( September 30, 2010 ) - Valiant Health Care, Inc. Annouces Execution Of Term Sheet To Acquire Atlantic Medical Supply, Inc.

Coral Springs, Florida. September 30, 2010 (MARKETWIRE) - Valiant Health Care, Inc. (VHCI:OTCBB) announces that it has executed a term sheet with Atlantic Medical Supply, Inc., a Florida corporation (”AMS”), under which it will acquire all of the outstanding shares of AMS in exchange for cash, shares of Valiant’s common stock and options to purchase shares of Valiant’s common stock. Atlantic is a Joint Commission Accredited, Medicare Certified firm serving South Florida’s home medical equipment and supply needs since 1993. As one of the area’s largest retail suppliers of home health products and services, they provide superior customer service and top quality, state-of-the-art medical equipment and supplies.

The parties intend to quickly negotiate the stock purchase agreement and hope to close the transaction as quickly as possible, but no later than six months from the signing of the term sheet. Specific terms of the purchase will be provided when the stock purchase agreement is completed and filed with the SEC as required.

Ms. Salem, Co-founder of Accessible stated that “Acquisition of Atlantic a DME provider is the next important step toward achieving our objective of being a “One Stop Provider” of home health care” she continued “We are looking forward to having the Founders of Atlantic join our team, they bring 17 years each of successful experience in the home health care industry.”

About Valiant Health Care, Inc.
Through our Accessible Home Health Care division, we offer and sell a proven one of its kind franchise opportunity to establish and operate a full service medical and personal care Accessible Home Health Care franchise, under our distinctive brand and system. As of the date of this press release, there are 96 Accessible Home Health Care franchise units and one company-owned unit in 24 states, as well as in India and Kenya.

Accessible’s business model is designed to lead and direct the 21st Century demands of the long term home health care industry by offering a “Complete Home Healthcare Package™” and being a “One Stop Provider™.” Accessible’s primary mission is to provide the highest quality home health care services and products to its patients while adding value to the payers by reducing direct costs and the potential for fraud.  Accessible’s next phase of growth includes an expansion of its company owned units by acquisition of Medicare certified home health care providers in strategic geographic markets.

Forward-Looking Statements
This release is not an offer to purchase or sell securities and may contain statements that are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Certain statements herein are or may be based on current estimates and projections about Valiant’s business, which are derived in part on assumptions of its management, and are not guarantees of future performance, as such performance is difficult to predict. Valiant assumes no obligation to update information concerning its expectations.

Contact:
Steven Turner, President
Valiant Health Care, Inc.
954-755-5564
www.accessiblehomehealthcare.com
www.valianthealthcare.com

( September 30, 2010 ) - New Drug Helps Treatment-Resistant Arthritis

In Study, R788 Helps Rheumatoid Arthritis Not Relieved by Methotrexate

By Daniel J. DeNoon
WebMD Health News

Reviewed by Laura J. Martin, MD

Sept. 28, 2010 — An experimental rheumatoid arthritis treatment helps two-thirds of patients getting too little relief from methotrexate.

The drug, from a company called Rigel, is R788 or fostamatinib disodium. The oral drug targets an enzyme called Syk. Nobody is exactly sure of the role Syk plays in rheumatoid arthritis. But there’s an overabundance of Syk in the fluid of arthritic joints, and the enzyme is part of the runaway immune machinery that increases joint inflammation.

In a pilot study, the drug appeared to reduce symptoms of rheumatoid arthritis. Now Harvard researcher Michael E. Weinblatt, MD, reports results from a phase II clinical trial in which 457 patients with active rheumatoid arthritis despite methotrexate treatment received R788 or placebo for six months.

For patients treated with the more active twice-daily dose of 100 milligrams of R788:

• 67% had at least 20% fewer arthritis symptoms, compared to 35% of patients getting a placebo.
• 43% had at least 50% fewer arthritis symptoms, compared to 19% getting a placebo.
• 28% had at least 70% fewer arthritis symptoms, compared to 10% getting a placebo.
  

The drug does have side effects. Among patients getting the twice-daily 100 milligram dose:

• 19% had diarrhea, compared to 3% getting a placebo.
• 14% had upper respiratory infections, compared to 7% getting a placebo.
• 6% had low white blood cell counts, compared to 1% getting a placebo.
• 23% had to start or increase blood pressure medication, compared to 7% getting a placebo.

There’s at least one theoretical concern about R788. Normally, the Syk enzyme helps suppress tumors. Women with breast tumors have low levels of Syk.

It’s not clear whether long-term use of R788 will increase cancer risk; longer-term clinical trials will have to evaluate this risk.

For now, R788 looks very promising, the researchers report.

“Inhibition of the Syk pathway offers a new drug target for rheumatoid arthritis,” Weinblatt and colleagues conclude.

The Weinblatt study and an editorial by NIH researchers Juan Rivera, PhD, and Robert A. Colbert, MD, PhD, appear in the Sept. 30 issue of the New England Journal of Medicine. Rigel funded the study, and three of the study’s six authors are Rigel employees. Weinblatt reports receiving grants, fees, or honoraria from a number of drug and biomedical companies, including Rigel.

SOURCES: Weinblatt, M.E. New England Journal of Medicine, Sept. 30, 2010; vol 363: pp 1303-1312.Rivera, J. and Colbert, R.A. New England Journal of Medicine, Sept. 30, 2010; vol 363: pp 1362-1364.

©2010 WebMD, LLC. All Rights Reserved.

Article URL - http://bit.ly/9kiH3d

( September 29, 2010 ) - Exercise Helps Prevent Fractures

Regular Exercise Reduces Risk of Fractures in Elderly Women With Osteopenia

By Bill Hendrick
WebMD Health News

Reviewed by Laura J. Martin, MD

Sept. 27, 2010 — Elderly women with osteopenia, a condition with low levels of bone mineral density, can reduce their risk of hip fractures with regular daily exercise, a new study says.

In people diagnosed with osteopenia, bone mineral density is lower than normal, but not low enough to be classified as osteoporosis.

Researchers in Finland studied 160 elderly women with osteopenia, 84 of whom were assigned to an exercise group and 76 who didn’t receive training in how to work out.

Women in the exercise group attended supervised balance, leg strength, and impact training weekly for a six-month period from October to March each year from 1998 to 2001. Both the exercise and control groups were followed for a period of about seven years.

During that time, 17 women trained in how to do proper exercises were treated in hospitals for fractures, compared to 23 in the control group.

No hip fractures occurred in the exercise group during the follow-up, compared to five hip fractures in the control group. This is significant, the researchers say, because broken hips increase mortality risk in elderly women.

The women who exercised also “demonstrated a significant gain compared with the control group in mean leg strength.”

During the follow-up period, only one woman in the exercise group had died, compared with eight among those in the control group.

The authors write that 30 months of supervised, mainly home-based exercising methods followed by voluntary training at home had a positive long-term effect on balance and gait in high-risk elderly women.

What’s more, “life-long physical activity was associated with reduced risk of fractures,” the authors say.

The researchers say that regular daily exercise should be recommended for elderly women with osteopenia.

The authors write that falls cause at least 90% of all hip fractures, which have a high mortality rate.

SOURCES: News release, Archives of Internal Medicine.Korpelainen, R. Archives of Internal Medicine, Sept. 27, 2010; vol 170: pp 1548-1556.

©2010 WebMD, LLC. All Rights Reserved.

Article URL - http://bit.ly/cvJP1C

( September 28, 2010 ) - As Science Unlocks Secrets, Cancer Rates Fall

FRIDAY, Sept. 24 (HealthDay News) — Cancer is one of the most feared diseases on the planet, and the second leading cause of death in the United States.

But medical science is slowly conquering cancer, according to an assessment of cancer trends produced by the U.S. National Cancer Institute in conjunction with the U.S. Centers for Disease Control and Prevention, the American Cancer Society and the North American Association of Central Cancer Registries.

Death rates and diagnosis rates from all cancers combined are declining significantly, both for men and women overall, and for most racial and ethnic populations within the United States, the report found.

New diagnoses for all types of cancer combined decreased an average of almost 1% a year from 1999 to 2006, and deaths attributed to cancer decreased 1.6% a year from 2001 to 2006, according to the report, an annual evaluation released each December.

Doctors predict that the rates will keep falling because research has begun unlocking the secrets of how different cancers begin and develop.

“We’re beginning to understand that each cancer has an individual pathway to development,” said Dr. Alan G. Thorson, president of the American Cancer Society, a clinical professor of surgery and director of colon and rectal surgery at Creighton University in Omaha, Neb. “We know now how to look at cancer, find its source and go for that source, which makes all the difference in the world.”

The decrease in cancer incidence and deaths has been driven mainly by advances in detecting and treating the major types of cancer in men and women, according to the report.

Incidence and death rates are declining for lung, prostate and colorectal cancer in men, and for breast and colorectal cancer in women, the report said. Also, increases in the other major cancer for women, lung cancer, have tapered off, with rates remaining stable since 2003.

There’s no single explanation for the decrease in these major cancers, doctors said. Rather, the decreases are chalked up to effective detection and treatment tools designed for each form of cancer.

For example, public tobacco policy has been crucial in reducing lung cancer rates in men and leveling them out for women, said Dr. Brenda Edwards, associate director of the Surveillance Research Program at the U.S. National Cancer Institute.

“The biggest risk factor for lung cancer is smoking,” Edwards said. “We’ve begun to see the impact of efforts to limit tobacco use.” She noted that the reduction in smoking rates has accompanied laws designed to prohibit public smoking.

Colorectal cancer has decreased because of increased efforts to screen for the cancer using colonoscopy and other methods, Thorson said. Colonoscopy has made colorectal cancer completely preventable, he explained, because doctors can remove precancerous polyps from the colon during the procedure.

A number of factors account for the decrease in breast cancer rates. Mammograms are providing earlier detection of breast cancers, and earlier detection most often results in more successful treatment, Thorson said.

On top of that, fewer women are using hormone replacement medications after menopause, and “the sudden shift away from hormone replacement therapies in women affected incidence rates,” Edwards said.

Prostate cancer rates have fallen as the result of improved detection through the use of tests that measure the level of prostate-specific antigen (PSA) in a man’s blood, which can indicate cancer likelihood, and improved treatment procedures, Edwards said.

Both Edwards and Thorson believe the key to keeping cancer in decline involves molecular and genetic research that is unlocking the way cancer cells function.

“We’re beginning to understand what’s going wrong inside of the cells to make them behave in a bad manner,” Thorson said. This type of research will result in targeted therapies that will attack cancer cells while leaving healthy cells alone, he said.

Increased understanding of the human genome also will help in cancer prevention, Thorson said. Using knowledge of the genetics of cancer, doctors might soon be able to identify people who are at high risk for certain types of cancer and provide them with the tools to prevent its occurrence.

Other breakthroughs along the way also should help. For example, doctors are using vaccines to prevent the occurrence of cervical cancer in women and are researching ways other vaccines might stop other forms of cancer.

But Thorson said the biggest breakthroughs in cancer prevention could be ones that people undertake in their everyday lives.

If people begin eating right, exercising and avoiding bad habits such as smoking, then cancer rates will continue to fall, he explained.

“We have the ability to significantly reduce cancer available right now,” Thorson said. “Those are things we can do to prevent cancer, which is infinitely better than creating new ways to treat cancer once it’s there.”

“People forget how much power we do have right now through simple lifestyle changes,” he added.
Copyright © 2010 HealthDay. All rights reserved.

SOURCES: Alan G. Thorson, M.D., president, American Cancer Society, clinical professor, surgery, Creighton University and University of Nebraska, Omaha, Neb.; Brenda Edwards, Ph.D., associate director, Surveillance Research Program, U.S. National Cancer Institute, Bethesda, Md.; December 2009, U.S. National Cancer Institute, Annual Report to the Nation on the Status of Cancer

Article URL - http://bit.ly/dqy1cq

( September 28, 2010 ) - Scientists Discover Gene That Controls Stem Cells In Central Nervous System

Scientists at the Medical Research Council (MRC) have discovered that a gene called Sox9 plays a critical role in how stem cells behave and is crucial in the development of the central nervous system. These results could potentially help researchers manipulate stem cells in the brain and develop new regenerative treatments for stroke, Alzheimer’s disease or brain tumours. Human embryos develop their nervous systems very early on, from just after two weeks into a pregnancy. From this stage, until about five weeks, the nervous system is largely made up of so-called neuroepithelial cells, which grow rapidly and lay the foundations for our brains and spinal cord. However, it is only after this stage that the various types of nerves and supporting cells seen in the central nervous system begin to appear. These come from stem cells that have the potential to differentiate into different cell types or create more of themselves.

This study shows for the first time in mice is that the gene Sox9 is required for the neuroepithelial cells to turn into these stem cells, and that it continues to be required throughout development and stem cells in the adult brain to retain their properties, such as the ability to self-renew and differentiate.

The study has also established that a gene known as Sonic Hedgehog (Shh) is needed for Sox9 to work. By inducing Sox9 or Shh in neuroepithelial cells, the team found they could kick-start this process early and convert them into neural stem cells. They also found that if there was a genetic defect in Sox9, it was much harder for the mouse to renew damaged nerve cells later on.

This knowledge will be vital for finding new ways to regenerate damaged nerve cells in neurodegenerative diseases such as Alzheimer’s or in cases where the brain has had a severe trauma such as a stroke. It could also pave the way for treatments for certain kinds of brain tumours caused by out-of-control stem cells.

Dr James Briscoe from the MRC National Institute for Medical Research said:

“With the knowledge that the gene Sox9 plays a central role in the development of our nervous system, we are one step closer to being able to control stem cells in the brain and regenerate different kinds of nerve cells. Being able to correct damaged nerve cells would be a huge leap forward for the millions of people with Alzheimer’s, stem cell-related brain tumours or who have suffered from a stroke.”

Stem cell research offers the potential for new treatments for many diseases that currently have no effective cure. MRC researchers are working hard to integrate such cells in living systems so that they can regain function of cells in the spinal cord and brain among others, transforming the opportunities for cell and tissue-based treatments.

1. Neural stem cells are defined by their ability to renew themselves and their potential turn into several different kinds of other cells.

Source:
Medical Research Council

Article URL - http://bit.ly/aFce10

( September 27, 2010 ) - Acetylation May Contribute To Dementia And Alzheimer’s Disease

A new study uncovers a protein modification that may contribute to the formation of neuron-damaging neurofibrillary tangles in the human brain. The research, published by Cell Press in the September 23 issue of the journal Neuron, may lead to new strategies for treatment of neurodegenerative diseases that result from pathological aggregation of tau protein. Tau protein is common in the central nervous system where it helps to stabilize microtubules that form the neuronal cytoskeleton. Tau mutations have been linked with dementia and Alzheimer’s disease (AD), and accumulation of phosphorylated tau protein (p-tau) has been implicated in neurodegeneration. However, the molecular mechanisms that underlie abnormal tau aggregation have not been elucidated.

“We know that an enzyme called SIRT1 is reduced in the AD brain and that this reduction correlates with the accumulation of p-tau. Further, overexpression of SIRT1 protects against neuronal loss in a mouse model of AD,” explains senior study author, Dr. Li Gan from the Gladstone Institute of Neurological Disease in San Francisco, California. “However, how SIRT1 protects against tau-mediated neurodegeneration is not clear.”

SIRT1 is a deacetylase, an enzyme that removes acetyl groups from proteins. Like phosphorylation, acetylation regulates many different cellular functions, including cytoskeleton dynamics. “To determine whether tau is acetylated and whether tau acetylation contributes to tau accumulation, we investigated tau acetylation in neurons, mouse models of tauopathy, and AD brains,” says Dr. Gan.

Dr. Gan’s group found that tau acetylation prevents degradation of p-tau, and patients at early and moderate stages of tauopathy exhibited elevated tau acetylation. The researchers went on to show that inhibiting SIRT1 increased levels of acetylated and pathogenic tau while a small molecule inhibitor of p300, an enzyme known to attach acetyl groups to proteins, promoted tau deacetylation and eliminated p-tau associated with pathological conditions.

While the link between tau acetylation and tau phosphorylation is not known, the results provide new insight into tau-mediated neuropathology. “Our findings support the model that the abnormally elevated acetylation at an early stage of the disease could block clearance of p-tau from neurons, leading to its accumulation,” concludes Dr. Gan. “Our observation that p300 diminished tau acetylation and effectively eliminated p-tau supports the idea that interfering with tau acetylation may be a new approach for reducing tau-related pathology.”

The researchers include Sang-Won Min, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; Seo-Hyun Cho, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; Yungui Zhou, Gladstone Institute, University of California, San Francisco, CA; Sebastian Schroeder, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; Vahram Haroutunian, The Mount Sinai School of Medicine, New York, NY; William W. Seeley, University of California, San Francisco, CA; Eric J. Huang, University of California, San Francisco, CA; Yong Shen, Haldeman Laboratory of Molecular and Cellular Neurobiology, Sun Health Research Institute, Sun City, AZ; Eliezer Masliah, University of California at San Diego, La Jolla, CA; Chandrani Mukherjee, Johns Hopkins University, School of Medicine, Baltimore, MD; David Meyers, Johns Hopkins University, School of Medicine, Baltimore, MD; Philip A. Cole, Johns Hopkins University, School of Medicine, Baltimore, MD; Melanie Ott, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; and Li Gan, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA.

Source:
Cathleen Genova
Cell Press

Article URL - http://bit.ly/bJLLGk

( September 24, 2010 ) - Novel Rheumatoid Arthritis Drug Shows Early Promise

By Madonna Behen WEDNESDAY, Sept. 22 (HealthDay News) — A new targeted medication for rheumatoid arthritis (RA) may benefit patients with this chronic autoimmune disease who aren’t adequately helped by standard RA drug therapy, researchers say.

The oral medication, known as fostamatinib or R788, is part of a new class of drugs known as spleen tyrosine kinase (Syk) inhibitors, which work on the cellular level to block specific pathways that are responsible for joint inflammation. The drugs are similar to the breakthrough cancer drug Gleevec, which inhibits the growth of malignant cells.

“Our findings highlights the fact that there are other pathways that can be utilized in order to improve disease activity among people with rheumatoid arthritis,” said Dr. Michael E. Weinblatt, a professor of medicine at Harvard Medical School and the lead author of the study, which was published September 23 in the New England Journal of Medicine.

In this phase 2 multi-center clinical trial, patients with RA who took fostamatinib along with methotrexate were twice as likely as those taking methotrexate and a placebo to have a clinically significant improvement in their disease after six months of treatment, the researchers found. What’s more, roughly one third of the patients taking methotrexate and fostamatinib showed measurable benefits after just one week of therapy.

“This drug is particularly promising because it’s an oral medication rather than an injectable therapy,” added Weinblatt, who is co-director of clinical rheumatology at Brigham and Women’s Hospital in Boston.

Currently, some RA patients take injectable medications in a class of drugs called biologic response modifiers, which have been available for roughly a decade. Weinblatt said although these medications are effective, they are expensive (around $25,000 a year).

An estimated 1.3 million Americans have RA, which is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Inflammation can develop in other organs as well. The disease typically affects women twice as often as men.

For their research in the double-blind, placebo-controlled trial, Weinblatt and his colleagues studied 457 patients who were taking methotrexate but still had active RA. Patients were randomly assigned to be given either 100 mg of fostamatinib twice daily, 150 mg of the drug once a day, or placebo, for six months. At the end of the study, 67 percent of the patients taking 100 mg twice a day showed a clinically significant improvement (including at least a 20 percent reduction in the number of both tender and swollen joints) versus 35 percent in the placebo group. And 43 percent of the patients taking the combination of active drugs had at least a 50 percent reduction in tender and swollen joints, versus 10 percent in the placebo group. A third of patients had a clinically significant benefit after just one week of treatment, the researchers said.

The most common side effects were diarrhea, which occurred in roughly 20 percent of those taking the active drug, and an increase in blood pressure, which was seen in about a quarter of the patients taking fostamatinib; a larger percentage of the patients also developed neutropenia, but no infections were associated with it. Weinblatt said the increaes in blood pressure was seen primarily in people with a history of hypertension and that all the patients were able to control their blood pressures with antihypertensive medication.

In an editorial accompanying the study, the authors said that fostamatinib and similar drugs currently in development “have considerable promise as new drugs in the treatment of rheumatoid arthritis,” but that more studies are needed to prove their long-term safety as well as efficacy.

One issue of concern involves a theoretical increased risk of cancer, according to the editorial co-author Juan Rivera, deputy scientific director at the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

“Since Syk kinase seems to have tumor suppressive ability in breast cancer cells and its expression is inversely correlated with invasive growth and metastasis, there is the concern that suppressing its function in individuals carrying breast cancer susceptibility genes could result in increased susceptibility to the development of cancer,” Rivera said. “This is speculative, but it merits close scrutiny in the use of this drug in the treatment of RA in such individuals.”

Rheumatologists said that although the findings so far are intriguing, it’s too soon to tell what place, if any, Syk inhibitors will have in treating RA.

“This drug is particularly promising because it is taken orally and it works very fast, but until more studies prove that it has long-term safety and efficacy, we really don’t know where it’s going to fit in our armamentarium of treatments for RA,” said Dr. Jon T. Giles, assistant professor of medicine in the division of rheumatology at the Johns Hopkins School of Medicine in Baltimore.

The study was funded by the drug’s manufacturer, Rigel Pharmaceuticals. Earlier this year, Rigel and AstraZeneca entered into a licensing agreement under which AstraZeneca will develop and market the drug. The company said it expects to begin a phase 3 clinical trial before the end of this year.

Copyright © 2010 HealthDay. All rights reserved.

SOURCES: Michael E. Weinblatt, M.D., Brigham and Women’s Hospital, Boston, Mass.; Juan Rivera, Ph.D., Deputy Scientific Director, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Md., Jon T. Giles, M.D., M.P.H., assistant professor of medicine, division of rheumatology, Johns Hopkins School of Medicine, Baltimore, Md.; Sept. 23, 2010, New England Journal of Medicine

Article URL - http://bit.ly/coRgKc

( September 23, 2010 ) - Milk Drinkers May Lose More Weight

Study Shows Milk and Other Dairy Products May Have Weight Loss Benefits By Denise Mann
WebMD Health News

Reviewed by Laura J. Martin, MD

Sept 22, 2010 — Drinking milk may help you get rid of unwanted weight.

Drinking higher amounts of milk or eating other dairy foods may help you win the battle of the bulge, according to new research published online in the American Journal of Clinical Nutrition.

Adults who ate or drank the highest amount of dairy per day — about 12 ounces of milk or 580 milligrams of dairy calcium — at six months lost about 12 pounds at the end of the two-year study. People who got the least amount of calcium from dairy foods — about 150 milligrams of dairy calcium, or half of a glass of milk per day — lost 7 pounds after two years. Higher levels of vitamin D in the blood were also linked with successful weight loss, the study showed.

More than 300 overweight men and women aged 40 to 65 followed a low-fat diet, a low-carb diet, or a Mediterranean-style diet. All foods were readily available in the cafeteria at their workplace.

Participants filled out questionnaires regarding how many dairy products (and other foods) they ate or drank. The dairy section comprised 12 foods, such as low- and regular-fat milk, chocolate milk, low- and regular-fat yogurt, and yellow and white hard cheeses. Researchers also measured participants’ blood levels of vitamin D and body mass index (BMI).

“Our study suggests that both higher dairy calcium intake and increased [blood] vitamin D are related to greater diet-induced weight loss,” conclude the researchers, who were led by Danit R. Shahar, of Ben-Gurion University of the Negev in Beer-Sheva, Israel.

Exactly how — or if — dairy foods aid in weight loss is not fully understood. Several theories exist, including the possibility that eating more calcium results in losing more fat via the stool, the study researchers say.

Overweight participants had lower blood levels of vitamin D when the study began, but vitamin D levels increased among those who lost more weight. The higher the blood levels of vitamin D, the greater the weight loss, the study showed.

Vitamin D is also known as the sunshine vitamin because our bodies make it when exposed to sunlight. Recent studies have linked vitamin D deficiency to a host of medical problems, including heart disease and certain cancers.

“Low vitamin D is associated with weight gain, and raising vitamin D is looking more and more like it is able to help with weight loss,” says Vincent Pera, MD, director of the Miriam Hospital Weight Management Program in Providence, R.I.

“I am more and more convinced that there is something helpful about vitamin D at regulating weight,” he says.

“Milk is a great source of vitamin D, and it is also taking the place of other foods that are higher in fat and calories,” he tells WebMD.

“This study is part of an emerging body of research that suggest boosting key milk nutrients like calcium and vitamin D could aid weight loss,” says Constance Brown-Riggs, RD, a diabetes educator in Massapequa, N.Y.

“The 2005 Dietary Guidelines for Americans recommend three cups of milk daily and this study provides consumers another good reason to grab a glass of low-fat milk — especially if you are trying to lose weight,” she tells WebMD in an e-mail.

“A lot of times with weight maintenance and management, there is so much focus on what you should not eat, but we have to look for more tools in the box,” says Carolyn O’Neil, MS, RD, an Atlanta-based dietitian and the author of The Dish on Eating Healthy and Being Fabulous.

Milk is chock full of important vitamins and nutrients, she says. “It’s rich in vitamin D, protein for satiety, and is one-stop-shopping for nine different nutrients, which can fill in gaps that may be created when cutting back on calories.”

Some weight loss experts, including David Katz, MD, MPH, director and co-founder of the
Yale Prevention Research Center and an adjunct associate professor of public health at Yale University School of Medicine in New Haven, Conn., urge caution in interpreting these new findings.

“This is not a cause-and-effect study,” he tells WebMD in an email.

“It may mean the dairy helps with weight loss or it may be that what is not being eaten helps with weight loss,” he says. “For instance, more dairy intake may mean less soda intake.”

The vitamin D effect seen in the study could be a result of sun exposure as we make vitamin D when we are exposed to sunlight, he says. “Perhaps the people who lost the most weight were the ones who spent the most time walking outdoors.”

Katz is not sold on dairy as a miracle weight loss aid, but he does think it can be “a very nutritious choice that provides valuable nutrients at a low cost in calories or unwelcome nutrients such as added sugar, sodium, and harmful fats,” he says. High levels of dairy have been linked to increased risk for certain cancers, he points out.

The new study was supported by the Israel Ministry of Health, the Israel Dairy Council, the Israel Chief Scientist Office, German Research Foundation and the Dr. Robert C. and Veronica Atkins Research Foundation.

SOURCES: Shahar, D.R. American Journal of Clinical Nutrition, 2010.David Katz, MD, MPH, director; co-founder, Yale Prevention Research Center; adjunct associate professor, public health, Yale University School of Medicine, New Haven, Conn.Carolyn O’Neil, MS, RD, dietitian.Constance Brown-Riggs, RD, dietitian, Massapequa, N.Y.Vincent Pera, MD, director, Miriam Hospital Weight Management Program, Providence, R.I.

©2010 WebMD, LLC. All Rights Reserved.

Article URL - http://bit.ly/cZYFt0

( September 23, 2010 ) - Ginger May Soothe Aching Muscles

Daily Dose of Ginger May Act as Pain Reliever

By Jennifer Warner
WebMD Health News

Reviewed by Laura J. Martin, MD

Sept. 20, 2010 — Ginger’s soothing properties may not be limited to the stomach. A new study shows that ginger may also be an effective pain reliever for sore muscles.

Ginger has been a favorite remedy of Chinese medicine for centuries and is often used to treat nausea and upset stomach. However, researchers say, it hasn’t been widely studied as a pain reliever until now.

The study, published in The Journal of Pain, showed a daily dose of ginger eased muscle pain caused by exercise-induced muscle injury. In two separate experiments, researchers looked at the effects of two grams of raw or heat-treated ginger in supplement form on muscle pain caused by exercise in 74 healthy adults. The participants performed a variety of exercises designed to induce muscle pain over a period of 11 days while taking ginger supplements or a dummy pill.

“Daily consumption of raw or heat-treated ginger resulted in moderate-to-large reductions in muscle pain following exercise-induced muscle injury,” write researcher Christopher D. Black, of the department of kinesiology at Georgia College and State University in Milledgeville, and colleagues.

The results showed that raw and heat-treated ginger reduced muscle pain by 25% and 23%, respectively.

Researchers say previous studies in animals have shown that ginger has anti-inflammatory properties, which might help explain its beneficial effects on muscle pain.

Although some studies have suggested that heat treatment may enhance ginger’s impact on pain, researchers say their findings show heat treatment had little effect on ginger’s effectiveness as a pain reliever.

SOURCES: Black, C. The Journal of Pain, September 2010; vol 11: pp 894-903.News release, American Pain Society.

©2010 WebMD, LLC. All Rights Reserved.

Article URL - http://bit.ly/db50CI

( September 22, 2010 ) - Scientists Identify A New Target For Alzheimer’s Disease

Neurological researchers at Rush University Medical Center have found a new therapeutic target that can potentially lead to a new way to prevent the progression of Alzheimer’s disease. The target called neutral sphingomyelinase (N-SMase) is a protein that when activated, can cause a chain of reactions in the cell leading to neuronal death and memory loss. Results from the study funded by the National Institutes of Health and the Alzheimer’s Association will be published in the September 22 issue of the Journal of Neuroscience.

“There are multiple, neurotoxic, disease-causing pathways that converge on the neutral sphingomyelinase that can cause neuronal loss in the brain of an Alzheimer’s patient,” said Kalipada Pahan, PhD, neurological researcher and lead investigator at Rush. “If we can stop the activation of the neutral sphingomylinase, we may be able to stop memory loss and the progression of Alzheimer’s disease.”

In the brain of a patient with Alzheimer’s disease, two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. While neurons die, other brain cells like astroglia and microglia do not die. These cells become activated and glial cell activation plays a key role in the destruction of neurons. However, the molecular mechanisms by which activated glial cells can kill neurons have been poorly understood until now.

Beta-amyloid, which is a protein fragment deposited in the brains of patients who have Alzheimer’s disease, causes the activation of glial cells. Neuritic plaques are mainly composed of aggregates of beta-amyloid. When healthy nerve cells in the brain are exposed to beta-amyloid, they exhibit a number of pathological changes that are characteristic of Alzheimer’s pathology.

Researchers at Rush were able to determine that the neutral sphingomyelinase is triggered by the activated brain cells and beta-amyloid. However, when the neutral sphingomyelinase was inhibited by using a small molecule inhibitor and a chemical inhibitor, the activated brain cells and beta amyloid were unable to kill neurons.

Experts tested the two inhibitors using human brain cells in a mouse model and a cell culture model.

“Understanding how the disease process works is important in identifying effective approaches to protect the brain and stop the progression of Alzheimer’s disease,” said Pahan. “The results of this study are very promising and our next step is to translate these findings to the clinic.”

“If we can develop and test a clinical medication that can target the neutral sphingomyelinase, we may be able to halt memory loss in Alzheimer’s disease patients,” said Pahan.

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills, and eventually even the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear after age 60.Alzheimer’s disease is the most common cause of dementia among older people. Alzheimer’s disease affects as many as 5.3 million Americans.

Source: Rush University Medical Center

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