RxPG News : Musculoskeletal

Physiotherapy after surgery best for shoulder problems

Tue, 21 Jun 2011 04:00:00 PST

( from http://www.rxpgnews.com ) Most patients who receive physiotherapy after surgery experience that pain is reduced by a half within a few months. Most of them are free of pain after one to two years. This is the conclusion of a thesis presented at the University of Gothenburg, Sweden.

Age-related changes in tissue combined with acute trauma can contribute to shoulder problems. The most common cause of such problems, however, is compression of the tendons in the shoulder due to a reduction in the space available, says Ingrid Hultenheim Klintberg, physiotherapist and researcher at the Institute of Neuroscience and Physiology.

Patients with these symptoms should initially be treated by physiotherapy. Those for whom physiotherapy does not have an adequate effect are offered surgical treatment, in which the space available is enlarged and the tendons repaired, if necessary. The two most common procedures are known as arthroscopic subacromial decompression and rotator cuff repair.

The aim is that the patient should become free of pain, regain muscular strength, regain mobility, and be able to resume work and leisure activities. Patients who undergo either of these two procedures are offered physiotherapy, following a tailored programme of treatment.

The results presented in the thesis show that most patients state that pain and discomfort are reduced by 50%, 3-6 months after the surgery. They had achieved full mobility and muscle strength compared with reference values at the two-year follow up after the surgery, says Ingrid Hultenheim Klintberg.

Follow up 8-11 years after the surgery showed that many of the patients had retained good shoulder function, mobility and strength.

Their quality of life was good and they display the same pattern of physical activity as do Swedish people in general, states Ingrid Hultenheim Klintberg.

ACSM: Yoga helped older stroke victims improve balance, endurance

Sat, 04 Jun 2011 04:00:00 PST

( from http://www.rxpgnews.com ) An Indiana University study that exposed older veterans with stroke to yoga produced exciting results as researchers explore whether this popular mind-body practice can help stroke victims cope with their increased risk for painful and even deadly falls.

The pilot study involved 19 men and one woman, average age of 66. For eight weeks, they participated in a twice weekly hour-long group yoga class taught by a yoga therapist who dramatically modified the poses to meet the veterans' needs.

A range of balance items measured by the Berg Balance Scale and Fullerton Advance Balance Scale improved by 17 percent and 34 percent respectively by the end of the program. But equally exciting to lead researcher Arlene A. Schmid, rehabilitation research scientist at the Richard L. Roudebush VA Medical Center in Indianapolis, was the measurable gain in confidence the study participants had in their balance.

It also was interesting to see how much the men liked it, said Schmid, assistant professor of occupational therapy in the School of Health and Rehabilitation Sciences at Indiana University-Purdue University Indianapolis. Many of the veterans wanted the study to continue or asked for a take-home exercise plan so they could continue the practice. They enjoyed it so much partly because they weren't getting any other treatment. They had already completed their rehabilitation but felt there still was room for improvement.

Schmid will discuss her findings on Saturday during the American College of Sports Medicine meeting in Denver. Her poster presentation, Preliminary Evidence of Yoga on Balance and Endurance Outcomes for Veterans with Stroke will be from 7:30 a.m.-11 a.m. in Hall B in the session for Fitness and Performance Testing for Posture, Stability and Balance.

Statistics concerning strokes and falls are grim, with studies showing that strokes can quadruple the risk of falling and greatly increase the risk of breaking a hip after a fall. An estimated 80 percent of people who have strokes will also have some degree of impaired balance.

The study participants performed poses initially while seated in chairs and then progressed to seated and standing poses. Eventually, they all performed poses on the floor, something Schmid considers significant because of a reluctance many older adults have to working on the floor.

Everything was modified because we wanted them to be successful on day one, Schmid said. Everyone could be successful at some level.

A score of less than 46 on the Berg Balance Scale indicates a fall risk. Schmid said the study participants on average began the study with a score of 40 and then improved to 47, moving them past the fall risk threshold. The study participants also showed significant improvements in endurance based on a seated two-minute step test and a six-minute walk test.

Schmid said research into therapeutic uses for yoga is really taking off, particularly in mental health fields. Clinically, she has been watching a small trend of occupational therapists and physical therapists also becoming yoga therapists. The yoga performed in the study was modified to the extent that Schmid said it would be very difficult to find a comparable class offered publicly. Such a class should be taught by a yoga therapist who has had additional training in anatomy and physiology and how to work with people with disabilities. Schmid hopes to expand the study so she and her colleagues can explore whether such classes are effective on a larger scale.

Large study of arthroscopic rotator cuff repair reveals some surprises

Sat, 19 Feb 2011 05:00:00 PST

( from http://www.rxpgnews.com ) Arthroscopic rotator cuff repair is highly effective and provides durable results five years after surgery, according to a large, prospective study by Hospital for Special Surgery investigators. The study also surprisingly revealed that the rotator cuff has the ability to heal even when early imaging studies have found a defect at the site of repair. The research will be presented at the upcoming American Shoulder and Elbow Surgeons (ASES) 2011 Specialty Day meeting, to be held Feb. 19 in San Diego, Calif., following the annual meeting of the American Academy of Orthopaedic Surgeons.

Our study demonstrates that arthroscopic rotator cuff repair results remain excellent when followed over five years, and we found that some tendons that were incompletely healed at two years appeared to heal fully by five years, suggesting that rather than deteriorating over time, results may in fact improve over time, said David Altchek, M.D., attending orthopedic surgeon and co-chief in the Sports Medicine and Shoulder Service at Hospital for Special Surgery (HSS) in New York, who was involved with the study.

These days, arthroscopy is the standard of care for repairing rotator cuffs. Most patients who have this procedure have excellent clinical results, but surprisingly the results sometimes don't correlate to whether the rotator cuff is healed or not. When your rotator cuff is torn, you attribute all your pain and dysfunction to your torn rotator cuff, then you have it fixed and you feel better, but sometimes when you take an ultrasound or an MRI, the rotator cuff looks exactly like it did before you had the surgery, said Lawrence Gulotta, M.D., who led the study and is a sports medicine and shoulder surgeon at HSS. Before this study, we thought that once a rotator cuff had re-torn or failed to heal following surgery, it had no capacity to heal in the future. Now we know that the rotator cuff does have the capacity to heal itself, even if early radiographic studies showed there was a defect at the repair site.

At one year following surgery, ultrasound results showed that 64.3 percent of patients had a healed rotator cuff. This percentage went up to 75.4 percent at two years and 81.2 percent at five years.

The study involved 193 patients who underwent arthroscopic rotator cuff repair at HSS and then were evaluated annually for five years. In 2003, HSS established the Arthroscopic Rotator Cuff Registry to prospectively evaluate the functional and radiographic outcomes of patients undergoing this procedure and this study comes from that registry. When the study was started, arthroscopic rotator cuff repairs were really just coming onto the scene, so the HSS Sports Medicine and Shoulder Service decided to start a prospective study to evaluate the outcomes of them, Dr. Gulotta said.

Common hip disorder can cause sports hernia

Sat, 19 Feb 2011 05:00:00 PST

( from http://www.rxpgnews.com ) Sports hernias are commonly found in individuals with a mechanical disorder of the hip and can be resolved with surgery to fix the hip disorder alone in some cases, according to a recent study. The research, conducted by investigators at Hospital for Special Surgery, will be presented at the American Orthopedic Society for Sports Medicine 2011 Specialty Day meeting, held Feb. 19 in San Diego following the annual meeting of the American Academy of Orthopaedic Surgeons.

If individuals have symptoms of athletic pubalgia otherwise known as sports hernia, doctors should carefully assess their hip joint to make sure there is not an underlying mechanical problem in the hip that may be the bigger problem in the overall function of the athlete, said Bryan Kelly, M.D., co-director of the Center for Hip Pain and Preservation at Hospital for Special Surgery who led the study. If patients present with both sports hernia and femoro-acetabular impingement symptoms, you have to consider what the order of treatment should be or whether you should just treat one. He said the research suggests that treating the joint mechanics first is optimal and if problems persist, doctors can then try surgery for the sports hernia.

In recent years, a hip condition known as femoro-acetabular impingement (FAI) or hip impingement has become widely recognized in the medical community. The hip is a ball-and-socket joint where the upper end of the thigh bone fits into the cup-shaped socket of the pelvis. In a healthy hip joint, the ball rotates freely in the cup, but in some people a bony bump on the upper thigh bone produces a situation where there is inadequate space for the hip bone to move freely in the socket. The result is damage to the socket rim and the cartilage that lines the bones, which can lead to hip arthritis. In the past few years, doctors have thought that this condition may also cause sports hernias. A sports hernia is a tearing of the tissue that forms the inner part of the abdominal wall and inserts into the pubic bone.

To investigate how often FAI is associated with sports hernia, researchers examined the records of all professional athletes who underwent arthroscopic surgery at HSS for symptomatic FAI between April 2005 and April 2010. Patients were included if their FAI limited their ability to return to competitive play. The group, 38 in total, included nine baseball players, 13 football players, eight hockey players, five soccer players, two basketball players, and one skater. Retrospective data regarding prior athletic sports hernia surgery, ability to return to play, and duration until return to play was collected from all patients.

The investigators found that while 32 percent of the athletes had previously undergone surgery for their hernia, none of them had been able to return to their previous level of competition with the hernia surgery alone. One patient underwent hernia surgery at the same time as the FAI surgery. Thirty-nine percent of patients had hernia symptoms that resolved with FAI surgery alone and 36 of 38 patients were able to return to their previous level of play. All 12 patients that had both hernia and FAI surgery were able to return to professional competition. On average, athletes were able to return to their sport 5.9 months after arthroscopic surgery.

This is the first paper that has looked at the coincidence of FAI and sports hernia, and has practical implications for practice. Groin pulls and lower abdominal muscle strains are frequently associated with hip joint mechanical problems, and patients should make sure that doctors are looking at both those locations as potential sources of the pain, said Dr. Kelly, who is also in the Sports Medicine and Shoulder Service at HSS. Before this study we knew that both impingement in the hip joint and athletic pubalgia were the cause of decreased function and pain in athletes. Now we recognize that there is a close relationship between those two, and oftentimes the problems coexist and need to be looked at when treatment options are being discussed.

Duchenne muscular dystrophy - also a disease of stem cells

Fri, 10 Dec 2010 08:26:15 PST

( from http://www.rxpgnews.com ) Researchers have long known that the devastating disease called Duchenne muscular dystrophy (DMD) is caused by a single mutation in a gene called dystrophin. The protein encoded by that gene is critical for the integrity of muscle; without it, they are easily damaged. But new findings in mice reported online in the journal Cell on December 9th by researchers at Stanford suggest that disease symptoms, including progressive muscle weakening leading to respiratory failure, only set in when skeletal muscle stem cells can no longer keep up with the needed repairs.

"This is not just a disease of dystrophin deficiency" said Helen Blau of Stanford University School of Medicine, who led the study. "It's also a disease of stem cells." That means that successful treatments would likely need to target muscle stem cells, not just muscle fibers, she says.

"These findings are critical for thinking about how to treat the disease and when," added Jason Pomerantz, the study's co-corresponding author who is now at the University of California, San Francisco. "It predicts any treatment designed solely to build muscle or enhance muscle function without replenishing the stem cell compartment is likely to fail and may even accelerate the decline. It's like pushing the gas pedal to the floor when there is no reserve."

The new study also answers a long-standing puzzle in the field that has stymied basic studies in search of potential treatments or treatment strategies: Mice carrying the same dystrophin mutation found in human patients show only mild symptoms of the disease.

"It has been a mystery for the past 25 years that mice with the genetic defect show minimal or no symptoms," Blau said, "and consequently there has been no mouse model in which to study the pathophysiology of the disease or potential treatments." People thought maybe it was because mice are smaller or don't live as long, but there was no real explanation. That is, until now.

The new findings attribute the discrepancy between the mouse and human symptoms to a characteristic of chromosomes. Regions of repetitive DNA found at the tips of chromosomes, known as telomeres, are longer in mice than they are in humans. Blau and her team have found that mice with the dystrophin mutation and another that leads them to have shortened telomeres have severe symptoms of the disease that worsen with age just as they do in human patients.

Telomeres protect chromosomes from deterioration and they tend to get shorter each time a cell divides. When telomeres become critically shortened, it triggers events that lead cells to die. The longer telomeres normally found in mice apparently give their muscle stem cells greater staying power and a greater capacity to repair the damage caused by the deficiency of dystrophin.

"Mice with shorter telomeres show all the parameters of the disease," Blau said. The animals won't run on a treadmill, their strength is really diminished, and their diaphragms (the muscle needed to breathe) are reduced to the point that they are "thin remnants, or strips of tissue." This muscle weakening paralleled a decline in the regenerative capacity of their muscle stem cells.

"There is continuous damage due to the loss of dystrophin," Pomerantz explained. "When the stem cell reserve is depleted, the symptoms emerge. The mice are spinning their wheels in a cycle of damage, repair, damage, repair, until the ability to repair gives out. In these mice [with shortened telomeres], it gives out earlier."

When the researchers isolated and transplanted healthy muscle stem cells into the sick mice, it alleviated symptoms of the disease.

The mice are now the first tractable model system for studying the disease, and that should come as good news to families affected by this form of muscular dystrophy, the researchers say.

"Our new mouse model changed the way we were thinking about the pathophysiology of the disease," said Foteini Mourkioti of Stanford who is the co-first author on the paper. "We now understand that muscle stem cells are an essential component of this dystrophin-deficient disease and we can now start thinking of more precise ways to treat Duchenne muscular dystrophy."

Treatments intended to restore muscle will likely work only temporarily or not at all. In fact, they are likely to exacerbate the problem by exhausting muscle stem cells more rapidly. Timing will also be key.

"Therapeutic strategies aimed at intervening early in DMD patients, in the first years of their life, are more likely to have a better outcome as they would act before this end-stage tissue failure is reached," said Alessandra Sacco, the study's first author who is now at the Sanford-Burnham Medical Research Institute.

Laboratory studies show promise for new multiple sclerosis treatment

Thu, 18 Nov 2010 05:00:00 PST

( from http://www.rxpgnews.com ) Successfully treating and reversing the effects of multiple sclerosis, or MS, may one day be possible using a drug originally developed to treat chronic pain, according to Distinguished Professor Linda Watkins of the University of Colorado at Boulder.

Watkins and her colleagues in CU-Boulder's department of psychology and neuroscience discovered that a single injection of a compound called ATL313 -- an anti-inflammatory drug being developed to treat chronic pain -- stopped the progression of MS-caused paralysis in rats for weeks at a time.

Lisa Loram, a senior research associate who spearheaded the project in Watkins' laboratory, presented the findings at the Society for Neuroscience's annual meeting held in San Diego this week.

MS is an inflammatory disease where the body's immune system attacks a protective sheath called myelin that encompasses nerves in the spinal cord and brain. As the disease progresses, the myelin develops lesions, or scars, that cause permanent neurological problems.

What happens now with MS drugs is they slow or stop the progression of MS, but they don't treat it, Watkins said. They don't take people back to normal because the lesions caused by MS don't heal.

Watkins, Loram and their colleagues hope to use spinal cord and brain-imaging technology to extend their studies to determine if lesions are being healed in rats that received an ATL313 injection.

If we have a drug that is able to heal these lesions, this treatment could be a major breakthrough in how we treat the symptoms of MS in the future, she said.

The new findings were quite a surprise to Watkins. The team had originally wanted to look at the drug's potential in treating pain associated with MS, because about 70 to 80 percent of MS patients suffer from chronic pain that is not treatable.

What we had originally thought about this class of compounds is that they would calm down glial cells in the spinal cord because their pro-inflammatory activation is what causes pain, she said.

Under normal circumstances glial cells are thought to be like housekeepers in the nervous system, Watkins said, essentially cleaning up debris and providing support for neurons. Recent work by Watkins and others has shown that glial cells in the central nervous system also act as key players in pain enhancement by exciting neurons that transmit pain signals.

What's become evident is that glial cells have a Dr. Jekyll and Mr. Hyde personality, Watkins said. Under normal circumstances they do all these really good things for the neurons, but when they shift into the Mr. Hyde formation they release a whole host of chemicals that cause problems like neuropathic pain and other chronic pain conditions.

They discovered that ATL313 appears to reset the glial cells from an angry activated state to a calm anti-inflammatory state that may heal MS lesions.

NIH awards Muscular Dystrophy Cooperative Research Center grants

Wed, 29 Sep 2010 04:00:00 PST

( from http://www.rxpgnews.com ) Three grants totaling more than $4.5 million, from agencies of the National Institutes of Health, will be used to explore novel treatment strategies for muscular dystrophy.

The grants were awarded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute of Neurological Disorders and Stroke (NINDS) and Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) for year one of five-year cooperative agreements.

The grants designate Nationwide Children's Hospital, Columbus, Ohio, as a Senator Paul D. Wellstone Muscular Dystrophy Cooperative Research Center (MDCRC), and continue funding of crucial research by two previously established MDCRCs at the University of Pennsylvania, Philadelphia and the University of Iowa, Iowa City.

Researchers at Nationwide Children's Hospital, under the direction of Jerry Mendell, M.D., will further develop methods to overcome immune barriers to gene correction for Duchenne muscular dystrophy (DMD). A form of muscular dystrophy that affects children and young adults, DMD is caused by an absence of dystrophin, a protein that helps keep muscle cells intact. Gene therapy for DMD includes injecting genes for a functional version of the muscle protein dystrophin, encased in a virus designed to deliver the gene into the muscle cells. In an early trial of this experimental therapy, blood analyses and biopsy slides showed that the immune system in more than half of the children mounted a response to dystrophin or the viral delivery vehicle.

The goal of the research will be to see how many patients have pre-existing immunity to dystrophin that could block the gene transfer. Researchers also will determine if the immune reaction could be circumvented by removing antibodies with a blood-purifying procedure called plasmapheresis or administering drugs that suppress the immune response.

At the University of Pennsylvania, researchers led by H. Lee Sweeney, Ph.D., will research treatments to inhibit muscle fibrosis, or scarring, that causes muscle dysfunction. By reducing scar formation, such treatments may not only improve muscle function, but may also enhance muscle regeneration and increase the effectiveness of drug, gene and stem cell therapies for muscular dystrophies (MD). The research aims to identify existing drugs that inhibit fibrosis, as well as drive the development of new classes of fibrosis inhibitors. The center's goal is to develop non-invasive imaging techniques to assess the replacement of skeletal and cardiac muscle with fat and scar tissue associated with MD progression.

Research at the University of Iowa, directed by Kevin Campbell, Ph.D., will explore therapeutic strategies for the treatment of various muscular dystrophies arising from the abnormal processing of muscle proteins called dystroglycans. This will involve investigating what happens on a molecular level in these dystrophies (called dystroglycanopathies) and evaluating various treatment strategies, using mouse models and cells with known mutations from dystroglycanopathy patients. It will also entail identifying and characterizing dystroglycanopathy patients and developing infrastructure for trials of dystroglycanopathy treatment in defined patient groups.

Muscular dystrophy is a group of debilitating, and often fatal, diseases characterized by progressive weakness and degeneration of the skeletal or voluntary muscles, which control movement and breathing. MD can affect people of all ages. Although some forms first become apparent in infancy or childhood, others may not appear until middle age or later.

Simple, accurate in-office tool predicts athletes at high-risk for ACL injury, study details

Sat, 17 Jul 2010 04:00:00 PST

( from http://www.rxpgnews.com ) PROVIDENCE, R.I. -- Previously, determining athletes at high-risk for ACL (anterior cruciate ligament) injuries required expensive and complex laboratory-based motion analysis systems, such as those used in creating video games. But a new study presented today at the American Orthopaedic Society for Sports Medicine's (AOSSM) Annual Meeting, offers physicians a low-cost, in-office, tool to help identify athletes at increased risk.

ACL injuries are devastating to athletes, and the risk factor for female athletes is much higher, said Greg Myer, sports biomechanist at the Cincinnati Children's Hospital. In an earlier study, we used motion analysis systems to measure and calculate torques on ligaments which accurately predicted which athletes are high-risk, but this method was expensive, labor intensive and required sophisticated equipment. So in this study, we looked for a low-cost, in office, simpler method to predict which athletes are high-risk.

Unfortunately, women are two to eight times more likely to injure their ACL than men, according to recent studies. Researchers believe this may be due to differences in hormone levels on ligament strength and stiffness, neuromuscular control and fatigue, lower limb biomechanics, ligament strength, as well as a difference in neuromuscular control in women when landing jumps (women appear to have less hip and knee flexion or bending and land more knock kneed than men.)

The good news, according to Myer, is that those athletes who have the higher risk factors of increased knee torques or load are those who also benefit the most from the remedy of neuromuscular training in jumping, posture and building landing strength.

The simpler, lower-cost measure to predict high-risk athletes for ACL injury provides the next critical step to bridge the gap between expensive in-laboratory identification of injury and identification of these injuries in the doctor's office. The simplified method, which can be done in the doctor's office combines measuring the tibia or shin bone with a standard measuring tape and an athlete's weight in combination with motions of the knee during landing captured with standard camcorders. These simple factors can quickly identify young females who demonstrate a primary risk for ACL injury. The in-office method strongly correlated to the expensive laboratory method with variables that ranged from 0.87 to 0.98.

This method may be used as a training camp protocol in partnership with team clinicians or set up and run in the athletic training setting, said Myer. Current evidence indicates that athletes identified as high-risk for ACL injury using this approach are more responsive to neuromuscular training aimed at reducing this risk factor. This tool can also be used to get high-risk athletes into appropriate interventions to further reduce their potential of injury risk which may increase both the efficacy and efficiency of future interventions aimed to prevent ACL injury in female athletes.

New surgery improves outcomes for severe flat foot deformity

Thu, 08 Jul 2010 04:00:00 PST

( from http://www.rxpgnews.com ) A surgery developed at Hospital for Special Surgery can improve patient outcomes in individuals with severe adult flat foot deformity, a problem that is increasingly being seen inhospitals across the country. Patients who undergo the new surgery have better long-term outcome and mobility than those who undergo traditional surgery. The paper will be presented at the annual meeting of the American Orthopaedic Foot and Ankle Society (AOFAS, abstract 348) in National Harbor, Md., on July 8.

Before this study, we were not sure whether you could salvage patients with flat foot and ankle deformity and correct their ankle as well as their foot deformity, said Jonathan Deland, M.D., chief of the Department of Foot and Ankle Surgery at Hospital for Special Surgery (HSS). Now we know that with this technique you can save the ankle, and it provides a correction of the deformity even at nine years after surgery. Dr. Deland developed the surgery and is senior author of the study.

Adult acquired flat foot deformity is basically a severe type of flat foot that develops for unknown reasons in individuals who have had flat feet all their life. It is more prevalent in women and those who are overweight, and it usually develops in individuals in their 40s and 50s. In stage I of the deformity, the tendon that runs along the inside of the ankle begins to degenerate. In stage II, the arch starts to fail, and a person develops a more severe case of flat foot. As the arch continues to collapse and the flat foot becomes more pronounced, mobility becomes difficult, and the foot becomes stiff, which is considered stage III.

In the most severe stage, stage IV, the ankle starts tilting and is at risk of developing arthritis as a result of the deformity. These people have tremendous flat foot to the point that their ankle is involved, said Scott Ellis, M.D., foot and ankle orthopedic surgeon at HSS and first author of the study. In these people, the extreme flat foot has injured the deltoid ligament, a strong, flat triangular ligament that is located on the inside of the ankle that provides support to prevent the ankle from over pronating. In stage IV, the deltoid ligament has become stretched and incompetent, which is what allows the ankle to tilt.

If the ankle deformity is severe and symptomatic enough, then surgeons either perform an ankle replacement, which is very difficult, or, more commonly, fuse the ankle. The fusion is not ideal because it takes all the motion away in the ankle in a patient who already has a foot problem, Dr. Ellis said. Imagine walking without motion in your ankle. It changes your gait and it leads to arthritis in the other joints of the foot over time, eight to 10 years down the line, because you start having to use those joints to take up the slack of motion that is not occurring in the ankle.

In the new surgery for stage IV deformity developed at HSS, surgeons not only reconstruct the flat foot deformity, but they also reconstruct the deltoid ligament using a tendon that runs along the outside of the calf called the peroneus longus. A person can function without their peroneus longus. Alternatively, the peroneus longus can be kept and a cadaver tendon used.

In the study presented at the AOFAS meeting, HSS investigators conducted the new surgery in five patients, four men and one woman, and monitored the surgery's success. The mean age was 67 years. Patients underwent X-rays that showed the surgery improved the alignment in the ankle and the effects were long-lasting. The X-rays showed the maintenance of the correction of the tilt. The alignment was still improved nine years later, Dr. Ellis said. Patients had excellent mobility at eight to 10 years following the surgery and none of the patients had arthritis.

Doctors also measured outcomes through several questionnaires including the Foot and Ankle Orthopedic Survey, an outcome scale that assessed 42 items divided among six categories. The average FAOS scores were 61.4 for symptoms, 1.5 for stiffness, 78.3 for pain, 87.9 for function/daily living, 71.7 for function/sports/recreational activities, and 42.1 for quality of life. The FAOS scores were good, Dr. Ellis said.

Patients were asked how far they could walk in blocks or miles and the cohort of patients was able to walk an average of 25 blocks (range 10 to 40), equivalent to 1.25 miles, after surgery. Two patients continued to play golf without significant problems, another exercised regularly on a treadmill, one was involved in circuit training, and the final patient played volleyball, although he did notice some stiffness. All patients reported they were satisfied with the procedure and, given the result, would have the operation again.

Dr. Ellis says he thinks the new surgery may be increasingly useful with stage IV flat foot deformity. No surgeons that the authors know of at other hospitals are currently using the surgery. The procedure is expected to become more popular. I see a lot of this deformity in my office. It's one of the major problems I deal with, Dr. Ellis said, pointing out that it is very prevalent.

Hip exercises found effective at reducing, eliminating common knee pain in runners

Fri, 04 Jun 2010 04:00:00 PST

( from http://www.rxpgnews.com ) A twice weekly hip strengthening regimen performed for six weeks proved surprisingly effective at reducing -- and in some cases eliminating -- knee pain referred to as patellofemoral pain (PFP) in female runners.

The study by Tracy Dierks, assistant professor in the Department of Physical Therapy at Indiana University-Purdue University Indianapolis, was based on the theory that stronger hips would correct running form errors that contribute to PFP, even though study participants were given no instruction in gait training. The study used a pain scale of 0 to 10, with 3 representing the onset of pain and 7 representing very strong pain -- the point at which the runners normally stop running because the pain is too great. The injured runners began the six-week trial registering pain of 7 when they ran on a treadmill and finished the study period registering pain levels of 2 or lower; i.e. no onset of pain.

I wasn't expecting such huge reductions, to be honest, Dierks said. We've had a couple of runners who have been at level 2, but the overwhelming majority have been a 2 or below.

PFP, one of the most common running injuries, is caused when the thigh bone rubs against the back of the knee cap. Runners with PFP typically do not feel pain when they begin running, but once the pain begins, it gets increasingly worse. Once they stop running, the pain goes away almost immediately. Dierks said studies indicate PFP essentially wears away cartilage and can have the same effect as osteoarthritis. His study participants showed many of the classic signs of PFP, the most prominent being their knees collapsing inward when running or doing a squat exercise move.

The pilot study thus far involved five runners and a control group that comprised another four runners. Hip strength measurements were taken before and after the runners in the control group maintained their normal running schedule for six weeks. Hip strength measurements were taken for all of the runners before and after the next six-week period in which they all performed the hip-strengthening exercises. The exercises, performed twice a week for around 30 to 45 minutes, involved single-leg squats and exercises with a resistance band, all exercises that can be performed at home. This study is part of an ongoing study involving hip exercises and PFP pain, with 11 runners successfully using the intervention. Dierks said he plans to seek funding to test the exercises on a larger group of runners.

Earlier research had focused on the feet as a possible root of PFP, with studies only recently looking more closely at the hips. Dierks said studies have found an association between PFP in women and weak hips, but his study is the first to test a possible treatment. He noted that PFP is considered multi-factorial, so his study is examining one of several possible causes of the pain.

NIH awards $7.5 million to study MRI as a tool to evaluate children with muscular dystrophy

Fri, 07 May 2010 04:00:00 PST

( from http://www.rxpgnews.com ) Duchenne muscular dystrophy research at the University of Florida got a major boost with the award of $7.5 million in National Institutes of Health funding to study the use of magnetic resonance imaging in determining the natural progression of the disease.

UF scientists will assess whether MRI technology can be used as a precise, noninvasive measure of muscle tissue in children with Duchenne muscular dystrophy. Understanding how the disease affects muscle tissue could help facilitate the testing of new therapies in clinical trials, researchers say.

Duchenne muscular dystrophy affects about one of every 3,500 to 5,000 boys born each year in the United States, according to the Centers for Disease Control and Prevention. The disease causes the muscles that control movement to progressively weaken and lose the ability to regenerate after an injury, eventually replacing critical muscle tissue with fat and collagen. By age 12, many patients need a wheelchair. As the disease advances, the heart and respiratory system are affected and patients often die of cardiorespiratory failure in their 20s.

The lack of a reliable assessment tool for measuring muscle function in patients with Duchenne inhibits the transfer of new therapies from the lab to clinical trials, said the study's lead investigator KristaVandenborne, Ph.D., an associate dean for research and planning at the UF College of Public Health and Health Professions and chair of the department of physical therapy. MRI allows you to look at the structure of a muscle tissue in a very objective way with a large amount of detail. Our goal is to develop MRI as a tool to see the progression of the disease, but more importantly, to determine if a new treatment is effective or not, giving researchers rapid feedback about potential new drugs.

The study is funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases and the National Institute of Neurological Disorders and Stroke and will include researchers at Oregon Health and Science University, Children's Hospital of Philadelphia and the University of Pennsylvania. Researchers at the four sites will conduct MRI measurements of muscle in 100 boys with Duchenne, ages 5 through 14, over a five-year period.

We are confident that by the end of the study we will be able to provide clear guidelines for how MRIs should be performed in Duchenne muscular dystrophy and that MRIs will be a valuable tool in clinical trials and drug tests targeting potential Duchenne treatments, Vandenborne said.

Preliminary studies, funded by Parent Project Muscular Dystrophy and the Muscular Dystrophy Association, involved about 30 boys and demonstrated that MRI had many advantages over traditional muscle biopsies, Vandenborne said. Biopsies are invasive and do not give researchers a complete view of all the muscle tissue.

NIH is excited to award this important research grant to Dr. Vandenborne, said Glen Nuckolls, Ph.D., program director of the Muscle Disorders and Therapies Program at the National Institute of Arthritis and Musculoskeletal and Skin Diseases. It is the type of thorough observational study that will collect data needed to design better clinical trials for DMD. Magnetic resonance imaging and spectroscopy are powerful tools to look inside the muscles of patients and measure chemicals in the muscles, and this study has the potential to show that these would be very valuable tools in determining whether an experimental therapy is working to improve the muscles of boys with DMD.

Using stem cells to mend damaged hips

Tue, 23 Mar 2010 04:00:00 PST

( from http://www.rxpgnews.com ) Bone stem cells could in future be used instead of bone from donors as part of an innovative new hip replacement treatment, according to scientists at the University of Southampton.

A team from the University's School of Medicine believe that introducing a patient's own skeletal stem cells into the hip joint during bone grafting would encourage more successful regrowth and repair.

The grafting technique is used to repair the thigh bone and joint during replacement (known as 'revision') hip replacement therapy, a procedure in which surgeons introduce donor bone to the damaged area to provide support for the new hip stem.

In this collaborative study between the University of Southampton and The University of Nottingham, researchers will use adult stem cells from bone marrow in combination with an innovative impaction process and polymer scaffolds.

In a two-year study, funded by the Medical Research Council (MRC), researchers aim to improve the outcomes of this high impact procedure.

Surgeons currently use bone from donors during bone grafting, so introducing a patient's own stem cells to create a living cell or material composite would be a totally new approach, comments Professor Richard Oreffo, an expert in musculoskeletal science at the University of Southampton, who is leading the project.

This is very much the beginning of a project to investigate the potential for this new technique, but our preliminary work suggests this may have significant therapeutic implications.

When a hip joint is damaged, part of the thigh bone or femur, including the ball, can be removed and a new, artificial joint fixed to the remaining thigh bone. Revision hip replacement occurs when that artificial joint needs to be changed.

Professor Oreffo will introduce the stem cells to the hip joint using a scaffold, or support structure, which is designed to protect them, and a new impaction process. The polymer scaffolds will be developed by Professors Steve Howdle and Kevin Shakesheff, experts in chemistry and tissue engineering at the University of Nottingham.

Professor Howdle explains: Building upon strong collaborations with tissue engineering experts, this new grant will allow researchers at Nottingham to take their materials nearer to the clinic.

This could have great benefits for patients, and also offer a significant cost saving for healthcare authorities; but first we need to verify and build upon our preliminary data.

A major part of the work at Nottingham will involve scaling up the supercritical fluid processing apparatus to create larger and more uniform batches of polymer scaffolds for testing.

Dr Chris Watkins, MRC's Translation Theme Leader, says: Resilience, repair and replacement is a priority research area in the MRC's strategic plan, 'Research Changes Lives'. This study highlights how a regenerative approach can offer real hope in addressing a significant problem for an ageing population.

This funding will allow the groups to build on initial studies that show that degradable polymer scaffolds prepared using supercritical carbon dioxide technology can have a dramatic effect on surgical procedures, such as inserting a hip implant in revision hip surgery.

The provisional studies carried out in Southampton show that the polymers can aid bone formation through the creation of a living cell/material composite and aid attachment of the hip implant.

Quantity vs. quality: Long-term use of bone-building osteoporosis drugs

Wed, 10 Mar 2010 05:00:00 PST

( from http://www.rxpgnews.com ) Bisphosphonate treatments, proven to enhance bone density and reduce fracture incidence in post-menopausal women, may adversely affect bone quality and increase risk of atypical fractures of the femur when used for four or more years, according to preliminary research presented today at the 2010 Annual Meeting of the American Academy of Orthopaedic Surgeons (AAOS).

Bisphosphonates are designed to slow or stop the bone loss that occurs during the body's bone remodeling cycle, or the natural process that involves removal and replacement of bone tissue.

Two separate studies by researchers from Hospital for Special Surgery (HSS) and Columbia University Medical Center revealed data suggesting that long-term suppression of bone remodeling by bisphosphonate treatments may alter the material properties of bone, potentially affecting the bone's mechanical integrity and potentially contributing to the risk of atypical fractures.

Although bisphosphonates have demonstrated an improvement in bone quantity, little if anything is known about the effects of these drugs on bone quality, said Brian Gladnick, BS, representing a team of investigators at HSS in New York.

Researchers at Columbia evaluated the bone structure of 111 postmenopausal women with primary osteoporosis, 61 of whom had been taking bisphosphonates for a minimum of four years and 50 controls taking calcium and vitamin D supplements.

This study found that bisphosphonate use improved structural integrity early in the course of treatment, but those gains were diminished with long-term treatment.

In the early treatment period, patients using bisphosphonates experienced improvements in all parameters, including decreased buckling ratio and increased cross-sectional area, said Melvin Rosenwasser, MD, orthopaedic surgeon for Columbia University Medical Center. However, after four years of use, these trends reversed, revealing an association between prolonged therapy and declining cortical bone structural integrity.

Scientists at both institutions noted that the culprit behind the diminishing results may be the fact that bisphosphonates suppress the body's natural process of remodeling bone. Recent research suggests that suppressed bone remodeling from long-term bisphosphonate use might result in brittle bone that is prone to atypical fractures, said Gladnick.

The investigators added that more research is needed to determine the true efficacy of the long-term clinical use of bisphosphonates for the treatment of osteoporosis, and that the results of their studies will not likely affect clinical practice in the near future.

Bisphosphonate use still is a very effective solution that prevents bone loss in most patients and no one is recommending that physicians avoid prescribing these, said Dr. Rosenwasser. However, as baby boomers age and continue to remain active, it is important that we conduct more research and develop sustainable, safe and effective treatments for osteoporosis.

In a second unrelated prospective pilot study, conducted at HSS and funded in part by the NIH, researchers evaluated the bone composition of 21 post-menopausal women who were treated for femoral fractures. Of these, 12 patients had a history of bisphosphonate treatment for an average of 8.5 years, while nine had not had bisphosphonate treatment.

Samples of bone were removed from each patient's femur during surgical placement of a femoral nail. Both micro-architecture and material properties of the bone were analyzed.

The study found that, although there were no differences in bone micro-architecture between groups, the material properties of bone in bisphosphonate-treated patients displayed reduced bone tissue heterogeneity, which may be associated with reduced strength and potentially may contribute to the presentation of atypical fractures.

Patients who had been treated with bisphosphonates showed a reduction in tissue heterogeneity, specifically with mineral content and crystal size compared with the control group, Gladnick said. This tells us that there may be some measurable differences in bone quality parameters in patients on long-term bisphosphonate therapy, which might contribute to the development of atypical fractures.

Osteoporosis drug improves healing after rotator cuff surgery

Wed, 10 Mar 2010 05:00:00 PST

( from http://www.rxpgnews.com ) Tears in the shoulder's rotator cuff, a common sports injury, are painful and restricting. Surgery to repair the damage is successful for pain management, but in many patients it does not result in full recovery of function due to poor healing. New research shows an approved therapy for osteoporosis, Forteo, may speed healing and improve patient outcomes. The preliminary study from Hospital for Special Surgery in New York is being presented at the American Academy of Orthopaedic Surgeons (AAOS) meeting in New Orleans March 9-13.

According to a previous study, only 69 percent of rotator cuff repairs were completely healed when evaluated two years after the surgery, said Scott Rodeo, M.D., co-chief of the Sports Medicine and Shoulder Service at Hospital for Special Surgery and senior author on the study. Although not all of the patients with failed rotator cuff tendon healing had poor clinical outcomes, we wanted to look for ways to further improve patient outcomes.

The rotator cuff is a set of four smaller muscles in the shoulder that rotate the upper arm. A rotator cuff tear happens when the tendon part of the muscle tears away from the bone of the upper arm. The repair surgery reattaches the tendon to the bone, but the success depends on how well the interface between the tendon and bone heals. Much of the time scar tissue forms at that interface, which is not as strong as the original tissue and can lead to a failed repair.

The healing process occurs from both the bone and the tendon, which is made up of collagen, said Carolyn Hettrich, M.D., MPH, fifth year resident in orthopedic surgery at Hospital for Special Surgery and lead author. We knew the drug Forteo is osteogenic and can stimulate bone growth, but we found reports in the literature that it is also chondrogenic, so it can promote cartilage formation as well.

Forteo is a synthetic version of parathyroid hormone, which is the body's primary regulator of calcium and phosphate levels in bone. Recently approved by the FDA, it is prescribed for osteoporosis as it not only stimulates bone growth but it also slows the rate of bone loss.

The researchers hypothesized that because Forteo stimulated both bone and cartilage formation, it might enhance the healing process after rotator cuff surgery. Using a rat model, they performed the surgery and then gave some rats Forteo injections in amounts comparable to human doses.

Initially, at two weeks after the surgery, the repair was not as strong in the rats who received the Forteo. But when the researchers looked at weeks four through eight, the tendon to bone interface in those rats appeared much more like normal tissue. Closer examination showed that not only had those rats that received Forteo produced more bone and cartilage cells, but the organization of the tissue was better and more closely resembled normal tissue. The tendon was also significantly stiffer, a sign of proper healing, at 8 weeks.

The results are positive, but now we want to understand why at week two the tendon wasn't healing as well, said Dr. Hettrich. Our next experiments will look to pinpoint these causes and determine the optimum delivery time of the drug after surgery.

The researchers caution that it would be risky to use Forteo in patients undergoing rotator cuff surgery just yet as further studies are needed. Instead, they encourage patients to talk to their surgeons about other steps they can do to improve healing, such as not smoking after the surgery to optimize their biology.

Athletes who use overhead movements, like baseball or tennis players, are prone to this injury. It is also common in adults over 40 because the tendons begin to degenerate and weaken.

Electromagnetic pulses provide pain relief for osteoarthritis

Sat, 06 Mar 2010 05:00:00 PST

( from http://www.rxpgnews.com ) Electromagnetic pulses significantly decrease pain and inflammation associated with osteoarthritis of the knee, according to Henry Ford Hospital researchers.

In the double-blind, randomized placebo-controlled study, 34 patients used a portable battery-operated device that emits a low-intensity pulsating electromagnetic frequency and experienced more than 40 percent pain relief on their first day.

Our results show pulsed electromagnetic fields caused a significant decrease in pain says Fred Nelson, M.D., associate program director for research and director of the Osteoarthritis Center, Department of Orthopaedics, Henry Ford Hospital.

Dr. Nelson will present the results this week at the Orthopaedic Research Society's annual meeting in New Orleans.

Dr. Nelson explains that in the laboratory, electromagnetic signals have been shown to decrease calcium in cartilage cells. This sets off a series of chemical events that can lead to reduced inflammation. Previously, the electromagnetic fields have been used to control pain related to cosmetic surgery.

We are really fine-tuning what we are doing to the cell environment with a very specific pulse sequence and frequency, says Dr. Nelson.

Patients strapped the small, ring-shaped plastic device around their knees for 15 minutes, twice daily for six weeks. The device was lightweight and patients could position the device directly over clothing. All participants were given a device with a coil that appeared to work but some were assigned active coils and others were given non-active coils. The electromagnetic device was developed by Ivivi Health Sciences of Montvale, New Jersey.

Osteoarthritis of the knee is a leading cause of disability and loss of independence. It is a slow, progressively degenerative disease in which the joint cartilage gradually wears away due to trauma, aging or infection. As the cartilage thins, the surrounding bone thickens and often bones rub against one another, causing additional wear. Normal activity becomes painful and difficult.

Current treatments include drug therapies like anti-inflammatory medication or pain relievers; physical therapy; support devices; health and behavioral modifications such as weight loss; surgery and joint replacement.

Dr. Nelson explains that medications often have variable success and can produce considerable side effects such as changes in kidney and liver function, a reduction in the ability of blood to clot as well as abdominal pain, nausea and indigestion.

The exciting thing about this new approach is that it has been found to have no side effects, it is relatively low-cost in the long-run and the onset of pain relief is immediate, says Dr. Nelson. We look at electromagnetic pulses as a potential way to improve quality of life and independence for those who suffer from osteoarthritis of the knee.

Dr. Nelson says researchers will continue to look at the consistency of the relief, how long the pain relief lasts and if electromagnetic pulses might affect other joints.

Multicenter study finds little effect of soy isoflavones on bone loss in postmenopausal women

Tue, 09 Feb 2010 05:00:00 PST

( from http://www.rxpgnews.com ) AMES, Iowa -- A previous six-month study by Iowa State University researchers had indicated that consuming modest amounts of soy protein, rich in isoflavones, lessened lumbar spine bone loss in midlife, perimenopausal women. But now an expanded three-year study by some of those same researchers does not show a bone-sparing effect in postmenopausal women who ingested soy isoflavone tablets, except for a modest effect at the femoral (hip) neck among those who took the highest dosage.

The multi-center clinical trial of 224 postmenopausal women -- led by D. Lee Alekel, professor of nutrition and interim associate director of the Nutrition and Wellness Research Center (NWRC) at Iowa State, and supported by the National Institute of Arthritis, Musculoskeletal and Skin Diseases, one of the research institutes of the National Institutes of Health (NIH) -- was the longest ever conducted on the effects of soy isoflavones on bone mineral density (BMD). It compared the effects of either ingesting daily 80-mg daily or 120-mg soy isoflavone tablets, compared to placebo tablets on BMD and other health outcomes.

Iowa State NWRC researchers collaborated with research physiologist Marta D. Van Loan and her colleagues at the USDA Agricultural Research Service's Western Human Nutrition Research Center, located at the University of California, Davis. The primary results of their study were published in the January issue of The American Journal of Clinical Nutrition.

Our six-month preliminary study, published in 2000, indicated that soy protein, rich in isoflavones, exerted the greatest impact in slowing the loss of bone mineral density in the lumbar spine, Alekel said. But we believed that we needed to replicate these results in a study with a greater sample size and longer duration, which is what we did with this three-year intervention.

In this longer study, we had sufficient power to detect change, she continued. We monitored adverse events, had excellent compliance throughout, and accounted for potential confounding factors.

NWRC research staff members Laura Hanson, Jeanne Stewart and Kathy Hanson also joined Kenneth Koehler and C. Ted Peterson from statistics as part of the eight-member ISU team that conducted the research.

The researchers ran statistical analyses to determine change in BMD at the lumbar spine, total proximal femur (hip), femoral neck and whole body. They accounted for treatment, age, whole body fat mass and bone removal (using a biochemical marker).

While the 120-mg dose soy isoflavones did reveal a small protective effect on femoral neck bone BMD, researchers found no significant effect of treatment on lumbar spine, total hip, or whole-body BMD.

This trial used isoflavones extracted from soy protein, compressed into tablet form, consumed over the course of three years, which is very different than either providing soy protein or soy foods, Alekel said. In our recent study, we did not demonstrate an important biological effect on BMD or bone turnover.

The new study calls into question the value of postmenopausal women consuming soy isoflavone tablets to help lessen bone loss and minimize the effect of osteoporosis.

The preponderance of studies that have been published -- particularly the longer term, more carefully conducted studies, like our own -- have shown little to no biological effects of soy isoflavones on BMD, she said. This field of research has attracted 'believers,' making it difficult to convince them otherwise. They may continue to believe what they want to believe, rather than what the evidence shows.

And when it comes to minimizing the consequences of osteoporosis in postmenopausal women, Alekel urges a more holistic approach.

People in general, would like an easy fix. We would all like soy isoflavones to be that magic pill, but this study has found that they are not, she said.

Results from other health outcomes from this research have been published in six manuscripts to date, with six additional manuscripts underway. The NWRC research team will continue to study factors that influence bone mineral density and health outcomes in postmenopausal women.

Extremity war injuries symposium seeks to improve patient care for wounded warriors

Wed, 27 Jan 2010 05:00:00 PST

( from http://www.rxpgnews.com ) WASHINGTON, D.C. - Since the beginning of Operations Iraqi Freedom and Enduring Freedom, there have been nearly 36,000 battle- injured warriors, of which approximately 82 percent suffer extremity trauma. Many of these injuries are complicated by the effects of improvised explosive devices which cause injury patterns distinct from civilian trauma. Traditional wound-management guidelines simply fall short. In an effort to address the increasing number and severity of extremity war injuries among the nation's warriors serving in Iraq and Afghanistan, the American Academy of Orthopaedic Surgeons (AAOS), the Society of Military Orthopaedic Surgeons (SOMOS), the Orthopaedic Trauma Association (OTA), and the Orthopaedic Research Society (ORS) will bring together the nation's top civilian and military orthopaedic trauma surgeons and researchers for a two-day symposium January 27 - 29 to discuss barriers of return of function and duty and develop treatment principles.

Over the past several years, peer-reviewed orthopaedic research has been an essential element of our continued efforts to encourage researchers to focus on improving the treatment of high-energy extremity war injuries, said Michael Bosse, MD, CAPT, USNR (Ret.), past OTA President and co-chair of the EWI Symposium. The EWI Symposium gives us a valuable opportunity to discuss this type of research and to learn more about helping our military orthopaedic surgeons discover new and innovative ways to best treat these complex injuries. To improve the quality of life for these injured troops, we have to recognize the need for sustained, robust investment in this type of research.

The distinguished service of our military surgeons never ceases to amaze me, noted COL James R. Ficke, MD, current Chairman of the Department of Orthopaedic Surgery and Rehabilitation at Brooke Army Medical Center, the Orthopaedic Surgery Consultant to the US Army Surgeon General, and co-chair of the EWI Symposium. The continued dedication of surgeons and the incredible courage of our patients inspires advances that enhance the treatment, research, and knowledge of blast injuries. The body of research to characterize these injuries demonstrates that the majority of battlefield wounds affect extremities. Extremity wounds are responsible for two-thirds of inpatient hospital and disability costs, and are the main reasons why up to one third of our warriors never fully recover. This underscores the fact that current therapy options are not capable of restoring full function after these devastating injuries.

In January 2006, AAOS, SOMOS, and OTA hosted the first Extremity War Injuries (EWI) symposium in Washington, DC, which defined current knowledge of the management of extremity war wounds and produced a prioritized list of objectives for future research. Now in its fifth year, the EWI symposium will focus on barriers to return of function and duty and will include a session on disaster preparedness and response. The session is co-moderated by Christopher T. Born, MD, Director of Orthopaedic Trauma at Rhode Island Hospital, who will discuss his recent experiences in Haiti after the earthquake disaster.

Startup at UCLA tech incubator to begin clinical trials for wireless body-monitoring system

Tue, 12 Jan 2010 05:00:00 PST

( from http://www.rxpgnews.com ) MediSens Wireless, a startup company in UCLA's on-campus technology incubator at the California NanoSystems Institute, has obtained approval under federal Food and Drug Administration guidelines to begin clinical trials on its novel wireless body-monitoring system, which assesses muscle and neuromotor functions in the upper extremities.

The Clinical Movement Assessment System (CMAS) is designed for a wide variety of medical applications and could potentially benefit health care professionals and facilities specializing in the areas of physical medicine and rehabilitation, neurology, orthopedics, and physical and occupational therapy, among others.

MediSens moved to the new CNSI incubator in 2009 to begin commercializing licensed technology originally invented by a team led by Majid Sarrafzadeh, a UCLA professor of computer science and engineering and co-director of the Wireless Health Institute at UCLA. The company's mission is to design and deliver personal medical monitoring systems that advance human health.

The data gathered by our monitoring system, CMAS, has the potential to enable health care professionals to improve care through early intervention and better tracking of outcomes and response to treatment, said Dr. Jay Rindenau, M.D., the company's chief medical officer.

The system also has potential for in-home use to assess patient progress following neurotraumas and as a rehabilitative tool to expand the reach of telemedicine. In addition, CMAS could possibly be used to differentiate and help diagnose diseases states, such as Parkinson's disease, at an early stage with sensitive assessments of fine movements, according to Reggie Edgerton, Ph.D., a professor of neurophysiology at UCLA and co-inventor of CMAS.

The CMAS system consists of a clinical assessment device and associated software that will allow health care providers to capture current and ongoing muscle and neuromotor functions, thereby providing them with quantifiable, real-time data for their decision-making.

Clinical trials will establish the viability of CMAS. It is anticipated that the system will provide clinical assessments of fine motor movement, gross muscle strength, hand-eye coordination and patient response to treatment. Closely captured repeat assessments will lead to early warning and detection of deteriorating conditions.

According to MediSens' medical director, Dr. Nick Terrafranca, D.P.M., the trials are planned as a multicenter, multidiscipline study that will involve community hospitals and public health facilities, as well as Ronald Reagan UCLA Medical Center.

The first phase of the trial will deal with baseline evaluations and therapeutic exercise. The second phase will involve an in-depth analysis of different sensory-motor pathways. The success of the trial will be evaluated by the efficacy and cost effectiveness of the system in testing early interventions for better outcomes and long-term patient care.

Tarantula venom-based MD therapy to be advanced by UB scientists' biotech company

Tue, 29 Dec 2009 05:00:00 PST

( from http://www.rxpgnews.com ) BUFFALO, N.Y. -- University at Buffalo biophysicists have found a protein in tarantula venom that shows promise as a potential therapy for muscular dystrophy (MD). They have formed a start-up biotech company in Buffalo -- Rose Pharmaceuticals -- to advance the drug to clinical trials.

Fredrick Sachs, PhD, professor of physiology and biophysics at the University at Buffalo, and colleagues in his laboratory, discovered the peptide, called GsMTx4.

Therapies for muscular dystrophy are classed as orphan drugs by the FDA, allowing a shorter testing period than normal drugs. Sachs said he anticipates Rose Pharmaceuticals may be able to obtain FDA approval of the peptide for human use within two years.

The new company is named for Rose, the pet tarantula that has been in residence in Sachs' lab for nearly 20 years.

The first target of the peptide is MD, a condition Sachs has been investigating for several years, but the peptide also has potential as a therapy for several other conditions, such as neuropathic pain and atrial fibrillation. Formation of the company was motivated by the goal of finding an MD therapy for the grandson of Sachs' friend Jeffrey Harvey.

The start-up is a collaboration between Sachs, Harvey, Thomas Suchyna, PhD, and Philip Gottlieb, PhD. Suchyna and Gottlieb, UB research scientist and UB research associate professor, respectively, have been working with Sachs at the university for several years to develop the peptide. Their work was supported by a grant from UB's Interdisciplinary Research and Creative Activities Fund.

In collaboration with Eric Hoffman, PhD, director of the Wellstone Muscular Dystrophy Center at Children's National Medical Center in Washington, D.C., the team tested the effect of GsMTx4 on MD mice extensively. Results showed that the drug increased muscle strength and caused no mortality, morbidity or toxicity.

Rose Pharmaceuticals now is concentrating on developing methods to administer the drug. The peptide and its mirror image are covered by U.S. patents obtained by UB's Office of Science, Technology Transfer and Economic Outreach (STOR), and licensed to Rose Pharmaceuticals. Sachs noted that there are no other drugs known to act specifically on mechanosensitive ion channels, the target of GsMTx4.

Unlike most drugs, GsMTx4 seems to generate only positive side effects, said Sachs. In addition to its effectiveness in MD, it inhibits atrial fibrillation, a cardiac arrhythmia that affects 2 million Americans, and for which there currently is no reliable drug therapy.

In a second application, research groups in Korea and UC San Francisco have shown that GsMTx4 can inhibit mechanically induced pain (pain originating in nerve fibers), he said. This therapy is at least half as effective as morphine, but does not act on the brain, only at the site of increased sensitivity. Mark Kristal, PhD, UB professor of psychology, has been collaborating on the pain testing.

GsMTx4 appears to have additional applications. Robert Plunkett, MD., UB associate professor of neurosurgery, has shown that the peptide stimulates neuronal growth, and may be useful for the treatment of Parkinson's disease.

Drug could provide first treatment for scleroderma

Sat, 17 Oct 2009 04:00:00 PST

( from http://www.rxpgnews.com ) Investigators have identified a drug that is currently approved to treat certain types of cancer, Gleevec, that could provide the first treatment for scleroderma, a chronic connective tissue disease for which a treatment has remained elusive. The news will be presented at the annual meeting of the American College of Rheumatology on October 18 in Philadelphia.

There has never been a drug that has been shown to be effective for this condition. I think there is a very good chance of Gleevec becoming a real treatment for a previously untreatable disease, said Robert Spiera, M.D., an associate attending rheumatologist at Hospital for Special Surgery who led the study.

For the study, investigators at Hospital for Special Surgery enrolled 30 patients with diffuse scleroderma, a widespread severe form of the disease, and gave them 400 mg of Gleevec per day. Patients were evaluated monthly for 12 months during treatment and were seen for follow-up three months after discontinuing the drug.

To measure the effectiveness of the drug, researchers used a tool known as the modified Rodnan skin score, a measure of how much skin is affected by the disease. The skin score seems to be a very good marker of disease status and most scleroderma trials use this as an outcome measure, said Dr. Spiera, who is also an associate professor at Weill Cornell Medical College. The investigators also measured lung function using tests for forced vital capacity (FVC), the maximum volume of air that a person can exhale after maximum inhalation, and diffusion capacity, a measurement of the lung's capacity to transfer gases. Lung disease is the main cause of mortality in scleroderma.

The investigators reported an interim analysis of their results, although the study is ongoing. At one year, the investigators saw a 23 percent improvement in skin scores. The researchers also saw an improvement in forced vital capacity scores by 9.6 percent and diffusion capacity scores by 11 percent in the 18 patients who had completed one year of treatment.

The lung function data was really exciting, Dr. Spiera said. In patients with scleroderma, you usually see lung function tests getting worse over time, and if doctors try a therapy for a year and a patient doesn't get any worse, we get pretty excited. What is amazing to me in this study is that we actually saw improvements in both lung function tests.

The study is the largest single center trial of Gleevec in scleroderma to date with the longest duration of treatment and follow-up. Before this trial, test tube studies of human cells indicated that Gleevec might have some activity in combating the disease, and the drug was shown to be effective in a rodent model of the disease. Only anecdotal evidence, however, had been published on the drug's effectiveness in treating the disease in humans. Dr. Spiera said the findings of his open-label study need to be interpreted cautiously, and ultimately corroborated by evidence from a randomized controlled trial, the gold standard of clinical trials.

Until now, no drug has been shown to be effective in treating scleroderma in a clinical trial. Several years ago, a small study provided some evidence that a chemotherapy drug called cyclophosphamide may help scleroderma patients, but the benefit was minimal and this drug causes side effects including infertility and secondary cancers.

Dr. Spiera's study was funded primarily through the Rudolph Rupert Scleroderma Program at the Hospital for Special Surgery. Novartis, the manufacturer of Gleevec, provided some monetary support and donated drug. The company is not involved in the design or analysis of the trial. Gleevec is approved in the United States for two types of cancer: chronic myeloid leukemia and gastrointestinal stromal tumor.

Systemic scleroderma affects not only the skin, but also underlying blood vessels, and often muscles and joints, as well as the gastrointestinal tract, kidneys, lungs and heart. According to the Scleroderma Foundation, roughly 300,000 individuals have scleroderma in the United States and roughly a third of these have the systemic kind. The disease typically strikes in the prime of patients' lives, when they are 30-50 years old.

Advances in treating hip pain to be focus of International Society for Hip Arthroscopy meeting

Sat, 26 Sep 2009 04:00:00 PST

( from http://www.rxpgnews.com ) Recent advances in diagnostic imaging techniques and hip arthroscopy procedures are giving physicians and surgeons better tools with which to treat hip pain. The 2009 International Society for Hip Arthroscopy meeting, hosted by Hospital for Special Surgery in New York, brings together leading surgeons from all over the world to take an in-depth look at hip arthroscopy and its potential benefits.

This inaugural meeting by the International Society for Hip Arthroscopy will concentrate on the rapidly changing field of arthroscopic hip surgery, said Robert Buly, M.D., attending orthopedic surgeon at Hospital for Special Surgery and course director of the ISHA meeting. Presentations will be focused on the current research and outcomes data associated with both common and new procedures.

Hip arthroscopy, a minimally invasive treatment option, is an alternative for some patients over open, invasive surgery. Through a few tiny incisions, doctors are able to insert tools to trim bone or repair cartilage. Previously, surgeons only had the option of opening up the entire hip with a large incision and dislocating the hip to access the joint. This procedure can be used to treat patients with femoro-acetabular impingement (FAI), also known as hip impingement, where there is a change in the bony form of the hip joint causing a decreased range of motion and pain, damage to the cartilage within the hip joint, such as labral tears, and other conditions.

It is not uncommon for hip pain due to hip impingement or labral tears to be misdiagnosed. The difficulty in diagnosing the underlying causes of hip pain doesn't affect only professional athletes like Alex Rodriguez, Carlos Delgado or Mike Lowell, who have been in the news for their injuries and subsequent treatment, but week-end warriors and everyday active individuals as well. Hospital for Special Surgery's Center for Hip Pain and Preservation uses the latest imaging technology and arthroscopic techniques to provide those experiencing hip pain with proper diagnosis and treatment.

Research highlights include outcomes data presented by Special Surgery's Dr. Buly and Bryan Kelly, M.D., co-director of the Center for Hip Pain and Preservation at Hospital for Special Surgery and a study by Marc Philippon, M.D., of the Steadman Hawkins Research Foundation in Colorado, on how to assess the ability of a patient to return to sports after arthroscopy. Two imaging advances, one on techniques that allow greater visibility into the hip joint and a second on a method that may identify the earliest onset of arthritis will be presented, as well as a British study on siblings that addresses the genetics underlying hip impingement.

The meeting will take place in New York on October 9 and 10, 2009 at the Roosevelt Hotel on Madison Avenue and 45th Street.

Artificial gravity prevents muscle loss in space

Thu, 06 Aug 2009 13:31:15 PST

( from http://www.rxpgnews.com ) When the Apollo 11 crew got back from the moon some 40 years ago, they showed no ill effects from a week spent in weightlessness. But as space men began conducting longer-duration space flights, scientists noticed a disturbing trend: the longer humans stay in zero gravity, the more muscle they lose.

Space travellers exposed to weightlessness for a year or more -- such as those on a mission to Mars, for example -- could wind up crippled on their return to Earth, unable to walk or even sit up.

Now, researchers at the University of Texas Medical Branch-Galveston - have conducted the first human experiments using a device intended to counteract this effect.

It is a NASA centrifuge that spins a test subject with his or her feet outward 30 times a minute, creating an effect similar to standing against a force two and half times that of gravity.

Working with volunteers kept in bed for three weeks to simulate zero-gravity conditions, they found that just one hour a day on the centrifuge was sufficient to restore muscle synthesis.

'This gives us a potential countermeasure that we might be able to use on extended space flights and solve a lot of the problems with muscle wasting,' said Douglas Paddon-Jones, senior study co-author.

'This small amount of loading, one hour a day of essentially standing up, maintained the potential for muscle growth,' he added.

Fifteen healthy male volunteers participated in the study.

The results showed that members of the centrifuge group continued to make thigh muscle protein at a normal rate, while the control group's muscle synthesis rate dropped by almost half.

Paddon-Jones cautioned that the rate of muscle protein synthesis alone does not necessarily predict changes in muscle function.

But, he pointed out, it was still a strong indicator that a relatively brief intervention could have a positive effect in preventing zero-gravity muscle loss -- one that might also be applied on Earth.

These findings were published in the July issue of the Journal of Applied Physiology.

Study to assess hip exercises as treatment for osteoarthritis in the knee joints

Wed, 15 Jul 2009 04:00:00 PST

( from http://www.rxpgnews.com ) Researchers at Rush University Medical Center are testing a novel regimen of hip-muscle exercises to decrease the load on the knee joints in patients with osteoarthritis. The goal is not only to relieve pain but also, possibly, to halt progression of the disease.

Each time you take a step, a load, or force, is placed on the knee joints. How much load depends not just on your weight, but also on the way you walk and the alignment of your leg, said Laura Thorp, PhD, assistant professor of anatomy and cell biology at Rush Medical College and principal investigator for the study. If we can appropriately alter the gait patterns of patients with osteoarthritis, we can minimize the load and relieve pain.

Ultimately, we're hoping we can prevent the disease from advancing. No treatment currently exists that can stop osteoarthritis from progressing in the knees, other than joint replacement surgery.

Osteoarthritis is the most common form of arthritis and a significant source of disability and impaired quality of life. A higher-than-normal load on the knees during walking is a hallmark of the disease, associated with both the severity of the osteoarthritis and its progression, according to Thorp.

Thorp is enrolling patients with mild to moderate osteoarthritis in their knees in a research study to determine the effectiveness of certain hip exercises in treating the disease. Study participants have their knees x-rayed and undergo an initial assessment in Rush's Human Motion Laboratory to measure the load on their knee joints while walking. Participants then follow a specific regimen of hip exercises for four weeks under the direction of Charles Cranny, clinical manager of outpatient physical therapy.

The exercises focus on strengthening the hip abductor muscles, such as the gluteus medius, a broad, thick, radiating muscle that helps to stabilize the pelvis during ambulation. In patients with osteoarthritis in the knees, these muscles tend to be weak, causing the pelvis to tilt toward the side of the swing leg when walking, instead of remaining level with the ground, which increases the load on the knee joints. Strengthening these muscles helps the pelvis and the knee remain in better alignment, and thereby lessens the load.

After the four weeks of supervised physical therapy, participants are reassessed to determine whether the load on the knees has decreased, and whether the pain has subsided.

The trial continues for another four weeks, with patients exercising at home to determine whether the adjustments in gait can be maintained.

According to Thorp, exercise regimens to date have focused largely on strengthening the quadriceps and hamstring muscles, which stabilize the knee joint but likely do little to correct alignment with the rest of the leg or alter the load on the joint.

Preliminary evidence in the present trial has already shown that a decrease in load is attained with hip-muscle exercises.

By lessening the load on the knees, we can remove one of the major known risk factors for the progression of osteoarthritis, Thorp said.

Study to assess hip exercises as treatment for osteoarthritis in the knee joints

Wed, 15 Jul 2009 04:00:00 PST

Surgery may not be necessary for Achilles tendon rupture

Thu, 14 May 2009 04:00:00 PST

( from http://www.rxpgnews.com ) The two ends of a ruptured Achilles tendon are often stitched together before the leg is put in plaster, in order to reduce the risk of the tendon rupturing again. However, Katarina Nilsson Helander, MD, PhD at the Sahlgrenska Academy, University of Gothenburg, Sweden, now suggests that surgery may be unnecessary. Patients who do not undergo surgery have just as good a chance of recovery.

The Achilles tendon, which attaches the calf muscle to the heel, is the body's strongest tendon. The tendon may rupture on sudden tensing of the muscle, something that affects middle-aged men in particular, typically when playing badminton or tennis.

When the Achilles tendon ruptures, it feels like a sudden, violent and intensely painful snap in the calf or tendon above the heel. It is an injury that has become increasingly common in recent years, probably because exercise is increasingly popular. But whether or not one should operate has been the subject of debate for quite some time, says orthopaedic surgeon Katarina Nilsson Helander, MD, PhD.

When the Achilles tendon has ruptured, the foot is put in plaster with the toes pointing downwards, so that the torn ends of the tendon come into contact and join together as they heal. The torn ends of the tendon are often stitched together before the foot is put in plaster, to make sure they stay in place. In recent times, a removable orthosis has begun to replace plaster casts, making it possible for the patient to start to move the foot sooner. Other studies have shown that early motion stimulates healing.

Surgery increases the risk of infections and sores but is often carried out anyway, as studies have shown that the operation reduces the risk of the tendon rupturing again.

One hundred patients were randomly assigned to surgery with early mobilisation or to early mobilisation alone with the removable orthosis and without prior surgery. In every other respect, all the patients in the study had the same treatment. The thesis shows that there is no difference in the re-rupture rate. A year after the injury, there was no difference in the patients' own impression of symptoms and function, but irrespective of which treatment the patient received, the function tests showed that there remained a substantial difference between the healthy and the injured foot.

I have concluded that not everybody needs to have surgery, but it is important that those who suffer an Achilles tendon rupture discuss the treatment options with their orthopaedic surgeon, says Katarina Nilsson Helander.

Risk of vibration-induced vascular injuries linked to vibration frequency differences

Sun, 19 Apr 2009 04:00:00 PST

( from http://www.rxpgnews.com ) Speaking on April 19 at the Experimental Biology 2009 meeting in New Orleans, Dr. Kristine Krajnak, a team leader in the Engineering and Control Technologies Branch of the Health Effects Laboratory Division of NIOSH in Morgantown, West Virginia, describes results from the first study to directly link the different physical responses of tissue that occur with exposure to different vibration frequencies with biological mechanisms underlying the development of vascular dysfunction. Her presentation is part of the scientific program of The American Physiological Society.

The study, along with results of other studies conducted by NIOSH, supports the importance of reducing job-related exposure to vibration. Ongoing research is evaluating the effectiveness of anti-vibration devices, such as anti-vibration gloves and tools.

Higher frequency vibrations produced by an electric sander (greater than 100 Hz) are smoother than the slower vibrations of an electric hand drill (approximately 63 Hz) and therefore are less likely to cause users discomfort.

Don't let that fool you into not using protective devices that can reduce your exposure to vibration, she says. The new research study conducted at the National Institute for Occupational Safety and Health (NIOSH) suggests that exposure to high and low frequencies cause different physiological responses, but both may affect the risk of developing vibration-induced peripheral vascular dysfunction.

Of the 1.1 to 1.5 million U.S. workers exposed to hand transmitted vibration on a fairly regular basis, approximately half eventually develop some disorder such as Vibration White Finger, in which a single finger or sometimes the entire hand turns white and numb when exposed to the cold, due to restricted blood flow.

Workers also may experience reductions in tactile sensitivity, grip strength, and/or manual dexterity. Earlier studies have shown that risk goes up with frequency and duration of exposure, although NIOSH studies are underway to determine why certain people appear more susceptible to shorter exposure durations.

Dr. Krajnak's team looked at two aspects of vibration injury about which very little is known: the mechanisms of injury and the differences in response to frequency of vibration. The researchers used rats, since the tissues, nerves and arteries of rat-tails are similar to those in human fingers and the tails are known to respond to vibration in a way similar to that seen in fingers.

For four hours a day (the longest time a human can be exposed to workplace vibration according to U.S. and international standards) for 10 days, 15 rats (five in each group) were placed in a container where their tails were vibrated at either 63, 125 or 250 Hz. One control group of five rats accompanied them to the experimental area, to make sure any results seen were not related to noise or change of locale. A second control group stayed in their home cages, uninvolved in the activity.

After the last exposure, the scientists examined the tail arteries for changes. Neither control group had changes, suggesting the changes seen were directly related to the effects of vibration. The rats that experienced high frequency (125 and 250 Hz) vibration had higher levels of measures of oxidative stress, while rats that experienced the lower frequency (65 Hz) vibration showed higher levels of pro-inflammatory factors.

The changes seen following higher frequency vibration are associated with more immediate changes in the peripheral vascular system, such as those seen in workers with vibration injury, says Dr. Krajnak, but the changes following lower frequency vibration also can lead to vascular problems.

Biomedical engineering student recognized as IEEE's 'New Face of Engineering'

Tue, 17 Mar 2009 04:00:00 PST

( from http://www.rxpgnews.com ) WASHINGTON (17 March 2009) -- Guruprasad Madhavan is working on neuromuscular stimulation approaches that may help prevent osteoporosis, heart failure and mild cognitive impairment -- all related to low blood pressure.

Madhavan's research is a major reason why he was selected the IEEE/IEEE-USA's 2009 New Face of Engineering.

My energy to perform better has multiplied, and so has my responsibility to better communicate engineering, Madhavan said after being selected.

The New Faces of Engineering is sponsored by the National Engineers Week Foundation, a coalition of engineering societies, major corporations and government agencies. The program highlights the vitality, diversity and rich contributions of engineers under 30.

Each engineering society's top choice must hold an engineering degree, be employed as an engineer from two to five years, and have worked with projects that significantly affect public welfare or further professional development and growth.

Madhavan is one of 14 engineers recognized for this international honor. They were featured in a full-page ad that ran in USA Today on 16 February.

Madhavan, 29, is completing his doctoral degree in biomedical engineering at Binghamton University, State University of New York. His research is focused toward non-invasively and non-pharmacologically stimulating the calf muscle pump -- also referred to as the second heart -- to enhance circulation.

The contractions of calf muscles help in propelling deoxygenated blood back to the heart against gravity. External stimulation of the lower leg musculature could help enhance venous return and cardiovascular recirculation of oxygen-rich blood.

Madhavan was born in a village in Tamil Nadu, a state in southern India. He became the first person in his family's history to earn an engineering degree when he received his bachelor's (honors with distinction) in instrumentation and control engineering from the University of Madras (India) in 2001. He added a master's degree in biomedical engineering from Stony Brook (N.Y.) University in 2002 and an MBA in leadership and healthcare management from Binghamton in 2007. He has also worked in the medical device industry as a research scientist.

In November 2007, Madhavan became the first person in the United States to receive the United Kingdom's Institute of Engineering and Technology's Mike Sargeant Career Achievement Award. The honor is given to the young professional deemed to have made the most significant career progress over a number of years. Madhavan, who received the award in London, was recognized for his medical device research.

Last fall Madhavan was selected for a science, technology and economic policy fellowship at the National Academies in Washington. He believes that this experience has helped prepare him for a career in public policy related to economic development and sustainability issues.

Madhavan is also senior editor of Career Development in Bioengineering and Biotechnology (Springer, 2008), a volume designed to introduce students, professionals and the public to the diverse career and sustainable-development opportunities within bioengineering, biotechnology and related fields.

An ad hoc committee of IEEE members Paul Kostek of Seattle; Sarah Rovito of Arlington, Va.; Abby Vogel of Atlanta; and Terry Malkinson of Calgary, Alberta, Canada, selected Madhavan as the IEEE/IEEE-USA's New Face.

A couple of glasses of red wine a day keep disabilities away!

Thu, 15 Jan 2009 14:47:51 PST

( from http://www.rxpgnews.com ) It is well known that moderate drinking can have positive health benefits — for instance, a couple of glasses of red wine a day can be good for the heart. But if you're a senior in good health, light to moderate consumption of alcohol may also help prevent the development of physical disability.

That's the conclusion of a new UCLA study, available in the online edition of the American Journal of Epidemiology, which found that light to moderate drinking among these seniors reduced their odds of developing physical problems that would prevent them from performing common tasks such as walking, dressing and grooming.

"If you start out in good health, alcohol consumption at light to moderate levels can be beneficial," said lead study author Dr. Arun Karlamangla, an associate professor of medicine in the division of geriatrics at the David Geffen School of Medicine at UCLA. "But if you don't start out healthy, alcohol will not give you a benefit."

The researchers based their study on data from three waves of the National Health and Nutrition Examination Survey's Epidemiologic Follow-up Study (1982󈟀, 1987 and 1992). The sample, which included 4,276 people split evenly between male and female, was about 92 percent white, with a mean age of 60.4 years.

Drinkers were classified as light to moderate if they consumed less than 15 drinks per week and less than five drinks per drinking day (less than four per day for women). Heavy drinkers were those who consumed 15 or more drinks per week or five or more per drinking day (four or more for women). Abstainers were those who drank fewer than 12 alcoholic beverages the previous year.

Having a physical disability means having trouble performing, or being unable to perform, routine tasks such as dressing and grooming, personal hygiene, arising, eating, walking, gripping, reaching, and doing daily errands and chores. Participants were asked if they experienced no difficulty, some difficulty, much difficulty or were unable to do these activities at all when alone and without the use of aids.

At the start of the survey, 32 percent of men and 51 percent of women abstained from drinking, 51 percent of men and 45 percent of women were light to moderate drinkers, and 17 percent of men and 4 percent women were heavy drinkers.

No one had any disabilities at the outset, but 7 percent died and 15 percent became disabled over five years.

The researchers found that light to moderate drinkers in good health had a lower risk for developing new disabilities, compared with both abstainers and heavy drinkers.

In unadjusted analyses, light to moderate drinkers had a 17.7 percent chance of becoming disabled or dying in five years, compared with 26.7 percent for abstainers and 21.4 percent for heavy drinkers. Among survivors, the risk for new disability was 12.5 percent for light to moderate drinkers, compared with 20 percent for abstainers and 15.6 percent for heavy drinkers.

However, after controlling for confounding variables such as age, smoking, exercise, heart attacks and strokes, the benefits of alcohol consumption were seen only in seniors who rated their health as good or better: There was a 3 to 8 percent reduction in the odds of developing disability with each additional drink per week in older men and women in good or better health who were not heavy drinkers, but there was no such benefit seen in those who rated their health as fair or poor.

"Light to moderate alcohol consumption appears to have disability prevention benefits only in men and women in relatively good health," the researchers wrote. "It is possible that those who report poor health have progressed too far on the pathway to disability to accrue benefits from alcohol consumption and that alcohol consumption may even be deleterious for them."

Sarcospan may help in Duchenne muscular dystrophy

Mon, 03 Nov 2008 00:01:09 PST

( from http://www.rxpgnews.com ) The overlooked and undervalued protein, sarcospan, just got its moment in the spotlight. Peter et al. now show that adding it to muscle cells might ameliorate the most severe form of muscular dystrophy.

In Duchenne muscular dystrophy (DMD), the mutated dystrophin protein fails to anchor correctly to its membrane glycoprotein complex. And without this anchoring, muscle cells experience severe contraction-induced damage. Sarcospan is part of the anchoring complex, but because mice without sarcospan don't seem any worse for its absence, it hasn't received much attention. Sarcospan's structure, however, suggests it might help stabilize the membrane complex, so the authors decided to test the effects of increasing sarcospan expression in a DMD mouse model.

The increase did not improve the dystrophin–glycoprotein interaction, but instead, the team was surprised to find sarcospan coaxed a dystrophin relative called utrophin to spread out on the muscle membrane. Utrophin is normally restricted to the neuromuscular junction, where it serves a role similar to that of dystrophin.

The extra sarcospan prompted higher levels of utrophin in the cell, but not by increasing its expression. Sarcospan instead stabilized extrajunctional utrophin complexes, which normally form early in development and then disappear after the first few weeks of life.

Mouse muscle cells were protected by sarcospan, but the true importance of this discovery will lie in its potential for human therapeutics, specifically gene therapy. In that regard, sarcospan's small gene size is significant—at 600 bp, it is easily packaged into the safest viral vectors, unlike either dystrophin or utrophin, which are about 700 times larger and require more immunogenic vectors.

'Wildcat Power Cord' repairs cruciate ligament in dairy cow's knee

Thu, 27 Mar 2008 04:00:00 PST

( from http://www.rxpgnews.com ) MANHATTAN, KAN. -- An 8-year-old Jersey dairy cow is back at her Kansas farm thanks to a decade of research and an experimental surgery performed at Kansas State University's Veterinary Medical Teaching Hospital.

The cow, named Wilhelmina Jolene by the veterinary students assigned to her case, sustained a breeding injury in December 2007 when the cruciate ligament in her right knee ruptured. Dr. David Anderson, professor and head of agricultural practices at K-State's College of Veterinary Medicine, replaced the ligament using synthetic material called monofilament nylon. The procedure's success could have enormous implications for breeding quality cows and bulls with the same injury.

Fortunately, Wilhelmina's owner recognized the value of saving her. Mike Frey is the son of Dr. Russ Frey, a prominent professor at K-State's College of Veterinary Medicine. She's owned by the son of an important faculty member in our college's history, Anderson said. It's wonderful that there is a connection to Dr. Frey with this case and that Mike understands the teaching value.

Mike Frey said he was happy to be part of an effort that could help animals, producers and students.

I was always under the assumption that an animal with this problem was going to be heading down the road, he said. If they could perfect this so that a cow could be kept in production, that would be worth quite a bit.

The cruciate ligament is a dense tissue that connects the bones in the knee joint. Injuring it can be career-ending and often life-ending - until now, Anderson said.

The three surgical techniques for cruciate ligaments in large animals have a failure rate of approximately 50 percent, Anderson said. This fact caused him and surgery colleagues Drs. Guy St-Jean and Andre Desrochers to investigate alternatives in the 1990s. That's when the team designed a cruciate ligament using braided polyester; however, the material was not strong enough for heavy cattle.

Anderson continued to experiment with a variety of materials until he discovered an unusual form of nylon monofilament, a solid material about the diameter of a coffee straw. But the question remained: Could this man-made material replace the natural ligament of a 1,500 pound animal?

On Jan. 17, Anderson replaced Wilhelmina's torn ligament with the artificial one, dubbed the Wildcat Power Cord. Anderson's surgery team included surgery residents Drs. Kara Schulz and Jose Bras, intern Dr. Manuel Chamorro, along with anesthesiologists, veterinary students and technicians.

The next day, the Jersey cow was led across the hospital's video synchronization pressure mat to determine her level of lameness. Her stride length had increased 30 percent, and she bore 25 percent more weight on her operated leg, Anderson said. To have that much improvement is spectacular.

His long-term goal is to develop a replacement ligament strong enough for bulls. Lab tests reveal that the Wildcat Power Cord can withstand up to 12,000 newtons of pressure - roughly 50 percent more than an adult bull requires.

Wilhelmina retuned home and was kept in a box stall for a week or so, Mike Frey said. After that, she had the run of the free stall. It's been a tough winter with all of the snow and ice, he said. I didn't think she'd get around as good as she did.

Shelby Reinstein, a senior veterinary student from Tulsa, Okla., was one of the K-State students who worked with -- and named -- Wilhelmina the cow.

Reinstein said she appreciated the learning opportunities this case presented, especially those relative to anatomy of the stifle and monitoring Wilhelmina for specific conditions dairy cows are at risk for developing. These include inflammation of the udder (mastitis) or of the uterus (metritis), a metabolic imbalance (ketosis), ulcers and displacement of the abomasum, the fourth compartment of a ruminant's stomach.

We worked really hard for her and spent long hours at the hospital, but it was definitely worth it after seeing how well she did post-op, Reinstein said. I love being part of the discovery aspect of veterinary medicine, and it is always really rewarding to try something you're not sure about and have it work. And, my parents were quite impressed that I could milk a cow!

Lithium chloride slows onset of skeletal muscle disorder

Tue, 18 Mar 2008 04:00:00 PST

( from http://www.rxpgnews.com ) Irvine, Calif., March 18, 2008 -- A new UC Irvine study finds that lithium chloride, a drug used to treat bipolar disorder, can slow the development of inclusion body myositis, a skeletal muscle disease that affects the elderly.

In the study by scientists Frank LaFerla and Masashi Kitazawa, mice genetically engineered to have IBM demonstrated markedly better motor function six months after receiving daily doses of lithium chloride, compared with non-treated mice. The muscles in treated mice also had lower levels of a protein that the study linked to muscle inflammation associated with IBM.

These data are the first to show that lithium chloride is a potential IBM therapy.

Lithium chloride is an approved drug for treating humans. We already know it is safe and can be used by people, said LaFerla, professor of neurobiology and behavior at UCI and co-author of the study. Given our findings, we believe a clinical trial that tests the effectiveness of lithium chloride on IBM patients should be conducted as soon as possible.

Results of the study appear online this month in the journal Annals of Neurology.

IBM is the most common skeletal muscle disorder among people older than 50. People with IBM experience weakness, inflammation and atrophy of muscles in their fingers, wrists, forearms and quadriceps. There is no cure for IBM, nor is there an effective treatment, according to the National Institutes of Health.

LaFerla, a noted Alzheimer's disease researcher, began studying IBM about 10 years ago after learning the disorders have similar tissue characteristics. In the brain, a buildup of phosphorylated tau protein leads to the development of tangles, one of the two lesions that are hallmarks of Alzheimer's disease. High phospho-tau levels also are present in IBM, though patients do not experience dementia or memory loss. In a previous study,

LaFerla found that lithium chloride reduced phospho-tau levels in mice genetically engineered to develop Alzheimer's disease. LaFerla and his research team then wondered: Could lithium chloride also reduce phospho-tau levels and symptoms in mice with IBM?

First, they sought to determine how the inflammation affects the skeletal muscle fibers. They injected the mice with a drug to trigger muscle inflammation, then put them on tiny treadmills to test their motor function. As expected, mice with inflammation could not keep up with the control mice, indicating reduced motor function. Examining their brain tissue, the scientists discovered the mice with muscle inflammation also had higher levels of phospho-tau.

Through additional testing, they discovered an enzyme called GSK-3 beta was responsible for increasing the tau phosphorylation. Previous studies have shown that same enzyme to cause tau buildup in the Alzheimer's brain.

Next, the scientists sought to block the accumulation of phospho-tau in the IBM mice with the goal of curbing motor function loss. In mice six months of age, one group was fed lithium chloride-laced food for six months, and a second group was fed regular food. At 12 months of age, mice in the first group performed on the treadmill as if they were six months of age, while mice in the second group had reduced motor function. Lithium chloride, the scientists found, blocked the GSK-3 beta enzyme that caused higher levels of phospho-tau.

The older animals were performing as if they were younger animals, said Kitazawa, a postgraduate researcher of neurobiology and behavior at UCI and co-author of the study. Lithium chloride was delaying their rate of decline.

The scientists then sought evidence that their results in mice might translate to humans with IBM. They performed tests on human muscle tissue samples and found the GSK-3 beta enzyme again played a role in the phosphorylation of tau. That was not the case, though, in patients with other muscle disorders. This suggests that our IBM mouse model may have the same skeletal muscle mechanism as in human cases, LaFerla said.

Massive microRNA scan uncovers leads to treating muscle degeneration

Wed, 17 Oct 2007 04:00:00 PST

( from http://www.rxpgnews.com ) Researchers have discovered the first microRNAs � tiny bits of code that regulate gene activity � linked to each of 10 major degenerative muscular disorders, opening doors to new treatments and a better biological understanding of these debilitating, poorly understood, often untreatable diseases. The study, to be published online this week by the Proceedings of the National Academy of Sciences, was led by Iris Eisenberg, PhD, of the Program in Genomics at Children�s Hospital Boston. Louis Kunkel, PhD, director of the Program in Genomics and an investigator with the Howard Hughes Medical Institute, was senior investigator.

The disorders include the muscular dystrophies (Duchenne muscular dystrophy, Becker muscular dystrophy, limb girdle muscular dystrophies, Miyoshi myopathy, and fascioscapulohumeral muscular dystrophy); the congenital myopathies (nemaline myopathy); and the inflammatory myopathies (polymyositis, dermatomyositis, and inclusion body myositis). While past studies have linked them with an increasing number of genes, it's still largely unknown how these genes cause muscle weakness and wasting, and, more importantly, how to translate the discoveries into treatments.

For instance, most muscular dystrophies begin with a known mutation in a �master gene,� leading to damaged or absent proteins in muscle cells. In Duchenne and Becker muscular dystrophies, the absent protein is dystrophin, as Kunkel himself discovered in 1987. Its absence causes muscle tissue to weaken and rupture, and the tissue becomes progressively nonfunctional through inflammatory attacks and other damaging events that aren�t fully understood.

�The initial mutations do not explain why patients are losing their muscle so fast,� says Eisenberg. �There are still many unknown genes involved in these processes, as well as in the inflammatory processes taking place in the damaged muscle tissue.�

She and Kunkel believe microRNAs may help provide the missing genetic links. Their team analyzed muscle tissue from patients with each of the ten muscular disorders, discovering that 185 microRNAs are either too abundant or too scarce in wasting muscle, compared with healthy muscle.

Discovered in humans only in the past decade, microRNAs are already known to regulate major processes in the body. Therefore, Eisenberg believes microRNAs may be involved in orchestrating the tissue death, inflammatory response and other major degenerative processes in the affected muscle tissue. The researchers used bioinformatics to uncover a list of genes the microRNAs may act on, and now plan to find which microRNAs and genes actually underlie these processes.

The findings raise the possibility of slowing muscle loss by targeting the microRNAs that control these �cascades� of damaging events. This approach is more efficient than targeting individual genes.

The team also defined the abnormal microRNA �signatures� that correspond to each of the ten wasting diseases. They hope these will shed light on the genes and disease mechanisms involved in the most poorly understood and least treatable of the degenerative disorders, such as inclusion body myositis.

�At this point, it�s very theoretical, but it�s possible,� says Eisenberg.

FDA approves knee-injury device for humans

Tue, 02 Oct 2007 04:00:00 PST

( from http://www.rxpgnews.com ) COLUMBIA, Mo. � A new knee-surgery device investigated by University of Missouri-Columbia researchers that will help to repair meniscus tears, which were previously defined as irreparable, has been approved by the FDA for use in humans.

Previous treatment options forced surgeons to completely remove the damaged portion of the meniscus. Typically the removal of the meniscus leads to painful, debilitating arthritis in the knee. Herb Schwartz, president and CEO of Schwartz Biomedical, LLC, and James Cook, MU professor of veterinary medicine and surgery and William C. Allen Endowed Scholar for Orthopedic Research in MU�s College of Veterinary Medicine, developed the BioDuct Meniscal Fixation Device. Schwartz and Cook believe that patients with meniscus tears will now be able to have their meniscus saved along with long-term knee function.

�In the past, when faced with meniscus injuries, surgeons were often forced to completely remove the torn meniscal cartilage, leaving a deficient knee that was doomed to develop arthritis,� Cook said. �With the BioDuct Meniscal Fixation Device, surgeons will be able to repair torn menisci and induce healing. People with meniscus injuries now have a better future ahead.�

The meniscus, a padding tissue that provides shock absorption and joint stability in the knee, is crucial for normal knee function. Surgeries for meniscus tears are common with approximately one million occurring in the United States each year. When meniscus function is deficient, bone rubs on bone and arthritis is likely to develop and progress. Because two-thirds of the meniscus is avascular (lacks a blood supply), a tear in that region will not repair itself. This new device will transport blood and cells from the vascular portion of the knee to the avascular portion of the meniscus. Supplied with blood and cells for healing, the previously untreatable meniscal tear now has the potential for allowing the knee joint to be saved.

Cook�s research team performed the BioDuct surgery on 25 dogs that had worst-case scenario meniscal tears. With the BioDuct Meniscal Fixation Device, the meniscus in the dogs� knees had complete or partial repair after a few weeks in all cases.

�Currently, there are no other devices that can provide improved fixation over time,� Schwartz said. �Therefore, the BioDuct device is set apart from the rest of the field.�

In his research, Cook found that the device will significantly improve healing of avascular meniscal tears both biologically and biomechanically, which should lessen the long-term effects of meniscus injuries, including osteoarthritis. Cook�s recent findings were published in the American Journal of Sports Medicine.

�The BioDuct device could impact the industry by improving repairs of the meniscus to such an extent that fewer patients develop arthritis that results from removing the meniscal tissue,� Schwartz said. �Thus, with fewer patients developing arthritis, the result could be fewer total joint replacements or at least delaying the need for a total joint replacement.�

Brain abnormalities found in people with writer's cramp

Mon, 23 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) People with serious cases of writerï¿½s cramp have brain abnormalities, according to a study published in the July 24, 2007, issue of Neurology, the medical journal of the American Academy of Neurology. People with writerï¿½s cramp had less brain tissue than healthy people in three areas of the brain that connect the senses and movement with their affected hand.

Writerï¿½s cramp is a form of dystonia, an involuntary, sustained muscle contraction. Writerï¿½s cramp often occurs in people who have used the same muscles repeatedly for years.

The study involved 30 people who had writerï¿½s cramp for an average of seven years with no other forms of dystonia. Using brain imaging, the researchers compared the brains of those with writerï¿½s cramp to 30 healthy people.

The researchers found that those with writerï¿½s cramp had less grey matter in three areas of the brain: the cerebellum, the thalamus, and the sensorimotor cortex.

ï¿½Itï¿½s not clear whether these abnormalities are a cause or a result of the disease,ï¿½ said study author Stï¿½phane Lehï¿½ricy, MD, PhD, of Salpï¿½triï¿½re Hospital in Paris, France. ï¿½The fact that the brain abnormalities are in the areas that control the affected hand suggests that these differences are specific to this problem.ï¿½

ï¿½Another theory is that the brain structure changed and adapted as a result of the sustained repetitive movement,ï¿½ Lehï¿½ricy said. ï¿½Studies have shown that people with no dystonia can experience brain changes due to learning new information, which supports this theory.ï¿½

Sports hernia repair technique coupled with innovative rehabilitation program speeds return to play

Sun, 15 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) CALGARY, Alberta -- Surgical repair of athletic hernia using tension-free mesh and a standardized rehabilitation protocol are successful in returning athletes to competition, according to new research released today at the 2007 Annual Meeting of the American Orthopaedic Society for Sports Medicine at the Telus Convention Center (July 12-15).

Dr. Brunt and colleagues studied the results of more than 60 athletic hernia repair surgeries to evaluate the experience of athletes undergoing tension-free mesh surgical repair using a standardized rehabilitation protocol. The investigators found a high rate of successful return to athletic competition. They also determined that the standardized rehabilitation protocol was useful in providing consistency in postoperative management and a structured approach to activity.

Using a tension-free mesh repair and a standardized rehabilitation protocol we have successfully returned athletes to competition in more than 90% of cases, says principal investigator L. Michael Brunt, M.D., professor of surgery at Washington University School of Medicine in St. Louis.

Athletic hernia is not a true hernia in a strict sense, which is defined as a protrusion through a hole or defect in underlying tissue or lining. People with athletic hernia have exertion-related pain in the lower abdominal and groin region that is associated with deterioration of the muscle layers. Without treatment, these athletes typically cannot perform at high levels and may no longer be successful at their sport.The standardized rehabilitation protocol is more structured than what has been previously reported. Athletic trainers, physical therapists and athletes appear to have the most success when given well-structured guidelines about what can and cannot be expected or allowed at each stage after hernia surgery.

An athletic trainer for the St. Louis Blues hockey team, Ray Barile, developed the multistep, graduated program used in this study to return the athletes to activity following repair. The program starts with early ambulation and motion and works toward resistance and core muscle building while later progressing to speed and functional activities. The hope is that this program can facilitate a faster rehabilitation and return to sport.

The three main groups of athletes who develop athletic hernias are hockey, soccer and football players. Sprinting, kicking, and skating are the activities that appear to be most problematic, explains Dr. Brunt. The athletes we see have usually undergone an extensive period of conservative management and having failed that, should be considered for surgical repair. On average, athletes in our series had experienced symptoms for more than eight months before undergoing surgery.

Pain from an athletic hernia, or pubalgia, is in the lower abdominal region and pubic bone. Typically this pain has been unexplained for a period of time, and there are few indications of the condition in the patients personal history, physical exam, or imaging scans. Making an accurate diagnosis often involves excluding other reasons for pain and identifying the few subtle findings that make the diagnosis.

Sports hernias have received recent media attention because several high-profile athletes, including tight end L.J. Smith of the Philadelphia Eagles, have been diagnosed with the condition. Athletic hernia can occur in athletes who are not necessarily at the elite level and who play sports only recreationally, Dr. Brunt notes.

Tension-free mesh is used for repair of other types of hernias. With no tension on the repair, the athlete can return to play earlier than when only sutures are used. Less pain is reported in the post-operative period when the mesh is used. Using the mesh helps restore strength and stability to the area affected, allowing easier recovery.

Other surgeons have been successful with different approaches including primary repair and repair with laparoscopic techniques, Dr. Brunt comments. For us, tension-free mesh has resulted in a consistent return to athletic competition and earlier activity than a primary approach could yield.

Dr. Brunt says that proper management of athletes with athletic hernia requires a multidisciplinary approach including sports orthopedists, physical therapists, and surgeons. It is important that physicians who see athletes with groin problems understand the entire spectrum of groin injuries. There are many different types of injuries that can occur, which makes it difficult to make the correct diagnosis since the imaging findings can be relatively nonspecific.

Sports hernia repair surgery plus innovative rehab program helps athletes return to play

Sun, 15 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) St. Louis, July 15, 2007 In recent years, sports hernias have sidelined many high-level athletes for months and, occasionally, prevented a return to competitive sports all together. New research at Washington University School of Medicine in St. Louis shows that surgical repair of sports hernias using tension-free mesh, coupled with an innovative rehabilitation program, successfully returned athletes to competition in 93 percent of cases.

Lead investigator L. Michael Brunt, M.D., professor of surgery, presented the study Sunday, July 15 at the annual meeting of the American Orthopaedic Society of Sports Medicine, held in Calgary, Alberta, Canada.

He and his colleagues evaluated the results of 61 sports hernia repair surgeries and a follow-up rehab program to determine how quickly they speed an athletes return to play. The surgeries were performed at Barnes-Jewish Hospital.

Sports hernias have received a lot of attention recently because of some high-profile athletes that have been sidelined with this condition, Brunt says. The benchmark for these athletes is return to play in their sport at the same level they were before the injury. By using the tension-free mesh to strengthen and reinforce the groin and lower abdominal muscles, we found that most athletes were back to their sport within eight weeks of surgery.

A sports hernia is not a true hernia because there is no hole in the abdominal wall through which underlying tissues protrude. A diagnosis can be tricky because symptoms particularly pain in the groin and lower abdomen can masquerade as a groin pull, strained abdominal muscle or other injury.

Those with sports hernias typically experience intense pain only at extreme levels of exertion. The condition is most common among hockey, football and soccer players. Repetitive twisting, turning or kicking motions at high speed are most likely to contribute to the condition.

Usually there is no discomfort walking around but significant pain when an athlete moves from a stationary position to full stride, Brunt says. For a high-performance athlete that can be enough to make a difference in their ability to compete successfully.

Although sports hernias occasionally occur among recreational athletes, it is far more common among those who play professional or college sports. In recent years, quarterback Donovan McNabb (Philadelphia Eagles) has had surgeries to repair sports hernias, as have forward Darren McCarty of the Calgary Flames and Los Angeles Galaxy soccer players Joseph Ngwenya and Benjamin Benditson.

The injury may also be related to changes in strength training. Most athletes focus more on the lower body and less so on the trunk. This lack of balance can create extra stress across the pelvis that is transmitted to the abdomen and the pelvic floor, which may be a factor in the development of a sport hernia, Brunt adds.

On average, the athletes Brunt operated on had experienced symptoms for eight months and most had undergone conservative management and rest during that time. A full 70 percent played at the college or professional level, and 95 percent were men. Because women have a different pelvic structure, they may be less vulnerable to sports hernias, he notes.

The surgery involves a two-inch incision to remove some of the damaged muscle tissue and instead of a primary repair with stitches, tension-free mesh is used to strengthen and reinforce the area. We think the mesh provides considerable support to let the area heal, Brunt says. Because theres no tension on the repair, this helps athletes return to full physical activity faster than surgery with a sutured repair alone.

The rehabilitation protocol used in the study was developed by Ray Barile, an athletic trainer for the St. Louis Blues hockey team. The multistep, graduated program is more structured than others used to return athletes to activity after groin surgery. It starts with early walking and movement and gradually moves athletes to resistance and core muscle building before progressing to speed and functional activities. Athletic trainers, physical therapists and athletes appear to have the most success when they are given well-structured guidelines about what can and cant be expected or allowed at each stage after hernia surgery, Brunt says.

A survey of athletic trainers who treated 21 of the athletes after surgery showed they rated the program highly (average score 4.5/5.0) in its ability to quickly and safely return athletes to their sport.

More recently, Brunt and his colleagues have accelerated the rehabilitation program to help athletes in midseason get back to competition sooner. This has helped some athletes return to play as early as five weeks after surgery. The tension-free nature of the repair helps facilitate a more aggressive progression to full activity, but Brunt cautions that the proper treatment of athletes with sports hernias requires a multidisciplinary approach. This includes sports orthopaedists, physical therapists and surgeons. It is important that physicians who see these athletes understand the entire spectrum of groin injuries and the methods that work best for returning them to competitive play, he says.

Tennis elbow procedure demonstrates long-term success

Sat, 14 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) CALGARY, Alberta -- Arthroscopic treatment of tennis elbow has shown to be successful at long-term follow-up, according to new research released today at the 2007 Annual Meeting of the American Orthopaedic Society for Sports Medicine at the Telus Convention Center (July 12-15).

This is the first longitudinal study of arthroscopic treatment of tennis elbow, says lead investigator Champ L. Baker, III, M.D., an orthopaedic resident at the University of Pittsburgh. The initial success from our original short-term study was maintained long term. I am happy to say that arthroscopic release is a good treatment option for lingering tennis elbow. The patients were enrolled through the Hughston Clinic in Columbus, Ga., where Dr. Bakers father and the senior study investigator, Champ L. Baker, Jr., M.D., practices orthopaedic sports medicine surgery.

Tennis elbow, a potentially debilitating condition, is common and can be successfully managed without surgery in almost 90% of cases. When it cannot be controlled by nonoperative measures, including rest, the arthroscopic technique used in this study is one of the many different surgical options that have good outcomes.

Investigators studied the long-term (130 month) pain and functional scores of 30 patients who underwent arthroscopic release for tennis elbow. The short-term results from this patient group were published in The Journal of Shoulder and Elbow Surgery in 2000 (9:475-82).

The researchers found that arthroscopic treatment provided very good results in terms of long-term pain relief and functional restoration. There were no repeat surgeries or injections. Satisfaction rates were also high, with 93% of the patients stating that they would have the surgery again if needed.

Athletes are not the only population vulnerable to tennis elbow. People in their 40s and 50s who do repetitive activities are often afflicted. Such activities can range from repetitively lifting boxes to repetitive wrist extension during long-term keyboard use. Tennis elbow pain is generally felt on the outside of the elbow.

In 1880, lateral epicondylitis was termed tennis elbow, but it could just as easily be called politicians elbow, because they run for office with their right hands 500 handshakes a day, explains the elder Dr. Baker, immediate past president of the AOSSM. This condition is caused by repetitive motion with the arm extended and the wrist moving up and down.

If youve had tennis elbow for more than a year and cant get better, then it would be a good idea to investigate having this procedure done by an orthopaedic surgeon skilled in arthroscopy. Patients should get better with very few complications, if any, continues Dr. Baker.

Dr. Baker adds that there are other advantages to arthroscopic surgery: I can look inside the joint to spot additional problems. Arthroscopic surgery speeds up the rehabilitation. In all published studies, return to work and play is much quicker with arthroscopic technique versus open surgery, while the complication rate is equal or less.

Women and arthritis sufferers have poorer short-term recovery from arthroscopic knee surgery

Sat, 14 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) CALGARY, Alberta -- The factors associated with poor short-term recovery from knee surgery appear to be different than those found to mar long-term outcome from the same surgery, according to new research released today at the 2007 Annual Meeting of the American Orthopaedic Society for Sports Medicine at the Telus Convention Center (July 12-15).

We found that women showed poorer short-term recovery than men in the first year following arthroscopic meniscal tear removal surgery, and people with osteoarthritis also did not do as well as others, says principal investigator Peter Fabricant, BS, a medical student at Yale University School of Medicine in New Haven, Conn. The factors associated with a poorer long-term outcome, such as larger tear size, greater amount of tissue removed, advanced patient age, and higher Body Mass Index, are not the same as those we can associate with short-term surgical recovery.

The meniscus is the shock-absorbing tissue that cushions the knee joint preventing the bones from rubbing. Tears in this tissue can cause pain and loss of function. In arthroscopic partial meniscectomy, the surgeon inserts small surgical instruments and a camera through tiny incisions in the knee to remove torn tissue. An estimated 636,000 arthroscopic knee procedures are performed annually, according to the American Academy of Orthopaedic Surgeons.

Fabricant and colleagues at Yale University studied 126 patients who underwent arthroscopic partial meniscectomy to assess the impact of obesity, age, gender, amount of tissue removed, and degenerative joint changes on short-term recovery. They found that being female and the extent of osteoarthritis were associated with a less-than-optimal first-year recovery.

Other studies have shown that advanced age, obesity, and the amount of meniscal tissue removed all negatively affect long-term outcome from arthroscopic meniscal repair. In our study these variables did not affect short-term recovery. Conversely, gender and osteoarthritis appear to play a role in short-term recovery, as they have been shown to do in the long-term, Fabricant comments.

The current medical literature only offers research findings on long-term outcomes following arthroscopic meniscal repair. We couldnt find anything in the literature to predict recovery during the first year, explains Fabricant. Physicians need to be able to discuss with patients how long it might be before they can return to optimal function levels in work and activities of daily living.

Fabricant and colleagues suggest that severe osteoarthritis in the knee may be a contraindication to surgery. Arthritis may be a marker for a degenerated knee, which may not be able to recover as well as a healthy, non-arthritic knee, Fabricant says.

Osteoarthritis may also be a marker for worse overall knee function in general. Patients with severe osteoarthritis already have loss of cartilage and soft tissue. Further tissue removal appears to have minimal impact on patient knee pain and function during the year following surgery.

The investigators say that it is unclear exactly how female gender complicates surgical recovery. Fabricant notes that there are gender differences both in surgical outcome and possibly in the biomechanics resulting in how the knee was initially injured. Even before surgery, women typically reported more knee pain and decreased knee function compared to men.

Serica scientists win AOSSM Award for ACL tissue regeneration in preclinical study

Fri, 13 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) MEDFORD, MA and CALGARY, CANADA, JULY13, 2007 -- Serica Technologies, Inc., a growth-stage medical device company developing silk-based biomaterial platforms for tissue regeneration, today announced that its scientists received the Cabaud Memorial Award from the American Orthopedic Society for Sports Medicine (AOSSM), for their pre-clinical research demonstrating the potential of Sericas SeriACL Graft to regenerate or re-grow anterior cruciate ligament (ACL) tissue in the knee, in a large-animal model.

Results from the award-winning paper were highlighted in a podium presentation during the AOSSM annual meeting. In this study, 43 goats were implanted with the SeriACL Graft and followed over 3, 6 and 12 months; results demonstrated the safety of the device, with initial indications of efficacy in the animal model. The SeriACL Graft, a new biomaterial made from natural silk protein, is installed using a standard surgical procedure to repair a torn ACL and is designed to provide a strong yet temporary support structure that replaces the torn ACL and stabilizes the knee joint.

This study provides the first evidence of sustainable ACL tissue engineering, said Gregory H. Altman, PhD, President and CEO, Serica Technologies, and senior author of the paper. Through advances in biomedical engineering, we now have a more thorough understanding of the bodys own capacity for ACL healing, if provided the correct impetus. We believe our proprietary technology can provide a long-term bioresorbable graft scaffold that anticipates the defect sites biological and mechanical requirements for ACL regeneration. We are extremely pleased with the results of this study and are aggressively moving forward with our development program, including the initiation of a study with the SeriACL Graft in humans.

Results from this study showed that all animals were weight bearing at 3, 6 and 12 months, with 95% returning to normal gait by 6 months; the majority of knees were clinically stable at all points. Range of motion assessment indicated the knees maintained a normal range flexion and extension at all points. By 12 months, the initial SeriACL graft structure was not evident, indicating the devices ability to provide sufficient direction and space for substantial ligament ingrowth while being bioresorbed.

Current ACL repair options either an autograft or allograft each have well-documented, debilitating side effects, said Rebecca Horan, PhD, the studys lead author and Sericas Senior Director of Research and Development. Our goal with the SeriACL Graft is to provide a scaffold, or biomechanical support structure, implanted during a standard surgical procedure, which supports the development of functional ACL tissue, thereby avoiding the limitations and lengthy rehabilitation associated with existing options.

The SeriACL Graft or the surgical procedure did not induce early signs of acute inflammation, swelling or initial scar formation in the goat model, as indicated by rapidly declining scores for pain and knee size.

The primary focus of our work over the past ten years has been to solve the unmet clinical need in ACL repair, offering surgeons and patients a device that would create the correct environment within the knee to regenerate ACL tissue, while supporting the mechanical structure of the joint during the healing process. Our ultimate goal is for the SeriACL Graft to serve the patient over his or her lifetime, Altman added. Prior to our study, no one has shown successful 12 month ACL regeneration data in a large-animal model with an off-the-shelf product, due to the demanding mechanical and biological requirements of a functional ACL. We are delighted that the AOSSM has recognized this important work, which brought to bear the combined disciplines of mechanical, biomedical, chemical and textile engineering for the development of our SeriACL Graft.

This study, Clinical, Mechanical and Histopathological Evaluation of a Bioengineered Long-Term Bioresorbable Silk Fibroin Graft in a One Year Goat Study for Development of a Functional Autologous Anterior Cruciate Ligament, was funded by a grant from the National Institutes of Health (NIH) and Serica Technologies, Inc. The very first source of funding which helped to initiate the broader research program began with a $15,000 First Time Investigator Grant from the AOSSM in 1999.

Since 1986, the Cabaud Memorial Award has been presented annually, by the American Orthopedic Society of Sports Medicine, for work that best exemplifies clinically relevant hypothesis-driven basic science research.

This award symbolizes what can be accomplished with a strong collaboration between engineers, scientists and surgeons who share a vision to advance medical science and improve patient care, said John C. Richmond, MD, Chair, Department of Orthopedics, New England Baptist Hospital, Boston, MA, and a co-author of the paper. We are excited by the potential of this device in ACL repair. An acknowledged expert in this area of medicine, Dr. Richmond has conducted more than 5,000 ACL and Rotator Cuff Tendon (RCT) reconstructive surgeries over the past 25 years.

Dr. Altman founded Serica in 1998, after completing his undergraduate and graduate studies at Tufts University, where he ruptured his ACL playing varsity football. His ACL repair surgery was performed by Dr. Richmond. Following knee surgery, Dr. Altman experienced the debilitating side effects of ACL reconstruction. This experience inspired his doctoral work, during which time he developed the concept and technology that became the platform for the current Serica product portfolio under development.

The ACL, one of the four major ligaments of the knee, is the second most commonly injured knee ligament, and is a very common injury among athletes. Female athletes are known to have a higher risk of injuring their ACL. Currently, 200,000 surgeries are performed each year in the U.S. to repair a torn or damaged ACL.

Groin injuries averted by preseason injury prevention

Thu, 12 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) CALGARY, Alberta -- Professional soccer players who participated in a special preseason groin injury prevention program had fewer groin injuries during that subsequent season than those who were not in the program, according to new research released today at the 2007 Annual Meeting of the American Orthopaedic Society for Sports Medicine at the Telus Convention Center (July 12-15).

The researchers enrolled 315 major league soccer players in a preseason groin injury prevention program to evaluate the effectiveness of the program. The 20-minute program was used as a prepractice warm-up two to three times a week during the preseason period. It included three phases warm-up, dynamic stretching, and strengthening.

The participating athletes had a groin injury incidence of 0.44 injuries per 1,000 hours, while a control group had a groin injury rate of 0.61 injuries per 1,000 hours.

Our 28% injury reduction rate is highly significant, says principal investigator Michael B. Gerhardt, M.D., director of the Center for Athletic Hip and Groin Disorders in Santa Monica, Calif., and team physician for US Soccer and Chivas USA, a major league soccer team. We were anticipating a 5-10% reduction rate, so we were pleasantly surprised that the injury reduction number was so high.

Most professional soccer teams in Europe and the United States recognize groin injury as a major problem, according to Dr. Gerhardt. Groin injury accounts for a large amount of lost playing time. They are common in elite soccer players and especially problematic among male soccer players. The term groin injury encompasses a wide range of injuries ranging from minor groin strains to chronic groin injuries, such as sports hernias, which often require surgery.

The number of groin surgeries was also evaluated. Although not statistically significant, the athletes in the prevention session had fewer surgeries (0.13/1,000 hours) than the control subjects (0.18/1,000) who did not participate in the program. While we were able to prevent the total number of groin injuries, we were unable to significantly reduce the number of surgeries, comments Dr. Gerhardt. Once an injury reaches the chronic stage it is hard to manage with any treatment regimen, including ours. These players typically go on to require surgery.

Chronic injuries are defined as lasting a month or longer. Avoiding acute injuries, which the studys preseason injury prevention program was able to reduce, can hopefully prevent them.

If a simple 15- to 20-minute program can reduce the number of groin injuries that are occurring in professional athletes, I think it will gain widespread use, notes Dr. Gerhardt. Weve seen this with ACL prevention programs, which have been implemented successfully by a variety of teams around the world. I anticipate that professional soccer teams will want their players to participate in a program if it is simple, cost effective, and, most importantly, proven to reduce groin injury.

Dr. Gerhardt attributes the success of the prevention program to the multidisciplinary efforts of several expert therapists, trainers, and physicians.

Neoprene sleeve equal to knee brace during recovery from ACL surgery

Thu, 12 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) CALGARY, Alberta -- Users of functional knee braces and neoprene sleeves have similar recoveries from anterior cruciate ligament (ACL) reconstruction, according to new research presented today at the 2007 Annual Meeting of the American Orthopaedic Society for Sports Medicine at the Telus Convention Center (July 12-15).

For patients returning to sport after ACL reconstruction, a functional knee brace, which is sturdy, elaborate, and expensive, does not provide advantages over a soft neoprene elastic sleeve, says principal investigator Trevor Birmingham, Ph.D., P.T., Canada Research Chair in musculoskeletal rehabilitation at the University of Western Ontario and the Fowler Kennedy Sport Medicine Clinic in London, Ontario.

ACL reconstruction surgery is common, particularly in young, athletic individuals. The ACL is an important ligament inside the knee that helps keep it stable. ACL reconstruction involves replacing the torn ACL with a strip of tendon called a graft. Approximately 100,000 ACL reconstructions are performed annually according to the American Academy of Orthopaedic Surgeons.

It is widely believed that the rigid support provided by a functional knee brace protects the graft and improves knee stability and function when the patient returns to sport after surgery and rehabilitation, explains Dr. Birmingham. Others believe that the additional support provided by a brace is not necessary.

To address this uncertainty, Dr. Birmingham and colleagues studied 150 athletes preparing to return to sport following ACL reconstruction. Seventy-six patients were randomized to receive a functional knee brace and 74 to receive a neoprene sleeve. The patients were instructed to wear the orthosis during all physical activities. The researchers found no significant differences between the groups at the one- and two-year follow-up visits.

Based on our clinical experience, we were not completely surprised by the results, Dr. Birmingham comments. These findings provide strong evidence that the average patient does not require a functional knee brace when returning to sport after ACL reconstruction. There may be some patients who will benefit from a brace, and identifying these individuals requires further research. Until then, these decisions are left to the surgeons discretion.

ACL functional knee braces are made by several different companies and have a variety of looks and fitting instructions. They are intended to limit abnormal movement of the knee and prevent excessive strain on the ACL or new graft. They generally provide a rigid support to restrain the knee, although they may also improve neuromuscular control of the knee. Most laboratory studies suggest that different types of functional knee braces perform similarly.

Neoprene sleeves are also made by several different companies and have different looks. Rather than providing rigid support, they are only intended to gently compress the area around the knee and improve neuromuscular control.

The study was large enough and had enough statistical power to detect even slight differences between the functional knee brace and sleeve groups. We can be confident that even if small but true differences between these groups exist, these differences are not large enough to be clinically important, concludes Dr. Birmingham. He notes that the study was not designed to test whether using a neoprene sleeve was better than using nothing at all.

Penn researchers find a new target for muscular dystrophy drug therapy

Thu, 12 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) PHILADELPHIA - Researchers at the University of Pennsylvania School of Medicine report how the gene for utrophin, which codes for a protein very similar to dystrophin, the defective protein in Duchenne muscular dystrophy (DMD), puts the brakes on its own expression in muscle cells, thereby suggesting a new target for treatment. The findings were published online in Molecular Biology Cell, in advance of print publication.

The production of utrophin slows in fetal muscles soon after birth, after which dystrophin takes over as the primary muscle-associated protein. How this normal utrophin silencing occurs has been a mystery, until now. If the brakes on utrophin production could be removed by drug intervention, then increased utrophin expression could substitute for dystrophin as a possible therapy for DMD, which affects 1 in 3,500 males.

Utrophin is normally made at the junction where nerves meet muscles, an area called the neuromuscular junction or synapse. In the present study, the Penn team discovered that silencing is applied by a protein called Ets-2 repressor factor (ERF) sitting on a small piece of the utrophin gene called the N-box.

We demonstrated that ERF significantly reduces or represses the activity of utrophins N-box in muscle cells of mice, says senior author Tejvir S. Khurana, MD, PhD, Associate Professor of Physiology and Member of the Pennsylvania Muscle Institute. When the N-box was deleted from the utrophin gene, ERF had no effect on silencing the utrophin gene, as measured by an increase in utrophin gene-promoter activity. In another experiment in which ERF was repressed, the researchers found utrophin mRNA production increased.

This approach of repressing the repressor is medically relevant to treating muscular dystrophy in that we hope to one day be able to upregulate utrophin production, explains Khurana.

Because utrophin is over 80 percent identical to dystrophin in its gene sequence, utrophin could substitute for it in muscle cells. In normal muscle cells dystrophin is part of a large complex of proteins that attaches muscle cells to surrounding tissues. In DMD muscle cells, dystrophin cannot perform this function and the muscles slowly fall apart. DMD patients begin to have muscle weakness and motor difficulties as children, and the condition worsens with age, eventually proving fatal around the third decade of life.

Dr. Khurana's work hints at what could be an important new drug target for DMDthe more options we have with this disease, the better, says Sharon Hesterlee, PhD, Vice President for Translational Research at the Muscular Dystrophy Association. We've known for a while that increasing utrophin expression can reduce symptoms of the disease, but it's very difficult to use a drug to increase gene activity. What's nice about this work is that now we can try to block a blocker to get the same effectit's a more drug-friendly approach.

Other therapeutic strategies for DMD involve muscle-cell implantation, stem-cell treatment, and gene therapy. While there has been some progress with these approaches, there have been many difficulties with graft vs. host rejection and gene delivery. This new research suggests that blocking ERF, either with drugs or by interfering with its RNA, may be more generally feasible in most DMD patients.

There are several animal models of DMD, most notably the mdx mouse. Khurana and his colleagues are currently investigating whether repressing ERF in mdx mouse muscle reduces muscle deterioration.

We have worked on this problem for a number of years, and our current findings are a logical incremental step in understanding how utrophin could become an effective tool for treating DMD, states Khurana. He cautions that while he hopes his work will lead to an effective treatment someday, there are many steps and hurdles to get through first.

Anti-malarial drug may reduce risk of diabetes for patients with rheumatoid arthritis

Tue, 10 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) Preliminary research suggests that use of the anti-malarial drug hydroxychloroquine may help reduce the risk of the development of diabetes in patients with rheumatoid arthritis, according to a study in the July 11 issue of JAMA.

Type 2 diabetes mellitus affects nearly 8 percent of US adults, and its prevalence has been increasing.Antimalarials such as hydroxychloroquine, a long-standing safe and inexpensive treatment for an autoimmune disease such as rheumatoid arthritis, theoretically may improve glucose tolerance and prevent diabetes mellitus, according to background information in the article. In vitro and animal studies indicate that antimalarials improve insulin secretion and peripheral insulin sensitivity.

Mary Chester M. Wasko, M.D., M.Sc., of the University of Pittsburgh, Pa., and colleagues examined the association between hydroxychloroquine therapy and risk of diabetes in patients with rheumatoid arthritis. The study included 4,905 adults with rheumatoid arthritis (1,808 had taken hydroxychloroquine and 3,097 had never taken hydroxychloroquine) with no initial diagnosis or treatment for diabetes, with 21.5 years of follow-up (Jan. 1983 through July 2004).

During the observation period, incident diagnoses of diabetes were reported by 54 patients who had taken hydroxychloroquine and by 171 patients who had never taken it. Analysis indicated that patients who had taken hydroxychloroquine had a 38 percent lower risk of developing diabetes, compared with those who had not taken hydroxychloroquine. This risk was further reduced with increased duration of hydroxychloroquine use. Patients who took hydroxychloroquine for more than four years had a 77 percent lower risk of diabetes compared with those who had never taken hydroxychloroquine.

We report herein the first evidence, to our knowledge, suggesting that use of hydroxychloroquine is associated with a reduced risk of developing diabetes in patients with rheumatoid arthritis, the authors write. Moreover, risk reduction increased with duration of hydroxychloroquine exposure, supporting a biological action of this drug on glucose metabolism.

While our study showed a reduction in diabetes incidence specifically in a rheumatoid arthritis cohort taking hydroxychloroquine, these findings also may be expected to occur in patients without rheumatoid arthritis. The beneficial changes in glucose metabolism and insulin sensitivity reported among patients with lupus, patients with type 2 diabetes, and in animal models suggest that these effects are not specific to rheumatoid arthritis.

Antimalarial drugs may have a role in treating rheumatoid arthritis not only to suppress synovitis [inflammation around the joints] but also to reduce the likelihood of developing glucose intolerance and dyslipidemia [abnormal concentrations of lipids]. As quality of life and life expectancy improve for patients with rheumatoid arthritis, and health care costs escalate, the use of inexpensive, safe therapies that have multiple beneficial effects is attractive. Further prospective studies are needed to determine whether this treatment option should be considered a standard component of rheumatoid arthritis combination therapy in the future, and to evaluate the potential role of hydroxychloroquine as a preventive agent for diabetes among high-risk individuals in the general population, the researchers conclude.

More muscle for the argument to give up smoking

Mon, 09 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) Researchers at The University of Nottingham have got more bad news for smokers. Not only does it cause cancer, heart attacks and strokes but smokers will also lose more muscle mass in old age than a non-smoker. The effect of this predisposes smokers to an accelerated decline in physical function and loss of independence.

Research has already established that smokers tend to have a lower muscle mass than non-smokers but no one has been able to explain why.

Now, Michael Rennie, a Professor of Clinical Physiology, and Dr Philip Atherton, a Research Fellow, both from the universityï¿½s School of Graduate Entry Medicine and Health at Derby, have, with collaborators in Denmark and the USA, discovered that smoking impairs the day to day upkeep of muscle. Their research shows that smoking is likely to speed up a condition known as sarcopenia ï¿½ the loss of muscle mass with ageing which is linked to poor balance, gait speed, falls, and fractures.

16 people took part in the study which was part funded by the Biotechnology and Biological Sciences Research Council. The men and woman in their mid sixties were selected because of their similar lifestyles in terms of alcohol consumption and physical activity. They were all considered to be healthy, with no symptoms of lung disease. They were studied in two equal groups: heavy smokers, who had smoked at least a pack of 20 cigarettes a day for at least 20 years: and non-smokers.

To measure the synthesis of muscle protein they were given an intravenous infusion of blood with a tagged amino acid (one of the building blocks of protein). Samples of muscle were taken from their thighs before and after the infusion to follow how much had ï¿½stuckï¿½ in muscle protein. This measured the rate of synthesis of muscle protein which contributes to the daily maintenance of the muscle mass. The researchers found that it was substantially less in smokers than non-smokers.

During extensive studies, carried out in collaboration with Washington University, St Louis and Copenhagen University, Professor Rennie and Dr Atherton discovered that the amounts of myostatin, a muscle growth inhibitor and MAFbx enzyme, which breaks down muscle protein, were higher in smokers than non-smokers.

Dr Philip Atherton said: ï¿½From our tests, we can conclude that smoking slows the muscle protein synthesis machinery ï¿½ probably impairing day to day upkeep of muscle. We are all well aware of the ill affects of smoking on the lungs but our study reveals yet another cause of ill-health associated with smoking. Hopefully the UK smoking ban will encourage people to quit while they are still young, helping them to keep in good health in later lifeï¿½.

Faulty cell membrane repair causes heart disease

Tue, 03 Jul 2007 04:00:00 PST

( from http://www.rxpgnews.com ) During vigorous exercise, heart muscle cells take a beating. In fact, some of those cells rupture, and if not for a repair process capable of resealing cell membranes, those cells would die and cause heart damage (cardiomyopathy).

Researchers at the University of Iowa Roy J. and Lucille A. Carver College of Medicine have discovered a specific repair mechanism in heart muscle and identified a protein called dysferlin that is critical for resealing heart muscle cell membranes.

The study, led by UI researcher and Howard Hughes Medical Institute investigator Kevin Campbell, Ph.D., also shows that loss of dysferlin causes cardiomyopathy in mice. Furthermore, heart damage in these mice is exaggerated by vigorous exercise or by inherent muscle weakness caused by a muscular dystrophy defect. The results are published in the July 1 issue of the Journal of Clinical Investigation.

Active tissues, like a beating heart or contracting muscle, need mechanisms to repair the inevitable cell membrane tears caused by physical stress and strain. In 2003, Campbell and his colleagues identified dysferlin as a key protein in this vital repair mechanism in skeletal muscle. In humans, dysferlin deficiency -- which leads to faulty muscle membrane repair -- causes three types of muscular dystrophy.

The new study expands knowledge of dysferlin function, showing that dysferlin-mediated membrane repair is also important in heart muscle cells and suggests that inadequate membrane repair can also lead to cardiomyopathy.

If we could boost this repair mechanism, it might be possible to slow cardiac and skeletal muscle damage in muscular dystrophy patients, said Campbell who also holds the Roy J. Carver Biomedical Research Chair in Molecular Physiology and is head of the department and a UI professor of neurology.

The UI team initially found that young mice that lacked dysferlin showed no heart damage, which is consistent with what is seen in humans with dysferlin mutations. However, a case study describing late-onset cardiomyopathy in a Japanese patient with a dysferlin deficiency prompted the UI team to look at the mice as they aged.

They found that the mice started to develop cardiomyopathy at about one year of age (middle aged for a mouse). The team also found that exercise exaggerated the stress-induced injury in these mice, suggesting that inadequate membrane repair led to cardiomyopathy.

The research team also bred mice that lacked both dysferlin and the protein dystrophin, which is missing in patients with Duchenne muscular dystrophy. These double knockout mice had early onset cardiomyopathy, which was much more severe than in mice with either of the single mutations. The results suggest that dysferlin might provide some protection against heart damage in Duchenne patients, at least at a young age, by delaying the onset of cardiomyopathy.

We hope these findings will stimulate clinicians to look at the cardiac health of muscular dystrophy patients and the overall muscle health of patients with cardiomyopathy, Campbell said.

New dynamic brace developed to advance clubfoot treatment

Thu, 28 Jun 2007 04:00:00 PST

( from http://www.rxpgnews.com ) A new brace that maintains correction for clubfoot, a birth defect in which the foot is turned in toward the body, has shown better compliance and fewer complications than the traditional brace used to treat the condition.

Matthew B. Dobbs, M.D., associate professor of orthopedic surgery at the School of Medicine, designed the new dynamic brace, called the Dobbs brace, to allow active movement, preserve muscle strength in the foot and ankle and be less restrictive to the child than the traditional brace.

Dobbs tested the brace on 28 patients who had already received non-surgical treatment for their clubfeet at St. Louis Children's Hospital and St. Louis Shriners Hospital. Over a two- to three-year follow-up period, Dobbs and his colleagues found that the Dobbs brace is at least as effective as the traditional brace and resulted in better compliance by parents.

Results of the study appear in the July/August issue of the Journal of Pediatric Orthopaedics. Dobbs is senior author.

Dobbs first treated children with clubfoot deformity using the Ponseti method. The treatment, developed in the 1950s by Ignacio Ponseti, M.D., professor emeritus of orthopedics and rehabilitation at the University of Iowa, involves weekly casting and manipulation of the clubfoot soon after birth. When done correctly, the Ponseti method greatly reduces the need for extensive surgery, which can contribute to painful and arthritic feet in adulthood. The children with clubfoot whom Ponseti treated with this method were likely to have normally functioning, pain-free, flexible feet in adulthood.

Traditionally, children who have been treated for clubfoot using the Ponseti method must wear a nighttime brace that turns their feet away from the body for three to four years following the initial casting treatment. The brace has open-toed, high-top shoes attached to a shoulder-width fixed metal bar. Because of skin blistering and the brace's restriction of leg motion, many parents used the brace less than had been prescribed, which can allow recurrent clubfoot deformities that may require extensive surgery. In fact, past studies had shown that about 30 percent to 40 percent of families do not use the traditional brace as prescribed.

In contrast, the new brace has a soft, custom-molded interface that is placed inside of a solid ankle-foot orthosis, an orthopedic appliance designed to maintain alignment of the bones in the foot and ankle. The bar connecting the feet has a release mechanism that allows parents to easily detach and reattach the bar to place the child in a car seat or high chair or change a diaper without removing the entire brace. Other differences from the traditional brace is that the Dobbs brace also allows children to move their legs independently while wearing the brace.

Dobbs said these changes are key to preventing a recurrence of clubfoot.

While we've had good success in obtaining correction in clubfeet, maintaining that correction has been more challenging, Dobbs said. If the child is tolerating the brace well, there is a higher likelihood of parental compliance.

All 28 patients in the study had reached full correction for their clubfoot before being fitted for the brace. Eighteen patients who had not been wearing the traditional brace as prescribed were fitted for the Dobbs brace. The remaining patients were fitted only for the Dobbs brace. All but two patients wore the brace as prescribed.

Of the two patients who were noncompliant in wearing the brace, one patient had skin blistering due to improper use of the brace, which was eventually corrected, while the other patient was not kept in the brace because of the caregiver's work schedule.

The newly designed, more flexible foot abduction orthosis is equally effective, or more so, than the traditional brace, considering rates of clubfoot relapse were less with the new orthosis than those reported in several series using the traditional brace, Dobbs said. Although our experience with the dynamic brace has been favorable, a randomized study comparing the dynamic orthosis to the traditional brace would provide a more accurate assessment of outcome.

Dobbs said the bar connecting the feet can be used with other types of corrective footwear for clubfoot.

Just having the flexible bar makes a huge difference in compliance and convenience, he said.

The Dobbs brace was patented and is licensed through the University's Office of Technology Management.

New genetic test developed at Emory advances detection and diagnosis of muscular dystrophy

Wed, 27 Jun 2007 04:00:00 PST

( from http://www.rxpgnews.com ) A new genetic test targeting the most common types of muscular dystrophy--those caused by mutations in the dystrophin gene--is far quicker with greater accuracy and sensitivity than existing tests. It can be used to confirm clinical diagnoses, to test female family members who may be carriers, and to perform prenatal testing.

The test was developed by Michael Zwick, PhD, and Madhuri Hegde, PhD, assistant professors in the Department of Human Genetics and the Emory Genetics Laboratory in the Emory University School of Medicine.

Muscular dystrophy includes more than 30 genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles that control movement. Some forms are seen in infancy or childhood, while others may not appear until middle age or later.Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy and primarily affects boys. It is caused by absence of dystrophin, an important muscle protein involved in maintaining the strength of muscle fibers.

According to the National Institute of Neurodegenerative Diseases and Stroke (NINDS), DMD onset is between 3 and 5 years, with rapid progression. Most boys are unable to walk by age 12 and later need a respirator to breathe. Girls in these families have a 50 percent chance of inheriting and passing the defective gene to their children. Becker muscular dystrophy, which is similar to Duchenne but less severe, results from faulty or not enough dystrophin.

As currently implemented the new test, called Em Dystrophin, detects 99 percent of mutations in the dystrophin gene including deletions, duplications and point mutations.

The Em Dystrophin test uses a new kind of microarray technology that contains the entire sequence of the dystrophin gene, the largest known gene in humans, on a chip the size of a microscope slide. The test initially detects deletions and duplications, then microarray-based resequencing is used to rapidly identify subtle genetic variations that may cause muscular dystrophy.

The Em Dystrophin test confirms clinical diagnosis of Duchenne and Becker muscular dystrophy in a male and characterizes the type and size of the mutation. Women with a family history of Duchenne or Becker who are at risk to be carriers can be tested, then, if found to be carriers, can have prenatal testing.

Previously, access to prenatal testing was limited for some women when the affected male relative was not available for testing. The Em Dystrophin test greatly improves access to prenatal and carrier testing for women without the need to test a male relative, in a rapid timeframe, according to Vanessa Rangel Miller, MS. In addition to improved testing, the Emory Genetics Laboratory, Parent Project Muscular Dystrophy, leading researchers and clinicians are working together to develop a database for mutations and clinical data.

Our new genetic test, along with new therapies currently in clinical trials, is a very positive development for muscular dystrophy patients and their families, says Dr. Hegde.

In the last five years DMD research has accelerated, resulting in more knowledge about the role of the dystrophin gene and an increased understanding about what happens to a muscle cell lacking the dystrophin protein. Researchers around the world are investigating a number of different treatment strategies, all with the goal of slowing or stopping muscle degeneration. Several clinical trials are underway and many others are in development, including testing of an oral medication intended to circumvent mutations in the dystrophin gene and increase normal gene expression.

According to Dr. Hegde, about 13 percent of mutations in the dystrophin gene are nonsense mutations--point mutations in a sequence of DNA that can result in mistakes in gene expression and nonfunctional proteins. New data published online in the current edition of the journal Nature show that PTC124, an investigational new drug designed to bypass dystrophin nonsense mutations and restore a functional protein, was effective in a preclinical (animal) model of Duchenne muscular dystrophy (DMD). (www.clinicaltrials.gov).

Mouse model points to possible new strategy for treating rare muscle disease, kidney disorders

Fri, 01 Jun 2007 04:00:00 PST

( from http://www.rxpgnews.com ) Based on clues provided by a study with transgenic mice, a research group at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health (NIH), has developed a strategy that will be tested as the first treatment for people with hereditary inclusion body myopathy (HIBM), a rare, degenerative muscle disease. In an unexpected finding, the research indicates that the approach also might benefit patients with certain kidney disorders.

The scientists, led by Marjan Huizing, Ph.D., an associate investigator in NHGRIs Medical Genetics Branch, report their findings in the June issue of the Journal of Clinical Investigation. The study was supported by the NHGRI Division of Intramural Research and was conducted in collaboration with researchers supported by the Howard Hughes Medical Institute (HHMI), Bethesda, Md., and the HIBM Research Group, Encino, Calif.

It is gratifying to see how the tools and technologies generated by the sequencing of the human genome are being used to uncover new strategies for treating genetic human disease, said NHGRI Director Francis S. Collins, M.D., Ph.D. This work also underscores the value of animal models in learning more about the pathways involved in human disease and how to target therapies that affect those pathways.

NHGRI Scientific Director Eric D. Green, M.D., Ph.D. said, We are excited by the possibility that this study may lead to new treatments for those who suffer from either HIBM or kidney dysfunction. This work is a solid example of translational research, where discoveries in the laboratory provide a way forward to aid patients dealing with a frustrating and debilitating inherited disorder.

HIBM is a genetic disease with non life-threatening symptoms that emerge in adulthood and lead to slowly progressive muscle weakness. Most patients develop symptoms while in their early 20s and become wheelchair-bound by the time they reach 40, as their arm, hand, leg and core muscles progressively weaken. It is caused by a mutation in the GNE gene, which codes for two enzymes that produce sialic acid, a sugar important to muscle development and kidney function.

The new research focused on a form of HIBM in Iranian-Jewish families, which is caused by a specific mutation in the GNE gene known as M712T. Numerous other GNE mutations can cause HIBM and occur in populations worldwide. At this time, there is no treatment available for any type of HIBM.

In their search for potential HIBM treatments, the researchers drew upon previous evidence that impairment of the enzymes that promote sialic acid production causes low sialic acid levels in muscle proteins. They hypothesized that a compound called N-acetylmannosamine, or ManNAc, a sugar that is naturally converted to sialic acid, might have an impact on the muscle weakness caused by HIBM.

To help test that hypothesis, Dr. Huizing and her colleagues created a transgenic mouse model in which M712T GNE gene mutation was introduced into a strain of mice. However, the researchers were surprised to find that, instead of developing adult-onset muscle disease as expected, the transgenic mice developed a kidney condition that caused them to die just a few days after birth. When the researchers supplemented the diets of pregnant transgenic mice with ManNAc, sialic acid production improved in the fetuses, and they were born with markedly improved kidneys.

We were surprised that the HIBM mutation had such a detrimental impact on kidney function in the transgenic mice, said Dr. Huizing. Structural elements in the kidney that are important for filtering waste from the blood in these animals were severely impaired and we linked this to sialic acid deficiency. This outcome demonstrates the significance of the ability of the body to synthesize sialic acid for kidney development and function.

NHGRI Clinical Director William Gahl, M.D., Ph.D., who was a co-author of the study, said, With respect to the disease HIBM, we are hoping that humans with the same genetic mutation as in our mouse model will also respond to ManNAc. The availability of these transgenic mice will assist us greatly in assessing the appropriate dosage of the drug to test in HIBM patients.

To date, none of the offspring born to transgenic mice who received ManNAc supplementation have gone on to develop muscle weakness, but the mutant mice remain smaller than their unaffected siblings. Studies are currently ongoing in Dr. Huizings laboratory to study the mutant mice until they reach an older age when researchers can assess any onset of muscle weakness. In addition, NHGRI clinical researchers recently observed a temporary, but significant, improvement in muscle strength among HIBM patients who received intravenous immune globulin G an effect that researchers suspect was mediated through the provision of sialic acid present in the immune globulin.

NHGRI researchers expect the clinical trial of ManNAc for HIBM to begin in late summer or early fall. Based on their findings, the group is also exploring the possibility that ManNAc may benefit people suffering from diseases that involve damage to the cell layers of the kidney that are required for filtering the blood.

When the villain becomes your friend: The strange tale of muscle lactate

Thu, 31 May 2007 04:00:00 PST

( from http://www.rxpgnews.com ) In a paper published this week in The Journal of Physiology, Frank de Paoli and colleagues, working at the University of Aarhus in Denmark, add to the growing literature leading to a more complete understanding of the physiological role of lactic acid production in muscle.

In the late 19th century, fermentation chemists realized that juice left to ferment without adequate oxygen resulted in acid products. Then, in the early 20th century, when physiologists stimulated isolated frog muscles to contract until exhaustion, they found that the tissues had accumulated high amounts of lactic acid. Since then, the idea that lactic acid accumulation causes muscle fatigue has persisted. But did early scientists fail to address the various issues adequately and interpret the results appropriately Did they fail to ask the essential question Why does nature make lactic acid, and did they in effect put one and one together and make them a minus

De Paoli and colleagues looked at the effects of lactic acid and adrenaline on the processes that signal contractions in skeletal muscles. Using rat muscles, the study examined the combined effect of potassium ions, lactic acid and adrenaline on the electrical signalling system that serves to forward the activating signals from the brain to the muscle fibres where contraction takes place. They showed that in combination, lactic acid and adrenalin serve to help working muscles ward off the effects of potassium ions which leak from the inside to the outside of working muscle cells and negatively effect the signaling process by which muscles contract. In this, the latest of a series of reports from the Aarhus group, in combination with reports from other scientists in Scandinavia, the UK, US and Canada, long-standing ideas about the role of lactic acid in muscle are being overturned.

So, why do muscles contract Usually, muscles contract because the central and peripheral nervous system signals them to do so. Why do the muscles make lactic acid Lactic acid is the result of the glycolytic energy production system. It is an energy source to be used in muscle cells of origin, or adjacent fibres (cells), or fibres in the heart and cells in the brain. Lactic acid is also the material that the liver prefers to make glucose (sugar) for the blood when exercise is prolonged. Lactic acid production in muscle is stimulated in part by circulating adrenalin. Now, from de Paoli and colleagues we learn that adrenalin and lactic acid also help protect against the electrolyte imbalance across muscle membranes brought on by the loss of potassium.

Why does potassium have such a negative effect? In the study, when potassium ions outside the muscle fibres were increased to levels seen during intense exercise, the ability of the signalling system to forward electrical signals was profoundly reduced and the muscle became paralysed. If, however, lactic acid and adrenaline were added in combination, the function of the signalling system was largely recovered and the contractile response of the muscles restored. It was further shown that the positive effect of lactic acid was specifically related to an acidification of the interior of the muscle cells, which is one of the hallmarks of intense exercise.

The muscle lactic acid story, however, is still incomplete. It may even be found that lactate production is adaptive because its presence signals the activation of genes responsible for controlling muscle function. So, it seems that there is wisdom in the way that the body functions, a retrospective realisation that seems obvious, and which for lactic acid is supported by a century of strides even after a few false steps.

Existence of muscle-building stem cells points to regenerative therapies for muscular disease

Thu, 31 May 2007 04:00:00 PST

( from http://www.rxpgnews.com ) A new report in the June 1 issue of the journal Cell, a publication of Cell Press, confirms the existence of some apparently uncommitted stem cells amongst cells responsible for generating the bulging biceps of body builders and the rippling abs of fitness buffs. The findings could lead to new muscle-regenerating therapiesincluding cell transplantation regimens and stem cell-replenishing drugsfor people with various muscle-wasting diseases, including muscular dystrophies. Ultimately, such treatments might also help keep people strong as they age, according to the researchers.

A team led by Michael Rudnicki of the Ottawa Health Research Institute in Canada found that so-called satellite cells in muscle actually include a mix of cells already committed to their muscular fate and others that behave like more versatile stem cells. The cells had widely been considered by scientists as a homogeneous population of dedicated muscle progenitors. Moreover, Rudnickis team showed that injection of the satellite stem cells into the muscles of mice successfully replenished the animals regenerative reservoir of cells.

Weve found that there are two types of satellite cell90% that are already committed to becoming muscle and another 10% with characteristics normally attributed to stem cells, Rudnicki said. Its not been shown yet, but these muscle stem cells might even have the capacity to make other tissues, such as bone and fat.

Weve also shown that these satellite stem cells, when transplanted into muscle, can repopulate the regenerative cell niche. This is a very significant advance in our understanding of satellite cell biology that will require us to rethink decades of research. It also opens new avenues for therapeutic treatment of muscular diseases.

Skeletal muscle fibers are essentially long, tubular cells, each of which includes hundreds of nuclei. The fibers are surrounded by a coating of collagen and other glycoproteins with satellite cells sandwiched in between. First discovered in the 1960s, satellite cells are known to be responsible for the growth, maintenance, and repair of skeletal muscle after birth. The normally quiet restorative cells spring into action in response to the stress of weight-bearing or trauma.

Yet much about the mechanisms controlling satellite cells identity and development had remained uncertain, Rudnicki said. Earlier studies had even suggested that satellite cells might originate from muscle cells that had essentially regressed, or dedifferentiated, to a more primitive developmental state.

In the new study, the researchers took a closer look at the molecular profiles of satellite cells isolated from mouse muscle. They showed that the satellite cells consist of two classes defined by the activity or inactivity of a gene called Myf-5.

Moreover, that genetic difference gave rise to an important distinction in the satellite cells behavior. Cells without active Myf-5 divide asymmetricallya characteristic commonly seen among stem cells. That lopsided cell division produced one daughter like its parent, exhibiting a stem cell-like capacity for self renewal, and another Myf-5 positive cell.

The researchers also showed that satellite cells in which Myf-5 was switched on, when injected into the muscles of mice, continued down the road toward becoming muscle. In contrast, transplantation of Myf-5 negative cells extensively contributed to the satellite cell reservoir throughout the injected muscle.

The findings led the researchers to conclude that satellite stem cells could be used for direct transplantation into diseased muscle, noting that molecular characterization of satellite stem cells should lead to identification of markers enabling their prospective isolation from human muscle tissue.

Alternatively, they added, understanding the molecular regulation of satellite stem cell symmetric versus asymmetric cell division will lead to identification of biologics or small drugs that specifically target the relevant pathway leading to satellite stem cell expansion.

Research shows aerobic exercise helps maintain muscle in elderly

Wed, 30 May 2007 04:00:00 PST

( from http://www.rxpgnews.com ) GALVESTON, Texas Why do older people tend to lose muscle mass and grow frail? One important factor identified by medical science is the reduced ability of the elderly to respond to the muscle-building stimulus of the hormone insulin.

Insulin is best known for its link to diabetes a condition in which either a complete lack of insulin or systemic resistance to the hormone's activity (as in type 2 diabetes) causes blood sugar levels to soar out of control. Recent studies have shown, however, that insulin also provides crucial assistance in building muscle, and that its ability to do so drops off dramatically in the elderly.

Now, a small but provocative study by medical researchers in Texas and California suggests that a simple, cost-free therapy appears to largely overcome that drop-off in insulin response: moderate aerobic exercise such as walking.

Experiments at the University of Texas Medical Branch at Galveston (UTMB) and the University of Southern California, Los Angeles conducted on 13 healthy volunteers in their late 60s showed that 45 minutes of walking 20 hours before exposure to insulin restored the muscle-growth-stimulating effects of the hormone to levels comparable to those seen in normal young adults.

Prior research had suggested that a large part of the problem older people experience lies in the tiny blood vessels that feed the muscles protein-building amino acids, glucose and insulin (which itself also works within muscle cells as a powerful protein growth factor). In young adults, these normally closed vessels open wide in response to the insulin increase generated by a meal, providing clear passage for muscle-making materials. In elderly people, however, this process, known as vasodilation, is much less pronounced.

We thought, let's see what happens if we use aerobic exercise, one of the interventions that has been shown in the past to improve vasodilation, to find out whether we can get insulin to stimulate muscle synthesis in older people, said UTMB professor Elena Volpi, senior author of a paper on the experiments appearing in the June issue of the journal Diabetes. It turned out that a fast walk restored the insulin response quite well.

To test their hypothesis, the researchers first required six of their 13 subjects to walk for 45 minutes on a treadmill quickly enough to keep their hearts beating at 70 percent of their maximum rate the same aerobic intensity level recommended to maintain cardiovascular fitness. The other seven subjects simply rested.

On the following morning, the researchers sampled the blood going into and coming out of thigh muscle in each of the volunteers, while supplying via the femoral artery a concentration of insulin similar to that released after a typical meal. They also took three small muscle tissue samples from each subject.

Tracer techniques enabled the scientists to track amino acids (the building blocks of muscle proteins) and determine muscle-protein synthesis and breakdown rates from the blood and muscle samples, while measuring blood flow at the same time. These revealed that the volunteers who exercised had both higher blood flow and net muscle protein growth. In addition, the researchers screened the muscle biopsy samples for signals associated with insulin's ability to stimulate the assembly of muscle protein from amino acids. This test also showed that exercise boosted insulin's role as a muscle protein growth factor.

We already know that moderate aerobic exercise reduces cardiovascular disease, improves glucose uptake, and improves endurance, Volpi said. Now it looks like it may also slow the rate of muscle loss in aging. We need to test this hypothesis further with larger trials, but still, it's one more reason why elderly people ought to be regularly walking, swimming or cycling.

Biofeedback on abnormal mechanics lowers risk for stress fractures, pain under kneecap

Mon, 30 Apr 2007 04:00:00 PST

( from http://www.rxpgnews.com ) More than seven out of 10 runners will sustain an injury over the course of a year, many of these injuries preventable without any adverse effects on running distance or performance, according to Dr. Irene Davis, director of the Running Injury Lab at the University of Delaware, and director of Research for Drayer Physical Therapy Institute.

In earlier studies, Dr. Davis identified the specific gait mechanics associated with common injuries. Now, in a study reported at the Experimental Biology meeting in Washington, DC, she explains how she successfully retrained runners to change their faulty gaits in eight half hour sessions, reducing leg shock by 50 percent and completely eliminating pain under the kneecap.

Her Experimental Biology presentation on April 30 is part of the scientific program of the American Association of Anatomists.

In the laboratory, Dr. Davis uses sophisticated biofeedback devices and monitors, but she says she does similar - and also effective - retraining in the physical therapy clinic at the University of Delaware using basic mechanical information, mirrors and advice to listen to the sound of ones own feet hitting the ground.

The two studies underway in Dr. Davis' laboratory now are with runners who were selected for the study because they were experiencing or had been identified as high risk for one of the two most common running-related injuries: tibial stress fractures (microfractures of the lower leg bone) and patellofemoral pain syndrome (pain under the kneecap).

Each runner undergoes an analysis of their gait. Runners then come to the laboratory for two days, take a day off, return for two, until they have had eight retraining sessions on a special treadmill. The first sessions last 15 minutes, and the final ones 30 minutes. Runners are not allowed to run outside the laboratory during retraining for fear of reinforcing old gait habits.

Dr. Daviss earlier gait mechanics research had found that individuals with tibial stress fractures tend to land harder when each foot hits the ground, and in fact about half of the at-risk runners who have completed the study so far already had experienced microfractures. During their retraining sessions, the runners wore a shock measuring device on their lower legs while they ran on a tread mill. A monitor on the front of the treadmill showed the force of each footstrike measured against a line of what a normal, healthy footstrike should look like. The runners task was to constantly adjust the force with which each of their own feet hit the ground to keep it at or below the line on the screen.

With this feedback, all runners immediately were able to modify the hardness of their footstrike to meet the desired level, but all reported that the softer footstrike level did not feel normal. By the end of the eighth session, however, even when they were receiving relatively little feedback, all runners had adjusted the force of their footstrike by half. Furthermore, they reported that they found the new gait now felt more normal.

The runners experiencing pain under the kneecap followed the same protocol. Dr. Davis earlier gait mechanics studies had found that individuals with kneecap pain (patellofemoral pain syndrome) demonstrate poor hip stability, hips rotating inward, causing a knock-kneed type running gait. On the laboratory treadmill, these runners watched a monitor that compared their gait, measured by markers on their legs, to a normal angular curve.

By keeping their knees apart, not letting them collapse inward, they soon were able to make the two images merge. Before retraining, the group had classified their kneecap pain from five to seven on a ten point scale, ten being the worst. In every case, after retraining, the runners reported zero pain.

A month after the retraining, during which runners had resumed their regular running schedule, they returned to the laboratory treadmill. All had retained the lessons learned.

Dr. Davis recommends that runners without access to gait analysis and biofeedback do a little of what she does in the clinic at the University of Delaware.

For people with or at risk for stress microfractures, we ask them to listen to their footstrikes and simply make the sound softer, says Dr. Davis. For people with pain under the kneecap, we tell them to run in place in front of a mirror and concentrate on keeping their knees apart.

In the meantime, back at the laboratory, she is continuing to recruit patients into the study. Funded by both the Department of Defense and the National Institutes for Health in the interest of helping individuals to remain physical fit throughout their lives, the studies eventually will include 60 runners. Data reported at the Experimental Biology 2007 meeting were for five patients in each group.

Free weight training gets workers with rotator cuff injuries back on the job

Sun, 29 Apr 2007 04:00:00 PST

( from http://www.rxpgnews.com ) Resistance training, some of it job-specific, was successful in getting 90 percent of workers with severe rotator cuff injuries back to work, the majority (75 percent) at their previous job, after traditional physical therapy had failed to do so. Furthermore, all but one of the 42 employees in the study (98 percent) reported satisfaction with the resistance-training program and its outcome.

Dr. Jamie Stark described this and five related studies of workers suffering work-related rotator cuff and lumbar fusion injuries at Experimental Biology 2007, meeting in Washington, DC. His presentations, on April 29, are part of the scientific program of The American Physiological Society.

Participants in the rotator cuff study represent a class of worse-case-scenarios of work-related injuries. Rotator cuff injuries involve those muscles and tendons that stabilize the shoulder and can be caused by pulling the arm out of place, by falls and other accidents. All 42 of the employees had been through surgery to repair their torn muscles or ligaments. All had already gone through weeks of traditional rehabilitation and physical therapy. Even so, none had been judged capable of going back to work and thus were eligible for disability and workmen's compensation settlements.

This was just the patient population Dr. Stark, director of Research and Development at the Athletic and Therapeutic Institute in Chicago and his colleagues at the research division of the Institute wanted. Nothing had worked for these patients, and the researchers figured that what would work for them also would work for employees with less severe injuries.

The injured employees attended the Institute program four hours a day, five days a week, on average for six weeks. Their daily training began with warm up, stretching, and core exercises for balance and proper biomechanics, then moved to free weight resistance training of the upper and lower body. Unlike traditional physical therapy programs after injuries, this program was a modified version of what professional and collegiate athletes do using free weights. On the third day of the week, the exercises involved less weight than the previous two days but were much more dynamic, addressing specific injury and biomechanical patterns related to the workers' previous jobs. A drywaller, for example, would work muscles used in lifting large sheets of drywall overhead and in place. During the last two days of each week, the amount of weight used durinig free weight lifting was heavier than that of the first two days of the week.

At the end of the six weeks training, the workers were tested on physical function (a four hour protocol based on U.S. Department of Labor classifications of different types of work, re specific amounts of weight lifted for specific percentages of time). Ninety-six percent of patients met or exceeded the physical function levels of their previous job, and 90 percent went back to work, most at their previous job. Almost all employees were satisfied with the program, and so were employers.

Dr. Stark says We are at a new era in which we can develop standardized exercise prescriptions that produce desired, achievable functional goals. He believes doing that will meet the goals of all key stakeholders. Patients want to regain full function as soon as possible and be satisfied with their physical and work outcomes. Employers want workers to come back to work as soon as possible, as fully as possible, at a cost that prevents escalation in insurance premiums.

And payors, whether insurance companies or self-insured employers, are interested in the cost benefit between getting a worker back to the job at a functioning level (costs of medical, physical therapy, and other rehabilitation programs such as those these workers went through) and a worker's not being able to go back to work at all or at his or her previous level (costs of long-term disability settlement, workman's compensation). To date, says Dr. Stark, this model of rehabilitation using intense free weight training has proved objective, measurable, and successful in patient satisfaction, return to work, and cost benefit.

The researchers now hope to test the model in a larger prospective trial of workers at varying levels of injury in order to demonstrate increased outcome efficacy with a standardized prescription and concurrently measure cost-benefit to the worker's compensation system.

Green tea compound suppresses factors causing cartilage, bone destruction in arthritis

Sun, 29 Apr 2007 04:00:00 PST

( from http://www.rxpgnews.com ) In rheumatoid arthritis, a person's own immune system attacks the joints by activating the synovial tissue that lines the body's movable joints, causing inflammation, swelling, pain and eventually erosion of the bone and cartilage and deformation of the joint. It is among the most debilitating forms of arthritis, often making difficult even the simplest of daily activities.

In a study presented April 29 at Experimental Biology 2007, University of Michigan Medical School scientist Dr. Salah-uddin Ahmed reports that a compound derived from green tea was able to inhibit production of several immune system molecules involved in inflammation and joint damage. The compound, named epigallocatechin-3-gallate (EGCG), an active principal of green tea extract, is a potent anti-inflammatory molecule, and also was able to inhibit production of interleukin-6 (IL-6) and prostaglandin E2, the inflammatory products found in the connective tissue of people with rheumatoid arthritis.

Dr. Ahmed's Experimental Biology presentation was part of the scientific program of the American Society for Nutrition.

Synovial fibroblasts (cells that form a lining of synovial tissue surrounding the capsule of the joints) were isolated from the joints of the patients suffering from rheumatoid arthritis, cultured in growth medium, and incubated with EGCG. Synovial fibroblasts were then stimulated with pro-inflammatory cytokine IL-1ß, a protein of the immune system known to play an important role in causing joint destruction in rheumatoid arthritis.

In an earlier study published by Dr. Ahmed's research group last fall, the researchers showed some interesting and novel findings when EGCG pretreated synovial fibroblasts were stimulated with the cytokine IL-1ß to study the protective effect of this green tea compound. Compared to untreated synovial fibroblasts, the cells treated with EGCG markedly blocked IL-1ß's ability to produce the proteins and enzymes that infiltrate the joints of persons with rheumatoid arthritis causing cartilage degradation.

The scientists decided to extend their study to see if the green tea compound also has the capability to block the activity of two other potent molecules, IL-6 and cyclooxygenase-2 (COX-2), actively involved in causing bone erosion in the RA joint. In the new study presented at Experimental Biology, the scientists once again isolated synovial fibroblasts taken from the joints of patients suffering from rheumatoid arthritis and incubated these cells with the green tea compound. When untreated cells were stimulated with IL-1ß, a sequence of molecular events occurred that resulted in production of the bone-destructive molecules. But the scientists found that pre-incubation with EGCG was capable of blocking the production of these molecules in a dose-dependent manner. Furthermore, EGCG also inhibited the production of prostaglandin E2, which causes inflammation in the joints.

The cell signaling pathways that regulate levels of these immune system molecules under both normal and rheumatoid arthritis situations is well established, and the researchers were able to trace the effects of the green tea compound infusion to see that it worked by inhibiting these pathways.

Dr. Ahmed says that these studies suggest that EGCG or molecules that could be derived synthetically from the EGCG found in green tea may be of therapeutic value in inhibiting the joint destruction in this challenging disease. The laboratory now is focused on the inhibitory role of EGCG in gene expression. The scientists plan to give EGCG orally to mice genetically bred to be animal models of rheumatoid arthritis to see if it provides similar therapeutic or preventive effects. Dr. Ahmed believes these studies will form a strong foundation for future testing of green tea compounds in humans with rheumatoid arthritis.

Measuring calcium intake can help to identify osteoporosis in men with prostate cancer

Tue, 10 Apr 2007 04:00:00 PST

( from http://www.rxpgnews.com ) Measuring a mans daily calcium intake is an effective way of identifying prostate cancer patients with a higher than average risk of osteoporosis, according to the April issue of the urology journal BJU International.

Researchers from the Autonoma University School of Medicine, Barcelona, Spain, looked at a cross-section of 372 men with prostate cancer. 72 per cent were receiving androgen-deprivation therapy (ADT) and 28 per cent had undergone a radical prostatectomy. Their average age was just under 70.

They found that 49 per cent of the men had osteoporosis, including 55 per cent of those who had received the ADT hormone therapy and 35 per cent of those who had had a prostatectomy.

These figures are considerably higher than the prevalence of osteoporosis in the general male population, where its estimated that about 20 per cent of all male osteoporosis cases occur in the 61 to 70 age group.

A dietary questionnaire revealed that only seven per cent of the men were consuming more than 1000 mg of calcium a day - the average daily calcium intake was 610mg in men with osteoporosis and 683mg in those without.

These levels are well below the 1000mg recommended for all 25-65 year-olds by the US National Institutes of Health and the 1500mg recommended for men over 65.

Our research showed a significant relationship between a low daily calcium intake and higher levels of osteoporosis in men with prostate cancer says lead researcher Dr Jacques Planas from the Universitys Department of Urology.

Men who had undergone ADT hormone therapy were particularly at risk and longer treatment and increased age were also related to higher levels of osteoporosis.

What was particularly interesting was the fact that more than a third of the patients who hadnt received hormone treatment also developed osteoporosis.

Osteoporosis is caused by loss of bone mineral density, which makes bones brittle and significantly more likely to fracture. It is more common in older people and has been strongly linked to hormonal changes, such as the female menopause.

Links to ADT hormone therapy have also been reported, but the Barcelona study is thought to be the first to look at using daily calcium as a diagnostic tool to identify prostate cancer patients who face an increased risk of osteoporosis, including those who have not received ADT.

Men account for about a third of all hip fractures, but they are much more likely to die after an injury of this nature than women, so it is important to identify possible risks at an early stage adds Dr Planas.

Hormone treatment ranged from 12 to 98 months, with an average of just over 42 months. Men with bone disorders or secondary causes of osteoporosis were excluded from the study.

As well as the dietary questionnaire, the men taking part in the study had their bone mineral density measured at the lumbar spine and four different hip sites in line with the guidelines developed by the International Society for Clinical Densitometry for the diagnosis of osteoporosis.

We carried out our research to discover whether there was a relationship between low daily calcium intake and reduced bone mineral density, which there clearly was say Dr Planas.

We also wanted to know if daily calcium intake could be used as a prognostic factor for osteoporosis, especially for patients receiving ADT. Our research suggests that it does provide a good pointer to whether a prostate cancer patient also has osteoporosis.

The authors suggest that patients with prostate cancer should be routinely advised to take at least 1000mg of calcium a day and that their bone mineral density should be assessed, particularly before starting ADT, and monitored at regular intervals after the treatment begins.

The sturdier sex? -- Study by Pittsburgh scientists finds female stem cells work better

Mon, 09 Apr 2007 04:00:00 PST

( from http://www.rxpgnews.com ) PITTSBURGH April 4, 2007 -- Female stem cells derived from muscle have a greater ability to regenerate skeletal muscle tissue than male cells, according to a study at Childrens Hospital of Pittsburgh of UPMC.

The study, which is being published in the April 9 issue of the Journal of Cell Biology, is the first ever to report a difference in regenerative capabilities of muscle stem cells based on sex.

This finding could have a major impact on the successful development of stem cells as viable therapies for a variety of diseases and conditions, according to the studys senior author, Johnny Huard, PhD, director of the Stem Cell Research Center at Childrens and the Henry J. Mankin Professor and Vice Chair for Research in the Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine.

Regardless of the sex of the host, the implantation of female stem cells led to significantly better skeletal muscle regeneration, said Dr. Huard, also the deputy director of the McGowan Institute of Regenerative Medicine. Based on these results, future studies investigating regenerative medicine should consider the sex of the stem cells to be an important factor. Furthermore, investigations such as ours could lead to a better understanding of sex-related differences in aging and disease and could explain, at least partially, the high variability and conflicting results reported in the literature on stem cell biology.

Dr. Huards team, and the studys first author, Bridget Deasy, PhD, director of the Live Cell Imaging Lab at Childrens Stem Cell Research Center, made the discovery while working with a population of stem cells they isolated in the lab while searching for a cure for Duchene muscular dystrophy (DMD). DMD is a genetic disease estimated to affect one in every 3,500 boys. Patients with DMD lack dystrophin, a protein that gives muscle cells structure. Using an animal model of the disease, his laboratory is using stem cells to deliver dystrophin to muscles.

In this study, Dr. Huards team injected female and male muscle-derived stem cells into dystrophic mice and then measured the cells ability to regenerate dystrophin-expressing muscle fibers.

They then calculated the regeneration index (RI) the ratio of dystrophin-positive fibers per 100,000 donor cells. Only one of the 10 male populations of implanted stem cells had an RI over 200. In contrast, 40 percent of the female stem cell populations had an RI higher than 200, and 60 percent of the female populations of stem cells had an RI higher than the mean RI of the male cells (95).

This difference may arise from innate sex-related differences in the cells stress responses, according to Dr. Deasy, an assistant professor in the Departments of Orthopaedic Surgery and Bioengineering at the University of Pittsburgh School of Medicine and School of Engineering, respectively.

The investigators examined several aspects of stem cell behavior. They screened for differences in thousands of genes, and they also looked for differences related to estrogen. In many ways the male and female stem cells were similar, Dr. Deasy said.

The major difference was what we observed after exposing the cells to stress or after cell transplantation in the animals that have muscular dystrophy. Transplantation of female cells leads to a much more significant level of skeletal muscle regeneration, she said. The male cells exhibited increased differentiation after exposure to oxidative stress, which may lead to cell depletion and a proliferative advantage for female cells after cell transplantation.

Stevens and Connecticut Innovations agree to investment of $500,000 in SPOC Inc.

Mon, 02 Apr 2007 04:00:00 PST

( from http://www.rxpgnews.com ) HOBOKEN, N.J. -- Stevens Institute of Technology and Connecticut Innovations (CI), the states quasi-public authority responsible for technology investing and innovation development, today announced that they had completed an agreement for a seed-stage investment of $500,000 in Stevens Proof of Concept Inc. (SPOC), a Technogenesis® Company founded at Stevens Institute of Technology. CI made this investment through its Connecticut BioSeed Fund.

SPOC was formed in July 2005 at Stevens by Vice President Helena S. Wisniewski in the Office of University Research and Enterprise Development, along with Dr. Norman Marcus, a leader in pain management, and a team of Stevens undergraduate students in biomedical engineering. SPOC has developed a proprietary point-of-care medical diagnostic system, consisting of a medical device and methodology that pinpoint the specific myofascial (muscle) trigger points causing pain. The patent pending device is the first use of electroneural stimulation for diagnostic purposes.

SPOCs diagnostic system will benefit patients by helping to eliminate treatments that prove to be ineffective, such as surgical procedures, and by allowing physicians to locate and treat more effectively muscles that generate pain.

Since approximately 100 million people in the United States suffer from chronic pain and approximately 80 percent of Americans suffer from some form of pain in their lifetime, the potential market for such a system is enormous.

SPOCs diagnostic device is disruptive it will revolutionize neck and back pain diagnosis and treatment practices, said Dr. Wisniewski, who launched SPOC and serves as a member of the board. Wisniewski added, We are very pleased to enter into a relationship with CI, an organization committed to commercializing technologies for the public good, which is aligned with Stevens Technogenesis paradigm.

SPOCs CEO, Dr. Vikki Hazelwood, said, The entrepreneurial environment within Stevens has fostered a very successful collaboration between Stevens Biomedical Engineers and Dr. Marcus. Now, with the financial support from CI, I am confident that we have extremely solid footing upon which we can commercialize the product.

We are very excited to be investing in a company that has developed a tool that allows for a revolution in the accuracy and precision of muscle pain diagnosis, said Peter Longo, executive vice president and chief investment officer of Connecticut Innovations. And we are delighted that the management of SPOC, whose technology was developed at the Stevens Institute of Technology in New Jersey, has decided to locate the company in Connecticut. Longo added, We hope that SPOCs diagnostic tool will become as common as the stethoscope and that all doctors will carry one in their pocket.

Switching genes to overdrive improves muscular dystrophy symptoms in mice

Sat, 31 Mar 2007 04:00:00 PST

( from http://www.rxpgnews.com ) BOSTON -- Scientists at Dana-Farber Cancer Institute have shown in a laboratory study that revving up a crucial set of muscle genes counteracts the damage caused by a form of muscular dystrophy.

Reporting in the April 1 issue of Genes and Development, the researchers demonstrated that manipulating a genetic molecular switch increased the genes activity in the muscles of mice with Duchenne muscular dystrophy, slowing the disease-associated muscle wasting. The authors caution that they have not yet found a way to tweak the switch, known as PGC-1alpha, in humans.

I think that if we could elevate the levels of PGC-1alpha in the muscles of patients with Duchenne muscular dystrophy, it is likely that we could slow or reduce the course of the disease, said Bruce Spiegelman, PhD, the Dana-Farber researcher who led the team along with Christoph Handschin, PhD, formerly of Dana-Farber and now at the University of Zurich. Other authors are from the University of Iowa College of Medicine.

Duchenne muscular dystrophy (DMD) is the most common type of muscular dystrophy in children, occurring once in about every 5,000 live births of boys, and is ultimately fatal. The average age of death is the mid-teens, and most patients die by their 30s. In the United States, about 400 to 600 boys are born each year with DMD or Becker Muscular Dystrophy, a milder form of the disease. The cause is a mutation, either inherited or occurring spontaneously, that affects a muscle protein called dystrophin.

Spiegelman, whose laboratory discovered PGC-1alpha in 1998, led the new study which was aimed at determining whether increasing levels of PGC-1alpha in the muscles of mice could increase the activity of genes that are known to behave abnormally in muscular dystrophy.

PGC-1alpha is known as a transcriptional coactivator that functions as a switch, or perhaps more accurately, like a light dimmer that increases or decreases the activity of genes under its control. Exercising a muscle raises PGC-1alpha levels, causing the formation of more mitochondria, the chemical power plants that create energy in cells.

PGC-1alpha is also required for the normal operation of genes that control the development of neuromuscular junctions (NMJ) sites on muscle fibers where nerves attach and signal the fibers to contract. Part of the reason that exercise builds stronger muscles is that it increases PGC-1alpha activity. Conversely, disease or lack of exercise reduces PGC-1alpha activity, causing a loss of NMJ function and weakening, or atrophying, of muscles.

Spiegelmans team had previously bred a strain of mice with higher-than-normal levels of PGC-1alpha in their muscles. Also available for the research was a mouse model of Duchenne muscular dystrophy, the MDX mouse. In the new experiment, the scientists bred male high-PGC-1alpha mice with female MDX mice (the muscular dystrophy gene is carried by females in mouse and in humans.) As a result, the offspring of these matings had muscular dystrophy but also had elevated PGC-1alpha. Using exercise and chemical tests, the researchers compared muscle function in the offspring with MDX mice having no additional PGC-1alpha.

Both sets of rodents were run on a treadmill for one hour, then again 24 hours later. Normal mice completed the runs easily on both days, while untreated MDX rodents were exhausted halfway through each run. The MDX mice with increased PGC-1alpha activity performed almost as well as normal mice on the first day; their performances decreased on the second day, but they still did better than the untreated MDX mice on both runs.

The exercise tests and microscopic and chemical examinations of the muscles showed that boosting PGC-1alpha caused a clear and substantial improvement in the structure and function of skeletal muscle in this disease model, the scientists wrote.

Women need expanded musculoskeletal care during pregnancy, study finds

Tue, 06 Mar 2007 05:00:00 PST

( from http://www.rxpgnews.com ) (Arlington, Va.) -- Despite the high prevalence of musculoskeletal pain during pregnancy, few women in underserved populations receive treatment for their low back pain, according to a February 2007 study in the Journal of Manipulative and Physiological Therapeutics (JMPT). Moreover, researchers found that pain in a previous pregnancy may predict a high risk for musculoskeletal complaints in future pregnancies.

According to Clayton Skaggs, DC, the studys chief author, 85 percent of women surveyed reported that they had not received treatment for their musculoskeletal pain, and of the small percentage who perceived that their back complaints were addressed, less than 10 percent were satisfied with the symptom relief they obtained.

Based on the findings of this study, doctors of chiropractic and other health care professionals need to expand the musculoskeletal care available during pregnancy, especially in underserved populations, Dr. Skaggs said. As a proactive step, health professionals should consider including back pain screening as part of early obstetrical care to help identify musculoskeletal risk factors and allow for early education and/or treatment.

Researchers surveyed more than 600 women at a clinic that serves predominantly an uninsured, underinsured or Medicaid-insured population. Surveys were offered to all obstetrical patients and were designed to collect information about pregnancy-related pain and quality of life issues. Of those women who responded to the survey, two-thirds reported back pain and nearly half of all women reported pain at two or more locations, including pelvic pain and mid-back pain.

The study findings suggest that pregnant women with back pain are predisposed to sleep disturbances. In the survey, close to 80 percent of women reporting sleep disturbances had back pain, whereas only 8 percent of women without pain reported problems sleeping. More alarming was the significant relationship between reports of musculoskeletal pain and the use of pain medication. Three-fourths of the women who reported pain also described use of pain medication.

We saw a direct association between sleep deficiency and back pain, the authors said. These results raise the question of whether or not the high incidence of pain medication use reflects a lack of education about potential risks of medications or more an inability for the pregnant women to cope with the pain.

The studys authors also found a relationship between pain in a previous pregnancy and pain in the current pregnancy. Similar to the results of other studies, researchers found that 85 percent of women who experienced pain in a previous pregnancy reported pain during their current pregnancy.

Modified ligament surgery improves outcomes for baseball pitchers, other athletes

Wed, 28 Feb 2007 05:00:00 PST

( from http://www.rxpgnews.com ) In the largest study of its kind, surgeons at Hospital for Special Surgery have determined that by modifying a classic ligament surgery, they can return more athletes, such as baseball players, to their prior level of competition. The modified surgery repairs a torn medial collateral ligament (MCL), which links and stabilizes bones of the lower and upper arm where they meet at the elbow.

Less traumatic than the classic Tommy John surgery, the modified surgery called the docking procedure, with time, is likely to become the gold standard for treating these injuries.

This paper, in the largest series of patients ever published, shows that this particular operation in throwing athletes demonstrates better results than the classic operation, said David W. Altchek, M.D., senior author of the study and co-chief of the Sports Medicine and Shoulder Service at Hospital for Special Surgery (HSS) in New York. The study was presented at a special session of the American Shoulder and Elbow Surgeons, held during the American Academy of Orthopedic Surgeons annual meeting.

MCL injury is most common in professional and amateur athletes involved in so-called overhead throwing sports, such as baseball, softball, football, lacrosse and tennis. These sports involve a throwing motion at high velocity that exerts an exceptional force at the elbow. Repeated over time, this motion can cause inflammation and microtrauma, which can eventually lead to an MCL tear. When this ligament is torn, an individual has a full range of motion and can go about daily life, but a professional or semi-professional athlete cannot perform at their usual level because they cannot exert a significant force.

Specifically, the MCL attaches the ulna, one of two long bones that run from the elbow down to the wrist, with the humerus, the bone of the upper arm. For 30 years, athletes have undergone the Tommy John surgery or Jobe surgery (named after its inventor), in which a tendon is taken from a person's forearm or hamstring and then grafted into the elbow to act as a replacement for the injured ligament. Surgeons weave the harvested tendon in a figure eight pattern through bone tunnels drilled in the ulna and humerus bones and suture the tendon into place. Dr. Altchek's technique modifies the Jobe procedure in several ways. First, he begins with an arthroscopic evaluation of the elbow to examine and fix residual problems. An unstable ligament leads to a shifting elbow, which can cause further problems such as cartilage damage.

Second, Dr. Altchek gains access to the bone in a different way. In the Jobe surgery, surgeons detach major muscles and move the so-called ulnar nerve out of the way to gain access to the bone. Dr. Altchek uses a muscle splitting technique through which surgeons can gain access to the bone by gently prying apart muscle fibers, similar to the way you can poke a finger through a knitted sweater. He doesn't have to detach major muscles and, in most cases, the nerve can be left intact, reducing the problems of postoperative nerve damage. Damage to the ulnar nerve results in numbness and tingling in the ring and small fingers.

Dr. Altchek's procedure also differs from the traditional Jobe surgery by minimizing the number of holes drilled into the bones, thus decreasing the risk of postoperative bone fracture. In Dr. Altchek's surgery only one hole instead of three is drilled into the humerus. Instead of a figure eight design, one can think of the pattern as an elongated D, says Christopher Dodson, M.D., a resident in the Department of Orthopaedic Surgery at HSS and an author of the study.

In the classic operation, the graft enters the humerus bone in one hole, exits in another and goes into another and then the graft gets tied to itself, Dr. Altchek explained. In the docking procedure, the graft enters the humerus bone, but never exits. Instead, sutures secure the tendon and exit the bone through much smaller exit punctures.

Dr. Altchek first developed the docking surgery in 1994, but it wasn't until now, that it was tested in such a large patient population.

In a study of 100 athletes (mean age 22) who had the docking surgery, with an average follow-up of three years, 90 percent had an excellent result (returned to the same or higher level of competition) and 7 percent had a good result (able to compete at a lower level for more than 12 months). Only 3 percent had postoperative nerve complications. With the traditional Jobe surgery, studies have shown that only 68 percent of elite level throwers return to either their prior or a higher level of throwing and 20 percent have nerve complications.

Surgeons and athletes have applauded Dr. Altchek's modifications. Many surgeons have already been employing his technique in the clinic to improve outcomes, and with time, it is likely that the docking procedure will become the gold standard for treating these athletes.

This study recently appeared in the December issue of the American Journal of Sports Medicine (Am J Sports Med 2006;34(12):1926-1932). The Institute for Sports Medicine Research supported the work.

An attending orthopaedic surgeon at Special Surgery, Dr. Altchek serves as medical director for the New York Mets professional baseball team and medical director for the Nets professional basketball team.

Power-boosting signal in muscle declines with age

Tue, 06 Feb 2007 05:00:00 PST

( from http://www.rxpgnews.com ) As people age, they may have to exercise even harder to get the benefits afforded to younger folk. That's the suggestion of a report in the February issue of the journal Cell Metabolism, published by Cell Press, showing that a signal that gives muscles a kind of metabolic boost in response to exercise is blunted in older animals.

The researchers found that so-called AMP-activated protein kinase (AMPK) slows down in the skeletal muscle of 2-year-old rats relative to 3-month-old rats. A chief regulator of whole-body energy balance, AMPK in skeletal muscle stimulates the oxidation of fatty acids and the production, or biogenesis, of power-producing mitochondria that burn fat and fuel cells, according to the researchers.

The new findings might help to explain what happens as we age, said Gerald I. Shulman, a Howard Hughes Medical Institute investigator at Yale University School of Medicine.

Earlier studies have shown that, in comparison to 20-year-old adults, even lean and healthy people in their seventies show a higher incidence of fat buildup in their muscle and livers and a deficiency in mitochondrial function, Shulman explained. These metabolic shifts have been implicated in the increased prevalence of insulin resistance and type 2 diabetes that occurs with aging.

The message of this paper is that, with aging, the AMPK pathway has reduced activity, Shulman said. So, one probably has to work harder to maintain the same level of fat oxidation and mitochondrial biogenesis in muscle.

The number of mitochondria within muscle largely determines its metabolic capacity. The mitochondrial composition of fibers in different muscles corresponds to the jobs that they do, and muscle can be reprogrammed through exercise.

For example, Shulman said, the skeletal muscles of marathon runners typically have much greater mitochondrial content and a greater capacity to burn fat. Those properties can most likely be attributed to chronic activation of the AMPK pathway.

In regards to insulin resistance and type 2 diabetes, having more AMPK activity in our skeletal muscle is probably a good thing because AMPK activation stimulates glucose uptake, increases fat oxidation, and promotes mitochondrial biogenesis, he said.

In the current study, the researchers set out to determine whether the declining mitochondrial function and increased intracellular fat content seen with aging could be traced back to deficiencies of AMPK. They compared AMPK activity in young and old rats following three perturbations that normally stimulate the enzyme and, in turn, mitochondria production. The treatments included acute exposure to an AMPK-stimulating chemical, chronic exposure through feeding of another chemical that induces AMPK by mimicking an energy shortage, and exercise.

In every case, older rats showed a decline in AMPK activity compared to younger animals. Young rats infused with a stimulatory chemical showed an increase in muscular AMPK activity not seen in old rats, they found. Similarly, the muscle of exercise-trained young rats showed more than a doubling in AMPK activity. In older rats, that AMPK hike with exercise was severely blunted. The muscles of young rats fed the AMPK-stimulating chemical also showed an increase in AMPK and a 38% increase in mitochondrial density, they reported. In contrast, older animals' AMPK activity and mitochondrial numbers held steady.

These results suggest that aging-associated reductions in AMPK-stimulated activity may be an important contributing factor in the reduced mitochondrial function and dysregulated intracellular fat metabolism associated with aging-induced insulin resistance and type 2 diabetes, the researchers concluded.

Common blood pressure drug reduces progressive muscle degeneration in mice

Fri, 02 Feb 2007 05:00:00 PST

( from http://www.rxpgnews.com ) Scientists supported in part by the National Institutes of Health's National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and National Institute of Neurological Disorders and Stroke (NINDS) have found that that the commonly prescribed blood pressure medication losartan improves muscle regeneration and repair in a mouse model of Duchenne muscular dystrophy (DMD), a devastating disease characterized by rapid progression of muscle degeneration in boys and young men. The research is based on similarities in the mechanism of DMD and another rare disease Marfan syndrome and the discovery that losartan is effective in blocking the key mechanism in animal models of both diseases. Further studies of the drug, scientists emphasize, are needed to assess its value in patients.

Marfan syndrome is a heritable connective tissue disorder affecting many organ systems, resulting in dislocation of the lens of the eye; progressive dilation of the aorta, which puts the aorta at risk of rupture; and small, weak muscles, says Harry C. Dietz, M.D., an author of the study in the February 2007 edition of Nature Medicine. Until recent years, scientists believed that Marfan syndrome was caused by weakness of tissues, says Dr. Dietz, the Victor A. McKusick professor of genetics in the McKusick-Nathans Institute of Genetic Medicine at the Johns Hopkins University School of Medicine and director of the William S. Smilow Center for Marfan Syndrome Research. But research by Dr. Dietz and his colleagues, and funded by the National Heart, Lung, and Blood Institute, NIAMS and others, has shown that the disease is the result of excessive activity of a growth factor called TGF-beta in the muscles. We found that muscles were abnormal; they had very small fibers and excess fibrosis excessive connective tissue, or scarring between the fibers. What we learned was that high TGF-beta levels were preventing a process called muscle regeneration.

Normally, when a person damages their muscle or when they exercise and send a signal to the muscle to get bigger, the muscle is able to mobilize a population of muscle stem cells that proliferate and then fuse to each other and to damaged muscle fibers to rapidly accomplish muscle repair or muscle growth. In the presence of too much TGF-beta, however, the cells simply do not get the signal to accomplish this regenerative process, says Dr. Dietz. We learned that simply blocking TGF-beta in a mouse model of Marfan syndrome could rescue muscle regeneration, normal architecture and muscle function.

Previous studies have demonstrated that the muscles of dystrophic mice lose their ability to repair and regenerate efficiently, and as in the human, the muscle tissue is progressively replaced by scar tissue. Knowing that the same phenomenon occurred in Marfan syndrome, Ronald D. Cohn, M.D., assistant professor of pediatrics and neurology at Johns Hopkins' McKusick-Nathans Institute of Genetic Medicine, and Dr. Dietz and their colleagues tried to see if they could extrapolate findings from the Marfan syndrome mouse model to a mouse model of DMD. Their research paid off. They were able to find evidence that excessive TGF-beta had a role in limiting muscle regeneration in response to damage in DMD as well. When the researchers gave the mice losartan to inhibit TGF-beta, they showed that the muscle was able to regenerate and repair much more efficiently. What's more, when they treated the mice with the drug over a period of time, the entire disease was attenuated, says Dr. Cohn. Here we had two completely different myopathies muscle diseases that seemed to show a common pathway, which inhibits the repair process of skeletal muscle.

Losartan, a frequently prescribed and well-tolerated drug in humans, works to reduce high blood pressure by blocking a molecule called angiotensin II, which has been found not only to regulate blood pressure but also to work against TGF-beta by a number of mechanisms. Now that the drug has proven useful in mouse models of the two diseases, the next step is to test them in people with the diseases. A clinical trial of losartan for Marfan syndrome is scheduled to begin later this month. Researchers are in the process of organizing a clinical trial for DMD; patient recruitment is not yet underway. If the drug proves useful in humans, as it has in mouse models, it will represent a huge advance in the treatment of both diseases.

Current treatment for DMD is steroids. For many people with DMD, steroids seem to bring improvement in muscle function, but that improvement is offset by the drugs' side effects, and the effects are short-lived in some patients. In long-term treatment of mice with losartan, however, the researchers have seen a sustained significant improvement in muscle function. In fact, at about a year of age which would be equivalent to middle age in a person the mice with DMD actually had muscle function that was indistinguishable from a normal mouse, says Dr. Dietz. So I think that it has the strong potential to not only have a more enduring effect, but also to have a more profound effect on maintenance of muscle function he says. Losartan's safety profile is also more favorable than that of steroids. In 20 years of use in all human age groups, it has shown a remarkable tolerance profile, he says. The most common side effect of the drug low blood pressure can usually be managed by simply lowering the dose of the drug, says Dr. Cohn.

While much prior work in Marfan syndrome and DMD has been focused on trying to replace the product of genes (for Marfan syndrome a deficient protein called fibrillin-1; for DMD, a protein called dystrophin), Dr. Dietz says this new research is reflective of an emerging shift in attitude: to treat the disease as well as possible with what is available now. Right now, we don't have the technology to replace the deficient gene product to cure the disease, but we might have the technology to prevent other secondary events that contribute to the disease process, he says. In essence, we are focusing on the low-hanging fruit that we can currently address and that will have the strong potential to improve the length and quality of life while we are tackling some of the obstacles for a cure at the current time.

NIAMS Director Stephen I. Katz, M.D., Ph.D., is cautiously optimistic about the findings. This treatment in mice is derived from knowledge of the diseases' mechanisms, he says. It has been shown to be highly effective in mouse models. But we need to do clinical studies first. If they are successful, this therapy has the potential to help many people with devastating diseases for which there has really been no good treatment.

Pat Furlong, president and CEO of Parent Project Muscular Dystrophy, adds a similar perspective. The success of losartan in the mouse model of Duchenne muscular dystrophy has been received with great enthusiasm. Researchers and physicians who care for children with DMD recognize the excitement as well as the sense of urgency within the DMD community. Many parents are urging their primary care physicians to agree to add losartan to their son's current regimen. While this approach is understandable, there is concern that extensive off-label use will compromise clinical trials. Unfortunately, the only way to understand if losartan will be effective in DMD boys is clinical trials. Without evidence, we will not understand the interaction of losartan with other compounds, and the use of the drug will be limited to those families who are able to secure and afford the drug. It is generally believed that treatments for DMD will involve combination therapies, and to that extent promising strategies must be methodically evaluated so that all children might receive benefit.

Smoking worsens knee osteoarthritis

Thu, 07 Dec 2006 05:00:00 PST

( from http://www.rxpgnews.com ) ROCHESTER, Minn. -- New findings from a study led by a Mayo Clinic rheumatologist indicate that men with knee osteoarthritis who smoke experience greater cartilage loss and more severe pain than men who do not smoke. Results will be published online this week in the Annals of the Rheumatic Diseases.

Knee osteoarthritis is one of the leading causes of disability in elders.

This is a novel finding, says Shreyasee Amin, M.D., Mayo Clinic rheumatologist and lead study researcher. Previous studies showed no association between cigarette smoking and knee osteoarthritis or even a protective effect of smoking.

The finding that cigarette smoking plays a role in the worsening of knee osteoarthritis is important, says Dr. Amin, as it is a potentially modifiable risk factor.

To conduct this study, the researchers examined 159 men with symptomatic knee osteoarthritis who participated in a prospective study on the natural history of the condition, the Boston Osteoarthritis of the Knee Study. The current study focused on men, as there were too few women in the original group studied who smoked (4 percent). The researchers took MRIs (magnetic resonance images) of the more symptomatic knee of each patient at the study beginning, and also 15 and 30 months later. Cartilage loss over follow-up, based on knee MRIs, was determined at the tibiofemoral joint (the connection between the thighbone and shinbone) and the patellofemoral joint (the junction of the knee cap and the thigh bone) in the knees, and a scoring tool was used to assess knee pain severity. Nineteen, or 12 percent, of the men were current smokers at the studys start. These men also were leaner and younger than other study participants, so the researchers adjusted for these factors. The investigators found current smokers had a 2.3 fold increased risk of cartilage loss at the medial tibiofemoral joint and a 2.5 fold increased risk of cartilage loss at the patellofemoral joint compared to the men who had quit smoking or never smoked. Current smokers also had higher pain scores than men who were not current smokers, at the beginning of the study (60.5 vs. 45.0, with 100 as the highest possible pain score) and at follow up (59.4 vs. 44.3).

The association between smoking and cartilage loss in knee osteoarthritis could be explained by one or more of the following theories, according to the researchers:

Improperly sized tennis racket grip doesn't cause tennis elbow

Fri, 01 Dec 2006 05:00:00 PST

( from http://www.rxpgnews.com ) Rosemont, Ill. December 1, 2006 Researchers apparently have gotten a grip on the relationship between the development of tennis elbow (tendonitis) and the size of the grip on the racket a player uses.

A grip that is either too big or too small for the player's hand is not a factor in whether or not a player may develop tennis elbow, according to a study published in the December issue of The American Journal of Sports Medicine. An optimal grip size may influence the force with which a player hits the ball, but variations in grip size are unlikely to be contributing factors in overuse injuries such as tennis elbow, concludes George F. Hatch III, MD, currently of the Department of Orthopaedic Surgery, University of Southern California Keck School of Medicine, Los Angeles, and colleagues. (Dr. Hatch conducted the study while in training at the Kerlan-Jobe Orthopaedic Clinic in Los Angeles.)

Clinicians who treat patients with tennis elbow often tell them to try a different size grip in order to alleviate muscle fatigue, says Dr. Hatch. Our study demonstrates that those recommendations have no scientific basis. Therefore, it is reasonable to recommend whatever grip size feels most comfortable for them.

Tennis elbow (lateral epicondylitis) is the most common upper extremity complaint among recreational players, accounting for 75% to 85% of elbow injuries. Researchers believe it results from repetitive impacts between the ball and racket coupled with poor wrist stability especially during the backhand swing. The backhand stroke seems to be the culprit because it results in overexertion and micro-tearing within two primary muscles inside the forearm.

Hatch and coauthors at Kerlan-Jobe Orthopaedic Clinic studied 16 NCAA Division I and II tennis players (10 men, 6 women) with no prior history of elbow problems. Twelve players were right-handed; four left-handed. All players were proficient at using a one-handed backhand. Players' recommended grip size was determined using an industry standard: measuring the distance from the bottom lengthwise crease in the palm to the tip of the ring finger with a ruler.

The researchers inserted electrodes into five different muscles in each player's dominant arm to measure the firing pattern of their muscles (electromyogram, EMG). After a warm-up period, players then performed three single-handed backhand strokes using identical model rackets with three different grip sizes: the recommended grip size, a small grip size (1/4 inch smaller than recommended), and a large grip size (1/4 inch larger than recommended). One-quarter inch size variations were chosen because most commercially available adult-sized rackets have grip sizes ranging from 4 inches to 4 5/8 inches. A ball machine set at a constant speed and angle provided consistent ball delivery. Each player's strokes were captured on high speed video which was then synchronized with the corresponding EMG.

Of the five forearm muscles studied, none showed significant variations in firing patterns during three phases of the backhand stroke: accelerated forward motion of the racket, ball impact, and early follow-through. Close attention was paid to two specific muscles, the extensor carpi radialis brevis (ECRB) and the extensor digitorium communis (EDC), which are located beside each other in the forearm and originate from the bony prominence on the outside of the elbow. Overuse, microtrauma, and failed healing in both of these muscles can result in tendonitis. Yet larger and smaller grip sizes did not affect the activity of these two muscles, the authors found.

Based on our data, we recommend recreational tennis players use the currently accepted grip size measurement technique as a starting point in when picking a grip size, says Dr. Hatch. However, the player should feel free to increase or decrease the size of the grip based upon what feels most comfortable. Previous studies have shown that improper form is one of the biggest risk factors for the development of tendonitis.

Helping muscle regenerate

Wed, 01 Nov 2006 05:00:00 PST

( from http://www.rxpgnews.com ) Muscle wasting can occur at all ages as the result of genetic defects, heart failure, spinal injury or cancer. A therapy to cure the loss of muscle mass and strength, which has a severe impact on patients' lives, is desperately sought. Blocking a central signal molecule, researchers from the Mouse Biology Unit of the European Molecular Biology Laboratory (EMBL) in Monterotondo, Italy, have now found a way to protect muscle from degenerating after injury and to improve muscle healing in mice. The study appears in the current issue of the Journal of Clinical Investigation and suggests two molecules with the potential to speed up the regeneration of damaged muscle as promising drug targets for new therapies against muscle wasting.

We don't realise it when it is working fine, but our muscle is an intricate system that depends on a well regulated balance of protein production and breakdown. When this balance gets disturbed by disease or injury our muscles fade away, and with them our strength. A crucial player in this process is the signalling molecule NF-kB. It is well known as a messenger of inflammation and has recently been implicated in other degenerative conditions such as multiple sclerosis. The groups of Nadia Rosenthal and Manolis Pasparakis at the EMBL Mouse Biology Unit have now investigated the role NF-kB plays in muscle wasting.

First, they genetically removed NF-kB from the leg muscles of mice by blocking IKK2, a protein needed to activate the signal. Then, to mimic spinal injury, they blocked the communication between the spinal cord and the lower leg muscle an intervention that under normal circumstances inevitably leads to muscle wasting.

What we observed was truly amazing, says Rosenthal, Head of EMBL's Mouse Biology Unit. The mice showed hardly any muscle wasting after the injury; their muscle fibres maintained almost the same size, strength and distribution as in a healthy muscle. But that's not all; blocking IKK2 also helped muscle healing. Without the NF-kB signal the muscle regenerated much better and faster.

In response to injury or inflammation, NF-kB shuts down the production of proteins and stimulates their breakdown, which leads to the loss of muscle substance. Blocking NF-kB has the reverse effect, protects muscle from wasting and improves healing of already degenerated muscle.

Protection against muscle atrophy was even stronger when a gene encoding growth factor IGF-1 was added to muscle tissue lacking NF-kB. Rosenthal and her lab have been studying IGF-1 for a long time and have shown in previous studies that the molecule is very good at promoting repair of skeletal and cardiac muscles.

The fact that NF-kB reduction helps maintain our muscle mass is a useful starting point to develop new therapies against muscle diseases, says Foteini Mourkioti, who carried out the research in Rosenthal's lab. Adding IGF-1 has a similar effect as blocking NF-kB, but it must act, at least in parts, independently of NF-kB, because we observed a clear improvement when using the two treatments together, she explains.

A combination of IKK2 inhibitors with growth factors like IGF-1, then seems to be the most promising basis for new therapies against muscle diseases. The human NF-kB and growth factor signaling networks are very similar to those of mice, so compounds interfering with them are likely to show the same positive effects in humans.

Trichostatin A (TSA) Can Counteract Muscular Dystrophy in Mice

Thu, 05 Oct 2006 01:08:00 PST

( from http://www.rxpgnews.com ) Scientists at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and other institutions have demonstrated for the first time that a single drug can rebuild damaged muscle in two strains of mice that develop diseases comparable to two human forms of muscular dystrophy. This advance, which is reported online in Nature Medicine, is the latest from a research collaboration that began several years ago by the teams of Vittorio Sartorelli, M.D., at NIAMS and Pier Lorenzo Puri, M.D., Ph.D., now at Dulbecco Telethon Institute (DTI) in Rome, Italy and The Burnham Institute in La Jolla, Calif.

The scientists tested trichostatin A (TSA), an inhibitor of the enzyme deacetylase, in two mouse models of muscular dystrophy (MD): one that naturally develops a disease similar to Duchenne muscular dystrophy in humans, the other genetically altered to develop a form of dystrophy similar to the human limb-girdle muscular dystrophy. At 45 to 90 days of age, the muscles of the MD mice showed much fibrous tissue and infiltration of inflammatory cells. Unlike healthy mice, the mice with MD were unable to either run on a treadmill or swim. MD mice given TSA daily for two to three months, however, were virtually indistinguishable from healthy mice, and biophysical studies showed virtually no difference between the muscle strength of the mice with MD given the deacetylase inhibitor and healthy mice.

This is the first example of using a drug to counteract muscular dystrophy in mouse models, says Dr. Sartorelli. Yet he points out that the drug is only promoting muscle regeneration it is not curing the defect that causes muscle deterioration. Further studies are needed to determine how long the drug works and if it works in larger animals with bigger muscles, such as dogs, before such drugs can be tested in people.

The finding has its roots in several of the groups earlier advances, the first of which was reported in 2002 in the Proceedings of the National Academy of Sciences 1. The scientists found that treating muscle cells with deacetylase inhibitors caused the cells to grow larger and differentiate better, says Dr. Sartorelli, the group leader of the Muscle Gene Expression Group in NIAMS Laboratory of Muscle Biology. The next advance, published two years later in the journal Developmental Cell 2, was the discovery that the inhibitor worked by changing gene expression, causing some genes to be upregulated, or make more protein, and others to be downregulated, or make less protein. Among the genes positively regulated by the inhibitors was a gene for a key protein called follistatin.

It was known that follistatin had a role in muscle development, so by understanding normal muscle development we knew that follistatin would block the activity of another protein called myostatin, says Dr. Sartorelli. If you block myostatin, you get big muscles.

One way of inactivating myostatin is to upregulate follistatin. Basically, what follistatin does is to prevent myostatin from working, says Dr. Sartorelli. When his group treated the cells with deacetylase inhibitors, they saw that the cells became large and that follistatin was overexpressed. However, when the group treated the cells with the inhibitors and then used other agents to block follistatin, the cells didnt become bigger, showing that one of the most important pathways the inhibitors use to create bigger muscles involves the activation of follistatin. If you didnt have follistatin anymore, these drugs didnt work, he says.

Moreover, Drs. Sartorellis and Puris groups were able to show that in normal animals, follistatin is upregulated when muscle is damaged. When the researchers induced muscle damage and then gave the inhibitors, follistatin was even more expressed, as were two proteins that reflect increased muscle regeneration.

Scientists show drug can counteract muscular dystrophy in mice

Wed, 04 Oct 2006 04:00:00 PST

( from http://www.rxpgnews.com ) Scientists at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and other institutions have demonstrated for the first time that a single drug can rebuild damaged muscle in two strains of mice that develop diseases comparable to two human forms of muscular dystrophy. This advance, which is reported online in Nature Medicine, is the latest from a research collaboration that began several years ago by the teams of Vittorio Sartorelli, M.D., at NIAMS and Pier Lorenzo Puri, M.D., Ph.D., now at Dulbecco Telethon Institute (DTI) in Rome, Italy and The Burnham Institute in La Jolla, Calif.

The scientists tested trichostatin A (TSA), an inhibitor of the enzyme deacetylase, in two mouse models of muscular dystrophy (MD): one that naturally develops a disease similar to Duchenne muscular dystrophy in humans, the other genetically altered to develop a form of dystrophy similar to the human limb-girdle muscular dystrophy. At 45 to 90 days of age, the muscles of the MD mice showed much fibrous tissue and infiltration of inflammatory cells. Unlike healthy mice, the mice with MD were unable to either run on a treadmill or swim. MD mice given TSA daily for two to three months, however, were virtually indistinguishable from healthy mice, and biophysical studies showed virtually no difference between the muscle strength of the mice with MD given the deacetylase inhibitor and healthy mice.

This is the first example of using a drug to counteract muscular dystrophy in mouse models, says Dr. Sartorelli. Yet he points out that the drug is only promoting muscle regeneration it is not curing the defect that causes muscle deterioration. Further studies are needed to determine how long the drug works and if it works in larger animals with bigger muscles, such as dogs, before such drugs can be tested in people.

The finding has its roots in several of the group's earlier advances, the first of which was reported in 2002 in the Proceedings of the National Academy of Sciences . The scientists found that treating muscle cells with deacetylase inhibitors caused the cells to grow larger and differentiate better, says Dr. Sartorelli, the group leader of the Muscle Gene Expression Group in NIAMS' Laboratory of Muscle Biology. The next advance, published two years later in the journal Developmental Cell , was the discovery that the inhibitor worked by changing gene expression, causing some genes to be upregulated, or make more protein, and others to be downregulated, or make less protein. Among the genes positively regulated by the inhibitors was a gene for a key protein called follistatin.

It was known that follistatin had a role in muscle development, so by understanding normal muscle development we knew that follistatin would block the activity of another protein called myostatin, says Dr. Sartorelli. If you block myostatin, you get big muscles.

One way of inactivating myostatin is to upregulate follistatin. Basically, what follistatin does is to prevent myostatin from working, says Dr. Sartorelli. When his group treated the cells with deacetylase inhibitors, they saw that the cells became large and that follistatin was overexpressed. However, when the group treated the cells with the inhibitors and then used other agents to block follistatin, the cells didn't become bigger, showing that one of the most important pathways the inhibitors use to create bigger muscles involves the activation of follistatin. If you didn't have follistatin anymore, these drugs didn't work, he says.

Moreover, Drs. Sartorelli's and Puri's groups were able to show that in normal animals, follistatin is upregulated when muscle is damaged. When the researchers induced muscle damage and then gave the inhibitors, follistatin was even more expressed, as were two proteins that reflect increased muscle regeneration.

Muscle cells self-destruct rather than grow with use

Wed, 30 Aug 2006 04:00:00 PST

( from http://www.rxpgnews.com ) Muscle cells that should grow stronger with use instead self-destruct when a protein called BAG3 isn't around, researchers have shown.

Mice missing BAG3 seem fine at birth, but when they start using their muscles to breathe and stand, muscle cells rapidly degenerate and cannot regenerate, says Dr. Shinichi Takayama, cell and molecular biologist at the Medical College of Georgia.

The finding illustrates BAG3's importance in maintaining mature skeletal muscle, researchers say in the September issue of the American Journal of Pathology.

They hope it will lead to prevention of muscle atrophy that characterizes diseases such as muscular dystrophy, heart failure and a lesser-known condition called myofibril myopathy, which affects the tiniest muscle fibers. Dr. Takayama believes his BAG3 knockout is a model for the worst case of this rare disease.

Basically we think that the degeneration starts because of usage of muscles, which should make them stronger, Dr. Takayama says. Instead, cells previously dormant in utero start dying. They cannot breathe, they cannot use their muscles and they die quickly, he says of BAG3 knockout mice.

When a muscle contraction happens, cytoskeletal degeneration occurs naturally, he says. Interestingly, degeneration normally stimulates regeneration, but not in these mice. Instead cells take another option: when they can't be fixed, they kill themselves.

This mass suicide in the absence of BAG3 is not a huge surprise. Dr. Takayama, the first to clone five members of the BAG family, says the proteins help regulate heat shock protein 70, which helps other proteins fold and function properly. The BAG family also has an anti-death function called antiapoptosis. Dr. Takayama is still dissecting the relationship between the anti-death function and BAG's regulatory role with the heat shock protein. If protein folding is not happening to a cell, that cell should die, so I think the two functions are related, he says.

Without BAG3, researchers believe something goes wrong in the supporting structure of Z-discs, which help muscles contract. The structure is tightly regulated by cytoskeletal proteins and something is wrong in the cytoskeleton of these mice, he says. They found evidence of changes in the Z-discs that predate cell death, leading them to postulate that BAG3 is required for maintaining the integrity of Z-discs and other supporting components of the muscle cytoskeleton that helps strengthen and organize cells. The muscle, in structure, seems normal at birth, Dr. Takayama says. But after four days, their Z-disc structure is disrupted. Myofibrils, thin, cylindrical filaments that run the length of muscle cells, then begin to degenerate.

He first cloned BAG1 as an antiapoptotic protein more than 10 years ago while looking for a way to kill cancer cells. BAG is one of the things that helps cancer cells survive, says Dr. Takayama. In fact, BAG3 is highly expressed in cancer cells.

Last year, his group's work published in Nature Neuroscience showed a BAG1 knockout experiences massive brain cell death as an embryo. He's working on a mouse that over expresses BAG in muscle only, saying that should prevent cell death and atrophy.

Women show 47 percent greater persistence with osteoporosis drugs if offered monthly tablet, support

Thu, 20 Jul 2006 04:00:00 PST

( from http://www.rxpgnews.com ) Women who took an osteoporosis drug once a month and received extra telephone support from trained nurses showed 47 per cent greater persistence with their drug treatment than those who took a weekly tablet, according to a study in the August issue of IJCP, the International Journal of Clinical Practice.

103 primary care centres across the UK took part in the PERSIST study between January 2005 and January 2006, with 1,076 women each agreeing to participate for a six-month period.

542 were prescribed a single 70mg dose of alendronate once a week and the remainder received a single monthly 150mg dose of ibandronate and were enrolled in a free patient support programme designed to complement the drug.

The monthly ibandronate group received a welcome pack providing basic information about osteoporosis and a monthly reminder call from a trained nurse one to three days before the dose was due.

The nurses also used the opportunity to confirm dosing instructions, provide further information about osteoporosis and stress the importance of adhering to the treatment regime.

835 women completed the study, leaving 440 in the monthly ibandronate group and 395 in the weekly alendronate group.

Of these, just under 57 per cent of patients receiving monthly ibandronate tablets, together with patient support, were taking the medication after six months. The persistence rate for patients on weekly alendronate tablets was 39 per cent.

Getting patients to continue taking prescribed medication is a major problem for healthcare professionals says lead author Dr Alun Cooper, a family doctor from the Bridge Medical Centre in Crawley, UK.

The World Health Organization estimates that only 50 per cent of patients with chronic diseases in developing countries stick to treatment regimes. And the American Heart Association has identified failing to take medication correctly as the number one problem in treating ill health today.

According to the International Osteoporosis Foundation one in three women over 50 suffer from osteoporosis worldwide.

Sufferers find that their bones become increasingly brittle and this increases the risk of serious factures, especially if they don't take their medication on a regular basis says Dr Cooper. It's estimated that one in two women over 50 will experience a fracture at some time because of fragile bones, so any treatment regime that improves compliance is to be welcomed.

The women who took part in the study had an average age of 68 and more than a third had a family history of osteoporosis.

45 per cent had already suffered a fracture, with just under a third reporting one incident and a further ten per cent reporting two. Four per cent had experienced three to five factures.

Our study clearly shows that women who were prescribed monthly doses of ibandronate, and enrolled on a patient support programme, were much more likely to continue taking their medication than those on weekly doses of alendronate concludes Dr Cooper.

Evidence suggests that adhering to regular treatment for osteoporosis improves bone mass density and reduces fracture rates. This, in turn, reduces the social and economic burden of this very common and debilitating chronic condition.

Solitons could power molecular electronics, artificial muscles

Thu, 06 Jul 2006 04:00:00 PST

( from http://www.rxpgnews.com ) Columbus, Ohio -- Scientists have discovered something new about exotic particles called solitons.

Since the 1980s, scientists have known that solitons can carry an electrical charge when traveling through certain organic polymers. A new study now suggests that solitons have intricate internal structures.

Scientists may one day use this information to put the particles to work in molecular electronics and artificial muscles, said Ju Li, assistant professor of materials science and engineering at Ohio State University.

Li explained that each soliton is made up of an electron surrounded by other particles called phonons. Just as a photon is a particle of light energy, a phonon is a particle of vibrational energy.

The new study suggests that the electron inside a soliton can attain different energy states, just like the electron in a hydrogen atom.

While we know that such internal electronic structures exist in all atoms, this is the first time anyone has shown that such structures exist in a soliton, Li said.

The soliton's quantum mechanical properties -- including these newly discovered energy states -- are important because they affect how the particle carries a charge through organic materials such as conducting polymers at the molecular level.

These extra electronic states will have an effect -- we just don't know right now if it will be for better or worse, he said.

Li and his longtime collaborators from MIT published their findings in a recent issue of the Proceedings of the National Academy of Sciences (PNAS).

The name soliton is short for solitary wave. Though scientists often treat particles such as electrons as waves, soliton waves are different. Ordinary electron waves spread out and diminish over time, and soliton waves don't.

It's like when you make a ripple in water -- it quickly spreads and disappears, Li said. But a soliton is a strange kind of object. Once it is made, it maintains its character for a long time.

In fiber optics, normal light waves gradually flatten out; unless the signal is boosted periodically, it disappears. In contrast, solitonic light waves retain their structure and keep going without assistance. Some telecommunication companies have exploited that fact by using solitons to cheaply send signals over long distances.

Before solitons can be fully exploited in a wider range of applications, scientists must learn more about their basic properties, Li said. He's especially interested in how solitons carry a charge through conducting polymers, which consist of long, skinny chains of molecules.

The tiny chains are practically one-dimensional, and this calls some strange physics into play, Li said.

In their PNAS paper, Li and MIT colleagues Xi Lin, Clemens Först, and Sidney Yip describe a detailed calculation of what happens to solitons at a quantum-mechanical level as they travel along a chain of the organic polymer polyacetylene.

Their mathematical model builds upon a 1979 model called the Su-Schrieffer-Heeger (SSH) model. Alan Heeger, a University of California, Santa Barbara physicist who discovered solitons, won the Nobel Prize in 2000 for his pioneering work on conducting polymers.

Li said the new work extends the SSH model by including the full flexibility of the polymer chain, as well as interactions between electrons.

The finding will likely affect the development of molecular electronics -- devices built from individual molecules.

Because polymer chains tend to bend and twist as solitons pass through them, scientists have wondered whether solitons could be used to power artificial muscles for high-tech robots and devices to aid human mobility. Such muscles would be made of organic polymers, and flex in response to light or electrochemical stimulation.

If fully understood, solitons may also be harnessed to drive molecular motors in nanotechnology, Li said.

Fibromyalgia often misdiagnosed in pregnant women

Thu, 06 Jul 2006 02:58:00 PST

( from http://www.rxpgnews.com ) Pregnant women with fibromyalgia (FM) experience significant pain, fatigue and psychological stress, symptoms that are often misdiagnosed or undertreated as a normal part of pregnancy, according to a pilot study by Karen M. Schaefer, D.N.Sc., R.N., assistant professor of nursing at Temple University's College of Health Professions. Her research, the first to look at the impact of pregnancy on women with FM, was recently presented at the 2006 Association of Women's Health, Obstetrics and Neonatal Nurses' convention in Baltimore.

Fibromyalgia is a chronic condition commonly found in women that causes pain in the muscles and soft tissues of the body. Many sufferers feel weak from fatigue, and the condition, at its worst, can lead to disability.

"Until now, there was only anecdotal evidence suggesting that women with FM had a rougher time during pregnancy," said Schaefer. "This data is the first step toward gathering hard evidence of FM effects on this group and will hopefully help us identify ways to reduce the impact of fibromyalgia during pregnancy."

For this study, Schaefer recruited pregnant women with and without FM through an Internet announcement on a fibromyalgia Web site. Study subjects were between the ages of 29 and 31, in their third trimester, with no history of stillbirth and free of chronic illnesses other than FM.

The women were then mailed a questionnaire about fatigue, depression, pain and ability to function. A demographic form was also used to assess the number of painful areas in the body as well as age, marital status, education, hours slept and use of medication.

Schaefer's results revealed that the pregnant women with fibromyalgia had a hard time functioning, felt more stiff and tired, and experienced pain in more body areas than women without FM.

"Most women with FM have trouble getting this condition properly diagnosed, let alone knowing where to turn for help once their condition is identified. We need to start looking at how FM affects all areas of these women's lives and come up with ways to provide as much comfort and support as possible," she said.

Schaefer, whose research focuses on women with chronic illness (fibromyalgia, lupus, ovarian cancer) is currently expanding her study to include a larger group of subjects.

Valproate effective in adult spinal muscular atrophy (SMA)

Sat, 24 Jun 2006 03:00:00 PST

( from http://www.rxpgnews.com ) An epilepsy drug that has been on the market for decades can ease the symptoms of adult sufferers with a genetic disorder that seriously weakens muscles.

Scientists at Washington University School of Medicine in St. Louis retrospectively reviewed results from off-label use of the drug valproate to treat seven adult spinal muscular atrophy (SMA) patients. Clinicians offered the drug to patients on the basis of research conducted elsewhere that showed the drug increased levels of a key protein in cell cultures.

"The treatment has been fairly successful," says lead author Chris Weihl, M.D., Ph.D., a postdoctoral fellow in neurology. "The drug appeared to be well-tolerated and increased the strength of the patients who took it."

The study, now available online, will appear in the August 8 issue of Neurology.

Weihl notes that a larger, prospective trial is needed to firmly establish valproate as a treatment of choice for sufferers of this type of SMA.

Such trials are already underway elsewhere in pediatric patients who suffer from a different type of SMA that begins earlier in life. Weihl and his colleagues are concerned that valproate may not work as well in those patients. They wanted to make sure that researchers did not discard the possibility that valproate could help older sufferers even if the trials in pediatric patients went poorly.

"Based on what we know of the unique genetics of this disease, there was reason to think that this drug could be more helpful to patients who develop SMA later in life," Weihl says.

Patients with all forms of SMA, which affects approximately one of every 6,000 babies born in the U.S., are missing the SMN1 gene, which makes the survival motor neuron (SMN) protein. This progressively weakens the muscles, leading to difficulty in walking, eating, clearing the air passageway, and other essential functions.

Based on when the symptoms of SMA first manifest, physicians divide SMA into four subtypes. SMA I, for example, strikes very young children, causing weakness in the womb, preventing children from ever walking and typically resulting in death at an early age. Patients with SMA IV, in contrast, don't develop weakness until adulthood. The seven patients studied were either SMA III or SMA IV, and ranged in age from 17 to 54.

Differences in age of SMA onset have been directly linked to a second human gene that also makes the SMN protein. That gene, SMN2, isn't as efficient at making the SMN protein as SMN1. Patients who develop SMA early in life have only one copy of the SMN2 gene in their DNA, leaving them with very low levels of the SMN protein. Patients who get the disorder later in life have more copies of the SMN2 gene, increasing the amount of SMN protein made in their cells and delaying onset.

"Because we have learned so much about SMA over the last decade, there's been a big push at NIH to cure this disease," Weihl says. "The search has been on to find a treatment that can increase the amount of SMN2 protein synthesized by SMN2 genes. This rapid bench-to-bedside transition for valproate is a good example of the kind of progress that is encouraged both by NIH and the University's Biomed 21 initiative."

In addition to its use as an epilepsy treatment, valproate, which is sold under the brand name Depakote, has been used to treat bipolar disorder, migraine headaches and other neurological conditions. The drug's effects include increasing the number of times protein-building instructions are read from genes, which is the first step in creating copies of proteins like SMN.

As patients took the drug, clinicians regularly gave them a series of strength tests. When Weihl reviewed the data from those tests, he found patient strength had increased significantly over the course of eight to 15 months of treatment with the drug.

According to Weihl, simply increasing the strength of an SMA patient's cough might enable them to clear their lungs better and reduce incidence of pneumonia, the most common killer of patients with SMA III and IV.

Valproate's side effects can include weight gain, hair loss and acne. One patient stopped taking the drug because she was concerned about weight gain.

"Adding weight can be a problem in patients who are already weak, and it's certainly a legitimate reason to stop taking the drug, but overall we didn't see significant weight gains in patients taking the drug," Weihl says.

Weihl and his colleagues are continuing to follow the seven patients reviewed in the study, who are still taking a daily maintenance dose of the drug.

Cherry Juice May Prevent Muscle Damage Pain

Fri, 23 Jun 2006 00:03:00 PST

( from http://www.rxpgnews.com ) The familiar "no pain, no gain" phrase usually associated with exercise may be a thing of the past if results from a study on cherry juice published today in the online version of the British Journal of Sports Medicine prove true in future research.

Historically, a number of approaches to prevent exercise-induced muscle pain and damage have been examined, but few have been effective. Declan Connolly, associate professor of education and director of the human performance laboratory at the University of Vermont and colleagues at New Yorks Nicholas Institute of Sports Medicine and Athletic Trauma and Cornell University, evaluated the efficacy of a fresh, highly-concentrated, specially- processed tart cherry juice blend in preventing the symptoms of muscle damage in a randomized, placebo-controlled study in 14 male college students.

"The anti-inflammatory properties of cherry juice have been examined before, but the focus of this research was on a new area muscle damage repair," said Connolly. "Only two species of mammals suffer this type of muscle damage horses and humans."

The study participants were asked to either drink a bottle of the cherry juice blend twice a day for three days before exercise and for four days afterwards, or to drink a placebo juice containing no cherries. The 12-ounce bottle of juice contained the liquid equivalent of 50 to 60 tart cherries blended with commercially available apple juice.

The participants performed a type of muscle-damaging exercise flexing and tensing one arm 20 times that creates contractions in which the muscle is lengthened. Muscle tenderness, motion, and strength were assessed on each of the days before and after exercise, using standard pieces of equipment designed for the purpose. Study participants rated their muscle soreness on a scale of one to ten. The whole process was repeated all over again two weeks later, with those who had taken the placebo juice taking the cherry juice blend instead, and vice versa. The other arm was also used.

There was a significant difference in the degree of muscle strength loss between those drinking the cherry juice blend and those taking the placebo juice. This fell by 22 percentage points in those drinking the placebo juice, but only by four percentage points in those drinking cherry juice. Muscle strength had slightly improved after 96 hours in those drinking cherry juice. The degree of soreness differed little between the two groups, but the average pain score was significantly less in those drinking cherry juice. Average pain scores came in at 3.2 for those drinking the placebo juice and 2.4 for those drinking cherry juice. Pain also peaked at 24 hours for those drinking cherry juice, but continued to increase for those on the placebo juice for the subsequent 48 hours.

According to Connolly, next steps include identifying funding sources and collaborators to continue study of the cherry juices effectiveness in muscle damage repair and possibly arthritis, as well as research involving race horses.

"Current anecdotal evidence suggests the drink may be effective in treatment of arthritis and gout, and thus offer a potentially safer alternative than prescription drugs," said Connolly.

Natural pine bark extract Pycnogenol relieves muscle cramp and pain in athletes and diabetics

Sat, 17 Jun 2006 01:41:00 PST

( from http://www.rxpgnews.com ) A study published in this month's issue of Angiology shows that supplementation with the pine bark extract Pycnogenol® (pic-noj-en-all) improves blood flow to the muscles which speeds recovery after physical exercise. The study of 113 participants demonstrated that Pycnogenol significantly reduces muscular pain and cramps in athletes and healthy, normal individuals.

"With the millions of athletes worldwide, this truly is a profound breakthrough and extremely significant for all individuals interested in muscle cramp and pain relief with a natural approach. These findings indicate that Pycnogenol can play an important role in sports by improving blood flow to the muscles and hastening post-exercise recovery," said Dr. Peter Rohdewald, a lead researcher of the study.

Researchers at L'Aquila University in Italy and at the University of Würzburg in Germany studied the effects of Pycnogenol on venous disorders and cramping in two separate studies.

The first study consisted of 66 participants who had experienced normal cramping at some point, had venous insufficiency, or were athletes who suffer from exercise-induced cramping. The first two weeks of the study was an observation period and participants did not supplement with Pycnogenol. Symptoms related to venous disorders, and the number of cramping episodes each participant experienced over the two observation weeks was recorded.

Next, all the participants were given 200 mg of Pycnogenol once a day for four weeks. After the treatment phase, participants' symptoms and cramping episodes were recorded for one week without any Pycnogenol supplementation.

The researchers found a significant decrease in the number of cramps the participants experienced while supplementing with Pycnogenol. Participants who had experienced normal cramping had a 25 percent reduction in the number of cramps experienced while taking Pycnogenol.

Participants with venous insufficiency experienced a 40 percent reduction in the number of cramps, and athletes with frequent cramping experienced a 13 percent reduction in the number of cramps while on Pycnogenol.

The second study involved 47 participants with diabetic microangiopathy (a disorder of the smallest veins commonly associated with diabetes), or intermittent claudication (a blood vessel disease that causes the legs to easily cramp).This study also used a two-week pre-trial observation period followed by a week of supplementing with Pycnogenol (200 mg per day for one week), followed by a week of observation without Pycnogenol supplementation.

Patients with diabetic microangiopathy had a 20.8 percent reduction in pain, while participants with claudication experienced a 21 percent decrease in the amount of pain experienced while supplementing with Pycnogenol. Results indicated participants who took placebo experienced no decrease in pain.

Cramps are a common problem for people of all ages, ranging to the extreme fit and healthy to people who suffer from health problems. Previously, magnesium was hailed as the natural approach for relieving muscle cramps, however studies continue to show magnesium to be inefficient for reducing muscle cramps.

"Pycnogenol improves the blood supply to muscle tissue creating a relief effect on muscle cramping and pain. Poor circulation in the muscle is known to cause cramps and Pycnogenol improved the cramping in patients due to a stimulation of blood flow to their muscle tissue. Nitric oxide (NO) a blood gas, is well known to enhance blood flow and Pycnogenol may be influencing the activity of NO," said Rohdewald. "The insufficient production of NO is the common denominator responsible for impaired blood flow in vascular disease."

Strenuous exercise is known to involve muscle damage which may be followed by symptoms of inflammation. In separate studies published this year and in 2004 and 2005, Pycnogenol demonstrated its anti-inflammatory effects in clinical trials for asthma, dysmenorrhea and osteoarthritis.

Ninety-six percent of minimally invasive knee replacement patients leave same day, no complication

Mon, 19 Dec 2005 05:00:00 PST

( from http://www.rxpgnews.com ) Lead author surgeon Richard A. Berger says it's not just the surgeon's skills and techniques that help patients avoid a hospital stay.

It's a comprehensive management pathway helps the patient avoid an overnight stay. It's optimal sequencing and timing of interventions by the nursing, physical therapy, anesthesia surgical team; it's a team approach of equally weighted preoperative, intraoperative, and postoperative care.

Patients meet with the physical therapist and nurse prior to surgery. The nurse time is invaluable to patient before going into surgery, says Berger. They attend a class led by with a nurse where potential surgical complications and postoperative care are discussed.

Patients spend an hour learning about the surgery, asking questions about pain, recovery and surgery. We reassure patients that their pain will be controlled, that they will be carefully monitored for the occurrence of complications or delayed recovery due to early discharge, and explain how will be able to move around independently after surgery.

After class with the nurse, patients have a physical therapy session for instruction in gait training with crutches and a cane. An internist also evaluates patients as part of our hospital's policy. Lastly, the hospital discharge planner calls the patient at home before surgery to make sure all someone can take him or her home after surgery.

The 50 study patients (20 female, 30 males) had surgery between August 2003 and August 2004. The average age was 68 years old, average weight of 203 lbs. with a body mass index of 29.2. Forty-eight of the patients had osteoarthritis. Each patient was the first surgical case of the day.

Berger, who pioneered and perfected minimally invasive outpatient surgery, explains his technique for total knee arthroscopy (TKA) does not cut the quadriceps muscle and quadriceps tendon.

The only incision is from the joint line to the superior pole of the patella. The quadriceps tendon is not cut or split. The knee is not dislocated; instead, in situ cuts are made. The patient is out of surgery in less than two hours.

After surgery, patients see an occupational and physical therapist. To be released, patients must be able to independently get in and out of bed, rise from a chair, walk 100 feet, and walk up and down a full flight of stairs. Patients are then asked if they feel comfortable and would like to go home and are released with pain medication.

Patients receive home physical therapy until they can drive; then, outpatient physical therapy is started. Patients were evaluated clinically and radiographically in the office at one week, two weeks, six weeks, and three months.

Berger says this study demonstrates that, in these selected patients, outpatient TKA was safe with no short-term readmission or complications related to early discharge. New clinical pathways, including improvements in anesthetic techniques, postoperative pain management, and rehabilitation protocols, will make performing outpatient TKA a realistic goal. This comprehensive pathway may make it possible for this minimally invasive knee surgery to be done as an outpatient in specialized surgicenters in the future.

Muscular dystrophy - early cardiac screening shows better outcomes

Sun, 30 Oct 2005 15:02:00 PST

( from http://www.rxpgnews.com ) Early diagnosis and treatment of heart disease may lead to longer life in Duchenne and Becker muscular dystrophy patients, say experts at Baylor College of Medicine (BCM) and Texas Children's Hospital in Houston in a report that appeared online in the journal Circulation.

Cardiac disease, particularly dilated cardiomyopathy and heart failure, is the major cause of mortality in patients with muscular dystrophy and is present in most boys with Duchenne muscular dystrophy and approximately 70 percent of those with Becker muscular dystrophy. These are the two common forms of muscular dystrophy caused by defects in a gene called dystrophin.

"It should be the standard of care for all newly diagnosed Duchenne and Becker muscular dystrophy patients to be referred to a cardiologist for screening, probably by 10 years of age or earlier," says Dr. Jeffrey A. Towbin, professor of pediatrics at BCM and chief of pediatric cardiology at Texas Children's Hospital.

Towbin and his group studied 69 boys with DMD and BMD. After the first abnormal echocardiogram, which occurred at 14-15 years, 31 boys were started on ACE inhibitor or beta blocker therapy. During the follow-up two patients remained stable with their dilated cardiomyopathy, eight showed improvement and 19 normalized both heart size and function.

"This study also helped us realize that while some dystrophin-gene mutations are predictors of early onset cardiac abnormalities, others may actually protect against early development of these abnormalities," says Towbin.

Cardiac symptoms typically appear late in the course of cardiomyopathy, in part because affected individuals are usually wheelchairchair bound and often physically inactive. Heart disease progresses quickly, leading to premature death, often before 25 years of age.

Single Infusion of Zoledronic Acid More Effective in Pagets Disease

Thu, 08 Sep 2005 01:08:00 PST

( from http://www.rxpgnews.com ) Pagets disease is the second most prevalent bone disease after osteoporosis. Affecting more than one million people, the chronic bone disorder is marked by the malfunction of the bodys regular bone building process and may result in pain, deformities and fractures.

This pooled analysis of two identical double-blind, active-controlled studies compared a single 15-minute infusion of zoledronic acid 5 mg solution to oral risedronate (30 mg per day for 60 days) in 357 patients with Pagets disease. At six months, nearly all patients receiving one dose of zoledronic acid 5 mg solution were effectively treated. Specifically, 96 percent of patients treated with zoledronic acid 5 mg solution responded compared to 74 percent of patients who received risedronate (p<0<0<0

Studies confirm new treatments for Paget's disease

Mon, 05 Sep 2005 23:56:00 PST

( from http://www.rxpgnews.com ) Two studies led by researchers at The University of Auckland's Faculty of Medical and Health Sciences have pioneered new, more effective treatment for two forms of Paget's disease - a chronic and often painful bone disease.

The results of the studies, one led by Professor Ian Reid, who heads the University's Bone Research Group, and the other by his colleague, Professor Tim Cundy have been published in separate articles in the latest edition of the prestigious New England Journal of Medicine.

Professor Reid led an international study which confirmed a new treatment for Paget's disease, giving a more rapid, effective and longer-lasting result than existing medication.

Professor Cundy's research focused on Juvenile Paget's disease, a rare genetic bone disease with some similarities to adult Paget's. Having earlier been involved in the identification of the genetic cause of the disease, he used an experimental new treatment that substantially relieved bone pain, improved bone density and reversed the metabolic abnormalities of the disease in two patients.

Paget's disease is the second most prevalent bone disease after osteoporosis and affects up to five percent of the older population in New Zealand. It is caused by a malfunction of the body's regular bone building process and results in bone pain, skeletal deformity, bone fractures, deafness and neurological complications. Generally onset is in people over the age of 40.

Juvenile Paget's disease, although very rare is very debilitating. It usually presents in infancy or childhood and results in progressive deformity, growth retardation and deafness.

"Paget's is very painful, affects mobility and can greatly affect the quality of life for sufferers, which is why new treatments are so worthwhile," Professor Reid says.

Professor Reid's international study pioneered the use of zoledronic acid, and showed that a single injection gave a rapid and long-lasting improvement in bone health.

"The new treatment quickly gives sufferers a much improved quality of life, and has a much lower rate of relapse than the conventional treatment."

A further benefit is that it is much easier on the patients - the conventional treatment with tablets requires patients to take daily oral medication in a strict daily regimen for up to six months.

The study involved nearly 360 patients from 10 countries around the world, including 15 from New Zealand.

Based on the results of the study, the new drug under the brand name, Aclasta, was licensed for treatment of Paget's disease in the European Union in April this year, Canada in June and is currently under regulatory review in the United States.

It has not yet been made available in New Zealand for Paget's disease.

Professor Cundy's patients were a brother and sister, who had been wheel-chair bound with Juvenile Paget's since they were 15. He used an experimental new treatment giving them recombinant osteoprotergerin, the protein that is lacking in sufferers and deficiency of which causes the condition.

"While the disease in these patients was too advanced for any treatment to correct deformity, it made enough of an improvement in their bones, and reduction in bone pain for us to believe it could be very useful in halting progress of the disease in infants and children."

Gene therapy success for congenital muscular dystrophy (CMD)

Tue, 16 Aug 2005 19:46:00 PST

( from http://www.rxpgnews.com ) Researchers from the University of Pittsburgh report the first study to achieve success with gene therapy for the treatment of congenital muscular dystrophy (CMD) in mice, demonstrating that the formidable scientific challenges that have cast doubt on gene therapy ever being feasible for children with muscular dystrophy can be overcome. Moreover, their results, published in this week's online edition of the Proceedings of the National Academy of Sciences (PNAS), indicate that a single treatment can have expansive reach to muscles throughout the body and significantly increase survival.

CMD is a group of some 20 inherited muscular dystrophies characterized by progressive and severe muscle wasting and weakness first noticed soon after birth. No effective treatments exist and children usually die quite young.

Despite gene therapy being among the most vigorously studied approaches for muscular dystrophy, it has been beset with uniquely difficult hurdles. The genes to replace those that are defective in CMD are larger than most, so it has not been possible to apply the same methods successfully used for delivering other types of genes. And because CMD affects all muscles, an organ that accounts for 40 percent of body weight, gene therapy can only have real therapeutic benefit if it is able to reverse genetic defects in every cell of the body's 600 muscle groups.

By using a miniature gene, similar in function to the one defective in CMD, and applying a newly developed method for "systemic" gene delivery, the Pitt researchers have shown that gene therapy for muscular dystrophy is both feasible and effective in a mouse model of especially profound disease. Using this approach, the team, led by Xiao Xiao, Ph.D., associate professor of orthopaedic surgery and molecular genetics and biochemistry at the University of Pittsburgh School of Medicine, report that treated mice had physiological improvements in the muscles of the heart, diaphragm, abdomen and legs; and they grew faster, were physically more active and lived four times as long as untreated animals.

"While we have much farther to go until we can say gene therapy will work in children, we have shown here a glimmer of hope by presenting the first evidence of a successful gene therapy approach that improved both the general health and longevity in mice with congenital muscular dystrophy," said Dr. Xiao.

The most common form of CMD, and also one of the most severe, is due to a genetic mutation of laminin alpha-2, a protein that is essential for maintaining the structures that surround muscle cells and is an integral link in the chain of proteins that regulate the cell's normal contraction and relaxation. If the protein is defective, or is lacking, this outside scaffold, called the extra-cellular matrix, disintegrates, and the muscle cells become vulnerable to damage.

Simply replacing the defective gene with a good laminin alpha-2 gene is not possible because its size makes it impossible for researchers to get it to squeeze inside viral vectors disarmed viruses that are used to shuttle genes into cells. But the team found a good stand-in in a similar protein called agrin that when miniaturized could be inserted inside an adeno-associated virus (AAV) vector. Dr. Xiao's laboratory is known for its work developing this vector, which they have previously shown is the most efficient means for delivering genes to muscle cells.

In the current study, the authors show that two strains of AAV, AAV-1 and AAV-2, were effective in transferring the mini-agrin gene to cells in two mouse models. The AAV-1 vector was given by systemic delivery a single infusion into the abdominal cavity a method the authors only recently described and which they used for the first time in this study to transfer a therapeutic gene. The AAV-2 vector was delivered locally, given by intramuscular injection to different muscles of the leg. With both approaches, muscle cells were able to assimilate and copy the genetic instructions for making mini-agrin. Once produced, the mini-agrin protein functionally took the place of the laminin alpha-2 protein by binding to the key proteins on either end, thus restoring the cell's outside scaffolding and reestablishing the missing link to key structures inside the cell.

Clearly, the authors are most excited about the impressive results achieved in their experiments using systemic gene delivery, which proved there could be significant therapeutic improvements and even be life-saving. Yet they say their results are far from ideal and more work lies ahead.

"It's probably not realistic to expect that we can achieve complete success using the mini-agrin gene, which while somewhat similar, is structurally unrelated to laminin alpha-2. Unless we address the underlying cause of congenital muscular dystrophy we're not likely to be able to completely arrest or cure CMD," added Chungping Qiao, M.D., Ph.D., the study's first author and a research associate fellow in Dr. Xiao's lab.

Future directions for research include finding a way to engineer the laminin alpha-2 gene. For this study, the authors chose to use the mini-agrin gene because researchers from the University of Basel, Switzerland, had already demonstrated it could improve the symptoms of muscular dystrophy in a transgenic mouse model, which has little clinical relevance. The Pitt researchers might also explore approaches that combine genes that promote both muscle and nerve growth, as well as focus on improving the AAV vectors.

Avoid Falls!

Fri, 12 Aug 2005 00:26:00 PST

( from http://www.rxpgnews.com ) Whether it is caused by a wet floor, slippery throw rug, loose cord or objects in the wrong spot, falls in the home happen. The truth is, falls are not only the most common cause of injury among American adults age 65 and over, but are also the leading cause of death in the home, according to the National Safety Council. One in three adults over age 65 falls every year, and 90 percent of the 350,000 hip fractures that occur in the U.S. each year are the result of a fall. According to the American Academy of Orthopaedic Surgeons (AAOS), fall-related injuries can be reduced by removing clutter and items from the home, learning how to fall properly, and performing exercises that strengthen muscles and improve balance.

"It can take just one fall to lead to the loss of a person's independence and mobility," explained Richard F. Kyle, MD, first vice president of AAOS. "It is important to minimize obstacles in the home that often contribute to slips and falls. When simple safety measures are put in place, these mishaps can decrease significantly."

AAOS recommends following the below home safety checklist to fall-proof your home:

-- Get rid of clutter. Don't pile up items on the floor, stairway or pathways between rooms.

-- Keep appliance, lamp and telephone cords out of areas where you walk. Don't put them under rugs.

-- Use a rubber mat or put adhesive texture strips on the bottom of the tub or shower. Install grab bars on the walls for additional support. Place a slip-resistant rug on tile floor to safely get in and out of the bathtub.

-- Attach non-slip treads to bare-wood steps, and remove small area rugs at the top and bottom of stairs.

-- Good lighting is essential, so it is important to install glow-in-the-dark light switches at both the top and bottom of stairways. Also, place a night-light along the route between the bedroom and bathroom.

-- Keep a flashlight and new batteries by the bed in case of a power outage.

-- Clean up spills in the kitchen immediately. Use a step stool or low stepladder -- not chairs or boxes -- to reach items in upper cabinets. Use non-skid wax on the kitchen floor.

-- Wear proper footwear around the home and outside. Never walk around in stocking feet. Consider sneakers and shoes with laces. Avoid higher heels or platform shoes.

Of course, even the most careful people are still susceptible to trips and falls. With that in mind, there are "correct" ways to fall to minimize potential injury. Below are some recommended techniques to follow if you cannot prevent a slip or fall:

-- If possible, try to fall on your side or buttocks. Roll over naturally, turning your head in the direction of the roll.

-- Keep your wrists, elbows and knees bent. Do not try to break the fall with your hands or elbows.

-- Take several deep breaths after falling. If you feel you have suffered an injury, do not try to get up. Call 911 or a family member for help.

-- If you feel you are not injured and are able to get up, crawl to a strong, stable piece of furniture, like a chair, that you can use as a support to help pull yourself up. Place both hands on the seat.

-- Slowly begin to raise yourself up. Bend whichever knee is stronger, keeping the other knee on the floor. Finally, slowly twist and sit in the chair.

The Academy recommends that everyone, especially seniors, get regular physical check-ups. A healthcare provider may discover problems that can make someone more prone to falling. A provider can also monitor side effects from any prescriptions and over-the-counter medications, such as sleep aids, that might affect balance. People of all ages can reduce their risk of falls through regular exercise, as even moderate physical activity can help maintain strength, coordination, agility and balance. Exercises that improve balance and coordination are the most beneficial. A sedentary lifestyle -- at any age -- leads to weakness and increased chances of falling.

Genes may ultimately dictate seniors' mobility

Wed, 10 Aug 2005 00:28:00 PST

( from http://www.rxpgnews.com ) Genes can keep elderly people from benefiting equally from exercise, no matter how much effort they expend, according to research findings published in today's (Aug. 10) Journal of the American Medical Association.

Of nearly 3,000 seniors studied, those who exercised stayed healthier than their couch potato peers, but those born with a certain gene benefited the most from physical activity, said Marco Pahor, M.D., director of University of Florida's Institute on Aging and the multi-institutional study's senior author.

"To our knowledge, this is the first study to show behavioral and genetic interaction in functioning and aging, and shows people are already pre-selected, that there are genes that interact with behavior to affect mobility," Pahor said.

Decreasing mobility, along with lack of muscle strength and a decline in aerobic ability, are common aspects of aging that can lead to loss in quality of life, Pahor said. Understanding the mechanisms of how people lose mobility may lead to ways to help people remain independent longer, he added.

Federal health statistics have shown that about 34 percent of the U.S. population aged 70 or older reports difficulty walking a quarter of a mile. These individuals are at much greater risk of moving into a nursing home or dying over a two-year period, compared with their counterparts who do not report trouble walking the distance.

And despite the undisputed benefits of exercise, not everyone responds the same, even when they do lead active lives - for reasons that have not been entirely clear.

In the current study, researchers assessed seniors in an effort to better understand the relationship between genetic makeup, intensity of physical activity and functional decline. Twice a year throughout the four-year study, participants ages 70 to 79 reported their level of activity and their ability to walk a quarter mile or up 10 stairs.

Researchers also tested the blood of each study subject to identify which version of a gene long associated with exercise performance they had. About a third of the population possesses the DD genotype of the gene, named for the angiotensin-converting enzyme, or ACE. The rest have the II or ID versions of the ACE gene.

Study participants were categorized according to their exercise intensity and their genetic makeup. Overall, about 41 percent of study participants became less mobile over the four-year period. Even though people who exercised were less likely to develop substantial physical limitations, not everyone received the same benefits, even if they exercised with the same intensity.

About a third of the seniors engaged in significant physical exercise including walking and strenuous exercise, and they preserved their mobility longer than the 70 percent who engaged in little or no physical activity. Researchers also evaluated the 8 percent who reported participating in weight training.

But genetic makeup influenced long-term physical function. Among exercisers, the DD and ID genotypes were more likely to remain fit than those with the II genotype, who developed mobility problems at a 45 percent higher rate, researchers found. No difference in mobility according to genotype was found among non-exercisers, suggesting function was influenced by an interaction between exercise intensity and genetic make-up.

In addition, seniors who reported weight training and had the DD or ID genotype displayed the lowest rate of mobility loss in any exercise category. In contrast, weight trainers with the II genotype developed physical limitations similar to those experienced by seniors who were relatively inactive.

What differences in body composition the genotype creates also may yield clues to what causes mobility limitations to develop with age, and what people can do to stay active, Pahor said. Those with the II genotype, for example, tended to have higher total body fat.

"The good news is that regardless of genotype, the physically active people were at lower risk of losing mobility, suggesting that everyone should exercise to preserve mobility," said Pahor, a professor and chairman of the College of Medicine's department of aging and geriatric research.

The study's lead author, Stephen Kritchevsky, Ph.D., a professor and director of the Sticht Center on Aging at the Wake Forest University School of Medicine, said that people respond differently to exercise and that the implications of that response may change as they age.

"In our study, the II genotype is associated with increased fat in the leg muscles," Kritchevsky said. "Now energy storage near muscles may benefit young athletes engaged in endurance activities, but in older persons, accumulation of leg fat has been linked to poorer muscle function and metabolic diseases like diabetes."

The study, funded by the National Institute on Aging and the Claude D. Pepper Older Americans Independence Center and conducted in conjunction with researchers at several other institutions, including the University of Tennessee and the University of Pittsburgh, opens the door to more research on the interaction of behavior and genes and how that changes with age, Pahor said.

"This report is one step," he said. "It is necessary to do more research to determine whether there are other genes that may affect the benefits of physical activity on functioning of older adults."

Frequent falls?....Try Tai Chi

Tue, 28 Jun 2005 00:24:00 PST

( from http://www.rxpgnews.com ) Older people who took part in a structured programme of Tai Chi found that their balance and physical strength improved, reducing the risk of falls, according to a paper in the latest Journal of Advanced Nursing.
Researchers studied a group of fall-prone adults, with an average age of 78, living in residential care. 29 undertook a 12-week Tai Chi course three times a week and 30 formed the non-exercise control group.

They found that the physical fitness of the exercise group showed significant improvement, with stronger knee and ankle muscles, improved mobility and flexibility and better balance.

For example, after the exercise programme had finished, the time taken by the exercise group to walk six metres had fallen by 25 per cent, while the control group took 14 per cent longer.

"As people get older they are more likely to experience falls and this can lead to some very serious health issues" says co-author Professor Rhayun Song from the Chung Nam National University in South Korea.

"Figures published in the United States estimate that 30 per cent of people over 65 living in the community fall each year and this rises to up to 50 per cent for people in long-term care facilities, such as residential homes. One in ten falls results in a fracture.

"Regular exercise is very important as we get older because when we get to 65 we start losing muscle strength at a rate of up to two per cent per year."

Tai Chi, an ancient Chinese martial art consisting of a series of slow, gentle, continuous movements, is particularly suitable for older people as it helps them to develop stronger muscles and better balance and concentration.

The exercise programme used in the research consisted of 10 minutes of warming up exercises, 20 minutes of Sun-style Tai Chi movement and five minutes of cooling down exercises. Traditional instrumental music was used to help the group maintain slow and continuous movements and provide a soothing effect.

Both groups underwent a series of tests before the 12-week exercise programme and once it had been completed. This measured their muscle strength, balance and confidence in avoiding falls.

Participants were also asked to report any falls they experienced during the test period. 31 per cent of the exercise group said they had had a fall, compared with 50 per cent of the control group.

In the year before the research started, 66 per cent of the exercise group had reported a fall, together with 57 per cent of the control group.

"Our study shows that low-intensity exercise such as Tai Chi has great potential for health promotion as it can help older people to avoid falls by developing their balance, muscle strength and confidence" says Professor Song.

"We believe that regular exercise should be a fundamental part of caring for older people living in the community and in residential care."

European Commission Approves Zoledronic acid for the Treatment of Paget's Disease of Bone

Sun, 24 Apr 2005 08:13:00 PST

( from http://www.rxpgnews.com ) Novartis Pharma AG announced today that Aclasta® (zoledronic acid 5mg solution for infusion) has been granted Marketing Authorization by the European Commission for the treatment of Paget's disease of the bone in all 25 European member states, as well as Norway and Iceland. This represents the first approval for Aclasta.

In a head-to-head comparison versus the commonly used oral bisphosphonate risedronate, a single, 15 minute IV infusion of Aclasta showed superior efficacy1 and faster onset of action2, with longer remission following a single dose.3 Aclasta's unique molecular structure and IV administration enable fast and enduring efficacy.1 Aclasta, in clinical trials, was found to be generally safe and well tolerated.4

Bisphosphonates are well established as the standard of care for Paget's disease. However, oral risedronate requires daily administration for two months and for patients to avoid eating or drinking for 30 minutes prior to intake.5

"Oral bisphosphonates have limitations as not everyone responds well to them, or respond only very slowly and many relapse over time. In addition, they require complex administration regimens and are often associated with gastrointestinal discomfort, which can lead to poor compliance. The availability of a single intravenous infusion such as Aclasta that demonstrated superior efficacy, faster onset of action and longer remission in clinical studies compared to risedronate will be welcomed by patients and physicians," commented Professor Johann D Ringe, Klinikum Leverkusen, Germany. "Aclasta offers real benefits over oral bisphosphonates in the treatment of Paget's disease and resolves the issue of compliance."

"If you suffer from Paget's disease, you can't enjoy everyday activities such as tennis, walking or digging in the garden," added Dr. David Birch, who has been suffering from Paget's disease for 33 years. "The oral therapies currently available are associated with a lot of constraints."

In pivotal clinical studies, at six months, 96 percent of patients taking a single dose of Aclasta showed a therapeutic response, compared to 74 percent of patients taking 30 mg of risedronate, for 60 days.1 After more than 12 months, the vast majority of patients responding to Aclasta continued to maintain therapeutic response.3 At six months, serum alkaline phosphatase (SAP) levels - a key marker for bone turnover - were normal in 89 percent of Aclasta patients, compared with 58 percent of risedronate patients.1

Paget's disease, the second most common metabolic bone disease after osteoporosis6, can lead to serious consequences if not treated appropriately. It is a chronic skeletal disorder which in many patients causes pain, fractures and deformities that can seriously impede their ability to perform routine activities of daily living.7 This is a disease that can be difficult to diagnose, as not all patients experience noticeable symptoms7, leaving many untreated.

RxPG News : Musculoskeletal

Physiotherapy after surgery best for shoulder problems

ACSM: Yoga helped older stroke victims improve balance, endurance

Large study of arthroscopic rotator cuff repair reveals some surprises

Common hip disorder can cause sports hernia

Duchenne muscular dystrophy - also a disease of stem cells

Laboratory studies show promise for new multiple sclerosis treatment

NIH awards Muscular Dystrophy Cooperative Research Center grants

Simple, accurate in-office tool predicts athletes at high-risk for ACL injury, study details

New surgery improves outcomes for severe flat foot deformity

Hip exercises found effective at reducing, eliminating common knee pain in runners

NIH awards $7.5 million to study MRI as a tool to evaluate children with muscular dystrophy

Using stem cells to mend damaged hips

Quantity vs. quality: Long-term use of bone-building osteoporosis drugs

Osteoporosis drug improves healing after rotator cuff surgery

Electromagnetic pulses provide pain relief for osteoarthritis

Multicenter study finds little effect of soy isoflavones on bone loss in postmenopausal women

Extremity war injuries symposium seeks to improve patient care for wounded warriors

Startup at UCLA tech incubator to begin clinical trials for wireless body-monitoring system

Tarantula venom-based MD therapy to be advanced by UB scientists' biotech company

Drug could provide first treatment for scleroderma

Advances in treating hip pain to be focus of International Society for Hip Arthroscopy meeting

Artificial gravity prevents muscle loss in space

Study to assess hip exercises as treatment for osteoarthritis in the knee joints

Study to assess hip exercises as treatment for osteoarthritis in the knee joints

Surgery may not be necessary for Achilles tendon rupture

Risk of vibration-induced vascular injuries linked to vibration frequency differences

Biomedical engineering student recognized as IEEE's 'New Face of Engineering'

A couple of glasses of red wine a day keep disabilities away!

Sarcospan may help in Duchenne muscular dystrophy

'Wildcat Power Cord' repairs cruciate ligament in dairy cow's knee

Lithium chloride slows onset of skeletal muscle disorder

Massive microRNA scan uncovers leads to treating muscle degeneration

FDA approves knee-injury device for humans

Brain abnormalities found in people with writer's cramp

Sports hernia repair technique coupled with innovative rehabilitation program speeds return to play

Sports hernia repair surgery plus innovative rehab program helps athletes return to play

Tennis elbow procedure demonstrates long-term success

Women and arthritis sufferers have poorer short-term recovery from arthroscopic knee surgery

Serica scientists win AOSSM Award for ACL tissue regeneration in preclinical study

Groin injuries averted by preseason injury prevention

Neoprene sleeve equal to knee brace during recovery from ACL surgery

Penn researchers find a new target for muscular dystrophy drug therapy

Anti-malarial drug may reduce risk of diabetes for patients with rheumatoid arthritis

More muscle for the argument to give up smoking

Faulty cell membrane repair causes heart disease

New dynamic brace developed to advance clubfoot treatment

New genetic test developed at Emory advances detection and diagnosis of muscular dystrophy

Mouse model points to possible new strategy for treating rare muscle disease, kidney disorders

When the villain becomes your friend: The strange tale of muscle lactate

Existence of muscle-building stem cells points to regenerative therapies for muscular disease

Research shows aerobic exercise helps maintain muscle in elderly

Biofeedback on abnormal mechanics lowers risk for stress fractures, pain under kneecap

Free weight training gets workers with rotator cuff injuries back on the job

Green tea compound suppresses factors causing cartilage, bone destruction in arthritis

Measuring calcium intake can help to identify osteoporosis in men with prostate cancer

The sturdier sex? -- Study by Pittsburgh scientists finds female stem cells work better

Stevens and Connecticut Innovations agree to investment of $500,000 in SPOC Inc.

Switching genes to overdrive improves muscular dystrophy symptoms in mice

Women need expanded musculoskeletal care during pregnancy, study finds

Modified ligament surgery improves outcomes for baseball pitchers, other athletes

Power-boosting signal in muscle declines with age

Common blood pressure drug reduces progressive muscle degeneration in mice

Smoking worsens knee osteoarthritis

Improperly sized tennis racket grip doesn't cause tennis elbow

Helping muscle regenerate

Trichostatin A (TSA) Can Counteract Muscular Dystrophy in Mice

Scientists show drug can counteract muscular dystrophy in mice

Muscle cells self-destruct rather than grow with use

Women show 47 percent greater persistence with osteoporosis drugs if offered monthly tablet, support

Solitons could power molecular electronics, artificial muscles

Fibromyalgia often misdiagnosed in pregnant women

Valproate effective in adult spinal muscular atrophy (SMA)

Cherry Juice May Prevent Muscle Damage Pain

Natural pine bark extract Pycnogenol relieves muscle cramp and pain in athletes and diabetics

Ninety-six percent of minimally invasive knee replacement patients leave same day, no complication

Muscular dystrophy - early cardiac screening shows better outcomes

Single Infusion of Zoledronic Acid More Effective in Pagets Disease

Studies confirm new treatments for Paget's disease

Gene therapy success for congenital muscular dystrophy (CMD)

Single Infusion of Zoledronic Acid More Effective in Pagets Disease