Most Recent Links
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
|By Jenni Laidman During the second and third trimester of pregnancy, the outer layer of the embryo's brain, the cortex, assembles itself into six distinct layers. But in autism, according to new research, this organization goes awry—marring parts of the brain associated with the abilities often impaired in the disorder, such as social skills and language development. Eric Courchesne, director of the Autism Center of Excellence at the University of California, San Diego, and his colleagues uncovered this developmental misstep in a small study that compared 11 brains of children with autism who died at ages two through 15 with 11 brains of kids who died without the diagnosis. The study employed a sophisticated genetic technique that looked for signatures of the activity of 25 genes in brain slices taken from the front of the brain—an area called the prefrontal cortex—as well as from the occipital cortex at the back of the brain and the temporal cortex near the temple. The researchers found disorganized patches, roughly a quarter of an inch across, in which gene expression indicated cells were not where they were supposed to be, amid the folds of tissue in the prefrontal cortex in 10 of 11 brains from children with autism. That part of the brain is associated with higher-order communication and social interactions. The team also found messy patches in the temporal cortices of autistic brains but no disorder at the back of the brain, which also matches typical symptom profiles. The patches appeared at seemingly random locations within the frontal and temporal cortices, which may help explain why symptoms can differ dramatically among individuals, says Rich Stoner, then at U.C. San Diego and the first author of the study, which appeared in the New England Journal of Medicine. © 2014 Scientific American
By JOSHUA A. KRISCH An old stucco house stands atop a grassy hill overlooking the Long Island Sound. Less than a mile down the road, the renowned Cold Spring Harbor Laboratory bustles with more than 600 researchers and technicians, regularly producing breakthroughs in genetics, cancer and neuroscience. But that old house, now a private residence on the outskirts of town, once held a facility whose very name evokes dark memories: the Eugenics Record Office. In its heyday, the office was the premier scientific enterprise at Cold Spring Harbor. There, bigoted scientists applied rudimentary genetics to singling out supposedly superior races and degrading minorities. By the mid-1920s, the office had become the center of the eugenics movement in America. Today, all that remains of it are files and photographs — reams of discredited research that once shaped anti-immigration laws, spurred forced-sterilization campaigns and barred refugees from entering Ellis Island. Now, historians and artists at New York University are bringing the eugenics office back into the public eye. “Haunted Files: The Eugenics Record Office,” a new exhibit at the university’s Asian/Pacific/American Institute, transports visitors to 1924, the height of the eugenics movement in the United States. Inside a dimly lit room, the sounds of an old typewriter click and clack, a teakettle whistles and papers shuffle. The office’s original file cabinets loom over reproduced desks and period knickknacks. Creaky cabinets slide open, and visitors are encouraged to thumb through copies of pseudoscientific papers. © 2014 The New York Times Company
Keyword: Genes & Behavior
Link ID: 20204 - Posted: 10.14.2014
By GINA KOLATA For the first time, and to the astonishment of many of their colleagues, researchers created what they call Alzheimer’s in a Dish — a petri dish with human brain cells that develop the telltale structures of Alzheimer’s disease. In doing so, they resolved a longstanding problem of how to study Alzheimer’s and search for drugs to treat it; the best they had until now were mice that developed an imperfect form of the disease. The key to their success, said the lead researcher, Rudolph E. Tanzi of Massachusetts General Hospital in Boston, was a suggestion by his colleague Doo Yeon Kim to grow human brain cells in a gel, where they formed networks as in an actual brain. They gave the neurons genes for Alzheimer’s disease. Within weeks they saw the hard Brillo-like clumps known as plaques and then the twisted spaghetti-like coils known as tangles — the defining features of Alzheimer’s disease. The work, which also offers strong support for an old idea about how the disease progresses, was published in Nature on Sunday. Leading researchers said it should have a big effect. “It is a giant step forward for the field,” said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher at Duke University. “It could dramatically accelerate testing of new drug candidates.” Of course, a petri dish is not a brain, and the petri dish system lacks certain crucial components, like immune system cells, that appear to contribute to the devastation once Alzheimer’s gets started. But it allows researchers to quickly, cheaply and easily test drugs that might stop the process in the first place. The crucial step, of course, will be to see if drugs that work in this system stop Alzheimer’s in patients. © 2014 The New York Times Company
Link ID: 20203 - Posted: 10.13.2014
Daniel Cressey Mirrors are often used to elicit aggression in animal behavioural studies, with the assumption being that creatures unable to recognize themselves will react as if encountering a rival. But research suggests that such work may simply reflect what scientists expect to see, and not actual aggression. For most people, looking in a mirror does not trigger a bout of snarling hostility at the face staring back. But many animals do seem to react aggressively to their mirror image, and for years mirrors have been used to trigger such responses for behavioural research on species ranging from birds to fish. “There’s been a very long history of using a mirror as it’s just so handy,” says Robert Elwood, an animal-behaviour researcher at Queen’s University in Belfast, UK. Using a mirror radically simplifies aggression experiments, cutting down the number of animals required and providing the animal being observed with an ‘opponent’ perfectly matched in terms of size and weight. But in a study just published in Animal Behaviour1, Elwood and his team add to evidence that many mirror studies are flawed. The researchers looked at how convict cichlid fish (Amatitlania nigrofasciata) reacted both to mirrors and to real fish of their own species. This species prefers to display their right side in aggression displays, which means that they end up alongside each other in a head-to-tail configuration. It is impossible for a fish to achieve this with their own reflection, but Elwood reasoned that fish faced with a mirror would attempt it, and flip from side to side as they tried to present an aggressive display. On the other hand, if the reflection did not trigger an aggressive reaction, the fish would not display such behaviour as much or as frequently. © 2014 Nature Publishing Group,
By David Leonhardt and Amanda Cox Like so many other parts of health care, childbirth has become a more medically intense experience over the last two decades. The use of drugs to induce labor has become far more common, as have cesarean sections. Today, about half of all births in this country are hastened either by drugs or surgery, double the share in 1990. Crucial to the change has been a widely held belief that once fetuses pass a certain set of thresholds — often 39 weeks of gestation and five and a half pounds in weight — they’re as healthy as they can get. More time in the womb doesn’t do them much good, according to this thinking. For parents and doctors, meanwhile, scheduling a birth, rather than waiting for its random arrival, is clearly more convenient. But a huge new set of data, based on every child born in Florida over an 11-year span, is calling into question some of the most basic assumptions of our medicalized approach to childbirth. The results also play into a larger issue: the growing sense among many doctors and other experts that Americans would actually be healthier if our health care system were sometimes less aggressive. The new data suggest that the thresholds to maximize a child’s health seem to be higher, which means that many fetuses might benefit by staying longer in the womb, where they typically add at least a quarter-pound per week. Seven-pound babies appear to be healthier than six-pound babies — and to fare better in school as they age. The same goes for eight-pound babies compared with seven-pound babies, and nine-pound babies compared with eight-pound babies. Weight, of course, may partly be an indicator of broader fetal health, but it seems to be a meaningful one: The chunkier the baby, the better it does on average, all the way up to almost 10 pounds. “Birth weight matters, and it matters for everyone,” says David N. Figlio, a Northwestern University professor and co-author of the study, which will soon be published in the American Economic Review, one of the field’s top journals. © 2014 The New York Times Company
By MOISES VELASQUEZ-MANOFF WHEN Andre H. Lagrange, a neurologist at Vanderbilt University in Nashville, saw the ominous white spots on the patient’s brain scan, he considered infection or lymphoma, a type of cancer. But tests ruled out both. Meanwhile, anti-epilepsy drugs failed to halt the man’s seizures. Stumped, Dr. Lagrange turned to something the mother of the 30-year-old man kept repeating. The fits coincided, she insisted, with spells of constipation and diarrhea. That, along with an odd rash, prompted Dr. Lagrange to think beyond the brain. Antibody tests, followed by an intestinal biopsy, indicated celiac disease, an autoimmune disorder of the gut triggered by the gluten proteins in wheat and other grains. Once on a gluten-free diet, the man’s seizures stopped; those brain lesions gradually disappeared. He made a “nearly complete recovery,” Dr. Lagrange told me. I began encountering case descriptions like this some years ago as I researched autoimmune disease. The first few seemed like random noise in an already nebulous field. But as I amassed more — describing seizures, hallucinations, psychotic breaks and even, in one published case, what looked like regressive autism, all ultimately associated with celiac disease — they began to seem less like anomalies, and more like a frontier in celiac research. They tended to follow a similar plot. What looked like neurological or psychiatric symptoms appeared suddenly. The physician ran through a diagnostic checklist without success. Drugs directed at the brain failed. Some clue suggestive of celiac disease was observed. The diagnosis was made. And the patient recovered on a gluten-free diet. The cases highlighted, in an unusually concrete fashion, the so-called gut-brain axis. The supposed link between the intestinal tract and the central nervous system is much discussed in science journals, often in the context of the microbial community inhabiting the gut. But it’s unclear how, really, we can leverage the link to improve health. © 2014 The New York Times Company
Link ID: 20200 - Posted: 10.13.2014
Ann Robinson Neuroscience research got a huge boost last week with news of Professor John O’Keefe’s Nobel prize for work on the “brain’s internal GPS system”. It is an exciting new part of the giant jigsaw puzzle of our brain and how it functions. But how does cutting-edge neuroscience research translate into practical advice about how to pass exams, remember names, tot up household bills and find where the hell you left the car in a crowded car park? O’Keefe’s prize was awarded jointly with Swedish husband and wife team Edvard and May-Britt Moser for their discovery of “place and grid cells” that allow rats to chart where they are. When rats run through a new environment, these cells show increased activity. The same activity happens much faster while the rats are asleep, as they replay the new route. We already knew that the part of the brain known as the hippocampus was involved in spatial awareness in birds and mammals, and this latest work on place cells sheds more light on how we know where we are and where we’re going. In 2000, researchers at University College London led by Dr Eleanor Maguire showed that London taxi drivers develop a pumped-up hippocampus after years of doing the knowledge and navigating the backstreets of the city. MRI scans showed that cabbies start off with bigger hippocampuses than average, and that the area gets bigger the longer they do the job. As driver David Cohen said at the time to BBC News: “I never noticed part of my brain growing – it makes you wonder what happened to the rest of it!” © 2014 Guardian News and Media Limited
By Meredith Levine, Word went round Janice Mackay's quiet neighbourhood that she was hitting the bottle hard. She'd been seen more than once weaving along the sidewalk in front of her suburban home in Pickering, just outside Toronto, in a sad, drunken stagger. But Mackay wasn't drunk. As it turned out, her inner ear, the body's balance centre, had been destroyed by medication when she was hospitalized for over a month back in May 2005. At the time, Mackay was diagnosed with a life-threatening infection in one of her ovaries, and so was put on a cocktail of medication, including an IV drip of gentamicin, a well-known, inexpensive antibiotic that is one of the few that hasn't fallen prey to antibiotic-resistant bacteria. A few weeks later, the infection was almost gone when Mackay, still hospitalized, suddenly developed the bed spins and vomiting. Her medical team told her she'd been laying down too long and gave her Gravol, but the symptoms didn't go away. In a follow-up appointment after her discharge, Mackay was told that the dizziness was a side effect of the gentamicin, and that she would probably have to get used to it. But she didn't discover the extent of the damage until later when neurotologist Dr. John Rutka assessed her condition and concluded that the gentamicin had essentially destroyed her vestibular system, the body's motion detector, located deep within the inner ear. © CBC 2014
Link ID: 20198 - Posted: 10.13.2014
By CATHERINE SAINT LOUIS Many cases of so-called crib death, about one in eight, occur among infants who have been placed on sofas, researchers reported on Monday. Dr. Jeffrey Colvin, a pediatrician at Children’s Mercy Hospital in Kansas City, Mo., and his colleagues analyzed data on 7,934 sudden infant deaths in 24 states, comparing those that occurred on sofas with those in cribs, bassinets or beds. Previous research had shown that couches were particularly hazardous for infants. The new analysis, published in the journal Pediatrics, tried to identify factors significant in these deaths. “It’s not only one risk that’s higher relative to other sleep environments,” said Barbara Ostfeld, a professor of pediatrics at Rutgers Robert Wood Johnson Medical School who was not involved in the new study. “It’s multiple risks.” Nearly three-quarters of the deaths occurred among infants age 3 months or younger, the researchers found. Pediatricians have long advised putting infants to sleep only on their backs, alone and on a firm, flat surface without a pillow. The new study found parents were more likely to lay their infants face down on a sofa than, for instance, face down in a crib. There’s a “fallacy that if I’m awake or watching, SIDS won’t happen,” Dr. Colvin said, referring to sudden infant death syndrome. © 2014 The New York Times Company
By MICHAEL S. A. GRAZIANO OF the three most fundamental scientific questions about the human condition, two have been answered. First, what is our relationship to the rest of the universe? Copernicus answered that one. We’re not at the center. We’re a speck in a large place. Second, what is our relationship to the diversity of life? Darwin answered that one. Biologically speaking, we’re not a special act of creation. We’re a twig on the tree of evolution. Third, what is the relationship between our minds and the physical world? Here, we don’t have a settled answer. We know something about the body and brain, but what about the subjective life inside? Consider that a computer, if hooked up to a camera, can process information about the wavelength of light and determine that grass is green. But we humans also experience the greenness. We have an awareness of information we process. What is this mysterious aspect of ourselves? Many theories have been proposed, but none has passed scientific muster. I believe a major change in our perspective on consciousness may be necessary, a shift from a credulous and egocentric viewpoint to a skeptical and slightly disconcerting one: namely, that we don’t actually have inner feelings in the way most of us think we do. Imagine a group of scholars in the early 17th century, debating the process that purifies white light and rids it of all colors. They’ll never arrive at a scientific answer. Why? Because despite appearances, white is not pure. It’s a mixture of colors of the visible spectrum, as Newton later discovered. The scholars are working with a faulty assumption that comes courtesy of the brain’s visual system. The scientific truth about white (i.e., that it is not pure) differs from how the brain reconstructs it. © 2014 The New York Times Company
Link ID: 20196 - Posted: 10.11.2014
By Melissa Hogenboom Science reporter, BBC News A small group of neurons that respond to the hormone oxytocin are key to controlling sexual behaviour in mice, a team has discovered. The researchers switched off these cells which meant they were no longer receptive to oxytocin. This "love hormone" is already known to be important for many intimate social situations. Without it, female mice were no more attracted to a mate than to a block of Lego, the team report in journal Cell. These neurons are situated in the prefrontal cortex, an area of the brain important for personality, learning and social behaviour. Both when the hormone was withheld and when the cells were silenced, the females lost interest in mating during oestrous, which is when female mice are sexually active. At other times in their cycle they responded to the males with normal social behaviour. The results were "pretty fascinating because it was a small population of cells that had such a specific effect", said co-author of the work Nathaniel Heintz of the Rockefeller University in New York. "This internal hormone gets regulated in many different contexts; in this particular context, it works through the prefrontal cortex to help modulate social and sexual behaviour in female mice. "It doesn't mean it's uniquely responsible because the hormone acts in several important places in the brain but it does show that this particular cell type is required for this aspect of female social behaviour," Dr Heintz told BBC News. To silence the neurons, the team used toxins that block the ability of the cells to transmit signals to other neurons - technology that has recently revolutionised the ability to study small populations of neurons. BBC © 2014
by Mallory Locklear Do you have an annoying friend who loves bungee jumping or hang-gliding, and is always blathering on about how it never scares them? Rather than being a macho front, their bravado may have a biological basis. Research from Stony Brook University in New York shows that not all risk-takers are cut from the same cloth. Some actually seem to feel no fear – or at least their bodies and brains don't respond to danger in the usual way. The study is the first to attempt to tease apart the differences in the risk-taking population. In order to ensure every participant was a card-carrying risk-taker, the team led by Lilianne Mujica-Parodi, recruited 30 first-time skydivers. "Most studies on sensation-seeking compare people who take risks and people who don't. We were interested in something more subtle – those who take risks adaptively and those who do so maladaptively." In other words, do all risk-takers process potential danger in the same way or do some ignore the risks more than others? To find out, the researchers got their participants to complete several personality questionnaires, including one that asked them to rank how well statements such as, "The greater the risk the more fun the activity," described them. Next, the team used fMRI imaging to observe whether the participants' corticolimbic brain circuit – which is involved in risk assessment - was well-regulated. A well-regulated circuit is one that reacts to a threat and then returns to a normal state afterwards. © Copyright Reed Business Information Ltd
By Carl T. Hall Even Clayton Kershaw, the Los Angeles Dodgers’ pitching ace, makes mistakes now and then. And although very few of his mistakes seemed to do Giants hitters much good this season, a team of San Francisco scientists found a way to take full advantage. A new study by UCSF researchers revealed a tendency of the brain’s motion-control system to run off track in a predictable way when we try to perform the same practiced movement over and over. The scientists found the phenomenon first in macaque monkeys, then documented exactly the same thing in Kershaw’s game video. Although he struggled in a playoff appearance last week, the left-hander’s pitching performance during the regular season was among the best on record. It included a minuscule 1.77 earned run average, a nearly flawless no-hitter in June, 239 strikeouts and only 31 walks. He led the major leagues with 10.85 strikeouts per nine innings pitched. In what turned out to be an early warm-up to the playoffs, UCSF scientists Kris Chaisanguanthum, Helen Shen and Philip Sabes delved into the motor-control system of the primate brain. Their study, published in the Journal of Neuroscience, could help design better prosthetic limbs — or make robots that move less like robots and more like Kershaw. Unlike most machines, our brains seem to never stop trying to adapt to new information, making subtle adjustments each time we repeat a particular movement no matter how practiced. This trial-by-trial form of learning has obvious advantages in a fast-changing world, but also seems prone to drift away from spot-on accuracy as those small adjustments go too far.
Keyword: Learning & Memory
Link ID: 20193 - Posted: 10.11.2014
By David Shultz The next time you see a fruit fly hovering around your pint of beer, don’t swat it—appreciate it. You’re witnessing a unique relationship between yeast and insect. A new study reveals that the single-celled organisms have evolved to secrete a fruity scent that attracts fruit flies, which they hitch a ride on for greener pastures. The findings may also explain the sweet aroma of some craft beers. Like many scientific discoveries, the new work was the product of a happy accident. Kevin Verstrepen, a geneticist at KU Leuven in Belgium, was working with two types of yeast: a normal strain and another with a mutation in a gene called ATF1 that causes the cells to produce fewer odors during fermentation. “Nobody really knew what was happening until I was lazy enough to leave the lab on a Friday with these yeast left out on the bench,” he says. By coincidence, a group of fruit flies (Drosophila melanogaster) chose that weekend to escape from a neighboring genetics lab. When Verstrepen returned to work on Monday, he discovered that the insects had found their way into the smelly yeast culture but had ignored the mutant colony. To probe further, Verstrepen and colleagues set up an enclosed “arena” and pumped ATF1 aromas, which are either fruity, flowery, or solventlike, into one corner. Another corner received a dose of odors from the ATF1-deficient yeast. The remaining two corners emitted odorless streams of air to serve as controls. As expected, the flies congregated almost exclusively in the corner emitting the fragrant odors of yeast with intact ATF1 genes. Analyses of the insects’ brains revealed that the neurons in flies exposed to smelly yeast responded in an entirely different way from those exposed to odorless air or the scent of ATF1-deficient yeast strain, the researchers report online today in Cell Reports. © 2014 American Association for the Advancement of Science
Keyword: Chemical Senses (Smell & Taste)
Link ID: 20192 - Posted: 10.11.2014
For decades, scientists thought that neurons in the brain were born only during the early development period and could not be replenished. More recently, however, they discovered cells with the ability to divide and turn into new neurons in specific brain regions. The function of these neuroprogenitor cells remains an intense area of research. Scientists at the National Institutes of Health (NIH) report that newly formed brain cells in the mouse olfactory system — the area that processes smells — play a critical role in maintaining proper connections. The results were published in the October 8 issue of the Journal of Neuroscience. “This is a surprising new role for brain stem cells and changes the way we view them,” said Leonardo Belluscio, Ph.D., a scientist at NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and lead author of the study. The olfactory bulb is located in the front of the brain and receives information directly from the nose about odors in the environment. Neurons in the olfactory bulb sort that information and relay the signals to the rest of the brain, at which point we become aware of the smells we are experiencing. Olfactory loss is often an early symptom in a variety of neurological disorders, including Alzheimer’s and Parkinson’s diseases. In a process known as neurogenesis, adult-born neuroprogenitor cells are generated in the subventricular zone deep in the brain and migrate to the olfactory bulb where they assume their final positions. Once in place, they form connections with existing cells and are incorporated into the circuitry.
by Andy Coghlan Ten years after the death of everyone's favourite Superman, Christopher Reeve, his son Matthew Reeve is pushing ahead with a spine-tingling clinical trial You're planning a large study of a paralysis treatment that has already helped four young men. What will it entail? This study will include 36 people with spinal cord injuries who will be treated with epidural stimulation – a technique in which a device is used to apply electrical current to the spinal cord. If we see the same results as we did in the first four, this therapy could have a profound impact on thousands of people living with paralysis. It has the potential to become as commonplace as the pacemaker is for cardiac patients. How well has the treatment worked for the four men who have already received it? Prior to epidural stimulation, they had all suffered chronic injuries caused by completely severed spinal cords. All four have seen dramatic improvements, including the ability to voluntarily move their toes, feet, ankles and legs, and even stand at times, when the device is on. One unexpected bonus has been the return of autonomic function, such as bladder and bowel control and sexual function. From a quality-of-life point of view, this is the biggest improvement. Also unexpectedly, these autonomic functions continue in all four men even when the device is switched off, although they still need it to stand, move their legs and do exercises. © Copyright Reed Business Information Ltd.
Posted by Rachel Dolhun, MD, The ability to quit smoking, especially “cold turkey” or on the first attempt, has been heralded as a marker of strong willpower and determination. But could the ease with which one eschews cigarettes also serve as an early sign of Parkinson’s disease (PD)? This is the conclusion drawn by Beate Ritz, MD, PhD, and colleagues from the University of California, Los Angeles in a recent study published in Neurology. Researchers compared lifelong tobacco use, use of nicotine substitutes, and individual’s rating of their difficulty in trying to quit tobacco among 1,808 Danish people with PD and 1,876 control volunteers. They found that those with PD were less inclined to ever pick up the smoking habit, but, even if they did, they were less likely to need nicotine replacement therapies and able to more effortlessly stop smoking cigarettes. Therefore, ease of quitting smoking may be a sign of early PD. This joins a short list of other symptoms — smell loss, constipation and REM sleep behavior disorder — that usually predate diagnosis and are strongly associated with PD. Physicians rely heavily on such information to help confirm the diagnosis of Parkinson’s, given that biomarkers, objective measurements of disease, are currently lacking. Research led by The Michael J. Fox Foundation is ongoing to identify biological markers of PD, which could help diagnose and treat people earlier. In the meantime, doctors must look for symptoms and behaviors to help identify Parkinson’s. Researchers have long known that tobacco use was linked to a lower risk of PD. An ongoing Foundation-funded study is investigating whether nicotine might guard against or slow the progression of PD.
BY Ashley Yeager A protein made by gut bacteria may trigger a chain of interactions in the body that contribute to eating disorders such as anorexia and bulimia. When the protein is produced, the body makes antibodies to bind to it, but the antibodies also attach to a hormone that controls fullness. In tests, mice given bacteria that produce the protein changed how much they ate compared with mice given bacteria that did not make the protein, a new study shows. Researchers also found that the antibodies to the protein were higher in patients with anorexia and bulimia. The results, which appear October 7 in Translational Psychiatry, seem to be some of the earliest to link gut bacteria to eating disorders. © Society for Science & the Public 2000 - 2014.
Keyword: Anorexia & Bulimia
Link ID: 20188 - Posted: 10.11.2014
By Elizabeth Pennisi Four years ago, Igor Spetic lost his right arm in an industrial accident. Doctors outfitted him with a prosthetic arm that restored some function, but they couldn't restore his sense of touch. Without it, simple tasks like picking up a glass or shaking hands became hit-or-miss propositions. The lack of touch also robs Spetic of basic pleasures. “I would love to feel my wife’s hand,” he says. In time, he may regain that pleasure: Two independent research teams have now equipped artificial hands with sensors that send signals to the wearer’s nerves to recreate this missing sense. The sensing technologies work only in the lab, but they have proved durable, and amputees who have tried them, including Spetic, say that they are effective. One technology advances the range of touch sensations available, while the other promises to enable touch through a better way to attach the prosthesis. “All of these results are very positive,” says Mandayam Srinivasan, a neuroengineer at the Massachusetts Institute of Technology in Cambridge, who was not involved in either project. “Each of them fills a piece of the puzzle in terms of [prosthesis] development.” Almost 40 years ago, researchers tried to provide sensory feedback by adding pressure sensors to prostheses that relayed the sensation through electrodes attached to nerves. But for the most part, they just made it seem like the hand was tingling. And durability has been an issue in such efforts, too. In February, Silvestro Micera, a neuroengineer at the Sant'Anna School of Advanced Studies in Pisa, Italy, and the Swiss Federal Institute of Technology in Lausanne and his team showed that it was possible for sensor-equipped prosthetic arms to gently or powerfully grab objects and even to distinguish a round from a square object. But the study lasted just 4 weeks, in part because of the delicate interface with the body. © 2014 American Association for the Advancement of Science.
|By Bret Stetka Multiple sclerosis (MS) is an electrical disorder, or rather one of impaired myelin, a fatty, insulating substance that better allows electric current to bolt down our neurons and release the neurotransmitters that help run our bodies and brains. Researchers have speculated for some time that the myelin degradation seen in MS is due, at least in part, to autoimmune activity against the nervous system. Recent work presented at the MS Boston 2014 Meeting suggests that this aberrant immune response begins in the gut. Eighty percent of the human immune system resides in the gastrointestinal tract. Alongside it are the trillions of symbiotic bacteria, fungi and other single-celled organisms that make up our guts’ microbiomes. Normally everyone wins: The microorganisms benefit from a home and a steady food supply; we enjoy the essential assistance they provide in various metabolic and digestive functions. Our microbiomes also help calibrate our immune systems, so our bodies recognize which co-inhabitants should be there and which should not. Yet mounting evidence suggests that when our resident biota are out of balance, they contribute to numerous diseases, including diabetes, rheumatoid arthritis, autism and, it appears, MS by inciting rogue immune activity that can spread throughout the body and brain. One study presented at the conference, out of Brigham and Women’s Hospital (BWH), reported a single-celled organism called methanobrevibacteriaceae that activates the immune system is enriched in the gastrointestinal tracts of MS patients whereas bacteria that suppress immune activity are depleted. Other work, which resulted from a collaboration among 10 academic researcher centers across the U.S. and Canada, reported significantly altered gut flora in pediatric MS patients while a group of Japanese researchers found that yeast consumption reduced the chances of mice developing an MS-like disease by altering gut flora. © 2014 Scientific American
Keyword: Multiple Sclerosis
Link ID: 20186 - Posted: 10.09.2014