cracked a front tooth, on a Kind bar of all things, and was told it could not be saved. Already had 3 front crowns that were over 10 years old so I decided to replace them at the same time as the implant. The cost was $7800 for all however I did it over 2 years so I could use my full dental benefit of $1500 per year. Stretching it out helped and I took money from my 401k to pay the rest. Hopefully these last for at least 20 years,started at age 59.
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Two implants in Mexico 🇲🇽
Amount: $3,700.00 not covered by insurance
Posted by: Jenni Murnin in Cancun, TX.
Posted: March 19th, 2020 10:03AM
Which Tooth: Back left two teeth bridge
So happy with Cancún Ocean Dental! All the people in the building are very professional and I felt extremely comfortable with all dentists in Implantology’s that I came into contact with. It does get a bit busy around Christmas and in the milder months. I noticed there were a lot of winter Texans in Mexico period. I need to go back to Cancun and get two more months for 2 implants. Really happy 😃
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Teeth
Amount: $2,000.00 not covered by insurance
Posted by: Carol Shaffer in Woodbridge, VA.
Posted: January 25th, 2020 06:01PM
Which Tooth: Molar’s top right
Need crown
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Nuts
Amount: $8,000.00 not covered by insurance
Posted by: Michael D in Raleigh, NC.
Posted: January 21st, 2020 11:01AM
Which Tooth: Front
It cost 611.00 for an implant in Budapest, Hungry. Take a trip... get your teeth fixed. There is a lot of greed here.
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Clear Choice Dental Implants
Amount: $20,000.00 not covered by insurance
Posted by: Milana Wilson in Cleveland, OH.
Posted: October 3rd, 2019 05:10AM
Which Tooth: four bottom teeth
I had my grandma's implants done with Clear Choice Cleveland. Her gums kept bleeding even after 2 years after the procedure. We called Clear Choice main office and were sent to another office and so on, and so on. We ended up going to another clinic and redoing the teeth. I would not recommend this company.
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High cost of dental implants and dental work in general
Amount: $1,000,000.00 not covered by insurance
Posted by: Gave up my 20's in Chicago, IL.
Posted: May 24th, 2019 01:05PM
Which Tooth: All
No disrespect to anyone needing dental care or teeth replaced with implants. I knew in my teens I wanted to be a dentist after having a great relationship with my orthodontist. I said no to many fun and material things as I was studying hard, working hard to pay for school tuition, books and living expenses, borrowing money for student loans and going to school for 8 years after high school just so I could graduate over $125,000.00 in debt in 1989. Then, I had to borrow another $500,000.00 to buy all the equipment, supplies, and construction costs to build my office-not knowing if enough people were going to show up to pay their bill. Again, no disrespect, but most people in their 20's do not have the focus or work ethic to stay the course to become a successful dentist, plus the extra $100,000.00 in training and medical equipment necessary to be able to competently place implants. Let 1 thing go wrong and see who gets sued. Sorry, but I doubt any Dr are going to do it for free.
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dental implants
Amount: $0.00 not covered by insurance
Posted by: front teethonlynow in Santa Maria, CA.
Posted: March 11th, 2019 01:03PM
Which Tooth: any
Come on already...could this procedure plus the implants literally cost into the tens of thousands of dollars to manufacture and place in the patients mouth....I doubt it...The cost is quite ridiculous...and frankly way out of hand...too bad...
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Dental work in general
Amount: $1,000.00 not covered by insurance
Posted by: FreeFreeFree in Nashville, TN.
Posted: March 9th, 2019 04:03PM
I feel very blessed. I have only had to have a few crowns in my 55 years and fortunately I have a very honest, competent and ethical Dentist with strong morals and values.
Even so, I have spent thousands of dollars. But we’ll worth it and much less than it would have cost at most other rip off artists.
Here’s the real pisser. While I and all of you are paying thousands of hard earned dollars to keep up our teeth, there are thousands of low life punk ass thugs walking around with beautiful smiles they got while in jail. Yes, you and I paid for their nice smiles. While we’re working 40 + hours a week to support our families and pay our high insurance premiums, these low life, scum bucket pukes, who violated our rights, get three hots, a cot and free dental work. Along with all the other free things they get because their entitled.
Remember this the next time you have to finance 1,000’s of $’s to pay for your Med. Or dental work and then remember it again when you go to the polls t
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Needing help getting all my teeth surgically removed and need permit inplants put inn
Amount: $0.00 not covered by insurance
Posted by: Becky Murray in Scottsboro, AL.
Posted: January 29th, 2019 09:01PM
Which Tooth: All of them
No dentist will remove any of my teeth cause they r so bad and most of them r broke off below the gum line and I have no income and no insurance to cover them don't know what to do with out the help and I am in desperate need of getting them out and implants put in so please help me.
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UNC Dental School
Amount: $0.00 not covered by insurance
Posted by: nancy brown in Chapel Hill, NC.
Posted: January 21st, 2019 02:01PM
Which Tooth: any
Do not trust what this article says about UNC Dental School. I went there with a full mouth of teeth, after telling me it would be easier to pull some & that they were not needed, the teeth were pulled (and a lot of pain). Next came plan of treatment, partial for top, dentures for bottom (they said too many teeth had been removed). I put up $5,000 up front which was supposed to cover all. One tooth that they crowned to hold partial, caused severe pain, after 1 year of doing nothing, they decided I needed exploratory surgery which they told me would not come out of the money I had given them. After 3 surgeries, a lot more pain, I was told I needed to see another specialist & that I needed another $500 to see the specialist. I told them to take it out of $5,000, they told me that had been used for the surgeries & biopsies (biopsies & 1 surgery would have been covered by insurance had I gone to a REAL dentist). I left program. You get what you pay for-nothing. Plus my identity was stolen.
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All-on-4 Nobel Biocare (upper & lower) Jaw in India
Amount: $11,000.00 not covered by insurance
Posted by: Dorothy Wilson in Mansfield, OH.
Posted: July 13th, 2018 01:07AM
Which Tooth: All
I got all on 4 from Center for Dental Implants & Esthetics. They have a package $11000 which includes Nobel Biocare All-on-4 for both the jaws including Zirconia teeth. This was unbelievable till I actually got it. Over this I had travel & stay costs, which will be another 3K so in less than 15K I got NEW teeth.
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Crooked teeth
Amount: $10,000.00 not covered by insurance
Posted by: Miss Redmon in Ellenwood, GA.
Posted: June 25th, 2018 07:06AM
Which Tooth: Two uppers and Two lowers
I had no idea it was so expensive to have a beautiful smile. I need to replace teeth and in need of financial support, I do have dental ins but like MCHammer, they won't touch that.
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Why?
Amount: $0.00 not covered by insurance
Posted by: DJ Moores in Booneville, MS.
Posted: June 16th, 2018 08:06AM
Which Tooth: All
My heart goes out to folks on here begging for teeth.So to the ones begging,let me know how that goes.Im a middle class dad that is sitting here trying to figure out how to afford getting my teeth fixed.I need a full set.From what I learned,if you don't get implants on the bottom,you get bone lose and look like Herman the gummy monster.I also am from the South so my advise to you all asking for money.Dont,we may be poor in wealth but let's not loose our self respect.
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All-on four: One full arch of teeth, four dental implants
Amount: $40,000.00 not covered by insurance
Posted by: cataj3 in Montclair, CA.
Posted: April 8th, 2018 10:04PM
Which Tooth: All
All-on four: One full arch of teeth, four dental implants. I’ve recieved 2 identical quotes of $42,000 for All-on four dental implants.Most recent quote 3/2018. I have dental insurance which will cover up to $2000 of dental work, extractions etc... The dilemma I am having Is financing the $40,000. My monthly /annual income is more than sufficient to pay back a $40,000 loan yet I was denied the 2 times I applied. The credit reporting company, Experian, Didnt find any credit history? I NEED either a Co-signer or a lender willing to work with me. For example setting up automatic monthly payments either thru payroll deduction or Bank Acct defuction. I can pay $800 - $1200 /
month. Please help.
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Dental implants/upper denture
Amount: $14,000.00 not covered by insurance
Posted by: Marti Mueller in Highlands Ranch, CO.
Posted: April 8th, 2018 05:04PM
Which Tooth: All upper
I am in Denver,CO.area.I found an awesome dental implant specialist. His name is Dr.Ian Topelson in Auroara at AFFORDABLE DENTURES.Ge owns the practice so forget about bad things associated w affordable denture name. This is a pvt.Franchise .He tries to help people especially seniors who medically need implant dentures due to tooth loss, aging, bone loss.It cost me right around 10,600 to have 12 extractions, 5 implants, snap on upper denture. Bone implant. I had to finance it but might be able to recoup half thru Medicare.They give you a detailed report if anesthesia, surgery, bone grafting and all. I had gotten 3 estimates over past 2 years. I had 4 decayed post root canal upper teeth. 3 infected. Terrible pain. Difficulty eating.1 cracked tooth in half. The other 3 quotes were $20-30,000.Half of the problems with my teeth and jawbone were missed by other oral surgeons who did extract,implant, followed by snap fit denture ( ultimate fit best possible denture).so It is horrendously .
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permanent implants
Amount: $55,000.00 not covered by insurance
Posted by: CHULA in ladson, SC.
Posted: March 23rd, 2018 11:03AM
Which Tooth: both upper and lower
Hi my name is Delilah M.I am 57 years old oh my stars didn't know how much it cost just to be able to have smile and myself confidence back. I have insurance but will not pay for what I need. Lord is like buying a new car I really cant afford a new car let alone 55,000.00 for implants. I play the lottery just wishing and hoping that my time will come but here I am writing to see if anyone can help me in any way possible. I know that this is farfetched but so isn't winning the lottery. Thank you so much for reading this comment god bless you all and hope that you get the help you all need .
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Please help
Amount: $12,000.00 not covered by insurance
Posted by: Carly Cantrell in Knoxville, TN.
Posted: January 16th, 2018 12:01PM
Which Tooth: Upper dental implants
Hi My name is Carly Cantrell I'm 35, I need an upper full dental implant. This is so embarrassing and humbling. I hate to ask but is there anyone that can help me come up with $12,000.00 or can donate ANY amount? I would be so thankful. I have prayed, entered every dental cost I could find for years I've even wrote Oprah Lol.I don't have Anyone to ask or help me. I don't have dental insurance I receive $ 1500.00 a month income $735.00 for myself and $737 for my son (where his father passed away) If you don't trust sending me money you can pay it directly to the dental office. My email address is tregen@att.net Thank you, Carly
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5 Implants
Amount: $35,000.00 not covered by insurance
Posted by: DENIS HOFFMAN in Knoxville, AL.
Posted: December 16th, 2017 03:12PM
Which Tooth: 7 upper teeth
I had 6 upper and 6 lower existing baby teeth removed with cross ways impacted baby teeth upper and lower removed plus bone grafts ($9,500.00 surgery). Had 4 plus 1 single implant because of cracked broken tooth after start of process ($10,000.00). A 6 tooth bridge over 4 implants and a single tooth implant with abutments over each implant ($15,000)
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dental implants
Amount: $27.12 not covered by insurance
Posted by: Kirk thole in ElCerrito, CA.
Posted: December 6th, 2017 09:12PM
Which Tooth: a brand new smile
I need help to raise $30.000 for dental implants to get a new smile. I got medi-cal I was told implants not cover by medical I got Kaiser but Kaiser don't got a dental business.i did not purchase because I can't afford it.
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Had all teeth removed and dental implants put in
Amount: $38,000.00 not covered by insurance
Posted by: brock Kearsley in Phoenix, AZ.
Posted: November 9th, 2017 12:11PM
Which Tooth: All Teeth removed
I had it all done. I live in AZ. I got 3 quotes for full dental implants in AZ. They Ranged from $46000-$60,000. I got in touch with a friend who knew somebody in Salt Lake City that did implants. He did it for $38000. IT sucked because I had to stay in a hotel for a week after the implant surgery. But I saved $16000. I couldn't be happier. Its a lot of money but in the long run well worth it. I can eat and no more tooth pain. I can smile for pictures now.
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Amount: $22,000.00 not covered by insurance
Posted by: navigatrix in San Jose, Other.
Posted: October 20th, 2017 02:10PM
Which Tooth: All
After getting an estimate of $65,000 in Seattle for a whole smile makeover, I researched other countries and decided on Costa Rica. Best investment I ever made - 5 implants, new crowns on all my teeth, including some design to improve my bite (not included in the local estimate). Expert and qualified dental specialists, and lifetime guarantee.
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Dental Implants
Amount: $16,000.00 not covered by insurance
Posted by: babysrn in Las Vegas, NV.
Posted: October 11th, 2017 04:10AM
Which Tooth: 2 upper and 2 lower teeth
I had 4 dental implants before it was cool!! Sitting down? it was 4500 per tooth. That did include everything. Titanium rod, the surgery, and the tooth. I will say I have had no problems with the implants themselves. Care is just like your real teeth. I can eat a steak and corn on the cob as well. No worries.... It is so worth it just shop around for the best Dentist. Cheapest is not always the best to go with. Ask your friends for a referral . If you find someone you trust and have faith in keep him. Forever. One negative comment Every implant has a tooth next to it that has chipped or gotten a cavity . Dentist says it has nothing to do with the implants . Interesting . 4 issues with teeth next to 4 implants . I think it is likely there is a connection between the two. Its a lot of money but how important is it to have a great smile and be able to chew/ eat your food. That alone is priceless
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Dental Implants
Amount: $72,000.00 not covered by insurance
Posted by: Jack Sprat in Mulberry, FL.
Posted: September 3rd, 2017 12:09PM
Which Tooth: Backed out
Why do full dental implants cost more than purchasing a condominium?
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External Resources:
dentalimplants.com/understanding-dental-implants.php
www.mayoclinic.com/health/dental-implant-surgery/MY00084/DSECTION=what-you-can-expect
www.ada.org/267.aspx
www.nidcr.nih.gov/oralhealth/popularpublications/findinglowcostdentalcare/
www.mayoclinic.com/health/dental-implant-surgery/MY00084/DSECTION=how-you-prepare
www.associationdigital.com/aaid/online/findadoctor/searchinput.aspx
www.perio.org/?q=locator-advanced
www.aaoms.org/findoms.php
www.gotoapro.org/find-a-prosthodontist/
www.mouthhealthy.org/en/find-a-dentist.aspx
dentalimplants.com/search.php
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msmarco_passage_01_503448601 | Cost of Human Papillomavirus Vaccine - CostHelper | Cost of Human Papillomavirus Vaccine - CostHelper
CostHelper > Health & Personal Care > Vaccinations > Human Papillomavirus Vaccine
Human Papillomavirus Vaccine Cost
How Much Does Human Papillomavirus Vaccine Cost?
With Insurance: $30-$120
Without Insurance: $400-$500
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HPV vaccination protects against the four strains of the human papillomavirus (HPV) that cause most cases of genital warts and cervical cancer. The U.S. Centers for Disease Control and Prevention (CDC) recommends that all girls receive the HPV vaccine, also known by the brand name Gardasil, at age 11 or 12; however, it can be given any time between ages 9 and 26.
Typical costs:
For patients not covered by health insurance, the cost of HPV vaccination typically includes: shot administration fees and the cost of the three required doses of the vaccine at about $125 each, for a total of $400 to $500.
Many health insurance plans cover HPV vaccination, but only for females in the recommended age group. For example, Aetna [ 1] considers the HPV vaccination medically necessary for girls and women aged 9 to 26, so it is covered by plans that include preventive benefits. And it is covered by most BlueCross BlueShield of Rhode Island plans.
For patients covered by health insurance, typical expenses include a copay for each shot. For example, students covered under the student health plan at the Massachusetts Institute of Technology [ 2] pay $20 per shot for a total of $60. For any patient covered by health insurance whose out-of-pocket cost per dose is more than $30, Gardasil offers a rebate that will cover the remainder of the cost, up to $130.
Related articles: Health Insurance
What should be included:
The HPV vaccination requires three shots. The second shot is given two months after the first, and the final shot is given six months after the first.
The vaccine is almost 100 percent effective in protecting against the four targeted strains of HPV. According to the American Cancer Society [ 3] , almost all cervical cancers are related to HPV, and the vaccine will protect against the two types of HPV that cause 70 percent of all cervical cancers as well as the two types that cause 90 percent of all genital warts.
Additional costs:
HPV vaccination can be done at a routine doctor visit; otherwise, the doctor visit fee or copay will be an additional cost.
According to a CDC fact sheet [ 4] , the HPV vaccine provides protection for at least five years, and more research is being done to see if it provides protection for longer. So, it is possible a booster shot will be needed.
Discounts:
Eligible children 18 and younger can get the HPV vaccination for free through the Vaccines for Children [ 5] program. Or, for eligible women older than 18, Merck offers Gardasil through its patient assistance program.
Shopping for human papillomavirus vaccine:
Check with your child's pediatrician or your family doctor. Or, many Planned Parenthood clinics offer HPV vaccination; Planned Parenthood [ 6] has a clinic locator by zip code.
Genital HPV is spread through sexual contact, so it is best for females to get vaccinated before they become sexually active.
HPV vaccination generally is considered safe, but side effects can include pain, swelling or redness at the injection site, nausea, vomiting, dizziness and fainting. It should not be given to pregnant women or to anyone who has had a serious allergic reaction to yeast or any component of the vaccine. The HPV vaccine is being tested for safety and effectiveness in males and in women over 26.
Material on this page is for informational purposes only and should not be construed as medical advice. Always consult your physician or pharmacist regarding medications or medical procedures.
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You may not be able to host the large family gathering for the holidays, but there are still many ways to pick up items curbside to spruce up your indoor space for your everyday enjoyment and to bring a more festive spirit. || Posted December 30 2020
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As they age, members of the Baby Boomer generation don't like to admit that they're senior citizens, but they love getting discounts. It's kind of a quandary, because some of the best deals available are reduced prices for older folks. || Posted October 21 2013
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What People Are Paying - Recent Comments
Univ of KS Medical center charges $1200 PER Gardasil injection
Amount: $729.76
Posted by: Sarah James, KCMO in Kansas City, KS.
Posted: April 22nd, 2020 03:04AM
I have health insurance through my out of state employer. I verified that my childrens' pediatrician at Univ of Kansas Health Systems was in network before taking my 11 year old for his well child visit. I received a $744.15 bill for UKH. My insurance company broke the charges down for me - UKH has already received $1918.25 from my insurance company for a well child visit. Insurance explained to me that UKH is charging $1200 for the first Gardasil shot and it's not considered preventive so my out of pocket for the Gardasil shot will be $729.76. These charges are for an hour long well child visit. This is OUTRAGEOUS!
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External Resources:
www.aetna.com/cpb/medical/data/700_799/0726.html
medweb.mit.edu/wellness/programs/sexual_health.html
www.cancer.org/cancer/cancercauses/othercarcinogens/infectiousagents/hpv/humanpapi...
www.cdc.gov/vaccines/vpd-vac/hpv/vac-faqs.htm
www.cdc.gov/vaccines/programs/vfc/
www.plannedparenthood.org/health-center/findCenter.asp
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msmarco_passage_01_503865482 | Cost of Permanent Makeup - 2021 Healthcare Costs | Cost of Permanent Makeup - 2021 Healthcare Costs
CostHelper > Health & Personal Care > Personal Care & Body Art > Permanent Makeup
Permanent Makeup Cost
How Much Does Permanent Makeup Cost?
Beauty Mark: $50-$150
Eyeliner: $200-$600
Full Lip Color: $600-$800
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Permanent makeup is cosmetic tattooing to create the appearance of makeup.
Typical costs:
Permanent makeup typically costs $50 to $800 per procedure, depending on the type of makeup, the body part and number of visits required.
A permanent beauty mark generally costs $50 to $150. For example, the Permanent Makeup Clinic in Virginia charges $50 for a beauty mark, and SD Permanent makeup [ 1] in San Diego, California, charges $100. The Triad Permanent Cosmetic Clinic in North Carolina charges $150.
Permanent eyebrows, which usually require two visits, usually cost $400 to $600. For example, the Permanent Makeup Clinic charges $400 for eyebrows, and SD Permanent makeup charges $400 to $450. The Triad Permanent Cosmetic Clinic charges $595.
Permanent eyeliner usually costs $200 to $400 for just upper or just lower eyeliner, or $400 to $600 for upper and lower. For example, the Permanent Makeup Clinic charges $250 for upper or lower and $450 for both. The Triad Permanent Cosmetic Clinic charges $395 for upper or lower and $595 for both.
Full lip color with liner, which typically requires two to three visits, typically costs $600 to $800. For example, the Permanent Makeup Clinic charges $600, the Triad Permanent Cosmetic Clinic charges $625, and SD Permanent Makeup charges $700.
Permanent makeup is considered a cosmetic procedure, so it generally is not covered by health insurance.
Related articles: Wedding Day Make-up, Tattoo Removal
What should be included:
To apply permanent makeup, also known as micropigmentation, the doctor or technician uses a handheld device with a very small needle that punctures the skin hundreds of times per minute to embed permanent pigment in the deeper skin layers known as the dermis.
Each procedure typically requires topical anesthetic and will take an hour and a half to two hours. After the procedure, normal activities can be resumed right away, though there might be some swelling or redness. The Society of Permanent Cosmetics Professionals [ 2] answers frequently asked questions about permanent makeup.
Additional costs:
As with any tattoo, color can fade over time and periodic touch-ups might be required. Touch-ups typically cost less than the initial application -- usually $100 to $250.
Discounts:
Some permanent makeup artists offer online specials or coupons. For example, SD Permanent makeup [ 3] has offered a $100 off special.
Shopping for permanent makeup:
Permanent makeup should be done by a doctor, clinic or other reputable provider. A board-certified plastic surgeon, who can be found through the referral services offered by the American Society of Plastic Surgeons [ 4] or the American Society for Aesthetic Plastic Surgery [ 5] , can provide a referral to a reputable provider. Or, the Society of Permanent Cosmetic Professionals [ 6] offers a technician locator. Because professionals of various backgrounds -- including physicians, nurses, cosmetologists and tattoo artists -- seek training and become permanent makeup providers, it is especially important to thoroughly investigate a provider before using their services. Dr. Laura Reed [ 7] , a permanent makeup provider in California, offers a guide to evaluating a permanent makeup professional.
The American Academy of Micropigmentation [ 8] recommends asking the provider for references and a portfolio, and offers a list of questions to ask, including: what is the provider's background, training and level of experience; whether disposable needles are used; what pigments are used; whether the provider can do advanced techniques such as hair strokes for brows; whether the dyes contain ink; and what kind of anesthesia is used.
Permanent makeup is a tattoo that can be very difficult and expensive to try to remove, and dissatisfaction with results is a possibility. RealSelf.com [ 9] offers reviews of permanent makeup by those who have had the procedure.
Risks are similar to those for other kinds of tattoos and include infection from dirty needles with diseases such as hepatitis or HIV, or allergic reaction that, in some cases, could lead to permanent disfigurement. The U.S Food and Drug Administration has not approved any colors for injection into the skin and, in an information sheet on permanent makeup [ 10] , notes that many colors have not been tested for safety.
Material on this page is for informational purposes only and should not be construed as medical advice. Always consult your physician or pharmacist regarding medications or medical procedures.
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You may not be able to host the large family gathering for the holidays, but there are still many ways to pick up items curbside to spruce up your indoor space for your everyday enjoyment and to bring a more festive spirit. || Posted December 30 2020
7 Lesser-Known Discounts for the 50+ Crowd
As they age, members of the Baby Boomer generation don't like to admit that they're senior citizens, but they love getting discounts. It's kind of a quandary, because some of the best deals available are reduced prices for older folks. || Posted October 21 2013
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What People Are Paying - Recent Comments
Cover up lip birthmark
Amount: $400.00
Posted by: Nliza19 in Cleveland, OH.
Posted: October 2nd, 2019 05:10AM
Type of Makeup: Tattoo
Number of Visits: 2
Did not make a real difference
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Permanent concealer on my birthmarks on face
Amount: $500.00
Posted by: Lutfun nahar in Dhaka, DC.
Posted: June 8th, 2019 11:06PM
Type of Makeup: Concealer on my light birthmarks on face
Number of Visits: 1
I have need details information Please contact with me
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How long should I stay out of direct sunlight
Amount: $2.50
Posted by: Francine Hackney in Washington, DC.
Posted: October 23rd, 2017 07:10AM
Type of Makeup: Permanent eyebrows
Number of Visits: 2
I got my eyebrows tattooed @ Lucy's nails Spa & Permanent Makeup and it is exactly what I wanted.
Lucy was very professional and friendly, she informed me as what she was doing and how much more time was needed to achieve the look that we were seeking. This look is permanent. In two years I may require a touchup. It was worth the time, money and I would do it again.
Lucy's is located in the 400 block of Massachusetts Ave.
N.W.
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Micropigmentation
Amount: $550.00
Posted by: Sarah Dickinson in Florence, OH.
Posted: November 6th, 2016 10:11PM
Type of Makeup: Eyebrows, eyeliner, lip liner
Number of Visits: 2
I was able to get a partial bottom liner. She was running a special for the 3. It was not the detailed type of eyebrow just basic.
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face
Amount: $150.00
Posted by: Tearea in Wonder, GA.
Posted: August 9th, 2015 07:08PM
Type of Makeup: Eyebrows
Number of Visits: 2
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External Resources:
www.sdpermanentmakeup.com/permanent_makeup_cost.html
www.spcp.org/thinking-of-getting-a-cosmetic-tattoo/permanent-makeup-faq/
www.sdpermanentmakeup.com/permanent_makeup_cost.html
www1.plasticsurgery.org/find_a_surgeon/
www.surgery.org/consumers/find-a-plastic-surgeon
www.spcp.org/thinking-of-getting-a-cosmetic-tattoo/find-a-technician/
www.californiahealthandbeauty.com/articles.asp?article=304
www.micropigmentation.org/consumer/consumer.php
www.realself.com/Permanent-makeup/reviews
www.fda.gov/ForConsumers/ByAudience/ForWomen/ucm118568.htm
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msmarco_passage_01_504590030 | Cost of a Wheelchair - 2021 Healthcare Costs - CostHelper | Cost of a Wheelchair - 2021 Healthcare Costs - CostHelper
CostHelper > Health & Personal Care > Medical Equipment and Orthopedics > Wheelchair
Wheelchair Cost
How Much Does a Wheelchair Cost?
Low: Basic Manual Chair $500
Medium: Manual Chair, Everyday Use $1,000-$2,000
High: Power Chair Averages $7,100
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Wheelchairs vary almost as much as the individuals who require them. Though the cost can be significant, the chairs can provide mobility and independence. Be sure to talk to a doctor before purchasing a wheelchair, for help deciding what type of chair is best.
Typical costs:
A standard, manual wheelchair costs an average of $500, according to the Robert Wood Johnson Foundation [ 1] . A chair meant for everyday use costs between $1,000 and $2,000 depending upon the features of the chair, which can include an individualized seat, various types of wheels and a lightweight frame. The Invacare Top End Crossfire All Terrain Rigid Wheelchair [ 2] retails for about $1,900 and includes knobby, all-terrain wheels, a lightweight frame and a variety of color options.
Costs for a power wheelchair vary tremendously, starting around $1,200-$1,500 and going as high as $30,000. One study, published in the Archives of Physical Medicine and Rehabilitation [ 3] , evaluated 15 electric-powered wheelchairs, with an average cost of $7,132.
Costs for power wheelchairs vary based on features such as an individualized seat, longer battery life, ergonomic features and types of wheels. The Permobile C500 Lowrider [ 4] costs about $10,000, with adjustable speeds, tight turning radius, higher weight capacity and an estimated 25-mile battery range.
Securing insurance coverage to purchase a wheelchair can be a challenge. According to the Mobility Advisor [ 5] , private insurers and government programs typically cover between 50 and 80 percent of the costs. A physician will need to send documents proving that the patient requires a wheelchair.
Related articles: Crutches, Cane, Hip Replacement, Broken Leg
What should be included:
A basic manual wheelchair includes a seat, handles, arm rests, foot rests, manual brake, four tires and a frame. Assembly may be required. Extra features can include a specialized ergonomic seat, leg rests or a pouch for carrying personal belongings.
A basic power wheelchair should include a seat, handles, arm rests, foot rests, tires, a motor, power supply, battery and maneuvering device. Power wheelchair extras can include a specialized maneuvering device, extra batteries, neck support or a lift device to assist with transfer from the chair.
Most wheelchairs are covered by a warranty. Look for a chair with at least a three-year warranty.
A physician, nurse or wheelchair company representative should provide a tutorial on using the chair, including information on charging the batteries, set-up requirements and a maneuvering tutorial.
Additional costs:
Securing coverage under insurance or a government program such as Medicare for a wheelchair requires a face-to-face visit with a physician, to get documentation of the need for a wheelchair. Normal fees will apply and will vary depending upon the physician's office and geographic location. For those with insurance, typical coinsurance and copay rates range from $5 to $50.
Though most power wheelchairs will come with a battery, replacements will be required and can cost between $70 and $450 depending upon the type of wheelchair.
A simple wheelchair cushion made of foam costs about $7 while a neoprene rubber wheelchair cushion designed to limit pressure point tenderness can cost more than $500.
Discounts:
Several national and regional programs offer low-income families free or reduced-cost wheelchairs, including LifeNets [ 6] and Chariots of Hope [ 7] . Eligibility varies.
Some local and regional associations also provide assistance to individuals who require a wheelchair due to a specific illness or accident. For example, the Muscular Dystrophy Association [ 8] and local chapters of the National Spinal Cord Injury Association [ 9] provide help for qualifying families and individuals.
Purchasing a used wheelchair can help defray the costs. According to the National Multiple Sclerosis Society [ 10] , used wheelchairs often cost half of the original price. Get a used wheelchair checked out by a certified dealer and ask a physical therapist to make sure the equipment will fit the patient's needs and body type. Insurance companies typically do not cover used medical equipment.
The cost of a wheelchair may be tax deductible if the individual has a physician's letter outlining the need.
Shopping for a wheelchair:
Talk to the doctor or physical therapist about the individual's needs. Ask if he or she recommends any specific brands or types of chair.
The University of Iowa provides a checklist of questions for individuals considering wheelchair purchase.
The University of Washington [ 11] recommends making several visits to a medical supply store, shopping online and even talking to other wheelchair users before making a purchase.
Some online retailers such as Spin Life.com [ 12] offer competitive prices and telephone advice regarding the many options.
Before making a purchase, check with an insurance representative about coverage options. Most insurance companies will cover between 50 and 80 percent of the cost, but only if the insurance guidelines are followed.
Material on this page is for informational purposes only and should not be construed as medical advice. Always consult your physician or pharmacist regarding medications or medical procedures.
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You may not be able to host the large family gathering for the holidays, but there are still many ways to pick up items curbside to spruce up your indoor space for your everyday enjoyment and to bring a more festive spirit. || Posted December 30 2020
7 Lesser-Known Discounts for the 50+ Crowd
As they age, members of the Baby Boomer generation don't like to admit that they're senior citizens, but they love getting discounts. It's kind of a quandary, because some of the best deals available are reduced prices for older folks. || Posted October 21 2013
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Linda L. Koski
Amount: $0.00
Posted by: L. Koski in Havre, MT.
Posted: October 11th, 2018 05:10PM
Manual or Power: Power
Brand: Quicky
Lower income paralyzed senior citizen. I need a chair with heavy duty features, six-wheels. Chair tilt, legs raised and lowered, back lowers. Easy arm lifts to make it easy to put patient in and out of bed. Capability of going at least 7 mph up to a 14 mile range.
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power wheel chair
Amount: $1,200.00
Posted by: ken akey in White Bluff, TN.
Posted: August 31st, 2018 03:08PM
Manual or Power: power
Brand: scooter chair
Model/Features: high back
my wife past away in april so i have a power wheel chair in elc shape and the rack gos on the back of car
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My power chair
Amount: $3,800.00
Posted by: TT2012 in Toledo, OH.
Posted: August 5th, 2015 11:08AM
Model/Features: Standard
My chair was in excellent condition. it was a accident with semi and insurance company doesn't want to pay a reasonable price. they want to pay me less than $1000 and I can't get a new chair until the end of next year.PLEASE HELP!
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External Resources:
pweb1.rwjf.org/reports/grr/029269s.htm
www.spinlife.com/Invacare-Top-End-Crossfire-All-Terrain-Rigid-Wheelchair/spec.cfm?...
www.ncbi.nlm.nih.gov/pubmed/15083438?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubm...
www.usatechguide.org/itemreview.php?itemid=1266
www.mobility-advisor.com/electric-wheelchair.html
www.lifenets.org/wheelchair/
www.chariotsofhope.org/
static.mda.org/publications/quest/q84wheelchair.html
www.spinalcord.org/chapters/
www.nationalmssociety.org/living-with-multiple-sclerosis/mobility-and-accessibilit...
sci.washington.edu/info/newsletters/articles/03sum_wheelchair.asp
www.spinlife.com/
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msmarco_passage_01_507220607 | Why does my stomach growl? | HowStuffWorks | Why does my stomach growl? | HowStuffWorks
Why does my stomach growl?
By: Jessika Toothman
A grumbling stomach can be a bit embarrassing in some situations.
Ableimages/Riser/ Getty Images
The human body is an amazing machine, and every once in a while it will do something to remind you that it's working hard to keep you alive and well. The stomach growl is one of these reminders. Loud, soft and sometimes for no good reason at all, your growling stomach has a lot to say.
Whether you call it grumbling, rumbling, gurgling or growling, from time to time everybody's belly chimes in. These noises might sound like they should be coming from a noisy pot of bubbling stew rather than your stomach.
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But the big question is, why does it growl in the first place? And why does your stomach seem to growl the moment a room grows quiet?
Your stomach doesn't have such perfect timing or such a malicious sense of sabotage. But there is a perfectly logical explanation why your stomach sometimes feels the need to be heard.
Let's examine this age-old question on the next page and discover why Winnie the Pooh isn't the only one with a rumbly in his tumbly.
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Causes of Stomach Growling
Your stomach and small intestine (seen here through a stylized x-ray image) are the sources of all that growling.
MedicalRF.com/ Getty Images
Stomach growling, which originates in the stomach and the small intestine, can be explained by a closer look at how the digestive system functions.
The digestive system is, in essence, a long tube that starts at the mouth and ends at the anus. This tube connects with the various organs and passages that play important roles in digestion. One of the most important things to know about the digestive system is the manner in which it propels food. Waves of muscle contractions move and push the contents continually downward in a process called peristalsis. In addition to moving your meal along its digestive path, these contractions also help churn food, liquid and different digestive juices together, rendering them into a gooey mix known as chyme.
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Stomach growling is the result of this process. Moving with those solid and liquid chyme ingredients are gasses and air. As all these ingredients get pushed around and broken down into easy-to-absorb bits, pockets of air and gas also get squeezed and create the noises we hear. Stomach growling can happen at any time -- not just when you're hungry -- but if there's food in your stomach or small intestine, the growling becomes quieter. It's like putting a pair of sneakers in the dryer by themselves versus with a load of towels. The towels muffle the noise of the shoes as they bounce around.
But you may be wondering -- if your stomach is empty, why are the muscle contractions that digest food happening to begin with? The reason has to do with hunger and appetite. About two hours after your stomach empties itself, it begins to produce hormones that stimulate local nerves to send a message to the brain. The brain replies by signaling for the digestive muscles to restart the process of peristalsis. Two results occur: First, the contractions sweep up any remaining food that was missed the first time around. Second, the vibrations of an empty stomach make you hungry. Muscle contractions will come and go about every hour, generally lasting 10 to 20 minutes, until you eat again. Learn more about the twists and turns your food takes after your first bite by reading How the Digestive System Works.
In some cases, excessive gurgling and grumbling may be a sign of an upset stomach or a medical condition like irritable bowel syndrome. In these cases, there are usually a number of additional gastrointestinal complaints accompanying a growling stomach.
So now that we know what causes stomach growling, is there any way to control it? One tip to mute a noisy belly is to eat many small meals instead of a few large ones. Your digestive system will have less opportunity to create those peristalsis rumbles if your body has something tasty in it. Also, eating less gaseous foods may help decrease the growling.
So, is your body making any other weird noises? Visit the links on the next page to learn more about the human body.
Word Origins
The technical name for the noises made by a grumbling stomach is borborygmi (borborygmus is the singular form). The term comes from the Greek word borborugmos, an example of onomatopoeia (a word created to imitate a sound). Borborygmi illustrates what stomach growling might sound like in word form.
Onomatopoeia is commonly used for animal sounds and other noises, and can differ between languages. Examples in the English language include bang, hiss, whisper and buzz.
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Jessika Toothman "Why does my stomach growl?" 30 April 2008.
HowStuffWorks.com. <https://health.howstuffworks.com/human-body/systems/digestive/stomach-growling.htm> 21 May 2021
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msmarco_passage_01_507863852 | Inotropic Drugs: What You Need to Know | HowStuffWorks | Inotropic Drugs: What You Need to Know | HowStuffWorks
Inotropic Drugs: What You Need to Know
NEXT PAGE
By: Jill Ferguson
Inotropic drugs alter the strength of your heartbeat.
Plush Studios/Riser/ Getty Images
An inotropic drug is a medicine that alters the force or strength of the heart 's muscular contractions (heartbeats). There are two different types of inotropic drugs: negative and positive. Negative inotropic drugs make the heart beat less strongly, and positive inotropic drugs make the heart beat more strongly. Both kinds are used in the management of various conditions that affect the function of the heart.
One of the most important factors affecting the strength of the heart's muscular contractions is the level of calcium in the fluid inside the heart's muscle cells. Calcium is one of the most common electrolytes in the human body. Other common electrolytes are sodium, potassium, chloride and magnesium. We need the right balance of these electrolytes for proper functioning of the heart, nerves, muscles and kidneys.
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Electrolytes are minerals that come from the foods we eat and fluids we drink. They're found in the fluids throughout the body -- not only in the blood and urine, but also inside the body's cells and in the space surrounding the cells.
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Drugs & Diseases > Endocrinology
Androgen Excess Clinical Presentation
Updated: Apr 07, 2020
Author: Mohamed Yahya Abdel-Rahman, MD, MSc; Chief Editor: Richard Scott Lucidi, MD, FACOG more...
Sections
Androgen Excess
Sections Androgen Excess
Overview
Practice Essentials
Pathophysiology
Epidemiology
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Presentation
History
Physical
Causes
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DDx
Workup
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Imaging Studies
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Procedures
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Treatment
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Consultations
Diet
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Medication
Medication Summary
Oral contraceptives
Antiandrogens
Aldosterone Antagonists, Selective
5-Alpha-Reductase Inhibitors
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Presentation
History
Detailed history taking from the patient is the cornerstone in patients with hirsutism. Most of the patients with hirsutism will develop excess hair around puberty or a few years thereafter. Onset of mild hirsutism with a slowly progressive course is usually associated with a functional disturbance. On the other hand, rapid progression of hair growth suggests an androgen secreting tumor. [ 28]
Location and rate of hair growth
Patients with hirsutism are often most concerned with unwanted hair in their face. However, areas covered by clothes may be less of a concern. Hence, it is important to ask about increased hair growth in other areas, including the upper chest, abdomen, inner aspects of the thighs, and the upper and lower back. The frequency and the method used to remove unwanted hair should be elicited because this often gives some idea of the extent of hair growth.
Rapid virilization associated with hirsutism is suggestive of androgen secreting neoplasm or exogenous androgenic drug use. History should include acne, alopecia, clitoromegaly, deepening of voice, masculinization, breast atrophy, and amenorrhea.
Menstrual abnormalities
Hirsutism is almost always a manifestation of other disease (more than 90% of the time). Because PCOS represents 80% of the etiology, it is important to ask about symptoms of this disorder. Oligomenorrhea or amenorrhea with hirsutism is sufficient to diagnose PCOS according to the revised Rotterdam criteria [ 29] after exclusion of other causes.
A study by Willis et al found that self-reported hirsutism in women, as measured using the modified Ferriman-Gallwey score, was associated with menstrual irregularity, bleed lengths of 7 days or more, and heavy menstrual bleeding. [ 30]
Regular menses, however, do not predict normal androgen status in hirsute women. Although 40% of women with hirsute have regular menses, half of them will be found to have elevated levels of one or more androgens. [ 31] Other cutaneous manifestations of PCOS like acne, oily skin, androgenic alopecia, seborrhea, and obesity may be present with hirsutism.
Family history
An increased prevalence of hirsutism, acne, and male pattern baldness have been found to run in some families. [ 32] PCOS often presents with familial clustering. However, it is unclear if this is due to genetic pattern alone or due to environmental factors such as diet. [ 33] Congenital adrenal hyperplasia also presents with familial clustering. The ethnic differences in hair quantity and distribution should be kept in mind.
Next: Physical
Physical
Focused physical examination is essential for the evaluation of women with hirsutism. The clinician should determine whether hirsutism is truly present, as many women who complain of excess hair growth might not actually have hirsutism, especially those with ethnic and genetic predisposition (South European, and Middle East). Excess hair should be established as villus or terminal. Also, hirsutism should be distinguished from hypertrichosis, where hair growth is not mediated by androgens and hairs are not distributed in an androgen sensitive (male) pattern. [ 34]
Height, weight, body mass index (BMI), and waist-to-hip ratio (WHR) should be determined. Increased BMI and WHR are associated with PCOS, insulin resistance, and increased risk of coronary artery disease. [ 35]
Hirsutism
Ferriman and Gallwey [ 36] published a hirsutism rating scale that is illustrated in the table below. This scale allows the physician to measure a response to therapy objectively. This system is the most widely used and evaluates body areas for absent-to-severe hirsutism with scores of 0-4, respectively. Scores of 8 and higher are consistent with a diagnosis of hirsutism. This scale does not measure the thickness of the hair, which is another way of objectively assessing excess hair.
Scoring systems are a useful aid in quantifying hirsutism and in evaluating treatment response. However, they are somewhat subjective, so the absolute score is not used to define hirsutism. Even with scores >8, the patient determines if she is hirsute. When evaluating treatment response, the patient can determine if he or she notices a difference. Photographs are helpful for documentation and for following the progress of therapy.
Table. Ferriman-Gallwey Scoring System (Open Table in a new window)
Body Area Evaluated
Score
(Graded from 0-4*)
Upper lip
Chin
Upper abdomen
Lower abdomen
Upper arm
Thighs
Upper back
Lower back/buttocks
*0 = No hirsutism, 4 = Severe hirsutism
Other signs of androgen excess
Acne and oily skin are both associated with hirsutism. Androgen acts on the PSU to increase sebum production and has an important role in acne development. However, many cases of acne are not associated with hyperandrogenism.
Androgenic alopecia is another distressing condition associated with androgen excess. It is characterized by hair loss from the crown of the scalp sparing the frontal and occipital hairline (male pattern baldness). [ 37]
Acanthosis nigricans is a mucocutaneous condition where velvety hyperpigmentation patches appear mainly in the skin of the base of the neck, axilla, antecubital fossae, and groin. Acanthosis nigricans is a marker of insulin resistance. [ 38] In contrast, acanthosis nigricans is rarely seen with androgen secreting tumors. [ 39]
Virilization
Virilization suggests an androgen secreting tumors. Features of virilization include temporal male pattern balding, laryngeal hypertrophy, loss of feminine body contour and clitoral hypertrophy. [ 40] Clitoromegaly is diagnosed when the clitoral length times diameter is >35 mm 2.
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Next: Physical
Causes
A specific underlying cause can be identified in most patients with androgen excess. [ 41]
Polycystic ovary syndrome (PCOS)
Approximately 80-90% of women with excess androgens have PCOS. [ 42, 41] PCOS is the most common endocrinological disorder affecting women in their reproductive years. [ 43] The prevalence in the United States has been estimated at 5-7% [ 44] and appears to be rising. Approximately 70% of women with PCOS are found to have mildly elevated free testosterone, and 20-30% have mildly elevated dehydroepiandrosterone sulphate (DHEAS). [ 45, 46]
Evidence suggests that hyperandrogenemia may be associated with chronic inflammation in PCOS by affecting adipocyte attributes and morphology. [ 47] Further, a study by Rudnicka et al indicated that increased androgen concentration is related to white blood cell (WBC) count in PCOS and therefore contributes to the mediation of chronic inflammation in this condition. [ 48]
A literature review by Escobar-Morreale and Roldán-Martín suggested that in women with type 1 diabetes mellitus, the prevalences of PCOS and associated traits, including hyperandrogenemia, are greater than in the general population without diabetes. The investigators found that out of 475 adolescent or adult women with type 1 diabetes, the prevalences of PCOS and hyperandrogenemia were 24% and 25%, respectively, while those for hirsutism, menstrual dysfunction, and polycystic ovarian morphology were 25%, 24%, and 33%, respectively. [ 49]
Hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN) syndrome
HAIR-AN syndrome is a subset of women with PCOS who present with hyperandrogenism, insulin resistance, acanthosis nigricans, and obesity in the absence of insulin receptor defect. [ 50] This syndrome is found in 1-3% of hyperandrogenic women. [ 51] HAIR-AN syndrome is characterized by high levels of post-glucose challenge insulin levels that may reach 300-500 µU/mL. [ 52]
Ovarian hyperthecosis
Ovarian hyperthecosis is another condition related to PCOS that most often presents in the perimenopausal period. This condition accounts for less than 1% of women with elevated androgens in their reproductive years, but most of the cases of hyperandrogenemia in postmenopausal women. [ 53]
Ovarian hyperthecosis is described when luteinized theca cell nests are present in the ovarian stroma. Although there is a considerable overlap between hyperthecosis and PCOS, hyperthecosis is associated with a more severe form of hyperandrogenism and virilization. Testosterone levels are much higher than PCOS and may reach levels greater than 200 ng/dL. [ 54]
Congenital adrenal hyperplasia
Approximately 2% of women with androgen excess are found to have late-onset, nonclassical, congenital adrenal hyperplasia. [ 42] Congenital adrenal hyperplasia is a group of autosomal recessive disorders resulting from mutations in the genes coding for steroidogenic enzymes. In these disorders, a block in cortisol biosynthesis leads to loss of negative feedback inhibition, increased ACTH secretion, and subsequent excessive adrenal androgen production. [ 55]
The most common cause of congenital adrenal hyperplasia is 21-hydroxylase deficiency, which accounts for 90-95% of patients with this condition. [ 55] The remaining patients with congenital adrenal hyperplasia have either 11 β-hydroxylase deficiency or 3 β-hydroxysteroid deficiency. [ 56, 57]
Cushing syndrome
Cushing syndrome is a rare but important cause of androgen excess, and hirsutism is present in approximately 81% of these patients. [ 58] Cushing syndrome (also called hypercorticism) is primarily the result of increasing levels of circulating cortisol or exogenous glucocorticoids. This syndrome can present insidiously with a spectrum of classic symptoms including rapid central weight gain (central obesity and “moon face”), abdominal striae, and signs of hyperandrogenemia including hirsutism, acne, and baldness.
Glucocorticoid therapy is currently the most common cause of Cushing syndrome but is unlikely to be associated with signs of increased androgens. In contrast, endogenous Cushing syndrome is often associated with hirsutism. Cushing syndrome can be secondary to an ACTH secreting pituitary tumor, which is called Cushing disease. Other cases of Cushing syndrome are related to autonomous cortisol secretion by the adrenal glands. [ 59] Adrenal tumors are associated with rapid onset of Cushing syndrome symptoms, often with hirsutism. [ 60] Rarely, Cushing syndrome is caused by ACTH secretion by other types of tumors such as small cell lung cancer.
Androgen secreting tumors
Androgen secreting tumors of the ovaries or adrenal glands are rare causes of hyperandrogenism that often mimic PCOS. Women with these tumors tend to have sudden onset of symptoms, rapid progression of hyperandrogenism and early development of frank virilization.
The most common virilizing ovarian tumors are Sertoli Leydig cell tumors and account for 0.5% of all ovarian neoplasms. [ 54] However, any type of ovarian tumor can present with signs of hyperandrogenism.
Androgen-secreting adrenal neoplasms are less common than ovarian neoplasms. [ 61] Patients with these tumors usually present with mixed picture of Cushing syndrome and virilization. [ 62]
Hyperprolactinemia
Elevated prolactin levels are found in as many as 6% of women with hirsutism. [ 63] The exact relationship between elevated prolactin levels and androgen excess is still unclear. Elevated prolactin levels might directly stimulate the adrenal cortex. [ 64]
Pregnancy
Testosterone rises throughout the normal pregnancy, reaching values around 600-800 ng/dL by term. The increase in SHBG and the placental aromatization of androgens to estrogens protect the mother and her fetus. Placental aromatase enzyme deficiency can cause hyperandrogenemia in both mother and fetus and result in virilization. [ 65]
Exogenous androgens
Ingestion of androgens or agents with androgenlike activity can result in hirsutism, acne, and virilization. Various anabolic steroids are used by professional athletes, both men and women, to attain a competitive edge or to assist in recovery from injury. These drugs are also used by a large number of noncompetitive body builders for cosmetic purposes and by women to increase libido.
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Differential Diagnoses
References
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Waldstreicher J, Santoro NF, Hall JE, Filicori M, Crowley WF Jr. Hyperfunction of the hypothalamic-pituitary axis in women with polycystic ovarian disease: indirect evidence for partial gonadotroph desensitization. J Clin Endocrinol Metab. 1988 Jan. 66 (1):165-72. [Medline].
Ibanez L, Potau N, Zampolli M, Prat N, Gussinye M, Saenger P, et al. Source localization of androgen excess in adolescent girls. J Clin Endocrinol Metab. 1994 Dec. 79 (6):1778-84. [Medline].
Shenenberger DW, Utecht LM. Removal of unwanted facial hair. Am Fam Physician. 2002 Nov 15. 66 (10):1907-11. [Medline].
Christ JP, Falcone T. Bariatric Surgery Improves Hyperandrogenism, Menstrual Irregularities, and Metabolic Dysfunction Among Women with Polycystic Ovary Syndrome (PCOS). Obes Surg. 2018 Mar 2. [Medline].
Pasquali R, Antenucci D, Casimirri F, Venturoli S, Paradisi R, Fabbri R, et al. Clinical and hormonal characteristics of obese amenorrheic hyperandrogenic women before and after weight loss. J Clin Endocrinol Metab. 1989 Jan. 68 (1):173-9. [Medline].
Pate RR, Pratt M, Blair SN, Haskell WL, Macera CA, Bouchard C, et al. Physical activity and public health. A recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA. 1995 Feb 1. 273 (5):402-7. [Medline].
Clark AM, Thornley B, Tomlinson L, Galletley C, Norman RJ. Weight loss in obese infertile women results in improvement in reproductive outcome for all forms of fertility treatment. Hum Reprod. 1998 Jun. 13 (6):1502-5. [Medline].
Lundgren JA, Kim SH, Burt Solorzano CM, McCartney CR, Marshall JC. Progesterone Suppression of Luteinizing Hormone Pulse Frequency in Adolescent Girls With Hyperandrogenism: Effects of Metformin. J Clin Endocrinol Metab. 2018 Jan 1. 103 (1):263-70. [Medline]. [Full Text].
Cumming DC, Yang JC, Rebar RW, Yen SS. Treatment of hirsutism with spironolactone. JAMA. 1982 Mar 5. 247 (9):1295-8. [Medline].
Board JA, Rosenberg SM, Smeltzer JS. Spironolactone and estrogen-progestin therapy for hirsutism. South Med J. 1987 Apr. 80 (4):483-6. [Medline].
Cusan L, Dupont A, Gomez JL, Tremblay RR, Labrie F. Comparison of flutamide and spironolactone in the treatment of hirsutism: a randomized controlled trial. Fertil Steril. 1994 Feb. 61 (2):281-7. [Medline].
Van der Spuy ZM, le Roux PA. Cyproterone acetate for hirsutism. Cochrane Database Syst Rev. 2003. CD001125. [Medline].
Wysowski DK, Freiman JP, Tourtelot JB, Horton ML 3rd. Fatal and nonfatal hepatotoxicity associated with flutamide. Ann Intern Med. 1993 Jun 1. 118 (11):860-4. [Medline].
Fulghesu AM, Melis F, Murru G, Canu E, Melis GB. Very low dose of flutamide in the treatment of hyperandrogenism. Gynecol Endocrinol. 2017 Nov 6. 1-5. [Medline].
Wong IL, Morris RS, Chang L, Spahn MA, Stanczyk FZ, Lobo RA. A prospective randomized trial comparing finasteride to spironolactone in the treatment of hirsute women. J Clin Endocrinol Metab. 1995 Jan. 80 (1):233-8. [Medline].
Erenus M, Yücelten D, Durmusoglu F, Gürbüz O. Comparison of finasteride versus spironolactone in the treatment of idiopathic hirsutism. Fertil Steril. 1997 Dec. 68 (6):1000-3. [Medline].
Erickson GF, Magoffin DA, Dyer CA, Hofeditz C. The ovarian androgen producing cells: a review of structure/function relationships. Endocr Rev. 1985 Summer. 6 (3):371-99. [Medline].
Nestler JE, Powers LP, Matt DW, Steingold KA, Plymate SR, Rittmaster RS, et al. A direct effect of hyperinsulinemia on serum sex hormone-binding globulin levels in obese women with the polycystic ovary syndrome. J Clin Endocrinol Metab. 1991 Jan. 72 (1):83-9. [Medline].
Ehrmann DA, Cavaghan MK, Imperial J, Sturis J, Rosenfield RL, Polonsky KS. Effects of metformin on insulin secretion, insulin action, and ovarian steroidogenesis in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 1997 Feb. 82 (2):524-30. [Medline].
Ibanez L, Valls C, Potau N, Marcos MV, de Zegher F. Sensitization to insulin in adolescent girls to normalize hirsutism, hyperandrogenism, oligomenorrhea, dyslipidemia, and hyperinsulinism after precocious pubarche. J Clin Endocrinol Metab. 2000 Oct. 85 (10):3526-30. [Medline].
Pasquali R, Gambineri A, Biscotti D, Vicennati V, Gagliardi L, Colitta D, et al. Effect of long-term treatment with metformin added to hypocaloric diet on body composition, fat distribution, and androgen and insulin levels in abdominally obese women with and without the polycystic ovary syndrome. J Clin Endocrinol Metab. 2000 Aug. 85 (8):2767-74. [Medline].
Sturrock ND, Lannon B, Fay TN. Metformin does not enhance ovulation induction in clomiphene resistant polycystic ovary syndrome in clinical practice. Br J Clin Pharmacol. 2002 May. 53 (5):469-73. [Medline].
Costello M, Shrestha B, Eden J, Sjoblom P, Johnson N. Insulin-sensitising drugs versus the combined oral contraceptive pill for hirsutism, acne and risk of diabetes, cardiovascular disease, and endometrial cancer in polycystic ovary syndrome. Cochrane Database Syst Rev. 2007 Jan 24. CD005552. [Medline].
Cosma M, Swiglo BA, Flynn DN, Kurtz DM, Labella ML, Mullan RJ, et al. Clinical review: Insulin sensitizers for the treatment of hirsutism: a systematic review and metaanalyses of randomized controlled trials. J Clin Endocrinol Metab. 2008 Apr. 93 (4):1135-42. [Medline].
Media Gallery
Androgen secretion pathway in adrenal glands and ovaries.
Chemical structures of spironolactone and drospirenone. The testosterone core is in black.
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Tables
Table. Ferriman-Gallwey Scoring System
Table. Ferriman-Gallwey Scoring System
Body Area Evaluated
Score
(Graded from 0-4*)
Upper lip
Chin
Upper abdomen
Lower abdomen
Upper arm
Thighs
Upper back
Lower back/buttocks
*0 = No hirsutism, 4 = Severe hirsutism
Back to List
Contributor Information and Disclosures
Author
Mohamed Yahya Abdel-Rahman, MD, MSc Research Fellow, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University Hospitals, Case Western Reserve University School of Medicine; Lecturer, Sohag University School of Medicine, Egypt
Mohamed Yahya Abdel-Rahman, MD, MSc is a member of the following medical societies: American Institute of Ultrasound in Medicine, American Society for Reproductive Medicine
Disclosure: Nothing to disclose.
Coauthor (s)
William W Hurd, MD, MSc, MPH Professor and Director, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Duke University Medical Center
William W Hurd, MD, MSc, MPH is a member of the following medical societies: American College of Surgeons, American Gynecological and Obstetrical Society, AAGL, Society of Reproductive Surgeons, Alpha Omega Alpha, American College of Obstetricians and Gynecologists, American Medical Association, American Society for Reproductive Medicine, Society for Reproductive Investigation
Disclosure: Nothing to disclose.
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Steven R Feldman, MD, PhD Professor, Departments of Dermatology, Pathology and Public Health Sciences, and Molecular Medicine and Translational Science, Wake Forest Baptist Health; Director, Center for Dermatology Research, Director of Industry Relations, Department of Dermatology, Wake Forest University School of Medicine
Steven R Feldman, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, North Carolina Medical Society, Society for Investigative Dermatology
Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbvie for consulting; Received honoraria from Galderma for speaking and teaching; Received consulting fee from Lilly for consulting; Received ownership interest from www.DrScore.com for management position; Received ownership interest from Causa Reseasrch for management position; Received grant/research funds from Janssen for consulting; Received honoraria from Pfizer for speaking and teaching; Received consulting fee from No.
Chief Editor
Richard Scott Lucidi, MD, FACOG Associate Professor of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Virginia Commonwealth University School of Medicine
Richard Scott Lucidi, MD, FACOG is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Society for Reproductive Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Arash Taheri, MD Research Fellow, Center for Dermatology Research, Department of Dermatology, Wake Forest University School of Medicine
Disclosure: Nothing to disclose.
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msmarco_passage_01_508780630 | How to Determine Your Skin Tone | HowStuffWorks | How to Determine Your Skin Tone | HowStuffWorks
How to Determine Your Skin Tone
By: John Barrymore
Our skin is our biggest organ, and it comes in many different colors. These different colors, referred to as skin tones, are determined by our outer layer's supply of a pigment called melanin. People with darker skin have more melanin than people with pale skin [source: National Geographic ]. To understand why there are so many different skin colors, it's important to understand how melanin works.
Melanin serves as your body's defense against ultraviolet rays, more commonly referred to as UV rays. These rays are incredibly damaging and can ultimately cause skin cancer if you don't protect yourself. That's where melanin comes in. You know that your skin changes color when you stay in the sun too long. When UV rays start penetrating our bodies, skin cells called melanocytes kick into high gear and start producing melanin, which results in a tan. People with fair skin, however, tend to burn, because they have fewer melanocytes and, thus, produce less melanin. Extreme burns can lead to all kinds of unpleasantness, including infections and shock.
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Some people just naturally have more melanin in their skin. They remain dark even in the absence of UV rays, and they don't burn as easily when they go out in the sun. Those whose families hail from Africa or India, for example, tend to have darker skin than European natives. Researchers believe this is the result of evolution: If you have dark skin, it's likely your ancestors once lived in tropical regions, where they were constantly bombarded with UV rays. Fair skin indicates you're a descendant of people who lived much farther from the equator.
Knowing your skin tone is important. Not only will you be able to better protect yourself from the sun's harmful rays and receive more accurate treatment for certain skin conditions, but you'll also be able to match clothing and hair color to better suit your body's biggest organ. It's not difficult to determine.
The simple distinction when referring to skin tone is warm or cool. To determine yours, simply look at your arm. What color are your veins? If they're blue, then you're a cool skin tone. If they're green, you've got yellow undertones, making you a warm skin tone. But, as you've probably noticed when make-up shopping or reading a fashion magazine, the descriptions and distinctions often go much deeper [source: CBS ].
Read on to find out more about skin tones and where you fall on the spectrum.
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Skin Types
While you can often look at your skin and give a general description of its color, you may not be able to communicate that in a way others would understand. For a long time, scientist's struggled to come up with a universal scale to describe the color of a person's skin. One of the first men who attempted to do so was German anthropologist Felix von Luschan. He created the Von Luschan chromatic scale in the early 20 th century. Unfortunately, his 36-tone scale eventually proved inexact and complicated. This system was abandoned during the 1950s, and people were left once again to ponder the significance of their skin tones [source: Jewish Museum ].
It wasn't long before Thomas B. Fitzpatrick, a Harvard-educated doctor, stepped up to the challenge. He designed the Fitzpatrick scale based on both a person's complexion and the way their skin reacts to sun exposure, specifically ultraviolet rays. This system of classification has become widely accepted, especially as a guideline for determining skin's susceptibility to the sun and other skin ailments. According to Fitzpatrick, skin tones fall into one of six major categories, or types. They are, in general, light, fair, medium, olive, brown and black. Light corresponds with type I on Fitzpatrick's scale while black corresponds with type VI [source: Commonwealth of Virginia ].
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When it comes to determining your skin tone, simply ask yourself three questions:
What color on the scale does my skin most resemble?
What is my pigmentation? People who are light, or type 1, have pale white skin and often have freckles as well, while those who are black, or type VI, have very dark skin.
How does my skin react to sun exposure? If you burn quite easily, you're probably type I. If you burn rarely -- or never -- then you're most likely type VI.
Read on to find out why it's so important to know your skin tone.
Plenty to Go Around
We have somewhere in the ballpark of 300 million skin cells. On average, that adds up to 8 pounds (17.6 kilograms) of skin, and if you could take it off and lay it flat on the floor, it would cover 22 square feet (2.04 square meters). Even more mind-boggling is the fact that we can shed up to 40,000 skin cells every minute -- that's 57.6 million cells every day [source: National Geographic ]. Think about that next time you get mad at your dog for shedding all over the house.
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Importance of Knowing Your Skin Tone
Knowing your skin tone is probably most important when it comes to preventing skin cancer. If you are a skin tone type I, II or III, you are at a much greater risk for developing skin cancer [source: American Cancer Society ]. You simply don't have as much melanin in your skin as people who are types IV, V or VI. That means you need to do more to protect yourself. It's as simple as wearing sunscreen every day.
Those with darker skin tones don't get off scot-free, either. No one is immune to ultraviolet rays. In other words, just because you're a type VI doesn't mean you can't get skin cancer [source: American Cancer Society ]. You might be able to get away with wearing a lower SPF sunscreen than your fair friends, though.
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Also, people with darker skin sometimes need different treatment for certain skin conditions than their pale counterparts. This is because melanin, which is located in the upper layer of the skin, tends to react when that area is irritated. Make sure a dermatologist has experience dealing with patients of your skin color before you go in for a visit [source: Marcus ].
It also helps to know your skin tone for cosmetic purposes. Face it: cosmetics cost money, so you might as well make sure you're using the products that suit you. Determining your correct skin tone will help you pick out more complementary shades of makeup and clothing. Doing some preliminary research before hitting the mall will better ensure you select items that make you look your best.
Determining your skin tone isn't hard. In fact, you've probably already done it. So put this knowledge to use. Protect yourself from UV rays, and make your natural skin type work for you. Every skin color has its advantages and disadvantages -- you just have to find out what they are.
Read on to learn more about skin tone.
Where's the Melanin?
In some extreme cases, melanin can be missing from a person's body all together. This condition is referred to as albinism, also known as being albino. The condition affects skin, hair and eye color. People with albinism are often incredibly pale, with light hair and light eyes. One in every 17,000 Americans has some form of the condition. Unfortunately, most people with albinism suffer from poor vision. Other than that, however, they can live a long and healthy life [source: Thompson ].
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msmarco_passage_01_509217388 | What does pH-Balanced mean? | HowStuffWorks | What does pH-Balanced mean? | HowStuffWorks
What does pH-Balanced mean?
By: Susan Sentry
You can use pH-Paper or litmus paper to find out the pH of your cleansers.
© iStockphoto.com /Sabine Kappel
If you think back to high school chemistry class, you may recall that pH is an abbreviation for potential hydrogen. A pH number measures from 0 to14 how acidic or alkaline a liquid is -- anything above 7 is alkaline and anything below 7 is acid. Water has a pH level of 7 -- it's neutral, meaning it has the same amount of acids and alkalis, which balance each other out.
When you're thinking about liquids in terms of their pH levels, going up or down one number on the scale represents a tenfold change in the acidity or alkaline nature of a liquid. For example, the pH level of milk is around 6. Because the pH level of water is 7, milk is 10 times more acidic than water. Vinegar has a pH of about 3, making it 40 times more acidic than water [source: Carpi ].
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On the other end of the spectrum, milk of magnesia is a base with a pH of 10, which is why it's soothing to an acidic stomach. Lye has a pH of 13 and can dissolve sticky substances like fat. As you can see, substances at either end of the pH spectrum can be corrosive -- but if you combine these substances, they neutralize and create salt water. They balance because they're at opposite ends of the scale [source: Ophardt ].
Now that you've had your general chemistry lesson, take a look at the next page to learn what pH-balanced means for your skin cleanser.
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pH-Balance and Skin Cleansers
Because buzzwords like "pH-balanced" are common advertising tools in the health and beauty industry, it's easy to ignore them and purchase a product regardless of its pH. However, when it comes to skin cleansers, pH levels do make a difference.
Your skin has a pH level of about 5.5. Skin -- or at least the outermost layer of it -- is slightly acidic [source: University of California Newsroom ]. The acidic layer helps your skin retain moisture and keeps germs out. To help maintain the skin's fatty protective layer, use a cleanser with a pH level similar to that of the skin itself. If you use a soap that's too alkaline, it will break up the acid in your skin, causing dryness.
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The pH level of most skin cleansers is slightly higher than 5.5, so the cleanser can break down dirt and oil on your skin. However, soap -- especially bar soap -- typically has a pH level of 9 to 12, which is too high if you're trying to keep your skin moist. Cleansers with lower pH levels leave your skin intact instead of breaking down the fatty tissue [source: Draelos ].
So, it must be important to use a skin cleanser that says it's pH-balanced, right? Yes and no. Most soap-free cleansers on the market today have balanced pH levels. Therefore, the words "pH-balanced" on a cleanser are more of a marketing ploy than anything else [source: Monroe ].
Now that you're clear on what pH balanced means to you and your skin, you can be savvy in the skin care aisle. For more information on how pH affects your skin, take a look at the links on the following page.
Finding a Product's pH Level
Beauty products -- whether they're skin cleansers or shampoos -- don't often list their exact pH levels on the label even when they claim to be balanced. If you're curious about a product's pH, you can use litmus paper to test if a liquid is an acid, neutral or base. For more specific results, use pH paper, which will turn different colors depending on the acid and alkaline levels [source: American Chemical Society ].
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msmarco_passage_01_510220455 | How to Get Rid of Age Spots | HowStuffWorks | How to Get Rid of Age Spots | HowStuffWorks
How to Get Rid of Age Spots
By: Alexander Page
Skin Problems Image Gallery Are you going to be stuck with those age spots forever? See more pictures of skin problems .
© iStockphoto.com /Fenykepez
Hitting the big 4-0 can mean a lot of different things to different people. Unfortunately, it can also mean age spots, which generally start popping up after the age of 40. They're sometimes called liver spots, which is a bit confusing considering the fact that they don't actually have anything to do with the liver. Perhaps a more fitting name would be sun spots -- sun exposure is what causes them in the first place. No matter what you call them, they're all the same thing: dark patches people get on their skin as they get older.
Age spots are usually brown or black, and they pop up on areas of the skin that are constantly exposed to the sun, like your hands and face. If you're good about protecting your skin from ultraviolet rays, you might be able to prevent them, but if you go out regularly without any sunscreen you'll probably develop them early on in life. Either way, they're painless. Aside from being unsightly, they won't really bother you -- but if you don't like the way they look, there are a few things you can do to try to get rid of them.
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If it's too late for you to prevent age spots, you're not out of luck. The good news is that they affect only the outermost layer of your skin, so there are several treatment options available to get rid of them. Think about it like spilling coffee on a pad of paper -- if you remove enough pieces of paper, you can get rid of the stain and the pad will look brand-new. Treatments that get rid of age spots work in a similar fashion -- they involve everything from freezing the top layer of your skin to getting underneath it with a laser. There are also a few homemade treatments you can try. Either way, you don't have to live with age spots unless you want to.
Keep reading to find out what specific treatment options are available.
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Age Spot Treatments
Age spots are really nothing more than a nuisance -- they won't hurt you. However, if you don't like they way they look, there are several ways to banish them from your skin. If you decide you want to get rid of them, you should consult a dermatologist to find out what treatment is best for you. Money might play a factor -- one of the procedures tends to be much more expensive than the others.
One of the most common treatments to fade age spots is a chemical peel. It uses acid to remove the top layer of your skin and allow newer, healthier skin to take its place. It may take several chemical peels before your age spot disappears, but it can be effective. A similar treatment that works is dermabrasion, which removes the top layer of skin with a rapidly rotating brush. Think of it like sandpaper for your face. The side effects associated with both of these treatments are scabbing and redness -- but many people think that's a small price to pay for blemish-free skin.
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From here the treatments get a little more complicated. Another way to get rid of age spots is to cover them with liquid nitrogen and freeze them. This destroys the pigment that turns your skin darker -- when your skin heals, it should be lighter. The only downside is the possibility of permanent scarring or discoloration of the skin, and isn't that the reason you were getting the treatment in the first place?
The final option has the fewest side effects, but it's also a lot more expensive than the others. A laser can actually remove age spots by destroying the cells that produce the pigment. This treatment shouldn't hurt your skin, but you'll need several treatments and the results aren't immediate. Sometimes it'll take months for an age spot to disappear.
If you don't like the sound of any of these treatments, keep reading to find out what home remedies are available.
Brrr, That's Cold!
Nitrogen makes up a large portion of the air we breathe. In its liquid form, however, it exists at a temperature of around -346 degrees Fahrenheit (-210 degrees Celsius) -- that's why it's so good at freezing things.
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Home Remedies for Age Spots
There aren't a ton of home remedies out there for getting rid of age spots, but if you have lemons, yogurt, honey and buttermilk you might be able to whip something up. Aside from that, there are several over-the-counter creams that can be effective.
Hydroquinone is one of the most common over-the-counter products for getting rid of age spots. According to the Food and Drug Administration, it's the only bleaching agent that's designed and thought to be safe for use on skin -- and it's incredibly effective. It also happens to be quite controversial. The European Union has already banned hydroquinone on the basis that it might cause cancer in lab animals. Dermatologists, however, continue to stand by hydroquinone as a safe and useful product as long as it's used in lower concentrations. Other over-the-counter products that can help reduce the appearance of age spots include topical tretinoin and adapalene gel. Both products are commonly used to treat acne, but they've also shown signs of improving skin that's been aged by the sun.
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If you're looking for a true home remedy to get rid of your age spots, there might be a few that can actually work. The first is lemon juice. It's acidic, and applying it to your age spots a couple times a day could help reduce their appearance. Similarly, buttermilk contains lactic acid, which can work in much the same way. Honey and yogurt combine to make another homemade bleach. Just mix a teaspoon of each and apply it to your age spots. Let it dry for half an hour and then rinse it off.
For more information about how to get rid of age spots, look over the links on the next page.
Age Spots and Cancer
Occasionally, what appears to be an age spot can actually turn out to be a cancerous lesion. So before you start trying any home remedies to get rid of yours, you may want to have them looked at by a doctor. They might be able to tell whether they're cancerous just by looking at them, but if not, a simple biopsy will do the trick.
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msmarco_passage_01_510313103 | How to Naturally Boost Collagen | HowStuffWorks | How to Naturally Boost Collagen | HowStuffWorks
How to Naturally Boost Collagen
By: Shannon Cicero
Getting Beautiful Skin Image Gallery Aging skin's loss of elasticity and firmness is partly related to the breakdown of collagen. See more pictures of ways to get beautiful skin .
© iStockphoto.com /Lubomir Lipov
Time and gravity will eventually leave you with hard evidence that you're growing older by the day -- fine lines, wrinkles and sagging skin. Blame it on genetics; if your parents developed wrinkles at an early age, chances are you will, too. You can also blame it on all the relaxing days you spent in the sun, or on bad luck and stress. No matter what the reason, wrinkles can be unpleasant and unwelcome. The good news is that it's possible to reduce those signs of aging with natural, noninvasive methods.
As you age, your skin loses some of its elasticity and firmness. Some of this is due to the loss and breakdown of collagen in the dermal layer of your skin. Collagen exists naturally in your skin as a structural support. As you lose collagen throughout the aging process, your skin gets thinner, and wrinkles begin to set in [source: New Zealand Dermatological Society ]. Furthermore, when collagen breaks down, your skin becomes weaker, and this can lead to sagging.
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There are a number of ways to slow down or turn back the hands of time. Modern science has provided plenty of options that attempt to deal with the inevitable signs of aging. Many plastic surgeons and dermatologists, for instance, can give you an injection of soft tissue filler, which is simply a shot of a flexible, tissue-like substance, such as human fat or cattle collagen [source: American Academy of Dermatology ]. But if you're not comfortable with needles or plastic surgery, you might find natural solutions to smooth out and tighten up your skin.
If you're ready to take on the effects of time and naturally boost your skin's collagen production, read on to find out about collagen supplements, creams and foods that can help you age a bit more gracefully.
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Contents
Collagen Supplements
Collagen Creams
Amino Acids and Collagen
Collagen Supplements
Even though your body may not produce the same levels of collagen as it once did, stimulating your collagen production has the potential to reverse some signs of aging. It might be easy to jump to the conclusion that taking collagen supplements for your skin would help, just as you can take calcium supplements to maintain strong bones.
However, the solution isn't as simple in the case of collagen, because you're trying to affect the way your body produces a protein, not just the way it absorbs a mineral. Collagen supplements come in pill and liquid form, and because collagen is found in your skin, bones and cartilage, you can combine it with other supplements. Collagen supplements may be mixed with glucosamine or chondroitin, two supplements used for joint and arthritis problems.
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Since collagen gives cartilage its strength, it can also be helpful for those suffering from osteoarthritis [source: WebMD ]. However, if you don't have joint problems, you might want to opt for collagen hydrolysate or collagen peptide supplements instead. Additionally, if you decide to give collagen supplements a try, you should also boost your vitamin C intake, as vitamin C helps the body produce collagen [source: Medline Plus ].
As with any treatment, how soon someone see results after taking collagen supplements will vary from person to person. Be aware that dietary supplements are not regulated by the United States Food and Drug Administration (FDA), and they do not undergo the same testing as prescription drugs. If you are not sure whether taking a collagen supplement is right for you, ask your doctor.
If taking a pill doesn't sound right for you, perhaps a topical treatment is more acceptable. Read on to find out about collagen boosting creams.
Gelatin and Collagen
Since gelatin is denatured collagen, it might just improve your body's own collagen levels. However, if gelatin is not your snack of choice, you can also use gelatine or gelatine hydrolysate supplements in pill or liquid form.
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Collagen Creams
If you've watched television or flipped through a magazine lately, you may have seen advertisements for anti-aging moisturizers and anti-wrinkle creams that claim to promote collagen production. The key to choosing the right product is studying what's on the label. If you're looking for an anti-aging moisturizer that will give your daily cleansing and moisturizing routine a collagen boost, look for these key ingredients:
Creams that contain retinoid or rentinol can speed up your skin's ability to turn over old skin cells and produce new skin cells [source: Bruno ]. These creams work on the layers of skin where new skin cells are formed and where collagen gives your skin the support and firmness it needs to appear young and wrinkle-free. By increasing skin cell turnover, retinoid helps stimulate your body's collagen production.
Prescription-strength creams containing tretinoin can also help replenish collagen in your skin cells [source: Mayo Clinic ]. Because they are prescription strength, they are stronger than over-the-counter retinoid creams. These types of creams can sometimes provide results where other collagen creams fail, as in the case of deep wrinkles or stretch marks.
Anti-aging creams containing copper peptides or other peptides have been known to increase collagen production. These creams help wounds heal faster, as well [source: Mayo Clinic ].
Collagen creams can help improve the firmness and texture of your skin in the short term, but the overall goal is to stimulate your body's ability to increase collagen production [source: American Academy of Dermatology ]. While creams can give your skin a healthy glow, however, there's no guarantee they will make you look like you're 20 again.
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Now that you've explored the possible benefits of supplements and creams, read on learn about how certain foods may increase collagen production.
Moisturizers vs. Collagen
Skin hydrated with moisturizer will most likely look younger, and fine lines and wrinkles will appear smaller and less visible. While moisturizers work on the outer layer of skin, creams and supplements that boost collagen production work on the deeper layers of your skin.
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Amino Acids and Collagen
The building blocks that make up all proteins, including collagen, are called amino acids. If you lack the amino acids that combine to form collagen, your body's cells can't produce enough of it. What are the amino acids necessary for collagen production, then, and how can you make sure you're getting enough for your body?
Threonine is an essential amino acid for collagen production. An essential amino acid is one your body cannot make, so you have to get it from food or dietary supplements. You can get threonine from foods such as lentils, peanuts, eggs, milk, pork, beef and chicken. If you prefer a vegetarian diet, you can also get threonine from soybeans, chickpeas, hummus, snap beans and asparagus [source: Das ]. Everything from a chicken dinner to a mid-day peanut snack may provide a benefit to your skin.
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Another amino acid that aids in collagen production is proline. Unlike threonine, proline is a nonessential amino acid; nonessential amino acids are ones that either the body or other essential amino acids can produce. You can also help your body by eating foods high in proline, such as gelatin, soy, milk, cheese, beef and cabbage [source: Nutrition Data ]. And as we mentioned before, vitamin C works along with proline to promote collagen production. Foods such as oranges, lemons and limes contain vitamin C.
You don't have to wait until the fine lines on your face turn into heavy wrinkles to think about preventing the signs of aging. You don't have to resort to expensive plastic surgery, either. To find out lots more information about collagen and basic skin care, see the links on the next page.
The Sun and Collagen
If you think your body's natural aging process is harsh on your collagen levels, you might want to stay out of the sun. The sun speeds up the breakdown of collagen, and if you want youthful skin later in life, you'll want to protect yourself daily with sunscreen [source: American Academy of Dermatology ].
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Shannon Cicero "How to Naturally Boost Collagen" 20 August 2009.
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msmarco_passage_01_511372799 | Cabbage: Natural Weight-Loss Food | HowStuffWorks | Cabbage: Natural Weight-Loss Food | HowStuffWorks
Cabbage: Natural Weight-Loss Food
By: the Editors of Publications International, Ltd.
Cabbage is a vegetable few people really appreciate, but it's truly a dieter's friend. It's strong-flavored, but it's this feature that makes it enjoyable in certain dishes.
This leafy vegetable ranks right up there with broccoli, cauliflower, and brussels sprouts with a reputation for fighting cancer. It's also a good source of vitamin C, fiber, potassium, and other nutrients. Cabbage also offers a major payoff -- the fewest calories and least fat of any vegetable. This powerful veggie is a must for dieters trying to lose weight.
Health Benefits
From green cabbage you'll enjoy a fiber boost and a respectable amount of vitamin C. Two types of cabbage, savoy and bok choy, provide beta-carotene -- an antioxidant that battles cancer and heart disease. For those who don't eat dairy products, bok choy is an important source of calcium, which may help prevent osteoporosis and aid in controlling blood pressure.
The phytochemicals in cabbage, called indoles, are also being studied for their ability to convert estradiol, an estrogenlike hormone that may play a role in the development of breast cancer, into a safer form of estrogen -- powerful incentives to add cabbage to your diet.
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Selection and Storage
There are literally hundreds of varieties of cabbage. Green cabbage is the most familiar kind, with Danish, domestic, and pointed being the top three picks of the cabbage family. All sport the familiar pale green, compact head; are similar nutritionally; and shine in fiber.
Red cabbage, a cousin of the green, has a bit more vitamin C, but the most nutritious is savoy cabbage, which has a pretty, dark-green, round head that's loose, ruffly, and prominently "veined." It is much higher in beta-carotene -- about 10 times more -- than green or red cabbage.
Napa cabbage, also known as celery cabbage or pe-tsai, is often incorrectly called Chinese cabbage. Nutritionally, it's equivalent to green cabbage.
Bok choy, or pak-choi, is true Chinese cabbage. As its dark green color suggests, it's rich in beta-carotene. It's also a good source of potassium and a particularly well-absorbed nondairy source of calcium, providing about 10 percent of a day's requirement. It only falls short in the fiber category.
When choosing green and red cabbage, pick a tight, compact head that feels heavy for its size. It should look crisp and fresh, with few loose leaves. Leafy varieties should be green, with stems that are firm, not limp. Store whole heads of cabbage in the crisper drawer of your refrigerator. If uncut, compact heads keep for a couple of weeks. Leafy varieties should be used within a few days.
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Preparation and Serving Tips
Discard outer leaves if loose or limp, cut into quarters, then wash. When cooking quarters, leave the core in as this prevents the leaves from tearing apart. If shredding cabbage for coleslaw, core the cabbage first. But don't shred ahead of time; once you do, enzymes begin destroying vitamin C.
Forget old-fashioned corned beef and cabbage recipes. More nutrients will be preserved and the cabbage will taste better if it is cooked only until slightly tender, but still crisp -- about 10 to 12 minutes for wedges, five minutes if shredded. Red cabbage takes a few minutes more; leafy varieties cook faster. To solve cabbage's notorious stink problem, steam it in a small amount of water for a short time and do not cook it in an aluminum pan. Uncover briefly, shortly after cooking begins, to release the sulfur smell.
Combine red and green cabbage for a more interesting cole slaw. Keep the calories down with a dressing of nonfat yogurt laced with poppy seeds. Bok choy and napa cabbage work well in stir-fry dishes. Savoy is perfect for stuffing. In place of the meat in traditional stuffed-cabbage recipes, use a grain like bulgur, quinoa, or buckwheat.
Cabbage is packed with good stuff. Its leaves are rich in vitamin A and vitamin C. Cabbage is like a health food weight-loss store in a compact edible package.
©Publications International, Ltd.
Nutritional Values Green Cabbage, Fresh, Cooked
Serving Size: 1/2 cup chopped
Calories: 16
Fat: <1 g
Saturated Fat: 0 g
Cholesterol: 0 mg
Carbohydrate: 4 g
Protein: 1 g
Dietary Fiber: 1.4 g
Sodium: 6 mg
Vitamin C: 15 mg
Bok Choy, Fresh, Cooked
Serving Size: 1/2 cup chopped
Calories: 10
Fat: 1 g
Saturated Fat: 0 g
Cholesterol: 0 mg
Carbohydrate: 2 g
Protein: 1 g
Dietary Fiber: 1 g
Sodium: 29 mg
Vitamin A: 3,612 IU
Vitamin C: 22 mg
Calcium: 79 mg
Iron: 1 mg
Potassium: 315 mg
Carotenoids: 261 mc
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the Editors of Publications International, Ltd. "Cabbage: Natural Weight-Loss Food" 28 April 2006.
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msmarco_passage_01_518888994 | Honest Kitchen Dog Food Review - Best Dog Foods and Holistic Dog Health Remedies | HealthierDogs.com | Honest Kitchen Dog Food Review - Best Dog Foods and Holistic Dog Health Remedies | HealthierDogs.com
Honest Kitchen Dog Food Review
Page may include affiliate links, and we may earn a commission from qualifying purchases.
Honest Kitchen dog food began with a search for a human grade pet food that would be good enough for their own pets to eat, one that resembles a home made diet in quality, encompasses variety, is economical, nutritionally balanced, and quick and easy to prepare.
Honest Kitchen Dog Food – It’s Dehydrated
Their motto is – Dehydrated raw pet food with passion and principles!
Honest Kitchen pet foods are made in an FDA approved, human-food-producing facility in Southern California, that makes the very same foods you eat. No processing in any pet food plant for Honest Kitchen dog foods or cat foods.
Honest Kitchen Dog Food x 8
There are now eight varieties of Honest Kitchen dog food to choose from and all contain a broad array of amino acids, phytonutrients, vitamins, minerals and enzymes to help achieve and maintain optimum health for your dog with natural dog food.
Verve was the original Honest Kitchen organic dog food. It contains organic rye, organic barley, hormone-free beef, organic flaxseed, organic oats, carrots,alfalfa, potatoes, eggs, red and green bell peppers, spinach, apples, cranberries, chicory, parsley, peppermint and rosemary. Yum! It’s best suited to adult and senior dogs with a low to moderate activity level.
Force – you could describe Force Honest Kitchen dog food as a force to be reckoned with! Its list of ingredients include hormone-free chicken, organic flaxseed, potatoes, celery, sweet potatoes, apples, alfalfa, organic kelp, honey, zucchini, green beans, cabbage, bananas, papayas, yogurt, basil, garlic and rosemary. Force was formulated specifically for dogs with sensitive stomachs, and allergies to wheat and gluten. It’s both wheat and gluten free.
Embark Honest Kitchen dog food was added to cater to active dogs, including puppies, and also for pregnancy and for nursing dogs where added nutrients are required for optimal nourishment of the unborn and newly born pups. It’s a low carbohydrate, grain free, dog food containing hormone-free USDA turkey, organic flaxseed, potatoes, celery, spinach, carrots, coconut, apples, organic kelp, eggs, sesame seeds, bananas, cranberries and rosemary.
Some dogs are intolerant of the usual meat protein sources, and some are intolerant of potatoes and flax. Preference was formulated by Honest Kitchen dog food for these dogs. Preference is a grain and meat free dog food base – you need to add your own protein. The beauty of this formulation is that if your dog does not tolerate chicken or turkey but can, for example tolerate venison or kangaroo, you can add the meat source your dog can tolerate. You can add eggs, fish, or even some cottage cheese, if your dog cannot tolerate any types of meat. What does Preference consist of? Alfalfa, sweet potatoes, cabbage, celery, apples, spinach, organic kelp, coconut, bananas, zucchini, and honey.
Thrive is a later edition to the Honest Kitchen dog food range. Like Embark, Thrive is also low carbohydrate and is gluten free, but contains some grain. The ingredients comprise Hormone-free Chicken, Organic Quinoa, Sweet Potatoes, Spinach, Parsley, Organic Kelp, Rosemary, Vitamins and Minerals. Because of its low carbs – just 37% carbohydrate, Thrive is not only good for active dogs, including pregnant and nursing dogs, but is also excellent as part of a cancer recovery regime.
More recent still are the Keen, Zeal and Love formulations.
Keen was created for dogs with common protein intolerances – often dogs with protein intolerances don’t do well with the more common proteins – chicken, beef, eggs and fish. Keen is formulated with cage-free turkey meat, plus low gluten organic oats, and garden vegetables such as carrots and cabbage. It also has herbs such as organic alfalfa, rosemary and kelp, as well as some apples.
The Zeal dog food by Honest Kitchen is another grain free food (like Embark) but this one is based on wild, line-caught white fish (Haddock and Whiting), with a touch of Salmon, mixed with some sweet potato, egg, organic coconut, organic alfalfa, apples, pumpkin, parsley, cabbage, bananas, cranberries, garlic, and rosemary – yum! Because it’s fish based, if your pooch is intolerant of any type of meat, this will be perfect. And most dogs love fish anyway, so it’s great for a change from whichever of the other Honest Kitchen formulations you usually feed your dog.
And last but not least – Love dog food. Love is a performance food for active dogs of all ages and life stages, including puppies and pregnant and nursing bitches and every other dog with an active lifestyle. Love is based on Midwestern beef with sweet potatoes, dandelion greens, parsley, papaya, cranberries, pumpkin and more. Love is gluten free, low carbohydrate, and is perfect for dogs with egg or poultry intolerances. Have an active dog? What better way to show your love to your dog than to give him Love!
Eight different varieties of natural dog food that you can really count on.
Honest Kitchen Dog Food AND Supplements!
Oh, and I almost forgot, Honest Kitchen also produces some excellent pet health supplements, and some really unusual and very yummy dog treats!
For more dog food reviews, and more on Honest Kitchen dog food and other types of natural dog food, click on any of the hyperlinks.
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How to Identify Dog Health Problems
Benefits Of Dog Obedience Classes
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msmarco_passage_01_523951352 | augmentin and sulfa allergy - MedHelp | augmentin and sulfa allergy - MedHelp
Augmentin and sulfa allergy
Common Questions and Answers about Augmentin and sulfa allergy
augmentin
A sulfite reaction is different from a sulfonamide allergy (a reaction to sulfa drugs) because sulfites and sulfonamides are entirely different chemicals and have unrelated mechanisms of reaction. A person sensitive to sulfites is no more likely to be allergic to sulfonamides than any other individual and vice versa. " http://www.itmonline.org/arts/sulfa.
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It is very difficult to precisely confirm a diagnosis without examination and investigations and the answer is based on the medical information provided. For exact diagnosis, you are requested to consult your doctor. I sincerely hope that helps. Take care and please do keep me posted on how you are doing.
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Some times yes, sometimes no. Generally diamox is not used with sulfa allergy unless no other good substitute is avalable.
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My big concern is that I was diagnosed with a Sulfa allergy as a child when a Sulfa Based Opthalmic Ointment was used to treat an eye infection and I broke out in hives after using the drug. My daughter used Sulfa Antibiotics to treat a UTI and over the course of a week her face swelled up. The pharmacist had mentioned taking the medication and trying benadryl and if I have a reaction to seek medical treatment immediately.
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I'm allergic to Penicillin and Sulfa, I just finished taking Doxycycline for a week and feel better. Thanks for the information.
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I was diagnosed with a sulfa allergy as a child and haven't had any problems since as my doctors know of this allergy when prescribing medication. However, due to the geothermal activity and potential exposure to sulphur related gases/water, I wanted to know if travelling to Iceland would pose any health risks. I know that sulfa and sulphur are related but not the same but I am still concerned that I might be exposed to problems when inhaling gases or drinking water.
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However, you mentioned an allergy to sulfa drugs; Lasix (Furosemide) has a sulfonamide in its structure and there is a concern of possible allergic reactions in a person with a Sulfa allergy. However, if she has taken the medication and only is experiencing gastrointestinal difficulties, this is not a concern about an allergic response to the medication.
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Yesterday I received a Lipo-Plex injection (B12 with Lipotropics) that contains Methionine a sulfur containing amino acid. I have a Sulfa allergy (normally get an extremely high fever). Should I be worried? I haven't had any side effects. Feeling a little flushed (hot) but that is about it. Otherwise I feel great. Can I continue with these shots? Thanks!
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Yes, it is true that you will not necessarily have a reaction to HCTZ if you have a sulfa allergy. A small percentage of people (< 15%) do have cross-reactivity to HCTZ when they have a sulfa allergy. If you have had a severe reaction to sulfa antibiotics then we would probably recommend avoiding HCTZ.
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About 3 months back i had a kidney infection, they put me on sulfa base medicine and i discovered i was allergic to the sulfa and had a drug.reaction toit. They had given me a steroid shot and steroid pills to continue taking for about 8-10 days. Along with a antihistamine. They worked and rash was cleared up. The same rash appeared about 2 weeks later again i went to the doctor and they did the same routine (steroid and antihistamine). Cleared up again.
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Drugs like penicillin and sulfa group of drugs are most common cause for hypersensitivity reaction. As you have a history of penicillin allergy. If your body is hypersensitive to sulfa, reaction will be similar to that you develop for penicillin. Each individual are known to respond to a drug differently in drug allergy. If the drug is too much sensitized then it can cause more severe reaction.
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My big concern is that I was diagnosed with a Sulfa allergy as a child when a Sulfa Based Opthalmic Ointment was used to treat an eye infection and I broke out in hives after using the drug. My daughter used Sulfa Antibiotics to treat a UTI and over the course of a week her face swelled up. The pharmacist had mentioned taking the medication and trying benadryl and if I have a reaction to seek medical treatment immediately.
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Hi, I was told when I discovered my allergy to Sulfa drugs that Neosporin is a No No. Maybe see if you have a sulfa allergy and don't mess with the vaccine until you get this figured out. I read about a healthy 61 year old woman developing shingles 3 months after the vaccine and it was excruciating. Best of luck.
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People with the sulfa allergy are not supposed to take lipotropic injections that include methionine. Please ask your regular doctor about it before taking an injection from a diet center that may not know enough about sulfa allergies.
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I found out the hard way in January that I have a severe allergy to sulfa antibiotics. It was hives head to toe for weeks and nothing really helped, I just had to wait it out. Well now that's gone but my system still isn't back to normal. I've switched, per a dermatologist's advice, to free and clear products, but four months down the road my hives have become chronic.
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I met my friend at an Irish Pub and had a fresh poured pint of Guinness. 3/4 of the glass down, my palms and neck was itching. I finished my pint and bought another round. 1/4 of the way into my next, my lips were swelling and my buddie noticed my eyes/ face were swelling. I tried to talk and within minutes my tongue had swollen to 2x the size and I could not speak. I was rushed to the ER where after 4 hours on an IV I returned to normal.
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t cystic, but a bit more problematic than mild acne. Also, a sulfa allergy limits that option for treatment. Current regimen includes Azelex (for redness and inflammation) and Tretinoin. I'm curious if there is an effective treatment that takes the fibromyalgia into consideration.
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Doctor, My dermatologist prescribed Augmentin 1g for 14 days for syphilis. I found out 4 days ago, both VDRL and FTA-ABS tests (IgG pos, IgM neg) confirmed that I do have a syphilis infection, and I was possibly infected 5 years ago ( am I way past the secondary stage? possibly latent?). The dermatologist says that Augmentin should work, but I'm worried. I will continue with the oral Augmentin, and re-test to see if it is working, but what are the chances it will?
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Stop the medication. And go to the FDA site and file an adverse reaction form. We don't know for certain that the antibiotic is linked to the red rashes, however if an allergy has developed there is a remote but unlikely possibility that the allergenic response may worsen and become life-threatening. You have already been on the antibiotic two weeks, which is long enough (under normal circumstances) to clear an infection. Sinus infections are notoriously difficult to destroy.
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I believe that primary care manager thinks I am hyper now because of side effects from hydrochlorothiazide (am deathly allergic to sulfa drugs and this is a sulfa drug - unbeknownst to me until today).
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A month ago, 2 parts (15 cent size) of my scalp started oozing, First Dr- said it is infection, gave me Bactrim (for 10 days) after 10 days scalp is still ozzing got bigger. Second Dr- said it is fungus,gave me Nizoral shampoo, after 3 days my face was having allergy reaction from the shampoo. stoped oozing is getting begger. Third Dr- said it is infection, gave me Augmentin. after 3 days i have rash all of my body start with lower arms and lower part of my leg.
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i recently found out that im 2 weeks pregnant and iwas on antibiotics (doxyclyn and metrronidazole) for bacterial infection before i took the test ,i want to know if this has affected the baby or me.
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I have white/clear mucous and have used augmentin and azithromax one course after another ( augmentin first and then azithromax) given by my doctor but the cough is not gone. My chest x ray is normal but the doctor could not do a pft because of my continuous cough at that time. My blood work for pneumonia diabetes and cholesterol are all good. sinus CT scan is normal too. Is this viral is it okay to take several months for cough to go away. I have no wheezing or asthma history.
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msmarco_passage_01_528387320 | is augmentin in the penicillin family - MedHelp | is augmentin in the penicillin family - MedHelp
Is augmentin in the penicillin family
Common Questions and Answers about Is augmentin in the penicillin family
augmentin
My lung Doctor called me in some augmentin because I have been coughing up thick yellow mucus. I just don't know if I can take it on treatment. Does anyone know??
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Penicillin is one of the meds prescribed to pregnant women with a Strep B infection.
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was aware I had the seizure problem and prescribed cipro, which I had to call and tell them to send me something different. The one at the pharmacy now is Augmentin. Just need a neurologist`s expert opinion as to whether or not it is alright to take Augmentin with my myoclonic seizure condition. Do not want to start up any seizures. However, this UTI is hurting so badly!!! If It is too risky then I can`t take it!!!! Please help me.
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Hi, antibiotics, such as amoxicillin for 2 weeks, have been the recommended first-line treatment of uncomplicated acute sinusitis. Amoxicillin-clavulanate ( Augmentin) is also an appropriate first-line treatment of uncomplicated acute sinusitis. Other options include cephalosporins such as cefpodoxime proxetil (Vantin) and cefuroxime (Ceftin). In patients allergic to beta-lactams, trimethoprim-sulfamethoxazole (Bactrim), clarithromycin (Biaxin), and azithromycin.
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Malarone is what landed me in the hospital that time. I had also tried mepron. I hadn't heard of that other drug but it seems you are on the right track and glad to hear it!
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augmentin would likely cure it if you had enough of it. I am just curious if you asked the doctors why are you asking us....... none of us are doctors.......you came for advice and the advice was sound. The cure for oral ghonnorhea is not augmentin as advised by the CDC and I think you will find if you rephrased your question and asked the docs what the reccomended cure would be they would not even list augmentin or amoxicillin.
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um yes she should not have had penicillian...your not suppose to take any antibiotics like that while pregnant...
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Month after the treatment the doctor made TPH tests and said that there is no difference at all, which is strange, because I was treated with penicillin. She added that one of the tests was negative, another will stay positive for life and there is no increase, neither decrease which I didn't understand. And she wanted me to have another treatment with penicillin depo...
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I'm getting a bit scared lately... I have been battling a recent UTI. I used to get them a lot when I was younger but haven't had one in about 2- 3 years. Anyway, took levaquin 500mg for about a week and felt much better then 4 days later it hit again. Did the AZO testing which tested positive for nitrate so went back on Levaquin and after two days of taking it I wasn't getting much relief so I went to my doctor.
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t wait too weeks and call your doctor when it is 72 hours past when you started the antibiotics. Is it your throat or your skin that is infected?
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I'm not buying your story about the er at all! First of all, there is no way that the nurse didn't know what a dry socket is, and two I doubt that they told you that penicillin only comes in an injection! I also don't believe that you are a health care provider, or you would know that amoxicillin is AUGMENTIN, & it has penicillin in it!!!.....
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Also I have minimal tooth pain but it is still there. Is it too soon to say that antibiotics are not working? The mucous thickening that the dentist saw will it go away with antibiotics or should it be removed surgically? I also got some Flonase yesterday hoping it will help. I do not get many sinus infections, I get allergies but I just let them run their course. Do you think this was caused by the root canal or did it aggravate it?
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Gotta love best friends, they will do you in!!! She is still taking the zyrtec, so that wasn't the culprit. It seems like the only thing it could have been was the augmentin. So even thought he rast was negative, some Drs. have said that that doesn't matter, I gusee that test isnot always accurate. I said what are the chances you would get ARS THE SAME TIME YOU ARE ON AN ANTIBIOTIC?!!!! Make me crazy!!!The angiodema is what made me lean towards allergic reaction, what do you think?
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5 weeks and my doctor detected strep b in my urine. i dont really feel too comfortable taking these in the first trimester even though they may be considered "safe". any insight would be great.
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I am leery of anything that could add to my liver damage and normally try to get an antibiotic in the penicillin family . There are times that the risk outweighs the benefit. Good luck to you.
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Your doc gave you augmentin because strep B is susceptible to that form of penicillin, but not in the prostate because it doesn't get inside in high enough quantity. But, Penicillin G administered by injection did for me. Prostatitis is curable, but you need a doctor that cares and uses science rather than witchcraft.
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It is now 5 days taking benadryl and the hives and itching have not stopped. What is in the clindamycin that I may be allergic to?
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She took it for one week, and on the seventh day of the ten day course is when she broke out in hives!!! She proceeded to tell me that they took 5 days to go away and that some who pop up here and there for a few weeks. The cortisone, steroid, and zyrtec halped to cure them, She also had angiodema around her eyes, the angiodema coupled with the hives responding to steroids and antihistmaines truly, to me, points to allergy.
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I have been fighting a bone infection in my jaw for 6 months - it wasn't identified until this past month but I'd been very sick this whole time. This past month I finally found a good oral surgeon who removed the 2 teeth causing the problem, and cleaned out the bone underneath.
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Hi, I have a sinus infection and the doctor has prescribed me Augmentin. I hate taking medication when I'm pregnant but I need to get better : ( I am only 8 weeks. Has anyone else taken antibiotics in their first trimester?
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t working, but Cephalexin is different enough it might work. You can tell if its working if the pain/swelling go away in 4-5 days.
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But 10-15% are resistant. Augmentin is active against even the resistant strains. Augmentin has not been studied for its effect against pharyngeal gonorrhea, but in the doses used for strep throat and respiratory infections, it probably would cure it. Asymptomatic urethral gonorrhea is uncommon in men, and testing is reliable. The asymptomatic person can be sure he doesn't have it. There is no point in you being tested while taking augmentin.
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t use my hands to open bottles and things of that nature due to tingling in my hands from the swellings and from the veins near surface of hands. Went to ER and they only visually looked and said they see nothing wrong with veins and swellings probably from eating to much salt, which is not true because my diet hasn't changed and I haven't experienced this before.
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msmarco_passage_01_534634274 | what is the fingernail quick - MedHelp | what is the fingernail quick - MedHelp
What is the fingernail quick
Common Questions and Answers about What is the fingernail quick
nail
Can HIV be transmitted if semen got underneath a fingernail? In otherwords, is the tissue underneath the fingernail vulnerable to passing HIV into the blood stream?
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Hsv is not concentrated in fluids. Genital hsv is an std and called this because that's what it takes to spread it. Hsv is not going to be transmited like you described. Even if you didn't wash your hands, the answer will remain the same. There isn't enough viral load.
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I have a small (maybe the length of my fingernail), half moon shaped white mark on the finger pad (tip) of my index finger. The mark is deep under the skin, with nothing bubbling up on the surface (yet). I have never had herpetic whitlow, but I have had several cold sores lately and am scared that this may be the start of one. My finger does not hurt or tingle though. Does this sound like it may be very early stages of whitlow?
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i was fingering a women with two bare fingers , she had some spotting from her period , i noticed a small amount of dry blood on my fingernail later in the day , I cleaned up after the fact with some wipes and did not notice any blood at that time , i am unaware of the womens HIV status although she says she is clean , should i worry about exposure and should i get tested
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Now the fingernail has a small hole in it and the nail felt soft. He is physically fine and there is no pain in the indicated finger. Please advise.
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it a nail coming off dear and it may be corsed by the washing powder soap you are using so change it...
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thanks for the quick response but I just read what I wrote again,and I see I put I think I had a small cut by fingernail,but I meant I did have one, I dont mean to bothersome,is your answer still the same?
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I was taking the fingernail polish off my toenails and I noticed one of them had a darker yellow color to it. The color of fingernail polish was red so it wouldn’t be a stain from the fingernail polish. I wish I could put a photo. It starts in th bottom corner and goes up a little. I don’t know. Please help.
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http://www.medhelp.org/posts/Dermatology/ what - is -this-in- the -tip-of-- fingernail /show/2234011#post_10720537 Thank you very much in advance.
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It is very difficult to precisely confirm a diagnosis without examination and investigations and the answer is based on the medical information provided. For exact diagnosis, you are requested to consult your doctor. I sincerely hope that helps. Take care and please do keep me posted on how you are doing.
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It's a wound under my fingernail and the blpod is really near it. Also I'm not trying to profile anyone I am just trying to give as much detail about him to see does he match HIV symptoms.
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If this is not a bone spur than the other possibility could be paronychia which is an infection that develops along the edge of the fingernail or toenail. The paronychia is first tried to control with the help of antibiotics if there is infection along with inflammation. Nail removal can help in such cases. If the podiatrist recommended nail removal then there is nothing to worry about as this is a simple procedure if done carefully with local anaesthetics and the nail will grow back quickly.
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Do you think the virus will transfer from my hand to zipper to then underneath my fingernail? Is it possible to get underneath the fingernail from a small metal zipper?
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Just wondering, what's the difference between the Weight Loss and the Dieting communities? I never know where to post.
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But since I have been able to scrape this white mucous like substance out of my mouth for a few weeks now it has me very concerned that I may have a Candida infection. Can anyone please verify what a thrush lesion would look like when it is scraped off the inner cheek. And does what I am describing sound like it might be thrush. Sometimes these white spots are easy enough to rub off with my tongue. My inner cheek feels raw like I have been biting it.
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There was no liquid from hsv2 on the zipper but can the virus still transfer from the hand to zipper to underneath fingernail with no liquid? Can the virus get underneath fingernails, are there any "opening" under the nail to let the virus in?
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It is exactly the consistency of healthy fingernail material. So my guess is that the hair follicle is defective and is producing fingernail keratin from the scalp. Maybe that means simply that the normal outer sheath of the hair is wildly thicker than it should be. Any help from anyone who knows would be appreciated! Thanks!
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Reread the advice because you asked the same question before.
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YESTERDAY I GOT A FINGERNAIL SIZE DISCHARGE AND IT WAS DARK BROWN IT WASNT A SHADE OF RED OR PINK JUST BROWN SOME PPL SAY NORMAL AND SOME PPL SAY GO TO THE DOCTOR QUICK. IM REALLY NERVOUS CAUSE I HAVE A MC IN FEB. AND I DONT WANT THAT HAPPENEING AGAIN. IT WAS HORRIBLE. I NEED HELP? SOMEONE PLEASE HELP ME?
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what are the chances of HIV infection for a female who had her vagina cut with a fingernail and was fingered with about a half tablespoon of pre-ejaculate right after?
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I have added a photo as I am not sure if everything is ok. I guess what is the nail is growing back but its like a half inch bump in the middle of the nail, Could anyone recommend if I should leave nature take it's course, or should I see a doctor?
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msmarco_passage_01_541206461 | The FDA Recommended Sodium Intake | Healthy Eating | SF Gate | The FDA Recommended Sodium Intake | Healthy Eating | SF Gate
The FDA Recommended Sodium Intake
Healthy Eating
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Nutrition
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Sodium
By Cindy Pineo Updated December 12, 2018
The U.S. Food and Drug Administration doesn’t develop nutritional guidelines itself, but rather advocates those in the Dietary Guidelines for Americans, a publication that the U.S. departments of Agriculture and Health and Human Services release every five years. The FDA does not actively regulate sodium content in food, but has issued guidance for companies voluntarily reducing their food's sodium content.
Tip
The FDA recommends that individuals consume no more than 2,300 milligrams of sodium per day, and that certain groups limit intake to 1,500 milligrams per day.
Upper Limit
The Dietary Guidelines for Americans 2015 address sodium intake in detail. The average daily sodium intake for Americans is 3,400 milligrams per day, an excessive amount that raises blood pressure and poses health risks. In general, Americans should limit daily sodium consumption to 2,300 milligrams, but this is an upper safe limit, not a recommended daily allowance. Even active people who lose lots of sodium through sweating require no more than 1,500 milligrams of sodium per day.
Sodium Sensitivity
Certain demographic groups are especially sensitive to sodium’s blood-pressure-raising effects, and members of these groups must limit sodium to 1,500 milligrams per day. Half of all Americans are subject to this limit, including African Americans, people over the age of 51 and anyone with high blood pressure, diabetes or kidney disease. Children also have lower sodium needs and should adhere to the 1,500-milligram maximum.
Cutting Sodium
Limiting sodium is challenging in a world full of fast food, prepared food and salty snacks. Cooking at home, eating mostly whole foods and scrutinizing food labels will help you take control. Be wary of restaurant foods and drinks, even those that don’t taste salty. Excessive sodium lurks in treats like sweet blended coffee drinks, doughnuts and cookies, which often contain several hundred milligrams per serving. Certain canned foods, such as soup and tomatoes, are always overloaded with sodium unless specifically labeled otherwise. Seek out low-sodium versions of these pantry staples.
Increasing Potassium
Dietary potassium -- another mineral salt and essential nutrient -- can balance sodium consumption by lowering blood pressure. Fruits and vegetables are naturally high in potassium. Some of the best sources are bananas, potatoes, prunes, oranges, beans and tomatoes. As an added safeguard against excess dietary sodium, include plenty of these tasty plant foods in your diet. Don’t take potassium supplements unless your doctor prescribes them, however, because potassium overdose from supplements is dangerous.
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References
U.S. Food and Drug Administration: Lowering Salt in Your Diet
U.S. Food and Drug Administration: Sodium Reduction
U.S. Food and Drug Administration: FDA Issues Statement on IOM Sodium Report
Dietary Guidelines for Americans, 2015-2020
ABC News: Beware of Hidden High-Sodium Foods
ChooseMyPlate.gov: Salt and Sodium
Linus Pauling Institute: Potassium
Writer Bio
Cindy Pineo has been writing about diet, wellness and culture since 2002. She is coauthor of the book "The Atkins Diet and Philosophy." Pineo holds a Master of Arts in English literature from the University of Illinois at Urbana-Champaign and a Master of Arts in humanities from the University of Chicago.
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msmarco_passage_01_542299275 | The Harmful Effects of Sodium Nitrite in Food | Healthy Eating | SF Gate | The Harmful Effects of Sodium Nitrite in Food | Healthy Eating | SF Gate
The Harmful Effects of Sodium Nitrite in Food
Healthy Eating
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Healthy Meals
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Planning Meals
By Christina Marie Updated December 14, 2018
The potential health effects of sodium nitrite, known more simply as nitrite, is confusing, but more research is bringing this compound into the spotlight. Excessive intake of sodium nitrite has been linked to diseases such as non-Hodgkin lymphoma, leukemia and esophageal, pancreatic, bladder and thyroid cancer, according to Healthy Child, Healthy World. Although sodium nitrite is largely unavoidable in the environment, exposure can be minimized to prevent harmful levels.
Sodium Nitrite Defined
Nitrates are chemical compounds found in the environment. The term nitrites is often used interchangeably with nitrates, due to the conversion in the body of nitrate to nitrite. Sodium nitrite is the product of bacterial microbes digesting waste that contains nitrogen. It is an inorganic material that can occur naturally but also as a byproduct of fertilizer application, decomposition of animal waste, sewage treatment facilities and septic systems, as well as a food preservative. Major sources of sodium nitrites include drinking water and food; sodium nitrate is added to cured meats as a preservative.
Sources of Sodium Nitrite
Diet is responsible for the highest level of exposure to nitrites, due to nitrate fertilizer on crops that accumulate in foods, according to the New Hampshire Department of Environmental Services. An average American diet accounts for 75 to 100 milligrams per day of nitrate exposure. Nitrates can be found naturally in some vegetables, including cauliflower, broccoli and collard, and they are used as preservatives in cured meats, such as deli meat and bacon. Drinking water is also a source of exposure, particularly well water from contaminated or shallow wells.
Health Effects of Sodium Nitrite
Exposure to nitrites poses the highest risk to infants and pregnant women, reports Healthy Child, Healthy World. In pregnant women, the harmful byproduct of nitrites known as methemoglobin accumulates in the body and deprives the cells of oxygen. Nitrate exposure during pregnancy can cause birth defects, according to a study published in 2004 in "Epidemiology," and high amounts in infants can lead to a serious respiratory condition known as blue-baby syndrome. When nitrites react with amine-containing food or drugs, they convert to compounds known as nitrosamines, which are known to cause cancer, according to the New Hampshire Department of Environmental Services.
Ways to Avoid Sodium Nitrite
An important measure to limit exposure to nitrites is to request information about the quality of your water, whether it comes from a private well or a municipal water system. By carefully reading labels, you can avoid purchasing foods and cured meats that contain these compounds. Choosing organic over conventionally grown foods will minimize your exposure to synthetic fertilizers, which contribute to the nitrite content. Eating a diet rich in antioxidants, such as vitamin C, will block the formation of harmful nitrosamines. If you suspect that you or a family member has nitrite poisoning, Delaware Health and Human Services recommends that you have a healthcare professional order tests to measure blood and urine levels.
References
U.S. Environmental Protection Agency: Nitrates and Nitrites
Healthy Child, Healthy World: Avoid Nitrates and Nitrites in Food
Delaware Health and Social Services: Nitrate and Nitrite
Epidemiology: Dietary Nitrites and Nitrates, Nitrosatable Drugs, and Neural Tube Defects
New Hampshire Department of Environmental Services: Nitrate and Nitrite: Health Information Summary
Writer Bio
Christina Marie is a health writer based in Buffalo, N.Y. She holds a Master of Science in nutrition science and enjoys helping others reach their own optimum wellness. She also works as a nutritionist and lactation consultant.
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msmarco_passage_01_542697685 | The Health Effects of Eating Raw Garlic Daily | Healthy Eating | SF Gate | The Health Effects of Eating Raw Garlic Daily | Healthy Eating | SF Gate
The Health Effects of Eating Raw Garlic Daily
Healthy Eating
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Diet
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Digestion
By Jill Corleone Updated November 21, 2018
Snacking on pita chips and garlicky hummus not only tastes good, but is good for you, too. Garlic is a natural source of many phytonutrients that may help improve heart health, reduce risk of cancer and fight off infection. However, to get the most benefits from garlic, you need to eat it raw, because cooking negatively alters the beneficial compounds.
Better for Your Heart
This little flavor enhancer is filled with nutrients that do your heart good, including lowering blood pressure and cholesterol, and reducing risk of atherosclerosis, which is hardening of the arteries. In test-tube studies, it's thought that γ-Glutamylcysteines in garlic may help prevent the constriction of your arteries, which in turn, helps lower blood pressure. The S -allylcysteine, or SAC, in garlic may help lower cholesterol by inhibiting the enzymes that produce cholesterol and lipids. And the acetone and chloroform compounds in raw garlic may help prevent the build up of plaque on your arteries, reducing risk of hardening.
Garlic and Cancer
A number of compounds found in garlic, including allicin, ajoene, and diallyl trisulfide, or DATS, may help protect you against cancer. Allicin may inhibit the growth of tumor cells, while ajoene and DATS kill cancer cells. In addition to decreasing growth and killing cancer cells, it's also thought that garlic may help protect against cancer by assisting in cell detoxification and working as an antioxidant.
Protection Against Infection
Garlic has been used as an anti-microbial agent for centuries, according to a 2014 review article on the health benefits of garlic published in Acivenna Journal of Phytomedicine. The allicin in garlic is believed to be the component that helps your body fight off bugs such as salmonella, E. coli and Staph aureus. Garlic is such a potent anti-bacterial that it's been shown to be beneficial in fighting off bacteria that have become resistant to certain antibiotics.
Garlic appears in a number of cooked foods, from spaghetti sauce to lo mein, but you might be struggling on how to add the bulb to your diet in raw form. In addition to hummus, guacamole and salsa are also dipping foods that use raw garlic. Also, you can add thinly-sliced raw garlic to your avocado toast or mix it into your cooled mashed potatoes. Minced garlic also adds a little punch to salad and soup. Or try adding a clove or two to your kale, carrot and tomato smoothie.
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References
Acivenna Journal of Phytomedicine: Garlic: A Review of Potential Therapeutic Effects
Writer Bio
Jill Corleone is a registered dietitian and health coach who has been writing and sharing her love of food, nutrition and health with anyone who'll listen for almost 20 years. Her work has been featured on the Huffington Post, Diabetes Self-Management and Working Mother.
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msmarco_passage_01_543710285 | List of Foods That Can Be Eaten on a Low-Purine Diet | Healthy Eating | SF Gate | List of Foods That Can Be Eaten on a Low-Purine Diet | Healthy Eating | SF Gate
List of Foods That Can Be Eaten on a Low-Purine Diet
Healthy Eating
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Nutrition
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Protein
By Erica Kannall Updated December 12, 2018
If you've recently been diagnosed with gout or kidney stones, your health care provider may recommend you follow a low-purine diet. Purines occur naturally in some foods, such as organ meats and anchovies, and contribute to uric acid production in your body, which aggravates both gout and kidney stones. But, you can safely eat a majority of fruits, vegetables, grains and dairy products while following a low-purine diet.
Proteins
You need to use caution when eating high-protein food, as some proteins are high in purines. You can safely eat about 6 ounces of poultry, fish, beef, lamb, veal, pork or eggs per day, according to the University of Pittsburgh Medical Center. Nuts and nut butters are a good vegetarian protein source. But, you'll want to limit your intake of dried beans and peas to two servings per week because of their purine content. You should avoid all organ meats, such as liver, as well as anchovies, herring, mackerel, scallops, mussels, shrimp and lobster.
Dairy
You can also safely eat dairy while following a low-purine diet. Milk, yogurt and cheese are a good way for you to get low-purine protein. They also provide you with much needed calcium. However, choose low-fat or fat-free varieties when possible and avoid cream. Full-fat versions of dairy products contain saturated fat, which may decrease excretion of uric acid and make your condition worse.
Fruits and Vegetables
Fruits and vegetables are some of the safest foods to eat while following a low-purine diet. The variety of fruits and vegetables to choose from is extensive and offers you a good source of vitamins, minerals, fiber and antioxidants. However, you should limit your intake of spinach, mushrooms, asparagus and cauliflower to two servings per week because of their purine content. But, you can freely can eat all the other fruits and vegetables you love.
Grains and Starches
Grains are another staple food while following a low-purine diet. You can have most bread, pasta, cereal and rice while sticking to your diet. Starchy vegetables, such as potatoes and winter squash provide another way to get in low-purine, complex carbohydrates. However, you should limit your intake of oats to 2/3 cup per day and your intake of wheat germ and wheat bran to 1/4 cup per day to prevent problems. Read the ingredient list of the food to determine if it's high in one of these grains. The ingredients are listed in descending order according to their concentration in the food. If you see oats or wheat bran at the top of the list, limit your intake of that food.
References
UPMC: Low-Purine Diet
Drugs.com: Low-Purine Diet
FamilyDoctor.org: Low-Purine Diet
Writer Bio
Erica Kannall is a registered dietitian and certified health/fitness specialist with the American College of Sports Medicine. She has worked in clinical nutrition, community health, fitness, health coaching, counseling and food service. She holds a Bachelor of Science in clinical dietetics and nutrition from the University of Pittsburgh.
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msmarco_passage_01_544067610 | What Is the Main Function of Phosphorus in the Body? | Healthy Eating | SF Gate | What Is the Main Function of Phosphorus in the Body? | Healthy Eating | SF Gate
What Is the Main Function of Phosphorus in the Body?
Healthy Eating
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Diet
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Fat
By Sue Roberts, M.P.H., R.D. Updated December 12, 2018
Phosphorus is an essential mineral primarily used for growth and repair of body cells and tissues. According to the University of Maryland Medical Center, all body cells contain phosphorus, with 85 percent found in bones and teeth. There, together with calcium, phosphorus provides structure and strength. Phosphorus is also required for a variety of biochemical processes including energy production and pH regulation.
Energy Production
Phosphorus is commonly found in the body as phosphate. Phosphates play an important role in energy production as components of ATP, or adenosine triphosphate. ATP is readily used to fuel your body's many functions. Structurally, ATP consists of adenosine, an organic compound, and three phosphate molecules. When bonding between one phosphate and adenosine is severed, energy is released which then fires cellular activity. According to the authors of "Nutrition," energy released from ATP is used quickly, so your body contains only a small amount at any one time.
Protein Synthesis
Phosphorus is a component of deoxyribonucleic acid, or DNA, and ribonucleic acid, or RNA, long molecules which carry genetic information used to make proteins. Synthesis begins in the cell nucleus, where a portion of DNA serves as a template for RNA manufacture. RNA then carries specific coding instructions for building needed body proteins to the ribosomes, where proteins are assembled from amino acids. Without sufficient phosphorus, body protein manufacture is impaired, which eventually affects overall health.
Secondary Functions
Phosphorus also acts as a buffer, neutralizing acids to maintain normal pH in the blood. Many enzymes and hormones also contain phosphorus as a structural component. Hemoglobin, the important oxygen-carrying protein in the bloodstream, also depends upon phosphorus contained in its structure for proper function.
Food Sources and Requirements
Good food sources of phosphorus include protein foods, such as meat, fish, eggs, milk, nuts and legumes, and also cereals and grains. Carbonated beverages supply significant amounts of phosphorus in the diet, too. Gordon Wardlaw and Anne Smith, in their book “Contemporary Nutrition,” report that between 20 and 30 percent of dietary phosphorus comes from food additives contained in processed foods. The Institute of Medicine’s Recommended Dietary Allowance for adults is 700 milligrams of phosphorus per day. The Tolerable Upper Intake Limit, or UL, also set by the Institute of Medicine, is 4 grams per day. Intakes above this are considered unsafe.
Precautions
Because phosphorus is found in a wide variety of foods, deficiencies are rare, except in diseases that affect absorption, such as diabetes or Crohn’s disease. In children, phosphorus deficiency affects normal bone and teeth development. According to the University of Maryland Medical Center, many individuals consume over twice as much phosphorus as they do calcium. Equal amounts of both minerals are necessary to avoid calcium depletion from bones. As your intake of phosphorus increases, so should your intake of calcium in order to prevent bone abnormalities.
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References
Oregon State University Linus Pauling Institute: Micronutrient Information Center; Phosphorus
Writer Bio
Sue Roberts began writing in 1989. Her work has appeared in such publications as “Today’s Dietitian” and "Journal of Food Science." Roberts holds a Bachelor of Science in nutrition from Pennsylvania State University, a Master of Public Health in nutrition from the University of Minnesota and a Master of Science in food science from Michigan State University. She is a registered dietitian and certified nutritionist.
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msmarco_passage_01_545211885 | How Much Sodium Is in Raw Green Bell Peppers? | Healthy Eating | SF Gate | How Much Sodium Is in Raw Green Bell Peppers? | Healthy Eating | SF Gate
How Much Sodium Is in Raw Green Bell Peppers?
Healthy Eating
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Nutrition
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Sodium
By Sara Ipatenco
You've probably heard over and over again that you should cut your sodium intake to improve your health and lower your risk of certain illnesses and diseases. It's sound advice, and eating more vegetables, such as green bell peppers, is one way to do that because fresh veggies are naturally low in sodium. As a bonus, adding raw green bell peppers to your diet also increases your intake of certain vitamins and minerals.
Sodium
A 1-cup serving of raw green bell peppers contains 4 milligrams of sodium. That translates to less than 1 percent of your daily 2,300-milligram sodium limit. In fact, you can eat an entire raw green bell pepper and consume just 5 milligrams of sodium.
Sodium Dangers
You need small doses of sodium to regulate your blood pressure, as well as to help your nerves and muscles work properly. When you consume more than you need, your kidneys aren't able to get rid of it efficiently. Over time, this can cause sodium to build up in your blood, which increases your blood pressure. High blood pressure puts you at an increased risk for heart disease and stroke. If you already have high blood pressure, heart problems or kidney disease, your doctor might recommend limiting your sodium intake to 1,500 milligrams or less per day to help prevent these potentially life-threatening health problems.
Vitamins and Minerals
While raw green bell peppers are low in sodium, they are high in other key vitamins and minerals. A 1-cup serving of chopped green peppers contains about 120 milligrams of vitamin C, which is more than the 75 milligrams women need each day and the 90 milligrams men should aim for. Vitamin C helps protect you from infection and aids in wound healing. The same serving of raw green bell pepper delivers 11 micrograms of vitamin K. That's 12 percent of the 90 micrograms women need each day and 9 percent of the 120 micrograms men require. Vitamin K is essential for proper blood clotting. Raw green bell peppers also supply vitamin A for healthy eyes and potassium, which regulates your heart beat.
Eating Raw Green Bell Peppers
Eat raw green bell pepper strips with hummus or low-fat ranch dressing for dipping, or sprinkle them with fresh black pepper for a tasty and low-sodium side dish. Chop the bell peppers and scatter them over a spinach or pasta salad. Toss diced green pepper with onions, jalapenos and mushrooms for a quick, healthy and low-sodium salad. Stir raw green bell peppers into cooked quinoa or rice to add a boost of flavor and nutrition.
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References
U.S. Department of Agriculture: Peppers, Sweet, Green, Raw
University of Maryland Medical Center: Sodium in Diet
University of Maryland Medical Center: Vitamin C
University of Maryland Medical Center: Vitamin K
National Institutes of Health: Dietary Supplement Fact Sheet: Vitamin A
Writer Bio
Sara Ipatenco has taught writing, health and nutrition. She started writing in 2007 and has been published in Teaching Tolerance magazine. Ipatenco holds a bachelor's degree and a master's degree in education, both from the University of Denver.
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High-Sodium Foods & Condiments |
msmarco_passage_01_548748008 | Whole Foods That Contain High Percentage of Monosaccharides | Healthy Eating | SF Gate | Whole Foods That Contain High Percentage of Monosaccharides | Healthy Eating | SF Gate
Whole Foods That Contain High Percentage of Monosaccharides
Healthy Eating
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Nutrition
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Sugar & Sweeteners
By Virginia Van Vynckt Updated December 12, 2018
A monosaccharide, also called simple sugar, is a carbohydrate that cannot be broken down into other carbohydrates. The most common monosaccharides provided by foods are glucose, fructose and galactose. Sweet foods such as honey and cane sugar are rich in monosaccharides, but a wide variety of other foods, such as dairy products, beans and fruit, also contain these simple sugars.
Sweeteners
Whole foods that act as natural sweeteners are the richest sources of the monosaccharides fructose and glucose, usually in combination. In addition to table sugar, which is made from either cane or beets, natural sweeteners such as honey and molasses are high in simple sugars. Honey is mostly fructose. Corn syrup -- the regular kind, not high-fructose -- and maple syrup are mostly glucose. Agave nectar, often touted as a more healthful alternative to table sugar, contains a high ratio of fructose to glucose.
Fruits
Fruits, especially apples, cherries, grapes, guavas, lichees, honeydew melon, watermelon, mangoes, papayas, pears, persimmons and pineapple, are the richest whole-food sources of the monosaccharide fructose. Unless you have a fructose intolerance, health professionals generally recommend getting most of your simple sugars from whole fruits, which contain fiber that slows down your body’s absorption of sugars, as well as healthful vitamins, minerals and antioxidants. Dried fruits and fruit juices are more concentrated sources of fructose.
Dairy Products and Meat
Dairy products are the richest food sources of galactose. Milk, butter, sour cream, ice cream, yogurt and other dairy products don’t contain actual galactose, but they do have a sugar called lactose, which the body breaks down into glucose and galactose. Ingredients derived from dairy products, such as whey protein, dry milk solids and casein, can also contribute galactose. Fermented and aged dairy products such as cheddar cheese and yogurt generally contain less sugar.
While meats generally contribute little in the way of sugars, organ meats such as liver are the exception. They’re rich in galactose.
Vegetables and Legumes
Generally, vegetables contain much less sugar than fruits, and don’t contribute many simple sugars to the diet. Vegetables that tend to contain more fructose include artichokes, asparagus, beans, broccoli, cabbage, chicory, onions and leeks, peanuts, tomatoes and zucchini. Beans, lentils, chickpeas and sugar beets also provide galactose.
References
Biology-Online.org: Carbohydrate Definition
Healthhype.com: Foods High in Fructose, Sorbitol, Fructans and FODMAPS
Writer Bio
From 1978 until 1995, Virginia Van Vynckt worked as a writer and editor at The Chicago Sun-Times. She has written extensively about food and nutrition, having co-authored seven cookbooks. She also published "Our Own," a book about older-child adoption. Van Vynckt holds a Bachelor of Arts degree in journalism from Indiana University.
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List of Non-Starchy Fruits
Negative Effects of Refined Sugar in Children
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Sucrose Vs Glucose
What Are the Products When Carbohydrates and Fats Are Metabolized? |
msmarco_passage_01_551999618 | How to Pick the Right Size Inner Tube for a Bike | Healthy Living | How to Pick the Right Size Inner Tube for a Bike | Healthy Living
How to Size Bike Tires to the Rim
How to Measure a Mountain Bike Wheel in Inches
How to Pick the Right Size Inner Tube for a Bike
by Karren Doll Tolliver
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A flat bike tire is an interruption at best and a disaster at worst. Unless your tire is heavily damaged, replacing the tube is usually all you need to get back on the bike path. You must know the diameter and width of the flat tire to select the appropriate replacement tube. Although mountain bikes have a standard 26-inch diameter, other types of bikes have different diameters, such as 27 inches or 700c. The widths also vary, even on mountain bike tires.
Step 1
Inspect the sidewall of the bicycle tire that needs a new tube. The sidewall is the area of the tire next to the rim on either side that does not touch the ground when the bike is in motion. The tire size will be printed there in raised numbers along with the recommended tire pressure and possibly other information. Alternatively, check the tube that needs replacing or your bike’s owner's manual for the information. The tire size notation will consist of the wheel diameter and the tube width separated by the letter "x." For example, 26 x 1.95 means that the wheel diameter is 26 inches and the tire width is 1.95 inches. Although mountain bike tires are 26 inches in diameter, you must still find the width.
Step 2
Choose a tube with the same diameter number and a range of widths into which your tire falls. In the previous example, a tube labeled 26 x 1.9-2.125 has the correct diameter of 26 inches. The width of your tire, 1.95 inches, falls within the range of the widths displayed on the tube package, or 1.9-2.125. This is the correct tube size for your bike.
Step 3
Learn what tubes will fit your tires if you can’t find the exact right size. Because the stated tire width is usually slightly larger than the actual tire and because the tube stretches, tubes close in width serve just as well. For example, choose a tube for a mountain bike if the width is within ¾ inch of the tire’s stated width. Use a tube within 3/8 inch of the stated width for road bikes. A tube with a close diameter measurement will also work. For example, a 700c tube can be substituted for a 27-inch tube and vice versa.
References
BikePro.com: Overview of Tubes
BicycleTires.com: Bike Tubes
How to Buy a Bike Tube (in Simple Pedal Queen Terms)
Sheldon Brown: Tire Sizing Systems
Tips
Always carry a spare tube of the correct size and a hand pump. It can mean the difference between continuing your ride or walking your bike home. Specialized bike bags that fit below the saddle carry your spare conveniently. Some bikers save weight by carrying a spare tube of the right diameter and the smallest possible width.
If your bike tire goes flat and there is no obvious puncture, air may have just escaped through the tube over time as part of a natural process. Always reinflate the tire before replacing the tube to see if the tube is still intact. You may not need a new tube, especially if your bike has been sitting in one place for a while.
Writer Bio
Karren Doll Tolliver holds a Bachelor of English from Mississippi University for Women and a CELTA teaching certificate from Akcent Language School in Prague. Also a photographer, she records adventures by camera, combining photos with journals in her blogs. Her latest book, "A Travel for Taste: Germany," was published in 2015.
Image Credit
David Greedy/Getty Images Sport/Getty Images
How to Tighten a BMX Bike Chain
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How to Size Bike Tires to the Rim
by Christina Shepherd McGuire |
msmarco_passage_01_552319647 | What Size Yoga Mat Is Standard? | Healthy Living | What Size Yoga Mat Is Standard? | Healthy Living
How Often Do You Change Yoga Mats?
DIY Yoga Mat
What Size Yoga Mat Is Standard?
by Aline Lindemann
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Yoga, whether you practice it in class or on your own, requires the use of a mat. A yoga mat provides a cushion against the hard floor and offers traction and stability for poses that might make you slip on a bare or carpeted floor. Look for specific features when choosing a yoga mat.
Length
The standard yoga mat length is 68 inches, but you should get a mat that suits your needs. Yoga mats come in lengths of 72, 74 and 84 inches. Look for a mat that allows both your head and your feet to be on the mat when lying flat. If you're tall, a longer mat is heavier and bulkier, but should also provide extra room for you to transition from one pose to another without having to step off the mat.
Width
The standard width for a yoga mat is 24 inches. Wider mats are available in 30 or 36 inch widths, but these widths might not fit into a standard yoga mat bag.
Thickness
Standard mats are 1/8-inch thick, providing optimal stability. You can find thicker mats that are 1/4-inch thick. Thicker mats do provide more cushion, but they can also make it more difficult to hold a pose, or asana, without wobbling. Travel mats are typically 1/16-inch thick, making them a little easier to roll up and fit into a suitcase.
Materials
Yoga mats come in a variety of colors, patterns and materials. Some are made of bamboo, cotton or jute, and some are made of latex or natural rubber. Many basic and less expensive mats are made of PVC, which is vinyl. PVC mats are known for being sticky, which prevents you from sliding and helps you hold your pose while you gradually transition from one asana to another.
References
Gaiam: How to Choose the Right Yoga Mat
Dear Lil Devas: Yoga Mats
Writer Bio
Aline Lindemann is a health, food and travel writer. She has also worked as a social worker, preschool teacher and art educator. Lindemann holds a Master of Liberal Studies in culture, health and creative nonfiction writing from Arizona State University.
Image Credit
Creatas/Creatas/Getty Images
How to Keep a Yoga Mat Sticky
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by Neville Smithson |
msmarco_passage_01_553318089 | Baked Chicken Breast: Easy, JUICY Recipe! | Healthy Recipes Blog | Baked Chicken Breast: Easy, JUICY Recipe! | Healthy Recipes Blog
Chicken Recipes » Juicy Baked Chicken Breast
Juicy Baked Chicken Breast
Last updated: Apr 3, 2021 · Recipes developed by Vered DeLeeuw and nutritionally reviewed by Rachel Benight MS, RD
Jump to Recipe Card
How to bake chicken breast so that it comes out nice and juicy? Bake it for a short time at a high temperature. It's the best way to avoid drying it out.
Chicken breast is so easy. I always have it on hand, and there are countless recipes where I can use it. But more often than not, I simply bake it in the oven. And when I do, I make sure not to dry it out. The secret? I bake it for a short time at a high temperature.
Baking the chicken for 30 minutes at 350 degrees F will yield dry meat. But baking it for just 15-20 minutes at 450 degrees will result in delightfully juicy chicken, every time.
Jump to:
Ingredients
Instructions
Expert tip: how to check for doneness
Frequently asked questions
Variations and substitutions
Recommended side dishes
Storing and using leftovers
Related recipes
Recipe card
Ingredients
You'll only need a few simple ingredients to make this tasty chicken recipe. The exact measurements are listed in the recipe card below. Here's an overview of what you'll need:
Chicken breasts: I use boneless skinless pieces in this recipe. I haven't experimented with bone-in pieces.
Olive oil spray: It's such a wonderful oil and I love its flavor and cook with it often. But if you prefer using an oil with a higher smoke point, which is perfectly understandable, you can use avocado oil instead.
Kosher salt and black pepper: If using fine salt, you should reduce the amount you use, or the dish could end up too salty.
Spices: I like to use garlic powder, onion powder, dried oregano, and paprika. Make sure the spices you use are fresh! A stale spice can easily ruin a dish. Speaking from experience...
Instructions
Scroll down to the recipe card for detailed instructions. Here are the basic steps for making this recipe:
Spray the chicken pieces with olive oil and sprinkle them with the seasonings.
Bake them uncovered until their internal temperature reaches 165°F. This should take about 20 minutes in a 450°F oven.
Loosely cover them with foil and let them rest before slicing and serving.
Expert tip: how to check for doneness
While you COULD cut a small slit in the thickest part of the chicken to make sure it's cooked through, the disadvantage of doing that is that juices will escape out and leave you with drier meat.
That's why the best method is to use an instant-read thermometer inserted into the thickest part. Aim for an internal temperature of 165°F.
Frequently asked questions
How do I bake chicken breast without drying it out?
The secret is to cook it in high heat for a short time. Moderate heat and prolonged cooking time will dry it out. Another tip is to allow the cooked chicken to rest before cutting it. If you slice into it right away, the yummy juices will escape.
Should you cover the chicken with foil when baking?
No, you shouldn't. You want it exposed to the dry heat of the oven. If you cover the pieces, they will steam in their own juices rather than bake. So you should leave them uncovered.
What's the best temperature to bake chicken?
When it comes to chicken breast, you should bake it in a 450°F oven. High-heat baking for a relatively short time will help it stay moist and juicy and help prevent it from drying out.
You basically have two choices - either bake the chicken for 30 minutes in a 350°F oven. Or bake it for about 20 minutes in a 450°F oven. I've tried both methods, and in my experience, the latter is much better at producing juicy chicken.
How long to bake chicken breast?
Bake it for a short time - 15-20 minutes. Medium, 8-oz pieces will need about 20 minutes in a 450°F oven. For smaller, 6-oz pieces, 15 minutes should be enough. The best way to make sure the chicken is done is to use an instant-read thermometer. Aim for an internal temperature of 165°F.
What if my chicken pieces are very large?
These days, many chicken breasts sold in the supermarket are huge. I've seen ones weighing 12 oz or even 13 oz!
If yours are this big, you will need to bake them for longer, probably around 30 minutes. So check after 20 minutes. And if you do need to bake them for longer, either flip them or loosely cover them with foil to prevent the tops from burning in the hot oven.
Variations and substitutions
I love this recipe as is and almost always make it as written. But in case you'd like to vary the basic recipe, here are a few ideas for you:
Rather than olive oil, you can brush the chicken pieces with melted butter. It's really good!
Experiment with the spices you use. Tasty options include smoked paprika, chili powder, cumin, and dried thyme.
Recommended side dishes
Anything goes, really! This main dish is incredibly versatile. But because I cook it in a 450°F oven, I like to serve it with a side that I can cook in the same oven, such as:
Buffalo cauliflower
Carrot chips
Roasted peppers
Roasted broccoli stalks
Eggplant chips
Zucchini pizza bites
Storing and using leftovers
You can keep the leftovers in the fridge, in an airtight container, for up to 4 days. You can also freeze them for up to 3 months. I like to make several of them at a time because leftovers are so incredibly versatile.
So what to do with the leftovers? I use them in lots of tasty recipes! Here are a few tasty ideas:
Stuffed poblano peppers
Enchilada casserole
Chinese chicken salad
Chicken chili
Chicken patties
Broiled Chicken Breast
Bacon-Wrapped Chicken Breast
Blackened Chicken
Keto Chicken Cordon Bleu
👩🏻🍳 I typically publish a new or an updated recipe once a week. Want these recipes in your inbox? Subscribe! You can unsubscribe at any time.
Recipe card
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Juicy Baked Chicken Breast
How to bake chicken breast? Bake it for a short time at a high temperature. You will get delightful results, every time.
Prep Time 10 mins
Cook Time 20 mins
Rest time 5 mins
Total Time 35 mins
Course: Main Course
Cuisine: American
Servings: 2 servings
Calories: 252kcal
Author: Vered DeLeeuw
INGREDIENTS
▢
2 boneless skinless chicken breasts 8 oz each
▢
Olive oil cooking spray
▢
½ teaspoon Diamond Crystal kosher salt
▢
¼ teaspoon freshly ground black pepper
▢
¼ teaspoon garlic powder
▢
¼ teaspoon onion powder
▢
¼ teaspoon dried oregano
▢
¼ teaspoon paprika
INSTRUCTIONS
Preheat your oven to 450 degrees F. Line a baking dish with foil.
Generously spray both sides of each chicken breast with olive oil, and sprinkle them with the seasonings.
Bake, uncovered, until the internal temperature reaches 160-165 degrees F and juices run clear when pierced with a fork, about 20 minutes. The center of the chicken breasts should be white and opaque.
Transfer the baked chicken breasts to a platter. Loosely cover with foil and allow to rest 5-10 minutes before slicing and serving.
WATCH THE VIDEO:
NOTES
If your chicken breasts are much larger than 8 oz, you will need to bake them for longer, probably around 30 minutes. So check after 20 minutes. And if you need to bake them for longer, either flip them or loosely cover them with foil, to prevent the tops (and especially the spices) from burning in the hot oven. While you COULD cut a small slit in the thickest part of the chicken to make sure it's cooked through, the disadvantage of doing that is that juices will escape out and leave you with drier meat. That's why the best method is to use an instant-read thermometer inserted into the thickest part. Aim for an internal temperature of 165°F.
NUTRITION INFO Most of our recipes are low-carb (or keto) and gluten-free, but some are not. Please verify that a recipe fits your needs before using it. Recommended and linked products are not guaranteed to be gluten-free. Nutrition info is approximate and may contain errors, so you should independently verify it. It is calculated using the SparkPeople.com recipe calculator and the carb count excludes sugar alcohols. Please read the disclaimers in our Terms of Use carefully before using any of our recipes.
Serving: 1chicken breast | Calories: 252kcal | Carbohydrates: 0.7g | Protein: 52g | Fat: 5g | Saturated Fat: 1g | Sodium: 406mg | Fiber: 0.2g
NEVER MISS A RECIPE! I typically publish a new or updated recipe once a week. Want them in your inbox? Subscribe!
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About the Author
Vered DeLeeuw, LL.M., CNC, has been following a low-carb real-food diet and blogging about it since 2011. She's a Certified Nutrition Coach (NASM-CNC), has taken courses at the Harvard School of Public Health, and has earned a Nutrition and Healthy Living Certificate from Cornell University. Her work has appeared in several major media outlets, including Healthline, HuffPost, Today, Women's Health, Shape, and Country Living. Click to learn more about Vered.
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msmarco_passage_01_556239737 | Grandparent Visitation Rights | Law Office of Heath L. Baker | Grandparent Visitation Rights | Law Office of Heath L. Baker
Grandparent Visitation Rights
The negative effects of divorce on spouses and children are well-documented, but people often forget that divorces are hard on grandparents, too. Many grandparents have strong emotional ties to their grandchildren, and losing contact with them due to a nasty divorce can be devastating.
Many grandparents already act in a parental role, making things even more difficult in a divorce. Nearly 5 million U.S. children live in households run by grandparents, and about 20 percent of those children (more than 960,000) have neither parent present in the home. Therefore, the grandparent acts as the sole caregiver and provides for the physical, psychological, and financial needs of the grandchildren. Many grandparents support their grandchildren on a day-to-day basis, and even grandchildren who don’t live with their grandparents full-time can suffer from having these emotional ties severed during the divorce process.
If you are a grandparent seeking grandparent visitation rights for your grandchild or have questions about your rights, the Law Office of Heath L. Baker is here to help. Call (951) 222-2228 or contact us online to schedule a free consultation to discuss grandparents’ rights with an experienced legal professional. We are proud to represent grandparents in Riverside and throughout Southern California, and we will work tirelessly on your behalf to ensure a fair visitation agreement.
Grandparents’ Rights and California Law
Compared to many other states, California law is relatively friendly to grandparents and their right to visitation or guardianship. A grandparent is allowed to petition the court for visitation rights after the divorce proceedings are over, so long as:
The court finds that there was a pre-existing relationship between the grandparent and grandchildren
The court finds that the existing relationship is positive and meaningful and that it would be beneficial for the child for it to continue
The court finds that granting visitation rights to the grandchild would be in the child’s best interest
If you can prove that you had a positive pre-existing relationship with your grandchildren and that your visitation rights would not infringe upon the parents’ rights, a California court can approve a visitation schedule.
However, there are certain situations in which the court will not want to award visitation rights to grandparents. Visitation rights are typically not granted to grandparents when the natural (or adoptive) parents are still married and caring for the child. Also, if both parents agree that the visits should not be granted, the court will typically not award visitation rights to the grandparent. Essentially, a grandparent’s visitation rights cannot conflict with the custody or visitation rights of the parents.
While California family courts typically do not award visitation rights when the grandchild’s parents are married, there are a few exceptions. The court may choose to award visitation rights when the parents are married if:
The parents are living separately
A parent’s whereabouts are unknown (and have been for at least a month)
One of the parents joins the grandparent’s petition for visitation
The child does not live with either of his or her parents
The grandchild has been adopted by a stepparent
Obtaining a Visitation Order
Before you start the process of filing for visitation rights, it is important to speak with an experienced family law attorney. Grandparents’ rights can be legally complex, particularly when the parents of the child are not on good terms with the grandparents, and it is in your best interest to have a solid case before you go to a judge. (In addition, if you fill out the forms incorrectly or do not have an argument prepared, your request may be denied on the first try. Getting back in court for another hearing is time-consuming, expensive, and may not even be possible unless you can show the judge that circumstances have changed substantially since your initial request was denied.)
Here is a quick look at the legal process of requesting visitation rights:
Find out if there is a family court case open. If there is a divorce case, parentage case, child support case, or domestic violence restraining order case open, a grandparent can request visitation under one of the existing cases. If there is not a case open, you and your attorney will have to open a new family court case.
Fill out the necessary forms. Grandparents seeking a visitation order must fill out the “Request for Order” form, in addition to any forms needed to open a case (if applicable). This form is the place to explain what kind of visitation schedule you would like and why visitation rights are appropriate in your case. It is important to answer any questions the judge may have when considering the case, such as: why it is in your grandchildren’s best interest to grant visitation; what is the nature of your relationship with your grandchildren; and any other relevant information that can help the judge understand your unique situation. You will also need to explain what type of visitation arrangement you are seeking, which can be done in a few different ways. You can use the “Child Custody and Visitation Application Attachment”, explain the type of order you are seeking on a “Declaration”, or attach your proposal for the visitation order.
File the forms. An attorney who is familiar with the family court system will be able to help you copy the forms correctly and get them filed with the appropriate court clerk.
Get a court date. The court clerk will usually give you a court date when you file your paperwork. Some court systems require the grandparent seeking visitation and the parents of the child to meet with a mediator before the court date, so make sure to ask your attorney or the court clerk if this applies to you.
Serve the papers. Once the paperwork is filed, you must give formal notice to the parents, stepparents, or whomever else has physical custody of your grandchildren. This requires having another adult (who is not party to the case) serve each parent with a copy of the appropriate forms and a blank “ Responsive Declaration to Request for Order .” The person who serves the papers must fill out proofs of service and file them with the court so there is an official record of the service.
Go to your hearing or mediation session. The next step is to attend your court date or mediation session, depending on the circumstances of your case. If you and the child’s parents are able to come to an agreement about visitation in mediation, your attorney can turn the agreement into an order for the judge to sign. If you are unable to agree, you can take the case to a judge, who will make the final ruling based on the best interests of the child.
Protect your Grandparent Visitation Rights With Our Help Today!
As a Riverside native himself, family law attorney Heath L. Baker is extremely knowledgeable when it comes to Southern California and California family law. He attended California Baptist University and California Southern Law School, and he is a member of the California State Bar, Riverside County Bar Association, San Bernardino County Bar Association, and U.S. District Court in the Central District of California.
Attorney Heath L. Baker has the investigative experience and “home team advantage” that you want on your side. Mr. Baker focuses exclusively on family law, so you can rest assured your case is in the best possible hands. During an emotionally trying time, you can count on Heath Baker to look out for you and your family’s best interests.
If you have questions about your visitation rights as a grandparent, the Law Office of Heath L. Baker is here to help. Attorney Baker is an experienced legal advocate, and he is proud to provide effective, thorough representation for clients throughout Southern California. The legal experts at the Law Office of Heath L. Baker will fight tirelessly to protect your rights as a grandparent, and we will work to come up with a solution that works for you and your family. Call (951) 222-2228 or contact us online to schedule a free consultation today. |
msmarco_passage_01_556934471 | Mike Fisher, Carrie Underwood Husband: 5 Fast Facts to Know | Heavy.com | Mike Fisher, Carrie Underwood Husband: 5 Fast Facts to Know | Heavy.com
Heavy.com
Entertainment
Celebrities
Mike Fisher & Carrie Underwood: 5 Fast Facts You Need to Know
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By Lauren Weigle
Updated Jun 10, 2015 at 10:23pm
View this post on Instagram
Mustache Madness!!!
A post shared by Carrie Underwood (@carrieunderwood) on May 3, 2013 at 10:02pm PDT
Mike Fisher and Carrie Underwood are a power couple. Fisher has an estimated net worth of $30 million, while wife Carrie Underwood reportedly has $70 million, which means these two could pretty much rule the world. Read on for all the facts on the amazing couple, the details on their wedding, their family news, and their views on gay marriage.
1. Fisher Met His Wife at One of Underwood’s Concerts
View this post on Instagram
Our little girl loves her Daddy almost as much as I do…
A post shared by Carrie Underwood (@carrieunderwood) on May 7, 2014 at 7:00pm PDT
Underwood and Fisher met backstage after one of Underwood’s concerts in 2008 and soon began dating after. They became engaged when Fisher proposed to his now wife on December 20, 2009. Fisher announced the big news the next morning during the Senators’ morning skate.
2. Fisher Is a Nashville Predator Hockey Player
View this post on Instagram
Uh-huh…you guessed it, another cookie! I'm going to be full of sugar for the show!
A post shared by Carrie Underwood (@carrieunderwood) on Feb 21, 2013 at 8:11pm PST
Fisher grew up playing hockey in the Peterborough Minor Hockey Association (OMHA) with the rep Minor Petes program and eventually he grew into a pro player. He played for the Ottowa Senators before being traded in February 10, 2011 to the Nashville Predators. In 2012, Fisher won the NHL Foundation Player Award and during his off-season, he underwent surgery for his Achilles tendon. Hey, at least he had a very pretty nurse by his side.
3. Underwood and Fisher Are Expecting a Baby Boy
View this post on Instagram
At the Jays game! Fun times! :)
A post shared by Carrie Underwood (@carrieunderwood) on May 24, 2013 at 6:37pm PDT
Underwood is hosting the 2014 CMA Awards for the seventh time with Brad Paisley, but this time there will be a third person in the mix – her baby. Underwood is rocking a baby bump at this year’s awards show as she and hubby Fisher are expecting their first baby. Enstarz writes:
This year is especially different for Underwood herself, who will be hosting the show while pregnant for the first time. Back in September the star announced that she and husband Mike Fisher, who plays in the NHL for the Nashville Predators, are expecting their first child together. As a result, the CMA Awards are bound to include a few baby jokes, as well as some alterations when it comes to Underwood’s costume changes. In previous years the singer changed half a dozen times throughout the evening, but being pregnant might limit the number of ensembles, or at least change the nature of them.
At tonight’s awards show, Underwood’s co-host Brad Paisley let the cat out of the bag on the sex of Underwood’s baby, revealing that she and her hubby Fisher are having a boy. Underwood has not let her pregnancy stop her from working. Just recently, she had another first – filming a music video while pregnant.
4. The Couple Are Huge Philanthropists
Help us shine a light on slavery tomorrow with a red X on your hand. We're in it to end it! #enditmovement pic.twitter.com/wSRbMNVkRu
— Mike Fisher (@mikefisher1212) February 27, 2014
Fisher and his wife are big on charity. In fact, in his off-seasons, Fisher goes back to his hometown to help out at hockey camps for kids. Underwood and Fisher made a video for the “Do It for Daron,” anti-bullying campaign, urging young people to stop bullying. They are also very supportive of the gay community. Underwood told British newspaper The Independent:
As a married person myself, I don’t know what it’s like to be told I can’t marry somebody I love, and want to marry. I can’t imagine how that must feel. I definitely think we should all have the right to love, and love publicly, the people that we want to love.” Underwood went on to say, “Our church is gay friendly. Above all, God wanted us to love others. It’s not about setting rules, or [saying] ‘everyone has to be like me’. No. We’re all different. That’s what makes us special. We have to love each other and get on with each other. It’s not up to me to judge anybody.
5. Underwood Surprised Her Husband at Their Wedding
Happy 4th wedding anniversary to @carrieunderwood and @mikefisher1212 ! pic.twitter.com/HSyLbSp5v7
— K99.1FM (@k99online) July 10, 2014
There are always surprises at weddings, but Underwood had a very thoughtful one for her husband at theirs. On July 10, 2010, Fisher married Underwood at The Ritz-Carlton Lodge, Reynolds Plantation in Greensboro, Georgia. It was a large wedding with 250 guests in attendance. Underwood surprised her new husband by having one of their favorite music artists, Brandon Heath, sing his song “Love Never Fails” for their first dance.
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Published Nov 6, 2014 at 10:05am |
msmarco_passage_01_559686276 | Stephen Curry: 5 Fast Facts You Need to Know | Heavy.com | Stephen Curry: 5 Fast Facts You Need to Know | Heavy.com
Heavy.com
Sports
5 Fast Facts
Stephen Curry: 5 Fast Facts You Need to Know
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By Danielle Dwyer
Updated Jun 1, 2015 at 9:02pm
Golden State Warriors Stephen Curry goes up for a shot in the NBA Playoffs against the New Orleans Pelicans. (Getty)
A name that continues to grab headlines not only in the NBA, but also in the sports world is Golden State Warriors’ Stephen Curry – better known as Steph Curry.
From his insane shot from the team’s run out tunnel last year, to his record-breaking performance this year, Curry has become a staple name in professional hoops.
Here’s what you need to know about this splash brother:
1. He Set The NBA Single-Season 3-Point Record…Again
Golden State Warriors Stephen Curry against the New Orleans Pelicans in the NBA Playoffs. (Getty)
In the 2012-13 season, the 27-year-old point guard bypassed Ray Allen ’s mark of 269 that he set in the 2005-06 season – Curry scored 272 baskets from behind the arc that year.
After knocking down 261 triples last year, Curry has followed up this season with breaking his own record. He reached No. 273 in his 45-point performance against the Portland Trail Blazers on April 9, 2015.
With the record-breaking performance, the Twittersphere blew up – one of the more interesting tweets was by Bleach Report’s Kelly Scaletta. It read:
Curry broke the record with 273 3-point makes tonight. Since the line was introduced, 373 teams have failed to hit that mark in a season.
— Kelly Scaletta (@KellyScaletta) April 10, 2015
Others tweeted about how he should be the NBA’s MVP and ESPN Stats & Info posted a tweet that showcased just how good Curry’s night and overall game is:
Stephen Curry is the first player to score 45 on a night in which he took 25 shots or fewer AND 5 or fewer FT attempts (via @eliassports)
— ESPN Stats & Info (@ESPNStatsInfo) April 10, 2015
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Frank Kaminsky: 5 Fast Facts You Need to Know
2. He Has a Net Worth of $8 Million
Stephen Curry's Pregame Routine Warriors guard Stephen Curry has a detailed pregame warm-up routine that includes several dribbling and shooting drills. 2015-03-25T21:00:46.000Z
According to Celebrity Net Worth, Curry has an overall net worth of $8 million and has a per year salary of $3.4 million.
Following his junior year of college, the 6-foot-3 two-time NBA All-Star was selected by the Warriors as the seventh pick in the first round of the 2009 NBA Draft.
Since then Curry has been a two-time NBA All-Star, 2014 All-NBA Second Team, 2015 NBA Three-Point Shootout champion, 2011 NBA Skills Challenge champion, 2011 NBA Sportsmanship Award recipient and 2010 NBA All-Rookie First Team.
And in 2012, Curry and the Warriors reached an agreement on a 4-year $44 million contract extension.
Oh, and that net worth number doesn’t really factor in his shoes, which were released by Under Armour on January 8, 2015.
Golden State Warriors Stephen Curry’s shoes – Curry Ones by Under Armour. (Instagram/wardell30)
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Jahlil Okafor: 5 Fast Facts You Need to Know
3. He Originally Wanted to Play College Ball at Virginia Tech
Golden State Warriors Stephen Curry during his career at Davidson College. (Getty)
Born in Akron, Ohio and raised in Charlotte, North Carolina native wanted to follow in his parents’ footsteps and attend Virginia Tech.
His mom, Sonya, was an outside hitter on the volleyball team from 1984-86, while his dad, Dell, is in the Hokies’ Hall of Fame for his basketball career. He played at Virginia Tech from 1982-86 before being drafted to the NBA by the Utah Jazz. After a season with the Jazz, Dell then played for the Cleveland Cavaliers, Charlotte Hornets and Milwaukee Bucks before closing out his career with the Toronto Raptors.
Although Curry wanted to play for the Hokies, he never got the opportunity because he only received three scholarship offers from Davidson, VCU and Winthrop.
He chose Davidson and during his freshman year, he was second in the nation in scoring among freshman. Who was No. 1? Well that would be another NBA standout, last season’s MVP Kevin Durant.
Also, during his three-year career with the Wildcats, Curry was held scoreless just one time. It was during his junior season when Loyola Maryland double teamed and face guarded him the entire game – whether he had the ball or not. How did he make a comeback in the next game? He shot a career-high 44 points of course.
Not only did Curry make his mark at Davidson with his scoring abilities, but he also helped lead the Wildcats to their first conference championship game in 38 years.
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Frank Kaminsky Jr., Frank’s Dad: 5 Fast Facts You Need to Know
4. He Is Married to Ayesha Alexander
Golden State Warriors Stephen Curry with wife Ayesha Alexander and daughter Riley. (Instagram/wardell30)
Curry met Ayesha Alexander in church at the age of 15. The high school sweethearts eventually tied the knot on July 30, 2011 in Charlotte, North Carolina.
Since then the couple has had one child – a daughter name Riley, who was born on July 19, 2012.
Read More From Heavy
Steph Curry’s Wife, Ayesha Alexander: 5 Fast Facts You Need to Know
5. His Real Name Isn’t Steph
Golden State Warriors Stephen Curry with dad Dell Curry. (Instagram/wardell30)
And we saved the best for last. Curry’s real first name isn’t even “Steph” or “Stephen.” Nope. It’s Wardell.
His full birth name is Wardell Stephen Curry II – named after his father. And speaking of his dad, yeah, he wore No. 30 as well. Like father, like son.
Read More From Heavy
Steph Curry vs. Lebron James: 5 Fast Facts You Need to Know
Published Apr 23, 2015 at 6:59pm |
msmarco_passage_01_56013995 | Diabetic Foot Ulcers Treatment & Management: Approach Considerations, Management of Systemic and Local Factors, Wound and Foot Care | Diabetic Foot Ulcers Treatment & Management: Approach Considerations, Management of Systemic and Local Factors, Wound and Foot Care
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Drugs & Diseases > Endocrinology
Diabetic Foot Ulcers Treatment & Management
Updated: Oct 15, 2020
Author: Tanzim Khan, DPM; Chief Editor: Romesh Khardori, MD, PhD, FACP more...
Sections
Diabetic Foot Ulcers
Sections Diabetic Foot Ulcers
Overview
Practice Essentials
Pathophysiology
Etiology
Epidemiology
Prognosis
Patient Education
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Presentation
History
Physical Examination
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DDx
Workup
Approach Considerations
Blood Tests
Plain Radiography
Computed Tomography and Magnetic Resonance Imaging
Bone Scans
Ankle-Brachial Index
Pulse-Volume Recording
Ultrasonography
Transcutaneous Tissue Oxygen Studies
Conventional Angiography
Alternatives to Conventional Angiography
Staging
Laboratory Studies
Other Tests
Procedures
Show All
Treatment
Approach Considerations
Management of Systemic and Local Factors
Wound and Foot Care
Surgical Care
Options for Soft Tissue Coverage of the Clean but Nonhealing Wound
Hyperbaric Oxygen Treatment
Dietary Changes
Restriction of Activity
Measures for Prevention of Diabetic Ulcers
Consultations
Long-Term Monitoring
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Guidelines
Medication
Medication Summary
Hemorrheologic Agents
Antiplatelet agents
Wound Healing Agents
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Questions & Answers
Media Gallery
Tables
References
Treatment
Approach Considerations
The management of diabetic foot ulcers requires offloading the wound, [ 6, 7] daily saline or similar dressings to provide a moist wound environment, [ 8] débridement when necessary, antibiotic therapy with or without surgical intervention if osteomyelitis or soft tissue infection is present, [ 9, 10] optimal control of blood glucose, and evaluation and correction of peripheral arterial insufficiency. [ 11]
To promote ulcer healing in a person with diabetes and a neuropathic plantar ulcer, consider, if nonsurgical offloading therapy is unsuccessful, Achilles tendon lengthening, metatarsal head resection (s), or joint arthroplasty.
Wound coverage by cultured human cells [ 40, 43] or biologic skin substitutes, application of recombinant growth factors, [ 44, 45, 46, 47] and hyperbaric oxygen treatments also may be beneficial at times, but only if arterial insufficiency is not present.
Physicians of diabetic patients with ulcers must decide between the sometimes conflicting options of (1) performing invasive procedures (eg, soft tissue and musculoskeletal reconstruction, angiography, bypass surgery) for limb salvage and (2) avoiding the risks of unnecessarily aggressive management in these patients, who may have significant cardiac risk. In general, the greatest legal risks are associated with delay in diagnosis of ischemia associated with diabetic ulceration, failure to aggressively debride and treat infection, and failure to treat the wound carefully.
If a patient presents with a new diabetic foot ulcer, he or she should receive care from a multidisciplinary team of physicians, surgeons, podiatrists, and pedorthotists who have an active interest in this complex problem.
IWGDF guidelines
The aforementioned IWGDF practical guidelines state the following with regard to pressure offloading in ulcer treatment [ 35] :
For patients with a neuropathic plantar ulcer, a nonremovable knee-high offloading device—ie, either a total contact cast (TCC) or a removable walker that is rendered irremovable by the provider who fits the device—is the preferred offloading treatment
In patients who cannot tolerate a nonremovable, knee-high offloading device, or if such a device is contraindicated, a removable version can be considered; should a removable device be contraindicated or if it cannot be tolerated, an ankle-high offloading device can be considered; patients must be educated with regard to the benefits of adherence to removable device use
In the absence of other forms of biomechanical relief, felted foam, in combination with appropriate footwear, can be considered
While offloading remains important in the presence of infection or ischemia, greater caution is necessary
Nonplantar foot ulcers, depending on their type and location, should be addressed with a removable, ankle-high offloading device, footwear modifications, toe spacers, or orthoses
With regard to restoration of tissue perfusion, the practical guidelines state the following [ 35] :
When ankle pressure is below 50 mmHg or the ankle brachial index (ABI) is less than 0.5, urgent vascular imaging and, in the presence of appropriate findings, revascularization, should be considered; revascularization should also be considered if the toe pressure is below 30 mmHg or the transcutaneous pressure of oxygen (TcpO 2) is less than 25 mmHg; however, revascularization may be considered at higher pressures should extensive tissue loss or infection occur
If optimal treatment does not result in ulcerative healing signs within 6 weeks, revascularization should be considered, regardless of the outcomes of the above-mentioned vascular tests
If an above-the-ankle amputation is being contemplated, revascularization should first be considered as an option
Revascularization should be avoided in patients with an unfavorable risk-benefit ratio
Individual factors (eg, morphologic distribution of peripheral artery disease, autogenous vein availability, patient comorbidities) and local operator expertise should be considered when selecting a revascularization technique
Following revascularization, perfusion should be objectively measured to assess the procedure’s effectiveness
Pharmacologic treatments have not been proven to benefit perfusion
Smoking cessation, hypertension and dyslipidemia control, and antiplatelet drug use, as the means to reduce cardiovascular risk, should be emphasized
With regard to treatment of infection, the practical guidelines state the following [ 35] :
For a superficial ulcer with limited soft tissue (mild) infection - The ulcer should be cleansed and all necrotic tissue and surrounding callus should be debrided; start empiric oral antibiotic therapy directed against Staphylococcus aureus and streptococci (unless there are indications that alternative or additional likely pathogens exist)
For deep or extensive (potentially limb-threatening) infection (moderate or severe infection) - The need for surgical intervention to remove necrotic tissue, including infected bone, should be urgently evaluated, and compartment pressure should be released or abscesses drained; assess for peripheral artery disease (with urgent treatment, including revascularization, to be considered if such disease is present); empiric, parenteral, broad-spectrum antibiotic therapy aimed at common gram-positive and gram-negative bacteria, including obligate anaerobes, should be initiated; the clinical response to empirical therapy, along with culture and sensitivity results, should be used to adjust (constrain and target, if possible) the antibiotic regimen
With regard to local ulcer care, the practical guidelines recommend the following [ 35] :
The ulcer must be inspected regularly by a trained health-care provider, with the severity of the ulcer, the underlying pathology, the presence of infection, the amount of exudation, and wound treatment provided determining the frequency of examination
Ulcer débridement and removal of the surrounding callus (preferably with sharp surgical instruments) should be carried out, with the procedure repeated as necessary
Selected dressings should control excess exudation and keep the environment moist
Foot soaking may cause skin maceration and so should not be employed in treatment
Negative pressure should be considered as an aid to healing postoperative wounds
If noninfected ulcers do not heal after 4-6 weeks of optimal clinical care, one of the following adjunctive treatments should be considered - If severe ischemia is not present in a neuro-ischemic ulcer, a sucrose octasulfate–impregnated dressing; if moderate ischemia is either present or absent, a multi-layered patch of autologous leucocytes, platelets, and fibrin; also in the presence of absence of moderate ischemia, placental membrane allografts; in ischemic ulcers in which revascularization has not led to healing, adjunctive treatment with systemic oxygen therapy
Next: Management of Systemic and Local Factors
Management of Systemic and Local Factors
Treatment of diabetic foot ulcers requires management of a number of systemic and local factors. [ 48, 49, 50, 51]
Precise diabetic control is, of course, vital, not only in achieving resolution of the current wound, but also in minimizing the risk of recurrence. Management of contributing systemic factors, such as hypertension, hyperlipidemia, atherosclerotic heart disease, obesity, or renal insufficiency, is crucial. [ 52, 53] Management of arterial insufficiency, treatment of infection with appropriate antibiotics, offloading the area of the ulcer, and wound care are also essential.
For more information, see Diabetes Mellitus, Type 1 and Diabetes Mellitus, Type 2.
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Next: Management of Systemic and Local Factors
Wound and Foot Care
The basic principle of topical wound management is to provide a moist, but not wet, wound bed. [ 8, 54]
It is prudent to address the underlying etiologies in diabetic foot ulcers for any of the following wound care modalities to be successful. Without addressing the osseous deformities and muscular imbalances, infections, and vascular insufficiency, there will be minimal benefit in employing advanced wound care dressings.
Wound coverage
After débridement, apply a moist sodium chloride dressing or isotonic sodium chloride gel (eg, Normlgel, IntraSite gel) or a hydroactive paste (eg, Duoderm). Optimal wound coverage requires wet-to-damp dressings, which support autolytic débridement, absorb exudate, and protect surrounding healthy skin. A polyvinyl film dressing (eg, OpSite, Tegaderm) that is semipermeable to oxygen and moisture and impermeable to bacteria is a good choice for wounds that are neither very dry nor highly exudative. Wound coverage recommendations for some other wound conditions are as follows (see the Table, below) [ 55] :
Dry wounds: Hydrocolloid dressings, such as DuoDERM or IntraSite Hydrocolloid, are impermeable to oxygen, moisture, and bacteria; maintain a moist environment; and support autolytic débridement. They are a good choice for relatively desiccated wounds.
Exudative wounds: Absorptive dressings, such as calcium alginates (eg, Kaltostat, Curasorb), are highly absorptive and are appropriate for exudative wounds. Alginates are available in a rope form, which is useful for packing deep wounds.
Very exudative wounds: Impregnated gauze dressings (eg, Mesalt) or hydrofiber dressings (eg, Aquacel, Aquacel-Ag) are useful for extremely exudative wounds. In these cases, twice-daily dressing changes may be needed.
Infected wounds: For infected superficial wounds, use Silvadene (silver sulfadiazine) if the patient is not allergic to sulfa drugs; if a sulfa allergy exists, either bacitracin-zinc or Neosporin ointment is a good alternative. Where heavy bacterial contamination of deeper wounds exists, irrigation using one-fourth strength Dakin solution and 0.25% acetic acid may be useful for a brief period of time; a hydrofiber-silver dressing (Aquacel-Ag) can help control wounds that are both exudative and potentially colonized.
Wounds covered by dry eschar: In this case, simply protecting the wound until the eschar dries and separates may be the best management. Occasionally, painting the eschar with povidone iodine (Betadine) is beneficial to maintain sterility while eschar separation occurs; an uninfected dry heel ulcer in a well-perfused foot is perhaps best managed in this fashion.
Areas that are difficult to bandage: Bandaging a challenging anatomical area, such as around a heel ulcer, requires a highly conformable dressing, such as an extra thin hydrocolloid; securing a dressing in a highly moist challenging site, such as around a sacrococcygeal ulcer, requires a conformable and highly adherent dressing, such as a wafer hydrocolloid.
Fragile periwound skin: Hydrogel sheets and nonadhesive forms are useful for securing a wound dressing when the surrounding skin is fragile.
Other topical preparations that occasionally may be useful in the management of diabetic foot ulcers are as follows:
Platelet-derived growth factors (PDGF): Topically applied PDGF has a modestly beneficial effect in promoting wound healing. Becaplermin gel 0.01% (Regranex), a recombinant human PDGF that is produced through genetic engineering is approved by the US Food and Drug Administration (FDA) to promote healing of diabetic foot ulcers. [ 45] Regranex is meant for a healthy, granulating wound, not one with a necrotic wound base, and is contraindicated with known skin cancers at the site of application.
Enzymatic débridement: Collagen makes up a significant fraction of the necrotic soft tissues in chronic wounds; the enzyme collagenase, derived from fermentation of Clostridium histolyticum, helps remove nonviable tissue from the surface of wounds. However, it is not a substitute for an initial surgical excision of a grossly necrotic wound.
Miscellaneous topical agents: Various other topical agents that have been used for wound management include sugar, antacids, and vitamin A and D ointment.
Cytotoxic agents, such as hydrogen peroxide, povidone iodine, acetic acid, and Dakin solution (sodium hypochlorite), should be avoided, except as noted above under infected wounds.
Table. Characteristics and Uses of Wound Dressing Materials (Open Table in a new window)
Category
Examples
Description
Applications
Alginate
AlgiSite
Comfeel
Curasorb
Kaltogel
Kaltostat
Sorbsan
Tegagel
This seaweed extract contains guluronic and mannuronic acids that provide tensile strength and calcium and sodium alginates, which confer an absorptive capacity. Some of these can leave fibers in the wound if they are not thoroughly irrigated. These are secured with secondary coverage.
These are highly absorbent and useful for wounds having copious exudate. Alginate rope is particularly useful to pack exudative wound cavities or sinus tracts.
Hydrofiber
Aquacel
Aquacel-Ag
Versiva
An absorptive textile fiber pad, also available as a ribbon for packing of deep wounds. This material is covered with a secondary dressing. The hydrofiber combines with wound exudate to produce a hydrophilic gel. Aquacel-Ag contains 1.2% ionic silver that has strong antimicrobial properties against many organisms, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus.
These are absorbent dressings used for exudative wounds.
Debriding agents
Hypergel (hypertonic saline gel)
Santyl (collagenase)
Accuzyme (papain urea)
Various products provide some degree of chemical or enzymatic débridement.
These are useful for necrotic wounds as an adjunct to surgical débridement.
Foam
LYOfoam
Spyrosorb
Allevyn
Polyurethane foam has some absorptive capacity.
These are useful for cleaning granulating wounds having minimal exudate.
Hydrocolloid
Aquacel
CombiDERM
Comfeel
Duoderm CGF Extra Thin
Granuflex
Tegasorb
These are made of microgranular suspension of natural or synthetic polymers, such as gelatin or pectin, in an adhesive matrix. The granules change from a semihydrated state to a gel as the wound exudate is absorbed.
They are useful for dry necrotic wounds, wounds having minimal exudate, and clean granulating wounds.
Hydrogel
Aquasorb
Duoderm
IntraSite Gel
Granugel
Normlgel
Nu-Gel
Purilon Gel
(KY jelly)
These are water-based or glycerin-based semipermeable hydrophilic polymers; cooling properties may decrease wound pain. These gels can lose or absorb water depending upon the state of hydration of the wound. They are secured with secondary covering.
These are useful for dry, sloughy, necrotic wounds (eschar).
Low-adherence dressing
Mepore
Skintact
Release
These are various materials designed to remove easily without damaging underlying skin.
These are useful for acute minor wounds, such as skin tears, or as a final dressing for chronic wounds that have nearly healed.
Transparent film
OpSite
Skintact
Release
Tegaderm
Bioclusive
These are highly conformable acrylic adhesive film having no absorptive capacity and little hydrating ability, and they may be vapor permeable or perforated.
These are useful for clean dry wounds having minimal exudate, and they also are used to secure an underlying absorptive material. They are used for protection of high-friction areas and areas that are difficult to bandage such as heels (also used to secure IV catheters).
For more information, see Diabetic Foot Infections.
Vacuum-assisted closure
Clean but nonhealing deep cavity wounds may respond to repeated treatments by application of negative pressure under an occlusive wound dressing (vacuum-assisted closure [VAC]). [ 56]
Hydrotherapy
Intractable, infected, cavity wounds sometimes improve with hydrotherapy using saline pulse lavage under pressure (PulsEvac).
Extracorporeal shock-wave therapy
Two multicenter, randomized, sham-controlled, double-blinded, phase III clinical trials by Snyder et al indicated that extracorporeal shock-wave therapy (ESWT) can effectively treat neuropathic diabetic foot ulcers that fail to heal with standard therapy alone. At 24 weeks, in patients with diabetic foot ulcers that had not been reduced by 50% or greater over the course of 2 weeks’ standard treatment, complete healing occurred in 37.8% of patients treated with ESWT and standard care, compared with 26.2% of patients treated with sham therapy and standard care. [ 57]
Treatment of Charcot foot
Charcot foot is treated initially with immobilization using special shoes or braces but eventually may require podiatric surgery such as ostectomy and arthrodesis.
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Surgical Care
All patients harboring diabetic foot ulcers should be evaluated by a qualified vascular surgeon and podiatric surgeon who will consider débridement, reconstructive surgery on bony architecture, vascular reconstruction, and options for soft tissue coverage.
For more information, see Perioperative Management of the Diabetic Patient.
Débridement
Débridement is indicated for preventing ulceration of nonviable and/or infected tissue. Hyperkeratotic tissue, fibrin, eschar, biofilm, and necrotic tissue need to be removed from the wound and periwound to facilitate wound healing. It is not uncommon for the wound to be larger in size following debridment, especially after the initial débridement. Chronic wounds such as diabetic foot ulcers are often arrested in the healing cascade, and with débridement there is the creation of a reservoir of growth factors to assist the wound in moving forward in healing. These include platelet-derived growth factor, which is excreted by small vessels in the fresh, bleeding edges of a debrided wound. [ 58]
Reconstructive foot and ankle surgery
Reconstructive surgery can be considered when nonremovable knee-high offloading devices are failing to achieve wound healing, when the patient is unable to transition from knee-high offloading devices to custom diabetic orthopedic shoes/insoles due to recurring pressure, or in the setting or pre-ulcerative lesions/calluses in the neuropathic patient. Prior to surgical intervention, a thorough musculoskeletal exam must be performed, and appropriate imaging such as plain radiographs, CT scans, and MRI scans must be reviewed to determine the surgical plan. Surgical options include arthroplasties, osteotomies, resection, arthrodesis, tenotomies, tendon transfers, and tendon lengthening. The goal is to rebalance the foot and create a plantigrade foot that distributes pressure appropriately. These procedures can be considered a type of internal, surgical offloading. [ 59]
Revisional surgery for bony architecture may be required to remove pressure points. [ 60] Such intervention includes resection of metatarsal heads or ostectomy. [ 61]
Vascular reconstruction
In general, the indications for vascular surgery in the presence of a reconstructible arterial lesion include intractable pain at rest or at night, intractable foot ulcers, and impending or existing gangrene. [ 17, 62, 63] Intermittent claudication alone is only infrequently disabling and intractable enough to warrant bypass surgery. Physicians must specifically ask for symptoms suggestive of intermittent claudication, such as pain in the buttocks and thighs while walking and abatement of pain when at rest.
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Options for Soft Tissue Coverage of the Clean but Nonhealing Wound
Once a wound has reached a steady clean state, a decision has to be made about allowing healing by natural processes or expediting healing by a surgical procedure. Clinical experience and observation of the healing progress in each case dictate the appropriate management. Surgical options include skin grafting, application of bioengineered skin substitutes, and flap closures. [ 64]
Clinicians have to treat the underlying etiology of these wounds for these modalities to work appropriately. This includes addressing osseous deformities and muscular imbalances, treating infection, and addressing any vascular compromise.
Skin grafts
The autologous split-thickness skin graft is the criterion standard for viable coverage of a full-thickness granular wound. The graft can be harvested under local anesthesia as an outpatient surgery. Meshing the graft allows wider coverage and promotes drainage of serum and blood. The surgery does create a secondary partial-thickness wound, which can be a site of pain and morbidity.
A cadaveric skin allograft is a useful covering for relatively deep wounds following surgical excision when the wound bed does not appear appropriate for application of an autologous skin graft. The allograft is, of course, only a temporary solution.
Tissue-cultured skin substitutes
Dermagraft (Smith & Nephew) is a cryopreserved human fibroblast–derived dermal substitute produced by seeding neonatal foreskin fibroblasts onto a bioabsorbable polyglactin mesh scaffold. Dermagraft is useful for managing full-thickness chronic diabetic foot ulcers. It is not appropriate for infected ulcers, those that involve bone or tendon, or those that have sinus tracts.
A multicenter study of 314 patients demonstrated significantly better 12-week healing rates with Dermagraft (30%) versus controls (17%). Allergic reactions to its bovine protein component have been reported.
Apligraf (Organogenesis) is a living, bilayered human skin substitute. [ 65, 43] It is not appropriate for infected ulcers, those that involve tendon or bone, or those that have sinus tracts. Allergic reactions to the agarose shipping medium or its bovine collagen component have been reported.
A prospective observational study by Hwang et al indicated that treatment with allogeneic keratinocyte dressings is effective in patients with chronic, intractable diabetic foot ulcers. Of the 71 patients in the study, all of whom underwent weekly keratinocyte therapy, 56 (78.9%) experienced complete wound healing, including 46 (64.8%) in whom complete healing occurred within an average of 6.1 weeks. [ 66]
The use of bioengineered skin substitutes has been questioned because the mechanism of action is not clear, the efficacy is questionable, and the cost is high.
Xenograft
Oasis (Smith & Nephew) is a xenogeneic, acellular collagen matrix derived from porcine small intestinal submucosa that allows an extracellular matrix and natural growth factors to remain intact.
Integra (Integra LifeSciences) is a bilayered skin substitute that is composed of bovine collagen and chondroitin 6-sulfate for dermal regeneration. The silicone top layer mimics epidermis, providing protection and preventing moisture loss.
Primatrix (Integra LifeSciences) is a collagen-based dermal repair scaffold that is derived from fetal bovine dermis. There is an option of obtaining this graft with ionic silver impregnation, which provides antimicrobial coverage for contaminated wounds.
ACell (ACell) is an acellular wound scaffold derived from porcine urinary bladder matrix that can be obtained in either fenestrated sheet form or in a particulate form that is useful for deep and tunneling wounds.
Surgical wound closure
Delayed primary closure of a chronic wound requires well-vascularized, clean tissues and tension-free apposition; it usually requires undermining and mobilization of adjacent tissue planes by creation of skin flaps, local muscle flaps, or myocutaneous flaps. [ 67]
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Hyperbaric Oxygen Treatment
Hyperbaric oxygen therapy is used rarely and is certainly not a substitute for revascularization. [ 68] In the presence of an intractable wound and associated noncorrectible ischemic arterial disease, hyperbaric oxygen therapy may be beneficial (in selected cases). [ 69] Löndahl et al found that 40 hyperbaric oxygen treatments (85 min daily, 5 d/wk for 8 wk) resulted in complete healing of chronic diabetic foot ulcers in 52% of patients in the treatment group. Among patients in the placebo group, 29% had complete healing at 1-year follow-up. [ 70] Although data are equivocal on the impact of hyperbaric oxygen therapy in ischemic and pressure ulcers, positive benefits have been documented in diabetic chronic foot ulcers. [ 71, 72]
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Dietary Changes
The recommended diet is diabetic and low in saturated fat.
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Restriction of Activity
Offloading of the ulcerated area is imperative. This may require non–weight-bearing or weight-bearing, as tolerated in appropriate offloading devices. Custom footwear, a custom clamshell orthosis (for severe deformities), or total contact casting (a fiberglass shell with a walking bar on the bottom) are required for patients who are ambulatory.
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Measures for Prevention of Diabetic Ulcers
The risk of ulceration and limb amputation in people with diabetes can be improved by routine preventive podiatric care, appropriate shoes, and patient education. [ 21] Diabetic clinics should screen all patients for altered sensation and peripheral vascular disease. [ 47] Of diabetic foot ulcers, 85% are estimated to be preventable with appropriate preventive medicine, including the following:
Daily foot inspection
Gentle soap and water cleansing
Application of skin moisturizer
Inspection of the shoes to ensure good support and fit: Medicare covers custom shoes with appropriate physician documentation confirming that the patient is at risk for ulceration.
Minor wounds require prompt medical evaluation and treatment.
Prophylactic podiatric surgery to correct high-risk foot deformities may be indicated.
Avoid hot soaks, heating pads, and irritating topical agents.
A literature review by Matos et al suggested that exercise and physical activity are effective against the complications of diabetic foot. The investigators found that patients involved in physical activity and exercise had a lower annual incidence of ulcers than other patients in the study (0.02 vs 0.12, respectively). Moreover, nerve velocity conduction, peripheral sensory function, and foot peak pressure distribution significantly improved in the physical activity/exercise group. [ 73]
Glycemic control
The Diabetes Control and Complications Trial, performed by the Diabetes Control and Complications Trial Research Group, studied the effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus (1993). [ 74] This trial found that uncontrolled hyperglycemia correlates with the onset of diabetic microvascular complications and that good glycemic control can reduce or even prevent the complications of diabetes, including nephropathy, neuropathy, and retinopathy.
Cigarette smoking should be stopped, and hypertension and hyperlipidemia should be controlled.
To see complete information on the conditions below, please go to the main article by clicking on the title:
Diabetic Neuropathy
Diabetic Nephropathy
Diabetic Retinopathy
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Consultations
Any of the following evaluations may prove productive:
Endocrinologist
Podiatrist
Orthopedist
Vascular surgeon
Interventional cardiologist/interventional radiologist
Infectious disease specialist
Plastic surgeon
Pedorthist
Wound care specialist
Physical therapist
Dietitian
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Long-Term Monitoring
For the most part, diabetic ulcers are managed in the outpatient setting, with brief hospital stays often occurring for initial evaluation and débridement; management of infection, including via intravenous antibiotics and amputations; and vascular evaluation and interventions.
Risk classification and follow-up based on the comprehensive foot examination [ 75] (Open Table in a new window)
Risk category
Definition
Suggested follow-up
0
No LOPS, no PAD, no deformity
Annually
1
LOPS ± deformity
Every 3–6 months
2
PAD ± LOPS
Every 2–3 months
3
History of ulcer or amputation
Every 1–2 months
LOPS = Loss of protective sensation
PAD = Peripheral arterial disease
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Guidelines
References
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[Guideline] Schaper NC, van Netten JJ, Apelqvist J, Bus SA, Hinchliffe RJ, Lipsky BA. IWGDF practical guidelines on the prevention and management of diabetic foot disease. International Working Group on the Diabetic Foot. Available at https://iwgdfguidelines.org/wp-content/uploads/2019/05/01-IWGDF-practical-guidelines-2019.pdf. 2019; Accessed: January 22, 2020.
Teodorescu VJ, Chen C, Morrissey N, Faries PL, Marin ML, Hollier LH. Detailed protocol of ischemia and the use of noninvasive vascular laboratory testing in diabetic foot ulcers. Am J Surg. 2004 May. 187 (5A):75S-80S. [Medline].
Legendre C, Debure C, Meaume S, Lok C, Golmard JL, Senet P. Impact of protein deficiency on venous ulcer healing. J Vasc Surg. 2008 Sep. 48 (3):688-93. [Medline]. [Full Text].
Christman AL, Selvin E, Margolis DJ, Lazarus GS, Garza LA. Hemoglobin a1c predicts healing rate in diabetic wounds. J Invest Dermatol. 2011 Oct. 131 (10):2121-7. [Medline]. [Full Text].
Lee YJ, Sadigh S, Mankad K, Kapse N, Rajeswaran G. The imaging of osteomyelitis. Quant Imaging Med Surg. 2016 Apr. 6 (2):184-98. [Medline]. [Full Text].
Brem H, Balledux J, Bloom T, Kerstein MD, Hollier L. Healing of diabetic foot ulcers and pressure ulcers with human skin equivalent: a new paradigm in wound healing. Arch Surg. 2000 Jun. 135 (6):627-34. [Medline].
Nelson A, Wright-Hughes A, Backhouse MR, et al. CODIFI (Concordance in Diabetic Foot Ulcer Infection): a cross-sectional study of wound swab versus tissue sampling in infected diabetic foot ulcers in England. BMJ Open. 2018 Jan 31. 8 (1):e019437. [Medline]. [Full Text].
Lam K, van Asten SA, Nguyen T, La Fontaine J, Lavery LA. Diagnostic Accuracy of Probe to Bone to Detect Osteomyelitis in the Diabetic Foot: A Systematic Review. Clin Infect Dis. 2016 Oct 1. 63 (7):944-8. [Medline]. [Full Text].
Veves A, Falanga V, Armstrong DG, Sabolinski ML. Graftskin, a human skin equivalent, is effective in the management of noninfected neuropathic diabetic foot ulcers: a prospective randomized multicenter clinical trial. Diabetes Care. 2001 Feb. 24 (2):290-5. [Medline].
Bennett SP, Griffiths GD, Schor AM, Leese GP, Schor SL. Growth factors in the treatment of diabetic foot ulcers. Br J Surg. 2003 Feb. 90 (2):133-46. [Medline].
Guzman-Gardearzabal E, Leyva-Bohorquez G, Salas-Colín S, Paz-Janeiro JL, Alvarado-Ruiz R, García-Salazar R. Treatment of chronic ulcers in the lower extremities with topical becaplermin gel .01%: a multicenter open-label study. Adv Ther. 2000 Jul-Aug. 17 (4):184-9. [Medline].
Platelet-derived growth factor for diabetic ulcers. Med Lett Drugs Ther. 1998 Jul 17. 40 (1031):73-4. [Medline].
Jirkovska A, Boucek P, Woskova V, Bartos V, Skibova J. Identification of patients at risk for diabetic foot: a comparison of standardized noninvasive testing with routine practice at community diabetes clinics. J Diabetes Complications. 2001 Mar-Apr. 15 (2):63-8. [Medline].
Muha J. Local wound care in diabetic foot complications. Aggressive risk management and ulcer treatment to avoid amputation. Postgrad Med. 1999 Jul. 106 (1):97-102. [Medline].
Pinzur MS, Slovenkai MP, Trepman E, Shields NN. Guidelines for diabetic foot care: recommendations endorsed by the Diabetes Committee of the American Orthopaedic Foot and Ankle Society. Foot Ankle Int. 2005 Jan. 26 (1):113-9. [Medline].
Edmonds M. Diabetic foot ulcers: practical treatment recommendations. Drugs. 2006. 66 (7):913-29. [Medline].
Bello YM, Phillips TJ. Recent advances in wound healing. JAMA. 2000 Feb 9. 283 (6):716-8. [Medline].
Frykberg RG, Armstrong DG, Giurini J, Edwards A, Kravette M, Kravitz S, et al. Diabetic foot disorders. A clinical practice guideline. For the American College of Foot and Ankle Surgeons and the American College of Foot and Ankle Orthopedics and Medicine. J Foot Ankle Surg. 2000. Suppl:1-60. [Medline].
Margolis DJ, Kantor J, Santanna J, Strom BL, Berlin JA. Risk factors for delayed healing of neuropathic diabetic foot ulcers: a pooled analysis. Arch Dermatol. 2000 Dec. 136 (12):1531-5. [Medline].
Brem H, Sheehan P, Rosenberg HJ, Schneider JS, Boulton AJ. Evidence-based protocol for diabetic foot ulcers. Plast Reconstr Surg. 2006 Jun. 117 (7 Suppl):193S-209S; discussion 210S-211S. [Medline].
Saco M, Howe N, Nathoo R, Cherpelis B. Comparing the efficacies of alginate, foam, hydrocolloid, hydrofiber, and hydrogel dressings in the management of diabetic foot ulcers and venous leg ulcers: a systematic review and meta-analysis examining how to dress for success. Dermatol Online J. 2016 Aug 15. 22 (8): [Medline].
Evans D, Land L. Topical negative pressure for treating chronic wounds: a systematic review. Br J Plast Surg. 2001 Apr. 54 (3):238-42. [Medline].
Snyder R, Galiano R, Mayer P, Rogers LC, Alvarez O, Sanuwave Trial Investigators. Diabetic foot ulcer treatment with focused shockwave therapy: two multicentre, prospective, controlled, double-blinded, randomised phase III clinical trials. J Wound Care. 2018 Dec 2. 27 (12):822-36. [Medline].
Steed DL. Debridement. Am J Surg. 2004 May. 187 (5A):71S-4S. [Medline].
Frykberg RG, Bevilacqua NJ, Habershaw G. Surgical off-loading of the diabetic foot. J Am Podiatr Med Assoc. 2010 Sep-Oct. 100 (5):369-84. [Medline].
Lipsky BA, Berendt AR, Deery HG, Embil JM, Joseph WS, Karchmer AW, et al. Diagnosis and treatment of diabetic foot infections. Plast Reconstr Surg. 2006 Jun. 117 (7 Suppl):212S-238S. [Medline].
Wieman TJ, Mercke YK, Cerrito PB, Taber SW. Resection of the metatarsal head for diabetic foot ulcers. Am J Surg. 1998 Nov. 176 (5):436-41. [Medline].
Faries PL, Teodorescu VJ, Morrissey NJ, Hollier LH, Marin ML. The role of surgical revascularization in the management of diabetic foot wounds. Am J Surg. 2004 May. 187 (5A):34S-37S. [Medline].
Marston WA, Davies SW, Armstrong B, Farber MA, Mendes RC, Fulton JJ, et al. Natural history of limbs with arterial insufficiency and chronic ulceration treated without revascularization. J Vasc Surg. 2006 Jul. 44 (1):108-114. [Medline].
Ehrenreich M, Ruszczak Z. Update on tissue-engineered biological dressings. Tissue Eng. 2006 Sep. 12 (9):2407-24. [Medline].
Streit M, Braathen LR. Apligraf--a living human skin equivalent for the treatment of chronic wounds. Int J Artif Organs. 2000 Dec. 23 (12):831-3. [Medline].
Hwang YG, Lee JW, Park KH, Han SH. Allogeneic keratinocyte for intractable chronic diabetic foot ulcers: a prospective observational study. Int Wound J. 2019 Jan 2. [Medline].
Demiri E, Foroglou P, Dionyssiou D, Antoniou A, Kakas P, Pavlidis L, et al. Our experience with the lateral supramalleolar island flap for reconstruction of the distal leg and foot: a review of 20 cases. Scand J Plast Reconstr Surg Hand Surg. 2006. 40 (2):106-10. [Medline].
Strauss MB. Hyperbaric oxygen as an intervention for managing wound hypoxia: its role and usefulness in diabetic foot wounds. Foot Ankle Int. 2005 Jan. 26 (1):15-8. [Medline].
Roeckl-Wiedmann I, Bennett M, Kranke P. Systematic review of hyperbaric oxygen in the management of chronic wounds. Br J Surg. 2005 Jan. 92 (1):24-32. [Medline].
Löndahl M, Katzman P, Nilsson A, Hammarlund C. Hyperbaric oxygen therapy facilitates healing of chronic foot ulcers in patients with diabetes. Diabetes Care. 2010 May. 33 (5):998-1003. [Medline]. [Full Text].
Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus SE. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2012 Apr 18. 4:CD004123. [Medline].
Stoekenbroek RM, Santema TB, Legemate DA, Ubbink DT, van den Brink A, Koelemay MJ. Hyperbaric oxygen for the treatment of diabetic foot ulcers: a systematic review. Eur J Vasc Endovasc Surg. 2014 Jun. 47 (6):647-55. [Medline]. [Full Text].
Matos M, Mendes R, Silva AB, Sousa N. Physical activity and exercise on diabetic foot related outcomes: A systematic review. Diabetes Res Clin Pract. 2018 Feb 23. 139:81-90. [Medline].
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Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care. 2008 Aug. 31 (8):1679-85. [Medline]. [Full Text].
Hiatt WR, Money SR, Brass EP. Long-term safety of cilostazol in patients with peripheral artery disease: the CASTLE study (Cilostazol: A Study in Long-term Effects). J Vasc Surg. 2008 Feb. 47 (2):330-336. [Medline].
Media Gallery
Diabetic ulcer of the medial aspect of left first toe before and after appropriate wound care.
Diabetic ulcer of left fourth toe associated with mild cellulitis.
Charcot deformity with mal perforans ulcer of plantar midfoot.
of 3
Tables
Table. Characteristics and Uses of Wound Dressing Materials
Risk classification and follow-up based on the comprehensive foot examination [ 75]
Table. Characteristics and Uses of Wound Dressing Materials
Category
Examples
Description
Applications
Alginate
AlgiSite
Comfeel
Curasorb
Kaltogel
Kaltostat
Sorbsan
Tegagel
This seaweed extract contains guluronic and mannuronic acids that provide tensile strength and calcium and sodium alginates, which confer an absorptive capacity. Some of these can leave fibers in the wound if they are not thoroughly irrigated. These are secured with secondary coverage.
These are highly absorbent and useful for wounds having copious exudate. Alginate rope is particularly useful to pack exudative wound cavities or sinus tracts.
Hydrofiber
Aquacel
Aquacel-Ag
Versiva
An absorptive textile fiber pad, also available as a ribbon for packing of deep wounds. This material is covered with a secondary dressing. The hydrofiber combines with wound exudate to produce a hydrophilic gel. Aquacel-Ag contains 1.2% ionic silver that has strong antimicrobial properties against many organisms, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus.
These are absorbent dressings used for exudative wounds.
Debriding agents
Hypergel (hypertonic saline gel)
Santyl (collagenase)
Accuzyme (papain urea)
Various products provide some degree of chemical or enzymatic débridement.
These are useful for necrotic wounds as an adjunct to surgical débridement.
Foam
LYOfoam
Spyrosorb
Allevyn
Polyurethane foam has some absorptive capacity.
These are useful for cleaning granulating wounds having minimal exudate.
Hydrocolloid
Aquacel
CombiDERM
Comfeel
Duoderm CGF Extra Thin
Granuflex
Tegasorb
These are made of microgranular suspension of natural or synthetic polymers, such as gelatin or pectin, in an adhesive matrix. The granules change from a semihydrated state to a gel as the wound exudate is absorbed.
They are useful for dry necrotic wounds, wounds having minimal exudate, and clean granulating wounds.
Hydrogel
Aquasorb
Duoderm
IntraSite Gel
Granugel
Normlgel
Nu-Gel
Purilon Gel
(KY jelly)
These are water-based or glycerin-based semipermeable hydrophilic polymers; cooling properties may decrease wound pain. These gels can lose or absorb water depending upon the state of hydration of the wound. They are secured with secondary covering.
These are useful for dry, sloughy, necrotic wounds (eschar).
Low-adherence dressing
Mepore
Skintact
Release
These are various materials designed to remove easily without damaging underlying skin.
These are useful for acute minor wounds, such as skin tears, or as a final dressing for chronic wounds that have nearly healed.
Transparent film
OpSite
Skintact
Release
Tegaderm
Bioclusive
These are highly conformable acrylic adhesive film having no absorptive capacity and little hydrating ability, and they may be vapor permeable or perforated.
These are useful for clean dry wounds having minimal exudate, and they also are used to secure an underlying absorptive material. They are used for protection of high-friction areas and areas that are difficult to bandage such as heels (also used to secure IV catheters).
Risk classification and follow-up based on the comprehensive foot examination [ 75]
Risk category
Definition
Suggested follow-up
0
No LOPS, no PAD, no deformity
Annually
1
LOPS ± deformity
Every 3–6 months
2
PAD ± LOPS
Every 2–3 months
3
History of ulcer or amputation
Every 1–2 months
Back to List
Contributor Information and Disclosures
Author
Tanzim Khan, DPM Assistant Professor of Clinical Surgery, Keck School of Medicine of the University of Southern California
Disclosure: Nothing to disclose.
Coauthor (s)
Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Integrated Vascular Surgery Residency and Fellowship, Department of Surgery, Division of Vascular Surgery and Endovascular Therapy, Keck School of Medicine of the University of Southern California
Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Surgical Association, Pacific Coast Surgical Association, Society for Clinical Vascular Surgery, Society for Vascular Surgery, Western Vascular Society
Disclosure: Nothing to disclose.
Chief Editor
Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School
Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society
Disclosure: Nothing to disclose.
Acknowledgements
Jeffrey Lawrence Kaufman, MD Associate Professor, Department of Surgery, Division of Vascular Surgery, Tufts University School of Medicine
Jeffrey Lawrence Kaufman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society for Artificial Internal Organs, Association for Academic Surgery, Association for Surgical Education, Massachusetts Medical Society, Phi Beta Kappa, and Society for Vascular Surgery
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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msmarco_passage_01_560562308 | How to Use Snapchat | Heavy.com | How to Use Snapchat | Heavy.com
Heavy.com
Tech
Android Apps
How to Use Snapchat
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By Karen Tumbokon
Updated Jul 18, 2014 at 12:56am
Curious about using the popular photo messaging app, Snapchat? Here’s a guide on how to use Snapchat and all of its latest features.
1. Download the Snapchat App
Head on over to the Play Store or App Store and download the Snapchat app. Once the app has downloaded, open up the app and create your account. You will need to create a username and verify your phone number. Snapchat will then access your contact list to find out who is on Snapchat.
To add friends, simply tap on the friend icon, which is located in the top right-hand corner on My Friends page. If one of your friends added you, and you haven’t added them back yet, select the icon next to their name. You can do this under “Snapchatters Who Added Me.” You can even search for friends in the search tab. Just typing in their user name. If you go to the My Friends screen, you can see who your best friends are. The score represents the amount of Snaps you have sent and received.
2. Take Photos and Videos
Snapchat is an ephemeral photo messaging app, which means that when you send photos or videos to someone using the app, they can view them for a very short amount of time before they’re permanently deleted. If you want to take a photo Snap, simply tap the circle button on the bottom of the screen. If you want to record a video, hold the circle button. The app also lets you draw on your Snap with the pen icon, add captions and set timers for a photo Snap. If you want to set a timer on a photo Snap, tap the timer icon, and select how long you want your Snap to last. You can add a caption by tapping the center of the photo.
You can also add filters to you photo, but filters are not turned on by default. To turn on the option for filters, access your settings by swiping left and tap the settings button. Then tap ‘Manage’ under ‘Additional Services’ and turn filters on. Once filters are turned on, return to your photo and swipe right to preview all of the filters. In addition to color filters you can also include the current temperature, time and how fast you’re moving.
3. Chat With Your Friends
By swiping to the right on a friends name, you can start chatting. Messages viewed by you and your friends will be cleared when you exit the chat session. To save a conversation, you can tap the screen to take a screenshot. You can easily clear conversations by going to Snapchat settings and tap on clear conversations. You can even chat face-to-face or share live video by a long press.
4. Post & View Stories
Snapchat Stories let you share your “snaps” for 24 hours with anyone in your contact list before it disappears.By adding a snap to your story you can view your snap an unlimited number of times. To manage who can see your story, just go to settings, and make the changes. To post a story, simply take a snap on the main camera page, tap the stories icon, and the snap will instantly be added to your story. If you want to view your friend’s stories, go to My Friends page and tap the circle next to their name.
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Published Jul 11, 2014 at 1:08am |
msmarco_passage_01_569797985 | Confused Henna Results | Henna Blog Spot | Confused Henna Results | Henna Blog Spot
Confused Henna Results
by Khadija | Sep 28, 2012 | Caring For Your Hair: The Henna Way, Henna for Hair | 9 Comments
Confused results : Please help and advise!!
Product: Fresh Jamila Henna Powder 2012
Posted By: Lo-Po
I purchased the Jamilla Henna a week ago, and received it from here on Saturday. So with that I give 5 stars and am satisfied. I purchased 4 of the 100g so that I could possibly have one for next 3-4mos. Anywho, so for the 1st batch I mixed the Henna w/coconut milk and made my mix too runny (my mistake)..however, I noticed after 2hrs the henna dyed my palm light orange so unsure whether to immediately put on my hair (some ppl mention it should stain pumpkin-orange or dark orange) I let it sit awhile more..and then placed on my hair for 8 hours!!! After this I rinse it out but to my dismay I did not receive any color deposit. Discouraged I decided at 11pm last night to make another batch and since it was BAQ henna to do the 12 hour overnight wait. So I mix another batch, let sit for 12hrs. This morning at 11 placed it on my hair evenly–this batch was correct and I mixed with just warm water and consistency was like a mud mask. After taking an hour to place throughout my hair evenly, I saran wrap, paper bag, and plastic cap for 4 1/2 hours. This evening at 5 after easily rinsing out the henna–I didn’t need to add conditioner or wash…just rinsed out from under my tub faucet–I was crushed again to see that I had absolutely NO color deposit indoors or outdoors and also did not see any more shine, strength, or anything phenomenal to my hair. It looked the exact same (My hair is wavy/curly natural black hair with natural shine, tight s-curls, and medium-length dense packed hair)
I really thought the first application didn’t take because I had not let the henna sit 12hrs although I had seen the dye release w/in 2hrs. Next application I followed precise rules and method on the sheet included in shipment and my paste didn’t drip AT ALL and I had no mess but the result was the same. I don’t know what to say you guys I am very disappointed with the fact I didn’t receive color (not important) and no other benefits (most important) or any immediate results.
I tried to reason that maybe it’s because my hair is very low porosity (even when I had chemically relaxed hair my hair never took chemical dye and I would have to use a booster) but even with that, 4.5 hrs on the head should yield something and I know we are all different but I am truly lost as to not receiving no results when ppl with similar porosity and/or pattern have amazing results. I also tried to reason that maybe my hair is in a pretty good condition so maybe that’s why I didn’t see any results?
IDK…but I have nothing against BAQ Jamila henna. It is very fine sifted and rinsing out with plain tub faucet water was terrific for me. Also, after rinse my hair was NOT stick dry and brittle at all…and this was after using henna w/just water mix…but as a safety I washed with a duo-poo/con-dish to amazing detangle results.
I have two more boxes in the freezer and in 2wks will try and re-visit but do not know what I can do to try and improve the release on my hair..I may try leaving on overnight after leaving out 12hrs but I don’t feel that would yield much.
Sorry for this long, ranting review but the short of it, the product itself is 5 stars in regard to being finely sifted, easy to use..etc but I can’t give it 5 stars for color and/or hair treatment results because my hair looks and feel the EXACT same..same softness, texture, shine, etc as before..
Replies and Advice:
HS Reply: Thank you for giving such an amazing informative and HONEST review!!
When concentrating on color results don’t use heavy liquids such as coconut milk nor honey etc…That was the first reason you didn’t get good color deposit.
Second you left your henna sit for 12 hours and Jamila has a fast dye release this year. It only needs 3-4 hours for hair use, and then you should use it for best results by that time frame.
You can email us at info@hennasooq.com for further assistance. I hope this helps! -Khadija
Hildegarde Franck reply: Thanks for the posting
Vanessa LeBlanc reply: Another thought: Very dark-black toned hair can take several lengthy applications until any colour is noticeable, even in the sun. Was the hair clarified before applying the henna? Sometimes previous build up may prevent any conditioning and staining of the hair. They key is multiple lengthy applications. Also, with porous hair, it may be a good idea to do a protein treatment before the henna. Lawsone bonds to the keratin inside the hair.
Next time, mix the Jamila with warm water and allow it to release until you get some orange staining, then pop the henna covered in the freezer. Defrost and use the next day.
I agree with the HS reply in regards to the coconut milk and over releasing. For this, it is best to mix the henna with warm water first, then add 2 TBS per of coconut milk to every 100g of henna powder mixed after the henna has released.
Bonnie Ross KIlberg reply: Vanaessa is right….especially with low porosity…you have to build up the Henna on the hair shaft….Using a harsh shampoo before hand can help open up the shaft as well….I use old fashioned Prell..you can also try adding various other natural hair products….I always mix mine with lemon juice, bakers suga (fine) ground cinnamon and hibiscus tea and coffee for liquid……Khadija is right abt the Jamila…I had good dye reliease after 3 hours….But I still like my Morrocan the best :o) Good Luck keep at it it take lots of experimenting to find ust the right method for your hair……
Hillery Kelly reply: I mix my Jamilla with hibicus tea which helps with die release and also increases the red staining of the henna. Like someone else said, for color benefits, you need multiple applications unless you have some grey hairs which will show color uptake almost immediately. Also, I sometimes apply my henna and then sit under my heat cap. The gentle warm heat helps open the hair shaft, allowing the lawsome molecule to penatrate deeper into the hair which = better staining and other hair benefits.
S Marie Haskins-Tucker Jr. reply: Also you may want to try leaving it on over night. I have low porosity hair and i do all my treatments overnight (sleep with hair wrapped in cling wrap, covered with a conditioning cap and wrapped with a towel) to get the most out of my henna. After 2 Yemeni applications i started seeing subtle red tones, especially in the sunlight. I knew it was starting to show when i went to a hairstylist and she asked what color i used on my hair.
Supriya Dixit Hayer reply: I made the same mistake the first time. I let it sit out too long. Now when I do use Jamila, I let it sit for 3 hours and put it on my hair overnight with my head covered in a turban of cling wrap. In the morning, I rinse it out with water only (I use a wide toothed plastic comb to help get the pieces out) and I actually use the Cocoveda oil from Henna Sooq as a leave in conditioner. I leave this in my hair all day (I go to work like this) and then in the evening I follow it up by washing with shampoo and conditioner. This has been the way I’ve gotten the Jamila to work for me. Hope this helps. =)
Kari Lee Berrow reply: I had the same problem with my Jamila not having any dye release at all, TWICE now. I am not a beginner user of Henna so I do know the information on the how to. I just received it two weeks ago and I really do like the product for ease of use, but no dye release even after trying to freeze it, which is very frustrating. It is expensive for me to continue ordering and not having products work! I am almost ready to give up on Henna.
This thread can be followed at Henna Sooq’s fan page. There is SO MUCH more on HS’s fan page. Specials, promotions, exclusives for fans only, recipes, tips, hints, inside scoop and those henna secrets we only share at HS’s fan page. We can’t wait to see you there!! Join us! |
msmarco_passage_01_571002506 | Herbal Tinctures | Herbal Tinctures
Herbal Tinctures
Apr 15, 2015
Tinctures are concentrated herbal extracts in liquid form that have alcohol as the solvent. Although generally if any other solvent is used, such as water, vinegar, or glycerin, it is considered an extract rather than a tincture. There are exceptions to the rule – vinegar and vegetable glycerine tinctures are also effective options. However, some herbs (roots, berries, barks, non-aromatic seeds) require the strength of alcohol to extract the medicinal properties.
Tinctures are extremely convenient and easy to use, as they are taken orally either straight or in teas. The preferred method is often taking the tincture straight (directly under your tongue by dropper), as this allows the tincture to enter your bloodstream faster and can produce quick results. For those that do not like drinking tea, don’t have the time to brew a cup, or are looking for fast results, straight tinctures are perfect. Less than a minute and you are done!
Of course, the time it takes to see results varies depending on the herb. While some herbs have immediate effects, others may take weeks of continual use before the results are noticeable.
Tincture teas are a different, popular way of taking an herbal tincture. Many people enjoy the flavors, and the act of sitting down and relaxing with a warm cup of tea can be very therapeutic and relaxing. Tinctures can be added to a warm cup of water to make an instant cup of tea. The tincture may also be diluted with a small amount of juice, or flavored with lemon or honey if necessary. Two droppersful of tincture is equal to one 8 oz. cup of tea.
Here’s the good news: one dose of alcohol-based tincture is equal in alcohol content to a very ripe banana, making tinctures safe for potentially everyone, including those who are pregnant or nursing, children, and babies. Non-alcoholic options are offered as well. Please be sure you are aware of the herbs that are discouraged for pregnant and lactating mothers.
For adults, the standard suggested dosage is two full droppers two to three times daily. For children under 12, weight and height must be taken into consideration to determine a dosage. Suggested dosage charts for children can be found online. For babies under 6 months, tinctures should only be administered through breastfeeding.
Remember – regardless of the size of the tincture bottle or dropper tube, the bulb determines the dosage amount and is the same size on every bottle.
Alcohol-based tinctures have an unlimited shelf life and do not require refrigeration if stored in a cool, dark location. Tinctures that are vegetable glycerine-based do not need to be refrigerated and can last from 3-5 years. Vinegar-based tinctures are recommended to be refrigerated, and can last up to a year. They can also be stored in a cool, dark cupboard. |
msmarco_passage_01_571467474 | Indian Rennet Herb Uses, Benefits, Cures, Side Effects, Nutrients | Indian Rennet Herb Uses, Benefits, Cures, Side Effects, Nutrients
Indian Rennet Herb Uses, Benefits, Cures, Side Effects, Nutrients
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General Name
Indian Rennet
English Name
Indian Rennet, Indian Cheese Maker
Botanical Name
Withania Coagulans
Hindi Name
Paneer Doda, Doda Paneer, Rishyagandha, Binputakah, Paneer Booti
Chinese Name
Ning Gu Shui Qie
Do you know this herb by any other name ? Click Here.
Indian Rennet Cures
Most Effective
Diabetes
Highly Effective
Indigestion
Liver Diseases
Effective
Anxiety
Asthma
Biliousness
Cancer
Colic
High Blood P...
Impotence
Insomnia
Intestinal D...
Low Back Pain
Lung Cancer
Menstrual Di...
Piles
Strangury
Stress
Teething Pro...
Toothache
Action of Indian Rennet
Most Effective
Antidiabetic
Highly Effective
Digestive
Hepatoprotective
Effective
Alterative
Anodyne
Anthelmintic
Antiasthmatic
Antibacterial
Antibilious
Antibiotic Whol...
Anticancer
Antifungal
Antiinflammatory
Antimicrobial
Antioxidant
Antistress
Antitumor or An...
Blood Purifier
Cardio Tonic or...
Cytotoxic
Depressant
Diuretic
Emetic
Emmenagogue
Febrifuge
Hypoglycemic
Hypolipidemic
Immunity Booster
Sedative
Stomachic
Nutrients in Indian Rennet
Effective
Alkaloids Amino Acids Arachidoni... Asparagine Aspartic Acid Beta Sitosterol Cysteine Essential Oil Fatty Acids Fatty Oil Galactose Glutamic Acid Glycine Hydroxyproline Linoleic Acid Oleic Acid Palmitic Acid Proline Stearic Acid Tyrosine Valine
Taste of
Indian Rennet
Bitter,Sweet,
Parts Used
Whole Plant , Roots, Leaves, Stem, Green Berrie, Fruits, Seed, Bark
Side Effects, Risk Factors of, and Cautions for Indian Rennet
Indian Rennet possesses the immuno suppressive ability. The ability may be useful during an organ transplant, when the immune system rejects the new organ thinking of it as an threat. In normal conditions the prolong use of Indian Rennet may make a person vulnerable to infection or other diseases.
Avoid its usage during Pregnancy.
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Description
Indian Rennet is a shrub.
It is perennial.
It grows in tropical, subtropical climate.
It grows up to 1.2 M.
Best used for Diabetes, Indigestion.
It is a member of the Solanaceae family
Has an Affinity to :
Pancreas
Origin
India
Grown In
Afghanistan
India
Pakistan
Common Names
Af Ghan
Akri
Ammukkura
Ashutosh Booti
Asvagandhi
Ayurvedic ...
Binputakah
Clustered ...
Cuajo indio
Desi Asgandh
Doda Paneer
Dodi Paneer
Ghoda Asoda
Ha B Kaknaj
Hab Kaknaj
Habb Kaknaj
Indian Che...
Indian Rennet
Javzulmizaja
Kaaknaj e Hindi
Kaknaj
Khamjaria
Khamjira
Ning gu sh...
Paneer Bandh
Paneer Booti
Paneer Dhodi
Paneer Doda
Paneer Dodi
Paneer Flower
Paneer ka Phool
Paneer Phool
Panir Bed
Panirband
Panner Doda
Panner Ka Phool
Panner Ka ...
Panner Ka Phul
Panneru Gadda
Physalis s...
Puni ke Bij
Punir Band
Punir Bandh
Punir Dodi
Punir ja Fota
Punirbad
Punirband
Punirjafota
Rishyagandha
Samm Al Rerakh
Spicebajja
Spiubajja
Tukhme Kak...
Tukhme Kak...
Tukhmekakn...
Turangi Ghanda
Vegetable ...
Withania
Withania C...
Withania C...
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Materia Medica : How to use Indian Rennet - Uses and Benefits
Indian Rennet General
Withania Coagulans or more popularly called Indian Rennet is a member of the Solanaceae family. Indian Rennet ( Panner Doda in India ) is a shrub. It is a common herb in India, Nepal and Afghanistan.
Indian Rennet is one of the best herb for treating Diabetes. It helps the body to absorb blood glucose. It repairs the beta cells of the Pancreas so that the body gets sufficient amount of insulin. Regular consumption of Paneer Doda cures Diabetes and gives relief from taking Antidiabetic medications.
Indian Rennet decoction is useful in combating Asthma.
The Febrifuge action of the leaves is beneficial in arresting Fever.
Indian rennet paste applied externally on the wounds speeds up the wound healing process.
The blood purifying quality of leaves keeps the blood clean from harmful toxins.
TheEmmenagogue action of the seeds helps in regulating Menstrual flow and keeps the Menstrual Disorders away.
The Antibacterial property of the Indian Rennet fruit is beneficial in combating Streptozotocin Aureus and Vibrio Cholerae bacteria.
Indian Rennet is a Diuretic plant. It increases the volume of urine and keeps the body clean of harmful toxins.
The stem of Indian Rennet is traditionally used in cleaning of teeth.
The plant is burnt and the smoke is inhaled in relieving toothache.
Keywords : Diabetes, Asthma, Fever, Wound, Menstrual Disorders, Toothache.
Single Herb
Indian Rennet for Diabetes
Take 9 pods of Indian Rennet. Soak overnight. Next morning, mash them. Strain. Drink daily. If acceptable. do not strain, drink the pulp as well.
Caution : Take care if you are on prescription medicines. Indian Rennet becomes effective immediately. Blood sugar may fall suddenly. Get your blood tested regularly. Adjust the dose of the remedies accordingly.
Queries on Indian Rennet
Shalini
27 Mar 2015
Dear Sir,
Please let us know where we can get Indian Rennet (Paneer Ka Phool) in Vadodara City.
Thanks,
Shalini
Reply
Murtuza Daruwala
08 Mar 2016
Its available at sariya stores at MG road vadodora.
Reply
Alpa
07 Feb 2017
G Y Hakim & Sons - RaopuraRaopura, Vadodara -
Reply
Piyush
12 Mar 2018
In any grocery store you can get
Reply
Hira
25 Apr 2019
This avalable 500gm is only 500 Rs + 150Shipping Extra. Send address on this no:- 9868065204 Amount Gpay on this no.
Reply
Ripudaman Singh
18 Oct 2020
Hi we can deliver you the best quality paneer ke phool at your address
Including shipping cost share your address at 7073330428
Rioudaman singh
Reply
Narendra
23 Apr 2015
I can send you by parcel, I am in Ahmadabad.
You can contact me on mobile number 9904643541 for more detail.
Thanks.
Narendra
Reply
Aslam
23 Mar 2016
shut up i already has
Reply
KK
08 Jan 2017
Where did you learn English?
Reply
Manoj
30 Dec 2017
Buy it Now from Amazon & Get maximum Discount + fast delivery
Visit: http://amzn.to/2Csbe9u
Reply
Jai ho
05 Nov 2018
In a madrasa.These moslems are all rude
Reply
Asma
13 Oct 2020
Excuse me! All the Muslims are not rude,true Muslims have good faith but some of them are still wanderers.
Reply
Rohan singh
02 Dec 2016
It is available in all india
Reply
J. Reuban chennai
14 Jun 2017
Sir i also need this Paneer phool
Reply
Kashvy
30 Dec 2017
NutrActive™ provides superb quality of Paneer Doda, Buy it Now from Amazon & Get upto 50 % Discount. http://amzn.to/2Csbe9u
Reply
Alagar
30 Sep 2018
Sir you can contact me 7010623464
Reply
Ramkumar
09 Nov 2017
If you want pls call me at 9382337474. I can sen you.
Reply
Shilpi Gautam
08 May 2015
It is good for diabetic person. I am taking this in pregnancy as well. However I reduced the quantity to half.
Reply
Mohit
14 Apr 2016
Hi, Do not consume it during Pregnancy...,
Reply
Sultan
16 May 2015
Try to find it at any "Dawa-saas" store in and around your area. It cost around
INR 130 to 150. Buy some and check, if its effective then you buy more. Good Luck.
Reply
Mariam mohd yunus
24 May 2015
I am taking paneer phool since 1.5 year. Is any side effects if we take it with other diabetes medicine. Please Tell.
Reply
Herbpathy Research Team
26 May 2015
Dear Mariam Mohd Yunus,
Firstly, let us know for what purpose you are taking Paneer Doda. Also tell us, if you have any other problem except that ( Like; High Blood Pressure ). So that, we may suggest you the suitable one.
Thanks and Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Sandeep
17 Jun 2016
i am sacrificing with acne problem , can i use this
Reply
Shweta
21 Aug 2016
I am suffering from acne? Is it helpfull in acne? How long i have to take the dose??
Reply
Aisha
01 Oct 2016
Take a jola every morning for acne in every summer season for 40 to 50 days. It will show it action after 2 years
Reply
Kiran
07 Jul 2017
Jola ??? What is this herb
Reply
Muskan gopang
17 Nov 2016
Would this help me to get fair complexion? I'm 16 year old, someone has told me to drink its water (soak paneer booti overnight in water and drink its water in morning without having any meal)..
Reply
Nil ratan brahma
26 May 2015
I am a 43 years old and a diabetic also fatings range is 170 and pp range is 240. After viewing your net reviews I feel hope to fight with diabetic and for that purpose I want to know what is the source of paneer ka phool and the doses also. I hope you will advise me and help me for that purpose.
Reply
Herbpathy Research Team
27 May 2015
Dear Nil Ratan Brahma,
Diabetes is a disease of Metabolism.
Yes, it is true, that cause of Diabetes is high glucose level in the blood. But do you know, this is not the exact reason behind it ?
The sole cause of diabetes is : The Cells unable to get the required amount of sugar.
Our body cells require Glucose for energy. And when, these Cells fail to absorb the required amount of sugar from the blood , they get starved. As a result, the sugar is still in the blood stream. When, more and more sugar gets accumulated in the Blood, and is not being absorbed by the cells. This leads to an increase of Glucose level in the Blood.
Paneer ka Phool is a good cure for Diabetes, but, is a palliative one. If you want a cure, you should try Giloy ( Tinospora Cordifolia ).
For Immediate results, buy a Tincture of Giloy and take 10 drops in water every day.
Giloy is very effective for Diabetes. Therefore, a caution is advised in case you are already taking any other medications for the same. It may lower the blood sugar levels below the normal.
Regards,
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Palak
23 Apr 2016
Where I get in Indore
Reply
Monika Arora
04 Jun 2015
Yes you can use paneer ka phool even if you are not a diabetic. It is a good herb with many more medicinal values. Paneer ka hool is known for its stress relieving property. It has anti cancer properties and purifies your blood. It is a good tonic for liver and cures the problems associated with liver. Twigs of this plant are also used for cleaning the teeth.
So over all it is a good herb to take.
Reply
Monika Arora
04 Jun 2015
Dear Pradeep,
Sorry i missed out your blood pressure problem. For Blood pressure Giloy also known as guduchi is beneficial. It regulates the blood pressure and also good for high cholesterol. You may have this herb.
Reply
Deepak Kumar
12 Jun 2015
Please confirm about ,what will side effect for using paneer phool for
Reply
Dilip
11 Apr 2018
Site effect not there but quantity will maintain most important 4 to 5 paneer phool good for all body remade don't fear
Reply
Shalini
12 Jun 2015
Dear Deepak,
As such paneer phool has no side effects. It is known as one of the best herbs for Diabetes.
But over use may cause complications. So it is better to consult a doctor before use.
Avoid if you are already taking any kind of medications for Diabetes, as it may lead to Kidney damage and Hepatotoxicity.
Reply
Har
25 Jun 2015
Dear Herbpathy
Can you please let me know if I can use PANEER DODA or PANEER PHOOL for controlling diabetes and reduce or eliminate the use of insulin and/or tablets?
Reply
Herbpathy Research Team
26 Jun 2015
Dear Har
This herbal flower is amazingly effective to cure Diabetes. Yes, you can use Paneer Phool for your disease.
The herb is known to bring down the sugar levels remarkably.
But, if you are using the herb with other medications, it may cause a sudden drop in sugar levels, below the normal range.
So, we suggest you to,
Keep a count of your Sugar and Cholesterol levels before beginning the administration of the medicine and then record the sugar level after 10 to 20 days, You will see the difference.
Once you start feeling any better, you may even stop the use of insulin or the tablets, and continue with this herb.
The herb really acts like a magic wand.
Dosage : Put 8-10 pieces of flower in a glass of water and keep it overnight.
In the morning, squeeze the flowers and mix them well, Now, strain it and drink the water.
The taste would be real bitter, but very effective.
For best results, use the herb regularly.
Please consult your health care provider, before using any of the remedies.
Regards
Herbpathy Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Jawad
30 Aug 2016
I am hi blood pressure problem , can i use it ?
Reply
Umarani
25 May 2016
What exactly it is? I am a south Indian and not able to find out what it is? Can any one explain what it is?
Reply
Dilip
11 Apr 2018
It is one type of flower it is available 7676266744 rs 200 kg delivery free
Reply
George Bush
09 Feb 2018
For better result soak paneer ke phool in half liter glass of water in the night, squeeze the phool in the morning, and boil it in a steel vasel 1/4 evaporate, remained 3/4 filter and after cooling drink it empty stomach ( without consuming water, tea, coffee or breakfast). God bless you.. Be healthy
Reply
MUKESH KUMAR
29 Jun 2015
Is there any side effect of pander ka phool
Reply
Herbpathy Research Team
30 Jun 2015
Dear Mukesh Kumar
Paneer ka Phool is an amazing herb for curing Diabetes and quite effective in curing other diseases like Asthma, Cancer, Impotence, etc.
As such the herb has no side effects. But as you know that excess of everything is bad. So, avoid the overuse of this herb.
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Anil
01 Jul 2015
I am taking Paneer ka phool regularly since 2 months. My sugar level is normal. It is most effective and economical herb
Reply
Priyam
24 Mar 2016
Hi ANIL please leave me your contact number please SMS me on9833990295. 9833990295
Reply
Swapnil Malhotra
01 Jul 2015
Yes, It is Anil . I absolutely agree with you Anil.
It indeed is a "Wonder Herb" for diabetes. I have seen drastic changes in my sugar levels. Very happy I am.
Reply
Sapna Bafna
27 Jul 2015
Thanks for Paneer ka phool remedy.
But i have never known that giloy is also effective.
Reply
Praveen
30 Jul 2015
Dear Sir,
I want to know, how effective is Paneer Doda in Anemia.
I have been told by somebody that it is also effective in anemia.
Reply
Rekha
30 Jul 2015
I am 8 week pregnant with gestational diabetes. Can I take Paneer doda during pregnancy ? Please suggest.
Reply
Herbpathy Research Team
31 Jul 2015
Dear Parveen
If you want to see better results, then try the following Herbs.
1. Eat one pomegranate every day for one month.
2. You may try Raisins. Dip 20 to 30 Raisins in water at night. Next morning drink that water and eat the Raisins.
3. You may try seasonal beet root juice and carrot juice.
After one month, get your blood test done and note the difference.
Regards,
Herbpathy Research Team
( Make Your Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Herbpathy Research Team
31 Jul 2015
Dear Rekha,
Our research team is working on it. We will get back to you as soon we find the best solution for your query.
Regards,
Herbpathy Research Team
( Make life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Bhavin
31 Oct 2016
Dear sir...I am taking 4 no Paneer ka phool daily with prescribed method. I am having diabetes for 10 years and taking medicines also. After I started taking paneer ka phool I had puss drain from below abdomen organs . If taken more than some blood.so I restricted it to 4 no. Do think it will be worse if I continue to have. My blood sugar although is under control.
Reply
Anil kumar
02 Aug 2015
Sir I am suffering from diabeties and high BP . Please suggest me can I use paneer ka phool.
Reply
Aruna
07 Apr 2019
My B p has increased Is it due to paneer doda
Reply
Herbpathy Research Team
05 Aug 2015
Dear Rekha
We would like to congratulate you for this wonderful news. We believe it is one of the most delicate and thrilling phases of your life. So, we wish you to have a great one.
We would like to tell you that Gestational Diabetes is similar to the Diabetes, when Insulin receptors fail to function properly.
It poses a threat to the child being Diabetic or Obese. So, we suggest you to take Astragalus, this is the best Herb for pregnant women. Infact, a super herb . You may take it in the form of decoction or tea.
Consume the dosage between low to moderate. Do not take high dosage of any herb during pregnancy.
You may prepare a tea of any of these herbs
Dandelion
Kelp
Alfalfa
Also, prior discussion with a medical professional is necessary before taking any Herb during this fragile period of pregnancy.
Take care. God Bless!!
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Khalid Suleria
05 Aug 2015
Dear Sir
very usful info many things were new to me never knew before
Excellent info on herbs
Reply
Herbpathy Research Team
06 Aug 2015
Dear Anil Kumar
Paneer ka Phool is a good herbal treatment for Diabetes. But if you want to combat both BP and Blood Sugar, then you may try Giloy ( Tinospora Cordifolia ) for 10 Days initially. It is good for Blood Pressure as well as blood sugar.Please check your BP and Blood Sugar Before taking it. And then monitor it regularly after every two days.
Please avoid the consumption, if you are taking other medications for your problem. As Giloy is very effective, it may lower the Blood Sugar and Blood Pressure than normal.
Always consult a doctor before taking any kind of medication.
Regards,
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
AbdulMunaf Shaikh
16 Feb 2016
I am using Paneer phool since last 6 months. It has helped me a lot for diabetics. My medications have reduced to 50 %. However my common cold sneezing has increased over last 2 to 3 months. My question is is it due to intake of paneer phool or due to something else. This cold which i suffer from is not recent but since last 2 to 3 months it has agrevated. Pl advise. Thanks and await your response.
Reply
Anil Roy
10 Aug 2015
I am taking paneer ka phool regularly from 3-4 months. I get benefit in diabetes but as a side effect, my ESR is high in blood.
Reply
Herbpathy Research Team
10 Aug 2015
Dear Anil Roy
We would like to know that are you taking any other Herb with Paneer ka Phool ? Any other medications ?
And what all other symptoms did you observe, please provide us with the details
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Subhash jain
11 Aug 2015
I am a 50 years old man ........I am taking paneer ka phool from a long time and i can also see good results of the same but one of the doctors i consulted said that paneer ka phool is good but it has adverse effects on kidney after a long time so i just wanted to know is this true or not
Reply
Anil Roy
12 Aug 2015
Dear Sir,
I am taking paneer ka phool and methi powder. i am facing pain in joint and backache. I am taking natralix sr 10 mg, storvas 10 mg and ecosprine since 5 year due to high tg and bp.
Reply
Shobhit Kalra
13 Aug 2015
Mr. Subhash Jain
There are really no side effects of Paneer Ka Phool. Just keep it in mind the dosage to be consumed. Over dose of any Herb is harmful for the body.
Also, I believe you should discontinue the Herb for sometime, because a prolonged use of it may affect Kidneys, and you have confirmed it with your doctor as well.
I took this Herb to cure my diabetes for about 6 months, then stopped. Shifted to Giloy, which is an amazing herb to cure diabetes. Why don't you try this ?
God Bless...........
Reply
D.Guhan.
12 Sep 2016
sir can you tell me the common name for Giloy.
Reply
Veekay kirti
14 Aug 2015
very useful information, thank you.
Please guide me from where to get giloy and how to use it ?
I have heard about it quite often.
I am suffering from diabetes,high blood pressure,very high LDL,
very low HDL and very high triglyceroids.
I need your guidance.
Thank you.
Reply
Sameer Batra
15 Aug 2015
Me (26 years) and my dad (60 ) are non diabetic, still have paneer doda everyday in morning just to be precautionary as my mom has high level of diabetic. The quantity involved is 10 seeds.we strongly feel it helps in reducing stress, bp, diabetes level in our body.
Suddenly we both felt we are loosing our weight. Can you please tell the side effects of paneer dhodha?
Reply
Shobhi Kalra
18 Aug 2015
Sameer
Its good that you are taking this herb as a precautionary measure against diabetes.. It is a good herb with many more medicinal values Paneer ka phool is known for its stress relieving properties as well. If your feel that you are shedding weight, why don't you make sure by weighing your body weight.
I suggest you to monitor your weight.
Just consume the herb for 15 days , then discontinue. check the weight. if you find no change, you may continue, if you see reduction in weight. discontinue the use.
There are no side effects of this herb. i have been taking this herb for years. Just don't take the overdose. okay!!
Take care. you seem to be a smart chap....decide for your self.
Reply
Neha
12 Nov 2016
Hello..shobhi kalra can u plz suggest us how many flowers shud we take?
Reply
Herbpathy Research Team
20 Aug 2015
Dear Veekay Kirti
Giloy is an amazing Herb which takes care of your Blood Pressure, elevates your HDL and lowers your LDL.
Giloy is a Rasayana Herb, which is used to cure multitude of problems. You can buy the tincture of this herb from any Homeopathic Store, it is known as Tinospora Cordifolia.
Add 10 drops of the tincture in half a glass of water. Drink it once in a day, for 3 months. And see the difference for yourself.
It is advised that you read Vibrant Health portal on our website. The link is given right next to the Home link, on the top most left corner of this page. And follow the regimen mentioned there. The regimen will make sure to provide you a holistic health and will take care of your other diseases as well.
In the mean time, you may try the following remedy to deal with HDL and LDL-
Eat walnuts, peanuts and almonds to raise your HDL to normal. Omega 3 fatty acids are essential for a balance between LDL and HDL levels, so consume diet rich in Omega 3, like fish and walnuts.
Since, the review section under Vibrant Health is not functional yet, therefore, we expect your reply here, under Indian Rennet.
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Herbpathy Research Team
20 Aug 2015
Dear Anil Roy
Indian Rennet is a harmless Herb. It really does not have any side effects. Unless you take it in a limit and do not take it while taking any other medications. As it is believed that any herb might show negative effects, when taken with other medications. So, caution is recommended. Also, the prolonged use of herb should be avoided. Discontinue the Herb after a month, then again,start administering it.
And the other 3 medicines, which you are administering for BP abd Tg , do have adverse impacts on the Liver and Kidney. So they should be avoided.
We advise you to read Vibrant Health. The link to Vibrant Health is to the right of the Home link, at the topmost left corner of the website. There, you will find the regimen to be followed to achieve holistic health and longevity.
God Bless....
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Anil
21 Aug 2015
guys, Here is something for If its diabetes.
Indian name Giloy, Homeopathic name Tinospora Cordifilia Q (Tincture). It is the 'Amrit' that will set you metabolism right. Take 10 drops of Tinospora Cordifolia in water daily for a month. Measure your blood sugar, early morning, after fasting for 10 hours. Then measure 2 hours after eating a major meal. Note it in your diary.
Now your body will be ready to accept the specific herb for Diabetes.
Indian name 'Gurmar', meaning kill sugar. Homeaopathic name Gymnema Sylvestre tincture. This is the magic herb that will see you through till the end. Take 5 drops of Gymnema Sylvestre tincture before every major meal. Measure your blood sugar every day. Slowly stop taking all other medicines and if required increase/decrease the 5 drops to 10, 7, 3 drops. Adjust the drops till the blood sugar reading are normal. Now take this herb for at least 3 months. Now stop for 10 days. If blood sugar starts going up. Start Gymnema Sylvestre tincture again for 3 months. You will know when to stop completely or not at all.
Why Gymnema Sylvestre ? I will tell you tomorrow.
Reply
George Bush
09 Feb 2018
Dear Mr. Anil thanks very good information you provided
Reply
Herbpathy Admin
24 Aug 2015
Dear Anil
Thank you so much for writing such an informative write up about Indian Rennet and how it is to be used for curing Diabetes. We really appreciate your effort of sharing knowledge with us and our users. Hope to receive such reviews from you in future as well... Keep visiting and dropping in such valuable comments.
Regards
Herbpathy Admin
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Anil Roy
04 Sep 2015
Dear Sir,
Presently I am taking Giloy Stem water and leaves since 2 weeks and stop to take Paneer ka phool. I find that our Sugar level increase gradually. What can I do. Restart taking Paneer ka phool.
Reply
Herbpathy Team
07 Sep 2015
Dear Anil Roy,
You should try Giloy Tincture. As the giloy tincture is supposed to have more beneficial effects then the boiled water. Take 5-10 Drops of giloy tincture in half cup of water. Try this for 10 days . Monitor your blood sugar levels regularly.
You can buy Giloy Tincture from any homeopathic shop . In homeopathy giloy tincture is known as Tinospora Cordifolia Tincture.
Regards
Herbpathy Team
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Anil Roy
07 Sep 2015
Dear Herbpathy Team,
I have purchased Tinospora Cordifilia Tincture and Gymnema sylvestre tincture. Can I take both ? Please advise .
Reply
Herbpathy Research Team
08 Sep 2015
Dear Anil
Yes, of course you can take both the tinctures. Tinospora Cordifolia will take care of your Blood Pressure and Gymnema Sylvestre for Diabetes.
Kindly go through the following procedure for 20 days. Revert back with results. We suggest you to follow the regimen given below-
Take 10 drops of Tinospora Cordifolia ( Giloy ) in the morning and evening for 20 days.
Take 5 drops of Gymnema Sylvestre ( Gudmar ) - morning and evening before meal for 20 days.
Keep a check on your Diabetes and Blood Pressure readings. Do not panic, if the readings fall below the normal range. Just skip the dosage for a few days and then restart it.
Decrease the dosage of your allopathic medications, as this may cause great drop in the sugar or Blood Pressure levels.
Write to us after 20 days, informing us about your condition. We will wait.
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Pratikash
17 Sep 2015
My husband is diabetic his sugar level is around 125 to 130 after dinner, he is taking tablets i can't ask the Doctor as i am in USA they may not know it. So how much phool should i soak to avoid any overdose.
Thanks
Pratiksha
Reply
Herbpathy Research Team
17 Sep 2015
Dear Pratiksha
Please stop taking tablets. The level of sugar is normal. By taking alopathic medicines, you are creating problem to yourself. There is no need of taking medicines.
If you continue the tablets, your husband's Heart and Kidneys will be harmed and will become very difficult to cure. His feet will be swelled.
Please note down the sugar level after 10 hours of eating food. Let us know and we will recommend you the remedy.
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
KATHIRAVAN V
23 Sep 2015
Is there any side effects if we consume Panneer Doda regularly.
Can Panneer Doda will reduce Blood Pressure ?
Reply
Herbpathy Research Team
23 Sep 2015
Dear Kathiravan V
As such there are no side effects of Paneer Doda, but yes, if we consume anything in excess, it may cause some side effects.
For High Blood pressure, You should go through the following procedure for 20 days-
Take 10 drops of Tinospora Cordifolia ( Giloy ) in the morning and evening for 20 days.
After 20 days monitor your Blood Pressure. Continue if there are positive results and you may reduce the dose accordingly.
Please let us know the results.
Kindly let us know the range of your Blood Pressure.
Please consult a doctor before taking any kind of Medicine.
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Anil Roy
28 Sep 2015
Dear Herbpathy team,
As suggested by you I am taking 10 drop twice Tinospora cardifolia Q in a day and Gymnema mother tincture 10 drop before each meal. But my Blood Pressure is 150/89 and BFs 112 , BPP 144 on 27.9.2015. I had start this after advise by you on 8.9.15. In early 10 days I took paneer ka phool in morning than my sugar was under control, I observed no beneficial Tinospora Coredifolia in Blood Pressure or sugar.
Reply
Herbpathy Team
06 Oct 2015
Dear Anil Roy,
Thanks for sharing your feedback. It is sad to know that the herbs mentioned did not benefit you. It rarely happens as Tinospora Cordifolia is considered an effective remedy for controlling Blood Pressure. For blood sugar you can continue to take Paneer ka Phool. As you already told, it is helping you, so it is good to continue that. One thing you may do, is take paneer ka phool for 15 days and then give a break of one week and, repeat. It gives the herb time to act on the body and avoids any possible ill effects.
If you are taking any other medications, then please consult with your doctor before using any herb. Regular Monitoring of Blood Pressure and Sugar is a good thing to do. It will be great if you can have a check up with some professional health care practitioner. So that you can get the exact readings and determine how much you have to work out.
Moreover you can still share your problems in case of any confusion or any query about your health. We are always here to help you.
Care and Regard
Herbpathy Team
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Ram shankar
09 Oct 2015
Dear Sir
My wife is diabetic in 1st stage.
From last 6 months sugar varies F 100-160 &pp 145 to 250 having no any allopathic medicine.
Before 6 months sugar was controlled by change in life style and powder made in home of karela Brij methi kanjar beej jaaun beej kumar buti and kali jiri.
Now started taking paneer doda from yesterday. Please give the suggestion for taking the medicine for blood pressure.
Reply
Nishtha Lamba
04 Jan 2016
Dear Ram Shankar Is your wife suffering from high Bp problem? Do not worry, there is a superb cure for it. Have you ever heard of Giloy ( Tinospora cordifolia ). The tincture can be bought from any homeopathic store. give her 10 drops daily in a glass of water. Check the readings, ask her to stop, when blood pressure is under control. Arjuna bark is also very very effective to cure high BP.
All the very Best to you and your wife
Reply
Herbpathy Research Team
09 Oct 2015
Dear Ram Shankar
As this is the initial stage of Diabetes, so they are easy to treat by an appropriate remedial treatment.
Please buy Tincture of Tinospora Cordifolia also known as Giloy.
Give 10 drops of Tinospora Cordifolia in half glass of water at morning and evening.
Repeat the process for 20 days and monitor her Blood Sugar levels on regular basis. If you see her sugar levels dropping below the normal range then please reduce the dose to five drops.
Consult a doctor before taking any kind of Medication.
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
George bush
09 Feb 2018
Dear sir, can you provide any informative guideline to prostate patients. Which indian herb is useful for enlarged prostate. I am taking paneer ke phool from last one year for sugar. But also suffering from prostate problem from two years. Please advice me. Waiting for your reply..
Reply
Bharat
17 Oct 2015
Is there any side effects of paneer doda to children as my daughter aged 6 is suffering from diabetes. Is paneer dodi useful for her ?
Reply
Neha gautam
19 Oct 2015
Dear Bharat
My son is also suffering from Juvenile Diabetes. Please share, since when is your daughter suffering from Diabetes. And, is it Type 1 diabetes or type 2. ? Is she taking any medicines ?
I am really worried about his condition, he is 11 years of age.
your review regarding your daughter, might help me dealing my problem.
This is sad.
Reply
C B Singh
04 Nov 2015
Dear Moderator of Herbpathy Research Team
Kindly see the adv. of Dr. Dave Gray. This will dent the image of the site. Kindly do not allow such adv. on this site. We are very confidently following the experiences shared by the different users. Such kind of luring advertisements will make the forum members loose their faith on the website.
Reply
Herbpathy Admin
05 Nov 2015
Dear C B Singh
Thank you so much for intimating us. It indeed is an egregious post. Herbpathy does not support such content at all. Users are requested not to post such advertisements as posted by Dr Dave gray.
You are free to express your queries, doubts, feedbacks,experiences, information. But luring someone to donate their body parts if in need of money or in debt, or anything detrimental post like this shall not be posted here at all.
We do not object your freedom of thoughts, but ,if it is tend to harm someone, then sorry, not here. Not permitted.
Thank you Mr. CB Singh, we appreciate it. Suitable action will be taken regarding that post.
Herbpathy Admin
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Sanjay chamoli
24 Nov 2015
Dear sir
Can u tell me what is the perfect dose of paneer doda for daily use and what is the over dose
Becase i ha v taken from fifteen days 6 to 8 phul daily please advice me.
Reply
Herbpathy Research Team
24 Nov 2015
Dear Sanjay Chamoli
Paneer ka Phool is known to bring down the sugar levels remarkably.
But, if you are using the herb with other medications, it may cause a sudden drop in sugar levels, below the normal range.
So, we suggest you to keep a count of your sugar levels.
Dosage : Put 8-10 pieces of flower in a glass of water and keep it overnight.
In the morning, squeeze the flowers and mix them well, Now, strain it and drink the water.
For best results, use the herb regularly.
The super effective herb to treat Diabetes is----- 'Gurmar', meaning kill sugar. Homeopathic name Gymnema Sylvestre tincture. This is the magic herb that will see you through till the end.
Take 5 drops of Gymnema Sylvestre tincture before every major meal. Measure your blood sugar every day. Slowly stop taking all other medicines and if required increase/decrease the 5 drops to 10, 7, 3 drops. Adjust the drops till the blood sugar reading comes to normal. Now take this herb for at least 3 months.
Please consult your health care provider, before using any of the remedies.
Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Atul
31 Dec 2015
Dear Sir,
I am female, 73, and a diabetic for 22 years. Am taking Glimipride 2 mg. pills morning & evening, plus Metformin 1000 twice daily and Sitaglyptin 100 once daily. I am also hypertensive, under control, and Hypothyroid patient also under control with Eltroxin. I have started taking Paneer Doda in the manner prescribed, early morning, for the last 2 weeks. The fasting diabetes has come immediately under control (90-91), but Post prandial it shoots upto, and even beyond 200 on a regular basis. I am taking the above mentioned Allopathic medicines also.
What should I do? Should I take Paneer Doda twice a day? Please advise. Thankyou.
Reply
Herbpathy Research Team
04 Jan 2016
Dear Atul
Paneer ka phool is a good herb, it is very effective, but since, you are 73 years of age, so we do not recommend you to take this Herb, it is quite a harsh Herb. The super effective herb to treat Diabetes is----- 'Gurmar',Homeopathic name Gymnema Sylvestre tincture. This herb will see you through till the end.
Take 5 drops of Gymnema Sylvestre tincture before every major meal. Measure your blood sugar every day. Slowly reduce the dosage of allopathic medicines and if required increase the 5 drops to 8,10,12 drops. Adjust the drops till the blood sugar reading comes to normal. Now take this herb for at least 3 months. If, the reading gets excessively low, you may reduce the drops to 6,4,3.
Tejpatta is another effective cure for diabetes. Boil 5 to 8 leaves of this plant in 3 cups of water for 15 minutes. Strain well. Drink the tea twice a day. Herbpathy Research Team
(Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Devendra
07 Jan 2016
Does paneer doda increase Cholesterol level ?
Reply
Prerna Kaul
07 Jan 2016
Dear Devendra
Paneer ka phool is known to treat high cholesterol. It does not raise cholesterol levels. But, is famous to reduce LDL levels, i.e. bad cholesterol... Are you suffering from high cholesterol ?
Reply
P k gupta
16 Jan 2016
Dear herbpathy research team
I am 29 year old male, was diagnosed having diabetes in fasting 248, after meal 364 & bp- 140/90 also high cholesterol - 256 and ldl -171, hdl - 35 , vldl- 49, triglicerides 249 on 9 the November 2015. After taking medicine in 15 days fasting comes
101 and after meal 112.
After this I start to take paneer doda with medicine from 30 December 2015 and madhusunya (meghdoot ayurvedic co.) From 7 Jan. 2016 with medicine and on 15 Jan. 2016 again checked without taking medicine and herb where fasting comes - 100 and after meal - 135.
Advice me
Thank you.
Reply
Pk gupta
17 Jan 2016
Dear herbpathy research team
I am waiting for your advice , am i to continue with medicine or medicine with herb or only herb and one question why my after meal increased when i was medicine and herb both only that day (when get blood taste) not taken.
Thank you.
Reply
Herbpathy Research Team
18 Jan 2016
Dear PK Gupta We did not get what you wanted to ask. It is all so confusing.... It is advised that you stop taking all the medicines and Herbs for a day. Monitor the sugar levels, if under control, skip the medicine for 3 more days and keep a note of your sugar levels. You have mentioned the readings, and medicine, but did not mention the name of the medicine you were taking...
Please write back to us the name of the medicine you took. Then only we would be able to suggest you. Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
P k gupta.
19 Jan 2016
Dear sir For blood sugar I am taking zoryl M1 forte. For blood pressure I am taking hopace 2.5 For cholesterol I am taking tg tor 10. Sir I want to know when my sugger level is under control than why feel symptoms like that dry throat. And also want to know is their any problem to take herbs with medicine ? And my pp was 112 with medicine and without medicine and herb its 135 so what it shows ? Please advice me. Thank you.
Reply
Pk gupta
22 Jan 2016
Dear sir
I am waiting for your response.
Thank you
Reply
Herbpathy Research Team
22 Jan 2016
Dear Pk Gupta
It is a good news, if your sugar levels are under control. Do not worry about this dryness of Throat , it will be set right when you regularly take Gudmar and reduce the dosage of allopathic medicines you have been taking.
If you take these drugs and Herbs together for a long run, then you are likely to face symptoms like pains all over the body, weak bones and joints, eyes will go bad too.
Once, readings get normal, dosage of Herbal medicine may be increased and that of drugs can be decreased.
However, it is always advised that you consult your health care provider before taking any Herb. Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Shareef
26 Jan 2016
what herb is Bandal Doda is it unani or Ayurveda, where i can find.
what is real name
Reply
Herbpathy Admin
27 Jan 2016
Dear Shareef We have forwarded your query to our Research Team. As for now, we are not aware of any Herb named Bandal Doda. A detailed research needs to be done on the subject.
If our Team comes up with something related to the Herb you mentioned, It would definitely be posted on Herbpathy. Thank You
Herbpathy Admin
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Vikas Chawla
27 Jan 2016
Dear sir,
This is a very informative site, thank you for that.
Could you please confirm if paneer Phool is safe for children with type 1 diabetes, who are insulin dependant.
If yes, what is the recommended dose for an 11 year old girl.
Thank you.
Reply
Herbpathy Research Team
27 Jan 2016
Dear Vikas Chawla We would not recommend Indian Rennet to your child. The Herbs to be give to your child are Gymnema Sylvestre- 5 drops of this tincture in half glass of water,should be given before every major meal. Measure the blood sugar every day. Slowly reduce the dosage of Insulin, as this Herb is known to drop sugar levels drastically. Adjust the drops from 5 to 3 till the blood sugar reading are normal. Your child might need to take this herb for at least 3 months. Do not consider this as incurable, it will be cured, but might take 3 to 6 months............
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Herbpathy Research Team
27 Jan 2016
Continued-------- Dear Vikas You may also give your daughter Velvet Beans capsules, give her one capsule daily for a month. It will prevent Hormonal imbalance in your child. Bay Leaf capsules are another cure for Diabetes, but not as effective as Gymnema Sylvestre. It is always advised that you consult your health care provider before giving any medicine to your daughter. Everything will be set right. The Herbs we have mentioned have shown miraculous effects in curing Diabetes. Wishing you good luck. Regards Herbpathy Research Team
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Vikas Chawla
28 Jan 2016
Dear sir,
Thank you for your prompt reply. I will start the herb and revert to you with the result. However, I gave rennet to my daughter, 8 pods in water overnight, and her sugar levels improved today..... Just one dose. So, please do confirm why you don't recommend it for her. Regards,
Reply
Pooja verma
31 Jan 2016
Dear sir.
My age is 31. I am 7 week pregnant. I am diabetic. My sugar level is always high fasting and pp both. My medical history i had an abortion in 6th month in early labour pain. Please sir suggest to me what should i do to control my sugar level. Dr. Started my insulin 4 unit in the morning before break fast. But it does not control. Should i take paneer ka phool to control my sugar.
Regards
Pooja
Reply
Herbpathy Research Team
01 Feb 2016
Dear Pooja Verma
Before we suggest you any Herb, a prior discussion with your Health care provider is always recommended. To control your blood sugar, the super effective Herb is Gudmar. Its homeopathic name is Gymnema Sylvestre, Take its tincture form. Start with 5 drops in a glass of water before every major meal. Monitor your sugar levels. If you find a drop in your sugar level, you may reduce the dosage of Insulin accordingly. If no difference, then herb's dosage may be increased to 6,8 and then 10 drops. You'd have to keep a check on your sugar level, and then adjust the dosage accordingly. Regards
Herbpathy Research Team
( Make Life Healthy )
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
DEEPAK GOEL
12 Feb 2016
Myself Deepak Goel, age-40 years, my sugar level is 223 fasting and 320 after meal...my cholesterol is also high, now a days I am taking only allopathic medicine...but still no improvement in my sugar level.
Please suggest me some ayurvedic medicine to control my sugar level.
Reply
Sangeeta Verma
17 Feb 2016
Dear Deepak Goel
To control your blood sugar, best Herb is Gudmar. Its homeopathic name is Gymnema Sylvestre, Take its tincture form. Start with 5 drops in a glass of water before every major meal. Monitor your sugar levels. If you find a drop in your sugar level, you may reduce the dosage of allopathic medicine accordingly. If no difference, then herb's dosage may be increased to 6,8 and then 10 drops. You'd have to keep a check on your sugar level, and then adjust the dosage accordingly. The Herb will considerably decrease the sugar level and bring the Cholesterol to normal.
Note : Monitor your sugar level, you may even stop taking allopathic medicines, once the sugar level gets under control. High Cholesterol can be treated by Shiiitake capsules. eat one daily. Include carrot and coriander in your daily diet. Good luck !!
Reply
Apurva
13 Feb 2016
Dear Sir,
i have been suffering from DVT in my right leg for last five years, is there any medicine to cure this
i have tried blood thiner (Wraf) and after that i started doing rakt motion, i tried many other things but its not helping me. can you please recommened me.
Reply
Shaurya Paul
18 Feb 2016
Apurva
Cayenne and Rosemary, Gingko are the best Herbs for you. Gingko-- it improves blood flow through dilation of blood vessels. Take one capsule per day ( 160 gm ). Eat it for a month Apply paste of cayenne and water on your leg. leave it for 10 minutes. Rinse off. Do this daily for 7 days. Do not smoke, don't take vitamin K food.
Do not sit with an obstruction to the thigh or leg muscle. Keep a check on your Blood Pressure. No alcohol please. Please share your feedback after 7 days.
Reply
Vivek
03 Nov 2017
DVT can be cured. I had the same problem. By the mercy of god, some homeopathic, ayurvedic medicines it is almost cured. My Doppler and d-dimer test reports showed negative result.
Reply
Hira
14 Feb 2016
Can i give paneer doda to my daughter age 3 yrs? She just diagnosed just 2 months ago
Reply
Herbpathy
18 Feb 2016
Hira
Diagnosed with what ?
You said your daughter has been diagnosed , what is it exactly.
Why do you wish to use Paneer ka phool ?
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
ABDULMUNAF SHAIKH
16 Feb 2016
I am using paneer phool since last 6 months. My diabetics is reduced to a reasonable extent no it hovers over 145 to 155 fasting and 150 to 175 ppbs. My medications reduced by 50 %.
However my common cold and sneezing, and nose overflow has increased.
Earlier i used to have this problem. But it has aggravated now and inspite of taking medicine it is not in control. Is it because of intake of paneer phool.
please advice
Reply
Herbpathy
17 Feb 2016
Dear Abdulmunaf Shaikh
Thanks for sharing the good news that your sugar is under control. As far as your common cold and sneezing are concerned, we can not comment if its because of paneer ka phool. As you have mentioned that you are already taking this Herb for the last 6 months, it is advised that you please stop its usage. Six months is a long period. As it is mentioned in the side effects of this Herb ( scroll up )that a prolonged use of the Herb may cause other diseases. So please STOP the usage . For diabetes Gudmar is the best Herb. Visit the Diabetes page in disease section of the website and check how to take this Herb. Also, you should get an allergy test done. The sneezing and cold might be because of some allergies or infections. Write back to us, once you get your test done, so that we may suggest you a cure.
Please consult your health care provider before taking any Herb. Regards
Herbpathy
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
AbdulMunaf Shaikh
18 Feb 2016
Thanks for the advice, will stop taking this herb. As advised pl tell from where in Hublj, karnataka state can i get Gudmar is available. Thanks
Reply
Loksh
03 Mar 2017
Buy Gudmar from any herbal store. It is very famous herb
Reply
Kumar
20 Nov 2016
Paneer Doda (fool) has immunosuppressive properties thats why your cough and cold has elevated.
Reply
Saleheen ( INDIA/W.BENGAL )
18 Feb 2016
I am having sugar fasting 120 and Pp 180 for that I am taking metformin 1gm 2 times. Also, I hv Bp n TG for that I m taking Olvan tri 20 n orvas 10 mg. Can I take paneer booty with these medicines. My dr. Never allows me to take herbal medicine and stop alopathy. What should I do.
Reply
Herbpathy Admin
19 Feb 2016
Saleheen The choice is yours. It is advised to always consult your health care provider before taking any medication.
You may write back to us, if you make up your mind to use Herbs to cure your Diabetes problem.
We would love to help you.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Saleheen akhter
03 Aug 2016
Dear Dr, I always want to stop alopathic. I am using paneer boot I more than 6 months. Sugar in fasting is 120, pp didn't check. What shall I do.
Reply
Mayank
27 Feb 2016
Dear research team
Can you give sucess story of giloy and gudmar.
Reply
Krish
05 Mar 2016
Dear team
I am 30 year old Before 6 month i come to know i have diabetic (fasting-248 pp-364) and high bp (140/90) but currently my fasting-91 and pp- 117 with medication (glimpride 1 mg metaformine 500mg) and bp 130/80 with medicine (vampiric 2.5mg)
I want to know:-
1. Can i move on to ayurvedic medicine if yes
2. Than which one is best for both diabetic and high bp.
3. Is there any sideeffect of ayurvedic medicine
4. And ayurvedic Medicine can also need to take lifetime.
Thanking you.
Reply
Bharati ( India )
05 Mar 2016
WIll Paneer Phool work on cases of Insulin Resistance and also someone with borderline sugar (Type 1)
Reply
Krish
06 Mar 2016
Sir
Waiting your kind response.
Reply
Herbpathy
08 Mar 2016
Dear Krish 1. Yes, you can move to Herbal medicines. 2. The best Herb for diabetes is Gudmar . You may take its capsule or its tincture which is known as Gymnea Sylvestre. Keep a check on your sugar levels . The dosage might be adjusted as per the readings. intially, you may start with 10 drops of th tincture in a glass of water. Then the dosage might be adjusted as per the readings. Similarly, you can lower the dosage of your allopathic medicines and then can ultimately stop taking them, once the sugar is under control. Monitoring your sugar levels is an important step. Bay leaf and Fever nut are other Herbs that assist in th curing Diabetes.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Herbpathy
08 Mar 2016
2. The Herb that is highly effective for High Bp is Giloy. It is known as Tinospora Cordifolia, in Homeopathy. Take 10 drops of this tincture in half glass of water daily for a month. Monitor your Bp levels regularly. And the dosage may be increased or decreased as per the readings. Rasayanas and Adaptogens are the Herbs that have no side effects and can be taken for life time. hose Herbs will boost up your metabolism and set your body right. you may refer to the portal Vibrant Health,and look for the Rasayanas That can be taken for life. It is advised that you consult your health care provider before taking any Herb. For any queries, you can always write back to us. Regards
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Krish
10 Mar 2016
Thanks for reply But you have not mentioned how it should be taken. Now these days i am feeling other complication.
1. Without GETTING full of urine blader i feel urination which happens little amount.
2. After rest again 10 to 15 min same feeling.
3.and their is no any burning feeling in urine.
4. My pulse rate and heart bitt getting fast some time So please advice me. I am waiting ur responset. Thank you.
Reply
Kriah
28 Mar 2016
I am Waiting ur response.
Reply
Shubham Patwa ( India,Maharashtra )
07 Mar 2016
Dear Team,
My dad is 53 yrs od and has type 2 diabetes. (Fasting is 120 but PP is 250-300)
His diet is just like a normal person, not like a diabetic person. (Vegetarian Diet)
He is taking paneer doda empty stomach in the morning for controlling sugar level and no other medicines.
But sugar not in control.
What can be the reason? What can be done? Please guide.
Reply
Roop
16 Mar 2016
Dear Shubham Patwa
My dad also had the same problem. It was by providence that i came across this beautiful website. And found a cure for my dad. Gymnema Sylvestre is the Herb, it is called Gudmar. It indeed is very famous Herb here on this website and all over the internet and research studies. give him 10 drops of this Herb daily, before every major meal. Monitor the sugar levels. If they drop, the dosage can be reduced to 7,5 or even 3. Give him bitter gourd juice daily on an empty stomach. Soak the Fenugreek seeds in water overnight and drink this water and chew on the seeds first thing in the morning. Take this thrice a week. Skip for 4 days and then again take it for next three days.
Reply
Shubham
22 Mar 2016
Dear Roop, Will try it out.
Thanks a lot.
Reply
Maha ( Uae )
07 Mar 2016
Im 40 yr old lady since my teen age im having acne problem.. It come and go but my skin do not 100% clear of acne . Still i got breakout.. Can i use paneer boti to cleanse my blood.. What should b the dose (how many paneer boti should use in water) and durration. Some body told me that put 10 paneer boti in a glass of water n drink in morning on empty stomach for one month. Is it ok? Plz reply
Reply
Krushi Kaul
16 Mar 2016
Dear Maha
You may try Tea Tree oil. The oil is very potent. So dilute this with water. wash your face with water, pat dry. Take one part of oil and 9 parts of water. Apply this on your face with a cotton ball. Leave it for 15 minutes and then you may wash it off with cold water. Remember, this oil is very strong, so dilution is very very important. You may even use Aloe vera gel instead of water. do it thrice a week. Drink loads of water. Papaya pulp may be applied daily before sleeping. massage your face with papaya pulp. wash the face after 15 minutes with luke warm water. Rub your acne with raw Garlic several times a day, it helps in healing them fast. All the very best...
Reply
Shraddha ( INDIA )
13 Mar 2016
can paneer ka phool be used to cure hypothyroidism...
shraddha
Reply
Ruchi Jain
16 Mar 2016
Consume 3 to 4 walnuts daily . It will help in balancing the functioning of Thyroid gland. The most effective Herb is Withania Somnifera. The tincture may be taken daily for a month. Add 10 drops of this tincture in half glass of water. and have it. Stinging Nettle is another Herb to cure Hypothyroidism. Consume Broccoli , either raw or cooked. Take it twice a week.
Reply
Srishti kalra ( India )
13 Mar 2016
Can i use this rennet in hemorrhoids n piles....
Reply
Herbpathy
16 Mar 2016
Dear Srishti Kalra.
Piles is the disease of Liver. It is a result of a Faulty Liver. No amount of local application or pain killers are going to help, until the Liver disorder is corrected.
Read the Liver Damage page under disease section on this website for information purpose. However, the course of action to be followed is - Take fresh Radish, grate it to squeeze the juice. Drink 40 ml or half a glass of this juice on an empty stomach for 3 days. Do not take it for a week. Now after skipping it for 7 days, again drink it for 3 days. Skip for a week. Again, take for 3 days.
Repeat this course for a month.
If the problem still persists, let us know. We will suggest you another cure. We advise you not to drink alcohol. Avoid spicy food, oily food, coffee and tea.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Sunil U
15 Mar 2016
Dear Team,
I am recently diagnosed with diabetes ( pp - 240) and not started any allopathic medication so far. Heard about Paneer Ke Phool and purchased and started having from today 10 flower in the early morning. How long should I have this or any break is required in-between?
I am under allopathic medication for BP & Cholesterol for last 10 years and can I have Paneer Ke phool along with this.
Now I heard about Ghiloy tincture and Gudmar tincture from this page and confused .. as to what to have to control diabetes. For diabetes.. not started any allopathic med and for BP & Cholesterol am under allopathic medication. Kindly advise a proper med for Diabetes.
Rgds,
Sunil
Reply
Shaurya Paul
16 Mar 2016
Dear Sunil U
You may take this Herb for 7 days. Keep a check on your sugar levels. If it falls and you see any improvement, usage may be continued for 10 days more. After that you may switch to Herbs like Bael-- They are proved to be anti-diabetic. Drink fresh juice of leaves with pinch of pepper, daily in the morning for 10 days. Yes, Gudmar is the super effective Herb for diabetes and Giloy is quite effective in curing High Blood Pressure. You may scroll up and look for the method to take the two Herbs. Both these Herbs can be used for 2 to 3 months. Without any risk of side effects. Just do not forget to monitor your sugar and bp levels. The dosage can be reduced or increased as per the readings.
Reply
Sunil U
27 Apr 2016
I tried Paneer Ke phool for about 3 weeks and not much of change in the PP sugar levels stopped the same .. then switched to Gurmar ( Mother Tincture) from schwabeindia .. 8-10 drops in empty stomach morning and evening before food... unfortunately not much of change in PP sugar level ( its abt 225)... kindly advise..
Reply
K H Joshi ( India )
17 Mar 2016
sir
I have diabetes type-2 with fasting sugar 204 as on today , not taking any medicine for fear of any side effects . my BP is hovering between normal to little below borderline for High side. sometimes stressful working conditions , sedentary work . weight is 80 kg. take Non-Veg food also. no other bad habits . I was suggested overnight soaking 5 flowers of paneer ka phool and drinking that water for curing diabetes .
kindly advise
Reply
Ronit Khosla
18 Mar 2016
Dear KH Joshi
Paneer ka Phool is a good cure for Diabetes. You may start with this Herb. Take this for one month. This Herb really has shown great positive results. Dosage : Put 5-6 pieces of flower in a glass of water and keep it overnight. In the morning, squeeze the flowers and mix them well, Now, strain it and drink the water. And, if you think you might have a problem of high bp, you should try Giloy ( Tinospora Cordifolia ). For Immediate results, buy a Tincture of Giloy and take 10 drops in water every day. Just keep a note of your Bp readings and reduce the dosage if the Bp falls considerably. And the intake might be stopped, once you think your BP becomes normal. All the very best.....
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Shomasree ( Maharashtra )
17 Mar 2016
I am diabetic for last 5 years and is on oral medication, I also have thyroid disorder and I am taking eltroxin 100. Since 2014 I am consuming early morning Paneer ka phool 5-6, daily. I do not crush it but I just remove the flowers and drink the water. My blood sugar is still in baseline...ff 126 / pp-156. I love having rice and usually consume some at night, but after boiling the rice I wash away the starch.
Could this be the reason for sugar level not coming down?
Where in Mumbai/ Thane can we buy Paneer ka Phool,
Reply
Arjun Rawat
14 Apr 2016
Dear Shomasree
Yes, right is known to increase the sugar levels. It is better if you take rice on alternatively . That too not too much. Instead of Paneer ka phool why don't you try the Herb Gudmar. Its tincture is known as Gymnema Sylvestre. Take 10 drops of it before every major meal. Try for 10 days. Keep a note of sugar levels. If it drops, then you may decrease the dose of the tincture.
Reply
PAM ( CANADA )
18 Mar 2016
I AM OVER WEIGHT,IS PANEER DODI HELPS TO REDUCE THE WEIGHT
Reply
Herbpathy
18 Mar 2016
Dear Pam
For reducing weight, drink green tea daily, early morning. Continue for 20 days.
Swallow a tablespoon of raw Fenugreek seeds daily. Eating 250 gm of Papaya daily for dinner will also help to reduce weight. Have you heard of a fruit called Avocado. This is a great fruit, which helps in reducing weight. It will suppress your hunger, reduces the urge to eat and will help to shed off extra calories, that too without any side effects.
Take Black Cumin seed oil-- Add half teaspoon of this oil in 2 spoons of honey. Mix them well. eat this paste with warm water, two times a day. Once in the morning, on an empty stomach and once in the night before going to bed.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
NAGAVENI. ( India )
19 Mar 2016
SIR I AM 30 YEARS OLD, SINCE 5 1/2 YEARS I AM HAVING SUGAR. my HBA1C IS 8.3, 7.8, 8.5 like it will come, can i take paneer dodi flower. plz replay me sir, i am waiting for the answer. please help me. how many quantity can i take in one day
Reply
Varooshi Kailker
12 Apr 2016
Dear Nagaveni
Paneer ka phool is quite effective in curing Diabetes. Dosage : Put 5-6 pieces of flower in a glass of water and keep it overnight. In the morning, squeeze the flowers and mix them well, Now, strain it and drink the water. You may take this drink for 20 days. Then you can stop and try with another super effective Herb called Gudmar. It indeed is very famous Herb here on this website and all over the internet and research studies. give him 10 drops of this Herb daily, before every major meal. Monitor the sugar levels. If they drop, the dosage can be reduced to 7,5 or even 3. Give him bitter gourd juice daily on an empty stomach.
Oh yes, and the homeopathic name of Gudmar is Gymnema Sylvestre. All the very best.......
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NAGAVENI
13 Apr 2016
Thank You Sir, Now I am taking 5-6 Paneer ka phool daily, Now i am feeling better,
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Shivangi ( Maharashtra )
06 Apr 2016
I'm pregnant in my 7th month with high diabetes. May I consume paneer phool? Please suggest.
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Sandeep ahuja ( Indore )
11 Apr 2016
i am sandeep , can u tell me the cost of getting paneer phool . how will it works if i take water of 5 -6 phools .plz reply
Reply
Herbpathy
12 Apr 2016
Dear Sandeep To know about the cost of this Herb, you'd have to do research on your own. You may visit the near by herbal stores or may check the price on the internet. We do not deal with buying or selling of Herbs. Your review has also been copied to Buy/ Sell Herbs portal of this website. There you may find the vendors for this Herb.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
LAVANYA ( INDIA, BANGALORE )
13 Apr 2016
Dear Sir, What should do for weight gain and which herb i can take. plz suggest me. my marriage is fixed.
Reply
Janghel
17 Apr 2016
Dear lavanya congratulation first for your marriage i want to suggest you drink milk with honey every morning.for one month.
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Preeti shah
23 Apr 2016
from last 10 days i have seen my husband's weight reduced he has been feeling more thirsty and drinking more water we went for check up . in report he has suffering from diabetes his HBA1C IS 11.5 % AND FASTING BLOOD SUGAR IS 282 AND POST MEAL BLOOD SUGAR IS 445AND WE STARTED MEDICINE PRESCIBED BY DOCTOR . WITH MEDICINE CAN WE START PANEER DODA PHOOL?? WAITING FOR NORMAL BLOOD SUGAR IN OUR FAMILY NO ONE HAS SUFFERING FROM DIABETES
Reply
Herbpathy
03 May 2016
Dear Preeti..
To control your blood sugar, the super effective Herb is Gudmar. Its homeopathic name is Gymnema Sylvestre, Take its tincture form. Start with 5 drops in a glass of water before every major meal. Monitor your sugar levels.. If no difference, then herb's dosage may be increased to 6,8 and then 10 drops. You'd have to keep a check on your sugar level, and then adjust the dosage accordingly.
Stinging Nettle is the other Herb for you-- It is known as Urtica Dioica. Take 10 drops of this tincture daily in a glass of water.. try for a week, if it suits you, continue for 20 days.........
Bitter gourd is another cure...
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Herbpathy
03 May 2016
Crush 5 to 7 bitter gourds in a food processor. Put this crushed herb in a tub of hot water. Now, your patient should dip his feet in the tub, keep them soaked, until he feels the bitterness of the herb in his mouth. Once, he gets the taste of the herb, he can take his feet out. ..... Use this water for 3 days, heat it and dip is feet in it...on the fourth day, prepare the water again by crushing the fresh Bitter Gourds. Continue for another 3 days. Keep a check on the sugar levels. It is advised that you consult your health care provider before giving him any medication.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Uma mahesh ( India,andhra pradesh )
25 Apr 2016
my wife is having diabetes from 25 years she on insulin take 60 in the morning and 60 in the afternoon and 60 in the night. She started using panner ka phool last 10 days,her diabetes levels are not coming down any reason
please let me know sugar level in morning are between 100-150 and after noon between 100-105 and in the evening
is between 140-190
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Sunil. U ( Karnataka )
27 Apr 2016
Hello,
For diabetes, I tried drinking Paneer Ke phool water in the early morning in empty stomach for about 3 weeks and not much of change in the PP sugar levels ( PP 225) hence stopped the same .. then switched to Gurmar, ( Gymnema Sylvestre - Mother Tincture) from schwabe india .. 8-10 drops in empty stomach morning and evening before food for 2 weeks ... unfortunately not much of change in PP sugar level and still its abt 220... kindly advise..
Thanks & Regards..
Reply
Paralin
28 Apr 2016
Dear Sunil . U Are you taking any other medication as well ? You know, you have to be patient. Your sugar level is quite high and it takes time for some medicines to act. Different herbs act differently on an individual. So patience is the key. You will have to give Gudmar some time to act. Since, This is a highly effective herb for diabetes. Good day !!
Reply
Sunil
02 May 2016
Hello Paralin,
Thank you so much for your advise. I am not taking any other medicine for diabetes. Shall continue with Gudmar for some more time and now I'am taking the same 3 times a day before food. Thanks & Regards...
Reply
Paralin
07 Jun 2016
Yes, you may continue with Gudmar. And can try the method given below---
50 leaves of each: Basil, Neem, Bael,Jamun. Prepare a decoction of these leaves and store in the refrigerator. Take teaspoons everyday, twice. Keep doing this for a month.
Keep a check on your sugar levels. Thai is must.
Good luck!! I really wish , you get cured...
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Sunil
17 Jun 2016
Thank you Paralin for your revert..!!!
Reply
Sunil ( Bangalore )
28 Apr 2016
Hi,
There is a new ayurvedic medicine named BGR-34 released by Amil Pharmaceuticals.
Is there any update/ feedback of the effectiveness about the medicine by anybody please..?
Thanks & Regards,
Reply
Sunil
17 Jun 2016
Hello,
Any update on the efficacy of BGR-34 on diabetes treatment...?
Kindly revert.
Reply
Monali ( Maharashtra )
05 May 2016
Hi,
My mom is having type 2 diabetes since 6-7 yrs. The last time we had it checked was on 30Jan'16, her fasting was 199 and pp was 191 of course which has reduced than before but keeps on fluctuating when we check at home. And her total cholestrol was 170.6, triglyceride 135.7, HDL 50.2 & LDL 113. She is taking allopathy medicines Glyciphage 500mg - 3 times daily, Reclide 80mg - 3 times daily, For cholestrol she is taking rosimit 10mg - once at night, trifeno 200mg - once at night and antacid pantoch DSR once daily and other multi vitamins as well. She has started having paneer ka phool since Sep'15 regularly but with intervals for some days. She has lost weight but the diabetes is still not in control...Allopathy doctors say no to stop the medicine.
Please advise your suggestion as to shall she continue to have paneer ka phool or swtich to some other herb like gurmar. Also is it ok to have allopathy along with these herb medicines. hope it wont have any adverse effects on her. we want to stop or atleast reduce her allopathy medicines due to its major side effects.
Await positive reply.
Reply
Monali
07 May 2016
Dear Team, Awaiting reply.
Reply
Monali
09 May 2016
Still awaiting reply.
Reply
Mahima
17 May 2016
Dear Monali
When you take Herbal remedies and Allopathy also, keep one thing in mind that you should check her Blood Sugar on regular intervals. As both will show the effects and there are chances that her blood sugar may drop down than the normal levels. And the Herbs that she is taking are strong enough. So, be careful about the dosages.
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Monali
24 May 2016
Inspite of all these allopathy medicines and paneer ka phool her fasting remains constant to 198-199 and post lunch is 154 now. Please advise shall we start with gymnema or giloy instead of paneer ka phool ???
Reply
Monali
02 Jun 2016
Awaiting reply from the team
Reply
Herbpathy
07 Jun 2016
Dear Monali
Yes, your mother can stop Paneer Ka phool. She can try Gudmar. It is a super effective Herb to cure diabetes. It is known as Gymnema Sylvestre in homeopathy. Buy this tincture and give her- 5 drops of this tincture in half glass of water,before every major meal. Measure the blood sugar every day. Herb is known to drop sugar levels drastically. Adjust the drops from 5 to 3 till the blood sugar reading are normal. Once, you see that her sugar readings are normal, then she may slowly reduce the dosage of allopathic medicines that she has been taking. Or, she may try the following-- this method has also proven to be very effective in curing many diabetic cases. 50 leaves of each: Basil, Neem, Bael,Jamun. Prepare a decoction of these leaves and store in the refrigerator. Take teaspoons everyday, twice. Keep doing this for a month. It is advised to consult your health care provider before trying any medication.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
VINOD BHARDWAJ ( CHANDIGARH )
14 May 2016
any herb to improve eye site
Reply
Daniel
17 May 2016
To improve your Eye Sight is, eat a lot of Green Vegetables, Foods rich in Vitamin A, Add carrot juice to your daily diet. Also do some exercises. Go for morning walk also.
Reply
Sobia ( Pakistan )
24 May 2016
Hi. I am 37 year old female. Have two kids.
My problem is that my digestion has suddenly because bad I feel bloated most of the time can't digest much. Although feel hungry as usual.
My body feels hot all the time as if I have fever and now that it is summers I feel burning inside me and can't sit without aircondition at all.
I have disc buldging in lower back and I am gaining weight. Current weight is 80 kg
Reply
Tina
26 May 2016
Dear Sobia
Take Aloe Vera and Aamla juice daily in the morning. This will help you out with your digestive problems. It will also makes your body cool. Drink a glass of butter milk and lemon juice daily. For you disc problem take Guggul tablets. take 1 tablet a day. Also drink a cup of green tea daily.
Reply
Viswanath ( India/Kerala )
07 Jun 2016
Hi all,
Good Day.
I am taking Paneer ka Phool regularly for more than 3 years. I started this herb on the advise of a Jaipur bound Sadhu, when my FBS crossed 200 and remained so for a couple of months or so. Then my doctor advised me to switch on to Insulin than oral medicine. I was continuing oral medicine and the above herb and my FBS came down to 130-145 range till a couple of months ago. Now it is high in the range of 190-210. Due to the ban on combination tablets, the tablet which I was using for 4-5 years is not available.
Any advise as to how I could bring down and maintain low FBS without changing over to Insulin?
Regards.
Reply
Paralin
07 Jun 2016
Dear Viswanath You may try the following-- a very effective in curing many diabetic cases, including mine. I am 52. My FBS ranged from 220-260. And now I am glad as my FBS is finally 120 to 140.. This formula has proven to be some magic tonic for me. Take 50 leaves of each: Basil, Neem, Bael,Jamun. Prepare a decoction of these leaves and store in the refrigerator. Take teaspoons everyday, twice. Keep doing this for a month. And monitor your sugar regularly. It is advised to consult your health care provider before trying any medication.
Reply
Goutham Mahaveer ( Tamilnadu )
13 Jun 2016
My wife is seven months pregnant, Today we went for a checkup and we came to know that she has sugar , the doctor told her to follow diet. There is no history of sugar in our family.
My question is
Is this temporary? Will it continue after pregnancy?
Reply
Komal
15 Jun 2016
Hello Goutham Mahaveer Diabetes in Pregnancy usually occurs between 26 and 30 weeks of pregnancy. Yes, this Gestational diabetes is temporary. But, there is strong need to take care of your diet. Along with this, regular exercise is necessary.
Reply
Pinky patel ( India )
15 Jun 2016
Is there any side effect of these flowers on kidney or any other?
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Herbpathy
16 Jun 2016
Hello Pinky There is no such side effect this herb. But,still sometimes it depends on individual person to person. On a large scale, this herb is safe to use.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Priyanka dhariwal ( India )
22 Jun 2016
Can we take panir doda if we are planning a baby?
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Sahil
22 Jun 2016
no, don't consume it during pregnancy.
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Firdous Ahmad
22 Jun 2016
can i use paneer dooda for weight loss
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Ankush
22 Jun 2016
Paneer dooda is not useful for weight Loss. To get the most relevant herb for weight loss, go to the disease " obesity" of Herbpathy
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Gururaj Jahagirdar ( India Karnataka )
24 Jun 2016
How long we have to take if diagnosed diabetic? Is it necessary to continue paneerphool till life .If we discontinue for few days ,what is the alternative herb to replace? pl reply=Gururaj
Reply
Matul Garg
24 Jun 2016
Gururaj
Paneer ka phool is known as one of the best herbs for Diabetes.
But over use may cause complications. So it is better to consult a doctor before use.
Avoid if you are already taking any kind of medications for Diabetes, as it may lead to Kidney damage and Hepatotoxicity. The substitue herb is Gudmar. you may check that page in the herb section of this website.
Reply
Gururaj Jahagirdar ( India )
03 Jul 2016
I have asked in my previous query that how long we shall take Paneerphool contineously & how long discontineu the Paneerphool & what is the replacement during discontined period.Your reply is very much awaited
Reply
Herbpathy
04 Jul 2016
You may take Paneer ka Phool for continuously. 2 months, if it suits you. Even if you wish to skip it, do it for 10 days, in the mean time you do not need any replacement. Do not take it for more than 4 months in total, as the long term usage may cause Kidney disorders. The super effective herb for diabetes is Gudmar. Only Rasayanic and Adaptogenic herbs can be taken for life.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Gururaj Jahagirdar ( Karnataka India )
06 Jul 2016
Sir, WHETHER is it more helpful in taking Tinospora Cardifolia Q Paneerphool Gymnemasylvestre Q for controlling bloodsugar with lower doses? Please reply immediately to start the course I await your reply.
Reply
Herbpathy
07 Jul 2016
The herb which has shown great results in reducing Blood sugar, is Gymnema Sylvestre. This is the homeopathic name of herb Gudmar. It is the super effective herb to cure Diabetes. Buy it's mother tincture and start taking 5 drops in a glass of water before every major meal. Keep a note of your sugar readings. and then adjust the dosage after a week , as per your readings. Continue it for a month and share the results here.
Good luck. Consult your health care provider before taking any medicine
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Gururaj Jahagirdar ( Karnataka India )
07 Jul 2016
Sir, Thanks for your reply.pl let me know shall I take Gudmar PaneerPhool Giloy each 5 drops (PaneerPhool5 phool) in the early morning on empty stomach.My fbs is 91& pbs is 138.This is controlled on food diet only Taking millets as main food
Reply
Herbpathy
08 Jul 2016
Dear Gururaj Initially start with Gudmar only. Giloy is recommended if you have high bp. This will lower your blood pressure. Try with Gudmar first. Take it for 15 days, you will see the results. Then you mat decide if you wish to continue with it or wish to take Paner ka Phool. Do not take Paneer ka Phool and Gudmar at the same time. As both have anti diabetic action and will lower the sugar level drastically.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Suman jain ( Toronto )
31 Jul 2016
HELLO my husband have stroke March 20 -2014 right side paralyzed he is little bits movement he have high blood pressure and sugar but doctor give him Madison to control he is 48 year old please can you tell me what I can do make him better he is is fele like wick selping all that time can you suggest me some thing to give him to eat I have one question can you tell me Isthere any deferent between planner dodi and / planner ki phool Is same I say people view so nice . thank you so much please send me email or call me to solve my problem 416 749 6742 . thanks again
Reply
Nishtha Gandhi
02 Aug 2016
Suman
I guess you meant paneer ka phool. Yes, paneer ka phool and paneer dodi are same. For high Bp you can give him Giloy. It is known as Tinospora cordifolia. 10 dops of this tincture in a glass of water, everyday for 15 days. Keep a note of his bp reading and reduce the dose when the bp comes back to normal.
For his heart, you may give him Hawthorn tea-- 2cups in a day. It is advised that you Consult your health care provider before giving him any herb. give him 2 walnuts everyday to eat. all these herbs have helped my father to a great extent. all the best.
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Tejashree ( Maharashtra )
02 Aug 2016
Can I roast these rennets as these are getting spoilt in humid weather
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Roshik
03 Aug 2016
store them in an air tight container. and if you are taking decoction, then refrigerate it. Roasting might change the action of the herb. For what purpose are you using this herb ??
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Rajendra ( USA )
08 Aug 2016
Is it available in U S A? And how much cost?
Reply
Swapnil
09 Aug 2016
Rajendra
You may check your local herbal store. If it is not available, then you may order it online. There are a number of websites like dragon herbs or amazon.
Research need to be done on your end.
Reply
Fizza Raza
19 Aug 2016
If we drink paneer bolti with water just like tablets instead of soaking it overnight!.. Will the effect be same?
Reply
Herbpathy
26 Aug 2016
Fizza
The method of taking a herb depends on the disease to be cured. Please mention your condition. The herb can be taken either in the form of pills, decoction, infusion or fresh as it is..
Mention the disease along with all the symptoms that you want to cure.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Shekhar ( India /Delhi )
18 Sep 2016
Dear sir/madam
I am 39 year old suffering from diabetes & high cholesterol. for diabetes i m taking in morning metformin 500 mg amaryl 2mg in afternoon metformin 500 mg galvas met 50mg/500mg in evening metformin 500mg for cholesterol tonact 10mg ecosprin 75mg. so can i take paneerdoda and tell me dose of it & is it safe to take with medicines.
Regards..
Shekhar
Reply
Deepak Lal
20 Sep 2016
No, it is not safe to take anti diabetic herbs if you already are on so much medication. As , this may lower the sugar levels beyond normal, drastically. The dosage of these drugs need to decreased with the intake of herbs.
Reply
Menka ( India/Delhi )
20 Sep 2016
Hi My Mom In Law Starting taking Panner ke Phool Last Week onwards and her sugar was 203
She just started with 3-4 phools everyday
After having Paneer ke phool she starts feeling energyless and she starts burping . She has complaints of BP but it is only when she is anxious otherwise she has no issue and she is also not on any medication of Sugar and Bp She starts feeling hungry and after 15-20 mins and feels that she is not keeping well
Is this a normal behavior?
Reply
Palash Mishra
22 Sep 2016
Menka
If the herb did not suit her then I think you should switch to other herbs for Diabetes. The most effective heard that I've heard of is Gudmar. you can buy it's tincture for your mother in law. A regular check on sugar levels is a must. It's tincture is : Gymnema Sylvestre. give her 5 drops of this tincture added to a glass of water. She may reduce the number of drops as per the reading. I hope you are getting what I 'm trying to say.
Reply
Ravikumar ( India , telangana )
27 Sep 2016
Sir, iam having thyroid. Will paneer ka doda helps in correcting thyroid. Can I have along with thyroxine tablet.
Reply
Manhar
28 Sep 2016
Ravi Kunar
You need to state that are you suffering from Hypothyroidism or is it Hyperthyroidism ?
Because, both has different cure.................
Reply
Ayan ( India )
28 Sep 2016
I just want to know, how to use paneer dodi for home cheese making.??
Thanks,
Regards,
AYAN.
Reply
Herbpathy Admin
30 Sep 2016
What ? Sorry we could not comprehend your query. Ayan, your question is not clear. Do you intend to ask anything about this herb called " Indian rennet " ?
Please write in detail
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
K.NARAYANASHAMI ( TAMILNADU )
29 Sep 2016
Sir where can i get this herb in Coimbatore -Tamil Nadu please guide me.
Reply
Kishorie Somti
30 Sep 2016
Dear SIr
Please visit your local herbal store. If you do not find it in your region , then do not worry. You may order it over the internet. There are many websites which sell herbs and herbal products. You can look on the internet. amazon.in is the website that sells almost everything. You can try that.
Reply
Lodha sm ( MAHARASHTRA, INDIA )
08 Oct 2016
I have high cholesterol LDL 215 hdl is 45.
Total cholesterol is 268.
Sugar 180
Reply
Mahuo Das
18 Oct 2016
For Diabetes, take Gymnema Sylvestre tincture everyday. For high Cholesterol take Spirulana capsules. One every day. Keep a note of your sugar level and adjust the dosage as per the readings. Take 5 drops of the tincture in a glass of water.
Reply
Misbah
09 Oct 2016
I'm gettin married in 4 months and pimples have started showing up on my face and I'm really concerned that they might leave marks. Someone suggested this herb and I've started taking it. I just wanna know how many of these should we keep in water overnight and in how much water. And is it any good for pimples and their marks? And how do we EXACTLY use em
I'll be waiting for a response and I hope I get one ASAP,do I'm really very concerned
Thanks :)
Reply
Sparsh
18 Oct 2016
Misbah The best herbs for you are:
Neem, turmeric,honey and lemon. Boil 5 to 8 Neem leaves. Once the water cools down, strain it and wash your face with this water, thrice in a day. Do not use any soap or face wash. Apply a mask made of honey and lemon on your face every night 15 minutes prior to sleep. Once you have applied the mask, leave it on the face for 15 minutes and then wash it off with plain water. Do this for a month
The herbs shall take care of your skin. Make sure you are not constipated and avoid foods that may cause constipation.
Reply
Anuradha Kalwar ( India )
02 Nov 2016
Dear Sir
My child 7 year old was down with high grade fever and urticaria. So I was advised to give him paneer phal.
Can you pls suggest how much can i give him.
Reply
Herbpathy
04 Nov 2016
Anuradha , you can give him Urtica Urens 30. Take 2 globules (pills ) of this medicine, add it to a glass of water. Give 2 teaspoons of this water, after every 2 hours.
Once the water is finished, do not repeat the dose.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
D.N jagga ( Haryana )
05 Nov 2016
dear sir,
i am suffering from high cholestrol and diabetes and i am taking medicine for the same .can i take doda paneer ? is doda paneer is also useful for decreasing the cholestrol level?
Reply
Jikiles
11 Nov 2016
For decreasing Cholesterol level, take Spirulana tea everyday for a month.
Also eat one Burdock capsule everyday for a month. Discuss with your doctor before you try any remedy.
Reply
Swastika jain ( India )
07 Nov 2016
I have severe gastric issuse with heart burn , burrps and stomuch ache , .can u help and sugest what medicine will help me .
Reply
Radhya Sen
16 Nov 2016
Drink Fennel water after every meal. Take 3 to4 4 Basil leaves, crush them and make a globule of it and swallow it with water. Do this everyday for 15 days. Since when are you suffering from stomach ache. Do you feel the pain going towards a particular side, like, right, left or the lower abdomen.
Reply
Ms.linda ( India )
09 Nov 2016
I am a diabetic since 9 years. Currently taking Zita plus 20 mg before breakfast and Volix Trio 1 after lunch and after dinner. My last b.sugar reading was fasting 173 and pp 193. Have been taking paneer doda 7 nos.daily since a month. Is it ok for me to continue taking paneer doda wih my meds.
Reply
Dheertha
16 Nov 2016
Dear
It is recommended that you reduce the dosage of your allopathic medicines.
As the level of sugar reduces, the dosage should be reduced.
Also, I would suggest that you please take the herb Gudmar.
Reply
Vasantben ( India )
29 Dec 2016
What is use of renet
Reply
Gururaj Jahagirdar ( Karnataka )
06 Jan 2017
Dear Sir,I have been advised to take paneer doda in the morning with empty stomach before fresh Now recently I am advlsed to take Kalonji seed oil Pl let me know whether I can replace kalonji oil in place of Paneer doda If so what is the dose & method how long I can take the Kalonji seed oil
Reply
Raman
19 Jan 2017
The usage depends on the disease to be cured. So, please specify the exact problem that you wish to use these herbs for.
Reply
Arvind kumar ( Mohali )
23 Jan 2017
Dear Sir, I have done ny HB A1c test and the result is fasting blood sugar 110mg% and HB A1C value is 6.4 (mean blood glucose 137mg/dL) so please suggest something to me to make it normal.
Reply
Sukrit Talwar
03 Feb 2017
Arvind Kumar. Please do not worry, you are prediabetic. I suggest that you please try Green Leaf juice for 15 days.
Please go to the portal Vibrant Health and read " The Genesis " page. That is the cure for you.
Reply
Anand Palkar ( India )
12 Feb 2017
Hi
I have type 2 diabeties since two years. I was on alopathy medicine called Diamicron XRMEX 500 before taking paneer dodha from last two months it was around 250 fasting now its reduced to 170 fasting and 180 pp. Please let me know for how long i need to continue paneer doda . Or shall i continue it til i get within specified limits.
Reply
Manisha Kakkar
21 Mar 2017
Take it for a month. And after a month switch on to Gudmar. It is the most widely used herb for Diabetes. Take its mother tincture for a month. It is known as Gymnema Sylvestre. Have 5 drops in a glass of water, daily. Adjust the dosage of the remedy as per your sugar readings Sir.
Reply
Ankush rastogi ( INDIA )
17 Mar 2017
sir i have a pancreatitis problem and i also have a diabetes my sugar remains uncontrolled
can i take paneer ka phool is it be beneficial for me
Reply
Liza Thakur
21 Mar 2017
Ankush.
You may drink a cup of Nut grass decoction every day for a month. This will cure Pancreatitis. For Diabetes I would like to tell you that take Metformin tablets one every day and also take Berberis Vulgaris mother tincture for a month. This will control your sugar. Make sure that you keep a note of your sugar readings.
Reply
Meera ( Canada )
19 Mar 2017
Hi there,
I am pregnant and may have gestational diabetes. Currently i am not on insulin but have to keep a check on my sugar levels 4 times a day. I have started having panner ka phool.
Please let me know if it is ok to have during pregnancy.
I take around 10 to 15 paneer ka phool soak them in water and then crush them , strain and have water.
Also can I have 2 times a day morning and night or only once. Please let me know.
Regards
Meera
Reply
Herbpathy
21 Mar 2017
Meera. It is suggested that you do not take Indian Rennet . The herb might not be safe to be consumed during Pregnancy. Take High fiber diet. Include Lentils in your diet. Eat foods rich in Vitamin D. Do gentle exercise every day. The herb which can help you is Astragalus. Have a cup of Astragalus tea every day. Consume it for a month.
It is your delicate period, so it is suggested that you consult your doctor before trying any remedy. Please let us know that which trimester is this ?
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Isela ( California )
21 Mar 2017
Can I use for 8 years old kids?
Reply
Meera Deol
21 Mar 2017
What Indian Rennet ?
but, what for ?
What is the problem that your kid is facing ?
Reply
Kiran sonawane ( India )
25 Mar 2017
Dear sir
my 4.5 years son is diagnosed with type 1 diabetes just 2. weeks ago now he is on insulin
doctors are saying his pancreas not making insulin
his blood glucose varies his blood sugar levels are much high ........he was hospitalized with kitoacidosis at that time his sugar level was 600
and hb1ac 10.56 after discharged from hospital
and now on insulin shots
2 points before breakfast 3 points before afternoon lunch and 2 points before night dinner and 9 points at night his sugar was 450 and 500 before dinner
i know paneer doda is very effective one ,,can this herb cure ..type 1 diabetes
Reply
Mahendra shah ( Canada )
05 Apr 2017
where do we get paneer dodi in Toronto, canada?
Reply
Mahendra Dubey ( Maharashtra/India )
07 Apr 2017
Dear Sir,
I am diagnosed with prediabetes since last 2 years. My FBS was 120 and PPBS was 200 on diagnosis. I am on combi of Metformin 500 Voglibose 0.3, one tablet a day. Off late i started experiencing dip in my blood sugar levels. I am also having high BP and borderline lipids, am on pinom-20 and rosuvastatin-5
Got to know about Paneer phool from a friend and started taking it since last 1 week (5-6 pods soaked overnight). I am monitoring my BS 2 hours after every meal and have stopped allopathy medication. Post meal BS is ranging between 120-147 since last one week.
I am feeling more energetic and much better now. Better than when I was on medication. I also had metabolism issue, chronic constipation and acidity. Now after starting Paneer phool I am observing better bowel movement and relief from constipation.
I have stopped metformin (consultation with my doc is pending). I am continuing with medication for BP and lipids (one tablet post dinner).
kindly suggest how long can I continue with Paneer Phool. Do i need to restart after some time.
Can you suggest anything better for my conditions.
Mahendra Dubey
Mumbai
Reply
Herbpathy
10 Apr 2017
Mahendra. It is good that your post meal readings are better.
Congrats!. Consume Paneer Ka Phool for 15 days. Then skip for a few days. Again continue for 15 more days.
After this, you can start with the herb called Gudmar ( Gymnema Sylvestre )
Read about it in the herb section or in the disease : Diabetes, given in the disease section of this website. It is one of the best herbs for Diabetes. We will also suggest that Metformin can be continued, just reduce its amount. Instead of 500 , take 250.
Monitor your sugar levels regularly. For constipation, take Green Leaf juice for 15 days.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Mahendra Dubey
04 May 2017
Thanx for your revert and advice related to my conditions.
Reply
Uzma salam ( Pakistan )
25 Apr 2017
Hey sir my name is uzma salam my mother is a suger patient and also having heigh blood pressure and she is also having UTI problem as well as H Phylori.... but the main problem is hwer bp and suger is out of controle . is she used this herb as a madicene or not. if its not good for her health then please recommend us the effective one for her' it will be a great pleasure for me if u reccomend it...
Reply
Ritvika Desai ( India)
05 May 2017
For High Blood Pressure give her Giloy. It is one of the best herbs for lowering the blood pressure.
You can give her tincture of Giloy . Buy mother tincture , it is known as Tinospora Cordifolia. Give her 5 drops in a glass of water,, every day for 2 weeks.
It is important that you keep a regular check on her blood pressure. For Diabetes give her Jarul tea, one cup everyday for a week. The dosage can be increased as per the sugar reading.
Is she taking any additional medicines for Blood Pressure control and for Diabetes.
Reply
Uzma salam
17 May 2017
thank you soo mush Ritvika Desai .the madicince yo recomend me for my mother is really good and benificial for her i m really thank ful to you thanks. and one thing more i want to ask for my self i m a lil bit fatty and i want to lose my fats if you know any herb for it or any madicine which is easily available in pakistan so plz recommend me my wait is 58 and my age is 23 im student of bs botany having my last semester plzz
recoment it to me
Reply
Uzma salam
17 May 2017
yeah she is taking dioplus 10/160 mg for bp and hemoline 70/30 inj for diabetes
Reply
Uzma salam
17 May 2017
sorry there is a mistake done by me my weight is 68 kg
Reply
Shahbaaz ( Haryana /India )
08 May 2017
I m suffering from diabetes last 11yrs and now having initial stage of liver cirrohsis and also my spleen inlarge. I m taking alopathy medicine metformin 500mg twice a day .my sugar level after meal 300 .but now i m taking paneer ke phool without medicine last 30days my sugar level is 280 .Please suggest me can i continue paneer ke phool daily. Is any side effect for liver desease or any other.
Reply
Saran Jaray
16 May 2017
Take Metformin every day. Do not stop. And, start taking Gudmar herb. You may take the capsules or the mother tincture which is known as Gymnema Sylvestre. Monitor you sugar reading after taking the tincture. For Liver, take Milk Thistle capsules, one daily for a month. Buy Kutki powder from a herbal store, take half teaspoon with a glass of water after breakfast for 7 days only.
These two herbs are excellent for Liver.
Reply
Mikhil
16 May 2017
For Enlarged Spleen take Sage tea , every day for 15 days . Drink Cranberry juice daily.
Reply
Falak
11 May 2017
Dear Sir / Madam ,
I have a friend who had a D&C done 3-4 years back and she is suffering from amenorrhoea ever since. Her ultrasound is normal. Every month there is a specific time when she feels menstrual cramps and other symptoms but there is no bleeding. 2 months back she took paneer k phool. She experienced some spotting in March and lesser amount in April (a delay of 5 days). I would like to know if she should continue taking paneer k phool. Also does paneer boti help resore menses and if so, how?
Looking forward to your reply,
-Falak
Reply
Madhuri ghosh ( India )
16 May 2017
Falak. Please mention the age of your friend. The reason that she is not getting her periods is the D & C treatment. First of all, it is recommended that you get her ultrasound done. She really needs to be examined by a doctor. The herb that can help her to get back her periods is Fevernut. You can give her that herb, but a diagnosis is still important.
Reply
Falak
17 May 2017
She is now 38 years old. Not menopausal as her FSH and estrogen levels are normal. Her ultrasound report is also normal.
Reply
Madhuri Ghosh ( India )
07 Jun 2017
It is a good news, if all her reports are normal. Give her Fever nut decoction until the menses resume. Once, her periods start, stop giving her the remedy. The problem might be due to some sort of hormonal imbalance.
Also, give her Chaste Berry tea, every day for a month.
Reply
Dr uday ( Delhi india )
23 May 2017
Hlo
My wife is diabetic on insulin ( both on basal and short acting ). Her creatinine is 3.04 and urea 70.
Will it b useful for her to use paneer Phool.
If yes how much quantity shouls she start with.
Her fasting sugar levels range 200 and pre dinner about same levels when seen in glucometer . Her hba1c was 7.8 about 4 weeks back.
She is also on anti hypertensive drugs
Reply
Sushma ( India )
13 Jun 2017
Is paneer ka phool good for treating allergy???
Reply
Meghna
06 Jul 2017
What type of Allergy are you talking about ?
Please be specific. List out the symptoms that you haver been suffering from.
Reply
Hisamuddin ( Pakistan )
13 Jun 2017
Under side effects Paneer Booti is stated as Immunity Suppressant, while in terms of actions it is described as Immunity Booster. I do not understand this because of my lack of knowledge in herbs. Please favor me and many others like me with more information.
Reply
Rupesh
20 Jun 2017
Dear Herbpathy Team,
Can a combination of Chirata (Botanical Name-Swertia perennis) and Paneer ka phool be taken to combat with Diabetes?
Reply
Deepti Khosla ( India )
10 Jul 2017
Yes, both of these herbs can be taken together. I have taken it for myself. I also took it for 20 days and then I switched to Galega Officinalis. And, now my Sugar level is in control now.
Reply
Sanjay Waghmare ( Maharashtra )
27 Jul 2017
I have diabetes. My fasting blood sugar is 128 and BSLPP is 233. I am taking allopathy medicine " Glimestar-PM 1mg and Glyciphage 500mg" since 1 year. Also I am taking paneer k pool since one month along with this medicine. Please advise me whether I should continue paneer k phool. Or advise any other hurb medicine to cure diabetes
Reply
Fuziah kamaruddin ( Singapore )
06 Sep 2017
Hi, I'm 48yrs old diabetic, hypothyroid and cholesterol patient. Im currently on 500mg metformin and 2.5mg glipzide twice a day, 50mg euthyrox and simvor 10. My question is can I take paneer doda?
Reply
Nouman ( Pakistan )
06 Oct 2017
Is this available in usa
Reply
Surya Rathore ( India )
30 Oct 2017
I am a 50 years old woman diagnosed with Type II diabetes with FBS 226 and HDL Cholesterol 36 and VLDL cholesterol 132.80 TSH 6.9. Allopathy doctor has written medicines but I want to get cure through homeopathy/natural herbs. Kindly advice. I stay in Hyderabad
Reply
Jwal ( India/Gujarat )
20 Dec 2017
Hi my wife is 27 she is 7 weeks pregnant and detect high blood sugar dr has recommended insulin so is it advisible to use panner ke phool to reduce it any effect on pregnancy.
Reply
Bhanumathi ( West Bengal India )
22 Feb 2018
If i have no diabetes can that lower my sugar level n harm my health??
Reply
Rhyaan
23 Feb 2018
What ? Are you asking about Indian Rennet ? Why do you want to take it?
It may be harmful. It is very effective for high Sugar, if you are not suffering from Diabetes, then you must not have it.
Reply
Uttam Sinha ( India. )
23 Feb 2018
I am suffering from diabetes and high blood pressure since 1 year. However since june 2017 I started taking paneer ka phool 4 times a week. Since August 2017 my crp level is high which means there is some infection in the body. Should I stop taking it. Because medicine and injections are not working.
Please help me.
Regards,
Uttam
Reply
S.ramesh kumar ( Tamil nadu )
07 Mar 2018
Sir iam daily iam having at early morning 6 clock iam having it without brushing it is good then I have stomach pain some time Even motion three times
Reply
Karundhi
12 Mar 2018
Why are you having Indian rennet ? You are taking too much of the medicine. Stop taking it and observe for a week
Reply
Devi ( India tamilnadu )
15 Mar 2018
Sir
I am 32 years old. diabetic last 4 years. Recently am using panned flower and maintain sugar in normal level. For this problem itself am avoiding second baby. I saw u r substitute herb like kelp dandelion. .... But I did not got this in my home near. Am from tamilnadu. Please suggest the herbs for my future life.
Reply
S RAMESH Kumar
27 Mar 2018
This will be available at country drugs shop
Reply
Rahul ( Maharashtra )
11 Apr 2018
Hello sir, can u tell the chemical properties of that flowers,..and we can separate by simple distiltion with water to make more benificial to health..reply asap....if yes then what the boilng range of this liquid
Reply
Krish ( Malaysia )
28 Apr 2018
Dear sir
Is paneer doda safe to be consumed by pregnant womans? If yes what would be the recommended dosage?
Thanks
Jega
Reply
Annie Chishti ( Canada )
04 May 2018
Can i use this herb for Uterine Fibroids ? plz reply
Reply
PRIYANKA DARYANANI ( India )
10 May 2018
Can the paneer fool be taken on daily basis..for pimples bearing skin?
Reply
Bhawthra ( Tamilnadu )
17 Jun 2018
i m 55 year old female i have high sugar 250 from last 1year onwards i took tablet for 4months and i stoppped to take tablets and i have weight loss . Can i take paneer phool and for how many days i should take a paneer phool in a week . I should take for a month or week ?
Reply
NITIN B BORULKAR ( India )
21 Jun 2018
HOW TO TAKE PANEER DODA AS MEDICINE? hFOR HOW MUCH TIME. IS IT INCREASES INSULIN IN BODY OR ACT AS INSULIN.
Reply
Shweta ( India )
10 Jul 2018
How to use paneer phool for curing asthma?
Can it be given to 13 year old child?
Reply
Parneet ( India )
25 Jul 2018
My son aged 14years is juvenile diabetic since last 5 years. He's on insulin 3times a day. Please advice what should he use paneer doda or gurmar.please reply ASAP
Reply
Jyoti ( India )
17 Aug 2018
I am suffering from Psoriasis is paneer doda is suitable for me.
please suggest.
Reply
Usha Mohan ( India )
19 Aug 2018
My RBS is 343..I'm not into any medicine..can I opt the paneer ke phool...I need to know how to take it...does it have any side effects??
Reply
Manish Goel ( INDIA )
30 Aug 2018
My father aged 69 is a patient of hypertension. In the recent ultrasound the doctor found that his prostate has increased. BUT his PSA levels in the blood tests are normal. taking cap.URIMAX for last fifteen years.
His RA factor is also high 89.90. No medication until now.
He works almost 13 hours a day. Running a retail shop.
Early this month his BP fluctuated from low to high. Since then he is feeling very weak. In the recent blood tests we got done, we got to see very high levels of vitamin B12. The levels were as high as 2700. (Probably because of multivitamins). Even after taking multivitamins and other allopathic medicines, we could not see better results. Please advise some Ayurvedic medicine.
Reply
Sourabh ( India )
04 Sep 2018
Hello All,
Myself Sourabh, age 37 Years from Noida, i have diagnosed diabities 4 months back (fast:- 278, PP- 450, Hb1ac-12.5,
lost almost 18 KG Weight) i was in deep mental trauma, what happened to me, then i visited Fortis noida and took Medicine from Dr.
after 15 days of allopathy Medicine, stopped it, and start taking Paneer ka phool early in the morning and cut carbs from my diat.
Start taking triphla powder and methi dana in night (before sleep), Keep AAk leaves on foot (around 8 hours)
After taking paneer ka phool for almost 1 week, it start working and lowering down my fasting to below 120,..100,..90,...85-86 (in 2 months).
and Hba1c 12.5 to 8.4, i will go for hba1c after 1 month then i will share the result.
I dont know whatever i did , its good or not but it works best for me.i am happy with its result.
As of now i am taking paneer ka phool twice in a week.
No Alopathy Medicine.
10000 Steps daily walk
Cut carbs from daily diat
I am not a doctor but writing this to help others.
How to take paneer ka phool, methi dana, aak leaves, you will get the method from youtube (i did the same).
I recommand to track your KFT and ESR during taking paneer ka phool.
if any question as
Reply
Garima ( India )
06 Oct 2018
Why is it not safe to consume Indian rennet during pregnancy
Reply
Kumararaja Devarajan ( India )
24 Oct 2018
Dear Sir
My sugar level after food 175 and bp is 136/91 and i am consuming alopathic medicine. In this condition can I take panneer khe phool if so how long I have to use it please let me suggest. Is there any side affect for kidneys if simaltaneiously taking both and panneer khe phool can reduce High BP
Reply
Mad Jamil Asghar ( India/Bihar )
02 Nov 2018
How can manage the energy label as well as the sugar label for diabetic patient. I have just got the findings that is 126 after fasting and 196 after two hours of flooding. Please let need have your best advise regarding the ailment, I have also the cervical problem since 2007, and I am 63yrs aged
Reply
Anil ( Gujarat )
19 Dec 2018
Hi sir,
I am using paneer dodi for acne ... Only paneer dodi is working for skin.
Actually I am a Hyderabadi and came to Ahmadabad on job purpose. But in Ahmadabad I am facing pimples (acne )problem only on face
to which going into depression.
One of my friend suggested to take paneer. And now I am using since 1 month. So I want to ask is there will be any side effects if I use in long term like one year. Because I am planning to stay in Ahmadabad for one year.
Pls reply to my mail I'd.
Thank u.
Regards,
AA
Reply
Anil
22 Dec 2018
Hi I am waiting for your reply
Reply
Inaya ( India )
24 Jan 2019
Hi I am 29 years suffering from diabetes and on oral medication please suggest some remedies for diabetic retinopathy and controlling sugar levels. Urgently needed
Reply
Divyesh ( Gujarat )
22 Apr 2019
My father has diabetes dependent on Insulin injections and FBS 200 and PPBS 300
can he take paneer phool?
If yes than from where I can buy from ahmedabad??
Please share dosage as well.
Reply
Mamta Chamoli ( India )
24 May 2019
Dear sir
My blood sugar fasting was ranging between119 to 124mg/dl since last one year.i didn't took it seriously.Two months back my fasting was 160 and pp 203 and my hba1c was 6.I showed to doctor he told me to make dietary changes and regular walks.
One of my friend suggested me to take paneer Doda.I started using it since yesterday.I have started with 10 flowers.
sir please guide as to how long should I take paneer Doda and when to get my blood sugar tested.I have also made dietary modification and go for regular walks now.
Regards
Reply
Nivedita
22 Dec 2019
Sir,
I am diabetic. I am consuming Paneer Dod, as prescribed bu soaking 5-6 pcs in wanter overnight and next morning drinking the water (by squeezing the soda out of it). I drink it on empty stomach. I have stated taking this for the last three weeks, However, I have developed a dull headache ever since I began taking it. Could this be a side effect?
I look forward to your answer
Reply
Herbpathy
24 Dec 2019
Dear Nivedita. It might be a side effect. You can try Gymnema Sylvestre- mother tincture ( Homeopathic medicine ) Gurmar ( Hindi name ). Take 5 drops in half a glass of water. Take it twice a day. It is a very effective herb. Keep a check on your blood sugar levels. If they go below normal, then reduce the dosage to 3 drops.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
SHAREEF ( SAUDI ARABIA )
30 Dec 2019
Sir
i am a diabetic since 9 years i am taking morning: sitagliptin / metformin hcl 1 tab with jardiance 10 mg 1 tab night : sitagliptin / metformin hcl 1 tab with pioglitazone HCL 15 mg 1 tab after food my levels are FBS-190 & PPS IS 286 after having this above medicine
can i use this paneer ke phool and how many in dosage BCZ i dont have any ayurvaid doctors hear
Reply
Sandra
30 Dec 2019
Hello friend. have Gymnema Sylvestre ( Gurmar ) - mother tincture. It is very very effective for diabetes. My father is having it for the last 1 year. He is very fine now. His sugar levels are stable. Take 5 drops daily in half a glass of water once daily.
Consult your doctor first if you are taking other medications or any homeopath near you. My father had cut down on his allopathic medication a little and then started, our doctor suggested so. You too have a consultation first.
Reply
Narmeen
02 Jan 2020
Is it same as "ghesso kay phool"?
Reply
Ketaki
25 Jun 2020
Sir, my 4 yr old son has been diagnosed with Type 1 diabetes last year. He is on insulin injections daily. Desperately searching for a cure for him. You had mentioned that Indian Rennet helps in the repair of beta cells of pancreas. Should I give that to him. If not , what is the best we can do for him/ cure him? I am v dedicatedly also administering wheatgrass juice every morning.
Reply
Herbpathy
02 Jul 2020
Dear Ketaki Please mention how did your son developed Diabetes, Is it by birth? Did he suffer illness after which he developed Diabetes? Did the mother face any trauma during Pregnancy? Meanwhile you can use Bittersweet Herb, Homeopathic name: Dulcamara- Mother tincture. It is good in treating Diabetes in children. Take time and read Diabetes under Disease section on this website. It may help you.
Write back with answers for further suggestions.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
R.sivam ( India tamilnadu )
21 Jul 2020
Shall i take panner phool twice a day morning and before lunch. My age 53. I am in advicate profession.my sugar level pp is 220. Fasting is 170.
Reply
Prakash ( India )
23 Jul 2020
Dear sir,
My diabetic mother is suffering from proteinuria, is it good for her to take panneer poo to reduce her blood glucose levels. Please give some medical advice.
Reply
Herbpathy
23 Jul 2020
Dear Prakash
Paneer Phool is good for Diabetes. However, Gurmar ( Gymnema Sylvestre ) is considered a more effective herb for Diabetes. Take homeopathic tincture- Gymnema Sylvestre -Mother tincture. Take 2-3 drops in half a glass of water. Keep a check on your sugar readings. If you are already taking medication, keepa thorough check or consult with your Health care practitioner first. For Proteinuria, take Punarnava herb extract (Boerhavia Diffusa- Homeopathic tincture ): Take 5 drops in a glass of water. Write back incase of query.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Anna mandoon ( Pakistan )
24 Jul 2020
can paneer booti's water be used in periods
Reply
Archana ( Haryana )
21 Aug 2020
My age is 25 and I am suffering from type 1 diabetes and I am on Ayurvedic treatment and don't take insulin but I drink it and my sugar gets normal. Should I take it daily empty stomach?
Is there any side effect of this?
Reply
Anisha
21 Aug 2020
Take Gurmar tincture ( Gymnema Sylvestre). Take 3-4 drops daily in a glass of water once in a day. Keep a note of your readings. It is known to super effective to lower the blood sugar levels.
Since you are already taking Ayurvedic treatment, please consult your Health care provider before taking other herbs.
However, the procedure to take Rennet is explained above.
Reply
Mona ( INDIA/UP )
04 Oct 2020
I want to grow paneer doda plant in my house. Where can i get its seeds or what is the way please guide
Reply
ZAHEER ( PAKISTAN )
14 Oct 2020
BEFORE A MONTH .I TRACED SUGAR AND MY SUGAR 319 MG/DL . I STARTED MEDICINE
NOW MY BLOOD SUGAR 125 MG/DL. DURING A MONTH I TEST 3 TIME .SOME 113 MD/DL. THREE MONTH TEST 10.80. MY BP 80-120 .PLEASE SUGGEST PRESCRIPTION I
WANT TO BLOOD SUGAR 80-90 MG/DL
Reply
Herbpathy
14 Oct 2020
Dear Zaheer. Gymnema ( Gurmar ) is the best suited herb for High blood sugar. You can take it in Homeopathic form- Gymnema Sylvestre. Take 5 drops in a glass of water twice a day. As you are taking medication already, take a note of the readings after meals for 2-3 days. Lower the dosage if the levels drop below normal. Do not stop the already taking medication without consult of your Health care provider.
-You can also take Black Plum Vinegar (Jamun Sirka ), Bitter Gourd juice on regular basis.
Write back for further queries.
This advice is for educational purpose only. It is not intended to replace a doctor. Please consult your doctor before taking any herb.
Reply
Zia ( PAKISTAN )
18 Nov 2020
Dear Sir
How can we use Paneer phool for wounds.
For Diabetic Patient.
Reply
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msmarco_passage_01_571782438 | How to Use Lemon Juice to Whiten Skin | LoveToKnow | How to Use Lemon Juice to Whiten Skin | LoveToKnow
How to Use Lemon Juice to Whiten Skin
By Jeanne Grunert
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If you'd like to know how to use lemon juice to whiten skin, the instructions aren't difficult. Not only is lemon juice useful for whitening skin and reducing freckles, it's also a time-honored treatment for oily skin. Just keep a few safety precautions in mind and you can try lemon juice to lighten skin coloration.
Whitening Skin with Lemon Juice
Lemon juice is an astringent juice. It has natural bleaching properties. If using lemon juice to whiten skin, know that you cannot drastically alter skin tone using lemons. At best, skin will brighten a few shades lighter. The effects aren't permanent. You can use lemon juice for overall skin brightening, as a freckle treatment, or to treat oily skin. It's very simple to learn how to use lemon juice to whiten skin.
Lemon Selection
Use only fresh lemons, never the bottled lemon juice from the store. Bottled lemon juice is often diluted with water and contains preservatives to maintain freshness. Lemons are fairly inexpensive. Plan to buy one lemon per day for this treatment. A hand juicing device, the kind your grandmother may have used to make fresh orange juice in the morning, is ideal.
Patch Test
Before trying to use lemon juice on your skin, conduct a patch test to make sure it's not too harsh for your skin. A patch test uses a product in a controlled area on the arm so you can see if you're allergic to it.
Clean the inside of the elbow and rub some lemon juice on the area.
Wait 24 hours. If the skin feels fine, it's probably okay to use it. If it stings or burns, rinse it off immediately and do not use it on your face or the skin anywhere else on your body.
Preparation
To create a whitening liquid, slice the lemon in half and remove the seeds. Using the manual juicer, juice the lemon until all juice is extracted from it. If you don't have a juicer, hold the lemon over a large bowl and squeeze it as hard as you can, wringing every little bit of juice from it.
Application
Wash your face clean and pat dry. Apply lemon juice to a clean face or to the area you'd like to lighten. If it stings, rinse it off immediately. It may be too harsh for your skin.
Using Lemon Juice for Freckles
Freckles are concentrated clusters of melanin, the pigment that colors human skin. These brown, light brown or reddish marks are most common in fair-haired people, and usually appear on the face, neck and shoulders. If you want to lighten your freckles naturally, you can use lemon juice to do so; the acidic properties of the lemons will lighten your skin, but it does take time to do so and any lightening is only temporary; once you go back into the sun without good sunblock, your freckles will return.
Simple Application
The easiest way to use lemon juice to lighten your freckles is to place fresh lemon juice in a spray bottle and spray it directly onto your skin in the areas you wish to lighten. Alternatively, using the same technique to lighten your skin, you can rub a sliced lemon onto the area, or rub a small portion of ground fruit and rind into your skin. Allow it to sit on your skin for approximately 10 minutes, then wash it off.
Oily Skin Lemon Juice Face Mask
If you wish to make a face mask that will help treat oily skin while lightening your freckles, try the following recipe:
Ingredients
1 teaspoon fuller's earth
2 teaspoons rose water
1 teaspoon lemon juice
Instructions
Mix the fuller's earth with rose water and lemon juice to form a paste.
Rub the paste onto the areas of skin you wish to lighten.
Leave the face mask in place for 10 to 15 minutes, then rinse off.
Dry Skin Lemon Juice Face Mask
The acids in the lemon juice may dry out your skin, particularly if you use it daily for an extended period of time. Try this face mask to help moisturize the skin while lightening your freckles.
Ingredients
1 teaspoon olive oil
1 teaspoon honey
1 teaspoon lemon juice
Instructions
Mix the olive oil, honey and lemon juice together to form a thin paste.
Massage the paste into your skin for two to three minutes.
Leave in place for 10 to 15 minutes, then rinse off.
Cautions
Lemon juice is a generally safe natural treatment, but as with all herbal remedies, if you've got any serious skin problems or you're allergic to lemons, don't use this treatment. Other cautions to consider include:
If a rash develops or your skin burns or stings, avoid it too.
Never go out into the sun with lemon juice on your face. Lemon juice can make your skin photo sensitive, or extra sensitive to sunlight, resulting in the opposite effect - discoloration or burns. Rinse off all traces of lemon juice from the skin before going outside.
Avoid getting lemon juice near the eyes or on your eyelids as it can burn or sting.
Because lemon juice has astringent qualities, people with dry skin may find lemon juice too harsh. If skin burns or stings, stop using it. Consult a dermatologist for any lingering skin irritation.
Temporary Solution
Lemon juice may not permanently change the color of your skin, but it can temporarily lighten it and brighten it.
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queenn • 6 years ago
it is okey if i use lemon juice in my skin, then i apply a sun block protection? and i use lemon in my face i use sunblock also?
answer • 6 years ago
Dony do like that if u r going out to sun at that time don't use the leamon only use sun blocks because it can damage ur skin and all sun blocks and fairness creams contains bleach normally
Brittney West • 5 years ago
Every one use to tease me a lot in my school by seeing my face with dark spots .I bought DermalMD Lightening Serum and applied twice a day for a week .My face looks very bright without any dark spots and I was really happy .This product contains no chemicals and made with all natural ingredients. Add colour to your life..don’t miss it.
Angel Sullivan • 6 years ago
I love how DermalMD Skin Lighting Serum easily starts fading your skin
to even out the tone. It isn’t too greasy or too dry and leaves my skin
feeling wonderful. It also has a fine fragrance that isn’t too heavy.
I’d definitely keep buying this to have because its one of the best
products I’ve found.
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msmarco_passage_01_577360565 | HIGHFERRITIN Web Server | HIGHFERRITIN Web Server
What is ferritin?
Iron is an essential bioelement for life; however, free ionic iron is toxic and must be correctly stored inside the cell. Ferritin is the main protein that stores safely the iron inside the cell. This protein is expressed in all the organism cells.
Tissue ferritin (ferritin that is inside the tissues) is composed by 24 subunits of two types of ferritins named: L chain ( light, 19 kDa, chromosome 19) and H chains ( heavy, 21 kDa, chromosome 11). The proportion of each subunit varies according to the need for storage and homeostasis of the cell. These subunits form a spherical cavity which stores the free iron (Fe 2+ ) and saves it therein in the form of Fe 3+, through the action of the H-ferritin ferroxidase activity. Thus, ferritin consists of a soluble protein (apoferritin) and an inner layer composed of ferric hydrophosphate.
Plasma or serum ferritin, is secreted by all ferritin-producer cells and unlike tissue ferritin it is partially glycosylated and nearly completely iron-free. Serum ferritin is currently regarded as the main test for deficiency states or body iron overload, since its value is proportional to iron stores, indicating the amount of iron available in the body. Each microgram of plasma ferritin per litre (µg;/L) is equivalent to between 8-10 milligrams of iron deposit. Normally, a low level of ferritin indicates a low level of iron ( Iron Deficiency Anaemia ). However, a high level of ferritin may indicate various pathologies, including inflammation or infection, since this protein is an acute phase reactant that increases its concentration in that context.
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What means high levels of serum ferritin?
High values of ferritin usually indicate high levels of iron, but this is not always the case. High levels of ferritin or hyperferritinemia is associated with diseases or conditions such as:
Hemochromatosis : A disease of excessive accumulation of iron in the organism that can be genetic ( Hereditary Hemochromatosis type 1, Hereditary Hemochromatosis type 2A, Hereditary Hemochromatosis type 2B , Hereditary Hemochromatosis type 3, Hereditary Hemochromatosis type 4) or acquired (Secondary Hemochromatosis). Excess iron inside the organs seriously affects their function and leads to the development of various clinical symptoms such as liver cirrhosis, heart disease, arthritis, impotence, diabetes, hypogonadism, dark skin pigmentation, and others.
In Hereditary Hemochromatosis type 1, 2A, 2B, 3 and 4B hyperferritinemia is present together with elevated transferrin saturation (> 45%). In Hereditary Hemochromatosis type 4A hyperferritinemia is present together with normal transferrin saturation (< 45%).
See treatment and recommendations
Hemosiderosis: Excess of hemosiderin (micellar aggregates of ferritin) in tissues, which is not a priori harmful, but can evolve to Hemochromatosis. It occurs when there is a systemic iron overload due to:
Transfusional hemosiderosis: caused by frequent red blood cell transfusions in patients with conditions that requires them (thalassemia, sickle cell anaemia, aplastic anaemia, myelodysplastic syndrome). Red blood cells or erythrocytes are a very important source of exogenous iron. ( See also multiple blood transfusions ).
Pulmonary hemosiderosis (Idiopathic pulmonary hemosiderosis and other diseases associated with pulmonary hemorrhage)
Chronic hemolyic anaemias ( See Hemolytic anaemias ).
See treatment and recommendations
Porphyria cutanea tarda (PCT): A condition in which the enzyme activity of hepatic URO decarboxylase is decreased. The UROD is an enzyme required in the synthesis of heme. There are genetic forms of PCT (with UROD gen mutations) and sporadic cases, which are the most common (about 80% of cases). Alcohol, estrogens, iron overload (including iron overload due to hemochromatosis) and hepatitis viruses are triggers for this disease. The PCT can have a toxic origin by exposure to chlorinated cyclic hydrocarbons. Photosensitivity and skin lesions with late onset are often seen in PCT as well as persistence of elevated transaminases.
See treatment and recommendations
Hereditary hyperferritinemia cataract syndrome (HHCS) : Rare genetic disease ( ORPHA163, OMIM #600886) characterized by a persistent increase in plasma concentrations of ferritin in the absence of iron overload and the presence of early onset cataracts (although usually absent at birth). This syndrome is an autosomal dominant inherited disease which is caused by mutations in the translation regulatory element called IRE (Iron-Responsive Element) of the gene encoding the ferritin-L subunit. It is unknown the precise prevalence of this disease; however it is estimated to be at least 1 in 200,000 individuals.
See treatment and recommendations
Benign hereditary hyperferritinemia: It is a genetic rare disease with autosomal dominant inheritance due to mutations in the coding region of the L-ferritin subunit.
See treatment and recommendations
Aceruloplasminemia: It is a rare and recessive genetic disease due to mutations in the gene encoding the ceruloplasmin protein that possesses ferroxidase activity and oxidizes Fe 2+ a Fe 3+ ( ORPHA48818, OMIM #604290 ). The aceruloplasminemia presents with iron overload in various organs including the liver and brain. The clinical manifestations of this disease are diabetes mellitus, moderate microcytic anaemia, and late-onset neurological abnormalities including retinal degeneration, ataxia, dementia and involuntary movements. Laboratory manifestations include low or absent serum ceruloplasmin, low levels of copper and iron in serum and high levels of serum ferritin without a rise in transferrin saturation.
See treatment and recommendations
Metabolic syndrome: This syndrome is due to genetic factors and/or poor eating habits and little exercise. Metabolic syndrome increases 2-5 times the risk of cardiovascular disease or diabetes mellitus. This syndrome is defined by the presence of three or more of the following criteria:
Increased waist circumference (taking into account the type of population and specific conditions, see table of normal waist circumference ). The measurement should be made at the midpoint between the lowest rib and the iliac crest (the navel).
High serum triglycerides > 150 mg/dL (> 1.7 mmol/L). Alternatively, patients on specific treatment, fibrates or nicotinic acid.
Decreased HDL cholesterol < 40 mg/dL (<1.0 mmol/L) in men and <50 mg/dL (<1.3 mmol/L) in women. Alternatively specific treatment.
High blood pressure: systolic ≥ 130 mmHg and/or diastolic ≥ 85 mmHg. Alternatively specific treatment history.
Elevated fasting glucose ≥ 100 mg/dL. Alternatively, treatment of diabetes.
See table of normal waist circumference.
See treatment and recommendations
Alcoholic hepatitis: Inflammation of the liver due to excessive intake of alcohol. Alcohol damages the liver resulting in an increase in liver enzymes detected in blood (ALT, AST and GGT) and increased serum ferritin levels since the liver is the main organ of iron storage. It is suspected in a patient with high alcohol consumption when this person shows the characteristic clinical symptoms (fever, hepatomegaly, jaundice and anorexia) and typical laboratory findings (ALT/AST>2, high GGT, MCV>100, high IgA, high serum ferritin with normal transferrin saturation).
See treatment and recommendations
Viral hepatitis: Liver inflammation due to viral infection mainly by hepatotropic viruses named hepatitis A, B, C, D or E. Other viruses can also cause liver inflammation. Viral infection results in liver damage and in an increase in liver enzymes detected in blood (ALT, AST and GGT) as well as in an increase of serum ferritin levels since the liver is the main organ of iron storage. Hepatitis virus serologies, sensitive molecular methods and liver function tests are laboratory tests to diagnose this condition.
See treatment and recommendations
Other hepatic diseases: Other diseases that damage the liver can lead to high levels of ferritin blood because the liver is the main organ that holds the iron in ferritin.
Iron poisoning: Iron poisoning can occur from the massive ingestion of drug preparations containing iron, such as vitamins and oral iron supplements. In severe iron poisoning it can be observed four phases:
First phase with nausea, vomiting, abdominal pain and diarrhea that may be bloody
Second phase of apparent recovery during which iron accumulates in mitochondria and in various organs
Third phase with gastrointestinal bleeding, hepatotoxicity, metabolic acidosis, hyperglycemia, coagulopathy, cardiovascular collapse, etc.
Fourth phase of wound healing or pyloric stenosis can cause liver cirrhosis
See treatment and recommendations
Inflammation: Complex biological response of vascular tissues to harmful stimuli such as injury or pathogens, damaged cells, or toxics. Inflammation is classified as acute (initial response of the organism to harmful stimuli) or chronic (prolonged inflammation). Ferritin is an acute phase response protein whose concentration is increased in inflammatory diseases (acute or chronic) and infections, therefore, in such circumstances it no longer reflects the magnitude of iron stores. The simultaneous measurement of protein acute phase response as C-reactive protein (CRP) or α1-acid glycoprotein (GPA) may facilitate the interpretation of serum ferritin concentrations.
See recommendations
Many diseases curse with inflammation including autoimmune diseases such as rheumatoid arthritis , systemic lupus erythematosus, Still’s disease, Macrophage activation syndrome .
Some diseases such as Still's disease, macrophage activation syndrome (MAS) and drug-induced hypersensitivity syndrome occurs with extreme hyperferritinemia (serum ferritin levels > 10,000 µg/L).
Still’s disease is an immune-mediated systemic disease with inflammatory arthritis and other symptoms. Extreme hyperferritinemia of >10,000 ug/L is found in Still’s disease where plasma ferritin is a marker of disease activity. Still's disease that occurs in children is called systemic juvenile idiopathic arthritis (SJIA).
Extreme hyperferritinemia of >10,000 ug/L can also be due to the Macrophage activation syndrome (MAS). MAS is a life-threatening genetic or acquired complication of rheumatic disease that, for unknown reasons, occurs much more frequently in individuals with systemic juvenile idiopathic arthritis (SJIA) and in those with adult-onset Still's disease. MAS is thought to be caused by the activation and uncontrolled proliferation of T lymphocytes and well-differentiated macrophages, leading to widespread hemophagocytosis (phagocytosis by histiocytes of erythrocytes, leukocytes, platelets, and their precursors in bone marrow and other tissues) and cytokine overproduction. MAS is associated with abnormally raised liver enzymes, hepatosplenomegaly, pancytopenia, hypertriglyceridaemia, coagulopathy and hypofibrinogenaemia, persistent fever and neurologic symptoms (eg, irritability, disorientation, lethargy, headache, seizures, coma).
Drug-induced hypersensitivity syndrome is a severe drug reaction characterized by fever and multiorgan failure, which occurs about a month after drug initiation (eg. anticonvulsant drugs). It is an immune-mediated process associated with activation of macrophages and T-lymphocytes, overproduction of cytokines and extreme hyperferritinemia.
Chronic kidney disease (CKD) : It is a progressive, irreversible loss of kidney function, including the production of erythropoietin required for erythropoiesis and the consequent development of anaemia (renal anaemia). In this disease the kidneys lose their ability to remove waste, concentrate urine and maintain blood electrolytes. The most common causes of CKD are diabetes mellitus, hypertension, and glomerulonephritis. Hyperferritinemia is commonly found in patients with chronic kidney disease regardless of their hemoglobin level, and is often considered to be related to chronic inflammatory status or neoplasias. However, patients with CKD under different forms of renal replacement therapy are also at a risk of developing secondary iron overload because for correction of renal anaemia they receive multiple red blood cell transfusions and routinely iron supplementations (oral or intravenous).
See treatment and recommendations
Neoplasia: Uncontrolled process of proliferation of cells in a tissue or organ that results in the formation of a neoplasm that can be benign, potentially malignant or clearly malignant. In the process of formation of a tumor, inflammation plays a major role. Ferritin is an acute phase response protein whose concentration is elevated in cancer-associated inflammatory processes, so that in such circumstances it does no longer reflects the magnitude of the iron stores.
See recommendations
Multiple red blood cells transfusions: Red blood cells or erythrocytes are a major source of iron, each transfusion (aprox. 500 ml of blood) contains about 250 mg of iron. Therefore, a high number of red cell transfusions lead to hepatic iron overload and high levels of serum ferritin. Multiple blood transfusions are needed to treat some hereditary anaemias such as thalassemia, sideroblastic anaemia and congenital dyserythropoietic anaemias and some acquired conditions such as myelodysplastic syndrome.
See recommendations
Hemolytic anaemia: Hemolytic anaemia is a type of anaemia that occurs when the bone marrow is unable to replace prematurely destroyed red blood cells because of attacks by the immune system (autoimmune hemolytic anaemia, for example in paroxysmal nocturnal hemoglobinuria or PNH), genetic defects (thalassemia, glucose-6-phosphate dehydrogenase, sickle cell anaemia), infections or exposure to certain drugs or toxins. In these diseases there is a secondary iron overload and increased serum ferritin levels due to the release of haemoglobin and the blood transfusions or iron supplements required to treat them.
See recommendations
Iron loading anaemias: Congenital sideroblastic anaemia (CSA), congenital dyserythropoietic anaemias (CDA), atransferrinemias, aceruloplasminemia and DMT1 deficiency are rare anaemias that present at the same time iron overload in parenchymal tissues (eg. liver). The iron overload in these diseases occurs regardless of the transfusion or iron treatments and it is exacerbated by them.
See treatment and recommendations
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What means VERY high levels of serum ferritin (>1000 µg/L)?
There are several evidences that indicate that a serum ferritin level greater than 1000 µg/L is highly associated with a severe impairment of the parenchyma, especially the liver parenchyma. These patients should be tested for liver iron concentration using a direct method. Types of medical tests that can be done are:
Liver biopsy procedure to obtain a small sample of liver tissue for direct examination under a microscope.
Advantages: Histology can be studied
Disadvantages: Invasive method, uncomfortable and not free of risk. A false estimation iron concentration can be given when the distribution of iron in the liver is heterogeneous, especially in cases of heterogeneous liver cirrhosis.
Magnetic resonance imaging (MRI): non-invasive technique that uses the phenomenon of MRI to obtain information on the structure and composition of the scanned body.
Advantages: Non-invasive method that allows a fully evaluate of the whole body.
Disadvantages: High cost. The availability of the necessary instrumentation is not always possible.
Quantification of iron and values in liver biopsy and MRI:
Patients with hemosiderosis
No significant iron overload: Values below 3 mg/g
Mild iron overload: between 3 and 7 mg/g
Moderate iron overload: between 7 and 14 mg/g
Hgh iron overload: Higher values of 14 mg/g
Patients with genetic hemochromatosis: As HH is a progressive accumulation disease, normally it is also calculated the hepatic iron index. This index is the result of dividing the hepatic iron concentration in mol/g by the patient's age in years.
The patient has hemochromatosis when HII values are greater than 1.9
The patient does not have hemochromatosis when HII values are less than 1.1
Intermediate values are indicative of moderate iron overload.
In those patients with significant iron overload demonstrated by biopsy or MRI further studies in specialized laboratories are required.
If the rate of transferrin saturation (TS) is greater than 45% the following genetic studies are recommended:
Hereditary Hemochromatosis type 1. HFE gene. HFE protein.
Hereditary Hemochromatosis type 2A. HFE2 gene. Hemojuvelin protein.
Hereditary Hemochromatosis type 2B. HAMP gene. Protein hepcidin.
Hereditary hemochromatosis type 3. TFR2 gene. Transferrin receptor protein 2
Hereditary Hemochromatosis type 4B. SLC40A1 gene. Protein ferroportin.
Atransferrinemia. TF gene. Transferrin protein
If the rate of transferrin saturation (ST) is less than 45% following genetic studies are recommended:
Hereditary Hemochromatosis type 4A. SLC40A1 gene. Protein ferroportin.
Aceruloplasminemia. CP Gen. Protein ceruloplasmin.
Genetic studies in specialized laboratories can confirm the disease diagnostic in iron loading anaemias and hereditary hemolitic anaemias. Genetic studies:
Congenital sideroblastic anaemia with microcytosis. Genes ALAS2, SLC25A38, ABCB7, GLRX5.
Congenital dyserythropoietic anaemias. Genes CDAN1, SEC23B, KLF1.
Aceruloplasminemia. CP gene. Protein ceruloplasmin.
Atransferrinemia. TF gene. Protein transferrin.
DMT1-deficiency anaemia. SLC11A2 gene.
Thalassemia and sickle cell anaemia. Globin genes.
Deficiency in Glucose 6-phosphate dehydrogenase. G6PD gene.
For other hereditary anaemias: see ENERCA.
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What kinds of tests are needed to do with people with high serum ferritin levels?
Anamnesis
Family history
Presence of cataracts at an early age (<35 years)
Alcohol intake
History of transfusional iron treatments
History of known cancers
History of liver diseases
Physical Examination
Abdominal exploration for searching of hepatomegaly
Examination for searching of adenopathies
Calculation of body mass index calculate BMI
Blood pressure
Measure waistlines ( see table)
Analytical tests
Hemogram or complete blood count (CBC)
Transferrin saturation
Glucose
Cholesterol, HDL cholesterol include
Triglycerides
Transaminases and GGT
C-reactive protein
Hepatitis serologies
If the ferritin level is greater than 1000 µg/L, assess level of ceruloplasmin and transferrin
If the ferritin level is greater than 1000 µg/L, consider perform relevant genetic tests
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msmarco_passage_01_578603395 | White Rocks and Sand Cave (Cumberland Gap) | Hiking Bill | White Rocks and Sand Cave (Cumberland Gap) | Hiking Bill
White Rocks and Sand Cave (Cumberland Gap)
Posted by Bill Fuller on October 1, 2011
On Top of the White Rocks Cliff
Near the Cumberland Gap, and located on the long Cumberland Mountain ridgeline, are two awesome formations known as White Rocks and Sand Cave. Both of these can be visited in the same day with a strenuous, ~9 mile hike within the Cumberland Gap National Historic Park from the trailhead in the Thomas Walker Civic Park. This is a tough hike with about 1700 feet in elevation gain, but the trails are well maintained and contain lots of switchbacks that make the climbing a little easier.
I decided to make a loop out of the hike, visiting Sand Cave first and then heading down the ridge to White Rocks. If you use my route, review the trail directions below carefully. The trails are in good shape and have signage at trail junctions, but they aren’t blazed, and I found some of the sign posts uprooted, which could leave you a little unsure at times.
Small Waterfall at Sand Cave Entrance
Inside Sand Cave
Over an Acre in Size
Sand Cave is truly a beautiful and unusual site. As you near the entrance you first drop down into a small, sand covered stream lined with bright green Hemlocks and Rhododendron, giving lots of contrast to the white sand stream. It’s definitely not the typical mountain stream you usually see at higher elevations in the Appalachians. Then at the lower opening of the cave there is also a small waterfall, which was not flowing very well when I was there, but still made for neat echos inside the cave itself from the falling water.
Colorful Ceilings and Walls
Neat Striations and Swirls on the Ceiling
Powdery Dry Sand
Sand Cave is not actually a limestone, water-eroded cave, but instead a huge rock overhang (made of Sandstone) that has been eroded out mostly by the wind. There is a lot of color in this “cave” from the numerous colors of sand on the floor to the unique swirls and striations all over the ceiling. The room itself is well over an acre in size, and one thing I noticed is that you really don’t get the full effect of its size unless you climb up inside to the back wall. It’s a large formation. I was also intrigued by how deep and dry the sand was inside the cave. It made for some tough climbing and exploring.
Looking Down Into the Powell River Valley
Another View from White Rocks
The White Rocks Cliffs Taken from Highway 58
After visiting Sand Cave I climbed back up to the main ridge of the Cumberland Mountain (which happens to be the Kentucky/Virginia border), and made my way to White Rocks. This overlook was also NOT a disappointment… It was another beautiful and breathtaking location… overlooking the historic Powell River Valley of Virginia, and on into Tennessee and Kentucky.
A Late Purple Aster Growing on Top of White Rocks
The White Rocks cliffs once served as a landmark for early settlers who were traveling to the Cumberland Gap… one of the early gateways through the southern Appalachian Mountains. It is estimated that around a quarter million settlers passed through the gap prior to 1810, on their way to Kentucky and the Ohio Valley. These massive cliffs made of (and named for) white quartzite pebbles imbedded in sandstone must have been nice site for these early travelers, meaning they were only a day’s walk away from the gap.
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Overall
Recommendation:
Advanced hikers only. Do this one on a weekday if possible to avoid crowds.
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Outstanding
Features:
Unique sandstone eroded cave, Sandstone cliffs with amazing vista, National Historic Park.
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Difficulty:
Difficult.
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Driving:
From the Tri-Cities, Get on I-26 heading to Kingsport and continue on into Gate City on 58 west. You will basically stay on US58 West the whole way. Once you get to Duffield, you will take a left to stay on 58 West. Continue through Sticklyville and then on to Jonesville where you will take a left in downtown Jonesville to stay on 58 West. After that, just stay on 58 West for about 25 more miles to Ewing. Then take a right at the traffic light onto VA724. Proceed for another mile or so to the Thomas Walker Civic Park. You can park in the grass lot beside the toilets if dayhiking. If staying overnight, then park in the lot before the gate. There are no fees or permits required unless you are camping overnight. In that case you will need a permit from the main park visitor’s center.
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Trails:
From the grass parking area, walk up to the covered pavilion and around behind it you will see a handicapped parking spot. The trailhead is beside that parking spot, though the gate. Continue up this trail for 0.5 miles, and you will come to a junction with a wider trail (this is Ewing trail… also a horse trail). Register in the trail register box, and then take a left. Continue for 2.4 miles and you will pass by the junction (with signs) to the White Rocks Trail (this is where you’ll eventually come out to complete your loop), but just keep going straight on the Ewing Trail. In about another half mile you will reach the top of the ridge, but just continue going straight, starting to descend again (which you are now heading down into the state of Kentucky). At the 3.6 mile mark you will reach the intersection with Ridge Trail. There are signs here designating this. Take a right (toward Sand Cave). Keep descending for about 0.1 mile and you’ll reach the Sand Cave Spur Trail. There are some horse hitching post here. Take this trail for a couple tenths of a mile and you’ll descend to Sand Cave. There are some steep steps here. Enjoy Sand Cave, then retraced your steps up the spur trail until you reach the Ridge Trail again. Take a left on the Ridge Trail and in 0.7 miles you will come to the upper end junction of the White Rocks Trail (and a sign and trail to the trail for White Rocks Campsite), but just keep going straight here to get to White Rocks. Go for another 0.2 mile and you will come to the base of White Rocks. There’s a sign here that says “200 feet to White Rocks”, but that is misleading because it’s longer and the final approach requires a steep climb up a crevice on the back side of White Rocks. Once you view White Rocks, turn around climb back down the trail and retrace your steps on the Ridge Trail to the junction of the White Rocks Trail and White Rocks Campsite. Take a left here on the White Rocks Trail, and in about a half mile you will end up back at the Ewing Trail. Take a left on the Ewing Trail and continue back down the mountain all the way to the trailhead.
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Needed
Gear & Tips:
Regular day-hiking gear. Again, this can be a crowded trail as it’s open to horseback riders and hikers. So go on a weekday if possible.
–
Distance:
Approximately 9.0 miles round-trip.
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Time
Allotment:
5-8 hours
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Type:
Out & Back with loop in between.
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Vista
Rating (1-5):
4.0
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Waterfall
Rating (based on a 1-50 scale):
Small waterfall at cave entrance, but was too small to rate at my visit.–
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Water
Crossings (one way):
A few very small streams, but you shouldn’t get wet. These streams are sometimes completely dry depending on weather conditions.
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Scrambling/Climbing:
Some moderate climbing as you work your way up the crevice to White Rocks.
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Hazards:
Some steep slopes. There is a short-cut to get into Sand Cave without going down to the waterfall entrance, but it requires crossing a narrow ledge. I wouldn’t recommend that route. White Rock is also a pure vertical cliff. Don’t explore too close to the edge, unless you have a parachute or hang-glider!
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Maps/GPS
info:
Park Trail Map
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More
Information:
Posted under Day-hike, Historical, Rock Formations, Vistas and tagged with Cumberland Gap National Historic Park, Cumberland Mountain, Sand Cave, White Rocks
Comments (13) |
msmarco_passage_01_579181686 | Attractions near Hilton Garden Inn Minneapolis Eagan | Attractions near Hilton Garden Inn Minneapolis Eagan
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MSPEHGI
Hilton Garden Inn Minneapolis Eagan
1975 Rahncliff Court, Eagan, Minnesota, 55122, USA TEL: +1-651-686-4605 FAX: +1-651-686-4662
Things To Do
The Hilton Garden Inn Minneapolis Eagan provides a central location when visiting the area. Attractions near Eagan include the Mall of America, Nickelodeon Universe theme park and of course, the Twin Cities. Not sure what to see and visit while in town? Ask our friendly hotel staff for recommendations on what to do near this Eagan hotel.
While you're in Town
Entertainment & Attractions
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Entertainment & Attractions Onsite Services
Restaurants/Lounges
Evening Room Service and On Site Catering
The Garden Grille & Bar
Nearby Services
Name
Distance
Heading
Buckhill Ski Area
10.0 MI
S
Cascade Bay Waterpark
5.0 MI
NE
City Center
25.0 MI
NW
Exel Energy Center
9.0 MI
N
Mall of America
5.0 MI
N
Minnesota Zoo
3.0 MI
E
Mystic Lake Casino
18.0 MI
SW
Science Museum of Minnesota
9.0 MI
N
Target Center
25.0 MI
NW
Target Field
25.0 MI
NW
Valleyfair
18.0 MI
SW
MI=Miles BLK=Block KM=Kilometers MT=Meters YD=Yards
Fitness & Recreation
View
Fitness & Recreation Onsite Services
Fitness Room
Pool
Nearby Services
Name
Distance
Heading
Basketball
5.0 MI
Beach
10.0 MI
Bicycling
0.5 MI
Bowling
3.0 MI
Driving Range
4.0 MI
Fishing
10.0 MI
Golf course
4.0 MI
Hiking Trail
8.0 MI
Horseback Riding
5.0 MI
Hunting
40.0 MI
Jet Skiing
25.0 MI
Jogging Track
5.0 MI
Playground
4.0 MI
Pool Table
3.0 MI
Putting Green
4.0 MI
Racquetball
5.0 MI
Sight Seeing Tours
15.0 MI
Snow Skiing
5.0 MI
Squash
5.0 MI
Tennis Court
10.0 MI
Video Arcade
5.0 MI
Walking Track
5.0 MI
Water Skiing
25.0 MI
MI=Miles BLK=Block KM=Kilometers MT=Meters YD=Yards
Local Businesses & Corporations
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Local Businesses & Corporations Nearby Services
Name
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Heading
Blue Cross Blue Shield
5.0 MI
N
Coca-Cola
6.0 MI
NE
Delta Airlines
5.0 MI
E
Hearth & Home Technologies
12.0 MI
S
Lockheed Martin
3.0 MI
N
PanAm/Spectrum Building
10.0 MI
NE
Pepsi Bottling Group
5.0 MI
W
Telex
8.0 MI
SW
Thomson Companies
8.0 MI
NE
Unisys
3.0 MI
N
MI=Miles BLK=Block KM=Kilometers MT=Meters YD=Yards
In and Around Town
Twin Cities Outlet Mall
Enjoy shopping just moments away at Twin Cities Premium Outlets.
Outlet Mall Deal |
msmarco_passage_01_581856692 | Theodore Roosevelt : Family Life | Theodore Roosevelt : Family Life
Theodore Roosevelt: Family Life
Figure 1.--President Rossevelt is pictured with his family about 1901. Note the tunic suit with short socks that Quentin is wearing. He was killed as a fighter pilot in France during World War I--changing his father's romantic view of war.
The Roosevelt family was a strong close-knit group. The President took a great interest in his children and was fascinating in watching them growup. His letters are full of comments about the children and many letters to them. The children for their part adored their parents, except perhaps Alice, and were very close to each other. The White House was sometimes a dull place, but this changed when presidents arrived with young children. Most presidents were married and had children. Often they were older men whose childen had grown up or in one tragic case died on the way to the White House. Some presidents were notable for adoring and romping with their children. One such father was Franlin Foosevelt, but his children had grown up by the time they reached the White House. Two presidents are notable for having a brood of younger children with him in the White House, Abraham Lincoln and Theodore Roosevelt. Tad and Willie's exploits were legend such as firing a toy but fully functional cannon at the President's cabinent. The Confederacy never got so close. The Roosevelt boys never topped that--but they came close and there were more of them. The President for his part was the kind of father every boy dreamed about. He joined right in when time allowed. Their father thoroughly enjoyed the boys and often joined them in their play, both at the White House and in near by Rock Creek Park.
The President's View
The Roosevelt family was a strong close-knit group. The President took a great interest in his children and was fascinating in watching them growup. His letters are full of comments about the children. And their are many letters wrtten bythe children to her parents. The children for their part adored their parents, except perhaps Alice, who proved more difficult to control than her brothers. The children were also very close to each other. A fascinating view of Roosevelt family life can be seen in this letter written by the President at Oyster Bay, Aug. 6, 1903. There is a real sweetness in the residet's lettrs to the children that is unmistakeable.
Play
The President was not a stand-off father. He enjoying play as much as the children. This was not all thast common at the time. The President was the kind of father every boy dreamed about. He joined right in when time allowed. And there were plenty of places to play, even when they were in Washington. Unfortunately, most of the photograohic images of them were formal portraits. We are guessing that photographs of the President romping with the children were seen as not politically advisable as they would detract from his image as aeriious statesman. The public loved to read about the children's antics, but images of the President playing with them may have been too much for the President's image.
The White House
Most presidents were married and had children. Often they were older men whose childen had grown up or in one tragic case died on the way to the White House. Some presidents were notable for adoring and romping with their children. One such father was Franlin Foosevelt, but his children had grown up by the time they reached the White House. Two presidents are notable for having a brood of younger children with him in the White House, Abraham Lincoln and Theodore Roosevelt. Tad and Willie's exploits were legend such as firing a toy but fully functional cannon at the President's cabinent. The Confederacy never got so close. The Roosevelt boys never topped that--but they came close and there were more of them. The White House was sometimes a dull place, but this changed when presidents arrived with young children. The McKinnely White House was a rather gloomy place. His wife was sick and he did not want her disturbed. And then tragically Presifent McKinnely was assasinated. The gloomy ambience changed when President Roosevelt arrived with him family. There were six children between 3 and 17, all but Alice boys. And the younger boys were to say the least not only active, but inventive to boot. As any parent will tell you, that combination makes for active parenting. The boys found that the White House could be turned into a huge play ground and their parents only somewhat or at least only succeeded in limited their activities to a degree. The East Room made a fine roller link and here we are not talking about staid little girl roller skating, it was sometimes more like Roller Derby. The attic could be converted into a secluded club house. The lawn made for a great place to race horses or play with other animals. Their father thoroughly enjoyed the boys and often joined them in their play. The President at times seemed just another obe of the children, only slightly larger.
Rock Creek Park
The President not only played with the children at the White House, but also at other sites as well. But there was a great place for their outings very close to the White House in Washington--nearby Rock Creek Park. This is a National Park that is not very well known. It is in fact the largest urban parl in the world. It is a heavily wooded park with a stream winding through it. It was a great place for family outings and only a short carriage ride from the White House. A favorite activity in the heavily wooded Park was cowboys and Indians. And their were great places to go swimming. After a day of tromping through Rock Creek Park and playing in Rock Creek the boys and the President himself would be dischelved and not uncommonly covered with mud. Thus they would delay their return to the White House until dusk so no one would see them.
The Potomac
The Potomas River was even closer than Rock Creek Park. The President would organize boat trips down the river where he and the boys would pretend to be pirates.
HPC
Navigate the Boys' Historical Clothing Web Site:
[Return to the Main Theodore Roosevelt page]
[Return to the Main President's page]
[ 18th Century ] [ 19th Century ] [ 20th Century ] [ 21st Century ]
Created: December 5, 1999
Last changed: 10:23 AM 10/10/2016 |
msmarco_passage_01_595276648 | Drop Everything And Read Day 2021 - Monday April 12, 2021 | Drop Everything And Read Day 2021 - Monday April 12, 2021
Holidays Of Year
Holidays on Monday, April 12
Drop Everything And Read Day 2021
Drop Everything And Read Day 2021 is on Monday, April 12, 2021: Baby Dropping?
Monday, April 12, 2021 is Drop Everything And Read Day 2021. ACC Literacy Drop Everything And Read
you cannot believe what you read, its not all true for everyone. and sometimes women get their dates wrong, you technically could be a little further along even. for me thats about when i started to drop and i went late both times. is this your first kid? everyone is different so its hard to tell. your doctor will be able to give you a better idea when they check you next, if your dilating any or if they can feel any of the head. i wouldnt be nervous but the baby is getting ready for the big day. talk to your doctor, thats the best advice i can give to you. good luck.
I dropped my PS3 slim?
The HDD isn't corrupted if the system can detect everything when it isn't busy giving you that message. Something on the inside has shifted enough for the system to read the HDD on and off though. Either way, unless you backed the data up (using an external storage device like a USB flash drive or external HDD) you cannot get anything back if you take the HDD out, or send it into Sony (because they will take the HDD out and potentially put a new HDD in anyway, which will be blank. And anytime an HDD is taken out, it will not keep the data it already has on it if put back into the same system or a different one because it's set to automatically want to reformat the HDD to support the system anyway). Your kinda screwed. I would send it into Sony though. The system won't last long enough for you to back anything up (unless manually IF your LUCKY). I would try to keep on seeing if you can back up a few saves you really would rather not lose BEFORE sending it into Sony. That way when you get the system back it will simply be a matter or naming the User back to the same name as the User it was copied from and as long as you put the PSN account onto the User you can simply copy the save to the User and it will work because it "syncs" with the online account so to speak. But the name of the User has to be the same. If the User's name was "Bob" make the User name "Bob" again. Then put the PSN account on the User.
Make sure the flash drive is formated to FAT32, or the PS3 won't be able to detect it. You only need a few minutes to back up certain saves, so hope it lasts. Go to Saved Data Utility (PS3), hover the cursor of the game you want to copy (so it's highlighted), click the triangle button, and click x on copy, save it to the flash drive. It should definitely work to at least back up saves for your games. The system will still need to be sent into Sony and repaired though. There's not much choice there.
Which of these Tight Ends should I drop?
drop olsen because tony gonzalez is good but trade gonzalez for antonio gates |
msmarco_passage_01_599051579 | Erik's Toyota Differential info
Toyota
Differential Info
* USA 4x4 trucks, except Landcruiser!
Last update 12/16/08
What type of diffs does my Toy
4x4 have?
What is the gear ratio of my
diff?
How wide are the various Toyota
axles?
Front Diffs
Rear Diffs
Electric-Locking
Diffs
ZUK's gear
install page
Breif Toyota 4x4 history/definition of terms (for North
America):
'79-85 pickups and 4Runners had front live-axle,
leaf-spring suspensions.
'86-95 4Runners, '86-95.5 mini-trucks, and '93-'98 T100's
have torsion bar Independent Front Suspensions (IFS).
'96-up 4Runners, '95.5-up Tacoma's, and 2000-up Tundra's,
Sequoia's and FJ Cruiser's have coil-sprung IFS.
"First genereation" 4Runners are '84-89, 2nd
gen are '90-95, 3rd gen are '96-03, and 4th gen are
'03-up.
"Mini-trucks" are Toyota pickups prior to the
'95.5 model year change to the "Tacoma."
The "mini-trucks" are also known as the
"Hilux" in other parts of the world.
Whattypeof
differential does my Toyota 4x4 have? (top)
'79-85 Truck or 4runner: Front, Rear
'85-95 4cyl Truck or 4Runner (non-turbo): Front,
Rear
'86-87 Turbo 4cyl Truck or 4Runner: Front,
Rear
'88-95 V6 Truck or 4Runner: Front, Rear
'95.5-up Tacoma: Front, Rear
'96-up 4Runner: Front, Rear
Tacoma "TRD", Tacoma "PreRunner" 4x2,
or
3rd gen. 4Runner w/ factory electric locking diff option:
Front, Rear
'93-98 T100 (2wd and 4wd): Front, Rear
'00-06 Tundra or Sequoia (2wd and 4wd): Front, Rear
'07+ Tundra 4.7L V8: Front, Rear
'07+ Tundra 5.7L V8: Front, Rear
What's my gear ratio? There are several ways figure it out:(top)
If you think your axle gearing has not been changed since
it left the factory, you can read and decode the
"axle code" from your vehicle information
plate. Off-road.com has some pretty good information how
to do this HERE(scroll down to the section titled "Gearing").
If your differential has been removed so that you can see
and count the teeth on the gears, you can divide the
number of teeth on the ring gear by the number of teeth
on the pinion gear to come up with their ratio. For
example, 41/10 gives you a 4.10:1 gear ratio (the
most common stock ratio).
To verify gear ratios w/ the diffs on the vehicle, there
is the "spin and count"method:
For
"open" diffs:
Block the tires at one end of the vehicle to keep
it from rolling, and then jack up a tire on the
other end.
Place the transmission in neutral and release the
parking brake if you are checking the rear diff.
Spin the tire exactly TWOfull
revolutions while at the same time counting
exactly how many revolutions the driveshaft spins
(marking the driveshaft and tires beforehand will
make it easier to count revolutions).
The number of revolutions the driveshaft spins is
your gear ratio.
If it spins just over 4 times, then the ratio is
probably 4.10; 4-1/3 = 4.30; 4-1/2 = 4.56; just
under 5 = 4.88; 5-1/3 = 5.29, etc.
For limited slip (LSD or "posi"), locking
differentials, spools, etc.:
With these types of diffs, you won't be able to
turn one tire w/o the tire on the opposite side
of the axle turning with it.
In this case, follow the directions above except
raise bothtires off the ground and
turn them exactly ONEfull
revolution while counting driveshaft revolutions.
Again, the number of driveshaft revolutions is
your gear ratio as mentioned above.
Toyota Axle Widths: (top)
(all widths are measured wms-wms, wms=wheel mounting
surface)
'79-85 front axle~ 55.5", rear axle~ 55"
'86-95 front IFS~ 59", rear axle~ 58.5"
Tacoma 4x4, '96-up 4runner front IFS~ ???, rear axle-
60"
T100 front IFS~ 65", rear axle~ 66.75"
Tundra front/rear~ ??
'90-97 Landcruiser FJ-80/FZJ-80 front axle~ 63.5"
*Another tidbit: 2wd4runners, Tacoma PreRunners, T100's, and Tundra's use 6-lug
wheels- same as the 4x4's
(the other 2wd's use 5-lug)
FrontDifferentials (top)
The 4cyl8" diff
'79-85 Trucks and 4Runners all have 4-cylinder
engines and use what most call the 4cyl8"
diff in the front (the same one they use in the rear)-
see "4cyl 8" diff"
below.
The 7.5" IFSdiff
'86-95 IFStrucks and 4Runners, and
all '93-98 T100s use a 7.5" front diff that is
offset to the passenger's side. Later models came with ADD (Automatic Differential
Disconnect) which uses a vacuum actuated mechanism to
disconnect the drivers side axle shaft from the
differential. Carriers and gear sets are interchangeable
between the two different versions (and also happen to be
the same as used in the 2wd Toyota pickup 7.5"
diffs). One difference between ADD and non-ADD diffs is
that the carrier in an ADD differential has needle
bearings supporting the axle shafts at the differential. The non-ADD diffs did not have this bearing and sometimes
the passenger side axle flange wears the carrier and
becomes loose or wobbly, eventually causing oil leaks,
noise, and possible spider gear damage. ADD and non-ADD
diffs are swappable as are most of their parts. This makes it possible to change your ADD diff to non-ADD
by simply swapping parts as I've done in the picture to
the right. This is desirable to some people since
some of the ADD stubs are smaller diameter than the
non-ADD stubs and are therefore slightly weaker.
- Passenger's side
- Low pinion
- 27 spline axles
* This diff is based on the 2wd
pickup 7.5" rear diff- same internals, different
housing.
Late-model 7.5" diff
'95-03 Tacoma, '00-04 Tundra,
?? Sequoia's, and 96-02 4Runners have a high-pinion
7.5" IFS front diff offset to the drivers side. The
high-pinion design is used so that the rack and pinion
steering and anti-sway bar on these vehicles can run
under the front driveshaft. The housing is a unique
bolt-together design. The carrier inside is exactly the
same as the '86-95 IFS diffs, so LSD's and lockers for it
are also the same. However, since this is a
high-pinion diff, the gears for it are different
(reverse-cut) than the earlier diff. There is an ADD and
non-ADD version of this diff as well.
These diffs use different gear sets than the earlier IFS
diff because of the high-pinion design.
- Driver's side
- High pinion
- 27 spline axles
- Bolt-together "clamshell" housing design.
8" IFS diff
'03+ 4runner, '04+ Tacoma, FJ Cruiser, '05-07 Tundra,
?? Sequoia: 8" IFS diff.
- Driver's side
- Mid-pinion
- Clamshell housing
- 30 spline axles
- Carrier break: 3.91 and up, 3.73 and down.
Postedby RockKrawler of Allpro
Offroad 1-25-07
"The front differential is an 8" mid pinion IFS
that uses a gear not available through the common
aftermarket. It is the same as the Non-US Toyota Prado
front differential. The only current ratios available are
4.56 from Toyota OEM Japan and 4.88 from Mossiero in
Italy. All Pro has 4.56 OEM Toyota Gears in stock, and
4.88 on the way in.
Front install kits are also not available from the common
aftermarket. It uses the rear 86-95 V6 pinion bearings,
but everything else is unique to the FJ/Prado. All Pro
has gathered the parts together and can assemble a kit
for you by special order, and have preassembled kits in
the works. No solid spacers are available for the front
differential
One last thing - there is a case break on the front
differential. This means there are 2 different cases, or
differential offsets: one that fits 3.73 and down, and
the other that fits 3.91 and up. So if you have an
Automatic FJ with 3.73 gears and want to go to a 3.91,
4.56 or 4.88 ratio, you need an open diff from a stick
shift wth the factory 3.91, or you can change to an
aftermarket diff like an ARB and get yourself some extra
traction at the same time.
The Hi-pinion8" diff
‘90-97 Landcruiser(FJ-80
and FZJ-80) uses a high pinion, reverse-cut front
diff based on the V6/Turbo rear diff. The high pinion design allows the steering on these
vehicles to run behind the axle and under the driveshaft. Carriers (i.e. lockers, LSD's) from the 8" V6/Turbo diffscan be
installed (direct bolt-in) in the hi-pinion diff. The
entire diff is also a direct bolt-in to all front and
rear axles that use an 8" diff.
This diff is desirable to some straight-axle mini-truck
and 4runner owners for a couple of reasons. First, the
reverse-cut design of the gears is stronger than simply
using a rear diff and gears up front as the factory did
since its not using the weaker "coast" side of
the gears when driving forward. For this reason, this
diff is generally only used in the front axle. Second,
the hi-pinion design gives very good ground clearance for
the pinion and driveshaft as well as improves driveshaft
operating angles.
In North America, almost all of these diffs came from the
factory with 4.10 gears. Aftermarket gears for this diff
are more expensive than most since they are either
imported or custom made in limited quantities. At
this time 4.88 and 5.29 are the only aftermarket ratios
available.
RearDifferentials (top)
8" Diff Housing (3rd member) Identification
4cyl has 3 ribs on each side. V6/Turbo has 4 ribs on
each side and the trapezoid shaped top rib. T100/Tundra/Tacoma diff has the characteristic bearing
truss.
Note-Starting in about '96, the V6 diffs
started using a casting that looks nearly the same as the
T100/Tundra casting from the outside. However, it doesn't
have the trussed bearing cap on the inside, and the
outside uses the smaller 8mm mounting studs.
Axle Housing Identification
4cyl/V6/E-locker
has a dome-shaped cover. Diff uses 8mm studs with 12mm
nuts.
T100/Tundra/non-TRD Tacoma has deeper, blocky cover to
accomodate the bearing truss. Diff uses 10mm studs with
14mm nuts.
The 4cyl 8"diff
All pre-'95 4-cylinder4wd mini-trucks &
4Runners use the Toyota 8" 2-pinion differential
front and rear (except turbo models). This is
known as the "4cyl diff. " This diff is
by far the most common diff in older Toyotas.
- Ten
10mm ring gear bolts
- 27 spline pinion
- 2-pinion carrier (case)
- V6 carriers can be used in this diff if the
correct bearings are used
* LPH/SPH gear info: http://www.pirate4x4.com/forum/showpost.php?p=1478223&postcount=73
** 4cyl diffs are swappable with the V6and high
piniondiffs.
The V6/Turbo 8"diff
'86-95 4cyl Turboand V6*trucks and 4runners, and ALL '96+ 4Runnersuse the Toyota 8" 4-pinion differential in the rear. This diff is known as the "V6/Turbo diff."
- Stronger housing than the 4cyl diff
- Larger carrier bearings than the 4cyl diff
- 30 spline axles
- 27 spline pinion (pre-'96)
- Ten 10mm ring gear bolts
- 8mm axle housing studs with 12mm nuts
- 4-pinion carrier (case)
- 4cyl 8" diff carriers (cases) do not fit without
custom carrier bearing adapters ($), try Inchworm
Gear
- A few pre-'96 V6 trucks and 4runners have been found to
have come with the 4cyl style diff from the factory. Nobody knows why.
* LPH/SPH gear info: http://www.pirate4x4.com/forum/showpost.php?p=1478223&postcount=73
'96-up 4runner V6 diffs:
- new improved housing that looks the same as the T100/Tundra/Tacomadiff on the
outside, internals are all the same as the regular V6
diff
- 30 spline pinion on OEM gears, swap pinion flange to 27
spline to use aftermarket gears
The FACTORY 4.88 V6 diff is unique!
- Axle code G144, white pinion paint code,
- generally came in 92-95 trucks/4runners with V6, auto
tranny, 31" tires, and tow package.
- Housing offsets pinion towards ring gear, allowing ring
gear to be thinner
- OEM Toyota gears are the ONLY gears that fit this diff
due to the thinner ring gear. All other gear sets have
thicker ring gears and do not fit.
- The carrier (case) is the same as the V6 diffs, so
normal V6 lockers, LSD's, etc. will work in this diff
**V6 diffs are swappable with 4cyl and high piniondiffs
The T100/Tundra/Tacomadiff
All 2wd and 4wd T100's, '00-06
Tundra's, and ?? Sequoia's use a
newer/stronger 8" 2-pinion diff. Tacoma4x4's
and TacomaPreRunner's that don't come with
the electric locker(aka
"non-TRD), as well as V6 Tacoma 4x2's also
came with this diff.
This diff commonly and mistakenlycalled an 8.4"or 8.25"diff, possibly to imply its extra
strength. The
ring gear actually measures 8". The extra
strength of this diff comes from the bearing cap/truss
and large diameter pinion gear shaft.
LSD's available is the TRD/Kazuma clutch-type 3-pinion
LSD, the OEM 4-pinion Tundra TRD
LSD, and the Detroit Trutrac.
Lockers available are the Powertrax
"Lock-right," "No-Slip," ARB Air Locker,
Detroit Softlocker.
This diff cannot be fitted to an
older style 8" axle because it uses a larger
diameter mounting bolt pattern and because more space
inside the housing necessary to accommodate the large
bearing cap. The different bolt pattern also makes it
very impractical to swap in an electric locking Toyota
diff (the whole mounting flange would have to be re-done
using a special jig).
- Carrier bearing truss and newer housing adds
significant strength over V6 and 4cyl diffs
- Uses V6 carrier bearings, larger pinion bearings
- Uses shims for backlash adjustment instead of threaded
adjusters
- Twelve 12mm Ring gear bolts
- 10mm axle housing studs with 14mm nuts
- 30 splilne axles
- 30 spline pinion
* 4Runners do NOT use this diff at all. Late-model 4Runners still use the V6
8" diffabove.
** This diff is NOT swappable with V6, 4cyl,
high-pinion, or electric locking diffs. This diff cannot
be fitted to an older style 8" axle because it uses
a larger diameter mounting bolt pattern and because more
space inside the housing necessary to accommodate the
large bearing cap.
Tundra 9.5"
'07+ Tundra 4.7L V8, Sequoia?
Tundra 10.5"
'07+ Tundra 5.4L V8, Sequoia?
http://www.4wheeloffroad.com/techarticles/drivetrain/2007_toyota_tundra_rear_axle/index.html
Toyota
Electric-Locking Differentials (top)
Electric Locker
A factory option on 3rd Gen. 4Runners, Tacoma 4x4's,
and Tacoma PreRunner 4x2's is an electric locking
rear differential. This diff is a 4-pinon design
based on the Turbo/V6 8" diffand uses the same gear sets and bearings (except for the
large bearing near the locking mechanism).
These locking diffs can be retrofitted into 8" diff
axles if the axle housing is modified (see
this article for more info). It cannot be
easily retrofitted into a T100/Tundra or open-diff Tacoma
style axle housing because the mounting bolt pattern is
smaller. It "could" be done by an axle builder
by doing major work to the mounting flange, but that is
not really a practical option.
- 30 spline pinion on OEM gears, swap pinion flange to 27
spline to use aftermarket gears
Hi-pinion Electric Locker
A factory option on ‘93-97 Landcruiser
FZJ-80's is a hi-pinion electric locking front
differential. It can be installed into modified
8" axle housings, similar to the 4Runner/Tacoma
locker mentioned above. The reverse-cut gear sets for
this diff are the same as for the standard hi-pinion diffmentioned earlier.
These
vehicles also had an optional 8.875" REAR electric
locker. This one has been retrofitted into other
Landcruiser models with considerable effort (see
this article), but it doesn't appear to be compatible
with any non-Landcruiser vehicles.
Electric Locker Info
Toyota Electric Locker Links: (sorry some of this is very old)
-4x4wire's
electric locker installation article
-Mike
Carter's E-locker install
-Ken
Emanuel's E-locker install
-Ed
& Judy's E-locker install
-Carl
Whitmore's CJ2a w/ dual hi-pinion electric lockers
-Landcruiser
FJ80 rear locker into FJ55 front
Tacoma/4runner- "The
Grey Wire Mod" to allow the factory locker to be
engaged w/o being in 4-low
- 4x4wire
- CustomTacos.com
- Offroaders.com
InchwormGear.comis a great vendor who has a lot of E-locker parts and
experience.
Toyota Electric Locker
E-mail Threads:
(lots of good info in these old
emails)
-Karl Bellve and myself
-Scott Muir and myself
-Carl Whitmore (taken
from the Toy4x4 list)
Home-fabbed wiring to control a
Toyota Electric Locker using relays:
(click to enlarge)
Designed by Scott Muir, drawn by Karl Bellve and I
Special
Thanks to Karl Bellve and Scott Muir for all the help
with the electric locker info!
I would also like to thank Sean(aka "GearMan") at River City
Differentials. He has been very helpful and doesn't seem to
mind answering my many questions. He and his shop are highlyrecommended by members of the Toy4x4 mailing list Pirate4x4.com
BBS, and others. Let him know his info is being put to good use!
River City Differentials
Rancho Cordova, CA
(916) 852-7109
"ZUK" also has a great Toyota
diff info web page with a ton of practical gear install info:
http://gearinstalls.com/
Back to the top
Back to Erik's
home page
Front
Differentials (top)
The 4cyl 8" diff
'79-85 Trucks and 4Runners all have 4-cylinder
engines and use what most call the 4cyl 8"
diff in the front (the same one they use in the rear)-
see "4cyl 8" diff"
below.
The 7.5" IFS diff
'86-95 IFS trucks and 4Runners, and
all '93-98 T100s use a 7.5" front diff that is
offset to the passenger's side. Later models came with ADD (Automatic Differential
Disconnect) which uses a vacuum actuated mechanism to
disconnect the drivers side axle shaft from the
differential. Carriers and gear sets are interchangeable
between the two different versions (and also happen to be
the same as used in the 2wd Toyota pickup 7.5"
diffs). One difference between ADD and non-ADD diffs is
that the carrier in an ADD differential has needle
bearings supporting the axle shafts at the differential.
The non-ADD diffs did not have this bearing and sometimes
the passenger side axle flange wears the carrier and
becomes loose or wobbly, eventually causing oil leaks,
noise, and possible spider gear damage. ADD and non-ADD
diffs are swappable as are most of their parts.
This makes it possible to change your ADD diff to non-ADD
by simply swapping parts as I've done in the picture to
the right. This is desirable to some people since
some of the ADD stubs are smaller diameter than the
non-ADD stubs and are therefore slightly weaker.
- Passenger's side
- Low pinion
- 27 spline axles* This diff is based on the 2wd
pickup 7.5" rear diff- same internals, different
housing.
Late-model 7.5" diff
'95-03 Tacoma, '00-04 Tundra,
?? Sequoia's, and 96-02 4Runners have a high-pinion
7.5" IFS front diff offset to the drivers side. The
high-pinion design is used so that the rack and pinion
steering and anti-sway bar on these vehicles can run
under the front driveshaft. The housing is a unique
bolt-together design. The carrier inside is exactly the
same as the '86-95 IFS diffs, so LSD's and lockers for it
are also the same. However, since this is a
high-pinion diff, the gears for it are different
(reverse-cut) than the earlier diff. There is an ADD and
non-ADD version of this diff as well.
These diffs use different gear sets than the earlier IFS
diff because of the high-pinion design.
- Driver's side
- High pinion
- 27 spline axles
- Bolt-together "clamshell" housing design.
8" IFS diff
'03+ 4runner, '04+ Tacoma, FJ Cruiser, '05-07 Tundra,
?? Sequoia: 8" IFS diff.
- Driver's side
- Mid-pinion
- Clamshell housing
- 30 spline axles
- Carrier break: 3.91 and up, 3.73 and down.Posted by RockKrawler of Allpro
Offroad 1-25-07
"The front differential is an 8" mid pinion IFS
that uses a gear not available through the common
aftermarket. It is the same as the Non-US Toyota Prado
front differential. The only current ratios available are
4.56 from Toyota OEM Japan and 4.88 from Mossiero in
Italy. All Pro has 4.56 OEM Toyota Gears in stock, and
4.88 on the way in.
Front install kits are also not available from the common
aftermarket. It uses the rear 86-95 V6 pinion bearings,
but everything else is unique to the FJ/Prado. All Pro
has gathered the parts together and can assemble a kit
for you by special order, and have preassembled kits in
the works. No solid spacers are available for the front
differential
One last thing - there is a case break on the front
differential. This means there are 2 different cases, or
differential offsets: one that fits 3.73 and down, and
the other that fits 3.91 and up. So if you have an
Automatic FJ with 3.73 gears and want to go to a 3.91,
4.56 or 4.88 ratio, you need an open diff from a stick
shift wth the factory 3.91, or you can change to an
aftermarket diff like an ARB and get yourself some extra
traction at the same time.
The Hi-pinion 8" diff
‘90-97 Landcruiser (FJ-80
and FZJ-80) uses a high pinion, reverse-cut front
diff based on the V6/Turbo rear diff.
The high pinion design allows the steering on these
vehicles to run behind the axle and under the driveshaft.
Carriers (i.e. lockers, LSD's) from the 8" V6/Turbo diffs can be
installed (direct bolt-in) in the hi-pinion diff. The
entire diff is also a direct bolt-in to all front and
rear axles that use an 8" diff.
This diff is desirable to some straight-axle mini-truck
and 4runner owners for a couple of reasons. First, the
reverse-cut design of the gears is stronger than simply
using a rear diff and gears up front as the factory did
since its not using the weaker "coast" side of
the gears when driving forward. For this reason, this
diff is generally only used in the front axle. Second,
the hi-pinion design gives very good ground clearance for
the pinion and driveshaft as well as improves driveshaft
operating angles.
In North America, almost all of these diffs came from the
factory with 4.10 gears. Aftermarket gears for this diff
are more expensive than most since they are either
imported or custom made in limited quantities. At
this time 4.88 and 5.29 are the only aftermarket ratios
available.
Toyota
Electric-Locking Differentials (top)
Electric Locker
A factory option on 3rd Gen. 4Runners, Tacoma 4x4's,
and Tacoma PreRunner 4x2's is an electric locking
rear differential. This diff is a 4-pinon design
based on the Turbo/V6 8" diff
and uses the same gear sets and bearings (except for the
large bearing near the locking mechanism).
These locking diffs can be retrofitted into 8" diff
axles if the axle housing is modified (see
this article for more info). It cannot be
easily retrofitted into a T100/Tundra or open-diff Tacoma
style axle housing because the mounting bolt pattern is
smaller. It "could" be done by an axle builder
by doing major work to the mounting flange, but that is
not really a practical option.
- 30 spline pinion on OEM gears, swap pinion flange to 27
spline to use aftermarket gears
Hi-pinion Electric Locker
A factory option on ‘93-97 Landcruiser
FZJ-80's is a hi-pinion electric locking front
differential. It can be installed into modified
8" axle housings, similar to the 4Runner/Tacoma
locker mentioned above. The reverse-cut gear sets for
this diff are the same as for the standard hi-pinion diff mentioned earlier. These
vehicles also had an optional 8.875" REAR electric
locker. This one has been retrofitted into other
Landcruiser models with considerable effort (see
this article), but it doesn't appear to be compatible
with any non-Landcruiser vehicles.
|
|
msmarco_passage_01_599751320 | 2021 Cost of Building a Custom Home - Estimates and Prices Paid | 2021 Cost of Building a Custom Home - Estimates and Prices Paid
CostHelper > Home and Garden > Construction & Renovation > Building a Custom Home
Building a Custom Home Cost
How Much Does Building a Custom Home Cost?
Low: As low as $100 per square foot
Average: $200-$400 per square foot
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Having a house built to specifications means you get exactly the features you've always dreamed of owning, such as inlaid hardwood or tile floors, custom cabinetry, granite or marble countertops, an oversized Jacuzzi tub, an indoor lap pool or more. However, a custom home also requires your active participation and decision-making during each phase of the project, plus patience and money.
Typical costs:
Residential construction costs vary considerably nationwide, but as a general rule custom-built homes are about twice as much as production homes in the same area, plus the price of the lot or acreage. (The price of land is almost never included in cost estimates for custom homes.) On average, a custom-built home with top-of-the-line materials is $200-$400 or more a square foot, or $700,000-$1 .4 million for a 3,500 square foot house. However, building a modest custom home in a low-cost area might drop costs as low as $100 a square foot, or $350,000 for 3,500 square feet. These price ranges usually include standard site preparation (foundation, utilities, etc.) but do not include the cost of the land, design plans, or loan fees (which can run $1,500-$7,000 or more).
A great deal depends on location plus the complexity of the project and the quality of the materials chosen. It's possible to custom-build an 800-square-foot dome house for $1 million or a 12,000-square-foot rural ranch house for $400,000. However, the $400,000 custom-built house is the exception rather than the rule. Typically, a landowner choosing to build a custom-designed home wants high-quality features which nudge the total costs toward $1 million.
Architects charge anywhere from 2-15 percent of the total construction costs to custom-design a home; one advantage is that their services should include overseeing the building process to be sure everything is done properly.
Thousands of custom home plans are available for $500-$2,000 or more, depending on style and complexity. But before building it's wise to pay an architect $50-$150 an hour to review the plans to be sure they fit your site and meet local building codes.
Check with the local planning department. Building permits vary widely by region but can add several thousand or tens of thousands of dollars to the building costs.
Related articles: Home Addition, Architect
What should be included:
From buying the land to moving into the finished product, having a home custom-built is an extremely complex process. The Arizona Home Builders Network lists factors that can influence a custom home's cost per square foot; B4UBuild.com [ 1] describes the various phases of the home building process, from research and pre-construction work to interior and exterior finishes and landscaping; and the National Association of Home Builders [ 2] explains what a custom builder does compared to a production home builder.
Financing and cash flow can be an important issue. Typically architects and builders require a deposit with additional payments scheduled as each phase of the project is completed.
Additional costs:
An itemized bid sheet listing everything from site preparation to debris removal is $15 from HomeAdditionsPlus [ 3] .
The DVD-ROM "Your Custom Home" [ 4] lists for $19.99 and includes design guides, a cost estimator, a home construction encyclopedia, and the ability to order from more than 6,200 home plans.
Making changes to the design or materials used after construction has begun adds to the total cost; the exact amount will depend on the nature and scope of the changes.
Shopping for building a custom home:
Read as much as possible about the custom home-building process; books are available through your local library, at bookstores or through Amazon [ 5] . Talk to other people who had their home custom-built, asking about any problems they encountered.
Contractor referrals are available through your local home building association [ 6] .
Get several estimates, making clear what is (and isn't) included in each quote. View other projects designed or built by the architect or contractor, and talk to people who have used their services to see how smooth the process was. Before hiring a designer or builder, ask about their training and the length and type of their experience. Be sure the contractor is properly bonded, insured and licensed in your state.
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You may not be able to host the large family gathering for the holidays, but there are still many ways to pick up items curbside to spruce up your indoor space for your everyday enjoyment and to bring a more festive spirit. || Posted December 30 2020
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As they age, members of the Baby Boomer generation don't like to admit that they're senior citizens, but they love getting discounts. It's kind of a quandary, because some of the best deals available are reduced prices for older folks. || Posted October 21 2013
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What People Are Paying - Recent Comments
Semi-custom home
Amount: $675,000.00 total
Posted by: Ma Washi in Kennesaw, GA.
Posted: February 8th, 2021 04:02PM
Square Feet: 3700
We are investigating in high grade interior accents in kitchen and bath, hardwood flooring,custom cabinets to ceiling in kitchen,stacked stone fireplace. Exterior stone some wood, metal sheeting and bronze gutters
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custom home
Amount: $550,000.00 total
Posted by: Tammy Hale in oxford, AL.
Posted: January 6th, 2021 10:01AM
Square Feet: 5700
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Custom Home in Central Florida (Sanford)
Amount: $564,429.00 total
Posted by: Custom Home in Sanford, FL.
Posted: June 19th, 2019 12:06PM
Square Feet: 3546
$159 living square feet by a custom home builder and a total of 5339 square feet.
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MY Custom HOME
Amount: $3,500,000.00 total
Posted by: Drake W in lake cormorant ms, MS.
Posted: June 4th, 2019 12:06PM
Square Feet: 20,000
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Custom Home
Amount: $400,000.00 total
Posted by: Justine Woods in Temple, TX.
Posted: January 31st, 2019 09:01PM
Square Feet: 5000
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Custom home
Amount: $319,000.00 total
Posted by: Stljay in Hillsboro, MO.
Posted: September 8th, 2018 07:09PM
Square Feet: 2030
2030 sqft ranch, high end finishes, fixtures, custom flooring, $31000 in hardwood flooring, custom cabinets, granite and marble, No carpet in the house. 9 ft ceilings on main floor, vaulted in family/grAte room, 9 ft tall basement. Brick exterior. This is with myself doing the hvac, landscaping,finish grading, and putting down sod. Bids from general contractors for this home ranged from $285000 to $365000. In the end do your own research on exactly what you want in your area. I never use the lowest estimates or highest. Pick the person or company you trust, after looking at at least 3 of their prior homes and talking to a few prior customers. Our contractor gives us all the receipts and tells us exactly what he will make on the home.
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CURIOUS
Amount: $0.00 total
Posted by: JONATHAN ANDREWS in LANCASTER, CA.
Posted: November 14th, 2017 04:11AM
Square Feet: 12,000 TO 16,000+
LOOKING FOR SOME INFORMATION ABOUT THE AMOUNT OF BUILDING A CUSTOM MADE HOME (3 STORY) IN THE LAS VEGAS NEVADA AREA
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Features expected in $165 schedule home in phx AZ
Amount: $450,000.00 total
Posted by: ron hastings in Gilbert, AZ.
Posted: October 1st, 2016 12:10PM
Square Feet: 2,600
Just trying to get a idea of whatfeaturesone would expect to get. Such as wall height, closet type, energy efficiency leval, photovoltaic system installed solar water install, grade of windows and foors. LOT NOT INCLUDED HOME ONLY
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Per sq ft Daytona Beach custom build Moore's
Amount: $240,000.00 total
Posted by: melea b moore in Daytona beach, NY.
Posted: July 1st, 2016 09:07AM
Square Feet: 1734
Estimated 138 per sq ft at KB Homes. Energy efficient homes
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new home
Amount: $450,000.00 total
Posted by: Glenn MCleod in loganville, GA.
Posted: June 7th, 2016 06:06PM
Square Feet: 4300 plus basement
plans already drawn
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Custom Home Pricing
Amount: $525,000.00 total
Posted by: Stranded1 in Orlando/Central Florida, FL.
Posted: April 25th, 2016 08:04AM
Square Feet: 3,500
Don't be under-educated by thinking you can build a custom home for $75.00 pr. sq. ft. Pricing varies greatly by region so always speak with a builder or designer in your area up front. Actual costs in the Orlando Area currently can run between $150.00 pr. sq. ft. to in excess of $400.00 depending on your finishes and all pricing is based on total area not just a/c or heated area. The $150.00 range will get you into your home with a mid finish level throughout the home but realistically the $200.00 top $225.00 range is where you want to be at. This usually gives you nice custom finishes everywhere that really counts. (i.e. kitchens and bathrooms).
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House build
Amount: $200,000.00 total
Posted by: Edward Diuga in Goodyear, AZ.
Posted: October 13th, 2015 12:10PM
Square Feet: 2500
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house
Amount: $450,000.00 total
Posted by: Hitesh Shah in Powell, TN.
Posted: February 6th, 2015 04:02PM
Square Feet: 6000
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Jacksonville, Florida cost per square foot 2015
Amount: $425,000.00 total
Posted by: Kevin Davis in JACKSONVILLE, FL.
Posted: January 15th, 2015 07:01PM
Square Feet: 5500 heated/cool
Can a modest custom home be build for this amount?
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custom home
Amount: $215,000.00 total
Posted by: adela Rodriguez in desoto, TX.
Posted: July 3rd, 2014 10:07AM
Square Feet: 3000
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External Resources:
www.b4ubuild.com/resources/index.shtml
www.nahb.org/generic.aspx?sectionID=182&genericContentID=3911
www.homeadditionplus.com/New%20Home%20Construction%20Bid%20Sheet.htm
www.amazon.com/Valusoft-10429-Your-Custom-DVD-Rom/dp/B0007U9BT4
www.amazon.com/s/ref=nb_ss_gw/104-2967680-0286341?url=search-alias%3Dstripbooks&fi...
www.nahb.org/local_association_search_form.aspx
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msmarco_passage_01_600274965 | 2021 Cost of Exterior Shutters - Estimates and Prices Paid | 2021 Cost of Exterior Shutters - Estimates and Prices Paid
CostHelper > Home and Garden > Roofing, Windows & Siding > Exterior Shutters
Exterior Shutters Cost
How Much Do Exterior Shutters Cost?
Low: Stock Sizes $20-$200 per pair
Medium: Custom Sizes $50-$320 per pair
High: Handcrafted $600-$4,000 per pair
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Exterior window shutters cover windows from the outside, providing privacy, energy savings, style and some protection from weather. Most exterior shutters are made of wood or vinyl, and come in a variety of styles. Storm (hurricane) shutters are used in areas where hurricanes can break exposed glass.
Typical costs:
Wooden or vinyl exterior window shutters in stock sizes cost $20-$200 per pair of panels. Price depends on materials, size, and brand name. Home improvement stores like Home Depot [ 1] carry exterior window shutters in a range of styles.
Custom size exterior shutters can cost from $50-$320 per pair of panels, depending on size, materials used, and quality of construction. ReadyShutters [ 2] and Shutter Land [ 3] let customers order custom sized shutters within specific parameters based on style and materials.
Designer branded, handcrafted exterior window shutters cost $600-$4000 per pair of panels. Companies such as Timberlane [ 4] can provide matches to existing shutters, historically accurate shutters, hand-forged hardware, exotic hardwoods, and precise decorative details.
Storm shutters cost $40-$400 per panel. Metal hurricane shutters can cost $40-$100, while certified reinforced/treated fabric hurricane shutters cost $50-$400 per panel. Home improvement stores also sell hurricane shutters. Check a local Lowes [ 5] or online at Stormshutters.com [ 6] or Hurricane Depot [ 7] .
Related articles: Painting a House, Handyman, Landscape Design
What should be included:
Stock size exterior window shutters include a pair of shutters and all needed installation hardware. Exterior shutters may be painted or stained, or may come uncolored so homeowners can paint them to match or compliment the exterior home paint colors.
Designer custom exterior window shutters should include necessary installation hardware, plus any additional hardware and decorative features purchased.
Complete service from a specialty window treatment retailer should include initial measuring for the exterior shutters, the shutters themselves, installation of the shutters, testing of mobility and function, and cleanup.
Additional costs:
Shutter locks keep exterior window shutters closed despite wind and storms. Locks cost $5 -20, depending on quality and style.
Decorative hardware can cost extra, from $8-$22 each.
Motorized exterior window shutters cost $800-$1000 per window and up. Motorized exterior window shutters can be opened and closed from inside the house using a wall switch or a remote control.
Professional installation of exterior shutters costs $100 and up for a complete job (whole house or all windows required), depending on the number of shutters to be installed and the complexity of the installation. Installing motorized shutters costs more, and a certified electrician may be required to run the wires from the motor to the switches or sensors (which would add to the cost).
Discounts:
DIY installation of exterior window shutters saves the cost of professional installation. This Old House provides instructions [ 8] on installing exterior shutters without professional assistance.
Shopping for exterior shutters:
All About Shutters [ 9] explians what exterior window shutters do, and describes different types of exterior shutters and the purpose of optional exterior shutter hardware.
Manufacturers of stock size exterior window shutters may have websites with instructions about measuring for and installing shutters. Buying from manufacturers such as ReadyShutters [ 10] or Shutter Land [ 11] costs less than using a local retailer that does all measuring and installation.
The National Oceanic and Atmospheric Association [ 12] explains how storm shutters work, the different types of shutters and who should install storm shutters. The South Florida Sun-Sentinel [ 13] describes the different types of storm shutters, including average price per square foot.
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10 Quick and Inexpensive Home Makeover Projects To Do While At Home
You may not be able to host the large family gathering for the holidays, but there are still many ways to pick up items curbside to spruce up your indoor space for your everyday enjoyment and to bring a more festive spirit. || Posted December 30 2020
7 Lesser-Known Discounts for the 50+ Crowd
As they age, members of the Baby Boomer generation don't like to admit that they're senior citizens, but they love getting discounts. It's kind of a quandary, because some of the best deals available are reduced prices for older folks. || Posted October 21 2013
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Comment On Your Experience With Exterior Shutters
External Resources:
www.homedepot.com/webapp/wcs/stores/servlet/Navigation?Ntk=AllProps&N=10000003+900...
www.readyshutters.com
www.shutterland.net?
www.timberlane.com/
www.lowes.com/StoreLocatorDisplayView
www.stormshutters.com
www.hurricanedepot.com
www.thisoldhouse.com/toh/how-to/intro/0,,20049877,00.html
www.allaboutshutters.com/exterior-shutters.htm
www.readyshutters.com/exterior_shutters_styles.html
www.shutterland.net?
www.aoml.noaa.gov/hrd/shutters/index1.html
www.sun-sentinel.com/news/broward/sfl-hc-shutterguide,0,4823608.htmlstory
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msmarco_passage_01_601290591 | 2021 Cost of a Quartz Countertop - Estimates and Prices Paid | 2021 Cost of a Quartz Countertop - Estimates and Prices Paid
CostHelper > Home and Garden > Kitchen & Bath > Quartz Countertop
Quartz Countertop Cost
How Much Does a Quartz Countertop Cost?
Average Kitchen: $1,500-$2,700
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Also called engineered stone, quartz countertops are man-made solid slabs composed of natural quartz crystals held together with resin. Engineered stone kitchen countertops provide a seamless work surface for cooking that is impervious to liquids and resistant to chips, cracks, and scratches. Because engineered stone is nonporous and resistant to bacteria, it makes for an easy-to-clean bathroom counter.
Typical costs:
Quartz countertops cost $50-$90 per square foot, or $1,500-$2,700 for a typical kitchen with 30 square feet of counter space, including professional installation.
Related articles: Stone Countertop, Granite Countertop, Solid Surface Countertop, Laminate Countertop, Kitchen Countertops, Kitchen Remodeling
What should be included:
Engineered stone countertops should be polished and the outer edges shaped. Quartz countertops do not need to be sealed.
Because installing most quartz countertops is not a DIY project, installation of an engineered stone countertop is included in the price of the countertops. Installation should include a professional measurement before the countertops are ordered, removal of old countertops, preparation of the cupboard surfaces (including leveling and shimming), installation, inspection, and cleanup.
Quartz countertops come with long-term limited warranties. Zodiaq countertops carry a 10-year warranty. Silestone includes a 15-year warranty.
Discounts:
Both Silestone and Zodiaq [ 1] have discounts and special offers available on their websites.
Shopping for a quartz countertop:
Before beginning to price engineered stone countertops, measure the countertop area. Home Depot provides a worksheet [ 2] to help calculate the measurements, including corners and tricky areas. The installer or contractor will do an official measurement later, but a good estimated area will help you estimate the cost of the countertops before making your purchase.
Home Depot [ 3] and Lowes [ 4] sell a variety of kitchen countertop materials. Other brands of engineered stone such as Cambria [ 5] , CaesarStone [ 6] and HanStone [ 7] are sold by specialty kitchen & bath remodeling stores.
Call ahead to schedule an appointment for a consultation at a kitchen & bath or home improvement store. Many stores get busy, especially on weekends.
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10 Quick and Inexpensive Home Makeover Projects To Do While At Home
You may not be able to host the large family gathering for the holidays, but there are still many ways to pick up items curbside to spruce up your indoor space for your everyday enjoyment and to bring a more festive spirit. || Posted December 30 2020
7 Lesser-Known Discounts for the 50+ Crowd
As they age, members of the Baby Boomer generation don't like to admit that they're senior citizens, but they love getting discounts. It's kind of a quandary, because some of the best deals available are reduced prices for older folks. || Posted October 21 2013
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Additional Costs
Amount: $835.00
Posted by: Freddie in gr in Grand rapids, MI.
Posted: February 22nd, 2016 12:02PM
Store: Home Depot
Installed By: Cameo
Like granite quotes, you have to pay for the 4x8 full slab whether its all used or not. You pay the square footage for the sink cutout, you pay pay for unused space to make the inside corner, you pay for full square corner when a rounded corner makes a cutaway . If the pieces are large there may be a third man charge ($400) just to get the pieces into the house. Oh, all plumbing is additional as is the new sink. Whatever the quote, add 25%.
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External Resources:
www2.dupont.com/Surfaces/en_US/where_to_buy/offers.html
www.homedepot.com/hdus/en_US/DTCCOM/Home_Services/Countertop_Installation/Docs/cou...
www.homedepot.com/webapp/catalog/servlet/ContentView?catalogId=&langId=-1&pn=SF_KB...
www.lowes.com/cd_Kitchen+Countertop+Buying+Guide_655374990_
www.cambriausa.com
www.caesarstoneus.com
www.hanstoneusa.com
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