Chapter 5. The Sensorimotor System
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Jasmin Fox-Skelly Scientists have found a way to beat back the hands of time and fight the ravages of old age, at least in mice. A new study finds that mice bred without a specific pain sensor, or receptor, live longer and are less likely to develop diseases such as diabetes in old age. What’s more, exposure to a molecule found in chili peppers and other spicy foods may confer the same benefits as losing this pain receptor—meaning that humans could potentially benefit, too. When you touch something hot or get a nasty paper cut, pain receptors in your skin are activated, causing neurons to relay a message to your brain: “Ouch!” Although pain protects your body from damage, it also causes harm. People who experience chronic pain, for example, are more likely to have shorter lifespans, but the reason for this has remained unclear. To investigate further, researchers from the University of California (UC), Berkeley, bred mice without a pain receptor called TRPV1. Found in the skin, nerves, and joints, it’s known to be activated by the spicy compound found in chili peppers, known as capsaicin. (When you feel like your mouth is burning after eating a jalapeño, that’s TRPV1 at work.) Surprisingly, the mice without TRPV1 lived on average 14% longer than their normal counterparts, the team reports today in Cell. (Meanwhile, calorie restriction—another popular way of lengthening mouse lifespans—can make them live up to 40% longer.) When the TRPV1-less mice got old, they still showed signs of fast, youthful metabolisms. Their bodies continued to quickly clear sugar from the blood—a trait called glucose tolerance that usually declines with age—and they burned more calories during exercise than regular elderly mice. © 2014 American Association for the Advancement of Science
Keyword: Pain & Touch
Link ID: 19652 - Posted: 05.23.2014
By MICHAEL BEHAR One morning in May 1998, Kevin Tracey converted a room in his lab at the Feinstein Institute for Medical Research in Manhasset, N.Y., into a makeshift operating theater and then prepped his patient — a rat — for surgery. A neurosurgeon, and also Feinstein Institute’s president, Tracey had spent more than a decade searching for a link between nerves and the immune system. His work led him to hypothesize that stimulating the vagus nerve with electricity would alleviate harmful inflammation. “The vagus nerve is behind the artery where you feel your pulse,” he told me recently, pressing his right index finger to his neck. The vagus nerve and its branches conduct nerve impulses — called action potentials — to every major organ. But communication between nerves and the immune system was considered impossible, according to the scientific consensus in 1998. Textbooks from the era taught, he said, “that the immune system was just cells floating around. Nerves don’t float anywhere. Nerves are fixed in tissues.” It would have been “inconceivable,” he added, to propose that nerves were directly interacting with immune cells. Nonetheless, Tracey was certain that an interface existed, and that his rat would prove it. After anesthetizing the animal, Tracey cut an incision in its neck, using a surgical microscope to find his way around his patient’s anatomy. With a hand-held nerve stimulator, he delivered several one-second electrical pulses to the rat’s exposed vagus nerve. He stitched the cut closed and gave the rat a bacterial toxin known to promote the production of tumor necrosis factor, or T.N.F., a protein that triggers inflammation in animals, including humans. “We let it sleep for an hour, then took blood tests,” he said. The bacterial toxin should have triggered rampant inflammation, but instead the production of tumor necrosis factor was blocked by 75 percent. “For me, it was a life-changing moment,” Tracey said. What he had demonstrated was that the nervous system was like a computer terminal through which you could deliver commands to stop a problem, like acute inflammation, before it starts, or repair a body after it gets sick. “All the information is coming and going as electrical signals,” Tracey said. For months, he’d been arguing with his staff, whose members considered this rat project of his harebrained. “Half of them were in the hallway betting against me,” Tracey said. © 2014 The New York Times Company
Link ID: 19649 - Posted: 05.23.2014
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
Four common chronic pain conditions share a genetic element, suggesting they could - at least in part - be inherited diseases, say UK researchers. The four include irritable bowel syndrome, musculoskeletal pain, pelvic pain and dry eye disease. The study of more than 8,000 sets of twins found the ailments were common in identical pairs sharing the same DNA. The King's College London team say the discovery could ultimately help with managing these debilitating diseases. While environmental factors probably still play a role in the four conditions, genes could account for as much as two-thirds of someone's chances of developing the disease, they believe. They told the journal Pain that more research is needed to pinpoint the precise genes involved. Chronic pain - pain which persists or recurs for months on end - is common and has many different causes, which can make it difficult to diagnose and treat. While the pain can be related to other medical conditions, it is thought to be caused by problems with the nervous system, sending pain signals to the brain despite no obvious tissue damage. Experts are keen to understand more about chronic pain to improve the quality of life of the millions of people who have to endure it. Some have suspected that some people may have a genetic predisposition to chronic pain since many sufferers share similar symptoms and often have more than one of the different types of chronic pain conditions. The team at King's College London decided to study identical and non-identical twins because these two groups provide an ideal comparison for investigating inherited genes - identical twins share the same DNA while non-identical twins do not. BBC © 2014
By JAMES GORMAN If an exercise wheel sits in a forest, will mice run on it? Every once in a while, science asks a simple question and gets a straightforward answer. In this case, yes, they will. And not only mice, but also rats, shrews, frogs and slugs. True, the frogs did not exactly run, and the slugs probably ended up on the wheel by accident, but the mice clearly enjoyed it. That, scientists said, means that wheel-running is not a neurotic behavior found only in caged mice. They like the wheel. Two researchers in the Netherlands did an experiment that it seems nobody had tried before. They placed exercise wheels outdoors in a yard garden and in an area of dunes, and monitored the wheels with motion detectors and automatic cameras. They were inspired by questions from animal welfare committees at universities about whether mice were really enjoying wheel-running, an activity used in all sorts of studies, or were instead like bears pacing in a cage, stressed and neurotic. Would they run on a wheel if they were free? Now there is no doubt. Mice came to the wheels like human beings to a health club holding a spring membership sale. They made the wheels spin. They hopped on, hopped off and hopped back on. “When I saw the first mice, I was extremely happy,” said Johanna H. Meijer at Leiden University Medical Center in the Netherlands. “I had to laugh about the results, but at the same time, I take it very seriously. It’s funny, and it’s important at the same time.” Dr. Meijer’s day job is as a “brain electrophysiologist” studying biological rhythms in mice. She relished the chance to get out of the laboratory and study wild animals, and in a way that no one else had. © 2014 The New York Times Company
Dr. Mark Saleh Bell's palsy is a neurological condition frequently seen in emergency rooms and medical offices. Symptoms consist of weakness involving all muscles on one side of the face. About 40,000 cases occur annually in the United States. Men and women are equally affected, and though it can occur at any age, people in their 40s are especially vulnerable. The facial weakness that occurs in Bell's palsy prevents the eye of the affected side from blinking properly and causes the mouth to droop. Because the eyelid doesn't close sufficiently, the eye can dry and become irritated. Bell's palsy symptoms progress fairly rapidly, with weakness usually occurring within three days. If the progression of weakness is more gradual and extends beyond a week, Bell's palsy may not be the problem, and other potential causes should be investigated. Those with certain medical conditions, such as diabetes or pregnancy, are at greater risk of developing Bell's palsy, and those who have had one episode have an 8 percent chance of recurrence. Bell's palsy is thought to occur when the seventh cranial (facial) nerve becomes inflamed. The nerve controls the muscles involved in facial expression and is responsible for other functions, including taste perception, eye tearing and salivation. The cause of the inflammation is unknown, although the herpes simplex virus and autoimmune inflammation are possible causes. © 2014 Hearst Communications, Inc.
Keyword: Movement Disorders
Link ID: 19637 - Posted: 05.20.2014
Katia Moskvitch The hundreds of suckers on an octopus’s eight arms leech reflexively to almost anything they come into contact with — but never grasp the animal itself, even though an octopus does not always know what its arms are doing. Today, researchers reveal that the animal’s skin produces a chemical that stops the octopus’s suckers from grabbing hold of its own body parts, and getting tangled up. “Octopus arms have a built-in mechanism that prevents the suckers from grabbing octopus skin,” says neuroscientist Guy Levy at the Hebrew University of Jerusalem, the lead author of the work, which appears today in Current Biology1. It is the first demonstration of a chemical self-recognition mechanism in motor control, and could help scientists to build better bio-inspired soft robots. To find out just how an octopus avoids latching onto itself, Levy and his colleagues cut off an octopus’s arm and subjected it to a series of tests. (The procedure is not considered traumatic, says Levy, because octopuses occasionally lose an arm in nature and behave normally while the limb regenerates.) The severed arms remained active for more than an hour after amputation, firmly grabbing almost any object, with three exceptions: the former host; any other live octopus; and other amputated arms. “But when we peeled the skin off an amputated arm and submitted it to another amputated arm, we were surprised to see that it grabbed the skinned arm as any other item,” says co-author Nir Nesher, also a neuroscientist at the Hebrew University. © 2014 Nature Publishing Group,
Link ID: 19623 - Posted: 05.15.2014
By KATIE THOMAS Almost overnight, a powerful new painkiller has become a $100 million business and a hot Wall Street story. But nearly as quickly, questions are emerging about how the drug is being sold, and to whom. The drug, Subsys, is a form of fentanyl, a narcotic that is often used when painkillers like morphine fail to provide relief. The product was approved in 2012 for a relatively small number of people — cancer patients — but has since become an outsize moneymaker for the obscure company that makes it, Insys Therapeutics. In the last year, the company’s sales have soared and its share price has jumped nearly 270 percent. Behind that business success is an unusual marketing machine that may have pushed Subsys far beyond the use envisioned by the Food and Drug Administration. The F.D.A. approved Subsys only for cancer patients who are already using round-the-clock painkillers, and warned that it should be prescribed only by oncologists and pain specialists. But just 1 percent of prescriptions are written by oncologists, according to data provided by Symphony Health, which analyzes drug trends. About half of the prescriptions were written by pain specialists, and a wide range of doctors prescribed the rest, including general practice physicians, neurologists and even dentists and podiatrists. Interviews with several former Insys sales representatives suggest the company, based in Chandler, Ariz., has aggressively marketed the painkiller, including to physicians who did not treat many cancer patients and by paying its sales force higher commissions for selling higher doses of the drug. Under F.D.A. rules, manufacturers may market prescription drugs only for approved uses. But doctors may prescribe drugs as they see fit. Over the last decade, pharmaceutical companies have paid billions of dollars to settle claims that they encouraged doctors to use drugs for nonapproved treatments, or so-called off-label uses, to increase sales and profits. © 2014 The New York Times Compan
By Suzanne Allard Levingston, Playing with bubble wrap is a silly activity that delights most preschoolers. But for one 21 / 2-year-old from Silver Spring, loud noises such as the pop of plastic bubbles were so upsetting that he would cover his ears and run away. Some days the sound of a vacuum cleaner would make him scream. The child so persistently avoided activities with too much noise and motion that his preschool’s administrators asked to meet with his family — and soon an assessment led to a diagnosis of sensory processing disorder, or SPD. SPD is a clinical label for people who have abnormal behavioral responses to sensory input such as sound and touch. Some children with SPD seem oversensitive to ordinary stimuli such as a shirt label’s scratching their skin. Others can be underresponsive — seemingly unaffected by the prick of a needle. A third group have motor problems that make holding a pencil or riding a bike seem impossible. Whatever the difficulty, such kids are often described as “out-of-sync,” a term popularized by Carol Stock Kranowitz’s 1998 book “The Out-of-Sync Child,” which has sold nearly 700,000 copies. As many as 16 percent of school-age kids in the United States may face sensory processing challenges. And yet there’s debate over whether these challenges constitute a discrete medical disorder. Some experts contend that SPD may be merely a symptom of some other ailment — autism, attention-deficit hyperactivity disorder, anxiety disorder or fragile X syndrome, for example — while others insist it is a separate condition that should be labeled a disorder when it interferes with daily life. The debate over how to classify SPD is not merely matter of semantics. Such discussions can affect research funding and can guide whether insurers will reimburse therapy costs. © 1996-2014 The Washington Post
By BARRY MEIER Four years and a lifetime ago, a new war began for Sgt. Shane Savage. On Sept. 3, 2010, the armored truck he was commanding near Kandahar, Afghanistan, was blown apart by a roadside bomb. His head hit the ceiling so hard that his helmet cracked. His left foot was pinned against the dashboard, crushing 24 bones. Sergeant Savage came home eight days later, at age 27, with the signature injuries of the conflicts in Iraq and Afghanistan: severe concussion, post-traumatic stress and chronic pain. Doctors at Fort Hood in Killeen, Tex., did what doctors across the nation do for millions of ordinary Americans: They prescribed powerful narcotic painkillers. What followed was a familiar arc of abuse and dependence and despair. At one point, Sergeant Savage was so desperate that he went into the bathroom and began swallowing narcotic tablets. He would have died had his wife, Hilary, not burst through the door. Today Sergeant Savage has survived, even prevailed, through grit, his family and a radical experiment in managing pain without narcotics. When off-duty, he pulls on cowboy boots and plays with his children, does charity work and, as part of a therapy program, rides horses. The only medication he takes for pain is Celebrex, a non-narcotic drug. “You have to find alternative ways to get out and do stuff to stay active, to get your brain off the thought process of ‘I’m in pain,’ ” said Sergeant Savage, whose ears push out from under a Texas A&M baseball cap. The story of Sergeant Savage illuminates an effort by experts inside and outside the military to change how chronic, or long-term, pain is treated. By some estimates, tens of millions of Americans suffer from chronic pain, and the use of opioids — drugs like hydrocodone, methadone and oxycodone (the active ingredient in painkillers like OxyContin) — to treat such conditions has soared over the last decade. © 2014 The New York Times Company
Jessica Morrison Interference from electronics and AM radio signals can disrupt the internal magnetic compasses of migratory birds, researchers report today in Nature1. The work raises the possibility that cities have significant effects on bird migration patterns. Decades of experiments have shown that migratory birds can orient themselves on migration paths using internal compasses guided by Earth's magnetic field. But until now, there has been little evidence that electromagnetic radiation created by humans affects the process. Like most biologists studying magnetoreception, report co-author Henrik Mouritsen used to work at rural field sites far from cities teeming with electromagnetic noise. But in 2002, he moved to the University of Oldenburg, in a German city of around 160,000 people. As part of work to identify the part of the brain in which compass information is processed, he kept migratory European robins (Erithacus rubecula) inside wooden huts — a standard procedure that allows researchers to investigate magnetic navigation while being sure that the birds are not getting cues from the Sun or stars. But he found that on the city campus, the birds could not orient themselves in their proper migratory direction. “I tried all kinds of stuff to make it work, and I couldn’t make it work,” Mouritsen says, “until one day we screened the wooden hut with aluminium.” Mouritsen and his colleagues covered the huts with aluminium plates and electrically grounded them to cut out electromagnetic noise in frequencies ranging from 50 kilohertz to 5 megahertz — which includes the range used for AM radio transmissions. The shielding reduced the intensity of the noise by about two orders of magnitude. Under those conditions, the birds were able to orient themselves. © 2014 Nature Publishing Group,
Keyword: Animal Migration
Link ID: 19590 - Posted: 05.08.2014
by Susan Milius Sometimes called the unicorn of the sea, the male narwhal’s tusk is actually a tooth, and it grows directly through the whale’s upper lip instead of pushing the lip aside. It’s an exuberantly large version of a canine tooth that grows in a spiral; the only tooth known to do so. Otherwise narwhals are practically toothless, with only vestigial stubs that stop growing during development and rarely emerge into the mouth. This extreme anatomy has captivated dentist Martin Nweeia, who practices in Connecticut and teaches at Harvard University. For more than a decade, he has pioneered ways to study these difficult-to-reach Arctic whales, and he and his colleagues now describe in the April Anatomical Record that narwhals can detect changes in water salinity using only their tusks. The animals “don’t have a good sense of humor,” though, about being temporarily restrained for the testing, Nweeia says. © Society for Science & the Public 2000 - 2013
Keyword: Pain & Touch
Link ID: 19571 - Posted: 05.05.2014
by Lisa Grossman Hasta la vista, nerve damage. Experiments with bullfrog nerves show that a Terminator-style liquid metal alloy could one day be placed in the body to help severed nerves reconnect. The alloy would stay in place until the nerve has healed, before being slurped back out with a syringe. The peripheral nervous system consists of nerves that carry electrical signals from the brain to the rest of the body. Because they aren't protected by the spine or the skull, peripheral nerves are more vulnerable to injuries than those in the central nervous system. Severed nerves can reconnect if treated quickly enough, but at a rate of just 1 millimetre per day. Also, existing methodsMovie Camera for grafting nerve ends back together have serious shortcomings. For instance, most existing scaffolds for grafts must ultimately be removed, requiring risky follow-up surgery. Even more worrisome, if the nerves don't pass signals to muscles during the healing process, the muscles can atrophy to the point where they never fully recover. Liu and his colleagues wondered if liquid metal could act as a backup system for damaged nerves, helping signals pass through a graft while the nerve healed. They used an alloy of gallium, indium and selenium, which is a very good electrical conductor. The alloy is liquid at room temperature, allowing it to be removed with a syringe when it's no longer needed. © Copyright Reed Business Information Ltd.
By JAN HOFFMAN How well can computers interact with humans? Certainly computers play a mean game of chess, which requires strategy and logic, and “Jeopardy!,” in which they must process language to understand the clues read by Alex Trebek (and buzz in with the correct question). But in recent years, scientists have striven for an even more complex goal: programming computers to read human facial expressions. We all know what it’s like to experience pain that makes our faces twist into a grimace. But can you tell if someone else’s face of pain is real or feigned? The practical applications could be profound. Computers could supplement or even replace lie detectors. They could be installed at border crossings and airport security checks. They could serve as diagnostic aids for doctors. Researchers at the University of California, San Diego, have written software that not only detected whether a person’s face revealed genuine or faked pain, but did so far more accurately than human observers. While other scientists have already refined a computer’s ability to identify nuances of smiles and grimaces, this may be the first time a computer has triumphed over humans at reading their own species. “A particular success like this has been elusive,” said Matthew A. Turk, a professor of computer science at the University of California, Santa Barbara. “It’s one of several recent examples of how the field is now producing useful technologies rather than research that only stays in the lab. We’re affecting the real world.” People generally excel at using nonverbal cues, including facial expressions, to deceive others (hence the poker face). They are good at mimicking pain, instinctively knowing how to contort their features to convey physical discomfort. © 2014 The New York Times Company
By Julie Steenhuysen CHICAGO (Reuters) - International teams of researchers using advanced gene sequencing technology have uncovered a single genetic mutation responsible for a rare brain disorder that may have stricken families in Turkey for some 400 years. The discovery of this genetic disorder, reported in two papers in the journal Cell, demonstrates the growing power of new tools to uncover the causes of diseases that previously stumped doctors. Besides bringing relief to affected families, who can now go through prenatal genetic testing in order to have children without the disorder, the discovery helps lend insight into more common neurodegenerative disorders, such as ALS, also known as Lou Gehrig's disease, the researchers said. The reports come from two independent teams of scientists, one led by researchers at Baylor College of Medicine and the Austrian Academy of Sciences, and the other by Yale University, the University of California, San Diego, and the Academic Medical Center in the Netherlands. Both focused on families in Eastern Turkey where marriage between close relatives, such as first cousins, is common. Geneticists call these consanguineous marriages. In this population, the researchers focused specifically on families whose children had unexplained neurological disorders that likely resulted from genetic defects. Both teams identified a new neurological disorder arising from a single genetic variant called CLP1. Children born with this disorder inherit two defective copies of this gene, which plays a critical role in the health of nerve cells. Babies with the disorder have small and malformed brains, they develop progressive muscle weakness, they do not speak and they are increasingly prone to seizures.
It takes a lot to deter a male from wanting sex. A new study has found that male mice keep trying to copulate even when they are in pain, whereas females engage in less sex. But when given drugs that target pleasure centers in the human brain, the females again became interested. The findings could shed light on the nature of libido across various animal species. To assess how pain influences sexual desire, researchers first identified pairs of mice that wanted to have sex. “What we found early on was not all mice will mate with each other,” says clinical psychologist Melissa Farmer, who led the study while earning her Ph.D. at McGill University in Montreal, Canada. The team set up the rodents on a series of “dates,” during which a male and female were paired together for 30 minutes. Couples that copulated for most of the session were deemed compatible and moved into a cage with separate rooms. A small doorway allowed a female mouse to freely cross over from her chamber, but the male—which is larger—could not. The scientists then induced pain in males or females by applying a small dose of inflammatory compounds to the cheek, tail, foot, or genitals. The sensation would primarily be soreness, like a bad sunburn, says Farmer, who now works at Northwestern University’s Feinberg School of Medicine in Chicago, Illinois. Female mice that were in pain, whether genital or nongenital, spent 50% less time with their male partners, implying a decrease in sexual motivation. Even when they did visit their paramours, females wouldn’t allow males to mount them with the same frequency, the team reports online today in The Journal of Neuroscience. © 2014 American Association for the Advancement of Science.
Chelsea Wald The sailfish’s sword-like bill looks as if it was made to slash at prey. But a study published today in Proceedings of the Royal Society B1 reveals that the bill is actually a multifunctional killing tool, enabling the fish to perform delicate, as well as swashbuckling, manoeuvres. By following throngs of predatory birds off the coast of Cancún, Mexico, the study’s authors were able to track Atlantic sailfish (Istiophorus albicans) hunting sardines, says co-author Alexander Wilson, a behavioural ecologist now at Carleton University in Ottawa, Canada. He and his colleagues made high-speed, high-resolution films in the open ocean over six days in 2012. Sailfish hunt in groups, taking turns to approach the ball of schooling fish. Their bodies darken and sometimes flash stripes and spots, perhaps to confuse the prey, or to signal to each other. “It’s a very orderly process,” Wilson says. “They don’t want to risk breaking their bills.” Although sailfish are among the fastest creatures in the ocean — they have been documented to swim at more than 110 kilometres per hour, or 60 knots — the new research shows that their strategy is to approach their prey slowly from behind and gently insert their bills into the school, without eliciting an evasive manoeuvre from the sardines. Then, by whipping their heads in powerful, sudden jerks, they can slash their bills left and right, with their upright fins providing stability. In fact, their bill tips slash with about the same acceleration as the tip of a swinging baseball bat, even in the water, says co-author Paolo Domenici, an environmental physiologist at the Institute for the Marine and Coastal Environment of Italy's National Research Council in Torregrande, on the island of Sardinia. The result is a scene of fishy carnage, as the surrounding water fills with iridescent fragments of sardine skin. © 2014 Nature Publishing Group,
Keyword: Pain & Touch
Link ID: 19523 - Posted: 04.23.2014
Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair, according to a study funded by the National Institutes of Health. In research conducted with rats, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration. “The finding gives insight into why chronic heavy drinking often saps muscle strength and it could also lead to new targets for medication development,” said Dr. George Koob, director of the National Institute on Alcohol Abuse and Alcoholism, the NIH institute that funded the study. The study is available online in the April issue of the Journal of Cell Biology. It was led by Dr. Gyorgy Hajnoczky, M.D., Ph.D., director of Thomas Jefferson University’s MitoCare Center, Philadelphia, and professor in the Department of Pathology, Anatomy and Cell Biology. Mitochondria are cellular structures that generate most of the energy needed by cells. Skeletal muscle constantly relies on mitochondria for power. When mitochondria become damaged, they can repair themselves through a process called mitochondrial fusion — joining with other mitochondria and exchanging material such as DNA. Although well known in many other tissues, the current study is the first to show that mitochondria in skeletal muscle are capable of undergoing fusion as a repair mechanism. It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle.
By Bill Briggs A Vietnam veteran swoops his hand through a row of baby vegetables, caressing the peppers on down to the kale. The plants are aligned in tidy, military order atop his backyard fence. He could spend hours describing his first garden. But he cannot utter a word. He can’t even eat his eventual harvest. So, Bob Hoaglan, 71, simply stands and grins at the spouts behind his Oxnard, Calif., home. Then, he grabs his primary communication tool, an LCD tablet, scribbling a stylus across the screen. He displays his words with a silent chuckle: “I don’t have a green thumb.” With a button click, he erases that sentence before composing another. His daily aim is to throw his body and brain into new pursuits. The crops — fresh life for a man facing mortality — help shove his disease to the back of his mind. He admits, though, he can’t keep it there: “I try,” he writes, “Sometimes it creeps up on me.” As he shows that message, the smile vanishes. Hoaglan was diagnosed with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, nearly a year ago. Inside a malady that offers no cure or explanation, he embodies two intriguing clues that, a top researcher says, may whisper answers: Hoaglan served in the military, and he is a nice man. U.S. veterans carry a nearly 60 percent greater risk of contracting ALS than civilians, according to a white paper published in 2013 by the ALS Association, citing Harvard University research that tracked ex-service members back to 1910.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 19509 - Posted: 04.19.2014
Scientists may have discovered how the most common genetic cause of Parkinson’s disease destroys brain cells and devastates many patients worldwide. The study was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS); the results may help scientists develop new therapies. The investigators found that mutations in a gene called leucine-rich repeat kinase 2 (LRRK2; pronounced “lark two” or “lurk two”) may increase the rate at which LRRK2 tags ribosomal proteins, which are key components of protein-making machinery inside cells. This could cause the machinery to manufacture too many proteins, leading to cell death. “For nearly a decade, scientists have been trying to figure out how mutations in LRRK2 cause Parkinson’s disease,” said Margaret Sutherland, Ph.D., a program director at NINDS. “This study represents a clear link between LRRK2 and a pathogenic mechanism linked to Parkinson’s disease.” Affecting more than half a million people in the United States, Parkinson’s disease is a degenerative disorder that attacks nerve cells in many parts of the nervous system, most notably in a brain region called the substantia nigra, which releases dopamine, a chemical messenger important for movement. Initially, Parkinson’s disease causes uncontrolled movements; including trembling of the hands, arms, or legs. As the disease gradually worsens, patients lose ability to walk, talk or complete simple tasks.
Link ID: 19477 - Posted: 04.12.2014