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Did I have a mole a wart or skin cancer?

March 1st, 2011 by admin

Moles and basal cell lesions can be hard to differentiate

Moles and basal cell lesions can be hard to differentiate

A little over a year ago I noticed what looked like a small pimple or possibly an infected hair follicle on my upper lip. I squeezed a little exudate out of it and cleaned it with alcohol and applied an antibiotic ointment, thinking that it would be gone in three or four days. It didn’t go away as quickly as things like that usually do. It grew fairly rapidly. It started to look like a pale-colored mole about 5 mm — less than a quarter of an inch — across. I tried to remove it a couple of times; once by using an over the counter wart-freezing spray and later a salicylic acid liquid-bandage type of product. Both times it got small enough that I thought it was about gone, but then it came right back to its original size in a few days.

While I was at the VA Outpatient Clinic in Charlotte for an annual physical, I asked Dr. Patel to take a look at the sore on my lip. She did and said she wasn’t sure what it was but that she would schedule an appointment with a dermatologist.  A few days later the dermatologist said that it would need to be removed just to be safe and made an appointment with the minor surgery department for me to have it taken care of the following Monday.

The surgeon looked at the sore on my lip in rapt attention, as if he were studying something for a final exam — like he was trying to memorize every detail. He was so focused on it that it made me feel uncomfortable. He finally looked up and said, “Yep, we need to take that out.”

I was glad that it was going to be taken care of. Still thinking that it might be a mole or some sort of persistent wart, I asked him if he had a diagnosis. Without skipping a beat of any kind he said, “You have a basal cell carcinoma. I’ll send a specimen to the lab to make sure — after we cut it out.”

I’ve had a mustache for over 40 years, so my image in the mirror this morning doesn’t look quite right without it. The bandage feels like it covers my whole face. The stitches are the type that will dissolve and it hurts a little, but I am more than glad to have this thing over and done with.

In retrospect, I was more concerned about my slightly elevated cholesterol, than I was about that thing on my lip. Now that I have proven that I can make cancer, I’ll be a little more careful about pooh-poohing any little lumps or bumps that might pop up in the future.

Thank God for annual checkups and the Veterans Administration.

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Study finds that the pesticides rotenone and paraquat are associated with Parkinson’s disease

February 11th, 2011 by admin


National Institutes of Health research shows a link between use of two pesticides, rotenone and paraquat, and Parkinson’s disease. People who used either pesticide developed Parkinson’s disease approximately 2.5 times more often than non-users.

The study was a collaborative effort conducted by researchers at the National Institute of Environmental Health Sciences (NIEHS), which is part of the National Institutes of Health, and the Parkinson’s Institute and Clinical Center in Sunnyvale, Calif.

“Rotenone directly inhibits the function of the mitochondria, the structure responsible for making energy in the cell,” said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author of the paper appearing online in the journal Environmental Health Perspectives. “Paraquat increases production of certain oxygen derivatives that may harm cellular structures. People who used these pesticides or others with a similar mechanism of action were more likely to develop Parkinson’s disease.

The authors studied 110 people with Parkinson’s disease and 358 matched controls from the Farming and Movement Evaluation (FAME) Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/fame/index.cfm) to investigate the relationship between Parkinson’s disease and exposure to pesticides or other agents that are toxic to nervous tissue. FAME is a case-control study that is part of the larger Agricultural Health Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/ahs/index.cfm), a study of farming and health in approximately 90,000 licensed pesticide applicators and their spouses. The investigators diagnosed Parkinson’s disease by agreement of movement disorder specialists and assessed the lifelong use of pesticides using detailed interviews.

There are no home garden or residential uses for either paraquat or rotenone currently registered. Paraquat use has long been restricted to certified applicators, largely due to concerns based on studies of animal models of Parkinson’s disease. Use of rotenone as a pesticide to kill invasive fish species is currently the only allowable use of this pesticide.

“These findings help us to understand the biologic changes underlying Parkinson’s disease. This may have important implications for the treatment and ultimately the prevention of Parkinson’s disease,” said Caroline Tanner, M.D., Ph.D., clinical research director of the Parkinson’s Institute and Clinical Center, and lead author of the article.

The NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit www.niehs.nih.gov. Subscribe to one or more of the NIEHS news lists (www.niehs.nih.gov/news/releases/newslist/index.cfm) to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications.

The National Institutes of Health (NIH) — The Nation’s Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.


Reference: Tanner CM, Kamel F, Ross GW, Hoppin JA, Goldman SM, Korell M, Marras C, Bhudhikanok GS, Kasten M, Chade AR, Comyns K, Richards MB, Meng C, Priestly B, Fernandez HH, Cambi F, Umbach DM, Blair A, Sandler DP, Langston JW. 2011. Rotenone, paraquat and Parkinson’s disease. Environ Health Perspect; doi:10.1289/ehp.1002839 [Online 26 January 2011].

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Study ties blood protein ApoE to Alzheimer’s brain abnormalities

December 20th, 2010 by admin

Alzheimer's specific protein called apolipoprotein E

Alzheimer's specific protein called apolipoprotein E

In NIH-supported study, blood test in symptom-free volunteers links levels of specific protein with beta amyloid deposits

Scientists are seeking ways to detect the earliest stages of Alzheimer’s disease, since harmful changes may be taking place in the brain years before symptoms appear. Now, researchers report that a blood test detecting a specific protein in blood samples from cognitively normal older people may reflect the levels of beta-amyloid protein in the brain — a hallmark of the disease. Supported in part by the National Institutes of Health, the findings may eventually lead to a blood test that helps predict risk for Alzheimer’s disease and who may be a good candidate for participating in clinical trials.

Madhav Thambisetty, M.D., Ph.D., of the Intramural Research Program at the National Institute on Aging (NIA), part of the NIH, was the lead author on the study with collaborators from the Institute of Psychiatry at King’s College, London, and the Department of Radiology at Johns Hopkins University, Baltimore. The study appears in the Dec. 20, 2010, issue of the Journal of Alzheimer’s Disease.

“Recent advances in imaging and biomarkers that help track the onset and progression of Alzheimer’s disease show promise for early detection of the disease process, and for tracking the effectiveness of early interventions,” said NIA Director Richard J. Hodes, M.D. “This is critically important in streamlining and conducting trials more efficiently so that we can find out about possible therapies that much sooner.”

Using proteomics technology, a method of studying hundreds of proteins from a small blood sample, the researchers analyzed blood samples of 57 older and symptom-free volunteers to determine whether specific proteins were associated with amyloid burden in the brain. They measured brain amyloid using PET (positron emission tomography) scans with Pittsburgh Compound B, a tracer that binds to amyloid plaques. The volunteers are participating in the NIA’s Baltimore Longitudinal Study of Aging (BLSA), America’s longest-running scientific study of human aging.

The researchers found the amount of a specific protein called apolipoprotein E, or ApoE, in the blood samples was strongly associated with the level of beta amyloid in the brain. Those with high blood levels of the protein had significantly greater deposits of amyloid in the medial temporal lobe, the region of the brain important to memory function.

“These results are especially intriguing as this protein is made by the APOE gene, the most robust genetic risk factor for late-onset Alzheimer’s,” Thambisetty said. Late-onset Alzheimer’s is the most common form of the disease and occurs around age 65 or later.

He now plans to test these findings in serial blood samples collected every year in BLSA volunteers to determine how changing blood levels of ApoE protein may relate to pathological changes in the brain over time.

“If the results are equally positive, we may be able to develop a blood test that provides a less invasive, inexpensive method that helps to detect the early pathological changes of Alzheimer’s disease,” he said.

The NIA leads the federal government effort conducting and supporting research on aging and the health and well being of older people. For more on health and on aging generally, go to www.nia.nih.gov. The NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer’s Disease Education and Referral (ADEAR) Center at www.nia.nih.gov/Alzheimers. To sign up for e-mail alerts about new findings or publications, please visit either website. To learn more about the BLSA, go to http://www.grc.nia.nih.gov/branches/blsa/blsanew.htm.

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Obesity patients are not victims

December 16th, 2010 by admin

by David Gratzer, MD

Call it the McVictim syndrome. Too many pundits, public health experts and politicians are working overtime to find scapegoats for America’s obesity epidemic.

In his latest book, former FDA Commissioner David A. Kessler argues that modern food is addictive. In it, he recounts how he was once helpless to stop himself from eating a cookie. In a paper in this month’s Journal of Health Economics, University of Illinois researchers join a long list of analysts who blame urban sprawl for obesity. In November, former Carter administration advisor Amitai Etzioni argued that it’s so hard for Americans to keep weight off that adults should simply give up and focus attention on the young instead.

The peak of the trend: A recently released Ohio study, using mice, suggests “fine-particulate air pollution” could be causing a rise in obesity rates.

How long before we’re told that the devil made us eat it?

The McVictim syndrome spins a convenient — and unhealthy — narrative on America’s emerging preventable disease crisis. McVictimization teaches Americans to think that obesity is someone else’s fault — and therefore, someone else’s problem to solve.

The truth: In the vast majority of cases, obesity is a preventable condition. So those of us in the medical community must be candid with overweight patients about the risks they face and the rewards of better health choices. But it’s also time for American policymakers to show the same level of candor.

All things being equal, the simplest explanation is often the right one. And the simplest explanation for the dramatic rise in obesity rates — roughly doubling as a percentage of the total population in just a quarter-century — is the surge in our daily caloric intake. Excess food now, excess weight later. And Americans won’t make better choices if the McVictim syndrome provides a convenient excuse to carry on as before.

Obesity is preventable, but its consequences seem difficult to avoid. Consider that the cost of treating resulting conditions such as diabetes is about 7% of all U.S. healthcare spending — and a significant drain on federal and state budgets. Obesity is a national security threat because it severely limits the pool of military recruits; in 2009, the Pentagon indicated that since 2005, 48,000 potential troops had flunked their basic physical exams because they weighed too much. Most important, obesity is a human threat, destroying otherwise healthy lives and increasing personal health costs, all for the sake of a few daily moments of instant gratification.

For these reasons, there is a role for government to play in attacking obesity. Public policy can help. School lunch programs shouldn’t push our children toward obesity at taxpayers’ expense. We should stop subsidizing agribusinesses; many are using taxpayer dollars to produce and market unhealthful foods. We should promote insurance reforms that support preventive medicine.

But we must also launch a direct attack on the philosophy behind the McVictim syndrome. Policymakers must accept the fact that a poor diet is almost always a poor personal choice.

Yes, it’s fair to say that many Americans try to choose better — and fail because they’ve chosen quack drugs or crash diets as the solution. Yes, it’s fair to say that losing weight solely for appearance’s sake isn’t a healthful choice. Yes, it’s fair to say we shouldn’t crush the self-esteem of those who’ve tried, and failed, to keep off excess weight. In other words, our society makes healthful choices tougher.

But even so, encouraging Americans to cut their dietary health risks is a responsible act of citizenship. And it’s absurd to pretend that Americans are helpless to make that choice — or that it’s too late for them to reap the benefits. Contrary to claims like Etzioni’s, even a modest, voluntary improvement in the average American diet could pay huge dividends.

Just as a little more weight causes more damage over time (to joints, to cardiovascular systems, to organs), a little less weight can produce dramatic health benefits. To take one example, a study cited in the Journal of the American College of Cardiology found that obese patients on a program of mild weight loss and modest exercise cut their odds of getting diabetes by as much as 60%. Imagine the benefits that would flow from keeping millions of future Medicare recipients from ever needing an insulin prescription.

The McVictim syndrome is far too prevalent, which promotes the notion that regulations and laws are the primary solution to the problem. But governments can’t micromanage your waistline for you. Even if governments could magically walk you to work, ban food advertising, regulate sugar out of food and suck those fat particles out of the air, in a free society you would still have the power to drive to the nearest restaurant, shake your salt shaker and order a second piece of pie.

That’s why understanding — and rejecting — the McVictim culture is crucial to obesity reduction policy. And the first step in that process is to reject the temptation to find an easy scapegoat.

David Gratzer is a physician and senior fellow at the Manhattan Institute. He is author of The Cure: How Capitalism Can Save American Health Care.

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Tinnitus (ringing in the ears) highlights poor doctor patient communication

November 11th, 2010 by admin

by Martin Young, MBChB, FCS(SA)

I’m both interested in and disturbed by what some doctors have said to patients at the first consultation for Tinnitus, an annoying perception of sound that comes from somewhere within their heads.  Not many of these patients are referred to me – most come of their own accord for a second opinion.  What they tell me their doctor said is a lesson in how not to communicate with patients, and I think worth repeating here.

The most common doctor diagnosis, treatment and reassurance is a curt, “You’ve got Tinnitus, and there’s nothing you or we can do.  Learn to live with it.”

Few patients can be more anxious.  For most, Tinnitus is a minor annoyance, no cause for concern, not due to any serious illness, and simple reassurance is all that is needed.  The unfortunate other end of the scale is the Tinnitus sufferer tormented by the incessant buzzing in his or her head, and whose life becomes consumed by efforts to escape the distraction.  Helping these patients is a real challenge, some driven as far as suicide.

At first glance certainly the first and last parts of the doctor’s statement are true. The middle is a common and mistaken assumption by many doctors, perhaps a bit of medical ignorance, but hardly negligent.  Or is it?  Overall, I’m disturbed by the callousness of this dismissal, for the following reasons.

Tinnitus is a symptom, not a disease.  The original statement is analogous to saying “You’ve got a backache.” Putting only a name to a symptom is a start, but not very helpful in the long term.

The possibility that Tinnitus is due to a disease process is ignored.  Tinnitus may be pulsatile or continuous.  If in time with a patient’s heartbeat, (i.e. pulsatile), there is a reasonable possibility of some disturbance in vascular flow in the neck, skull or brain, varying from as minor a problem as a small and insignificant kink in the normal internal carotid artery due to minor arteriosclerosis, to major challenges like vascular tumors filling large areas of the head and brain. Pulsatile Tinnitus should be investigated, by careful clinical examination and usually an MRI angiogram.

Continuous Tinnitus is often described as “buzzing, like the sea, or crickets” may be due to an abnormality anywhere in the hearing system.  It can be something as minor as wax in the ear canal.  Or as major as a tumor of the vestibulocochlear nerve – an acoustic neuroma. The commonest cause is going to be a degree of nerve deafness due to common everyday wear and tear.  But a diagnosis still needs to be made.  The statement closes the door on the possibility of diagnosing and removing the cause, and risks missing serious pathology.

“There’s nothing you or we can do.”  I guess what the doctor means is, “There’s no medication shown to reduce Tinnitus,” which at this point in time is generally true.  Intravenous lidocaine has been shown to be effective in the very short term, but is very toxic and impractical in any form for Tinnitus sufferers. There are other medications thought to have some benefit, but results of studies are variable.  Unfortunately for Tinnitus there is no magic bullet. But “we cannot write a prescription” should be very distinct from “there’s nothing you can do.”

There is a lot a doctor can do for a sufferer, given a basic understanding of Tinnitus, and a diagnosis is a good place to start.

First, for idiopathic or sensorineural hearing loss-related Tinnitus, the exclusion of serious pathology is very helpful for the anxious patient – an MRI scan of the brain has a good therapeutic effect in offering reassurance.  In my opinion, the worst sufferers have little chance of overcoming Tinnitus until an MRI scan convinces them there is no tumor inside their heads.  Second, an explanation as to why Tinnitus is there in the first place is essential, i.e. “sound perception due to nerve activity within the brain, which is usually not heard by the conscious brain, but which becomes heard due to other abnormalities” or, in other words, a “raising of sensitivity to natural brain ‘sound’, which is not usually heard.”

The majority of patients are happy with just an explanation, especially when they realize that if they focus attention on the Tinnitus, it will naturally become louder.  Advice to “learn to ignore Tinnitus” is very different to “learn to live with it.”

The latter advice is impossible to follow without a basic understanding of why the Tinnitus is there, and why distraction techniques are so important in learning to ignore it.  The patients have to be given the tools to “learn to live with it” – on its own that advice is as meaningless as is “learn to read” to someone who is illiterate.

Those seriously affected by Tinnitus may find wearing hearing aids or Tinnitus maskers – hearing-aid like fittings that mask the Tinnitus sound with another – very useful.  Some may need antidepressants to deal with the associated comorbidities.

And there are conditioning and behavior modification therapies specifically designed to treat Tinnitus – Tinnitus can and should be cured by, among others, audiologists and other professionals who are specially trained to deal with difficult cases.

The majority of my patients need little more than a history, quick physical examination, a hearing test, an MRI scan in selected cases, and then twenty minutes of detailed explanation and communication.  But omit the explanation, and all the rest is money and effort wasted, with little chance of cure.

I was taught to make my goal in medicine application of the three important principles – to do no harm, sometimes heal, and comfort always.

Saying, “You’ve got Tinnitus, and there’s nothing you or we can do.  Learn to live with it,” is a poor five-second substitute for a thirty-minute communication.

Martin Young is an otolaryngologist and founder and CEO of ConsentCare.

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Abbott Laboratories agrees to withdraw its obesity drug Meridia

October 12th, 2010 by admin

Meridia Capsules

Meridia Capsules

Abbott Laboratories has agreed to voluntarily withdraw its obesity drug Meridia (sibutramine) from the U.S. market because of clinical trial data indicating an increased risk of heart attack and stroke, the U.S. Food and Drug Administration announced today.

“Meridia’s continued availability is not justified when you compare the very modest weight loss that people achieve on this drug to their risk of heart attack or stroke,” said John Jenkins, M.D., director of the Office of New Drugs in the FDA’s Center for Drug Evaluation and Research (CDER). “Physicians are advised to stop prescribing Meridia to their patients and patients should stop taking this medication. Patients should talk to their health care provider about alternative weight loss and weight loss maintenance programs.”

Meridia was approved by the FDA in November 1997 for weight loss and maintenance of weight loss in obese people, as well as in certain overweight people with other risks for heart disease. The approval was based on clinical data showing that more people receiving sibutramine lost at least 5 percent of their body weight than people on placebo who relied on diet and exercise alone.

The FDA requested the market withdrawal after reviewing data from the Sibutramine Cardiovascular Outcomes Trial (SCOUT).  SCOUT was initiated as part of a postmarket requirement to look at cardiovascular safety of sibutramine after the European approval of this drug. The trial demonstrated a 16 percent increase in the risk of serious heart events, including non-fatal heart attack, non-fatal stroke, the need to be resuscitated once the heart stopped, and death, in a group of patients given sibutramine and another given placebo. There was a small difference in weight loss between the placebo group and the group that received sibutramine.

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ADHD Diet: Do food additives cause hyperactivity?

October 12th, 2010 by admin

ADHD Diet

ADHD Diet?

Question

I have a son with attention-deficit/hyperactivity disorder (ADHD). What does the research say about the relationship between food additives and ADHD?

Answer from  Mayo Clinic child psychiatrist John E. Huxsahl, M.D.

There’s no evidence that food additives cause attention-deficit/hyperactivity disorder (ADHD), but an increasing number of studies show that certain food colorings and preservatives may cause or worsen hyperactive behavior in some children. Because several studies looked at a combination of food additives and their possible effects on hyperactivity and ADHD, it isn’t clear which additives may affect behavior.

Food additives that may increase hyperactive behavior include:

  • Sodium benzoate
  • FD&C Yellow No. 6 (sunset yellow)
  • D&C Yellow No. 10 (quinoline yellow)
  • FD&C Yellow No. 5 (tartrazine)
  • FD&C Red No.40 (allura red)

FD&C Yellow No. 5, used in beverages, candy, ice cream, custards and other foods, may be more likely to cause reactions than other additives. The Food and Drug Administration requires that FD&C Yellow No. 5 be clearly labeled on food packaging along with other ingredients. But many colorings and food additives don’t require similar labeling, so it can be difficult to tell whether a food contains artificial coloring or other additives. One rule of thumb is that brightly colored processed foods are most likely to contain one or more coloring additives.

More research is needed regarding whether limiting certain foods helps prevent hyperactivity and ADHD symptoms. If you notice that a certain food causes a change in your child’s behavior, you may want to try eliminating it from your child’s diet to see if it makes a difference. However, consult with your child’s doctor before putting your child on a limited diet. A diet that eliminates too many foods can be unhealthy because it may lack necessary vitamins and nutrients.

The approach for your child’s overall health and nutrition is a diet that limits sugary and processed foods and is rich in fruits, vegetables, grains and healthy fats such as omega-3 fatty acids found in fish, flaxseed and other foods.

References

  1. McCann D, et al. Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: A randomised, double-blinded, placebo-controlled trial. The Lancet. 2007;370:1560.
  2. Bateman B, et al. The effects of a double blind, placebo controlled artificial food colourings and benzoate preservative challenge on hyperactivity in a general population sample of preschool children. Archives of Disease in Childhood. 2004;89:506.
  3. Schab DW, et al. Do artificial food colors promote hyperactivity in children with hyperactive syndromes? A meta-analysis of double-blind placebo-controlled trials. Journal of Developmental and Behavioral Pediatrics. 2004;6:423.
  4. Food ingredients and colors. U.S. Food and Drug Administration. http://www.fda.gov/Food/FoodIngredientsPackaging/ucm094211.htm. Accessed Sept. 24, 2009.
  5. Weber W, et al. Complementary and alternative medical therapies for attention-deficit hyperactivity disorder and autism. Pediatric Clinics of North America. 2007;54:983.

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Pharmageddon: America’s New Drug Crisis

October 6th, 2010 by admin

New Drug Pandemic strikes U.S.

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For the first time ever, the leading cause of accidental death has shifted from car accidents to involuntary overdose in fifteen states and the District of Columbia.

This drug abuse crisis sweeping the nation is so severe it has been coined as “Pharmageddon.”

Dr. Barbra Krantz, medical director of the Hanley Center, a drug treatment center in West Palm Beach, FL, explained that this issue arose in the 1990’s, and can be attributed to a number of factors, including a change in standard therapy practices for treating chronic pain, consumer-driven marketing campaigns for name-brand medications, and over-prescribing physicians.

These three factors contribute to what Krantz labels “the perfect storm.” In addition, the most common people suffering from prescription drug addiction are not street junkies but rather “people that are working, that are educated, that have had professions that are now looking for that better living through better chemistry,” said Krantz.

For more information click here.

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Big Breakthrough in Adult Stem Cell research

October 1st, 2010 by admin

By Dave Andrusko

Scientists reported more progress yesterday with a method of creating stem cells without using embryos

Yes, that is it in a nutshell, and what follows in TN&V today is simply an elaboration of an important breakthrough in what are known as induced pluripotent stem cells (iPS cells).

Everybody knows about the ultra-controversial Embryonic Stem Cell Research (ESCR). How could they not when we are told insistently that if you just are willing to pump federal money into hollowing out human embryos, you can use those stem cells to (eventually) cure most everything? This is all bunk, but… The proven alternatives to ESCR–by that I mean a source that is helping people here and now–are so-called adult stem cells. These non-controversial cells come from adult stem cells–bone marrow, umbilical cord blood and other tissues.

They “are treating thousands of patients around the globe, with an estimated 50,000 adult stem cell transplants occurring annually worldwide,” says David Prentice. “For some diseases, adult stem cell transplants have become the “standard of care,” meaning the treatments are so effective that they are a doctor’s best choice for sick patients.” For the most part, adult stem cells get a respectful response from the media, but hardly enthusiastic.

But the flashier alternative that is getting far more attention are induced pluripotent stem cells (iPS cells). That will only increase with today’s report published online by researchers at Children’s Hospital and the Harvard Stem Cell Institute.

In essence, in fashioning iPS cells scientists have “rewound” the clock on an adult cell (typically a skin cell), turning the cell back into something very, very close to an embryonic stem cell.

Without getting too technical, the hang-up–the reason it couldn’t be tested in humans–was that the technique carried a risk endemic to the embryonic stem cells they so closely resembled: the iPS cells could turn cancerous. (It had to do with the way four genes were injected and in the process “tampering with the DNA,” as Ritter put it.)

So scientists have tried a number of ways to more gently reprogram the cells, including a cold virus, plastimids (circles of DNA), and chemicals. The technique explained in the paper published today by the journal Cell Stem Cell “treats skin cells with modified forms of RNA, a chemical cousin of DNA that normally transmits instructions from genes to the protein-making machinery of the cell,” Ritter explains.

It gets better. Beyond being safer, this alternative strategy “coax[es] those cells to morph into specific tissues that would be a perfect match for transplantation into patients,” according to Rob Stein of the Washington Post. The trifecta was complete when it was found that the technique is much more efficient.

According to Stein, “[T] he researchers found that a daily cocktail of their creations were surprisingly fast and efficient at reprogramming the cells. The approach converted the cells in about half the time of previous methods - only about 17 days - with surprising economy - up to 100 times more efficient than the standard approach.”

All this is taking place against the backdrop of the ongoing controversy over federal funding of ESCR. As we noted several times in Today’s News & Views, last month Royce C. Lamberth, Chief Judge of the U.S. District Court for the District of Columbia, said that it appeared that the Obama Administration’s decision to fund embryonic stem cell research was inconsistent with a federal law known as the Dickey-Wicker Amendment.

The ruling was preliminary, but the judge ordered the funding to cease while the case progresses. Subsequently a different court ruled that funding could resume while legal arguments proceed.

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Menopause weight gain: Stop the middle age spread

September 22nd, 2010 by admin

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Most women gain weight as they age, but excess pounds aren’t inevitable. To minimize menopause weight gain, step up your activity level and enjoy a healthy diet.

By Mayo Clinic staff

Do you have to gain weight during menopause? - Health.com image

Do you have to gain weight during menopause? - Health.com image

As you get older, you may notice that maintaining your usual weight becomes more difficult. In fact, the most profound weight gain in a woman’s life tends to happen during the years leading up to menopause (perimenopause). Weight gain after menopause isn’t inevitable, however. You can reverse course by paying attention to healthy-eating habits and leading an active lifestyle.

What causes menopause weight gain?

The hormonal changes of menopause may make you more likely to gain weight around your abdomen, rather than your hips and thighs. Hormonal changes alone don’t necessarily trigger weight gain after menopause, however. Instead, the weight gain is usually related to a variety of lifestyle and genetic factors.

For example, menopausal women tend to exercise less than other women, which can lead to weight gain. In addition, muscle mass naturally diminishes with age. If you don’t do anything to replace the lean muscle you lose, your body composition will shift to more fat and less muscle — which slows down the rate at which you burn calories. If you continue to eat as you always have, you’re likely to gain weight.

For many women, genetic factors play a role in weight gain after menopause. If your parents or other close relatives carry extra weight around the abdomen, you’re likely to do the same. Sometimes, factors such as children leaving — or returning — home, divorce, the death of a spouse or other life changes may contribute to weight gain after menopause. For others, a sense of contentment or simply letting go leads to weight gain.

Click here to read the rest of this article

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