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BY Tina Hesman Saey SAN DIEGO — A Golden retriever that inherited a genetic defect that causes muscular dystrophy doesn’t have the disease, giving scientists clues to new therapies for treating muscle-wasting diseases. The dog, Ringo, was bred to have a mutation that causes Duchenne muscular dystrophy in both animals and people. His weak littermates that inherited the same mutation could barely suckle at birth. But Ringo was healthy, with muscles that function normally. One of Ringo’s sons also has the mutation but doesn’t have the disease, said geneticist Natassia Vieira of Boston Children’s Hospital and Harvard University October 19 at the annual meeting of the American Society of Human Genetics. The dogs without the disease had a second genetic variant that caused their muscles to make more of a protein called Jagged 1, Vieira and her colleagues discovered. That protein allows muscles to repair themselves. Making more of Jagged 1 appears to compensate for the wasting effect of the muscular dystrophy mutation, although the researchers don’t yet know the exact mechanism. The finding suggests that researchers may one day be able to devise treatments for people with muscular dystrophies by boosting production of Jagged 1 or other muscle repair proteins. N. M. Vieira. The muscular dystrophies: Revealing the genetic and phenotypic variability. American Society of Human Genetics Annual Meeting, San Diego, October 19, 2014. © Society for Science & the Public 2000 - 2014

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20226 - Posted: 10.22.2014

A drug to treat a particular form of Duchenne muscular dystrophy has been given the green light by the European Medicines Agency and could be available in the UK in six months. Translarna is only relevant to patients with a 'nonsense mutation', who make up 10-15% of those affected by Duchenne. The EMA decided not to pass the drug in January, but they have since re-examined the evidence. A campaign group said the drug must reach the right children without delay. There are currently no approved therapies available for this life-threatening condition. The patients who will benefit the most are those aged five years and over who are still able to walk, the EMA said. Duchenne muscular dystrophy is a genetic disease that gradually causes weakness and loss of muscle function. Patients with the condition lack normal dystrophin, a protein found in muscles, which helps to protect muscles from injury. In patients with the disease, the muscles become damaged and eventually stop working. There are 2,400 children in the UK living with muscular dystrophy, but only those whose condition is caused by a particular 'nonsense mutation' - namely 200 children - are suitable to use Translarna. The drug, ataluren, will be known by the brand name of Translarna in the EU. It was developed by PTC Therapeutics. The next step will see the European Commission rubberstamp the EMA's scientific 'green light' within the next three months and authorise the drug to be marketed in the European Union. At that point, individual member states, including the UK, must decide how it will be funded. The Muscular Dystrophy Campaign is calling for urgent meetings with National Institute of Health of Clinical Excellence (NICE) and NHS England to discuss how Translarna can be cleared for approval and use in the UK. It said families in the UK could have access to the drug by spring 2015. Robert Meadowcroft, chief executive of the campaign, said: "This decision by the EMA is fantastic news. BBC © 2014

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 19648 - Posted: 05.23.2014

By E. Paul Zehr As an infant, the Man Of Steel escaped Krypton’s red sun in a rocket lovingly prepared for him by his parents. Kal-L (but more commonly known as Kal-El) arrived under our yellow sun in Smallville to eventually become Clark Kent. Since his debut in Action Comics #1 in June of 1938, Superman has accumulated a pretty long list of “super abilities”. For me, though, I really like the list of his abilities that come from the 1940s radio serials. This was back when Superman was described as “faster than a speeding bullet, more powerful than a locomotive, and able to leap tall buildings in a single bound”. These descriptions all have to do with super-strength when you get right down to it. And with this summer’s “Man of Steel” Superman re-boot, super-strength is the focus of this post. I have to admit I’ve always found the explanation for Superman’s powers to be, well, a bit dubious. He has his powers because of our yellow sun. That is, because he was from a red sun planet (Krypton) somehow the yellow sun of Earth unleashes some inner super power mechanism that gives Superman all his…super-ness. Of course it’s a bit pure escapist fun. But what if there actually was something to that, though? I don’t mean something to the “yellow sun / red sun” stuff. You can just check in with our “friendly neighborhood physics” professor Jim Kakalios and his bok “Physics of Superheroes” for the real deal on that one. I mean rather the unleashing of some inner mechanism bit. What if something inside the human body could be unleashed—like removing the shackles from Hercules—and allow for dramatically increased strength? © 2013 Scientific American

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18273 - Posted: 06.15.2013

by Trisha Gura A rare genetic disease may be going to the dogs. About six in 100,000 babies are born with centronuclear myopathy, which weakens skeletal muscles so severely that children have trouble eating and breathing and often die before age 18. Now, by discovering a very similar condition in canines, researchers have a means to diagnose the disease, unravel its molecular intricacies, and target new therapies. The story began when Jocelyn Laporte, a geneticist at the Institute of Genetics and Molecular and Cellular Biology in Strasbourg, France, uncovered the genetic roots of an odd form of centronuclear myopathy that showed up in a Turkish family. Three children, two of them fraternal twins, were born normal. Then, at the age of 3-and-a-half, they grew progressively and rapidly ill. (Most forms of the illness do not come on so suddenly.) The twins died by the age of 9. Their younger brother recently reached the same age but is very ill. Investigators traced the problem to a mutation in a gene called BIN1, which makes a protein that helps shape the muscle so that it can respond to nerve signals that initiate muscle contraction. To find out how mutations in this gene could lead to such dire consequences, other researchers tried to genetically engineer mice models. But deleting the BIN1 gene failed to recreate the disease in mice, so the researchers had to look elsewhere. Laporte's team joined with geneticist and veterinarian Laurent Tiret, at the Alfort School of Veterinary Medicine in Paris, to tap a network of vets in the United States, United Kingdom, Canada, Australia, and France. The idea was to track down and analyze dogs that had spontaneously acquired a similar condition. Because of their longer lifespans and larger size, the canines could model how the disease progresses and might respond to new therapies. © 2010 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18272 - Posted: 06.15.2013

Linda Carroll TODAY contributor Each day brings Jenn McNary another dose of hope and heartache as she watches one son get healthier while the other becomes sicker. Both of McNary's sons were born with Duchene muscular dystrophy. Max, 11, is receiving an experimental therapy that appears to be making him better, while 14-year-old Austin is slowly dying. Austin was too sick to be included in the clinical trials for a promising new drug called Eteplirsen. “He can’t get into a chair, out of his wheelchair, into his bed and onto the toilet,” McNary told NBC’s Janet Shamlian. Max, however, was exactly what researchers were looking for. He was put on Eteplirsen, and now he's back to running around, climbing stairs and even playing soccer. “It’s a miracle,” McNary said. “It really is a miracle drug. This is something that nobody ever expected and he looks like an almost normal 11-year-old.” Eteplirsen is designed to partially repair one of the common genetic mutations that causes DMD. Even a partial repair may enough to improve life for boys struck by the condition, which results from a defect in the dystrophin gene. That gene resides on the X chromosome, which is why only boys end up with DMD. Boys get one X and one Y chromosome. Girls get two copies of the X chromosome — one from their mother and one from their father — so even if they inherit a defective copy from their mom, they get a healthy one from their dad. Although they won’t suffer symptoms, girls wind up with a 50 percent chance of being carriers for DMD.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 18196 - Posted: 05.28.2013

National Institutes of Health researchers used the popular anti-wrinkle agent Botox to discover a new and important role for a group of molecules that nerve cells use to quickly send messages. This novel role for the molecules, called SNARES, may be a missing piece that scientists have been searching for to fully understand how brain cells communicate under normal and disease conditions. "The results were very surprising,” said Ling-Gang Wu, Ph.D., a scientist at NIH’s National Institute of Neurological Disorders and Stroke. “Like many scientists we thought SNAREs were only involved in fusion." Every day almost 100 billion nerve cells throughout the body send thousands of messages through nearly 100 trillion communication points called synapses. Cell-to-cell communication at synapses controls thoughts, movements, and senses and could provide therapeutic targets for a number of neurological disorders, including epilepsy. Nerve cells use chemicals, called neurotransmitters, to rapidly send messages at synapses. Like pellets inside shotgun shells, neurotransmitters are stored inside spherical membranes, called synaptic vesicles. Messages are sent when a carrier shell fuses with the nerve cell’s own shell, called the plasma membrane, and releases the neurotransmitter “pellets” into the synapse. SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) are three proteins known to be critical for fusion between carrier shells and nerve cell membranes during neurotransmitter release.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 18115 - Posted: 05.04.2013

By James Gallagher Health reporter, BBC News A 'molecular scalpel' shows promise in patients with a deadly muscle wasting condition, according to researchers. The gene for the protein dystrophin is damaged in people with Duchenne muscular dystrophy. A drug trial on 19 children, published in the Lancet, used the 'scalpel' to removed the damage and restore dystrophin production. The charity Muscular Dystrophy Campaign said there was "real hope for the future". Duchenne muscular dystrophy affects one in every 3,500 newborn boys. Throughout life the muscle wastes away and children can need a wheelchair by the age of 10. The condition can become life-threatening before the age of 30, when it affects the muscles needed to breathe and pump blood around the body. New approach The instructions for making a protein are in the genetic code, but this can be disrupted by mutations or deletions in the code. Stem cell and gene therapy research has tried to find ways of introducing a functional dystrophin gene. This study tried to do the best it could with the damaged code. BBC © 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15590 - Posted: 07.25.2011

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.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 5: Hormones and the Brain
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.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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 BP7e: 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

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
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.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 5669 - Posted: 06.24.2010