Links for Keyword: Muscles
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A common question flowing across holiday tables trimmed with turkey this week may be "white meat or dark?" Now scientists have identified the genetic switch that governs the formation of the two types during development. White and dark meat differ in appearance because each is made up of a distinct type of muscle fiber. Dark meat comprises so-called slow twitch muscle fibers, which are specialized for extended exertion, whereas white meat is made up of fast twitch fibers that fuel short, intense bursts of energy. That much has been known for some time. The genetic mechanism underlying the specification of one muscle type versus the other was unclear, however. Philip Ingham of the University of Sheffield and his colleagues studied muscle cells of developing zebrafish and found that a gene dubbed u-boot (ubo ) plays a key role in determining what type of muscle develops by controlling the transcription factor protein known as Blimp-1. © 1996-2003 Scientific American, Inc.
Detergent delivers genetic medicine to mice with muscular dystrophy. HELEN R. PILCHER A mouse study raises hopes that injections of the DNA-like molecule RNA might one day help to treat the muscle-wasting disease Duchenne muscular dystrophy. For the first time in a live animal, RNA therapy has produced improvements that last for up to three months1. Duchenne muscular dystrophy is an inherited disease that affects 1 in 3,500 children, mainly boys. Sufferers inherit a fault in the gene encoding the protein dystrophin, causing most to die in early adulthood. The new approach effectively corrects the flawed gene. It targets RNA - the intermediate between DNA and protein. Snippets of RNA, injected directly into the muscle, help edit out damaged pieces of host RNA. Muscle cells can then produce the missing dystrophin protein. © Nature News Service / Macmillan Magazines Ltd 2003
-- A protein that plays a role in muscular dystrophies also may be involved in peripheral neuropathy - disorders of the nerves that carry messages between the brain and the rest of the body. The findings, by University of Iowa researchers and colleagues, may shed light on the causes and mechanisms of human peripheral neuropathies, which cause pain, numbness and muscle wasting. Peripheral neuropathies can be acquired as a result of diseases including diabetes and Hansen's disease (leprosy) or can be inherited. Some congenital peripheral neuropathies (those present at birth) can cause limb deformities. The UI study may suggest new treatment strategies for these conditions. In the peripheral nervous system, dystroglycan is found in Schwann cells, which wrap themselves around peripheral axons (nerve fibers) and protect them by producing a myelin sheath. The sheath allows nerve impulses to move faster and more efficiently along the nerves. If nerve fibers are the body's electrical wiring, then the myelin sheath represents the insulation. Copyright © 1992-2003 Bio Online, Inc.
A protein defective in two types of muscular dystrophy also appears to be important in repairing damaged muscle, according to Howard Hughes Medical Institute researchers at the University of Iowa College of Medicine. The discovery reveals the first known component of the machinery that repairs the damaged membrane in a muscle fiber. Further studies of this and related proteins could lead to a better understanding of disorders that affect cardiac and skeletal muscles. Howard Hughes Medical Institute investigator Kevin Campbell and Dimple Bansal led the research group that published its findings in the May 8, 2003, issue of the journal Nature. Campbell and his colleagues reported that their studies in mice showed that a mutant form of the muscle protein dysferlin prevents normal muscle repair in limb-girdle muscular dystrophy type 2B (LGMD2B) and Miyoshi Myopathy (MM). Campbell and his colleagues at the University of Iowa College of Medicine collaborated with Paul McNeil and his laboratory at The Medical College of Georgia. ©2003 Howard Hughes Medical Institute
HOUSTON - A newly identified gene, atrogin-1, is involved in muscle loss associated with cancer, diabetes, fasting and kidney disease as well as in the atrophy occurring with disuse, inactivity, and nerve or spinal injury. This discovery, funded by the National Space Biomedical Research Institute (NSBRI) and the Muscular Dystrophy Association, increases the understanding of how muscles atrophy and may lead to development of new treatments for muscle wasting on Earth and in space. "Through a study of rat muscles, we determined that atrogin-1 is found only in muscle," said Dr. Alfred Goldberg, professor of cell biology at Harvard Medical School and associate leader of NSBRI's team of scientists focusing on muscle loss in space. "In normal muscles, the amount is low; however, there is a dramatic increase in the production of the atrogin-1 protein in conditions where muscles lose size and strength." Copyright © 2000-2002 National Space Biomedical Research Institute
Scientists have found a way to block the genetic flaw that causes the most common form of muscular dystrophy. Tests on mice found injecting them with a compound that neutralises the faulty gene's activity led to muscle cells working more effectively. The US team's work, published in Science, could be a step towards treatments to reverse the symptoms of the disease. UK experts said the study results were "exciting". Around 7,500 children and adults in the UK have some form of muscular dystrophy. Myotonic dystrophy, like other forms of the condition, causes muscle weakness and wasting that is usually progressive. It typically affects muscles in the face, jaw and neck. Another symptom is muscle stiffness - myotonia - which tends to be seen in the hands. The condition can appear at any age, and currently there is no treatment that can halt its progress. It is caused by a mutation of a specific gene on chromosome 19. Scientists discovered RNA - which takes genetic messages from the nucleus to the rest of the cell in order to build proteins - was key to myotonic dystrophy. Each gene produces its own RNA. But in myotonic dystrophy, the genetic defect leads to production of a toxic RNA which blocks certain proteins from carrying out their normal functions by sticking to them like Velcro. In this study scientists from the University of Rochester in New York found the blocking of a protein called "muscleblind" causes the characteristic hand stiffness. The toxic RNA accumulates as deposits which are visible in the cell's nucleus. The team used a synthetic molecule, called an antisense morpholino oligonucleotide, that mimics a segment of the genetic code to break up these deposits and re-establish cellular activity. It was specifically designed to bind to the toxic RNA and neutralise its harmful effects. When it was injected into the muscle cells of mice with myotonic dystrophy, the stuck proteins were released and resumed their normal function. The abnormal electrical (myotonic) activity went away. (C)BBC
The anti-impotence drug Viagra may help save people with muscular dystrophy from an early death, a study suggests. Researchers found the way the drug works to combat impotence may also help ward off heart failure in muscular dystrophy patients. Tests on mice with a version of the disease showed the drug helped keep their hearts working well. The Montreal Heart Institute study appears in Proceedings of the National Academy of Sciences. Muscular dystrophy is a genetic condition causing wasting of the muscles. The first signs of muscular weakness appear at roughly age five, leading to a progressive loss in the ability to walk by the age of 13. People with the condition are also at a higher risk of heart failure due to a weakening of the muscles which keep the organ pumping strongly. For this reason, many people with Duchenne muscular dystrophy - the most common form of the condition - die in early life, often in their 20s or 30s. The Montreal team found that Viagra - known technically as sildenafil - prevents the loss of a molecule, cGMP, which plays a key role in keeping blood vessels dilated. In the penis, this increases blood flow, and helps to combat impotence. But in the heart it helps to ensure the organ itself receives a proper supply of blood, and remains healthy and strong. With the heart in a strong condition, it is more able to withstand the impact of weakening muscle cells caused by muscular dystrophy. (C)BBC
By GINA KOLATA One of the great unanswered questions in physiology is why muscles get tired. The experience is universal, common to creatures that have muscles, but the answer has been elusive until now. Scientists at Columbia say they have not only come up with an answer, but have also devised, for mice, an experimental drug that can revive the animals and let them keep running long after they would normally flop down in exhaustion. For decades, muscle fatigue had been largely ignored or misunderstood. Leading physiology textbooks did not even try to offer a mechanism, said Dr. Andrew Marks, principal investigator of the new study. A popular theory, that muscles become tired because they release lactic acid, was discredited not long ago. In a report published Monday in an early online edition of Proceedings of the National Academy of Sciences, Dr. Marks says the problem is calcium flow inside muscle cells. Ordinarily, ebbs and flows of calcium in cells control muscle contractions. But when muscles grow tired, the investigators report, tiny channels in them start leaking calcium, and that weakens contractions. At the same time, the leaked calcium stimulates an enzyme that eats into muscle fibers, contributing to the muscle exhaustion. In recent years, says George Brooks of the University of California, Berkeley, muscle researchers have had more or less continuous discussions about why muscles fatigue. It was his work that largely discredited the lactic-acid hypothesis, but that left a void. Copyright 2008 The New York Times Company
By Fergus Walsh A gene therapy trial for the fatal disorder Duchenne muscular dystrophy (DMD) is about to begin in London. In a world first, a small group of patients will be injected with an experimental drug which it is hoped will extend their lives. DMD, which affects boys, is caused by a single faulty gene, and results in progressive muscle wasting. The injection contains a "molecular patch" targeting the faulty gene so that it should work again. At first, minute quantities of the drug will be used - to check it is safe. If it works the drug will effectively knit together the key damaged section of DNA, allowing it to begin producing a protein that keeps the muscles strong. The hope is it could slow, or even halt the progression of muscle wasting, and give some patients the chance of living into old age. Animal trials of the drug have proved highly successful. If it works in humans, patients would need regular infusions of the drug. Lead researcher Professor Francesco Muntoni, of Imperial College London, has high hopes. He said: "It will be truly life changing, and life extending for these people. "Maybe this will not be a complete cure, but it could definitely buy a lot of time for these children." Professor Muntoni describes the gene therapy as like a piece of molecular velcro which will form a temporary repair. (C)BBC
Vitamin shots may help protect multiple sclerosis patients from severe long-term disability, a study suggests. Currently, there is no effective treatment for the chronic progressive phase of MS, when serious disability is most likely to appear. Researchers cut the risk of nerve degeneration in mice with MS-type symptoms by giving them a form of vitamin B3 called nicotinamide. The Children's Hospital Boston study appears in the Journal of Neuroscience. MS, which affects about 85,000 people in the UK, is a disease of the central nervous system. It causes the break down of the myelin sheath, a fatty protein, which coats nerve fibres, disrupting the ability to conduct electrical impulses to and from the brain. Many patients develop a form of the disease called relapsing-remitting MS, in which bouts of illness are followed by complete or partial recovery. In this early phase anti-inflammatory drugs can help. But eventually patients can enter the chronic progressive phase, for which there is no good treatment. The Boston team worked on mice with an MS-like disease called experimental autoimmune encephalitis (EAE). They found that daily nicotinamide shots protected the animals' nerve cells from myelin loss, and stabilised the condition of those cells that had already been affected. The greater the dose of nicotinamide, the greater the protective effect. Rating disability on a scale of one to five, mice receiving the highest doses of nicotinamide scored between one and two, while animals who received no shots at all scored between three and four. (C)BBC
US scientists have found a way to reverse muscular dystrophy (MD) in mice, offering hope of a cure for humans with muscle-wasting diseases. The animals in the Nature Genetics study had myotonic dystrophy - the most common form of MD in adults. The therapy targets a particular kind of toxic molecule to "silence" its presence in the diseased muscle. The University of Virginia team showed the treatment fully restored heart and skeletal muscle function in mice. In myotonic dystrophy, like the other types of MD, faulty DNA is to blame for the abnormalities that occur. Myotonic dystrophy occurs because of a large expansion of DNA code, which most likely causes an accumulation of toxic messenger RNA molecules in cells. Messenger or mRNA is a copy of the information carried by a gene on the DNA. If the DNA code is faulty then the mRNA will be faulty too. These abnormalities lead to the progressive muscle weakness and wasting and heart problems seen in myotonic dystrophy. Dr Mani Mahadevan and his team reasoned that eliminating the toxic mRNA molecules might help reverse the disease. They created mice with faulty DNA that could be turned on and off by adding or removing an antibiotic to their drinking water. In the "on" phase the mice showed all the cardinal features of myotonic dystrophy. When the DNA was turned off, normal skeletal and cardiac muscle function was restored in many, but not all of the mice. (C)BBC
A new gene therapy technique that has shown promise in skin disease and hemophilia might one day be useful for treating muscular dystrophy, according to a new study by researchers at Stanford University School of Medicine. In the study, scheduled to be published online in the Proceedings of the National Academy of Sciences the week of Jan. 2, the researchers used gene therapy to introduce a healthy copy of the gene dystrophin into mice with a condition that mimics muscular dystrophy. The dystrophin gene is mutated and as a result produces a defective protein in the roughly 20,000 people in the United States with the most common form of the disease. Using gene therapy to treat muscular dystrophy isn't a new idea. Thomas Rando, MD, PhD, associate professor of neurology and neurological sciences, said that researchers have tried several different techniques with variable success. One hurdle is getting genes into muscle cells all over the body. Another is convincing those cells to permanently produce the therapeutic protein made by those genes. The gene therapy technique Rando and postdoctoral fellow Carmen Bertoni, PhD, used was developed by Michele Calos, PhD, associate professor of genetics. One of the main advantages of this method is that it could potentially provide a long-term fix for a variety of genetic diseases, including muscular dystrophy.
Young blood could help revive tired ageing muscles, researchers suggest. Old people's muscles are known not to heal in the same way young people's do, but a Stanford University team suggests it is old blood that is to blame. The study found special stem cells come to the rescue of damaged young muscles, but are not triggered in older ones. Writing in Nature, the team say tests on mice suggest something in young blood spurs the stem cells into action to repair the muscle damage. It had been recognised that old muscles had the capacity to repair themselves, but that - for some reason - they failed to do so. The Stanford researchers focussed on muscle stem cells, called satellite cells, that are spread throughout muscle tissue. In young mice and humans, the cells come to life if they are needed to repair damaged muscle. But the team found that they fail to come to the rescue of older muscle - even though they are still present. In their tests, the team surgically connected the circulatory systems of an old mouse with that of a young one, or to another old mouse. They then damaged muscle in the older mice. If old mice were connected to young ones, and therefore had 'young blood' flowing through their bodies, healed normally. However, when old mice were connected to other old mice, and were sharing old blood, they healed slowly. (C)BBC
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: 7313 - Posted: 05.07.2005
Early treatment with a drug can delay the onset and progression of heart failure in children with Duchenne muscular dystrophy, research suggests. DMD is an incurable genetic disease causing muscle wastage, which often leads to fatal cardiac problems. The study shows the drug, perindopril, can slow heart muscle degeneration - and thus ward off heart failure. The research by Paris's Cochin Hospital involved 57 children, says the Journal of the American College of Cardiology. Lead researcher Professor Denis Duboc said: "For the first time, we have shown that it is possible to slow progression in this rare degenerative disease. "In DMD, the heart muscles are affected and cardiac problems are fatal in around 40% of children." The five-year study focused on the effect on perindopril, a drug from a class known as ACE inhibitors, widely used to treat high blood pressure and heart failure. Some 57 children with DMD received either perindopril, or a dummy drug. Eight in the dummy group went on to develop signs of heart failure, and three died from the condition. In contrast, just one of the perindopril group showed signs of heart failure, and none died from the condition during the study. Professor Duboc said the results suggested early treatment with perindopril might also benefit other people genetically predisposed to heart failure. DMD, one of the most common forms of muscular dystrophy, is caused by a lack of a protein called dystrophin which helps keep the muscles intact. It strikes children at a young age, and affects almost exclusively boys who rarely survive beyond their early 30s. (C)BBC
A study on mice suggests that a type of stem cells found in blood vessels may someday be able to regenerate wasting muscle in muscular dystrophy (MD) patients. The authors caution that more research must be done before researchers consider applying these findings to humans. Nonetheless, their results provide a possible new direction for efforts that have met largely with frustration thus far. The study appears in the journal Science, published by AAAS, the science society. The research team, led by Giulio Cossu of the Stem Cell Research Institute, in Milan, and the University of Rome and the Institute of Cell Biology and Tissue Engineering, in Rome, has found that these stem cells can cross from the bloodstream, into muscle tissue. There, they seem to take on a new identity, helping to generate new muscle fibers in mice with MD-like symptoms. MD is a collection of disorders caused by genetic defects that lead to increasing muscle weakness over time. These disorders currently have no cure.
Scientists are encouraged by the early success of treatment which may eventually help patients with a form of muscular dystrophy. Duchenne muscular dystrophy is a wasting disease caused by mutations on a particular gene. It is the most common muscular dystrophy, affecting one in 3,500 children - most of whom die early in life as a result. The mutations on the gene stop it producing the chemical needed to protect muscle cells and prevent wasting. Some experts believe that it may be possible to alleviate the disease by replacing the gene entirely. However, a slightly different strategy has paid dividends for researchers at the Medical Research Council's Clinical Sciences Centre Instead of trying to insert an entirely new version of the gene - called the dystrophin gene - which is problematic simply because of its large size, scientists are trying to issue the body instructions to ignore the faulty bits. While this, if successful, does not completely correct the problem, it does mean that a body chemical is produced that is almost as effective as the normal version. The technique, called "anti-sense" therapy, might also be easier to get working in a drug than full-blown gene therapy. (C) BBC
Jane Elliott, BBC News Online Health Staff When Catherine Crossin started suffering from fever, aching and exhaustion she thought she just had a bad case of flu. She took to her bed and waited for the illness to pass. Medics agreed it was probably flu, but soon her condition deteriorated, leaving her paralysed and unable to move even her little finger. She was so ill she needed 11 weeks in hospital to recover. "I couldn't bear anyone to touch me, I was so sensitive. My skin felt as if it was on fire." Her body became badly swollen and she was unable to move her muscles. For a while everyone was in the dark about Mrs Crossin's disease and she had a barrage of tests. "I had always been so healthy. I had never had colds and now I could not do anything," she said. Then doctors found she had a very serious case of polymyositis. Myositis is a relatively uncommon condition, which only affects about five new cases a year for every million people, leaving their muscles badly inflamed. (C) BBC
The discovery of genes that control the development of muscles in the fruit fly could help unravel the secrets of a devasting human disease. Cachexia is a severe wasting disorder normally linked to advanced cancer, Aids and a variety of chronic infections. It causes not just the loss of fat, but also of bone and muscle, and happens regardless of the amount the patient manages to eat. The patient's metabolism speeds up, burning more calories. The condition further robs patients of the ability to fight the disease which triggered the cachexia. It is believed that chemicals called cytokines released by the body in response to the underlying illness are responsible for the wasting illness. (C) BBC
Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 3394 - Posted: 02.03.2003
NASA researchers are learning new things about the human brain by studying how astronauts regain their balance. Balancing is not as easy as it seems--just try to stand on one foot for a full minute, and you'll get a sense of the constant effort involved. It's one of those complex skills like reading that becomes so automatic with practice, we simply forget how tricky they were to learn. And, like reading, you might suppose it would take something extraordinary to make you forget. Indeed it does. Like traveling to space. Researchers have found that astronauts who return from a space voyage can still balance, but they find it far more difficult. That's because, explains NASA neuroscientist Bill Paloski, their brains are no longer sure how to interpret the information that comes from their senses.
Related chapters from BP7e: Chapter 9: Hearing, Vestibular Perception, Taste, and Smell; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 6: Hearing, Balance, Taste, and Smell; Chapter 5: The Sensorimotor System
Link ID: 3092 - Posted: 12.02.2002
by Dennis Meredith Steven Vogel was suffering sore muscles -- ironic for a biologist who had just published a widely praised book on the science and history of muscles, from flies to humans. Ensconced in his comfortable office, the sinewy, fit scientist-author of Prime Mover: A Natural History of Muscle (Norton, 2002) revealed that he had been persuaded to walk down the Eiffel Tower. Ever the scientist, Vogel precisely explained the basis of his discomfort. "You're exerting more force when you decelerate them when you accelerate, but the aerobic cost is so low you don't notice that you're doing much," said the James B. Duke Professor of Biology, wincing. "You don't notice it until afterwards." [Steven Vogel, a Duke biologist and author of Prime Mover: A Natural History of Muscle Photo: Les Todd/ Duke Photography] Indeed, the phenomenon of sore muscles is only one scientific morsel Vogel offers in a smorgasbord of topics covered in his book, including that facts that