Archive for August, 2015

A major genetic study Tuesday confirmed a link between low vitamin D and a higher risk of multiple sclerosis, a finding which experts say could lead to better treatment and prevention.

Previous observational studies have found an association between a person's level of vitamin D, which comes from sunlight and from certain foods, and MS, a debilitating autoimmune disease that affects nerves in the brain and spinal cord, and has no known cause or cure.

But the problem with these studies was that they could not prove that low vitamin D caused MS, and may indeed have been showing simply that people who were sick tended to stay inside more and get less sunlight.

The latest study by Brent Richards, from McGill University, Canada, and colleagues published this week in PLOS Medicine, gets around that obstacle by analyzing the association between genetically reduced vitamin D levels and the likelihood of MS in a pool of 14,498 people with multiple sclerosis and 24,091 healthy controls.

The study found that people with genetically lower vitamin D levels face double the risk of getting MS, which is often diagnosed between age 20 and 50.

"The results show that if a baby is born with genes associated with vitamin D deficiency they are twice as likely as other babies to develop MS as an adult," explained Benjamin Jacobs, director of Children's Service at the Royal National Orthopedic Hospital in London.

Jacobs, who was not involved in the study, described its findings as "important."

"This could be because vitamin D deficiency causes MS or possibly because there are other complex genetic interactions," he said.

"We do not yet know if giving healthy children and adults vitamin D will decrease their risk of developing MS, but clinical trials are being conducted now to study this."

MS is a chronic disease that affects some 2.3 million people worldwide, causing blurred vision, slurred speech, tremors, extreme fatigue, problems with memory, paralysis and blindness.

Read more here:
Low Vitamin D Tied to Multiple Sclerosis

You probably know your nerves carry messages around your body. So if you stub your toe, your nerves deliver the message to your brain that says "Ouch!" Nerves also send signals that tell your muscles what to do when you want to walk and run.

In someone who has multiple sclerosis (MS), there are roadblocks in the pathways so the messages don't get to the brain like they should.

That leads to problems like:

MS is mostly a disease that adults get and is usually diagnosed between the ages of 20 and 50. It is more common in women than men.

If you know someone who has MS, you probably want to know what the disease will be like for them. The disease does tend to get slowly worse over time, but most people with MS have mild symptoms and live to be as old as people without MS.

Let's talk about what's causing those roadblocks for the signals. If a person has MS, the immune system which usually fights germs attacks nerves in the brain and spinal cord. It damages the layer of tissue, called myelin, which surrounds and protects the nerves.

When myelin becomes damaged, scars develop. The word sclerosis comes from the Greek word for scarring or hardening. And those scars can act like stones in the road, creating a bumpy ride for signals as they travel between the brain and body.

When those signals get slowed down or blocked, people with MS feel one or more symptoms, such as vision problems or feeling unsteady on their feet. The symptoms will vary depending on what nerves are affected.

There are four different categories of MS:

MS is rare in kids. About 5% of cases of MS are diagnosed in children. MS in kids tends to progress more slowly than MS diagnosed in adults.

Nobody knows exactly why a person gets multiple sclerosis. It is not contagious, so you can't catch it from someone who has it. And it's not hereditary. That means the disease is not passed on directly from one generation to the next, like eye color.

But your chances of developing MS are greater if a close relative, such as a parent or sibling, has it. Scientists are still studying why.

When people begin to experience what could be early signs of MS, such as vision or balance problems, doctors will take a careful history and do a complete physical exam. Since there is no one test that can determine if a person has MS, the doctor may order several tests, including blood tests, cerebrospinal fluid (the fluid that surrounds the brain and spinal cord) tests, and brain scans.

A brain MRI, or magnetic resonance imaging test, lets a doctor check for evidence of scars in the brain and spinal cord by taking detailed pictures of these body areas.

Another frequent stop on the way to an MS diagnosis is a series of evoked potentials (EP) tests, which test the time it takes for nerves to respond. If the response time is slow, the chances are greater that there's damage along the nerve pathways.

Currently, there is no known cure for multiple sclerosis, but medicines can help control symptoms. When a flare-up or relapse happens, steroids lessen inflammation and help speed up recovery. Several medicines can be given to reduce the number of relapses and slow down progression of the disease.

People with MS can take steps to manage symptoms, including physical and occupational therapy. Eating a balanced diet and exercising regularly are also important when it comes to overall health and well-being for people living with MS.

If someone you love has MS, you can be supportive in lots of ways. The person might appreciate some help with stuff like opening doors. If you live with this person, it's great to be quiet when he or she is resting.

As you get older, you might be able to help with other stuff, like getting groceries or doing other stuff around the house. But most of all, the person will like knowing that you're understanding and ready to help.

Reviewed by: Rupal Christine Gupta, MD Date reviewed: January 2015

More here:
Multiple Sclerosis - KidsHealth

Advanced Database Options Limit Articles Displayed by the Following Study Types Additional Research Available Sorting Options Limited to Members Only By default, all articles on GreenMedInfo.com are sorted based on the content type which best reflects the data which most users are searching for. For instance, people viewing substances are generally most interested in viewing diseases that these substances have shown to have positive influences. This section is for allowing more advanced sorting methods. Currently, these advanced sorting methods are available for members only. If you are already a member, you can sign in by clicking here. If you do not currently have a user account, and would like to create one/become a member, click here to begin the singup process. Currently Available Sorting Options

Cumulative Knowledge is determined by ascribing a numerical value to the various study types weighted in descending order as follows: (1) Meta-Analysis; (2) Human Study; (3) Human: Case Study; (4) Animal: Transgenic; (5) Animal; (6) In Vitro; (7) Review; and (8) Commentary.

Article Published Date : Nov 19, 2010

Study Type : Meta Analysis

Article Published Date : Jan 01, 2007

Study Type : Meta Analysis

Article Published Date : Jan 01, 2010

Study Type : Meta Analysis

Article Published Date : Dec 31, 2011

Study Type : Meta Analysis

Article Published Date : Jul 01, 2010

Study Type : Meta Analysis

Article Published Date : Aug 01, 2009

Study Type : Meta Analysis

Article Published Date : Jan 01, 2009

Study Type : Meta Analysis

Article Published Date : Oct 01, 2011

Study Type : Human Study

Article Published Date : Jun 01, 2009

Study Type : Human Study

Article Published Date : Jan 01, 2012

Study Type : Human Study

Article Published Date : Feb 28, 2015

Study Type : Human Study

Article Published Date : Sep 01, 2011

Study Type : Human Study

Article Published Date : Sep 01, 2010

Study Type : Human Study

Article Published Date : Aug 01, 2004

Study Type : Human Study

Article Published Date : Sep 27, 2005

Study Type : Human Study

Article Published Date : Oct 07, 2011

Study Type : Human Study

Article Published Date : Jan 01, 2009

Study Type : Human Study

Article Published Date : Feb 01, 2010

Study Type : Human Study

Article Published Date : May 01, 2009

Study Type : Human Study

Article Published Date : Aug 01, 1996

Study Type : Human Study

Article Published Date : Feb 28, 2015

Study Type : Human Study

Article Published Date : Dec 26, 2001

Study Type : Human Study

Article Published Date : May 01, 2002

Study Type : Human Study

Article Published Date : Feb 04, 2010

Study Type : Human Study

Article Published Date : Feb 04, 2010

Study Type : Human Study

See the rest here:
Multiple Sclerosis | GreenMedInfo | Disease | Natural Medicine

What do constant headaches, gum disease, sleep disorders, sore joints and other serious health conditions have in common? They all have chronic inflammation as the root cause.

Inflammation isnt always a bad thing. In fact, acute inflammation is normal for your body such aswhen you suffer a painful cut or bruise and your body fights to heal itself. The real trouble begins when inflammation becomes chronic. When this occurs, your immune system begins fighting against its own cells, leading to harmful effects on your health. (1)

Right now, if youre enduring one of the seven symptoms below, dont ignore them! These can be tell-tale signs that your body is chronically inflamed. Instead, try my favorite ways to help reduce inflammation and begin healing your body from the inside out.

Remember, one of the best things you can do to reduce overall inflammation is overhauling the way you eat. My healing foods dietwhich focuses on clean protein, healthy fats and low-glycemic carbohydrates is naturally anti-inflammatory. Give it a go if you have one of these seven symptoms!

If you find your head constantly throbbing, inflammation might be the cause. Not only are migraines and frequent headachesespecially painful, but they can also be precursors to more serious conditions. (2)

Help fight these headaches naturally by seeking out organic proteins like grass-fed beef and ingesting more high-fiber foods. In addition,because magnesium plays a vital role in keeping our bodies functioning properly and a deficiency can lead to headaches, takinga magnesium supplement mayhelp prevent recurring pains and reduce symptoms.

Constantly worried about bad breath or have you been diagnosed with gingivitis? Inflammation might be to blame. These periodontal diseases begin as bacterial infections that progress into inflammation. Not only are these conditions socially embarrassing, but they are also symptoms of inflammation that can lead to more widespread, systemic diseases in the body. (3)

Skip expensive treatments and help cure gum diseases naturally. Begin by flossing at least daily to get rid of errant food that can lead to bacterial growth. Usehomemade toothpaste,which can also help heal gum disease and even brighten teeth; or try coconut oil pulling to fight gum disease and keep gingivitis at bay.

Gut diseases are probably the most common of symptoms, andALL have inflammation at their roots. Unfortunately, these types of diseases are also becoming more common in society. (4) Things like preservatives in foods, toxin overload and an imbalance in bacteria are all to blame. (5,6)

My number one tried-and-true method of overcoming gut diseases is by sipping on bone broth. Its healing properties help sooth your guts lining, keeping toxins out of your bloodstream. Probiotics and enzymes are also useful in treating inflammatory bowel diseases naturally.

Have you been feeling the blues or been extra moody or anxious recently? Although it may surprise you, inflammation could be playing a role. Research shows that inflammatory cytokines, or proteins released by cells, can spur depression-like behavior. (7)

Help reduce anxiety by introducing ashwagandha, an adaptogenic herb, into your daily routine to ease stress. Eating more vitamin B-12 and omega-3 fatty foods are also great ways to fight depression and anxiety through nutrition.

Tossing and turning at night can also be attributed to inflammation. Persistent insomnia afflicts about 10 percent of American adults and has serious consequences; its been linked to a higher inflammation and a higher mortality rate. (8) (9)

Luckily, there are steps you can take to help fall asleep without habit-forming drugs. Setting the right room temperature, using essential oils and limiting caffeine can all help bring on the ZZZs. Check out my 20 favorite strategies to fall asleep fast.

No part of the body is safe from the effects of inflammation. Inflammation in other areas of the body can actually affect how tired you feel. One study found that in mice with inflamed livers behavioral changes like fatigue followed. (10) Gut inflammation is one of the symptoms that has also been linked with chronic fatigue syndrome. (11)

If youre just feeling plain ole drained all the time, try these 10 ways to boost energy levels. Those with chronic fatigue syndrome might opt for avoiding sugar, caffeine and gluten-containing grains, and instead addsuperfood powder and ashwagandha to their diets.

Both inflammatory arthritis (such as rheumatoid and psoriatic) and basic joint pain can be attributed to joint inflammation. (12) Help ease the effects of these taxing symptomsand reduce joint pain naturally by taking proteolytic enzyme supplements, eating more essential fatty acids, like those found in wild-caught salmon and grass-fed beef, and increasing your intake of potassium and sodium to revitalize your bodys cells and eliminate toxins.

Remember, your body is constantly communicating with you about what it needs its up to you to listen to what its saying!If you have any one of these symptoms, theres no need to suffer. Instead, start reducing inflammation and feeling better today.

Visit link:
What 7 Symptoms You Have Now That You Shouldn't Ignore

People usually volunteer to donate stem cells for an allogeneic transplant either because they have a loved one or friend who needs a match or because they want to help people. Some people give their stem cells so they can get them back later for an autologous transplant.

People who want to donate stem cells or join a volunteer registry can speak with their doctors or contact the National Marrow Donor Program to find the nearest donor center. Potential donors are asked questions to make sure they are healthy enough to donate and dont pose a risk of infection to the recipient. For more information about donor eligibility guidelines, contact the National Marrow Donor Program or the donor center in your area (see the To learn more section for contact information).

A simple blood test is done to learn the potential donors HLA type. There may be a one-time, tax-deductible fee of about $75 to $100 for this test. People who join a volunteer donor registry will most likely have their tissue type kept on file until they reach age 60.

Pregnant women who want to donate their babys cord blood should make arrangements for it early in the pregnancy, at least before the third trimester. Donation is safe, free, and does not affect the birth process. For more, see the section called How umbilical cord blood is collected.

If a possible stem cell donor is a good match for a recipient, steps are taken to teach the donor about the transplant process and make sure he or she is making an informed decision. If a person decides to donate, a consent form must be signed after the risks of donating are fully discussed. The donor is not pressured take part. Its always a choice.

If a person decides to donate, a medical exam and blood tests will be done to make sure the donor is in good health.

This process is often called bone marrow harvest, and its done in an operating room. The donor is put under general anesthesia (given medicine to put them into a deep sleep so they dont feel pain) while bone marrow is taken. The marrow cells are taken from the back of the pelvic (hip) bone. A large needle is put through the skin and into the back of the hip bone. Its pushed through the bone to the center and the thick, liquid marrow is pulled out through the needle. This is repeated several times until enough marrow has been taken out (harvested). The amount taken depends on the donors weight. Often, about 10% of the donors marrow, or about 2 pints, are collected. This takes about 1 to 2 hours. The body will replace these cells within 4 to 6 weeks. If blood was taken from the donor before the marrow donation, its often given back to the donor at this time.

After the bone marrow is harvested, the donor is taken to the recovery room while the anesthesia wears off. The donor may then be taken to a hospital room and watched until fully alert and able to eat and drink. In most cases, the donor is free to leave the hospital within a few hours or by the next morning.

The donor may have soreness, bruising, and aching at the back of the hips and lower back for a few days. Over-the-counter acetaminophen (Tylenol) or non-steroidal anti-inflammatory drugs (such as aspirin, ibuprofen, or naproxen) are helpful. Some people may feel tired or weak, and have trouble walking for a few days. The donor might be told to take iron supplements until the number of red blood cells returns to normal. Most donors are back to their usual schedule in 2 to 3 days. But it could take 2 or 3 weeks before they feel completely back to normal.

There are few risks for donors and serious complications are rare. But bone marrow donation is a surgical procedure. Rare complications could include anesthesia reactions, infection, transfusion reactions (if a blood transfusion of someone elses blood is needed this doesnt happen if you get your own blood), or injury at the needle insertion sites. Problems such as sore throat or nausea may be caused by anesthesia.

Allogeneic stem cell donors do not have to pay for the harvesting because the recipients insurance company usually covers the cost.

Once the cells are collected, they are filtered through fine mesh screens. This prevents bone or fat particles from being given to the recipient. For an allogeneic or syngeneic transplant, the cells may be given to the recipient through a vein soon after they are harvested. Sometimes they are frozen, such as when the donor lives far away from the recipient.

For several days before starting the donation process, the donor is given a daily injection (shot) of filgrastim (Neupogen). This is a growth-factor drug that causes the bone marrow to make and release stem cells into the blood. Filgrastim can cause some side effects, the most common being bone pain and headaches. These may be helped by over-the-counter acetaminophen (Tylenol) or nonsteroidal anti-inflammatory drugs (like aspirin or ibuprofen). Nausea, sleeping problems, low-grade (mild) fevers, and tiredness are other possible effects. These go away once the injections are finished and collection is completed.

Blood is removed through a catheter (a thin, flexible plastic tube) that is put in a large vein in the arm or chest. Its then cycled through a machine that separates the stem cells from the other blood cells. The stem cells are kept while the rest of the blood is returned to the donor through the same catheter. This process is called apheresis (a-fur-REE-sis). It takes about 2 to 4 hours and is done as an outpatient procedure. Often the process needs to be repeated daily for a few days, until enough stem cells have been collected.

Possible side effects of the catheter can include trouble placing the catheter in the vein, a collapsed lung from catheter placement, blockage of the catheter, or infection of the catheter or at the area where it enters the vein. Blood clots are another possible side effect. During the apheresis procedure donors may have problems caused by low calcium levels from the anti-coagulant drug used to keep the blood from clotting in the machine. These can include feeling lightheaded or tingly, and having chills or muscle cramps. These go away after donation is complete, but may be treated by giving the donor calcium supplements.

The process of donating cells for yourself (autologous stem cell donation) is pretty much the same as when someone donates them for someone else (allogeneic donation). Its just that in autologous stem cell donation the donor is also the recipient, giving stem cells for his or her own use later on. For some people, there are a few differences. For instance, sometimes chemotherapy (chemo) is given before the filgrastim is used to tell the body to make stem cells. Also, sometimes it can be hard to get enough stem cells from a person with cancer. Even after several days of apheresis, there may not be enough for the transplant. This is more likely to be a problem if the patient has had certain kinds of chemo in the past, or if they have an illness that affects their bone marrow.

Sometimes a second drug called plerixafor (Mozobil) is used along with filgrastim in people with non-Hodgkin lymphoma or multiple myeloma. This boosts the stem cell numbers in the blood, and helps reduce the number of apheresis sessions needed to get enough stem cells. It may cause nausea, diarrhea, and sometimes, vomiting. There are medicines to help if these symptoms become a problem. Rarely the spleen can enlarge and even rupture. This can cause severe internal bleeding and requires emergency medical care. The patient should tell the doctor right away if they have any pain in their left shoulder or under their left rib cage which can be symptoms of this emergency.

Parents can donate their newborns cord blood to volunteer or public cord blood banks at no cost. This process does not pose any health risk to the infant. Cord blood transplants use blood that would otherwise be thrown away.

After the umbilical cord is clamped and cut, the placenta and umbilical cord are cleaned. The cord blood is put into a sterile container, mixed with a preservative, and frozen until needed.

Remember that if you want to donate or bank (save) your childs cord blood, you will need to arrange it before the baby is born. Some banks require you to set it up before the 28th week of pregnancy, although others accept later setups. Among other things, you will be asked to answer health questions and sign a consent form.

Many hospitals collect cord blood for donation, which makes it easier for parents to donate. For more about donating your newborns cord blood, call 1-800-MARROW2 (1-800-627-7692) or visit Be the Match.

Privately storing a babys cord blood for future use is not the same as donating cord blood. Its covered in the section called Other transplant issues.

Read the original here:
Whats it like to donate stem cells?

Although the word "arthritis" means joint inflammation, the term is used to describe around 200 rheumatic diseases and conditions that affect joints, the tissues that surround the joint, and other connective tissue.5

The most common form of arthritis is osteoarthritis. Other common rheumatic conditions include gout, fibromyalgia and rheumatoid arthritis.4

You will also see introductions at the end of some sections to any recent developments that have been covered by MNT's news stories. Also look out for links to information about related conditions.

Fast facts on arthritis

Here are some key points about arthritis. More detail and supporting information is in the main article.

Typically, pain, aching, stiffness and swelling in and around one or more joints characterize rheumatic conditions. The symptoms can develop gradually or suddenly. Certain rheumatic conditions can also involve the immune system and various internal organs of the body.6

Some forms of arthritis, such as rheumatoid arthritis and lupus, can affect multiple organs and cause widespread symptoms.

Arthritis is more common among adults aged 65 years or older, but people of all ages (including children) can be affected.

There are 52.5 million adults in the US, equating to 22.7% of the population, reported to have a form of arthritis, rheumatoid arthritis, gout, lupus or fibromyalgia.1

With people living longer in the US, the prevalence of doctor-diagnosed arthritis is expected to increase. It has been estimated that by the year 2030, 67 million, 25% of the projected total adult population aged 18 years and older, will have doctor-diagnosed arthritis.

Arthritis has a significantly higher age-adjusted prevalence in women (23.9%) than men (18.6%), with the prevalence increasing with age and higher among women than men in every age group.

An estimated 294,000 children under the age of 18 have some form of arthritis or rheumatic condition; this represents approximately 1 in every 250 children in the US.4

Arthritis has a significant impact on individuals, for example:1

Impairment in the ability of people with arthritis to perform essential daily tasks may interfere with their work, their purpose in their community, or the care they can provide for their family.

Around 18% of total disabilities are caused by arthritis or rheumatism, making it the most common cause of disability in the US.

Arthritis has a strong association with major depression, with a risk of 18.1%. This could be due to its role in creating functional limitation. Around 6.6% of adults with arthritis report severe psychological distress.

Prevalence of arthritis increases with body mass index (BMI). Prevalence increases from 16.3% among underweight and normal adults to 20.3% of overweight adults and 28.9% of obese adults.

Reports among adults by BMI show the following groups express activity limitations:

Physical activity and exercise have been shown to benefit people with arthritis by improving pain, function and mental health. However, around 24% of adults with arthritis report being physically inactive compared with 18.6% of adults without arthritis.

By partaking in low levels of exercise, individuals with arthritis face placing themselves at risk of conditions associated with lack of activity such as cardiovascular disease, diabetes, obesity and functional limitations.

Certain factors have been shown to be associated with a greater risk of arthritis. Some of these risk factors are modifiable while others are not.

Non-modifiable risk factors:

Modifiable risk factors:

Cost attributable to arthritis and other rheumatic conditions (AORC) in the US in 2003 was approximately:2

The CDC reports that 47% of US adults with arthritis also have at least one comorbid condition (the presence of more than one disease or condition in the same person at the same time).3

Among people with arthritis the most common comorbidities are:

Risk factors for other chronic conditions are common among US adults with arthritis, such as:

More than half (53%) of US adult with arthritis report high blood pressure. High blood pressure is associated with heart disease - the most common comorbidity among adults with arthritis.

Approximately 1 in 5 (19%) of US adults with arthritis are smokers. Smoking is associated with chronic respiratory conditions - the second most common comorbidity among adults with arthritis.

In 2004, there were an estimated:4

In 2004, joint replacements for arthritis included:4

Between the years of 1979-1998, the AORC deaths increased from 5,537 to 9,367.4 The approximate death rate from AORC in 1979 was 2.46 per 100,000 population and 3.48 per 100,000 population in 1998. Both rates age-standardized to the year 2000 population were 2.75 and 3.51, respectively.

Using 10 categories of AORC, just three categories accounted for almost 80% of deaths:9

There is no one cause for arthritis; the cause depends on the type or form of arthritis. Potential causes for arthritis may include:

For many arthritis conditions, there is a strong element of chance involved as to what is the main cause. However, for most types of arthritis, the cause is a combination of many factors working together.

A person may naturally be more susceptible to certain conditions due to genetic makeup. If more susceptible, external factors such as previous injury, infection, smoking and physically demanding occupations could play a part.

There are some foods that appear to exacerbate arthritis, although diet or food sensitivity or intolerance is unlikely to cause arthritis.

Cartilage is a flexible, connective tissue in joints that absorb the pressure and shock created from movement like running and walking. It also protects the joints and allows for smooth movement.34

Some types of arthritis are caused by a reduction in the normal amount of cartilage tissue through wear and tear throughout life, such as osteoarthritis.

RA, on the other hand, occurs when the body's immune system attacks the tissues of the body.

On the next two pages we look at the types of arthritis, the signs and symptoms and the possible treatment options for arthritis.

Here is the original post:
Arthritis: Causes, Symptoms and Treatments - Medical News Today

All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms. It contains a detailed description of multiple sclerosis, a large archive of news stories about MS, an MS encyclopedia and a large links section containing hundreds of commented and rated links. It also has a list of famous people with multiple sclerosis and personal accounts, poems and essays by people with MS. The site receives no sponsorship from pharmaceutical or other financially interested companies and maintains absolute editorial independence.

Every effort is made to ensure that the information is medically up-to-date and accurate.

Please sign the guest book which is further on down this page.

Please read this Disclaimer

My Guestbook

Sign My Guestbook

View My Guestbook

Site Search Engine

There's quite a lot of stuff on these pages and there will be even more soon. You can use these search engines to find things that you are looking for.

What's New

And here's a list of all the pages that have been added or updated recently - this is updated every Saturday.

You can email me at jones.paul@btconnect.com. I cannot answer personal health queries - you should discuss these with your GP or neurologist. General health information and support is available from most national MS Societies. Here are details of some MS Society free telephone numbers:

View post:
All About Multiple Sclerosis : MS news and information on ...

http://www.baumanmedical.com - Hair loss affects tens of millions of American women, but new diagnostic procedures, effective treatments and tracking methods are available.

LaserCap delivers an effective, clinical dose of laser therapy anywhere, anytime because it is the first cordless, rechargeable, portable laser that has 224 separate laser diodes (not LEDs) that fits conveniently under a standard baseball hat. Laser treatments with LaserCap are 30 minutes, every other day. 650nm wavelength, 5mW per laser diode. Laser therapy does not regrow dead hair follicles, but it makes weaker hair follicles produce thicker, stronger and longer hair fibers. All laser patients should be measured in three areas using a HairCheck(TM) Cross sectional hair bundle measurement tool.

Female Androgen Sensitivity Genetic Testing is performed to determine if a women is likely to experience severe female hereditary hair loss and predict a post-menopausal woman's response to the off-label treatment finasteride (propecia). The female Androgen Sensitivity test is performed in minutes in the doctor's office using a cheek swab.

For more information on LaserCap, visit http://www.lasercap.info

To learn more about Hair Restoration Physician, Dr. Alan J. Bauman, M.D. visit http://www.baumanmedical.com

Read more from the original source:
Female Hereditary Hair Loss Treatment & Genetic Testing ...

Overview

Turmeric (Curcuma longa) has been used for 4,000 years to treat a variety of conditions. Studies show that turmeric may help fight infections andsome cancers, reduce inflammation, and treat digestive problems.

Many studies have taken place in test tubes and animals. Turmeric may not work as well in humans. Some studies have used an injectable form of curcumin, the active substance in turmeric, and not all studies agree. Finally, some of the studies show conflicting evidence.

Turmeric is widely used in cooking and gives Indian curry its flavor and yellow color. It is also used in mustard and to color butter and cheese. Turmeric has been used in both Ayurvedic and Chinese medicine as an anti-inflammatory, to treat digestive and liver problems, skin diseases, and wounds.

Curcumin is also a powerful antioxidant. Antioxidants scavenge molecules in the body known as free radicals, which damage cell membranes, tamper with DNA, and even cause cell death. Antioxidants can fight free radicals and may reduce or even help prevent some of the damage they cause.

In addition, curcumin lowers the levels of two enzymes in the body that cause inflammation. It also stops platelets from clumping together to form blood clots.

Research suggests that turmeric may be helpful for the following conditions:

Indigestion or Dyspepsia

Curcumin stimulates the gallbladder to produce bile, which some people think may help improve digestion. The German Commission E, which determines which herbs can be safely prescribed in Germany, has approved turmeric for digestive problems. And one double-blind, placebo-controlled study found that turmeric reduced symptoms of bloating and gas in people suffering from indigestion.

Ulcerative colitis

Turmeric may help people with ulcerative colitis stay in remission. Ulcerative colitis is a chronic disease of the digestive tract where symptoms tend to come and go. In one double-blind, placebo-controlled study, people whose ulcerative colitis was in remission took either curcumin or placebo, along with conventional medical treatment, for 6 months. Those who took curcumin had a significantly lower relapse rate than those who took placebo.

Stomach Ulcers

Turmeric does not seem to help treat stomach ulcers. In fact, there is some evidence that it may increase stomach acid, making existing ulcers worse. (See "Precautions" section.)

Osteoarthritis

Because ofturmeric's ability to reduce inflammation, researchers have wondered ifit may help relieve osteoarthritis pain. One study found that people using an Ayurvedic formula of herbs and minerals with turmeric, winter cherry (Withinia somnifera), boswellia (Boswellia serrata), and zinc had less pain and disability. But it's impossible to know whether turmeric, one of the other supplements, or all of them together, was responsible for the effects.

Heart Disease

Early studies suggested that turmeric may help prevent atherosclerosis, the buildup of plaque that can block arteries and lead to heart attack or stroke. In animal studies, an extract of turmeric lowered cholesterol levels and kept LDL (bad) cholesterol from building up in blood vessels. Because it stops platelets from clumping together, turmeric may also prevent blood clots from building up along the walls of arteries. But a double-blind, placebo-controlled study found that taking curcumin, the active ingredient in turmeric, at a dose of up to 4 g per day did not improve cholesterol levels.

Cancer

There has been a great deal of research on turmeric's anti-cancer properties, but results are still very preliminary. Evidence from test tube and animal studies suggests that curcumin may help prevent or treat several types of cancers, including prostate, breast, skin, and colon cancer. Tumeric's preventive effects may relate to its antioxidant properties, which protect cells from damage. More research is needed. Cancer should be treated with conventional medications. Don't use alternative therapies alone to treat cancer. If you choose to use complementary therapies along with your cancer treatment, make sure you tell all your doctors.

Bacterial and Viral Infections

Test tube and animal studies suggest turmeric may kill bacteria and viruses, but researchers don't know whether it would work in people.

Uveitis

A preliminary study suggests curcumin may help treat uveitis, an inflammation of the eye's iris. Preliminary research suggests that curcumin may be as effective as corticosteroids, the type of medication usually prescribed. More research is needed.

Neurodegenerative Conditions

Tumeric's powerful antioxidant, anti-inflammatory, and circulatory effects may help prevent and treat neurodegenerative diseases, including Alzheimer disease, Parkinson disease, multiple sclerosis, and other conditions.

A relative of ginger, turmeric is a perennial plant that grows 5 to 6 feet high in the tropical regions of Southern Asia, with trumpet-shaped, dull yellow flowers. Its roots are bulbs that also produce rhizomes, which then produce stems and roots for new plants. Turmeric is fragrant and has a bitter, somewhat sharp taste. Although it grows in many tropical locations, the majority of turmeric is grown in India, where it is used as a main ingredient in curry.

The roots, or rhizomes and bulbs, are used in medicine and food. They are generally boiled and then dried, turning into the familiar yellow powder. Curcumin, the active ingredient, has antioxidant properties. Other substances in this herb have antioxidant properties as well.

Turmeric is available in the following forms:

Bromelain increases the absorption and anti-inflammatory effects of curcumin, so it is often combined with turmeric products.

Pediatric

Turmeric supplements haven't been studied in children, so there is no recommended dose.

Adult

The following doses are recommended for adults:

The use of herbs is a time-honored approach to strengthening the body and treating disease. However, herbs can trigger side effects and may interact with other herbs, supplements, or medications. For these reasons, you should take herbs with care, under the supervision of a health care provider.

Turmeric in food is considered safe.

Turmeric and curcumin supplements are considered safe when taken at the recommended doses. However, taking large amounts of turmeric for long periods of time may cause stomach upset and, in extreme cases, ulcers. People who have gallstones or obstruction of the bile passages should talk to their doctor before taking turmeric.

If you have diabetes, talk to your doctor before taking turmeric supplements. Turmeric may lower blood sugar levels. When combined with medications for diabetes, turmeric could cause hypoglycemia (low blood sugar).

Although it is safe to eat foods with turmeric, pregnant and breastfeeding women should not take turmeric supplements.

Because turmeric may act like a blood thinner, you should stop taking it at least 2 weeks before surgery. Tell your doctor and surgeon that you have been taking turmeric.

If you are being treated with any of the following medications, you should not use turmeric or curcumin in medicinal forms without first talking to your health care provider.

Blood-thinning medications -- Turmeric may strengthen the effects of these drugs, raising the risk of bleeding. Blood thinners include warfarin (Coumadin), clopidogrel (Plavix), and aspirin, among others.

Drugs that reduce stomach acid -- Turmeric may interfere with the action of these drugs, increasing the production of stomach acid:

Diabetes Medications -- Turmeric may strengthen the effects of these drugs, increasing the risk of hypoglycemia (low blood sugar).

Aggarwal BB. Curcumin-free tumeric exhibits anti-inflammatory and anticancer activities: Identification of novel components of tumeric. Mol Nutr Food Res. 2013; 57:1529-42.

Aggarwal BB, Sundaram C, Malani N, Ichikawa H. Curcumin: the Indian solid gold. Adv Exp Med Biol. 2007;595:1-75.

Asai A, Miyazawa T. Dietary curcuminoids prevent high-fat diet-induced lipid accumulation in rat liver and epididymal adipose tissue. J Nutr. 2001;131:2932-2935.

Asher GN, Spelman K. Clinical utility of curcumin extract. Altern Ther Health Med. 2013;19:20-2.

Baum L, et al. Curcumin effects on blood lipid profile in a 6-month human study. Pharmacol Res. 2007;56:509-14.

Blumenthal M, Goldberg A, Brinckmann J. Herbal Medicine: Expanded Commission E Monographs. Newton, MA: Integrative Medicine Communications; 2000:379-384.

Bolognia: Dermatology, 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.

Curcuma longa (turmeric). Monograph. Altern Med Rev. 2001;6 Suppl:S62-S66.

Darvesh AS, Aggarwal BB, Bishayee A. Curcumin and Liver Cancer: A Review. Curr Pharm Biotechnol. 2011 Apr 5. [Epub ahead of print]

Davis JM, Murphy EA, Carmichael MD, Zielinski MR, Groschwitz CM, Brown AS, Ghaffar A, Mayer EP. Curcumin effects on inflammation and performance recovery following eccentric exercise-induced muscle damage. Am J Physiol Regul Integr Comp Physiol. 2007 Mar 1 [Epub ahead of print]

Dorai T, Cao YC, Dorai B, Buttyan R, Katz AE. Therapeutic potential of curcumin in human prostate cancer. III. Curcumin inhibits proliferation, induces apoptosis, and inhibits angiogenesis of LNCaP prostate cancer cells in vivo. Prostate. 2001;47:293-303.

Dorai T, Gehani N, Katz A. Therapeutic potential of curcumin in human prostate cancer. II. Curcumin inhibits tyrosine kinase activity of epidermal growth factor receptor and depletes the protein. Mol Urol. 2000;4:1-6.

Funk JL, Frye JB, Oyarzo JN, Kuscuoglu N, Wilson J, McCaffrey G, et al. Efficacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis. Arthritis Rheum. 2006;54:3452-64.

Gautam SC, Gao X, Dulchavsky S. Immunodilation by curcumin. Adv Exp Med Biol. 2007;595:321-41.

Gescher A J, Sharma R A, Steward W P. Cancer chemoprevention by dietary constituents: a tale of failure and promise. Lancet Oncol. 2001;2:371-379.

Goel A, Kunnumakkara AB, Aggarwal BB. Curcumin as "Curecumin": from kitchen to clinic. Biochem Pharmacol. 2008;75:787-809.

Hanai H, Iida T, Takeuchi K, Watanabe F, Maruyama Y, Andoh A, et al. Curcumin maintenance therapy for ulcerative colitis: randomized, multicenter, double-blind, placebo-controlled trial. Clin Gastroenterol Hepatol. 2006;4:1502-6.

Handler N, Jaeger W, Puschacher H, Leisser K, Erker T. Synthesis of novel curcumin analogues and their evaluation as selective cyclooxygenase-1 (COX-1) inhibitors. Chem Pharm Bull (Tokyo). 2007;55:64-71.

Heck AM, DeWitt BA, Lukes AL. Potential interactions between alternative therapies and warfarin. Am J Health Syst Pharm. 2000;57:1221-1227.

Jagetia GC, Aggarwal BB. "Spicing up" of the immune system by curcumin. J Clin Immunol. 2007;27:19-35.

Johnson JJ, Mukhtar H. Curcumin for chemoprevention of colon cancer. Cancer Lett. 2007 Apr 18; [Epub ahead of print]

Kapakos G, Youreva V, Srivastava AK. Cardiovascular protection by curcumin: molecular aspects. Indian J Biochem Biophys. 2012; 49:306-15.

Kim DS, Kim JY, Han Y. Curcuminoids in neurodegenerative diseases. Recent Pat CNS Drug Discov. 2012; 7:184-204.

Kim MS, Kang HJ, Moon A. Inhibition of invasion and induction of apoptosis by curcumin in H-ras-transformed MCF10A human breast epithelial cells. Arch Pharm Res. 2001;24:349-354.

Krishnaswamy K. Traditional Indian spices and their health significance. Asia Pac J Clin Nutr. 2008;17 Suppl 1:265-8.

Nagaraju GP, Aliya S, Zafar SF, Basha R, Diaz R, El-Rayes BF. The impact of curcumin on breast cancer. Integr Biol (Camb). 2012; 4:996-1007.

Pari L, Tewas D, Eckel J. Role of curcumin in health and disease. Arch Physiol Biochem. 2008;114:127-49.

Phan TT, See P, Lee ST, Chan SY. Protective effects of curcumin against oxidative damage on skin cells in vitro: its implication for wound healing. J Trauma 2001;51:927-931.

Rakel D. Rakel: Integrative Medicine, 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.

Rao CV. Regulation of COX and LOX by curcumin. Adv Exp Med Biol. 2007;595:213-26.

Sharma RA, Ireson CR, Verschoyle RD. Effects of dietary curcumin on glutathione S-Transferase and Malondialdehyde-DNA adducts in rat liver and colon mucosa: relationship with drug levels. Clin Cancer Res. 2001;7:1452-1458.

Sharma RA, Steward WP, Gescher AJ. Pharmacokinetics and pharmacodynamics of curcumin. Adv Exp Med Biol. 2007;595:453-70.

Shehzad A, Khan S, Shehzad O, Lee YS. Curcumin therapeutic promises and bioavailability in colorectal cancer. Drugs Today (Barc). 2010;46:523-32. Review.

Shehzad A, Lee J, Lee YS. Curcumin in various cancers. Biofactors. 2013; 39:56-68.

Shehzad A, Rehman G, Lee YS. Curcumin in inflammatory diseases. Biofactors. 2013; 39:69-77.

Shishodia S, Singh T, Chaturvedi MM. Modulation of transcription factors by curcumin. Adv Exp Med Biol. 2007;595:127-48.

Su CC, Lin JG, Li TM, Chung JG, Yang JS, Ip SW, et al. Curcumin-induced apoptosis of human colon cancer colo 205 cells through the production of ROS, Ca2+ and the activation of caspase-3. Anticancer Res. 2006;26:4379-89.

Suryanarayana P, Satyanarayana A, Balakrishna N, Kumar PU, Reddy GB. Effect of turmeric and curcumin on oxidative stress and antioxidant enzymes in streptozotocin-induced diabetic rat. Med Sci Monit. 2007;13:BR286-92.

White B, Judkins DZ. Clinical Inquiry. Does turmeric relieve inflammatory conditions? J Fam Pract. 2011;60:155-6. Review.

Zafir A, Banu N. Antioxidant potential of fluoxetine in comparison to Curcuma longa in restraint-stressed rats. Eur J Pharmacol. 2007;572:23-31.

Curcuma longa

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch)

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. 1997-2013 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

See the article here:
Turmeric | University of Maryland Medical Center

2

Florin I. Niculescu Eldersburg Arthritis 6190 Georgetown Blvd Ste 110 Sykesville, MD 21784 (410) 795-9700

3

Teodora M. Niculescu Eldersburg Arthritis 6190 Georgetown Blvd Ste 110 Sykesville, MD 21784 (410) 795-9700

4

Deepak Gupta Carroll Arthritis 412 Malcolm Dr Ste 306 Westminster, MD 21157 (410) 848-0364

5

Rosemarie A. Shaw Carroll Arthritis 412 Malcolm Dr Ste 306 Westminster, MD 21157 (410) 848-0364

6

Robert A. Shaw Carroll Arthritis 412 Malcolm Dr Ste 306 Westminster, MD 21157 (410) 848-0364

7

Melanie Chatterji Carroll Arthritis 412 Malcolm Dr Ste 306 Westminster, MD 21157 (410) 848-0364

8

Margret A. Fountain Gakuba & Fountain MDs 2 Reservoir Cir Ste 105 Pikesville, MD 21208 (410) 653-1822

9

Paul A. Gertler Arthritis Care Specialists Of Maryland 4801 Dorsey Hall Dr Ste 226 Ellicott City, MD 21042 (410) 992-7440

10

Moe Zan Arthritis Care Specialists Of Maryland 4801 Dorsey Hall Dr Ste 226 Ellicott City, MD 21042 (410) 992-7440

11

Thomas J. Lang Arthritis Care Specialists Of Maryland 4801 Dorsey Hall Dr Ste 226 Ellicott City, MD 21042 (410) 992-7440

12

Stephen W. George Arthritis Care Specialists Of Maryland 4801 Dorsey Hall Dr Ste 226 Ellicott City, MD 21042 (410) 992-7440

13

Melissa L. Hawkins-Holt Arthritis Care Specialists Of Maryland 4801 Dorsey Hall Dr Ste 226 Ellicott City, MD 21042 (410) 992-7440

14

David B. Arconti Arthritis Care Specialists Of Maryland 4801 Dorsey Hall Dr Ste 226 Ellicott City, MD 21042 (410) 992-7440

15

Jeffrey T. Landis Nasseri Clinic Arthritic & Rheumatology Diseases 700 Geipe Rd Ste 266 Catonsville, MD 21228 (410) 744-0661

16

Sharon D. Crum Nasseri Clinic Arthritic & Rheumatology Diseases 700 Geipe Rd Ste 266 Catonsville, MD 21228 (410) 744-0661

17

Leili Parsa Nasseri Clinic Arthritic & Rheumatology Diseases 700 Geipe Rd Ste 266 Catonsville, MD 21228 (410) 744-0661

18

Nasser Nasseri Nasseri Clinic Arthritic & Rheumatology Diseases 700 Geipe Rd Ste 266 Catonsville, MD 21228 (410) 744-0661

19

James R. Bellor Jr Columbia Medical Practice 610 Solarex Ct Frederick, MD 21703 (410) 964-6139

20

Chaim B. Mond Chaim B Mond MD 2835 Smith Ave Ste 207 Baltimore, MD 21209 (410) 580-1330

21

Rida A. Frayha Rida A Frayha MD 3640 Fords Ln Apt E Baltimore, MD 21215 (410) 358-2741

22

Raymond H. Flores Kernan Hospital Rheumatology 2200 Kernan Dr Gwynn Oak, MD 21207 (410) 448-6398

23

Violeta Rus Kernan Hospital Rheumatology 2200 Kernan Dr Gwynn Oak, MD 21207 (410) 448-6398

24

Jamal A. Mikdashi Kernan Hospital Rheumatology 2200 Kernan Dr Gwynn Oak, MD 21207 (410) 448-6398

25

Bernadette C. Siaton Kernan Hospital Rheumatology 2200 Kernan Dr Gwynn Oak, MD 21207 (410) 448-6398

26

Grace Ahn Falls Medical Specialists 10753 Falls Rd Ste 225 Lutherville-Timonium, MD 21093 (410) 583-2848

27

David E. McGinnis Falls Medical Specialists 10753 Falls Rd Ste 225 Lutherville-Timonium, MD 21093 (410) 583-2848

28

Ira T. Fine Falls Medical Specialists 10753 Falls Rd Ste 225 Lutherville-Timonium, MD 21093 (410) 583-2848

29

John O. Meyerhoff Sinai Hospital Rheumatology 2411 W Belvedere Ave Ste 401 Baltimore, MD 21215 (410) 601-8389

30

Primal K. Bhatia Arthritis & Osteoporosis Center 716 Maiden Choice Ln Ste 301 Baltimore, MD 21228 (410) 788-2000

31

Abdollah Shams-Pirzadeh Arthritis & Osteoporosis Center 716 Maiden Choice Ln Ste 301 Baltimore, MD 21228 (410) 788-2000

32

William L. Yap Cueto Miller & Yap MDs 724 Maiden Choice Ln Ste 204 Catonsville, MD 21228 (410) 744-6566

33

Andrea S. Marx Rheumatology Associates At Lutherville 1734 York Rd Lutherville, MD 21093 (410) 337-7780

34

Oliver J. Lawless Center For Arthritis Immunology & Enviornmental Diseases 18111 Prince Philip Dr Ste 310 Olney, MD 20832 (301) 774-2886

35

Anuradha D. Reddy Anuradha D Reddy MD 821 N Eutaw St Ste 303 Baltimore, MD 21201 (410) 225-8153

36

Mohammed Esfahani University Maryland Mid Town Campus Internal Medicine 827 Linden Ave Baltimore, MD 21201 (410) 225-8800

37

Marc Hochberg University Of Maryland Rheumatology 10 S Pine St MSTF 8-34 Baltimore, MD 21201 (410) 706-6474

38

Lawrence D. Weber Baltimore VA Medical Center Internal Medicine 10 N Greene St Baltimore, MD 21201 (410) 605-7000

39

Marlyn Lorenzo Rheumatology Associates 301 Saint Paul St Ste 411 Baltimore, MD 21202 (410) 332-9346

40

Peter A. Holt Peter A Holt Md 5601 Loch Raven Blvd Ste 509 Baltimore, MD 21239 (410) 734-4290

41

Gregory D. McCormack Rheumatology Associates 301 Saint Paul St Ste 411 Baltimore, MD 21202 (410) 332-9346

42

Nazi Farsi Rheumatology Associates 301 Saint Paul St Ste 411 Baltimore, MD 21202 (410) 332-9346

43

Lynn M. Ludmer Rheumatology Associates 1220B E Joppa Rd Ste 310 Towson, MD 21286 (410) 494-1888

44

Howard W. Hauptman Rheumatology Associates 1220B E Joppa Rd Ste 310 Towson, MD 21286 (410) 494-1888

45

Rebecca F. Marsden Rheumatology Associates 1220B E Joppa Rd Ste 310 Towson, MD 21286 (410) 494-1888

46

Tazeen Rehman Rheumatology Associates 1220B E Joppa Rd Ste 310 Towson, MD 21286 (410) 494-1888

47

Pamela Lentz Rheumatology Associates 1220B E Joppa Rd Ste 310 Towson, MD 21286 (410) 494-1888

48

Bansari Gujarat Rheumatology Associates 1220B E Joppa Rd Ste 310 Towson, MD 21286 (410) 494-1888

49

Michelle A. Petri Johns Hopkins Outpatient 601 N Caroline St FL 7 Baltimore, MD 21287 (410) 955-5268

50

Jazibeh A. Qureshi Harbour Hospital Arthritis Center 2900 S Hanover St Ste 100 Brooklyn, MD 21225 (410) 350-8280

51

Alan Baer John Hopkins University Rheumatology 4940 Eastern Ave Mason Lord Ste 1201 Baltimore, MD 21224 (410) 550-1887

Read the rest here:
Rheumatoid Arthritis Center - Eldersburg, MD

Surgeon performs bone marrow harvest

The terms "Hodgkin's Disease," "Hodgkin's Lymphoma," and "Hodgkin Lymphoma" are used interchangeably throughout this site.

Bone Marrow Transplants (BMT) and Peripheral Blood Stem Cell Transplants (PBSCT) are emerging as mainstream treatment for many cancers, including Hodgkin's Disease and Medium/High grade aggressive)Non-Hodgkin's lymphoma.

BMTs have been used to treat lymphoma for more than 10 years, but until recently they were used mostly within clinical trials. Now BMTs are being used in conjunction with high doses of chemotherapy as a mainstream treatment.

When high doses of chemotherapy are planned, which can destroy the patients bone marrow, physicians will typically remove marrow from the patients bone before treatment and freeze it. After chemotherapy, the marrow is thawed and injected into a vein to replace destroyed marrow. This type of transplant is called an autologous transplant. If the transplanted marrow is from another person, it is called an allogeneic transplant.

In PBSCTs, another type of autologous transplant, the patient's blood is passed through a machine that removes the stem cells the immature cells from which all blood cells develop. This procedure is called apheresis and usually takes three or four hours over one or more days. After treatment to kill any cancer cells, the stem cells are frozen until they are transplanted back to the patient. Studies have shown that PBSCTs result in shorter hospital stays and are safer and more cost effective than BMTs.

Read more here:
Bone Marrow and Stem Cell Transplants Lymphoma Info

Welcome to the worlds largest and most comprehensive back pain database. We are a completely free online community devoted to ending the epidemic of chronic pain. This web resource offers reliable and honest information in language you can easily understand. You are amongst friends here.

Our writing is highly critical of back pain treatment. The medical industry is broken and someone needs to speak up and inform people of the problems that exist. We are proud to be called healthcare renegades in the international press. We embrace our subversive point of view, since the accepted and traditional stance on chronic pain has fostered monumental suffering worldwide. We dont want to be part of a medical fraternity that has ruined more lives than it has helped. Our no-compromise attitude is what saves our readers from falling victim to the abuses of a healthcare system that has failed them on all fronts.

We are unique in the healthcare information sector. We do not have or want universal appeal, since there is no universally-applicable answer to back pain. Resources that promote a one size fits all approach to patient education fail miserably. We would rather educate the people who really want to be cured then to provide content that speaks to everyone, but helps no one. Our writing is different than what you might have read before. That is the whole idea, since thinking the same as everyone else seems to promote pain and leads to poor therapy outcomes in the general patient population.

All this being said, we do not outwardly reject any mainstream medical theory or practice. However, we are always mindful of the downsides of these ideas and methods, especially when they reflect the true financial motivations of the treatment industry more than the actual needs of patients. We do not provide an alternative view of back pain; merely an objective view.

Healthcare providers hate to be questioned. We go beyond merely questioning them. We demand answers and make them accountable for their opinions and decisions. Furthermore, we publicly expose their failings for all to see; not in an effort to discredit doctors, but instead to help improve treatment results for patients who are still not sure about the best approach to care for their own situations.

Despite our criticism, we find that year after year, our most loyal readers are doctors, chiropractors and various therapists. We know that so many healthcare professionals are dissatisfied with the present status quo and want to do better for their patients. These courageous professionals have chosen to be free of their egos in an effort to improve the lives of their patients. They know that change is needed and are working to implement better diagnostic and treatment protocols one patient at a time. We acknowledge and thank these caregivers for their efforts.

We have helped to cure hundreds of thousands of people over the past decade. No other health website dares to make this claim, because they all recycle the same old information that has not helped anyone to recover from back pain ever. This is exactly why you are here and ready to try something different

I have suffered with crippling lower back pain, neck pain and sciatica symptoms for most of my life. I know what you must endure every day while living with back problems. I have empathy for you. I understand because I was there myself. I lived the nightmare and was forever changed by the ordeal. I hope that this web resource can help you to achieve your goals of finding true back pain relief. I have been involved in spinal research and patient advocacy on an international level for over 25 years. I am passionate about my work because it is a reflection of the very fabric of my life. I am here to help you.

Sensei Adam Rostocki Founder and Editor-in-Chief

The navigation bar appears on every page of this site, so you will never get lost. Each navigation button corresponds to a different topic of discussion. Each of these main resource sections is broken down into several more focused guides, so it is best to read every article contained in the section in order to gain a full understanding of the diagnosed condition in its entirety. All the information is free, so you have nothing to lose. The time you invest in research will surely pay dividends in improved health.

Virtually all possible causes of back symptoms are detailed here, including degenerative disc disease, facet joint syndrome, fibromyalgia, herniated discs, lordosis, kyphosis, osteoarthritis, osteoporosis, pinched nerves, piriformis syndrome, sacroiliac joint pain, sciatica, scoliosis, spinal cord injury, spinal stenosis, spondylolisthesis and all varieties of pain in the coccygeal, sacral, lumbar, thoracic and cervical spinal regions.

There are also dedicated sections on diagnostic methods, back pain treatment options, mindbody medicine and back surgery. You can learn about the spinal anatomy and even read through an inspiring section devoted to recovering from chronic pain. You will never find a more comprehensive collection of back and spine pain reports anywhere.

Remember, it is vital to become more active in your own health and treatment. Learning more about your diagnosis is the best way to start and we have made it easy for you by organizing everything you need to know by topic. All you have to do is take the time to read. There are thousands of topics on this web resource. Make sure to check back often to stay up to date on all the latest research.

Share Your Story Share your own back pain story by taking part in our interactive forum. Speak out now and make a difference! You might be surprised how good it feels to vent about your pain. Go for it! Your experience will help other suffering patients.

Research Survey Take 1 minute to help others by sharing your own back ache experiences.

Healthcare providers, please add your practice details to our Doctor Directory

Updates are listed on theBack Pain Blog.

The complete list of site topics can be found on theSite Map.

We are not a dotcom. Many people do not realize that .com stands for company and this is simply not what we are all about. We are a grassroots organization (.org) which has grown from a humble single person project to one of the largest and most peer-respected health websites on the internet.

We are not going to market to you or try to take advantage of the trust you have placed in us. We do not have pages full of overpriced garbage to sell you. We do not want your money. You don't have to buy anything at all to benefit from this website.Enjoy the volumes of free information without any pressure.

Our writing is based on actual patient reports, citations and clinical evidence, not speculative or theoretic research designed to sell a product or treatment. We never confuse advertising with content and will never endorse anything in exchange for any financial compensation or other benefit.

This site is intensive, detailed and thought provoking. It is not the usual bland and useless information found everywhere else. We do not feel that the large commercial health websites provide any information about back pain that is not common knowledge or common sense, yet they are so prominently featured in search engine results. Most large search providers have hidden us away in their recesses, since we do not pay huge amounts of money to be featured on page 1 of their results. Just because a website pays does not mean it is truthful or useful. It just proves that it is out to make money and has done so effectively enough to silence its competitors. They can keep their stupid money. Making money is not our goal here. We rely on real people to spread our message, as well as support our cause, and real people have done so for us effectively for ten years now. We do not care about playing games to make search engines like us. We write for humans, not search algorithms.

The content of this site is 100% original and is self-written by the editorial board. Our content is never shared, distributed or syndicated.

Go here to see the original:
Back Pain

Genetic Engineering, the process of extracting DNA (deoxyribonucleic acid, which makes up the genes of all living things) from one organism and combining it with the DNA of another organism, thus introducing new hereditary traits into the recipient organism. The nature and characteristics of every living creature is determined by the special combinations of genes carried by its cells. The slightest alteration in these combinations can bring about significant changes in an organism and also its progeny. The science of devising techniques of modifying or controlling genes and genetic combinations is referred to as genetic engineering. It was practiced in one form or another in the past by farmers and agriculturists trying to create economically viable species of plants and animals through various breeding techniques Genetic engineering, as a science, was developed in the mid-1970's primarily to create new strains of microorganisms that produce certain chemicals useful in manufacturing or as drugs. Genetic engineering is now also applied to improving plants and creating transgenic animals (animals containing foreign genetic material).

Some persons oppose genetic engineering on religious, ethical, or social grounds. Among the religious questions is whether humans have the right to transfer traits from one organism to another. A social concern is the possibility of creating harmful organisms that, if accidentally released into the environment, could cause epidemics.The creation of human clones, for example, is facing serious opposition especially on moral grounds. Organizations, such as the National Institutes of Health (NIH), are seeking to control the harmful effects of genetic engineering by imposing guidelines and safety measures for genetic experimentation. Treatment of hereditary defects through gene transplantation and controlled interchange of genes between specified species was approved in 1985 and 1987 respectively by the NIH and the National Academy of Sciences. The USDA has framed regulations for the genetic alteration of plants by plant breeders.

The U.S. Supreme Court ruled in 1980 that genetically engineered microorganisms could be patented. In 1988 the U.S. Patent and Trademark Office issued its first patent for a higher form of life, a transgenic mouse that is highly susceptible to certain cancers that appear frequently in humans. This mouse is used in cancer research.

Original post:
Genetic Engineering - HowStuffWorks

Genetic tests have been developed for thousands of diseases. Most tests look at single genes and are used to diagnose rare genetic disorders, such as Fragile X Syndrome and Duchenne Muscular Dystrophy. In addition, some genetic tests look at rare inherited mutations of otherwise protective genes, such as BRCA1 and BRCA2, which are responsible for some hereditary breast and ovarian cancers. However, a growing number of tests are being developed to look at multiple genes that may increase or decrease a persons risk of common diseases, such as cancer or diabetes. Such tests and other applications of genomic technologies have the potential to help prevent common disease and improve the health of individuals and populations. For example, predictive gene tests may be used to help determine the risk of developing common diseases, and pharmacogenetic tests may be used to help identify genetic variations that can influence a persons response to medicines. There is much we still need to learn about how effective these new tests are, and the best way to use them to improve health. Learn more.

Despite the many scientific advances in genetics, researchers have only identified a small fraction of the genetic component of most diseases. Therefore, genetic tests for many diseases are developed on the basis of limited scientific information and may not yet provide valid or useful results to individuals who are tested. However, many genetic tests are being marketed prematurely to the public through the Internet, TV, and other media. This may lead to the misuse of these tests and the potential for physical or psychological harms to the public. At the same time, valid and useful tests, such as those for hereditary breast and ovarian cancer or for Lynch syndrome, a form of hereditary colorectal cancer, are not widely used, in part because of limited research on how to get useful tests implemented into practice across U.S. communities. Individuals can learn more about specific genetic tests by visiting the Web sites listed below or by talking with their doctor.

Top of Page

In 2008, the former Secretary's Advisory Committee on Genetics, Health and Society of the U.S. Department of Health and Human Services released a report identifying gaps in the regulation, oversight, and usefulness of genetic testing. They expressed the need for timely, reliable information that health care providers, payers, public health practitioners, policy makers, and consumers could use to make more informed decisions about the appropriate use of these tests in clinical and public health practice.

To begin addressing this need for reliable information, CDCs Office of Public Health Genomics (OPHG) established the Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Initiative project to systematically evaluate genetic tests and other applications of genomic technology that are in transition from research to clinical and public health practice. Since 2005, the independent EGAPP Working Group has released nine recommendations on the validity and utility of specific genetic tests.

The U.S. Preventive Services Task Force (USPSTF) has also released recommendations on specific genetic tests used in selected clinical scenarios involving breast cancer, colorectal cancer, and hemochromatosis.

In addition the Genetic Test Registry was developed by NCBI. The article "The NIH genetic testing registry: a new, centralized database of genetic tests to enable access to comprehensive information and improve transparency" in the journal Nucleic Acids Research describes in detail this database.

Top of Page

Also see the genetic testing and genetic counseling sections of CDCs Office of Public Health Genomics resource guide.

Top of Page

Excerpt from:
Genomics |Genetic Testing

Genetic testing is the process of using medical tests to look for changes (mutations) in a persons genes or chromosomes. Hundreds of different genetic tests are used today, and more are being developed.

Genetic testing can be used in different situations. The type of testing most often used to check for cancer risk is called predictive gene testing. Its used to look for gene mutations that might put a person at risk of getting a disease. Its usually done in families with a history that suggests theres a disease that may be inherited. An example is testing for changes in the BRCA1 and BRCA2 genes (known breast cancer genes) in a woman whose mother and sister had breast cancer.

Genetic testing is also used for other reasons:

All of these forms of genetic testing, including predictive gene testing, look for gene changes that are passed from one generation to the next and are found in every cell in the body. Except for the newborn screening tests, they are used mainly for people with certain types of disease that seem to run in their families. They are not needed by most people.

Cancer-related genetic tests are most commonly done as predictive genetic tests. They may be used:

Sometimes after a person has been diagnosed with cancer, the doctor will order tests to look for gene changes in a sample of the cancer cells. These tests can give information on a persons outlook (prognosis) and can sometimes help tell whether certain types of treatment might be useful.

These types of tests look for gene changes only in the cancer cells that are taken from the patient. These tests are not the same as the tests used to find out about inherited cancer risk.

This document does not cover gene testing done on cancer cells. For more about this kind of testing and its use in cancer treatment, see our information on specific types of cancer.

The rest of this document focuses on predictive genetic testing for inherited mutations as they relate to cancer.

Read the original here:
What is genetic testing? - American Cancer Society

Since 2003, AAG Health & Wellness has pioneered the field of health, vitality and wellness for men and women who want to achieve specific health goals.

We combine ongoing expertise in clinical research related to every area of wellness, with access to a unique team of board-certified physicians, wellness coaches and nutritionists at our hormone therapy clinics.

Our expertise is in the integrative field of age management and anti-aging. Our unique approach enables our clients to achieve optimum performance, productivity and appearance in the most efficient way possible.

Please find below a list of our most popular treatment plans designed to make you look good and feel better than ever:

We also offer a great selection of diagnostic tests at our clinics that are designed to identify health and wellness markers:

All of the above play a crucial role in our integrative wellness approach to age management. Here are some of the results our clients have reported after visiting our wellness centers:

If youre ready to supercharge your life, give us a call at (866) 734-5771 for a free consultation or to get more information about our integrative wellness programs.

Together, well help you feel young and stay healthy so you can accomplish more in life.

Originally posted here:
HGH Therapy | HGH Clinics | Human Growth Hormone Therapy

TV.NaturalNews.com is a free video website featuring thousands of videos on holistic health, nutrition, fitness, recipes, natural remedies and much more.

CounterThink Cartoons are free to view and download. They cover topics like health, environment and freedom.

The Consumer Wellness Center is a non-profit organization offering nutrition education grants to programs that help children and expectant mothers around the world.

Food Investigations is a series of mini-documentaries exposing the truth about dangerous ingredients in the food supply.

Webseed.com offers alternative health programs, documentaries and more.

The Honest Food Guide is a free, downloadable public health and nutrition chart that dares to tell the truth about what foods we should really be eating.

HealingFoodReference.com offers a free online reference database of healing foods, phytonutrients and plant-based medicines that prevent or treat diseases and health conditions.

HerbReference.com is a free, online reference library that lists medicinal herbs and their health benefits.

NutrientReference.com is a free online reference database of phytonutrients (natural medicines found in foods) and their health benefits. Lists diseases, foods, herbs and more.

Excerpt from:
Genetic engineering news, articles and information:

_______

GENE THERAPY:

______

______

Caveat:

Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. I have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publishing this article. However, in view of the possibility of human error or changes in medical sciences, I do not assure that the information contained herein is in every respect accurate or complete, and I disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. I have taken some information from articles that were published few years ago. The facts and conclusions presented may have since changed and may no longer be accurate. Questions about personal health should always be referred to a physician or other health care professional.

______

Prologue:

BLASPHEMY! some cried when the concept of gene therapy first surfaced. For them tinkering with the genetic constitution of human beings was equivalent to playing God, and this they perceived as being sacrilegious! On the other side was the scientific community, abuzz with excitement at the prospect of being able to wipe certain genetic disorders in humans entirely from the human gene pool. Although the term gene therapy was first introduced during the 1980s, the controversy about the rationality of this line of treatment still rages on. In the center of the debate lie the gene therapy pros and cons that derive opinions from religious, ethical and undoubtedly, political domains. The concept of genes as carriers of phenotypic information was introduced in the early 19th century by Gregor Mendel, who later demonstrated the properties of genetic inheritance in peas. Over the next 100 years, many significant discoveries lead to the conclusions that genes encode proteins and reside on chromosomes, which are composed of DNA. These findings culminated in the central dogma of molecular biology, that proteins are translated from RNA, which is transcribed from DNA. James Watson was quoted as saying we used to think that our fate was in our stars, but now we know, in large measures, our fate is in our genes. Genes, the functional unit of heredity, are specific sequences bases that encode instructions to make proteins. Although genes get a lot of attentions, it is the proteins that perform most life functions. When genes are altered, encoded proteins are unable to carry out their normal functions, resulting in genetic disorders. Gene therapy is a novel therapeutic branch of modern medicine. Its emergence is a direct consequence of the revolution heralded by the introduction of recombinant DNA methodology in the 1970s. Gene therapy is still highly experimental, but has the potential to become an important treatment regimen. In principle, it allows the transfer of genetic information into patient tissues and organs. Consequently, diseased genes can be eliminated or their normal functions rescued. Furthermore, the procedure allows the addition of new functions to cells, such as the production of immune system mediator proteins that help to combat cancer and other diseases. Most scientists believe the potential for gene therapy is the most exciting application of DNA science, yet undertaken.

__________

Note:

Please read my other articles Stem cell therapy and human cloning, Cell death and Genetically modified before reading this article.

__________

The rapid pace of technological advances has profound implications for medical applications far beyond their traditional roles to prevent, treat, and cure disease. Cloning, genetic engineering, gene therapy, human-computer interfaces, nanotechnology, and designer drugs have the potential to modify inherited predispositions to disease, select desired characteristics in embryos, augment normal human performance, replace failing tissues, and substantially prolong life span. As gene therapy is uprising in the field of medicine, scientists believe that after 20 years, this will be the last cure of every genetic disease. Genes may ultimately be used as medicine and given as simple intravenous injection of gene transfer vehicle that will seek our target cells for stable, site-specific chromosomal integration and subsequent gene expression. And now that a draft of the human genome map is complete, research is focusing on the function of each gene and the role of the faulty gene play in disease. Gene therapy will ultimately play Copernican part and will change our lives forever.

_

Gene therapy, the experimental therapy as on today:

Gene therapy is an experimental technique that uses genes to treat or prevent diseases. Genes are specific sequences of bases that encode instructions on how to make proteins. When genes are altered so that the encoded proteins are unable to carry out their normal functions, genetic disorders can result. Gene therapy is used for correcting defective genes responsible for disease development. Researchers may use one of several approaches for correcting faulty genes. Although gene therapy is a promising treatment which helps successfully treat and prevent various diseases including inherited disorders, some types of cancer, and certain viral infections, it is still at experimental stage. Gene therapy is presently only being tested for the treatment of diseases that have no other cures. Currently, the only way for you to receive gene therapy is to participate in a clinical trial. Clinical trials are research studies that help doctors determine whether a gene therapy approach is safe for people. They also help doctors understand the effects of gene therapy on the body. Your specific procedure will depend on the disease you have and the type of gene therapy being used.

______

Introduction to gene therapy:

Gene therapy is a clinical strategy involving gene transfer with therapeutic purposes. It is based on the concept that an exogenous gene (transgene) is able to modify the biology and phenotype of target cells, tissues and organs. Initially designed to definitely correct monogenic disorders, such as cystic fibrosis, severe combined immunodeficiency or muscular dystrophy, gene therapy has evolved into a promising therapeutic modality for a diverse array of diseases. Targets are expanding and currently include not only genetic, but also many acquired diseases, such as cancer, tissue degeneration or infectious diseases. Depending on the duration planned for the treatment, type and location of target cells, and whether they undergo division or are quiescent, different vectors may be used, involving nonviral methods, non-integrating viral vectors or integrating viral vectors. The first gene therapy clinical trial was carried out in 1989, in patients with advanced melanoma, using tumor-infiltrating lymphocytes modified by retroviral transduction. In the early nineties, a clinical trial with children with severe combined immunodeficiency (SCID) was also performed, by retrovirus transfer of adenosine deaminase gene to lymphocytes isolated from these patients. Since then, more than 5,000 patients have been treated in more than 1,000 clinical protocols all over the world. Despite the initial enthusiasm, however, the efficacy of gene therapy in clinical trials has not been as high as expected; a situation further complicated by ethical and safety concerns. Further studies are being developed to solve these limitations.

_________

Historical development of gene therapy:

Chronology of development of gene therapy technology:

1970s, 1980s and earlier:

In 1972 Friedmann and Roblin authored a paper in Science titled Gene therapy for human genetic disease? Rogers (1970) was cited for proposing that exogenous good DNA be used to replace the defective DNA in those who suffer from genetic defects. However, these authors concluded that it was premature to begin gene therapy studies in humans because of lack of basic knowledge of genetic regulation and of genetic diseases, and for ethical reasons. They did, however, propose that studies in cell cultures and in animal models aimed at development of gene therapies be undertaken. Such studiesas well as abortive gene therapy studies in humanshad already begun as of 1972. In the 1970s and 1980s, researchers applied such technologies as recombinant DNA and development of viral vectors for transfer of genes to cells and animals to the study and development of gene therapies.

1990s:

The first approved gene therapy case in the United States took place on 14 September 1990, at the National Institute of Health, under the direction of Professor William French Anderson. It was performed on a four year old girl named Ashanti DeSilva. It was a treatment for a genetic defect that left her with ADA-SCID, a severe immune system deficiency. The effects were only temporary, but successful. New gene therapy approach repairs errors in messenger RNA derived from defective genes. This technique has the potential to treat the blood disorder thalassaemia, cystic fibrosis, and some cancers. Researchers at Case Western Reserve University and Copernicus Therapeutics are able to create tiny liposomes 25 nanometers across that can carry therapeutic DNA through pores in the nuclear membrane. Sickle-cell disease is successfully treated in mice. The mice which have essentially the same defect that causes sickle cell disease in humans through the use a viral vector, were made to express the production of fetal hemoglobin (HbF), which normally ceases to be produced by an individual shortly after birth. In humans, the use of hydroxyurea to stimulate the production of HbF has long been shown to temporarily alleviate the symptoms of sickle cell disease. The researchers demonstrated this method of gene therapy to be a more permanent means to increase the production of the therapeutic HbF. In 1992 Doctor Claudio Bordignon working at the Vita-Salute San Raffaele University, Milan, Italy performed the first procedure of gene therapy using hematopoietic stem cells as vectors to deliver genes intended to correct hereditary diseases. In 2002 this work led to the publication of the first successful gene therapy treatment for adenosine deaminase-deficiency (SCID). The success of a multi-center trial for treating children with SCID (severe combined immune deficiency or bubble boy disease) held from 2000 and 2002 was questioned when two of the ten children treated at the trials Paris center developed a leukemia-like condition. Clinical trials were halted temporarily in 2002, but resumed after regulatory review of the protocol in the United States, the United Kingdom, France, Italy, and Germany. In 1993 Andrew Gobea was born with severe combined immunodeficiency (SCID). Genetic screening before birth showed that he had SCID. Blood was removed from Andrews placenta and umbilical cord immediately after birth, containing stem cells. The allele that codes for ADA was obtained and was inserted into a retrovirus. Retroviruses and stem cells were mixed, after which the viruses entered and inserted the gene into the stem cells chromosomes. Stem cells containing the working ADA gene were injected into Andrews blood system via a vein. Injections of the ADA enzyme were also given weekly. For four years T cells (white blood cells), produced by stem cells, made ADA enzymes using the ADA gene. After four years more treatment was needed. The 1999 death of Jesse Gelsinger in a gene therapy clinical trial resulted in a significant setback to gene therapy research in the United States. Jesse Gelsinger had ornithine transcarbamylase deficiency. In a clinical trial at the University of Pennsylvania, he was injected with an adenoviral vector carrying a corrected gene to test the safety of use of this procedure. He suffered a massive immune response triggered by the use of the viral vector, and died four days later. As a result, the U.S. FDA suspended several clinical trials pending the re-evaluation of ethical and procedural practices in the field.

2003:

In 2003 a University of California, Los Angeles research team inserted genes into the brain using liposomes coated in a polymer called polyethylene glycol. The transfer of genes into the brain is a significant achievement because viral vectors are too big to get across the bloodbrain barrier. This method has potential for treating Parkinsons disease. RNA interference or gene silencing may be a new way to treat Huntingtons disease. Short pieces of double-stranded RNA (short, interfering RNAs or siRNAs) are used by cells to degrade RNA of a particular sequence. If a siRNA is designed to match the RNA copied from a faulty gene, then the abnormal protein product of that gene will not be produced.

2006:

In March 2006 an international group of scientists announced the successful use of gene therapy to treat two adult patients for X-linked chronic granulomatous disease, a disease which affects myeloid cells and which gives a defective immune system. The study, published in Nature Medicine, is believed to be the first to show that gene therapy can cure diseases of the myeloid system. In May 2006 a team of scientists led by Dr. Luigi Naldini and Dr. Brian Brown from the San Raffaele Telethon Institute for Gene Therapy (HSR-TIGET) in Milan, Italy reported a breakthrough for gene therapy in which they developed a way to prevent the immune system from rejecting a newly delivered gene. Similar to organ transplantation, gene therapy has been plagued by the problem of immune rejection. So far, delivery of the normal gene has been difficult because the immune system recognizes the new gene as foreign and rejects the cells carrying it. To overcome this problem, the HSR-TIGET group utilized a newly uncovered network of genes regulated by molecules known as microRNAs. Dr. Naldinis group reasoned that they could use this natural function of microRNA to selectively turn off the identity of their therapeutic gene in cells of the immune system and prevent the gene from being found and destroyed. The researchers injected mice with the gene containing an immune-cell microRNA target sequence, and the mice did not reject the gene, as previously occurred when vectors without the microRNA target sequence were used. This work will have important implications for the treatment of hemophilia and other genetic diseases by gene therapy. In August 2006, scientists at the National Institutes of Health (Bethesda, Maryland) successfully treated metastatic melanoma in two patients using killer T cells genetically retargeted to attack the cancer cells. This study constitutes one of the first demonstrations that gene therapy can be effective in treating cancer. In November 2006 Preston Nix from the University of Pennsylvania School of Medicine reported on VRX496, a gene-based immunotherapy for the treatment of human immunodeficiency virus (HIV) that uses a lentiviral vector for delivery of an antisense gene against the HIV envelope. In the Phase I trial enrolling five subjects with chronic HIV infection who had failed to respond to at least two antiretroviral regimens, a single intravenous infusion of autologous CD4 T cells genetically modified with VRX496 was safe and well tolerated. All patients had stable or decreased viral load; four of the five patients had stable or increased CD4 T cell counts. In addition, all five patients had stable or increased immune response to HIV antigens and other pathogens. This was the first evaluation of a lentiviral vector administered in U.S. Food and Drug Administration-approved human clinical trials for any disease. Data from an ongoing Phase I/II clinical trial were presented at CROI 2009.

2007:

On 1 May 2007 Moorfields Eye Hospital and University College Londons Institute of Ophthalmology announced the worlds first gene therapy trial for inherited retinal disease. The first operation was carried out on a 23 year-old British male, Robert Johnson, in early 2007. Lebers congenital amaurosis is an inherited blinding disease caused by mutations in the RPE65 gene. The results of a small clinical trial in children were published in New England Journal of Medicine in April 2008. They researched the safety of the subretinal delivery of recombinant adeno-associated virus (AAV) carrying RPE65 gene, and found it yielded positive results, with patients having modest increase in vision, and, perhaps more importantly, no apparent side-effects.

2008:

In May 2008, two more groups, one at the University of Florida and another at the University of Pennsylvania, reported positive results in independent clinical trials using gene therapy to treat Lebers congenital amaurosis. In all three clinical trials, patients recovered functional vision without apparent side-effects. These studies, which used adeno-associated virus, have spawned a number of new studies investigating gene therapy for human retinal disease.

2009:

In September 2009, the journal Nature reported that researchers at the University of Washington and University of Florida were able to give trichromatic vision to squirrel monkeys using gene therapy, a hopeful precursor to a treatment for color blindness in humans. In November 2009, the journal Science reported that researchers succeeded at halting a fatal genetic disorder called adrenoleukodystrophy in two children using a lentivirus vector to deliver a functioning version of ABCD1, the gene that is mutated in the disorder.

2010:

A paper by Komromy et al. published in April 2010, deals with gene therapy for a form of achromatopsia in dogs. Achromatopsia, or complete color blindness, is presented as an ideal model to develop gene therapy directed to cone photoreceptors. Cone function and day vision have been restored for at least 33 months in two young dogs with achromatopsia. However, the therapy was less efficient for older dogs. In September 2010, it was announced that an 18 year old male patient in France with beta-thalassemia major had been successfully treated with gene therapy. Beta-thalassemia major is an inherited blood disease in which beta haemoglobin is missing and patients are dependent on regular lifelong blood transfusions. A team directed by Dr. Phillipe Leboulch (of the University of Paris, Bluebird Bio and Harvard Medical School) used a lentiviral vector to transduce the human -globin gene into purified blood and marrow cells obtained from the patient in June 2007. The patients haemoglobin levels were stable at 9 to 10 g/dL, about a third of the hemoglobin contained the form introduced by the viral vector and blood transfusions had not been needed. Further clinical trials were planned. Bone marrow transplants are the only cure for thalassemia but 75% of patients are unable to find a matching bone marrow donor.

2011:

In 2007 and 2008, a man being treated by Gero Htter was cured of HIV by repeated Hematopoietic stem cell transplantation with double-delta-32 mutation which disables the CCR5 receptor; this cure was not completely accepted by the medical community until 2011. This cure required complete ablation of existing bone marrow which is very debilitating. In August 2011, two of three subjects of a pilot study were confirmed to have been cured from chronic lymphocytic leukemia (CLL). The study carried out by the researchers at the University of Pennsylvania used genetically modified T cells to attack cells that expressed the CD19 protein to fight the disease. In 2013, the researchers announced that 26 of 59 patients had achieved complete remission and the original patient had remained tumor-free. Human HGF plasmid DNA therapy of cardiomyocytes is being examined as a potential treatment for coronary artery disease as well as treatment for the damage that occurs to the heart after myocardial infarction.

2012:

The FDA approves clinical trials of the use of gene therapy on thalassemia major patients in the US. Researchers at Memorial Sloan Kettering Cancer Center in New York begin to recruit 10 participants for the study in July 2012. The study is expected to end in 2014. In July 2012, the European Medicines Agency recommended approval of a gene therapy treatment for the first time in either Europe or the United States. The treatment, called Alipogene tiparvovec (Glybera), compensates for lipoprotein lipase deficiency (LPLD), which can cause severe pancreatitis. People with LPLD cannot break down fat, and must manage their disease with a restricted diet. However, dietary management is difficult, and a high proportion of patients suffer life-threatening pancreatitis. The recommendation was endorsed by the European Commission in November 2012 and commercial rollout is expected in late 2013. In December 2012, it was reported that 10 of 13 patients with multiple myeloma were in remission or very close to it three months after being injected with a treatment involving genetically engineered T cells to target proteins NY-ESO-1 and LAGE-1 which exist only on cancerous myeloma cells.

2013:

In March 2013, Researchers at the Memorial Sloan-Kettering Cancer Center in New York, reported that three of five subjects who had acute lymphocytic leukemia (ALL) had been in remission for five months to two years after being treated with genetically modified T cells which attacked cells with CD19 genes on their surface, i.e. all B-cells, cancerous or not. The researchers believed that the patients immune systems would make normal T-cells and B-cells after a couple of months however they were given bone marrow to make sure. One patient had relapsed and died and one had died of a blood clot unrelated to the disease. Following encouraging Phase 1 trials, in April 2013, researchers in the UK and the US announced they were starting Phase 2 clinical trials (called CUPID2 and SERCA-LVAD) on 250 patients at several hospitals in the US and Europe to use gene therapy to combat heart disease. These trials were designed to increase the levels of SERCA2a protein in the heart muscles and improve the function of these muscles. The FDA granted this a Breakthrough Therapy Designation which would speed up the trial and approval process in the USA. In July 2013 the Italian San Raffaele Telethon Institute for Gene Therapy (HSR-TIGET) reported that six children with two severe hereditary diseases had been treated with a partially deactivated lentivirus to replace a faulty gene and after 732 months the results were promising. Three of the children had metachromatic leukodystrophy which causes children to lose cognitive and motor skills. The other children had Wiskott-Aldrich syndrome which leaves them to open to infection, autoimmune diseases and cancer due to a faulty immune system. In October 2013, the Great Ormond Street Hospital, London reported that two children born with adenosine deaminase severe combined immunodeficiency disease (ADA-SCID) had been treated with genetically engineered stem cells 18 months previously and their immune systems were showing signs of full recovery. Another three children treated since then were also making good progress. ADA-SCID children have no functioning immune system and are sometimes known as bubble children. In October 2013, Amit Nathswani of the Royal Free London NHS Foundation Trust in London reported that they had treated six people with haemophilia in early 2011 using genetically engineered adeno-associated virus. Over two years later all six were still producing blood plasma clotting factor.

2014:

In January 2014, researchers at the University of Oxford reported that six people suffering from choroideremia had been treated with a genetically engineered adeno-associated virus with a copy of a gene REP1. Over a six month to two year period all had improved their sight. Choroideremia is an inherited genetic eye disease for which in the past there has been no treatment and patients eventually go blind. In March 2014 researchers at the University of Pennsylvania reported that 12 patients with HIV had been treated since 2009 in a trial with a genetically engineered virus with a rare mutation known to protect against HIV (CCR5 deficiency). Results were promising.

_

The three main issues for the coming decade will be public perceptions, scale-up and manufacturing, and commercial considerations. Focusing on single-gene applications, which tend to be rarer diseases, will produce successful results sooner than the current focus on the commoner, yet more complex, cancer and heart diseases.

______

What is Gene?

A gene is an important unit of hereditary information. It provides the code for living organisms traits, characteristics, function, and physical development. Each person has around 25,000 genes that are located on 46 chromosomes. Gene is a segment of DNA found on chromosome that codes for a particular protein. It acts as a blue print for making enzymes and other proteins for every biochemical reaction and structure of body.

What is allele?

Alleles are two or more alternative forms of a gene that can occupy a specific locus (location) on a chromosome.

What is DNA?

Deoxyribonucleic acid (DNA) is a nucleic acid that contains the genetic information used in the development and function of all known living organisms. The main role of DNA is the long-term storage of information. DNA is often compared to a set of blueprints or a recipe or code, since it contains the instructions needed to construct other components of cells, such as proteins. The DNA segments that carry this genetic information are called genes.

What are Chromosomes?

A chromosome is a singular piece of DNA, which contains many genes. Chromosomes also contain DNA-bound proteins, which serve to package the DNA and control its functions. Chromosomes are found inside the nucleus of cells.

What are Proteins?

Proteins are large organic compounds made of amino acids. They are involved in many processes within cells. Proteins act as building blocks, or function as enzymes and are important in communication among cells.

_

What are plasmids?

_

_

Plasmid is any extrachromosomal heritable determinant. Plasmids are fragments of double-stranded DNA that can replicate independently of chromosomal DNA, and usually carry genes. Although they can be found in Bacteria, Archaea and Eukaryotes, they play the most significant biological role in bacteria where they can be passed from one bacterium to another by horizontal gene transfer, usually providing a context-dependent selective advantage, such as antibiotic resistance.

_

In the center of every cell in your body is a region called the nucleus. The nucleus contains your DNA which is the genetic code you inherited from each of your parents. The DNA is ribbon-like in structure, but normally exists in a condensed form called chromosomes. You have 46 chromosomes (23 from each parent), which are in turn comprised of thousands of genes. These genes encode instructions on how to make proteins. Proteins make up the majority of a cells structure and perform most life functions. Genes tell cells how to work, control our growth and development, and determine what we look like and how our bodies work. They also play a role in the repair of damaged cells and tissues. Each person has more than 25,000 genes, which are made up of DNA. You have 2 copies of every gene, 1 inherited from your mother and 1 from your father.

_

_

DNA or deoxyribonucleic acid is the very long molecule that encodes the genetic information. A gene is a stretch of DNA required to make a functional product such as part or all of a protein. People have about 25,000 genes. During gene therapy, DNA that codes for specific genes is delivered to individual cells in the body.

_

The Human Genome:

The human genome is the entire genetic code that resides in every cell in your body (with the exception of red blood cells). The genome is divided into 23 chromosome pairs. During reproduction, two copies of the chromosomes (one from each parent) are passed onto the offspring. While most chromosomes are identical for males and females, the exceptions are the sex chromosomes (known as the X and Y chromosomes). Each chromosome contains thousands of individual genes. These genes can be further divided into sequences called exons and introns, which are in turn made up of even shorter sequences called codons. And finally, the codons are made up of base pairs, combinations of four bases: adenine, cytosine, thymine, and guanine. Or A, C, T, and G for short. The human genome is vast, containing an estimated 3.2 billion base pairs. To put that in perspective, if the genome was a book, it would be hundreds of thousands of pages long. Thats enough room for a dozen copies of the entire Encyclopaedia Britannica, and all of it fits inside a microscopic cell.

_

_

Our genes help make us unique. Inherited from our parents, they go far in determining our physical traits like eye color and the color and texture of our hair. They also determine things like whether babies will be male or female, the amount of oxygen blood can carry, and the likelihood of getting certain diseases. Scientists believe that every human has about 25,000 genes per cell. A mutation, or change, in any one of these genes can result in a disease, physical disability, or shortened life span. These mutations can be passed from one generation to another, inherited just like a mothers curly hair or a fathers brown eyes. Mutations also can occur spontaneously in some cases, without having been passed on by a parent. With gene therapy, the treatment or elimination of inherited diseases or physical conditions due to these mutations could become a reality. Gene therapy involves the manipulation of genes to fight or prevent diseases. Put simply, it introduces a good gene into a person who has a disease caused by a bad gene. Variations on genes are known as alleles. Because of changes in the genetic code caused by mutations, there are often more than one type of gene in the gene pool. For example, there is a specific gene to determine a persons blood type. Therefore, a person with blood type A will have a different version of that gene than a person with blood type B. Some genes work in tandem with each other.

_

Genes to protein:

Chromosomes contain long chains of DNA built with repeating subunits known as nucleotides. That means a single gene is a finite stretch of DNA with a specific sequence of nucleotides. Those nucleotides act as a blueprint for a specific protein, which gets assembled in a cell using a multistep process.

1. The first step, known as transcription, begins when a DNA molecule unzips and serves as a template to create a single strand of complementary messenger RNA.

2. The messenger RNA then travels out of the nucleus and into the cytoplasm, where it attaches to a structure called the ribosome.

3. There, the genetic code stored in the messenger RNA, which itself reflects the code in the DNA, determines a precise sequence of amino acids. This step is known as translation, and it results in a long chain of amino acids a protein.

Proteins are the workhorses of cells. They help build the physical infrastructure, but they also control and regulate important metabolic pathways. If a gene malfunctions if, say, its sequence of nucleotides gets scrambled then its corresponding protein wont be made or wont be made correctly. Biologists call this a mutation, and mutations can lead to all sorts of problems, such as cancer and phenylketonuria. Gene therapy tries to restore or replace a defective gene, bringing back a cells ability to make a missing protein.

_

Length measurements of DNA/RNA:

The following abbreviations are commonly used to describe the length of a DNA/RNA molecule:

bp = base pair(s) one bp corresponds to approximately 3.4 (340 pm) of length along the strand, or to roughly 618 or 643 daltons for DNA and RNA respectively.

kb (= kbp) = kilo base pairs = 1,000 bp

Mb = mega base pairs = 1,000,000 bp

Gb = giga base pairs = 1,000,000,000 bp.

For case of single-stranded DNA/RNA units of nucleotides are used, abbreviated nt (or knt, Mnt, Gnt), as they are not paired.

Note:

Please do not confuse these terms with computer data units.

kb in molecular biology is kilobase pairs = 1000 base pairs

kb in computer data is kilobytes = 1000 bytes

_

Read this article:
Dr Rajiv Desai Blog Archive GENE THERAPY

Every year, more than 10,000 people in the U.S. sustain a spinal cord injury (SCI). An SCI changes a persons life in an instant, creating new challenges for everyday life. Paralyzed Veterans of America membership offers resources and benefits to meet the needs of veterans who have sustained these injuries.

Explore our resources below about spinal cord injury, andtalk to us if you need help understanding and selecting treatment options.

When a person sustains an SCI, the communication between the brain and other parts of the body is disrupted, and messages no longer flow past the damaged area. The extent of the communication breakdown is dependent on both the severity and location of the injury. The human spinal cord is a bundle of nerve cells and fibers approximately 17 inches long that extends from the brain to the lower back. The spinal cord carries messages from the brain to all parts of the body and receives incoming messages from the body as well.

The nerves that lie only within the spinal cord itself are called upper motor neurons (UMNs). These run only between the brain and the spinal nerves. The spinal nerves branch out from the spinal cord into the tissues of the body. Spinal nerves are also called lower motor neurons (LMNs). In movement, the brain sends messages through the spinal cord (UMNs) to the spinal nerves (LMNs). The LMNs then carry these messages to the muscles to coordinate complicated movements such as walking. In this way, the brain can influence movement.

Most spinal injuries damage both UMNs and LMNs. A complete injury cuts or squeezes all the UMNs running down the spinal cord. In a UMN injury, control by the brain no longer exists because messages from the brain cant get through the point of injury. The LMNs act by themselves, causing reflexes without limit. One example is spasticity. Spasticity is the uncontrolled movement of the arms or legs. LMN injuries are a different story. This kind of injury is found, for the most part, at the lower tip of the spinal cord, or the cauda equina.

Spasticity is not found in LMN injuries as it is in UMN injuries, because muscles governed by these LMNs tend to shrink or atrophy. Stated simply, a UMN injury is one where the UMN pathway is broken, and the LMNs below the injury are intact and spasticity is noted. An LMN injury, usually at the cauda equina, abolishes nerve contact with muscles controlled below the injury and no spasticity develops.

There are many causes of these injuries, which can be traumatic or non-traumatic. Traumatic injuries include injuries sustained in military service, auto accidents, falls, sports injuries,or violence. Non-traumatic injuries may be caused by arthritis, cancer, infections, or disk degeneration of the spine.

Spinal cord injuries can occur at any level of the spinal cord, and the level of the injury will dictate which bodily functions are altered or lost. Damage to the spinal cord can cause changes in movement, feeling, bladder control, or other bodily functions. How many changes there are depends on where the spinal cord was injured and how severely the spinal cord was injured.

Immediately after a spinal cord injury, the spinal cord stops doing its job for a period of time called spinal shock. The return of reflexes below the level of injury marks the end of spinal shock. At this time, a doctor can determine if the injury is complete or incomplete. If the injury is incomplete, some feelings and movement may come back.

Rehabilitation begins immediately. The individual will be instructed in strengthening exercises, new styles of movement, and the use of special equipment. If additional recovery of feeling or movement does not occur, a rehabilitation team will help the individual to develop new goals.

View post:
Spinal Cord Injury Information - Paralyzed Veterans of America

Contents Spinal Cord Injury Overview

A spinal cord injury (SCI) is caused by damage or trauma to the spinal cord that results in a loss or impaired function causing reduced mobility or sensation.

Common causes of damage to the spinal cord are:

The spinal cord does not have to be severed in order for a loss of function to occur. In most people with SCI the spinal cord is intact, but the cellular damage resulting from compression or inflammation results in the loss of function. An SCI is very different from back injuries such as ruptured disks, spinal stenosis or pinched nerves. The later involves musculoskeletal and peripheral nerve changes where as a spinal cord injury involves damage to the central nervous system.

It is possible for a person to "break their back or neck" yet not sustain a spinal cord injury as long as only the bones (the vertebrae) around the spinal cord are damaged, but the spinal cord is not affected. In such cases the person may not experience paralysis after the affected vertebrae are stabilised. Fractured vertebrae and dislocated vertebrae can be stabilised using surgical management such as traction, vertebral fusion, fixation using titanium plates or rods and for less severe fractures of the vertebra bed rest.

The spinal cord is the major bundle of tightly compacted nerves contained within the vertebral column that carry nerve impulses to and from the brain throughout the body. The brain and the spinal cord constitute the central nervous system. Motor and sensory nerves outside the central nervous system constitute the peripheral nervous system, and another system of nerves that control involuntary functions such as blood pressure and temperature regulation are the sympathetic and parasympathetic nervous systems.

The spinal cord is about 18 inches in length and extends from the base of the brain vertically downwards through the middle of the spinal column to around the waist. The pathways that are situated within the spinal cord are called upper motor neurons (UMN's). Their function is to carry messages back and forth from the brain along spinal tracts within the spinal cord responsible for specific functions. The spinal nerves that branch out from the spinal cord to parts of the body are peripheral nerves called lower motor neurons (LMN's). These spinal nerves exit and enter between each vertebra and communicate with specific areas of the body. The sensory portions of the LMN carry messages about sensation from the skin and muscles such as pain, temperature, joint position and information from organs to the spinal cord and upwards via ascending spinal tracts to the brain. The motor portions of the LMN receive messages from the brain via descending tracts in the spinal cord to initiate actions such as muscle movement, gland functions and certain internal organ commands.

The spinal cord is surrounded by a hollow column of bones called vertebrae. These bones constitute the spinal column (back bones and neck bones). Generally the higher in the spinal column the spinal cord injury occurs, the more physical impairment a person will experience resulting in an increased level of paralysis. The vertebra are named according to their location. The seven vertebrae in the neck are called the cervical vertebrae. The top vertebra is called C1 or atlas vertebra and connects the top of the spinal column to the skull. The bottom cervical vertebra is called C7. Cervical SCI's usually result in loss of function in the arms and legs resulting in tetraplegia which is also referred to as quadriplegia. The next twelve vertebra are called the thoracic vertebra, T1-T12. The first thoracic vertebra T1 is the vertebra where the top rib attaches. There are 5 lumbar vertebrae, one fused sacral vertebra and one fused coccygeal vertebra.

So to recap, the five sections of the vertebral column are:

An injury to the spinal cord segments contained within the cervical spinal vertebrae C1-C7 usually result in paralysis of all four limbs to some degree resulting in tetraplegia (quadriplegia). Injuries in the thoracic region usually affect the chest and the legs and result in paraplegia. The vertebra in the lower back between the thoracic vertebra where the ribs attach and the pelvis are the lumbar vertebra. The sacral vertebra run from the pelvis to the end of the spinal column. Injuries to the five lumbar vertebra (L1 thru L5) and similarly to the five sacral vertebra (S1 thru S5) generally result in varying loss of function in the hips, legs, bladder, bowel and sexual function.

The spinal cord ends between L1-L2 where a mass of spinal nerves continue downwards inside the lumbar (L2-L5) and sacral (S1-S2) vertebrae. This mass of spinal nerves is referred to as the cauda equina and damage to these nerve roots is referred to as cauda equina syndrome.

The effects of SCI depend on the type of injury and the level of the injury. SCI can be divided into two types of injury: complete and incomplete. A complete injury results in no function below the level of neurological injury: no sensation and no voluntary movement. Both sides of the body are equally affected. An incomplete injury results in some preserved function below the level of neurological injury. A person with an incomplete injury may be able to move one limb more than another, may be able to feel parts of the body that cannot be moved, or may have more function on one side of the body than the other.

Types of incomplete spinal cord injury are:

With the recent advances in medical intervention and treatment of acute SCI, incomplete injuries are becoming more common. The most frequent spinal cord injury neurological classifications at time of discharge (2014) from a spinal injury centre is incomplete tetraplegia (31.6%), followed by incomplete paraplegia (18.6%), complete paraplegia (24.6%) and complete tetraplegia (19.3%). It is estimated that less than 1% of individuals diagnosed with a spinal cord injury experienced a complete neurological recovery at the time of hospital discharge. Over the last 20 years, the incidence of individuals with incomplete tetraplegia has increased whilst complete paraplegia and complete tetraplegia have decreased.

The level of injury is very helpful in predicting what parts of the body might be affected by paralysis resulting in loss of function. Remember that in incomplete injuries there can be a wide variation in the prognoses.

Cervical (neck) injuries usually result in Quadriplegia/Tetraplegia. Injuries to the spinal cord segments above the C4 level (C1,C2, C3) may result in the need of breathing aids such as mechanical ventilators or diaphragm pacemakers. Diaphragm pacemaker devices may be required to stimulate the phrenic nerve to initiate a persons breathing due to weak innervation of the diaphragm. C5 injuries often result in shoulder (deltoid) and biceps control, but no control of the wrist or hand. C6 injuries generally yield wrist control (wrist extensors), but no finger hand function. Individuals with C7-T1 injuries can straighten their arms (triceps) but still may have dexterity problems with the hand and fingers.

It is interesting to note that in the cervical area of the spine the nerve roots exit the spinal column above the vertebra, except for C7 where a pair of nerve roots also exit both above and below the vertebra. This is why there are seven cervical vertebrae but eight pairs of cervical nerve roots, C1-C8. From T1 downwards all spinal nerves then exit the spinal column below the vertebrae.

Injuries at the thoracic level and below result in paraplegia, with the hands not affected. At T1 to T8 whilst there is good control of the hands, trunk control may vary as the result of lack of abdominal muscle control. Lower thoracic injuries (T9 to T12) allow good truck control and good abdominal muscle control. Sitting balance is very good. Lumbar and sacral injuries yield decreasing control of the hip flexors and legs.

To reference the spinal segments discussed above, the 5 spinal segments are:

Sources

The above information has been written with reference from the following sources: https://www.nscisc.uab.edu/ Sekhon, Lali H.S.; Fehlings, Michael G. (2001). "Epidemiology, Demographics, and Pathophysiology of Acute Spinal Cord Injury". Spine 26 (24 Suppl): S212. doi:10.1097/00007632-200112151-00002. PMID11805601. Alexander Vaccaro; Michael Fehlings (2010). Spine and Spinal Cord Trauma: Evidence-Based Management. Thieme Publishers. ISBN9781604062229. Retrieved 2012-05-06.

Updated: May 2014

Showing the difference between spinal cord injury levels and the difference between tetraplegia (quadriplegia) and paraplegia. Note that there are seven cervical vertebrae, but eight pairs of cervical nerve roots due to how nerve roots exit the cervical vertebrae.

Any medical treatments or therapies discussed on this website should be reviewed by a medical professional before being acted upon.

View post:
What is a Spinal Cord Injury? - Apparelyzed

JavaScript must be enabled to use this site. Please enable JavaScript in your browser and refresh the page

Value Price: $18.75

Value Price: $17.79

Value Price: $22.49

Value Price: $22.50

Value Price: $25.99

Value Price: $34.99

Value Price: $34.99

Value Price: $17.99

Value Price: $8.99

Value Price: $15.49

Value Price: $23.49

Value Price: $16.99

Sale Price: $35.99

Value Price: $18.99

Value Price: $17.99

Value Price: $12.49

Value Price: $24.99

Value Price: $24.99

Value Price: $54.99

Value Price: $12.99

Value Price: $19.99

Value Price: $10.99

Value Price: $31.99

Value Price: $24.99

Value Price: $28.50

Value Price: $14.99

Value Price: $19.99

Value Price: $22.49

Value Price: $9.99

Value Price: $19.99

Sale Price: $54.49

Value Price: $27.00

Value Price: $15.99

Value Price: $17.99

Value Price: $21.99

Value Price: $29.99

Value Price: $44.49

Value Price: $22.50

Value Price: $59.99

Value Price: $31.99

Value Price: $10.99

Value Price: $17.99

Value Price: $29.99

Value Price: $25.99

Value Price: $42.49

Value Price: $24.99

Value Price: $30.99

Value Price: $21.99

Value Price: $56.49

Value Price: $12.99

Value Price: $45.99

Value Price: $22.99

Value Price: $35.99

Value Price: $7.99

Value Price: $29.99

Value Price: $57.99

Value Price: $34.49

Value Price: $47.99

Value Price: $10.49

Value Price: $81.99

Value Price: $41.99

Value Price: $17.49

Value Price: $39.99

Value Price: $34.99

Value Price: $17.99

Value Price: $7.45

Value Price: $19.99

Value Price: $28.49

Value Price: $34.99

Value Price: $76.99

Value Price: $23.49

Value Price: $27.99

Value Price: $42.99

Value Price: $30.99

Value Price: $18.99

Value Price: $19.99

Value Price: $20.49

Value Price: $16.99

Value Price: $22.50

Value Price: $33.49

Value Price: $32.99

Value Price: $31.99

Value Price: $14.99

Value Price: $16.99

Value Price: $29.99

Value Price: $12.99

Value Price: $55.99

Value Price: $22.49

Value Price: $23.99

Value Price: $12.99

Value Price: $19.99

View original post here:
Life Extension - Products on Sale, Coupons, Reviews, Free ...

The following is a guest post by Amber Larsen of Massage and Health by Amber Kim:

My body, my face, my features will never be repeated. How I look is not going to mimic the girl next to me in the gym. My body shape will not be the same as another female that I may be slightly jealous of because shes thinner than me. My ass is going to be bigger and there is nothing I can do about it.

My genetics did it.

It's amazing - on average, most women will have about thirteen negative thoughts about their appearance per day. If you break it down, it means that every waking hour we think negatively about ourselves. I cant lie; I know I have done the same. My ass is too big, my abs stick out, my latissimus dorsi is getting a bit too big because my bras are cutting into my skin (CrossFit did it).

According to cognitive behavioral psychology, the self-hate is called withdrawal emotions. These emotions make us want to withdraw from situations or things that are linked to the emotions that are causing us to feel this way. Essentially, you can say you can be withdrawing from yourself. This can cause us to either make drastic decisions, such as not to eat, or do things that can do us harm, or do the opposite - not take care of ourselves because we ask whats the use? I hope in writing this it can shed some light as to why you body looks the way it does, and how to embrace that you are unique and to work with your genetics.

What exactly is genetics? Genetics is a wide domain, but in short it is the study of heredity, more specifically the characteristics we inherit from our parents. Our appearance, abilities, susceptibility to disease, and even life span is influenced by heredity. That is just skimming the surface of genetics, but an overall view is that your body shape and your abilities in the gym are inherited from your parents. So what does that say about my personal body? My lower half will always be bigger because it is inherited from my father side. My upper body will always be a wee bit smaller because its inherited from my mothers side. The bottom line is, ladies, I will never weigh 110 pounds. Its not in my genetics, and you know what? Im okay with that.

Many times the media portrays an ideal size for a woman, but you know what? For a healthy woman who eats correctly and exercises on a regular basis there is no ideal size. The reason is because genetically we are all different. There is nothing wrong with a woman who has a leaner, thinner body, because she may be genetically predisposed to having a leaner frame. There is also nothing wrong with a woman who tends to be stronger looking with a larger frame for the same reason. Both body images are different, but both are ideal based on each individual womans inherited genetics.

Is your view on your body slowly changing?

So take a good look at my body (yes this is more difficult for me then you think). This photo is from 2012 and this is me at 140 pounds. If you see, my body is a bit stocky, bulky, and (since I am 53) technically overweight. By the way, you can see some of my cellulite and, yes, I did throw away my scale! My abs stick out and so does my ass.

You can see my body is made up of mostly fast-twitch muscle fibers, or type II muscle fibers. My muscles are different in that they contain a higher number of glycolytic enzymes, which means my muscles do very well anaerobically. Also, my body can be viewed as a bit of a subtype of fast twitch muscles in that I am efficient in strength movements and halfway decent at aerobic movements (not the best though). My body is adaptable with endurance training, but it will not be my strongest area of fitness. Bottom line, the body you see is genetically predisposed to strength work.

Now, a slow-twitch body will not look exactly like this. A slow-twitch body will be leaner because the muscle fibers tend to be longer. These muscles contain larger amounts of mitochondria and higher concentrations of myoglobin than my own body. Again, slow twitch muscle tissue is an inherited trait.

I am not super skinny (as you can see above), but its important to realize that each body is unique and has strengths and weaknesses. Each body is beautiful in its own right, and its important for all of you to embrace what makes you an individual. There is no ideal weight or look for any woman. Women look different based off of their genetic make up, and thats truly a beautiful thing. Just think - no one will ever look exactly like you. And you have automatically inherited strengths that will help you in your fitness goals.

Embrace the person you are. I know it can be difficult to stop the negative self talk that your body does not look like the skinny Victorias Secret model, but you know what? Maybe you were never meant to look that way based off of your genetic heredity. Maybe you were meant to look strong and maybe you were built for strength, which is beautiful. Even if you are a leaner person who wishes to look stronger, well you can, even with a leaner frame, and you can also embrace that your body allows you to work efficiently aerobically based on your genetic make-up.

The image you have of your body should be positive. No one can be you, and no one can look exactly like you because you are genetically different. There is so much beauty in that. Embrace the genetic make up that make your body unique to those around you. I hope you will not be afraid to wear that bikini this summer or to workout without a shirt on. Your body is beautiful because its uniquely you.

This is my body. I have learned to embrace the body that allows me to do amazing things. I hope you will do the same.

Read more from the original source:
The Female Form: Embrace Your Genetics and Find Beauty in ...

The Tahoma Clinic has a variety of programs for women who are interested in optimizing their health. The programs range from basic gynecological exams, menopausal support, gynecological conditions such as endometriosis and fibroids, to prevention against osteoporosis, Alzheimers, cardiovascular disease, and cancers. Each program is individualized to meet personal needs, as well as address your prior history and family history.

Our most popular program involves evaluation and use of Bio-identical natural hormone replacement therapy. The Tahoma Clinic offers the latest in Bio-identical natural hormone replacement therapy for women in a safe and effective manner. Dr. Jonathan Wright, MD originated the Triest blend of estrogens 25 years ago and is still leading the way today. Dr. Wright currently has two physicians on staff specializing in womens health, and has worked extensively with each of them in Bio-identical natural hormone replacement therapy.

Menopause is a natural process a womans body goes through as she ages. Many different approaches can be taken to help address this change. Diet and lifestyle are always at the core of the program. Vitamins, minerals, and other supplements as necessary are then added to support the foundation. Lastly, the Bio-identical hormones, which look exactly like the hormones you produce in your own body and originate from wild yam or soy, are formulated for you.

As we age, our hormone levels change. For example, as early as 30 years of age, our DHEA levels start declining. At the same time, our Cortisol starts to rise. This combination can result in weight gain, especially around the middle, increasing your risk of cardiovascular disease and insulin resistance. Other symptoms that occur with menopause include:

Each woman experiences these changes to varying degrees. There are many different approaches to managing your symptoms, and we will work with you to find the treatment that best supports your needs. To start, your hormone levels will be evaluated by a 24-hour urinalysis which allows for multiple metabolites to be measured accurately. Then, a physician will work with you to focus on methods to help you balance your hormones safely and effectively for your natural body composition.

Please , pleasecontact usto make an appointment with one of our doctors that specialize in womens health.

Learn more about the physicians at the Tahoma Clinic

See more here:
Bio-Identical Hormones & Women's Services at Dr. Wright's ...

Renal cell carcinoma (RCC, also known as hypernephroma, Grawitz tumor, renal adenocarcinoma) is a kidney cancer that originates in the lining of the proximal convoluted tubule, a part of the very small tubes in the kidney that transport waste molecules from the blood to the urine. RCC is the most common type of kidney cancer in adults, responsible for approximately 90-95% of cases.[1] Initial treatment is most commonly either partial or complete removal of the affected kidney(s) and remains the mainstay of curative treatment.[2] Where the cancer has not metastasised (spread to other organs) or burrowed deeper into the tissues of the kidney the 5-year survival rate is 65-90%,[3] but this is lowered considerably when the cancer has spread. It is relatively resistant to radiation therapy and chemotherapy, although some cases respond to targeted therapies such as sunitinib, temsirolimus, bevacizumab, interferon alfa and sorafenib which have improved the outlook for RCC.[4]

The body is remarkably good at hiding the symptoms and as a result people with RCC often have advanced disease by the time it is discovered.[5] The initial symptoms of RCC often include: blood in the urine (occurring in 40% of affected persons at the time they first seek medical attention), flank pain (40%), a mass in the abdomen or flank (25%), weight loss (33%), fever (20%), high blood pressure (20%), night sweats and generally feeling unwell.[1] RCC is also associated with a number of paraneoplastic syndromes (PNS) which are conditions caused by either the hormones produced by the tumour or by the body's attack on the tumour and are present in about 20% of those with RCC.[1] These syndromes most commonly affect tissues which have not been invaded by the cancer.[1] The most common PNSs seen in people with RCC are: anaemia (due to an underproduction of the hormone, erythropoietin), high blood calcium levels, polycythaemia (the opposite to anaemia, due to an overproduction of erythropoietin), thrombocytosis (too many platelets in the blood, leading to an increased tendency for blood clots and bleeds) and secondary amyloidosis.[6] When RCC metastasises it most commonly spreads to the lymph nodes, lungs, liver, adrenal glands, brain or bones.[6]

Historically, medical practitioners expected a person to present with three findings. This classic triad[7] is 1: haematuria, which is when there is blood present in the urine, 2: flank pain, which is pain on the side of the body between the hip and ribs, and 3: an abdominal mass, similar to bloating but larger. It is now known that this classic triad of symptoms only occurs in 10-15% of cases, and is usually indicative that the renal cell carcinoma (RCC) in an advanced stage.[7] Today, RCC is often asymptomatic (meaning little to no symptoms) and is generally detected incidentally when a person is being examined for other ailments.[8]

Other signs and symptom may include haematuria;[7] loin pain;[7] abdominal mass;[8]malaise, which is a general feeling of feeling unwell;[8] weight loss and/or loss of appetite;[9]anaemia resulting from depression of erythropoietin;[7]erythrocytosis (increased production of red blood cells) due to increased erythropoietin secretion;[7]varicocele, which is seen in males as an enlargement of the tissue at the testicle (more often the left testicle)[8]hypertension (high blood pressure) resulting from secretion of renin by the tumour;[10]hypercalcemia, which is elevation of calcium levels in the blood;[11] sleep disturbance or night sweats;[9] recurrent fevers;[9] and chronic fatigue.[12]

The greatest risk factors for RCC are lifestyle-related; smoking, obesity and hypertension (high blood pressure) have been estimated to account for up to 50% of cases.[13] Occupational exposure to some chemicals such as asbestos, cadmium, lead, chlorinated solvents, petrochemicals and PAH (polycyclic aromatic hydrocarbon) has been examined by multiple studies with inconclusive results.[14][15][16] Another suspected risk factor is the long term use of non-steroidal anti-inflammatory drugs (NSAIDS).[17]

Finally, studies have found that women who have had a hysterectomy are at more than double the risk of developing RCC than those who have not.[18] The reason for this remains unclear.

Hereditary factors have a minor impact on individual susceptibility with immediate relatives of people with RCC having a two to fourfold increased risk of developing the condition.[19] Other genetically linked conditions also increase the risk of RCC, including hereditary papillary renal carcinoma, hereditary leiomyomatosis, Birt-Hogg-Dube syndrome, hyperparathyroidism-jaw tumor syndrome, familial papillary thyroid carcinoma, von Hippel-Lindau disease[20] and sickle cell disease.[21]

The most significant disease affecting risk however is not genetically linked patients with acquired cystic disease of the kidney requiring dialysis are 30 times greater more likely than the general population to develop RCC.[22]

The tumour arises from the cells of the proximal renal tubular epithelium.[1] It is considered an adenocarcinoma.[6] There are two subtypes: sporadic (that is, non-hereditary) and hereditary.[1] Both such subtypes are associated with mutations in the short-arm of chromosome 3, with the implicated genes being either tumour suppressor genes (VHL and TSC) or oncogenes (like c-Met).[1]

The first steps taken to diagnose this condition are consideration of the signs and symptoms, and a medical history (the detailed medical review of past health state) to evaluate any risk factors. Based on the symptoms presented, a range of biochemical tests (using blood and/or urine samples) may also be considered as part of the screening process to provide sufficient quantitative analysis of any differences in electrolytes, renal and liver function, and blood clotting times.[21] Upon physical examination, palpation of the abdomen may reveal the presence of a mass or an organ enlargement.[23]

Although this disease lacks characterization in the early stages of tumor development, considerations based on diverse clinical manifestations, as well as resistance to radiation and chemotherapy are important. The main diagnostic tools for detecting renal cell carcinoma are ultrasound, computed tomography (CT) scanning and magnetic resonance imaging (MRI) of the kidneys.[24]

Renal cell carcinoma (RCC) is not a single entity, but rather a collection of different types of tumours, each derived from the various parts of the nephron (epithelium or renal tubules) and possessing distinct genetic characteristics, histological features, and, to some extent, clinical phenotypes.[21]

Clear Cell Renal Cell Carcinoma (CCRCC)

Array-based karyotyping can be used to identify characteristic chromosomal aberrations in renal tumors with challenging morphology.[28][29] Array-based karyotyping performs well on paraffin embedded tumours[30] and is amenable to routine clinical use. See also Virtual Karyotype for CLIA certified laboratories offering array-based karyotyping of solid tumours.

The 2004 World Health Organization (WHO) classification of genitourinary tumours recognizes over 40 subtypes of renal neoplasms. Since the publication of the latest iteration of the WHO classification in 2004, several novel renal tumour subtypes have been described:[31]

Laboratory tests are generally conducted when the patient presents with signs and symptoms that may be characteristic of kidney impairment. They are not primarily used to diagnose kidney cancer, due to its asymptomatic nature and are generally found incidentally during tests for other illnesses such as gallbladder disease.[33] In other words, these cancers are not detected usually because they do not cause pain or discomfort when they are discovered. Laboratory analysis can provide an assessment on the overall health of the patient and can provide information in determining the staging and degree of metastasis to other parts of the body (if a renal lesion has been identified) before treatment is given.

The presence of blood in urine is a common presumptive sign of renal cell carcinoma. The haemoglobin of the blood causes the urine to be rusty, brown or red in colour. Alternatively, urinalysis can test for sugar, protein and bacteria which can also serve as indicators for cancer. A complete blood cell count can also provide additional information regarding the severity and spreading of the cancer.[34]

The CBC provides a quantified measure of the different cells in the whole blood sample from the patient. Such cells examined for in this test include red blood cells (erythrocytes), white blood cells (leukocytes) and platelets (thrombocytes). A common sign of renal cell carcinoma is anaemia whereby the patient exhibits deficiency in red blood cells.[35] CBC tests are vital as a screening tool for examination the health of patient prior to surgery. Inconsistencies with platelet counts are also common amongst these cancer patients and further coagulation tests, including Erythrocyte Sedimentation Rate (ESR), Prothrombin Time (PT), Activated Partial Thromboplastin Time (APTT) should be considered.

Blood chemistry tests are conducted if renal cell carcinoma is suspected as cancer has the potential to elevate levels of particular chemicals in blood. For example, liver enzymes such as aspartate aminotransferase [AST] and alanine aminotransferase [ALT] are found to be at abnormally high levels.[36] The staging of the cancer can also be determined by abnormal elevated levels of calcium, which suggests that the cancer may have metastasised to the bones.[37] In this case, a doctor should be prompted for a CT scan. Blood chemistry tests also assess the overall function of the kidneys and can allow the doctor to decide upon further radiological tests.

The characteristic appearance of renal cell carcinoma (RCC) is a solid renal lesion which disturbs the renal contour. It will frequently have an irregular or lobulated margin and may be seen as a lump on the lower pelvic or abdomen region. Traditionally, 85 to 90% of solid renal masses will turn out to be RCC but cystic renal masses may also be due to RCC.[38] However, the advances of diagnostic modalities are able to incidentally diagnose a great proportion of patients with renal lesions that may appear to be small in size and of benign state. Ten percent of RCC will contain calcifications, and some contain macroscopic fat (likely due to invasion and encasement of the perirenal fat.[39] Deciding on the benign or malignant nature of the renal mass on the basis of its localized size is an issue as renal cell carcinoma may also be cystic. As there are several benign cystic renal lesions (simple renal cyst, haemorrhagic renal cyst, multilocular cystic nephroma, polycystic kidney disease), it may occasionally be difficult for the radiologist to differentiate a benign cystic lesion from a malignant one.[40] The Bosniak classification system for cystic renal lesions classifies them into groups that are benign and those that need surgical resection, based on specific imaging features.[41]

The main imaging tests performed in order to identify renal cell carcinoma are pelvic and abdominal CT scans, ultrasound tests of the kidneys (ultrasonography), MRI scans, intravenous pyelogram (IVP) or renal angiography.[42] Among these main diagnostic tests, other radiologic tests such as excretory urography, positron-emission tomography (PET) scanning, ultrasonography, arteriography, venography, and bone scanning can also be used to aid in the evaluation of staging renal masses and to differentiate non-malignant tumours from malignant tumours.

Contrast-enhanced Computed tomography (CT) scanning is a routinely used imaging procedure in determining the stage of the renal cell carcinoma in the abdominal and pelvic regions of the patient. CT scans have the potential to distinguish solid masses from cystic masses and may provide information on the localization, stage or spread of the cancer to other organs of the patient. Key parts of the human body which are examined for metastatic involvement of renal cell carcinoma may include the renal vein, lymph node and the involvement of the inferior vena cava.[43] According to a study conducted by Sauk et al., multidetector CT imaging characteristics have applications in diagnosing patients with clear renal cell carcinoma by depicting the differences of these cells at the cytogenic level.[44]

Ultrasonographic examination can be useful in evaluating questionable asymptomatic kidney tumours and cystic renal lesions if Computed Tomography imaging is inconclusive. This safe and non-invasive radiologic procedure uses high frequency sound waves to generate an interior image of the body on a computer monitor. The image generated by the ultrasound can help diagnose renal cell carcinoma based on the differences of sound reflections on the surface of organs and the abnormal tissue masses. Essentially, ultrasound tests can determine whether the composition of the kidney mass is mainly solid or filled with fluid.[42]

A Percutaneous biopsy can be performed by a radiologist using ultrasound or computed tomography to guide sampling of the tumour for the purpose of diagnosis by pathology. However this is not routinely performed because when the typical imaging features of renal cell carcinoma are present, the possibility of an incorrectly negative result together with the risk of a medical complication to the patient may make it unfavourable from a risk-benefit perspective.[11] However, biopsy tests for molecular analysis to distinguish benign from malignant renal tumours is of investigative interest.[11]

Magnetic Resonance Imaging (MRI) scans provide an image of the soft tissues in the body using radio waves and strong magnets. MRI can be used instead of CT if the patient exhibits an allergy to the contrast media administered for the test.[45][46] Sometimes prior to the MRI scan, an intravenous injection of a contrasting material called gadolinium is given to allow for a more detailed image. Patients on dialysis or those who have renal insufficiency should avoid this contrasting material as it may induce a rare, yet severe, side effect known as nephrogenic systemic fibrosis.[47] A bone scan or brain imaging is not routinely performed unless signs or symptoms suggest potential metastatic involvement of these areas. MRI scans should also be considered to evaluate tumour extension which has grown in major blood vessels, including the vena cava, in the abdomen. MRI can be used to observe the possible spread of cancer to the brain or spinal cord should the patient present symptoms that suggest this might be the case.

Intravenous pyelogram (IVP) is a useful procedure in detecting the presence of abnormal renal mass in the urinary tract. This procedure involves the injection of a contrasting dye into the arm of the patient. The dye travels from the blood stream and into the kidneys which in time, passes into the kidneys and bladder. This test is not necessary if a CT or MRI scan has been conducted.[48]

Renal angiography uses the same principle as IVP, as this type of X-ray also uses a contrasting dye. This radiologic test is important in diagnosing renal cell carcinoma as an aid for examining blood vessels in the kidneys. This diagnostic test relies on the contrasting agent which is injected in the renal artery to be absorbed by the cancerous cells.[49] The contrasting dye provides a clearer outline of abnormally-oriented blood vessels believed to be involved with the tumour. This is imperative for surgeons as it allows the patients blood vessels to be mapped prior to operation.[43]

The staging of renal cell carcinoma is the most important factor in predicting its prognosis.[50] Staging can follow the TNM staging system, where the size and extent of the tumour (T), involvement of lymph nodes (N) and metastases (M) are classified separately. Also, it can use overall stage grouping into stage I-IV, with the 1997 revision of AJCC described below:[50]

At diagnosis, 30% of renal cell carcinomas have spread to the ipsilateral renal vein, and 5-10% have continued into the inferior vena cava.[51]

The gross and microscopic appearance of renal cell carcinomas is highly variable. The renal cell carcinoma may present reddened areas where blood vessels have bled, and cysts containing watery fluids.[52] The body of the tumour shows large blood vessels that have walls composed of cancerous cells. Gross examination often shows a yellowish, multilobulated tumor in the renal cortex, which frequently contains zones of necrosis, haemorrhage and scarring. In a microscopic context, there are four major histologic subtypes of renal cell cancer: clear cell (conventional RCC, 75%), papillary (15%), chromophobic (5%), and collecting duct (2%). Sarcomatoid changes (morphology and patterns of IHC that mimic sarcoma, spindle cells) can be observed within any RCC subtype and are associated with more aggressive clinical course and worse prognosis. Under light microscopy, these tumour cells can exhibit papillae, tubules or nests, and are quite large, atypical, and polygonal.

Recent studies have brought attention to the close association of the type of cancerous cells to the aggressiveness of the condition. Some studies suggest that these cancerous cells accumulate glycogen and lipids, their cytoplasm appear "clear", the nuclei remain in the middle of the cells, and the cellular membrane is evident.[53] Some cells may be smaller, with eosinophilic cytoplasm, resembling normal tubular cells. The stroma is reduced, but well vascularised. The tumour compresses the surrounding parenchyma, producing a pseudocapsule.[54]

The most common cell type exhibited by renal cell carcinoma is the clear cell, which is named by the dissolving of the cells' high lipid content in the cytoplasm. The clear cells are thought to be the least likely to spread and usually respond more favourably to treatment. However, most of the tumours contain a mixture of cells. The most aggressive stage of renal cancer is believed to be the one in which the tumour is mixed, containing both clear and granular cells.[55]

The recommended histologic grading schema for RCC is the Fuhrman system (1982), which is an assessment based on the microscopic morphology of a neoplasm with haematoxylin and eosin (H&E staining). This system categorises renal cell carcinoma with grades 1, 2, 3, 4 based on nuclear characteristics. The details of the Fuhrman grading system for RCC are shown below:[56]

Nuclear grade is believed to be one of the most imperative prognostic factors in patients with renal cell carcinoma.[21] However, a study by Delahunt et al. (2007) has shown that the Fuhrman grading is ideal for clear cell carcinoma but may not be appropriate for chromophobe renal cell carcinomas and that the staging of cancer (accomplished by CT scan) is a more favourable predictor of the prognosis of this disease.[57] In relation to renal cancer staging, the Heidelberg classification system of renal tumours was introduced in 1976 as a means of more completely correlating the histopathological features with the identified genetic defects.[58]

The type of treatment depends on multiple factors and the individual, some of which include:[7][59]

Every form of treatment has both risks and benefits; a health care professional will provide the best options that suit the individual circumstances.

Active surveillance or "watchful waiting" is becoming more common as small renal masses or tumours are being detected and also within the older generation when surgery is not always suitable.[60] Active surveillance involves completing various diagnostic procedures, tests and imaging to monitor the progression of the RCC before embarking on a more high risk treatment option like surgery.[60] In the elderly, patients with co-morbidities, and in poor surgical candidates, this is especially useful.

Different procedures may be most appropriate, depending on circumstances.

Radical nephrectomy is the removal of the entire affected kidney including Gerota's fascia, the adrenal gland which is on the same side as the affected kidney, and the regional lymph nodes, all at the same time.[7] This method, although severe, is effective. But it is not always appropriate, as it is a major surgery that contains the risk of complication both during and after the surgery and can have a longer recovery time.[61] It is important to note that the other kidney must be fully functional, and this technique is most often used when there is a large tumour present in only one kidney.

Nephron-sparing partial nephrectomy is used when the tumor is small (less than 4cm in diameter) or when the patient has other medical concerns such as diabetes or hypertension.[7] The partial nephrectomy involves the removal of the affected tissue only, sparing the rest of the kidney, Gerota's fascia and the regional lymph nodes. This allows for more renal preservation as compared to the radical nephrectomy, and this can have positive long term health benefits.[62] Larger and more complex tumors can also be treated with partial nephrectomy by surgeons with a lot of kidney surgery experience.[63]

Laparoscopic nephrectomy uses laparoscopic surgery, with minimally invasive surgical techniques. Commonly referred to as key hole surgery, this surgery does not have the large incisions seen in a classically performed radical or partial nephrectomy, but still successfully removes either all or part of the kidney. Laparoscopic surgery is associated with shorter stays in the hospital and quicker recovery time but there are still risks associated with the surgical procedure.

Surgery for metastatic disease: If metastatic disease is present surgical treatment may still a viable option. Radical and partial nephrectomy can still occur, and in some cases if the metastasis is small this can also be surgically removed.[7] This depends on what stage of growth and how far the disease has spread.

Targeted ablative therapies are also known as percutaneous ablative therapies. Although the use of laparoscopic surgical techniques for complete nephrectomies has reduced some of the risks associated with surgery,[64] surgery of any sort in some cases will still not be feasible. For example, the elderly, people already suffering from severe renal dysfunction, or people who have several comorbidities, surgery of any sort is not warranted.[65] Instead there are targeted therapies which do not involve the removal of any organs or serious surgery. Rather, these therapies involve the ablation of the tumor or the affected area. Ablative treatments use imaging such as computed tomography (CT) or magnetic resonance imaging (MRI) to identify the location of the tumors, which ideally are smaller than 3.5cm and to guide the treatment. However there are some cases where ablation can be used on tumors that are larger.[65]

The two main types of ablation techniques that are used for renal cell carcinoma are radio frequency ablation and cryoablation.[65]

Radio frequency ablation uses an electrode probe which is inserted into the affected tissue, to send radio frequencies to the tissue to generate heat through the friction of water molecules. The heat destroys the tumor tissue.[7] Cell death will generally occur within minutes of being exposed to temperatures above 50C.

Cryoablation also involves the insertion of a probe into the affected area,[7] however, cold is used to kill the tumor instead of heat. The probe is cooled with chemical fluids which are very cold. The freezing temperatures cause the tumor cells to die by causing osmotic dehydration, which pulls the water out of the cell destroying the enzyme, organelles, cell membrane and freezing the cytoplasm.[65]

Immunotherapy is a method that activates the person's immune system and uses it to their own advantage. It was developed after observing that in some cases there was spontaneous regression.[66] That is, the renal cell carcinoma improved with no other therapies. Immunotherapy capitalises on this phenomenon and aims to build up a person's immune response to cancer cells.[66] Other medications target things such as growth factors that have been shown to promote the growth and spread of tumours.[67] They inhibit the growth factor in order to prevent tumours from forming.[68] There have been many different medications developed and most have only been approved in the last seven or so years.[69]

Some of the most recently developed treatments are listed below:[70]

Each of the treatments listed above is slightly different; some only work for a little while and others need to be used in conjunction with other therapies. There are also different side effects and risks associated with different forms of medication. As always, the advice of a health care professional should be sought if considering any of the therapies mentioned.

Chemotherapy and radiotherapy are not as successful in the case of RCC. RCC is resistant in most cases but there is about a 4-5% success rate sometimes, but this is often short lived with more tumours and growths developing later.[7]

Cancer vaccines are being developed but so far have been found to be effective for only certain forms of the RCC.[7] The vaccines are being designed to "prime" the immune system to provide tumour specific immunity.[66] They are still being developed but the present another treatment possibility.

Adjuvant therapy, which refers to therapy given after a primary surgery, has not been found to be beneficial in renal cell cancer.[72] Conversely, neoadjuvant therapy is administered before the intended primary or main treatment. In some cases neoadjuvant therapy has been shown to decrease the size and stage of the RCC to then allow it to be surgically removed.[68] This is a new form of treatment and the effectiveness of this approach is still being assessed in clinical trials.

Metastatic renal cell carcinoma (mRCC) is the spread of the primary renal cell carcinoma from the kidney to other organs. 25-30% of people have this metastatic spread by the time they are diagnosed with renal cell carcinoma.[73] This high proportion is explained by the fact that clinical signs are generally mild until the disease progresses to a more severe state.[74] The most common sites for metastasis are the lymph nodes, lung, bones, liver and brain.[8] How this spread affects the staging of the disease and hence prognosis is discussed in the Diagnosis and Prognosis section.

MRCC has a poor prognosis compared to other cancers although average survival times have increased in the last few years due to treatment advances. Average survival time in 2008 for the metastatic form of the disease was under a year[75] and by 2013 this improved to an average of 22 months.[76] Despite this improvement the 5 year survival rate for mRCC remains under 10%[77] and 20-25% of suffers remain unresponsive to all treatments and in these cases, the disease has a rapid progression.[76]

The available treatments for RCC discussed in the Treatment section are also relevant for the metastatic form of the disease. Options include interleukin-2 which is a standard therapy for advanced renal cell carcinoma.[72] In the past six years, seven new treatments have been approved specifically for mRCC (sunitinib, temsirolimus, bevacizumab, sorafenib, everolimus, pazopanib and axitinib).[4] These new treatments are based on the fact that renal cell carcinomas are very vascular tumors they contain a large number of blood vessels. The drugs aim to inhibit the growth of new blood vessels in the tumors, hence slowing growth and in some cases reducing the size of the tumors.[78] Side effects unfortunately are quite common with these treatments and include:[79]

Radiotherapy and chemotherapy are more commonly used in the metastatic form of RCC to target the secondary tumors in the bones, liver, brain and other organs. While not curative, these treatments do provide relief for suffers from symptoms associated with the spread of tumors.[76] Other potential treatments are still being developed, including tumor vaccines and small molecule inhibitors.[73]

The prognosis for renal cell carcinoma is largely influenced by a variety of factors, including tumour size, degree of invasion and metastasis, histologic type, and nuclear grade.[21] For metastatic renal cell carcinoma, factors which may present a poor prognosis include a low Karnofsky performance-status score (a standard way of measuring functional impairment in patients with cancer), a low haemoglobin level, a high level of serum lactate dehydrogenase, and a high corrected level of serum calcium.[80][81] For non-metastatic cases, the Leibovich scoring algorithm may be used to predict post-operative disease progression.[82]

Renal cell carcinoma is one of the cancers most strongly associated with paraneoplastic syndromes, most often due to ectopic hormone production by the tumour. The treatment for these complications of RCC is generally limited beyond treating the underlying cancer.

For those that have tumour recurrence after surgery, the prognosis is generally poor. Renal cell carcinoma does not generally respond to chemotherapy or radiation. Immunotherapy, which attempts to induce the body to attack the remaining cancer cells, has shown promise. Recent trials are testing newer agents, though the current complete remission rate with these approaches is still low, around 12-20% in most series. Most recently, treatment with tyrosine kinase inhibitors including nexavar, pazopanib, and rapamycin have shown promise in improving the prognosis for advanced RCC.[83]

The incidence of the disease varies according to geographic, demographic and, to a lesser extent, hereditary factors. There are some known risk factors, however the significance of other potential risk factors remains more controversial. The incidence of the cancer has been increasing in frequency worldwide at a rate of approximately 2-3% per decade[75] until the last few years where the number of new cases has stabilised.[14]

The incidence of RCC varies between sexes, ages, races and geographic location around the world. Men have a higher incidence than women (approximately 1.6:1)[72] and the vast majority are diagnosed after 65 years of age.[72] Asians reportedly have a significantly lower incidence of RCC than whites and while African countries have the lowest reported incidences, African Americans have the highest incidence of the population in the United States.[14] Developed countries have a higher incidence than developing countries, with the highest rates found in North America, Europe and Australia / New Zealand[84]

Daniel Sennert made the first reference suggesting a tumour arising in the kidney in his text Practicae Medicinae, first published in 1613.[85]

Miril published the earliest unequivocal case of renal carcinoma in 1810.[86] He described the case of Franoise Levelly, a 35 year old woman, who presented to Brest Civic Hospital on April 6, 1809, supposedly in the late stages of pregnancy.[85]

Koenig published the first classification of renal tumours based on macroscopic morphology in 1826. Koenig divided the tumors into scirrhous, steatomatous, fungoid and medullary forms.[87]

Following the classification of the tumour, researchers attempted to identify the tissue of origin for renal carcinoma.

The pathogenesis of renal epithelial tumours was debated for decades. The debate was initiated by Paul Grawitz when in 1883, he published his observations on the morphology of small, yellow renal tumours. Grawitz concluded that only alveolar tumours were of adrenal origin, whereas papillary tumours were derived from renal tissue.[85]

In 1893, Paul Sudeck challenged the theory postulated by Grawitz by publishing descriptions of renal tumours in which he identified atypical features within renal tubules and noted a gradation of these atypical features between the tubules and neighboring malignant tumour. In 1894, Otto Lubarsch, who supported the theory postulated by Grawitz coined the term hypernephroid tumor, which was amended tohypernephroma by Felix Victor Birch-Hirschfeld to describe these tumours.[88]

Vigorous criticism of Grawitz was provided by Oskar Stoerk in 1908, who considered the adrenal origin of renal tumours to be unproved. Despite the compelling arguments against the theory postulated by Grawitz, the term hypernephroma, with its associated adrenal connotation, persisted in the literature.[85]

Foot and Humphreys, and Foote et al. introduced the term Renal Celled Carcinoma to emphasize a renal tubular origin for these tumours. Their designation was slightly altered by Fetter to the now widely accepted term Renal Cell Carcinoma.[89]

Convincing evidence to settle the debate was offered by Oberling et al. in 1959 who studied the ultrastructure of clear cells from eight renal carcinomas. They found that the tumour cell cytoplasm contained numerous mitochondria and deposits of glycogen and fat. They identified cytoplasmic membranes inserted perpendicularly onto basement membrane with occasional cells containing microvilli along the free borders. They concluded that these features indicated that the tumours arose from the epithelial cells of the renal convoluted tubule, thus finally settling one of the most debated issues in tumour pathology.[85][90]

The rest is here:
Renal cell carcinoma - Wikipedia, the free encyclopedia

Graduate Medical Education (GME): Medical Genetics

Maximilian Muenke, MD

Eligibility CriteriaCandidates with the MD degree must have completed an accredited U.S. residency training program and have a valid U.S. license. Previous training is usually in, but not limited to, Pediatrics, Internal Medicine or Obstetrics and Gynecology.

OverviewThe NIH has joined forces with training programs at the Children's National Medical Center, George Washington University School of Medicine and Washington Hospital Center. The combined training program in Medical Genetics is called the Metropolitan Washington, DC Medical Genetics Program. This is a program of three years duration for MDs seeking broad exposure to both clinical and research experience in human genetics.

The NIH sponsor of the program is National Human Genome Research Institute (NHGRI). Other participating institutes include the National Cancer Institute (NCI), the National Eye Institute (NEI), the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), the National Institute of Child Health and Human Development (NICHD), the National Institute on Deafness and Other Communication Disorders (NIDCD), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and the National Institute of Mental Health (NIMH). Metropolitan area participants include Children's National Medical Center (George Washington University), Walter Reed Army Medical Center, and the Department of Pediatrics, and the Department of Obstetrics and Gynecology at Washington Hospital Center. The individual disciplines in the program include clinical genetics, biochemical genetics, clinical cytogenetics, and clinical molecular genetics.

The primary goal of the training program is to provide highly motivated physicians with broad exposure to both clinical and research experiences in medical genetics. We train candidates to become effective, independent medical geneticists, prepared to deliver a high standard of clinical genetics services, and to perform state-of-the-art research in the area of genetic disease.

Structure of the Clinical Training Program

RotationsThis three year program involves eighteen months devoted to learning in clinical genetics followed by eighteen months of clinical or laboratory research.

Year 1Six months will be spent on rotation at the NIH. Service will include time spent on different outpatient genetics clinics, including Cancer Genetics and Endocrine Disorders and Genetic Ophthalmology; on the inpatient metabolic disease and endocrinology ward; on inpatient wards for individuals involved in gene therapy trials; and on the NIH Genetics Consultation Service.

Three months will be spent at Children's National Medical Center and will be concentrated on pediatric genetics. Fellows will participate in outpatient clinics, satellite and outreach clinics. They will perform consults on inpatients and patients with metabolic disorders and on the neonatal service. Fellows will be expected to participate in the relevant diagnostic laboratory studies on patients for whom they have provided clinical care.

One month will be spent at Walter Reed Army Medical Center and will concentrate on adult and pediatric clinical genetics. One month will be spent at Washington Hospital Center on rotations in prenatal genetics and genetic counseling.

Year 2 Fellows will spend one month each in clinical cytogenetics, biochemical genetics, and molecular diagnostic laboratories. The remaining three months will be devoted to elective clinical rotations on any of the rotations previously mentioned. The second six months will be spent on laboratory or clinical research. The fellow will spend at least a half-day per week in clinic at any one of the three participating institutions.

Year 3This year will be devoted to research, with at least a half day per week in clinic.

NIH Genetics Clinic (Required)Fellows see patients on a variety of research protocols. The Genetics Clinic also selectively accepts referrals of patients requiring diagnostic assessment and genetic counseling. Areas of interest and expertise include: chromosomal abnormalities, congenital anomalies and malformation syndromes, biochemical defects, bone and connective tissue disorders, neurological disease, eye disorders, and familial cancers.

Inpatient Consultation Service (Required)Fellows are available twenty-four hours daily to respond to requests for genetics consultation throughout the 325-bed hospital. Written consultation procedures call for a prompt preliminary evaluation, a written response within twenty-four hours, and a subsequent presentation to a senior staff geneticist, with an addendum to the consult, as needed. The consultant service fellow presents the most interesting cases from the wards during the Post-Clinic Patient Conference on Wednesday afternoons during which Fellows present interesting clinical cases for critical review. Once a month the fellow presents relevant articles for journal club.

Metropolitan Area Genetics Clinics

Other Clinical Opportunities: Specialty Clinics at NIHThe specialty clinics of NIH treat a large number of patients with genetic diseases. We have negotiated a supervised experience for some of the fellows at various clinics; to date, fellows have participated in the Cystic Fibrosis Clinic, the Lipid Clinic, and the Endocrine Clinic.

Lectures, Courses and SeminarsThe fellowship program includes many lectures, courses and seminars. Among them are a journal club and seminars in medical genetics during which invited speakers discuss research and clinical topics of current interest. In addition, the following four courses have been specifically developed to meet the needs of the fellows:

Trainees are encouraged to pursue other opportunities for continuing education such as clinical and basic science conferences, tutorial seminars, and postgraduate courses, which are plentiful on the NIH campus.

Structure of the Research Training ProgramFellows in the Medical Genetics Program pursue state-of-the-art research related to genetic disorders. Descriptions of the diverse interests of participating faculty are provided in this catalog. The aim of this program is to provide fellows with research experiences of the highest caliber and to prepare them for careers as independent clinicians and investigators in medical genetics.

Fellows entering the program are required to select a research supervisor which may be from among those involved on the Genetics Fellowship Faculty Program. It is not required that this selection be made before coming to NIH.

In addition to being involved in research, all fellows attend and participate in weekly research seminars, journal clubs and laboratory conferences, which are required elements of each fellow's individual research experience.

Program Faculty and Research Interests

Examples of Papers Authored by Program Faculty

Program GraduatesThe following is a partial list of graduates including their current positions:

Application Information

The NIH/Metropolitan Washington Medical Genetics Residency Program is accredited by the ACGME and the American Board of Medical Genetics. Upon successful completion of the three year program, residents are eligible for board certification in Clinical Genetics. During the third residency year, residents may elect to complete either (a) the requirements for one of the ABMG laboratory subspecialties, such as Clinical Molecular Genetics, Clinical Biochemical Genetics or Clinical Cytogenetics, or (b) a second one year residency program (e.g., Medical Biochemical Genetics).

Candidates should apply through ERAS, beginning July 1 of the year prior to their anticipated start date. Candidates with the MD or MD and PhD degree must have completed a U.S. residency in a clinically related field. Previous training is usually in, but not limited to, Pediatrics, Internal Medicine or Obstetrics and Gynecology. Four new positions are available each year. Interviews are held during August and September.

Electronic Application The quickest and easiest way to find out more about this training program or to apply for consideration is to do it electronically.

The NIH is dedicated to building a diverse community in its training and employment programs.

NOTE: PDF documents require the free Adobe Reader.

Read more:
NIH Clinical Center: Graduate Medical Education (GME ...