by Nic Fleming At high altitude, even the fittest mountaineer's ability to move freely can vanish in the thin air. But it's not the fault of your muscles. In fact, this drop-off in athletic performance in low-oxygen conditions may be mostly in the mind: the brain kicks in to prevent potentially damaging overexertion. The cause of muscle fatigue has been the subject of much debate. Some researchers emphasise the importance of physical changes such as lactic acid build-up, while others back a "central governor" theory whereby fatigue is a sensation generated by the brain. Emma Ross of the University of Brighton, UK, and colleagues asked 11 men to carry out knee extensor muscle exercises while breathing normal air – which has 21 per cent oxygen – as well as mixes with 16 per cent, 13 per cent and 10 per cent oxygen to represent mild, moderate and severe hypoxia. As the oxygen levels fell, so did the forces the participants could generate voluntarily. To assess the role of the brain in muscle fatigue, the team repeated the experiment using non-invasive brain stimulation to artificially generate motor cortex signals, overriding voluntary control and triggering knee muscle contraction. Measuring the difference between the forces participants could generate voluntarily and those created by the brain stimulation helped Ross and colleagues establish that the brain contributes 18 per cent to muscle fatigue with normal oxygen, 25 per cent for mild to moderate hypoxia and 54 per cent for severe hypoxia (Journal of Applied Physiology, DOI: 10.1152/japplphysiol.00458.2010). © Copyright Reed Business Information Ltd.

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Link ID: 15563 - Posted: 07.16.2011

By Tina Hesman Saey Pumping up is easier for people who have been buff before, and now scientists think they know why — muscles retain a memory of their former fitness even as they wither from lack of use. That memory is stored as DNA-containing nuclei, which proliferate when a muscle is exercised. Contrary to previous thinking, those nuclei aren’t lost when muscles atrophy, researchers report online August 16 in the Proceedings of the National Academy of Sciences. The extra nuclei form a type of muscle memory that allows the muscle to bounce back quickly when retrained. The findings suggest that exercise early in life could help fend off frailness in the elderly, and also raise questions about how long doping athletes should be banned from competition, says study leader Kristian Gundersen, a physiologist at the University of Oslo in Norway. Muscle cells are huge, Gundersen says. And because the cells are so big, more than one nucleus is needed to supply the DNA templates for making large amounts of the proteins that give muscle its strength. Previous research has demonstrated that with exercise, muscle cells get even bigger by merging with stem cells called satellite cells, which are nestled between muscle fiber cells. Researchers had previously thought that when muscles atrophy, the extra nuclei are killed by a cell death program called apoptosis. © Society for Science & the Public 2000 - 2010

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Link ID: 14369 - Posted: 08.17.2010

By KENNETH CHANG For caterpillars, what you see on the outside as they crawl is not necessarily what Shaped something like an accordion, the tobacco hornworm caterpillar moves one segment at a time. First, the back legs on the last segment step forward, then the second-to-last segment and so on until finally the front segment with its head moves forward. Researchers at Tufts University and Virginia Tech were curious about the interior biomechanics of this form of movement, so they stuck the caterpillars on a treadmill within a powerful X-ray light source at Argonne National Laboratory in Illinois. For most creatures, including people, the innards and the outer parts are connected to something rigid like a skeleton or carapace, and the movements of the inside and the outside are synchronized. But caterpillars are almost entirely squishy, and the researchers were surprised when they saw that the guts of the caterpillar move differently. “It amazes me and blows my mind that there are still very unusual things to discover about such a humble creature,” said Michael A. Simon, a researcher at Tufts University in Boston who is the lead author of a paper describing the caterpillar locomotion, to be published in the journal Current Biology. Copyright 2010 The New York Times Company

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Link ID: 14288 - Posted: 07.27.2010

Durham, N.C. – Gene therapy methods that specifically target muscle may reverse the symptoms of a rare form of muscular dystrophy, according to new research in mice conducted by medical geneticists at Duke University Medical Center. Infants born with the inherited muscular disorder called Pompe disease usually die before they reach the age of two. The researchers also said their approach of targeting corrective genes to muscles may have application in treating other muscular dystrophies. Patients with Pompe disease have a defect in a key enzyme that converts glycogen, a stored form of sugar, into glucose, the body's primary energy source. As a result, glycogen builds up in muscles throughout the body, including the heart, causing muscles to degenerate. Using genetically altered mice in which the gene for the enzyme had been rendered nonfunctional, the researchers demonstrated they could introduce the functioning gene and correct glycogen buildup in heart and skeletal muscle. The findings suggest that such an approach should be considered as a potential gene therapy strategy for Pompe disease patients, the researchers report in a forthcoming issue of Molecular Therapy (now available online). © 2001-2005 Duke University Medical Center

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Link ID: 7094 - Posted: 06.24.2010

St. Paul, Minn. – Corticosteroids can be beneficial in the treatment of Duchenne muscular dystrophy and can be offered as a treatment option, according to the American Academy of Neurology and the Child Neurology Society in a new practice guideline published in the January 11 issue of Neurology, the scientific journal of the American Academy of Neurology. Duchenne muscular dystrophy is a genetic disorder linked to the X-chromosome. It is the most common form of muscular dystrophy in children and occurs when the protein dystrophin is missing. This causes a gradual breakdown of muscles and a decline in muscle strength. Duchenne muscular dystrophy mainly affects boys. An estimated one in 3,500 males worldwide has the disorder, and each year approximately 400 boys in the United States are born with it. Symptoms usually appear between ages two and five and include frequent falls, large calf muscles, and difficulty running, jumping, and getting up. There is no cure. The guideline authors reviewed all available research for the use of corticosteroids in the treatment of Duchenne muscular dystrophy. Corticosteroids are man-made drugs that are similar to the body’s hormone cortisone. Two corticosteroids, prednisone and deflazacort, were found to slow the rate of muscle deterioration, and are recommended as potential treatments to minimize the effect of Duchenne muscular dystrophy.

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Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 6706 - Posted: 06.24.2010

Researchers have found a delivery method for gene therapy that reaches all the voluntary muscles of a mouse – including heart, diaphragm and limbs – and reverses the process of muscle-wasting found in muscular dystrophy. "We have a clear 'proof of principle' that it is possible to deliver new genes body-wide to all the striated muscles of an adult animal. Finding a delivery method for the whole body has been a major obstacle limiting the development of gene therapy for the muscular dystrophies. Our new work identifies for the first time a method where a new dystrophin gene can be delivered, using a safe and simple method, to all of the affected muscles of a mouse with muscular dystrophy," said Dr. Jeffrey S. Chamberlain, professor of neurology and director of the Muscular Dystrophy Cooperative Research Center at the University of Washington School of Medicine in Seattle. He also has joint appointments in the departments of medicine and biochemistry. Chamberlain is the senior author of the paper describing the results, which will be published in the August edition of Nature Medicine. The paper describes a type of viral vector, a specific type of an adeno-associated virus (AAV), which is able to 'home-in' on muscle cells and does not trigger an immune system response. The delivery system also includes use of a growth factor, VEGF, that appears to increase penetration into muscles of the gene therapy agent. Chamberlain said the formula was the result of about a year of trying different methods.

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Link ID: 5880 - Posted: 06.24.2010

Expressing high levels of a sugar-adding protein known as LARGE in mice that lack the protein can prevent muscular dystrophy in these animals, according to studies by researchers at the University of Iowa Roy J. and Lucille A. Carver College of Medicine. Furthermore, the research suggests that LARGE protein also can restore normal function to a critical muscle protein that is disrupted by glycosylation (sugar-adding) defects in several different human muscular dystrophies. The team's findings, which appear June 6 in an advanced online publication of Nature Medicine and online in the journal Cell on June 3, might lead to new treatments for this particular class of muscular dystrophies and other muscle diseases caused by glycosylation defects. A group of muscular dystrophies, which include Fukuyama Congenital Muscular Dystrophy, Walker-Warburg Syndrome and Muscle-Eye-Brain disease, are caused by mutations in glycosylation enzymes – proteins that add sugars to other proteins. In these diseases, defects in the sugar-adding mechanism disrupt the properties of alpha-dystroglycan, a protein critical for normal muscle function.

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Link ID: 5602 - Posted: 06.24.2010

The increases in muscle fiber cross sectional area produced by dairy protein supplementation correlate very highly with superior increases in muscle strength (San Diego, CA) – Elizabethan England preferred it to milk; Miss Muffett enjoyed it on her tuffet before the spider showed up; now professional, collegiate, amateur, and recreational athletes combine it with creatine to supplement resistance training, with the expectation of improving gains in strength and muscle mass. The “it,” of course, is whey. Whey is a naturally occurring dairy protein found in bovine milk. Whey isolate, the highest quality form of whey that is extracted and purified during the cheese making process is shown in research to possess some extraordinary nutritional properties. In 2001 creatine supplement consumption in the US alone exceeded more than 2.5 thousand metric tons Researchers at Victoria University in Australia have previously shown that supplementation with creatine or a 100% whey isolate formulation significantly (P<0.05) increased levels of muscle force and mitochondrial energy production in rats as well producing significantly better (P<0.05) improvements in strength and body composition in bodybuilders during resistance training. Copyright © 2003, The American Physiological Society

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Link ID: 3674 - Posted: 06.24.2010

By GRETCHEN REYNOLDS Recently, researchers in England discovered that simply rinsing your mouth with a sports drink may fight fatigue. In the experiment, which was published online in February in the Journal of Physiology, eight well-trained cyclists completed a strenuous, all-out time trial on stationary bicycles in a lab. The riders were hooked up to machines that measured their heart rate and power output. Throughout the ride, the cyclists swished various liquids in their mouths but did not swallow. Some of the drinks contained carbohydrates, the primary fuel used during exercise. The other drinks were just flavored, sugar-free water. By the end of the time trials, the cyclists who had rinsed with the carbohydrate drinks — and spit them out — finished significantly faster than the water group. Their heart rates and power output were also higher. But when rating the difficulty of the ride, on a numerical scale, their feelings about the effort involved matched those for the water group. In a separate portion of the experiment, the scientists, using a functional M.R.I., found that areas within the brain that are associated with reward, motivation and emotion were activated when subjects swished a carbohydrate drink. It seems that the brains of the riders getting the carboyhydrate-containing drinks sensed that the riders were about to get more fuel (in the form of calories), which appears to have allowed their muscles to work harder even though they never swallowed the liquid. The role of the brain in determining how far and hard we can exercise — its role, in other words, in fatigue — is contentious. Until recently, most researchers would have said that the brain played littlerole in determining how hard we can exercise. Muscles failed, physiologists thought, because of biochemical reactions within the muscles themselves. They began getting too little oxygen or were doused with too much lactic acid or calcium. They stiffened and seized. Copyright 2009 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 13068 - Posted: 06.24.2010

By REED ABELSON For more than four decades, on telethons featuring celebrity performers and children in wheelchairs, Jerry Lewis has been raising money each Labor Day for the Muscular Dystrophy Association and the disease that helped make “poster child” part of the American idiom. On the most recent telethon, which was staged in Las Vegas and raised $63.8 million, the “Law and Order” actress Mariska Hargitay spoke of patients’ “hope that M.D.A. research will lead to treatments and cures.” Mr. Lewis, who has never disclosed why he chose this disease as his cause, once again closed the broadcast with an emotional rendition of the song “You’ll Never Walk Alone.” But for all the money collected toward a cure, Duchenne muscular dystrophy, the most common form of the disease, still confines thousands of boys in this country to wheelchairs in their early teens. Many do not live past their 20s. It is a stark reminder of how American medicine — with its focus on breakthrough treatments — can sometimes fail a complex, rare and stubbornly uncurable disease. Single-minded in their pursuit of a cure, doctors and researchers for years all but ignored the necessary and unglamorous work of managing Duchenne (pronounced doo-SHEN) as a chronic condition. Copyright 2008 The New York Times Company

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Link ID: 11314 - Posted: 06.24.2010

Helen Pearson A genetic tweak has converted mice into endurance runners by enriching a little-known form of muscle fibre. The discovery could help boost sporting abilities, or reveal ways to slow muscle wasting. Human muscles are made of four main types of fibre, including two 'slow-twitch' varieties and one 'fast-twitch' muscle type that are suited to endurance and sprint activities respectively. Little has been known about the fourth type, called IIX fibre, because it is scattered throughout different muscles. Now a Boston team has hit upon a genetic switch that converts almost all mouse muscle fibres into type IIX. The result is startling. "Damn, they're good athletes," says Bruce Spiegelman of Harvard Medical School, who led the team. The mice were able to run on a mouse treadmill for 25% longer than normal before reaching exhaustion. The discovery hints that the elusive type IIX muscle fibres are an underappreciated contributor to athletic ability. It is possible, for example, that world-class athletes are naturally endowed with more of these fibres than the average person — or that hard training generates more of them. If so, notes study researcher Zoltan Arany, also of Harvard Medical School, future athletes might try to take advantage of the discovery. It is possible, he predicts, that "someday we'll have drugs that switch on the production of these fibres and they'll be abused by sportsmen". ©2007 Nature Publishing Group

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Link ID: 9800 - Posted: 06.24.2010

— The octopus may have flexible arms, but it uses them in the same three-jointed way as vertebrates, a finding that sheds intriguing light on how limbs evolved, a new study says. An Israeli research team filmed octopuses as they stretched out an arm from a hidey-hole in an aquarium to grab a piece of food with their tentacles and bring it to their mouths. The octopuses, filmed about a hundred times, used a vertebrate-like strategy to carry out the complex movement. Even though their arms are supple and rubbery, the creatures stiffened the limbs through muscle control and articulated them in a way eerily like that of animals with rigid skeletons, the scientists found. To carry out the fetching movement, the octopus flexes its arm to form three "joints," located in similar locations to the shoulder, elbow and wrist in humans. Copyright © 2005 Discovery Communications Inc.

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Link ID: 6843 - Posted: 06.24.2010

By Michael Behar The chime on H. Lee Sweeney’s laptop dings again—another e-mail. He doesn’t rush to open it. He knows what it’s about. He knows what they are all about. The molecular geneticist gets dozens every week, all begging for the same thing—a miracle. Ding. A woman with carpal tunnel syndrome wants a cure. Ding. A man offers $100,000, his house, and all his possessions to save his wife from dying of a degenerative muscle disease. Ding, ding, ding. Jocks, lots of jocks, plead for quick cures for strained muscles or torn tendons. Weight lifters press for larger deltoids. Sprinters seek a split second against the clock. People volunteer to be guinea pigs. Gene therapy could do for athletes what photo manipulation has done for this runner. But performance-enhancing drugs would undermine amateur athletics, which by definition are supposed to show how far natural skills can be advanced, says Richard Pound, president of the World Anti-Doping Agency. “I want athletes,” he says, “not gladiators.” Sweeney has the same reply for each ding: “I tell them it’s illegal and maybe not safe, but they write back and say they don’t care. A high school coach contacted me and wanted to know if we could make enough serum to inject his whole football team. He wanted them to be bigger and stronger and come back from injuries faster, and he thought those were good things.” © 2003 The Walt Disney Company. All rights reserved.

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Link ID: 5669 - Posted: 06.24.2010

— Muscular dystrophy is a group of genetic diseases characterized by progressive muscle degeneration. Working with mice with a type of the disease, researchers have found that by expressing an enzyme that attaches sugar molecules to a protein essential for proper muscle structure, they can restore normal muscle function. Interestingly, the scientists found evidence of similar benefits when they expressed the protein, known as LARGE, in cells from patients with similar types of muscular dystrophies with distinct gene defects, suggesting that this approach may have clinical benefits for patients with the debilitating disease. The study, led by Howard Hughes Medical Institute investigator Kevin P. Campbell at the University of Iowa College of Medicine, was published online in the journal Nature Medicine on June 6, 2004. Campbell's co-authors on the paper were from the University of Iowa, the University of Toronto, Uppsala University in Sweden, and the National Center of Neurology and Psychiatry in Tokyo. The study complements additional work by Campbell and colleagues from the Scripps Research Institute in California, the California Pacific Medical Center Research Institute, and Uppsala University, which elucidated the critical role of LARGE in the processing of a protein required to link muscle cells to their surrounding matrix. This work was published in an advance online publication of Cell on June 3, 2004. ©2004 Howard Hughes Medical Institute

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Link ID: 5610 - Posted: 06.24.2010

— Subtle defects in the processing of a single protein that provides structural integrity to muscle cells can lead to several devastating forms of muscular dystrophy, according to studies by Howard Hughes Medical Institute researchers and their colleagues at the University of Iowa. The scientists reported in two papers published in the July 25, 2002, issue of the journal Nature that defects in enzymes responsible for the processing of the structural protein dystroglycan are the underlying cause of several rare forms of muscular dystrophy that affect muscles and cause additional developmental brain abnormalities including mental retardation. The new findings will immediately help doctors in providing accurate diagnosis and appropriate genetic counseling to patients and their families. In the longer term, knowing the underlying cause of the muscular dystrophies will help researchers tailor their interventions, according to Howard Hughes Medical Institute investigator Kevin Campbell . The disorder also disrupts an important component of learning and memory, so Campbell is hopeful that his team’s studies will improve understanding of possible links between muscle physiology and neurobiology. ©2002 Howard Hughes Medical Institute

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Link ID: 2369 - Posted: 06.24.2010

By DENISE GRADY Researchers in the Netherlands have developed a drug that may eventually be used to treat children with a severe and fatal type of muscular dystrophy. Times Health Guide: Duchenne’s Muscular DystrophyIn its first test in humans, a safety study in just four boys, the drug enabled patients to produce an essential muscle protein that is missing in Duchenne’s muscular dystrophy, a genetic disease. Not enough of the protein was produced to help the boys, but the presence of any at all was considered “proof of concept,” meaning that the approach has the potential to work and is worth pursuing. The experimental drug, called an “antisense” compound, works by canceling out the effects of certain genetic mutations. These types of drugs are being studied to treat cancer, heart disease, infections and other illnesses. “I don’t think you could ask for a better result from a preliminary study like this,” said Sharon Hesterlee, the vice president for translational research at the Muscular Dystrophy Association, which was not involved in the study but helped pay for an earlier phase of the work. Though promising, the research still has a long way to go. The four boys, ages 10 to 13, each received just one injection into a leg muscle. There were no adverse effects. But larger and longer trials with much higher doses, given systemically so that the drug reaches all muscles, are needed to test both safety and efficacy. If the treatment works, it will have to be given regularly, for life. Copyright 2007 The New York Times Company

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Link ID: 11146 - Posted: 06.24.2010

Roxanne Khamsi An experimental cancer drug has slowed muscular dystrophy in mice with the disease, raising hopes that a simple pill could one day treat the fatal condition in humans. “The results the researchers are reporting are very dramatic and impressive,” says Jeff Chamberlain at the University of Washington School of Medicine in Seattle, US. The researchers caution that the results are preliminary, but say that the approach might offer advantages over other medicines for muscular dystrophy currently in clinical trials. There are many forms of the muscle-wasting disease, but no cure for any of them. The most common form of the illness among children, known as Duchenne muscular dystrophy, involves a mutation for a muscle protein known as dystrophin. Without functioning copies of this protein, muscles weaken, leading to breathing problems and, ultimately, death in the victims' teens or early twenties. Pier Puri at the Burnham Institute in La Jolla, California and colleagues tried to boost muscle function in mice carrying a mutation in the dystrophin gene, by treating the animals with a cancer drug called trichostatin A (TSA). © Copyright Reed Business Information Ltd.

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Link ID: 9352 - Posted: 06.24.2010

Linda Geddes, reporter A gene therapy that appears to bulk up muscle mass and strength in monkeys - reported today in Science Translational Medicine - will undoubtedly raise fresh concerns about the potential for gene doping in sport. We already know that some athletes use drugs like erythropoietin to increase the amount of oxygen their blood delivers, and steroids to bulk up muscle mass. The big advantage with gene doping is that it should be harder to detect. That's because it's difficult to test for a protein that the body already produces, especially when its levels naturally vary between individuals - which might explain why some people are inherently better at sports than others. In the new study, Janaiah Kota and colleagues at Nationwide Children's Hospital in Columbus, Ohio, used gene therapy to add extra copies of the follistatin gene into the leg muscles of monkeys. Follistatin has been previously shown in mice to block myostatin, a protein that decreases muscle mass, resulting in bulked up "mighty mice". Monkeys injected with the gene also seemed to bulk up, and when Kota's team analyzed their leg muscles with a device that measures force, they found that the muscles injected with the follistatin gene were also stronger than normal muscles. They hope the approach could eventually be used to treat the severe muscle weakness associated with neuromuscular disorders like muscular dystrophy and multiple sclerosis. © Copyright Reed Business Information Ltd.

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Link ID: 13459 - Posted: 06.24.2010

Fenella Saunders The simple act of bending a knee requires the coordination of more strings than a symphony orchestra. Each muscle cell is made up of many tiny filaments of proteins. When a muscle contracts, these fibers change shape and slide past one another, creating vibrations. "It's like plucking a string, and the sound can tell you about the elastic properties of the muscle," says Karim Sabra, a mechanical engineer at the Georgia Institute of Technology. Sabra is measuring the noise from healthy muscles in the hope that this baseline information could be used in the future to help diagnose muscular diseases or injuries. It's possible to hear muscular noise for yourself. If you place your thumbs gently over your ear openings so they completely cover your ear canals, then with your elbows raised tighten your hands into fists, you will hear a sound that resembles distant rolling thunder, which becomes louder the tighter the fist is made. This phenomenon was first described in the late 1600s. Leg muscle sounds were first observed in the 1800s. During contraction, the overall volume of a muscle fiber stays the same. So in order to shorten, the fiber has to expand in width. The muscles become harder during this process. "Sound travels faster through stiffer muscles, and slower through softer ones," explains Sabra. © Sigma Xi, The Scientific Research Society

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Link ID: 11157 - Posted: 06.24.2010

By Steve Mitchell The recent breakthrough of skin cells reprogrammed to behave like embryonic stem cells has stolen the spotlight (ScienceNOW, 6 December), but adult stem cells are proving that they have advantages of their own. In the 13 December issue of Cell Stem Cell, researchers report using stem cells from patients afflicted with a form of muscular dystrophy to correct the disorder in mice. The results suggest that this strategy could one day treat muscular dystrophy in humans as well as other genetic disorders. Duchenne muscular dystrophy, which predominantly strikes boys, is caused by a mutation in the gene for a protein called dystrophin that is essential for proper muscle function. The condition leads to muscle degeneration, and patients usually die in their 30s. A particular type of stem cell found in muscle can give rise to new muscle tissue, so a team led by geneticist Luis Garcia of G�n�thon, a nonprofit biotechnology firm in �vry, France, investigated whether these cells could be used to reverse the dystrophin problems. The researchers first obtained the stem cells from patients via a muscle biopsy. Next, they used a virus to insert a gene into the cells that corrects the mutation in the dystrophin gene. The researchers then injected the modified stem cells into arteries of the legs of mice with muscular dystrophy. In just 3 weeks, muscles in the foot, shin, and thigh began expressing human dystrophin protein, indicating that the stem cells had given rise to muscle cells that had taken up residence in the muscles of the mice. © 2007 American Association for the Advancement of Science

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
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Link ID: 11085 - Posted: 06.24.2010