A new investigational anti-inflammatory drug has produced promising
results in scientific animal studies as an arthritis control therapy.
The new drug is a proprietary compound developed by Australian
biotechnology company Novogen Limited (Nasdaq: NVGN; ASX: NRT) from its
phenolic technology platform.
The effect of the new drug was examined using a well established model
of arthritis in rats which mimics the joint inflammation found in human
arthritis. A joint 'score' was determined based on the degree of swelling
and redness, as well as the number of joints involved. In the Novogen
study, the scoring was performed by an operator 'blinded' to the identity
of the treatment the rats received. A group of eight rats given the drug in
their feed showed significantly lower joint scores (p = 0.008) when
compared with the joint scores from another group of eight rats given
untreated feed.
The research, made public today, was conducted by Associate Professor
Michael James, the Chief Hospital Scientist at the Rheumatology Unit in the
Royal Adelaide Hospital. The study was conducted with the approval of the
Royal Adelaide Hospital Animal Ethics Committee according to National
Health and Medical Research Council guidelines.
The drug is one of a family of novel anti-inflammatory therapeutics
discovered by Novogen, known as FAIMs (flavonoid anti-inflammatory
molecules).
Professor James said that the FAIM concept involved a new approach to
treating arthritis, and other inflammatory conditions.
"These results are encouraging and suggest that the FAIM concept is
valid and could lead to a new class of anti-inflammatory drugs that would
not be expected to have the safety problems of the existing
anti-inflammatory agents," Professor James said.
FAIMs comprise a family of therapeutics presenting a new method of
treating inflammation. These compounds possess robust anti-inflammatory
activity in vitro and, as now demonstrated also in vivo, and are designed
to avoid cardiovascular, gastrointestinal and renal side effects and may
even be cardio-protective.
Inflammation and pain are currently most commonly treated with non-
steroidal anti-inflammatory drugs, or NSAIDs. However, these are associated
with undesirable side effects, including gastrointestinal bleeding and
ulcers, as well as kidney damage.
Recently, it has also been highlighted that these agents, particularly
the selective COX-2 inhibitors, are associated with an increase in heart
attacks and other adverse cardiovascular events. These problems occur
because NSAIDs all work by inhibiting the enzyme called COX.
Program Leader of the Novogen ant-inflammatory and cardiovascular drug
research program, Dr. Cath Walker, said the mechanism of action for the
anti- inflammatory effect of those FAIMs was now established within the
Novogen research program and had been accomplished by mechanisms other than
COX inhibition.
"This means they should not have the side effects of NSAIDS or
selective COX-2 inhibitors," Dr. Walker said.
"This result provides encouragement that the FAIM concept should be
pursued in human clinical studies.
"Our intention is to determine whether they will be effective in
treatment of arthritis, back pain and other inflammatory conditions," Dr.
Walker said.
About Novogen
Novogen is an Australian based biotechnology company in the business of
research and development of drugs derived from its phenolic technology
platform. The Company manages its research and development programs
utilizing the expertise and clinical research capabilities of universities
and hospitals in Australia, USA and Europe. Novogen's drug program is
researching and developing compounds for the treatment of cancer,
cardiovascular disease, inflammatory bowel disease and osteoarthritis. To
date Novogen has had 73 patents granted and a further 225 patents are
pending.
Novogen is the world leader in isoflavone research. From its original
technology platform of natural isoflavones (represented in OTC products
such as Promensil) the Company has developed a discovery program
surrounding novel chemical entities based on a flavonoid scaffold. One of
these compounds, phenoxodiol, is currently in Phase III clinical trialing
for treatment of late stage ovarian cancer.
Further information on the Novogen Group can be found at
novogen.
Statements included in this press release that are not historical in
nature are "forward-looking statements" within the meaning of the "safe
harbor" provisions of the Private Securities Litigation Reform Act of 1995.
You should be aware that our actual results could differ materially from
those contained in the forward-looking statements, which are based on
management's current expectations and are subject to a number of risks and
uncertainties, including, but not limited to, our failure to successfully
commercialize our product candidates; costs and delays in the development
and/or FDA approval, or the failure to obtain such approval, of our product
candidates; uncertainties in clinical trial results; our inability to
maintain or enter into, and the risks resulting from our dependence upon,
collaboration or contractual arrangements necessary for the development,
manufacture, commercialization, marketing, sales and distribution of any
products; competitive factors; our inability to protect our patents or
proprietary rights and obtain necessary rights to third party patents and
intellectual property to operate our business; our inability to operate our
business without infringing the patents and proprietary rights of others;
general economic conditions; the failure of any products to gain market
acceptance; our inability to obtain any additional required financing;
technological changes; government regulation; changes in industry practice;
and one-time events. We do not intend to update any of these factors or to
publicly announce the results of any revisions to these forward-looking
statements.
Novogen Limited
novogen
вторник, 12 апреля 2011 г.
Surgeon's Skill More Important Than Implant Design In Customized Knee Replacement
While the choices of knee implants are plentiful, the success of total knee replacement surgery still is dependent on the surgeon's skill, Henry Ford Hospital researchers say.
Researchers found that utilizing a series of common but nuanced surgical techniques is far more important to customizing the fit of a patient's implant than the implant's design.
The findings are displayed at the annual meeting of the American Academy of Orthopaedic Surgeons Feb. 15-18 in San Diego.
"Customized knee implants will not replace the need for precise, methodical surgical skill," says Jason Davis, M.D., a Henry Ford joint replacement surgeon and the study's lead author. "While improving outcomes will continue to evolve, getting back to the basics of surgery is still paramount to successful knee replacement."
Since the first knee replacement was performed in 1968, the procedure has greatly improved as have the design of implants. More than 580,000 knee replacements (an estimated two-thirds of patients are female) are performed each year in the United States, according to the AAOS, and more than 150 implant designs are available including ones that are gender- and patient-specific.
Relying on data collected from more than 20 joint replacement surgeons at an orthopaedic specialty hospital, researchers identified several surgical techniques that take into account a patient's individual knee characteristics and ensure that the implant is properly aligned and balanced with ligaments and soft tissue.
For instance, a gap-balancing technique provides better stability and overall functional performance. Several techniques aim to restore the "soft tissue personality" of the knee beyond just bone replacement. Another technique involves resecting the femur so the implant does not hang over the two sides of the bone. Additionally, researchers offer ways to enable surgeons to safely "downsize" components intraoperatively when needed while improving the balance of the knee.
"Customizing the surgery can be done effectively without the inventory or cost associated with gender- or patient-specific implants," Dr. Davis says. "By using some of these techniques surgeons can take steps to ensure the proper fitting of an individualized knee replacement."
The study was not funded.
Source:
David Olejarz
Henry Ford Health System
Researchers found that utilizing a series of common but nuanced surgical techniques is far more important to customizing the fit of a patient's implant than the implant's design.
The findings are displayed at the annual meeting of the American Academy of Orthopaedic Surgeons Feb. 15-18 in San Diego.
"Customized knee implants will not replace the need for precise, methodical surgical skill," says Jason Davis, M.D., a Henry Ford joint replacement surgeon and the study's lead author. "While improving outcomes will continue to evolve, getting back to the basics of surgery is still paramount to successful knee replacement."
Since the first knee replacement was performed in 1968, the procedure has greatly improved as have the design of implants. More than 580,000 knee replacements (an estimated two-thirds of patients are female) are performed each year in the United States, according to the AAOS, and more than 150 implant designs are available including ones that are gender- and patient-specific.
Relying on data collected from more than 20 joint replacement surgeons at an orthopaedic specialty hospital, researchers identified several surgical techniques that take into account a patient's individual knee characteristics and ensure that the implant is properly aligned and balanced with ligaments and soft tissue.
For instance, a gap-balancing technique provides better stability and overall functional performance. Several techniques aim to restore the "soft tissue personality" of the knee beyond just bone replacement. Another technique involves resecting the femur so the implant does not hang over the two sides of the bone. Additionally, researchers offer ways to enable surgeons to safely "downsize" components intraoperatively when needed while improving the balance of the knee.
"Customizing the surgery can be done effectively without the inventory or cost associated with gender- or patient-specific implants," Dr. Davis says. "By using some of these techniques surgeons can take steps to ensure the proper fitting of an individualized knee replacement."
The study was not funded.
Source:
David Olejarz
Henry Ford Health System
How Inflammatory Disease Causes Fatigue
New animal research in the February 18 issue of The Journal of Neuroscience may indicate how certain diseases make people feel so tired and listless. Although the brain is usually isolated from the immune system, the study suggests that certain behavioral changes suffered by those with chronic inflammatory diseases are caused by the infiltration of immune cells into the brain. The findings suggest possible new treatment avenues to improve patients' quality of life.
Chronic inflammatory diseases like rheumatoid arthritis, inflammatory bowel disease, psoriasis, and liver disease cause "sickness behaviors," including fatigue, malaise, and loss of social interest. However, it has been unclear how inflammation in other organs in the body can impact the brain and behavior.
The researchers found that in mice with inflamed livers, white blood cells called monocytes infiltrated the brain. These findings support previous research demonstrating the presence of immune cells in the brain following organ inflammation, challenging the long-held belief that the blood-brain barrier prevents immune cells from accessing the brain.
"Using an experimental model of liver inflammation, our group has demonstrated for the first time the existence of a novel communication pathway between the inflamed liver and the brain," said the study's senior author Mark Swain, MD, Professor of Medicine at the University of Calgary.
Swain and his colleagues found that liver inflammation triggered brain cells called microglia to produce CCL2, a chemical that attracts monocytes. When the researchers blocked CCL2 signaling, monocytes did not enter the brain despite ongoing inflammation in the liver.
Liver inflammation also stimulated cells in the blood to make an immune chemical (TNF?±). When the researchers blocked the signaling of this immune chemical, microglia produced less CCL2, and monocytes stayed out of the brain.
In the mice with inflamed livers, preventing the entry of monocytes into the brain reduced sickness behaviors; mice showed more mobility and social interaction. These findings suggest that people with chronic inflammatory diseases may benefit from treatments that limit monocyte access to the brain.
"Sickness behavior significantly impacts quality of life. Our findings further our understanding and may generate potential new avenues for treatment of these often crippling symptoms," said Swain.
"The brain is the master coordinator of many of our bodies' defense responses, so it must be able to sense injury and inflammation in distant body organs. This study starts to explain the peripheral communication signals that activate the brain," said Nancy Rothwell, PhD, DSc, at the University of Manchester, an expert on brain inflammation who is unaffiliated with the study.
The research was supported by the Canadian Institutes of Health Research, the Canadian Liver Foundation, and the Alberta Heritage Foundation for Medical Research.
The Journal of Neuroscience is published by the Society for Neuroscience, an organization of more than 38,000 basic scientists and clinicians who study the brain and nervous system.
Source: Todd Bentsen
Society for Neuroscience
Chronic inflammatory diseases like rheumatoid arthritis, inflammatory bowel disease, psoriasis, and liver disease cause "sickness behaviors," including fatigue, malaise, and loss of social interest. However, it has been unclear how inflammation in other organs in the body can impact the brain and behavior.
The researchers found that in mice with inflamed livers, white blood cells called monocytes infiltrated the brain. These findings support previous research demonstrating the presence of immune cells in the brain following organ inflammation, challenging the long-held belief that the blood-brain barrier prevents immune cells from accessing the brain.
"Using an experimental model of liver inflammation, our group has demonstrated for the first time the existence of a novel communication pathway between the inflamed liver and the brain," said the study's senior author Mark Swain, MD, Professor of Medicine at the University of Calgary.
Swain and his colleagues found that liver inflammation triggered brain cells called microglia to produce CCL2, a chemical that attracts monocytes. When the researchers blocked CCL2 signaling, monocytes did not enter the brain despite ongoing inflammation in the liver.
Liver inflammation also stimulated cells in the blood to make an immune chemical (TNF?±). When the researchers blocked the signaling of this immune chemical, microglia produced less CCL2, and monocytes stayed out of the brain.
In the mice with inflamed livers, preventing the entry of monocytes into the brain reduced sickness behaviors; mice showed more mobility and social interaction. These findings suggest that people with chronic inflammatory diseases may benefit from treatments that limit monocyte access to the brain.
"Sickness behavior significantly impacts quality of life. Our findings further our understanding and may generate potential new avenues for treatment of these often crippling symptoms," said Swain.
"The brain is the master coordinator of many of our bodies' defense responses, so it must be able to sense injury and inflammation in distant body organs. This study starts to explain the peripheral communication signals that activate the brain," said Nancy Rothwell, PhD, DSc, at the University of Manchester, an expert on brain inflammation who is unaffiliated with the study.
The research was supported by the Canadian Institutes of Health Research, the Canadian Liver Foundation, and the Alberta Heritage Foundation for Medical Research.
The Journal of Neuroscience is published by the Society for Neuroscience, an organization of more than 38,000 basic scientists and clinicians who study the brain and nervous system.
Source: Todd Bentsen
Society for Neuroscience
Treatments Can Improve Troublesome Aches
For many older adults, aching muscles and joints are common. Muscles weaken with age and become less flexible -- which can cause stiffness or soreness.
But in some cases, aches are a symptom of a disease or side effect from medication. Adults should check with a doctor when body aches have lasted more than a month; when aching is intense or interferes with normal activities; when morning stiffness lasts more than an hour; or when aching has come on suddenly with no obvious cause.
The March issue of Mayo Clinic Health Letter covers possible causes and treatments for body aches.
Polymyalgia rheumatica: This causes widespread, moderate to severe joint stiffness and muscle aching that often involves the neck, shoulders and hips. Symptoms are usually worse in the morning. Relatively low doses of the corticosteroid prednisone usually provide remarkable relief.
Infections: Short-lived body aches can accompany a bacteria or viral infection. Symptoms usually go away once the infection is gone.
Rheumatoid arthritis: This and other forms of inflammatory arthritis are considered autoimmune diseases. The immune system attacks parts of the body, causing inflammation and tissue damage, particularly in the joints. A wide variety of medications, including corticosteroids or drugs that affect the immune system, are used to reduce pain and inflammation.
Inflammatory myopathies: These autoimmune diseases, where the immune system attacks muscles, cause progressive muscle weakness over time. Treatments are corticosteroids or drugs that affect the immune system.
Depression: Aches and pains can be symptoms of depression. And people coping with chronic pain often can become depressed, worsening sensations of pain and aching. Combining antidepressant medication with psychotherapy can help ease pain.
Cholesterol-lowering medications: A possible side effect of statin drugs, commonly prescribed to reduce cholesterol, is muscle pain and weakness. Occasionally, statins may cause myopathy, characterized by severe muscle aching and weakness. To reduce pain, the patient may need to learn other ways to manage cholesterol levels.
Underactive thyroid disease: Most common in women over 60, this occurs when the thyroid gland isn't producing enough of the hormone thyroxine. Symptoms include constant fatigue, muscle aches and an inability to stay warm in cooler environments. Treatment involves a synthetic version of thyroxine, usually taken in pill form.
Vitamin D deficiency: Vitamin D is produced by the skin when it's exposed to sunlight. A deficiency can cause muscle weakness, aches and pains. Vitamin D supplements can ease pain.
Fibromyalgia: Symptoms often include fatigue and widespread pain and aching in joints and muscles. Treatment involves a variety of pain management techniques.
Mayo Clinic
200 First St. SW
Rochester, MN 55902
United States
mayoclinic/
But in some cases, aches are a symptom of a disease or side effect from medication. Adults should check with a doctor when body aches have lasted more than a month; when aching is intense or interferes with normal activities; when morning stiffness lasts more than an hour; or when aching has come on suddenly with no obvious cause.
The March issue of Mayo Clinic Health Letter covers possible causes and treatments for body aches.
Polymyalgia rheumatica: This causes widespread, moderate to severe joint stiffness and muscle aching that often involves the neck, shoulders and hips. Symptoms are usually worse in the morning. Relatively low doses of the corticosteroid prednisone usually provide remarkable relief.
Infections: Short-lived body aches can accompany a bacteria or viral infection. Symptoms usually go away once the infection is gone.
Rheumatoid arthritis: This and other forms of inflammatory arthritis are considered autoimmune diseases. The immune system attacks parts of the body, causing inflammation and tissue damage, particularly in the joints. A wide variety of medications, including corticosteroids or drugs that affect the immune system, are used to reduce pain and inflammation.
Inflammatory myopathies: These autoimmune diseases, where the immune system attacks muscles, cause progressive muscle weakness over time. Treatments are corticosteroids or drugs that affect the immune system.
Depression: Aches and pains can be symptoms of depression. And people coping with chronic pain often can become depressed, worsening sensations of pain and aching. Combining antidepressant medication with psychotherapy can help ease pain.
Cholesterol-lowering medications: A possible side effect of statin drugs, commonly prescribed to reduce cholesterol, is muscle pain and weakness. Occasionally, statins may cause myopathy, characterized by severe muscle aching and weakness. To reduce pain, the patient may need to learn other ways to manage cholesterol levels.
Underactive thyroid disease: Most common in women over 60, this occurs when the thyroid gland isn't producing enough of the hormone thyroxine. Symptoms include constant fatigue, muscle aches and an inability to stay warm in cooler environments. Treatment involves a synthetic version of thyroxine, usually taken in pill form.
Vitamin D deficiency: Vitamin D is produced by the skin when it's exposed to sunlight. A deficiency can cause muscle weakness, aches and pains. Vitamin D supplements can ease pain.
Fibromyalgia: Symptoms often include fatigue and widespread pain and aching in joints and muscles. Treatment involves a variety of pain management techniques.
Mayo Clinic
200 First St. SW
Rochester, MN 55902
United States
mayoclinic/
Pine Bark Naturally Reduces Osteoarthritis, Lowers Joint Pain, Improves Physical Function
More than 20 million Americans suffer from osteoarthritis, with half a million Americans having a total joint replacement each year. A new study to be published in the April 2008 edition (Volume 22, issue No 4) of the journal of Phytotherapy Research shows Pycnogenol (pic-noj-en-all), an antioxidant plant extract from the bark of the French maritime pine tree, was shown to reduce all osteoarthritis symptoms by 56 percent. The study revealed a particularly high efficacy of Pycnogenol for lowering joint pain by 55 percent. Moreover, patients required dramatically less standard pain medication (-58 percent), which greatly improved the gastrointestinal complications resulting from the pain medication by 63 percent.
"Pycnogenol seemed a natural fit for this study," said Dr. Gianni Belcaro, a lead researcher of the study. "There are a few main components contributing to the clinical picture of treatment management in osteoarthritis: inflammation causing a progression in the disease, alteration of fatigue resistance and muscular performance - reversing and blocking the vascular problems associated to altered mobility. Theoretically, a treatment with a compound specifically active on all those aspects could be highly effective, which is why we chose Pycnogenol."
The randomized, double-blind, placebo-controlled study, held at Italy's Chieti-Pescara University, sampled 156 patients with osteoarthritis of the knee (OA). Patients were administered 100 mg Pycnogenol or placebo, daily for three months. Symptoms were evaluated by WOMAC index scores and mobility by recording their walking performance on a treadmill. Patients were permitted to continue taking their choice of pain medication provided they recorded every tablet in a diary for later evaluation.
To describe and rate osteoarthritis symptoms (joint pain, stiffness and physical function), WOMAC questionnaires were evaluated by the investigator and patient at the start and after three months of treatment. Patients were trained on a treadmill test and performance evaluation was recorded on total distance that could be covered without pain. Measuring foot volume by the water-displacement method was used to evaluate ankle/foot edema in a randomly selected subgroup of subjects within the two treatment groups.
After three months, scores for pain dropped significantly for the Pycnogenol treatment group and no significant effects were recorded for the placebo group. Scores for stiffness were reduced by 53 percent. The scores for physical function were reduced by 57 percent in the Pycnogenol group and improvement under placebo was not significant. The global WOMAC score decreased following Pycnogenol treatment and very little in the placebo group, from 56 percent vs. 9.6 percent for Pycnogenol and placebo, respectively. Overall well-being of patients (emotional function) was significantly enhanced with the Pycnogenol group, by 64 percent and 15 percent for the placebo group.
Results of exercise tests on the treadmill demonstrated an increased performance after three months of Pycnogenol treatment. At the start of the study, patients could only walk a mean of 74 yards without feeling pain and after three months, they could walk 216 yards, compared to the placebo group that noted 71 yards at the beginning of the study and 96 yards at the end.
In addition to the osteoarthritis results, 76 percent of the patients in the Pycnogenol group and 79 percent in the placebo group showed visible ankle and foot edema at inclusion of the study. After the three months, edema decreased in 79 percent of the Pycnogenol patients and only one percent in placebo-treated patients.
Patients were allowed to use their regular dosage of NSAIDS. Usage dropped by 58 percent during treatment with Pycnogenol and one percent with the placebo. Evaluation of data demonstrated a decrease of gastrointestinal complications of 64 percent in the Pycnogenol group versus three percent in placebo.
"The results of this study are significant as they clearly demonstrate the clinical action of Pycnogenol on OA and management of symptoms. The use of Pycnogenol many reduce costs and side effects of anti-inflammatory agents and offer a natural alternative solution to people suffering from OA" said Dr. Belcaro.
A previous study on osteoarthritis which was carried out at the University of Arizona Tucson (published in Nutrition Research) had discovered that Pycnogenol was effective for improving pain and joint function. After three months in the Pycnogenol group, there was a reduction of 43 percent in pain, 35 percent in stiffness, 52 percent in physical function subscales, respectively. The placebo group showed no significant scores throughout the entire study. Dr. Belcaro confirms this earlier study with a much larger number of patients and with a more detailed investigation procedure.
The benefits of Pycnogenol for arthritic joints are suggested to result predominantly from the anti-inflammatory potency of Pycnogenol which was demonstrated in a series of clinical investigations in the past. There are more breakthrough studies on Pycnogenol and osteoarthritis expected to be published next year allowing for development of innovative, natural formulas for joint health. Additionally, Horphag Research, the exclusive worldwide distributor of Pycnogenol has filed for several patents for Pycnogenol's application for COX-1, COX-2 and treating osteoarthritis.
"The new research in the field of osteoarthritis has been a paradigm shift for Pycnogenol. We were able to demonstrate Pycnogenol's impact on all inflammatory parameters and have succeeded in providing strong clinical evidence of Pycnogenol efficacy in this field. It is obvious that Pycnogenol will have to be considered as an innovative ingredient of choice for the joint health market," said Victor Ferrari, CEO of Horphag Research, the exclusive worldwide supplier of Pycnogenol.
About Pycnogenol
Pycnogenol is a natural plant extract originating from the bark of the maritime pine that grows along the coast of southwest France and is found to contain a unique combination of procyanidins, bioflavonoids and organic acids, which offer extensive natural health benefits. The extract has been widely studied for the past 35 years and has more than 220 published studies and review articles ensuring safety and efficacy as an ingredient. Today, Pycnogenol is available in more than 600 dietary supplements, multi-vitamins and health products worldwide. For more information, visit pycnogenol/.
Natural Health Science Inc. (NHS), based in Hoboken, New Jersey, is the North American distributor for Pycnogenol (pic-noj-en-all) brand French maritime pine bark extract on behalf of Horphag Research. Pycnogenol is a registered trademark of Horphag Research Ltd., Guernsey, and its applications are protected by U.S. patents #5,720,956 / #6,372,266 and other international patents. NHS has the exclusive rights to market and sell Pycnogenol in North America and benefits from more than 35 years of scientific research assuring the safety and efficacy of Pycnogenol as a dietary supplement. For more information about Pycnogenol visit our Web site at pycnogenol/
Source: Melanie Nimrodi
MWW Group
"Pycnogenol seemed a natural fit for this study," said Dr. Gianni Belcaro, a lead researcher of the study. "There are a few main components contributing to the clinical picture of treatment management in osteoarthritis: inflammation causing a progression in the disease, alteration of fatigue resistance and muscular performance - reversing and blocking the vascular problems associated to altered mobility. Theoretically, a treatment with a compound specifically active on all those aspects could be highly effective, which is why we chose Pycnogenol."
The randomized, double-blind, placebo-controlled study, held at Italy's Chieti-Pescara University, sampled 156 patients with osteoarthritis of the knee (OA). Patients were administered 100 mg Pycnogenol or placebo, daily for three months. Symptoms were evaluated by WOMAC index scores and mobility by recording their walking performance on a treadmill. Patients were permitted to continue taking their choice of pain medication provided they recorded every tablet in a diary for later evaluation.
To describe and rate osteoarthritis symptoms (joint pain, stiffness and physical function), WOMAC questionnaires were evaluated by the investigator and patient at the start and after three months of treatment. Patients were trained on a treadmill test and performance evaluation was recorded on total distance that could be covered without pain. Measuring foot volume by the water-displacement method was used to evaluate ankle/foot edema in a randomly selected subgroup of subjects within the two treatment groups.
After three months, scores for pain dropped significantly for the Pycnogenol treatment group and no significant effects were recorded for the placebo group. Scores for stiffness were reduced by 53 percent. The scores for physical function were reduced by 57 percent in the Pycnogenol group and improvement under placebo was not significant. The global WOMAC score decreased following Pycnogenol treatment and very little in the placebo group, from 56 percent vs. 9.6 percent for Pycnogenol and placebo, respectively. Overall well-being of patients (emotional function) was significantly enhanced with the Pycnogenol group, by 64 percent and 15 percent for the placebo group.
Results of exercise tests on the treadmill demonstrated an increased performance after three months of Pycnogenol treatment. At the start of the study, patients could only walk a mean of 74 yards without feeling pain and after three months, they could walk 216 yards, compared to the placebo group that noted 71 yards at the beginning of the study and 96 yards at the end.
In addition to the osteoarthritis results, 76 percent of the patients in the Pycnogenol group and 79 percent in the placebo group showed visible ankle and foot edema at inclusion of the study. After the three months, edema decreased in 79 percent of the Pycnogenol patients and only one percent in placebo-treated patients.
Patients were allowed to use their regular dosage of NSAIDS. Usage dropped by 58 percent during treatment with Pycnogenol and one percent with the placebo. Evaluation of data demonstrated a decrease of gastrointestinal complications of 64 percent in the Pycnogenol group versus three percent in placebo.
"The results of this study are significant as they clearly demonstrate the clinical action of Pycnogenol on OA and management of symptoms. The use of Pycnogenol many reduce costs and side effects of anti-inflammatory agents and offer a natural alternative solution to people suffering from OA" said Dr. Belcaro.
A previous study on osteoarthritis which was carried out at the University of Arizona Tucson (published in Nutrition Research) had discovered that Pycnogenol was effective for improving pain and joint function. After three months in the Pycnogenol group, there was a reduction of 43 percent in pain, 35 percent in stiffness, 52 percent in physical function subscales, respectively. The placebo group showed no significant scores throughout the entire study. Dr. Belcaro confirms this earlier study with a much larger number of patients and with a more detailed investigation procedure.
The benefits of Pycnogenol for arthritic joints are suggested to result predominantly from the anti-inflammatory potency of Pycnogenol which was demonstrated in a series of clinical investigations in the past. There are more breakthrough studies on Pycnogenol and osteoarthritis expected to be published next year allowing for development of innovative, natural formulas for joint health. Additionally, Horphag Research, the exclusive worldwide distributor of Pycnogenol has filed for several patents for Pycnogenol's application for COX-1, COX-2 and treating osteoarthritis.
"The new research in the field of osteoarthritis has been a paradigm shift for Pycnogenol. We were able to demonstrate Pycnogenol's impact on all inflammatory parameters and have succeeded in providing strong clinical evidence of Pycnogenol efficacy in this field. It is obvious that Pycnogenol will have to be considered as an innovative ingredient of choice for the joint health market," said Victor Ferrari, CEO of Horphag Research, the exclusive worldwide supplier of Pycnogenol.
About Pycnogenol
Pycnogenol is a natural plant extract originating from the bark of the maritime pine that grows along the coast of southwest France and is found to contain a unique combination of procyanidins, bioflavonoids and organic acids, which offer extensive natural health benefits. The extract has been widely studied for the past 35 years and has more than 220 published studies and review articles ensuring safety and efficacy as an ingredient. Today, Pycnogenol is available in more than 600 dietary supplements, multi-vitamins and health products worldwide. For more information, visit pycnogenol/.
Natural Health Science Inc. (NHS), based in Hoboken, New Jersey, is the North American distributor for Pycnogenol (pic-noj-en-all) brand French maritime pine bark extract on behalf of Horphag Research. Pycnogenol is a registered trademark of Horphag Research Ltd., Guernsey, and its applications are protected by U.S. patents #5,720,956 / #6,372,266 and other international patents. NHS has the exclusive rights to market and sell Pycnogenol in North America and benefits from more than 35 years of scientific research assuring the safety and efficacy of Pycnogenol as a dietary supplement. For more information about Pycnogenol visit our Web site at pycnogenol/
Source: Melanie Nimrodi
MWW Group
Discovery Lays Groundwork For Better Understanding Of Protective Human Microbes In The Gut
Medical researchers have long suspected that obscure bacteria living within the intestinal tract may help keep the human immune system in balance. An international collaboration co-led by scientists at NYU Langone Medical Center has now identified a bizarre-looking microbial species that can single-handedly spur the production of specialized immune cells in mice.
This remarkable activation of the immune response could point to a similar phenomenon in humans, helping researchers understand how gut-dwelling bacteria protect us from pathogenic bacteria, such as virulent strains of E. coli. The study, published in the Oct. 30, 2009, issue of Cell, also supports the idea that specific bacteria may act like neighborhood watchdogs at key locations within the small intestine, where they sense the local microbial community and sound the alarm if something seems amiss.
In mice, at least, the newly identified neighborhood watchdog looks like something out of Disney's "The Shaggy D.A." Distinguished by long hair-like filaments, "These bacteria are the most astounding things I've ever seen," says Dan Littman, MD, PhD, the Helen L. and Martin S. Kimmel Professor of Molecular Immunology and a Howard Hughes Medical Institute Investigator.
Co-led by Dr. Littman's lab, the collaboration with researchers in Japan, California, and Massachusetts zeroed in on a little-known microbe named segmented filamentous bacterium, or SFB. In mice raised under germ-free conditions, the scientists found that adding SFB was sufficient to trigger the appearance of specialized T helper cells known as Th17 cells. These immune specialists, in turn, can send signals that tell epithelial cells lining the small intestine to increase their output of molecules targeting selected microbes.
For the study's mice, the infection-fighting response was enough to ward off the pathogen Citrobacter rodentium, considered a good model for the type of disease-causing E. coli found in contaminated foods like spinach or ground beef. Without SFB to protect them, mice infected with Citrobacter rodentium became ill before recovering.
In the same way, commensal microbes - beneficial bacteria - could decrease our susceptibility to various pathogenic invaders. "So you can immediately see some practical application of this, if one can mimic the presence of these commensal bacteria to strengthen resistance to pathogenic microbes," Dr. Littman says.
Thanks to rapid progress in the field of genomics, he expects the entire DNA sequence of the SFB species to be completed within a few months. Armed with the sequence, researchers could focus on specific proteins. "For example, can we identify a protein that, when we inject it into an epithelial cell, sets off in motion the whole pathway to make Th17 cells?" he says. "By knowing how to do this, you may be able to give people a peptide or a compound that induces Th17 cells by mimicking the bacterial product, and in that way either protect or ameliorate the effect of the infection."
Too much Th17 cell activation, however, can lead to harmful inflammation, Dr. Littman says. Excessive induction by specific microbes in the gut, then, could contribute to autoimmune diseases such as rheumatoid arthritis, psoriasis, Crohn's disease, and possibly even multiple sclerosis.
The study's co-authors include Ivaylo I. Ivanov and Nicolas Manel from NYU Langone Medical Center's Helen L. and Martin S. Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine; Kenya Honda, Koji Atarashi, Takeshi Tanoue, and Kiyoshi Takeda from Osaka University; Tatsuichiro Shima, Akemi Imaoka, and Yoshinori Umesaki from the Yakult Central Institute for Microbiological Research in Tokyo; Kikuji Itoh from the University of Tokyo; Eoin L. Brodie, Ulas Karaoz, Katherine C. Goldfarb, and Clark A. Santee from Lawrence Berkeley National Laboratory; Susan V. Lynch from the University of California at San Francisco; and Dongguang Wei at Carl Zeiss SMT Inc. in Massachusetts.
The study was supported by fellowships from the Crohn's and Colitis Foundation of America and the Cancer Research Institute, and by grants from the National Institutes of Health; the Japan Science and Technology Agency's PRESTO Program; the Ministry of Education, Culture, Sports, Science and Technology in Japan; the Senri Life Science Foundation; and the Naito Foundation
Source:
Dorie Klissas
NYU Langone Medical Center / New York University School of Medicine
This remarkable activation of the immune response could point to a similar phenomenon in humans, helping researchers understand how gut-dwelling bacteria protect us from pathogenic bacteria, such as virulent strains of E. coli. The study, published in the Oct. 30, 2009, issue of Cell, also supports the idea that specific bacteria may act like neighborhood watchdogs at key locations within the small intestine, where they sense the local microbial community and sound the alarm if something seems amiss.
In mice, at least, the newly identified neighborhood watchdog looks like something out of Disney's "The Shaggy D.A." Distinguished by long hair-like filaments, "These bacteria are the most astounding things I've ever seen," says Dan Littman, MD, PhD, the Helen L. and Martin S. Kimmel Professor of Molecular Immunology and a Howard Hughes Medical Institute Investigator.
Co-led by Dr. Littman's lab, the collaboration with researchers in Japan, California, and Massachusetts zeroed in on a little-known microbe named segmented filamentous bacterium, or SFB. In mice raised under germ-free conditions, the scientists found that adding SFB was sufficient to trigger the appearance of specialized T helper cells known as Th17 cells. These immune specialists, in turn, can send signals that tell epithelial cells lining the small intestine to increase their output of molecules targeting selected microbes.
For the study's mice, the infection-fighting response was enough to ward off the pathogen Citrobacter rodentium, considered a good model for the type of disease-causing E. coli found in contaminated foods like spinach or ground beef. Without SFB to protect them, mice infected with Citrobacter rodentium became ill before recovering.
In the same way, commensal microbes - beneficial bacteria - could decrease our susceptibility to various pathogenic invaders. "So you can immediately see some practical application of this, if one can mimic the presence of these commensal bacteria to strengthen resistance to pathogenic microbes," Dr. Littman says.
Thanks to rapid progress in the field of genomics, he expects the entire DNA sequence of the SFB species to be completed within a few months. Armed with the sequence, researchers could focus on specific proteins. "For example, can we identify a protein that, when we inject it into an epithelial cell, sets off in motion the whole pathway to make Th17 cells?" he says. "By knowing how to do this, you may be able to give people a peptide or a compound that induces Th17 cells by mimicking the bacterial product, and in that way either protect or ameliorate the effect of the infection."
Too much Th17 cell activation, however, can lead to harmful inflammation, Dr. Littman says. Excessive induction by specific microbes in the gut, then, could contribute to autoimmune diseases such as rheumatoid arthritis, psoriasis, Crohn's disease, and possibly even multiple sclerosis.
The study's co-authors include Ivaylo I. Ivanov and Nicolas Manel from NYU Langone Medical Center's Helen L. and Martin S. Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine; Kenya Honda, Koji Atarashi, Takeshi Tanoue, and Kiyoshi Takeda from Osaka University; Tatsuichiro Shima, Akemi Imaoka, and Yoshinori Umesaki from the Yakult Central Institute for Microbiological Research in Tokyo; Kikuji Itoh from the University of Tokyo; Eoin L. Brodie, Ulas Karaoz, Katherine C. Goldfarb, and Clark A. Santee from Lawrence Berkeley National Laboratory; Susan V. Lynch from the University of California at San Francisco; and Dongguang Wei at Carl Zeiss SMT Inc. in Massachusetts.
The study was supported by fellowships from the Crohn's and Colitis Foundation of America and the Cancer Research Institute, and by grants from the National Institutes of Health; the Japan Science and Technology Agency's PRESTO Program; the Ministry of Education, Culture, Sports, Science and Technology in Japan; the Senri Life Science Foundation; and the Naito Foundation
Source:
Dorie Klissas
NYU Langone Medical Center / New York University School of Medicine
Better Management More Important Than New Drugs For Arthritis
Although there has been an increase in the number of new arthritis treatments in recent years, the best results will come from more effective use of the drugs we have. Research published in BioMed Central's open access journal Arthritis Research and Therapy investigates the effectiveness of available arthritis drugs and concludes that better management is the most important factor.
Isidoro Gonz??lez-Alvaro from the Hospital Universitario de la Princesa, Spain, led a team of researchers who studied the treatment of 789 patients over four years between 2000 and 2004. He said, "Our work shows that the treatment of rheumatoid arthritis at tertiary hospitals in Spain has improved from the year 2000. It is likely that better management of available drugs, mainly methotrexate, has been learned during the last decade - along with the clinical development of most biologic agents."
The management of rheumatoid arthritis (RA) has changed a great deal over the last 10 years. The development of biologic therapies, as well as the rigorous clinical trials that have demonstrated their effectiveness, have probably contributed to this change. However, according to Gonz??lez-Alvaro, "In our study, we did not observe the amazing halt of radiological progression described in clinical trials."
When used outside trials, the effectiveness of new drugs may differ, since patients included in clinical trials are on average younger, have less comorbidity, and show greater disease activity than real-life patients. In order to ascertain the real-life effectiveness of new RA medication, the authors studied RA patients in terms of disease activity, disability and radiological progression in the period after the Spanish launch of Leflunomide and the TNF antagonists. They write, "The most relevant finding of our work is that disease activity in RA has improved, independently of the availability of new therapies, in patients with severe and mild disease."
The authors conclude, "It is clear that we need specific markers of RA severity that allow us to select adequate patients for early biologic treatment in order to improve their therapeutic response, as well as their functional outcome. These tools may also help to improve cost-effectiveness of these drugs avoiding unnecessary prescriptions."
Notes:
1. Trends towards improved disease state in Rheumatoid Arthritis over time: the influence of new therapies and changes in management approach. Analysis of the EMECAR cohort
Isidoro Gonzalez-Alvaro, Miguel A Descalzo, Loreto Carmona and the EMECAR group
Arthritis Research and Therapy (in press)
Article available at journal website: arthritis-research/
All articles are available free of charge, according to BioMed Central's open access policy.
2. Arthritis Research and Therapy is an international, peer-reviewed online and print journal, publishing original research, reviews, commentaries and reports. Studies relate to the rationale and treatment of arthritis, autoimmune disease and diseases of bone and cartilage. The journal is edited by Prof Peter E Lipsky (USA) and Prof Sir Ravinder N Maini (UK) and has an Impact Factor of 4.04.
3. BioMed Central (biomedcentral/) is an independent online publishing house committed to providing immediate access without charge to the peer-reviewed biological and medical research it publishes. This commitment is based on the view that open access to research is essential to the rapid and efficient communication of science.
Source: Graeme Baldwin
BioMed Central
Isidoro Gonz??lez-Alvaro from the Hospital Universitario de la Princesa, Spain, led a team of researchers who studied the treatment of 789 patients over four years between 2000 and 2004. He said, "Our work shows that the treatment of rheumatoid arthritis at tertiary hospitals in Spain has improved from the year 2000. It is likely that better management of available drugs, mainly methotrexate, has been learned during the last decade - along with the clinical development of most biologic agents."
The management of rheumatoid arthritis (RA) has changed a great deal over the last 10 years. The development of biologic therapies, as well as the rigorous clinical trials that have demonstrated their effectiveness, have probably contributed to this change. However, according to Gonz??lez-Alvaro, "In our study, we did not observe the amazing halt of radiological progression described in clinical trials."
When used outside trials, the effectiveness of new drugs may differ, since patients included in clinical trials are on average younger, have less comorbidity, and show greater disease activity than real-life patients. In order to ascertain the real-life effectiveness of new RA medication, the authors studied RA patients in terms of disease activity, disability and radiological progression in the period after the Spanish launch of Leflunomide and the TNF antagonists. They write, "The most relevant finding of our work is that disease activity in RA has improved, independently of the availability of new therapies, in patients with severe and mild disease."
The authors conclude, "It is clear that we need specific markers of RA severity that allow us to select adequate patients for early biologic treatment in order to improve their therapeutic response, as well as their functional outcome. These tools may also help to improve cost-effectiveness of these drugs avoiding unnecessary prescriptions."
Notes:
1. Trends towards improved disease state in Rheumatoid Arthritis over time: the influence of new therapies and changes in management approach. Analysis of the EMECAR cohort
Isidoro Gonzalez-Alvaro, Miguel A Descalzo, Loreto Carmona and the EMECAR group
Arthritis Research and Therapy (in press)
Article available at journal website: arthritis-research/
All articles are available free of charge, according to BioMed Central's open access policy.
2. Arthritis Research and Therapy is an international, peer-reviewed online and print journal, publishing original research, reviews, commentaries and reports. Studies relate to the rationale and treatment of arthritis, autoimmune disease and diseases of bone and cartilage. The journal is edited by Prof Peter E Lipsky (USA) and Prof Sir Ravinder N Maini (UK) and has an Impact Factor of 4.04.
3. BioMed Central (biomedcentral/) is an independent online publishing house committed to providing immediate access without charge to the peer-reviewed biological and medical research it publishes. This commitment is based on the view that open access to research is essential to the rapid and efficient communication of science.
Source: Graeme Baldwin
BioMed Central
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