By C. CLAIBORNE RAY Q. WHY WOULD A PAIN MEDICATION LOSE ITS EFFICACY AFTER WORKING WELL FOR SEVERAL YEARS? A. The mechanism is complex, said Dr. Shakil Ahmed, a pain medicine specialist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. “It is due to a phenomenon called tolerance,” in which there is a decrease in response over time to repeated exposures of the body to pain medication, he said. “This might be due to alteration in the way the body disposes of the medication,” Dr. Ahmed suggested. Or it could occur because drug interactions or bodily changes add a substance that induces an enzyme responsible for disposing of the drug. Another explanation is that long-term administration of pain medications results in a reduction of the number of target drug receptors or a drop in their responsiveness, and in desensitization to the pain medication in question. There is also an increase in the function of other nervous system receptors, called NMDA receptors , which may lead to the development of the tolerance, Dr. Ahmed said. Dr. Ahmed’s practice and research include several alternatives to conventional drug treatment for pain, including spinal cord stimulation, use of radio frequency to interrupt the nerve pathways of pain, delivery of pain medication with a pump directly to the space around the spinal cord, and non-invasive laser therapy. © 2014 The New York Times Company

Keyword: Pain & Touch
Link ID: 19666 - Posted: 05.28.2014

Pain is a symptom of many disorders; chronic pain can present as a disease in of itself. The economic cost of pain is estimated to be hundreds of billions of dollars annually in lost wages and productivity. “This database will provide the public and the research community with an important tool to learn more about the breadth and details of pain research supported across the federal government. They can search for individual research projects or sets of projects grouped by themes uniquely relevant to pain,” said Linda Porter, Ph.D., Policy Advisor for Pain at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health (NIH). “It also can be helpful in identifying potential collaborators by searching for topic areas of interest or for investigators.” Users of the database easily can search over 1,200 research projects in a multi-tiered system. In Tier 1, grants are organized as basic, translational (research that can be applied to diseases), or clinical research projects. In Tier 2, grants are sorted among 29 scientific topic areas related to pain, such as biobehavioral and psychosocial mechanisms, chronic overlapping conditions, and neurobiological mechanisms. The Tier 2 categories are also organized into nine research themes: pain mechanisms, basic to clinical, disparities, training and education, tools and instruments, risk factors and causes, surveillance and human trials, overlapping conditions, and use of services, treatments, and interventions.

Keyword: Pain & Touch; Development of the Brain
Link ID: 19665 - Posted: 05.28.2014

By Susana Martinez-Conde Expanding and contracting circles, mutating colors, and false image matches dominated the 2014 Best Illusion of the Year Contest, held on May 18th in the TradeWinds Island Grand in St. Petersburg, FL. One thousand perceptual scientists joined artists and the general public to determine the TOP THREE illusion masters from a pre-selected group of TOP TEN finalists, chosen by an international committee of judges. Each winner took home a trophy designed by the acclaimed Italian sculptor Guido Moretti: the trophies are visual illusions themselves. It was the 10th annual edition of the contest, which annually draws numerous accolades from attendees as well as international media coverage. Las Vegas magician Mac King was master of ceremonies for the event, hosted by the Neural Correlate Society, a non-profit organization whose mission is to promote public awareness of neuroscience research and discovery, and sponsored by Scientific American. Each of the 10 presenters displayed and described their creations for 5 minutes, to the sounds of music and confetti cannons, in an event unlike anything else in science. Afterwards, the audience voted on their favorite illusion while Mac King performed some of his signature magic tricks for the audience. The First Prize winner of the contest, an illusion by Christopher Blair, Gideon Caplovitz and Ryan Mruczek from University of Nevada Reno, took the classical Ebbinghaus illusion, where the perceived size of a central circle varies with the size of surrounding circles, and put it on steroids by making it into an ever-changing dynamic display. Blair rhymed his 5-minute presentation Dr. Seuss-style. Second Prize went to Mark Vergeer, Stuart Anstis and Rob van Lier from the University of Leuven, UC San Diego and Radboud University Nijmegen, for showing that a single colored image can produce several different color perceptions depending on the position of black outlines over the image. © 2014 Scientific American

Keyword: Vision
Link ID: 19664 - Posted: 05.28.2014

By JAMES GORMAN H. Sebastian Seung is a prophet of the connectome, the wiring diagram of the brain. In a popular book, debates and public talks he has argued that in that wiring lies each person’s identity. By wiring, Dr. Seung means the connections from one brain cell to another, seen at the level of the electron microscope. For a human, that would be 85 billion brain cells, with up to 10,000 connections for each one. The amount of information in the three-dimensional representation of the whole connectome at that level of detail would equal a zettabyte, a term only recently invented when the amount of digital data accumulating in the world required new words. It equals about a trillion gigabytes, or as one calculation framed it, 75 billion 16-gigabyte iPads. He is also a realist. When he speaks publicly, he tells his audiences, “I am my connectome.” But he can be brutally frank about the limitations of neuroscience. “We’ve failed to answer simple questions,” he said. “People want to know, ‘What is consciousness?’ And they think that neuroscience is up to understanding that. They want us to figure out schizophrenia and we can’t even figure out why this neuron responds to one direction and not the other.” This mix of intoxicating ideas, and the profound difficulties of testing them, not only defines Dr. Seung’s career but the current state of neuroscience itself. He is one of the stars of the field, and yet his latest achievement, in a paper published this month, is not one that will set the world on fire. He and his M.I.T. colleagues have proposed an explanation of how a nerve cell in the mouse retina — the starburst amacrine cell — detects the direction of motion. If he’s right, this is significant work. But it may not be what the public expects, and what they have been led to expect, from the current push to study the brain. © 2014 The New York Times Company

Keyword: Vision; Brain imaging
Link ID: 19663 - Posted: 05.27.2014

By JAMES GORMAN Crowd-sourced science has exploded in recent years. Foldit enlists users to help solve scientific puzzles such as how proteins are put together. Zooniverse hosts dozens of projects, including searching for planets and identifying images of animals caught on automatic cameras. Eyewire, which came out of H. Sebastian Seung’s lab at the Massachusetts Institute of Technology about a year and a half ago, is neuroscience’s entry into the field. The EyeWirers, as the players are called, have scored their first scientific success, contributing to a paper in the May 4 issue of Nature by Dr. Seung and his M.I.T. colleagues that offers a solution to a longstanding problem in how motion is detected. Anyone can sign up online, learn to use the software and start working on what Amy Robinson, the creative director of Eyewire, calls a “3-D coloring book.” The task is something like tracing one piece of yarn through an extremely tangled ball. More than 130,000 players in 145 countries, at last count, work on a cube that represents a bit of retinal tissue 4.5 microns on a side. The many branches of neurons are densely packed within. A micron is .00004 inches or, in Eyewire’s calculus, about one-tenth the width of a human hair. Some of the players spend upward of 40 hours a week on Eyewire. These cubes are created by an automated process in which electron microscopes make images of ultrathin slices of brain tissue. Computers then analyze and compile the data to create a three-dimensional representation of a cube of tissue with every neuron and connection visible. © 2014 The New York Times Company

Keyword: Vision; Brain imaging
Link ID: 19662 - Posted: 05.27.2014

By By Tanya Lewis, It's not every day you see a mouse with a mohawk. But that's what researchers saw while studying mice that had a genetic mutation linked to autism. The mohawks that the mice were sporting actually resulted from their "over-grooming" behavior, repeatedly licking each other's hair in the same direction. The behavior resembles the repetitive motions displayed by some people with autism, and the researchers say their experiments reveal a link between the genetic causes of autism and their effects on the brain, suggesting potential avenues for treating the disorder. "Our study tells us that to design better tools for treating a disease like autism, you have to get to the underlying genetic roots of its dysfunctional behaviors, whether it is over-grooming in mice or repetitive motor behaviors in humans," study researcher Gordon Fishell, a neuroscientist at NYU Langone Medical Center, said in a statement. Autism is a spectrum of developmental disorders that involve social impairments and communication deficits. People with autism may also engage in repetitive behaviors, such as rocking or hand flapping. In the study, detailed today (May 25) in the journal Nature, the researchers bred mice that lacked a gene for a protein called Cntnap4, which is found in brain cells called interneurons. Having low levels of this protein leads to the abnormal release of two brain-signaling molecules, known as dopamine and GABA. Dopamine is involved in sensations of pleasure; GABA (which stands for gamma-aminobutyric acid) dampens neural activity and regulates muscle tone. Mice that lacked the gene for this critical brain protein were found to obsessively groom their fellow animals' fur into mohawk-like styles, suggesting a link between genetics, brain function and autistic behaviors.

Keyword: Autism; Genes & Behavior
Link ID: 19661 - Posted: 05.27.2014

By Sandra G. Boodman, Cheron Wicker sank to her knees and began weeping, the contents of her purse and the bags of groceries she had dropped littering the floor of her suburban Maryland kitchen. As the searing pain in her index finger left her unable to reach the counter with the bags, Wicker felt an overwhelming sense of despair. Looking up, her gaze fell on a rack of kitchen knives. An idea that would have been unthinkable months earlier flickered through her mind. That morning in the fall of 2012 when she briefly considered cutting off her finger was the lowest point in her seven-year ordeal, recalled Wicker, a former public affairs official at the U.S. Maritime Administration. The Columbia resident had repeatedly consulted pain specialists and orthopedic surgeons, as well as her internist and endocrinologist; all were mystified by the persistence of her constant, excruciating pain. Wicker had even undergone two operations to replace the herniated disks in her neck that were believed to be the cause of the pain. She had taken all sorts of painkillers and become dependent on the sleeping pill Ambien to buy her a few hours of relief each night. She was increasingly convinced that she must be crazy; madness seemed to be the only reason that nothing had worked. The real reason, she would learn weeks later when she saw a new doctor, was simple: The pain in her fingertip was caused by something inside it, not by a pinched nerve in her neck. In December 2012, after a third surgery, her pain vanished. “I had to convince her that I knew what I was doing,” recalled Baltimore orthopedic surgeon Raymond Pensy, who diagnosed Wicker’s unusual disorder minutes after meeting her. “She was at her wit’s end.” © 1996-2014 The Washington Post

Keyword: Pain & Touch
Link ID: 19660 - Posted: 05.27.2014

By KATE MURPHY The baseball hurtles toward the batter, and he must decide from its rotation whether it’s a fastball worth a swing or a slider about to drop out of the strike zone. Running full speed, the wide receiver tracks both the football flying through the air and the defensive back on his heels. Golfers must rapidly shift visual focus in order to drive the ball at their feet toward a green in the distance. Many athletes need excellent vision to perform well in their sports, and now many are adding something new to their practice regimens: vision training. The idea has been around for years, but only recently have studies hinted that it might really work — that it might be possible to train yourself to see better without resorting to glasses or surgery. “Vision training has been out there for a long time,” said Mark Blumenkranz, a professor of ophthalmology at Stanford University Medical School. “But it’s being made more respectable lately thanks to the attention it’s been getting from psychophysicists, vision scientists, neurologists and optometrists.” Vision training actually has little to do with improving eyesight. The techniques, a form of perceptual learning, are intended to improve the ability to process what is seen. The idea is that if visual sensory neurons are repeatedly activated, they increase their ability to send electrical signals from one cell to another across connecting synapses. If neurons are not used, over time these transmissions are weakened. “With sensory neurons, just like muscles, it’s use or lose it,” said Dr. Bernhard Sabel, a neuroscientist at Otto von Guericke University in Magdeburg, Germany, who studies plasticity in the brain. “This applies both to athletes and the partially blind.” Vision training may involve simple strategies — for instance, focusing sequentially on beads knotted at intervals on a length of string with one end held at the tip of the nose. This is said to improve convergence (inward turning of the eye to maintain binocular vision) and the ability to focus near and far. © 2014 The New York Times Company

Keyword: Vision; Miscellaneous
Link ID: 19659 - Posted: 05.27.2014

Eliana Dockterman @edockterman A new study that could affect whether adoption agencies are willing to work with gay couples shows that after adopting, gay men's brain activity resembles that of both new moms and new dads Research has shown that a new mother’s brain activity changes after having a baby. Turns out, gay men’s pattern of brain activity also adapts to parenthood, and resembles that of both new moms and new dads, in findings published Monday. A study published Monday in the Proceedings of the National Academy of Sciences sought to determine whether mothers’ brains became hyper-reactive to emotional cues, like hearing their child cry after birth, because of hormonal changes or parenting experience. Researchers videotaped 89 new moms and dads taking care of their infants at home. They then measured parents’ brain activity in an MRI while the parents watched videos in which their children were not featured, followed by the footage shot in their home with their kids. The 20 mothers in the study—all of whom were the primary caregivers—had heightened activity in the brain’s emotion-processing regions; the amygdala, a set of neurons that processes emotions, was five times more active than the baseline. The 21 heterosexual fathers had increased activity in their cognitive circuits, which helped them determine which of the baby’s body movements indicated the need for a new diaper and which ones signaled hunger. The 48 gay fathers’ brain waves, on the other hand, responded similarly to both the heterosexual mom and dad. Their emotional circuits were as active as mothers’, and their cognitive circuits were as active as the fathers’. Researchers also found that the more time a gay father spent with the baby, the greater a connection there was between the emotional and cognitive structures.

Keyword: Sexual Behavior; Brain imaging
Link ID: 19658 - Posted: 05.27.2014

By IAN AUSTEN Hershey stopped producing chocolate in Smiths Falls, Ontario, six years ago. The work went to Mexico, but the factory remains, along with reminders of the glory days: A sign that once directed school buses delivering children for tours. A fading, theme-park-style entrance that marks what used to be the big attraction — a “Chocolate Shoppe” that sold about $4 million of broken candy and bulk bars a year. The once ever-present sweet smell of chocolate is gone, too. In the high-ceilinged warehouse, where stacks of Hershey’s bars and Reese’s Peanut Butter Cups once awaited shipment, the nose now picks up a different odor: the woody, herbal aroma of 50,000 marijuana plants. Clinical, climate-controlled rooms with artificial sunlight house rows upon rows of plants at various stages of growth. In the “mother room,” horticulturalists use cuttings to start new plants. The “flowering rooms” are flooded with intense light 12 hours a day to nurture nearly grown plants in strains with vaguely aristocratic names like Argyle, Houndstooth and Twilling. The new owner of this factory, at 1 Hershey Drive, is Tweed Marijuana. It is one of about 20 companies officially licensed to grow medical marijuana in Canada. A court ordered the government to make marijuana available for medicinal purposes in 2000, but the first system for doing so created havoc. The government sold directly to approved consumers, but individuals were also permitted to grow for their own purposes or to turn over their growing to small operations. The free-for-all approach prompted a flood of complaints from police and local governments. So the Canadian government decided to create an extensive, heavily regulated system for growing and selling marijuana. The new rules allow users with prescriptions to buy only from one of the approved, large-scale, profit-seeking producers like Tweed, a move intended to shut down the thousands of informal growing operations scattered across the country. © 2014 The New York Times Company

Keyword: Drug Abuse
Link ID: 19657 - Posted: 05.26.2014

Claudia M. Gold When Frank was a young boy, and he committed some typical toddler transgression such as having a meltdown when it was time to leave the playground, his father would slap him across the face, hurting and humiliating him in a very public way. When I spoke with Frank over 20 years later, in the context of helping him with his own son Leo's frequent tantrums in my behavioral pediatrics practice, he did not describe this experience as "trauma." Rather, he described it in a very matter-of-fact tone. But when we explored in detail his response to his son's tantrums, we discovered that, flooded by the stress of his own memories, Frank in a sense would shut down. Normally a thoughtful and empathic person, he simply told Leo to "cut it out." As we spoke he recognized how he was emotionally absent during these moments, which were increasing in frequency. It seemed as if Leo was testing Frank, perhaps looking for a more appropriate response that would help him manage this normal behavior. Once this process was brought in to awareness, Frank was able to be present with Leo- to tolerate his tantrums and understand them from his 2-year-old perspective. Soon the frequency and intensity of the tantrums returned to a level typical for Leo's developmental stage. Frank, greatly relieved, once again found himself enjoying his son. The upcoming Boston conference; Psychological Trauma: Neuroscience, Attachment, and Therapeutic Interventions, promises to offer insight in to the developmental neuroscience behind this story. What Frank experienced as a young child might be termed "quotidian" or "everyday" trauma. It was not watching a relative get shot, or having his house washed away in an avalanche. It was a daily mismatch with his father- he was looking for reassurance and containment and instead got a slap across the face. It was what leading researcher Ed Tronick would term "unrepaired mismatch." Frank, in a way that is extremely common- termed "intergenerational transmission of trauma"- was then repeating this cycle with his own child. When this dynamic was brought in to awareness, he was able to "repair the mismatch," setting his relationship with his own son on a healthier path. ©2014 Boston Globe Media Partners, LLC

Keyword: Stress; Development of the Brain
Link ID: 19656 - Posted: 05.26.2014

By JANE E. BRODY Bowels, especially those that don’t function properly, are not a popular topic of conversation. Most of the 1.4 million Americans with inflammatory bowel disease — Crohn’s disease or ulcerative colitis — suffer in silence. But scientists are making exciting progress in understanding the causes of these conditions and in developing more effective therapies. And affected individuals have begun to speak up to let others know that they are not alone. Abby Searfoss, 21, who just graduated from the University of Connecticut, shared her story not in a support group, but online. She was a high school senior in Ridgefield, Conn., when she became ill. After she researched her symptoms on the Internet, she realized that, like her father, she had developed Crohn’s disease. Her father had been very ill, losing 40 pounds, spending weeks in the hospital and undergoing surgery. Soon after Ms. Searfoss’s own diagnosis, her two younger sisters learned that they, too, had the condition. In Crohn’s disease, the immune system attacks cells in the digestive tract, most often the end of the small intestine and first part of the colon, or large intestine. Sufferers may experience bouts of abdominal pain, cramps and diarrhea, often accompanied by poor appetite, fatigue and anxiety. “You don’t go anywhere without checking where the bathroom is and how many stalls it has,” said Dr. R. Balfour Sartor, a gastroenterologist at the University of North Carolina School of Medicine and a patient himself. “The fear of incontinence is huge.” Neither Crohn’s disease nor its less common relative ulcerative colitis, which affects only the large intestine, is curable (except, in the latter instance, by removing the entire colon). But research into what predisposes people to develop these conditions has resulted in more effective treatments and has suggested new ways to prevent the diseases in people who are genetically susceptible. © 2014 The New York Times Company

Keyword: Stress; Neuroimmunology
Link ID: 19655 - Posted: 05.26.2014

By Neuroskeptic Nothing that modern neuroscience can detect, anyway. This is the message of a provocative article by Pace University psychologist Terence Hines, just published in Brain and Cognition: Neuromythology of Einstein’s brain As Hines notes, the story of how Einstein’s brain was preserved is well known. When the physicist died in 1955, his wish was to be cremated, but the pathologist who performed the autopsy decided to save his brain for science. Einstein’s son Hans later gave his blessing to this fait accompli. Samples and photos of the brain were then made available to neuroscientists around the world, who hoped to discover the secret of the great man’s genius. Many have claimed to have found it. But Hines isn’t convinced. Some researchers, for instance, have used microscopy to examine Einstein’s brain tissue on a histological (cellular) level. Most famous amongst these studies is Diamond et al, who in 1985 reported that Einstein’s brain had a significantly higher proportion of glial cells than those of matched, normal control brains. However, Hines points out that this ‘finding’ may have been a textbook example of the multiple-comparisons problem: Diamond et al. (1985) reported four different t-tests, each comparing Einstein’s brain to the brains of the controls. Only one of the four tests performed was significant at the .05 level. Although only the results of the neuron to glial cell ratios were reported by Diamond et al. (1985), the paper makes it clear that at least six other dependent measures were examined: (1) number of neurons, (2) total number of glial cells, (3) number of astrocytes, (4) number of oligodendrocytes, (5) neuron to astrocyte ratio and (6) neuron to oligodendrocyte ratio. Thus a total of seven different dependent measures were examined in four different brain areas for a total of 28 comparisons… one p less than 0.05 result out of 28 is not surprising. Other histological studies followed from other researchers, but Hines says that they do not present a coherent picture of clear differences:

Keyword: Intelligence; Glia
Link ID: 19654 - Posted: 05.26.2014

By DOUGLAS QUENQUA It’s easy to think of fruit flies as tiny robots that simply respond reflexively to their environment. But just like humans, they take time to collect information and to deliberate when faced with a difficult choice, according to a new study. The findings, published in the journal Science, could help researchers study cognitive development and defects in humans. Scientists have long been fascinated by decision-making, said an author of the study, Dr. Gero Miesenböck, a neuroscientist at the University of Oxford. “Going back to the 19th century, psychologists have measured how long it takes humans to make up their minds,” he said. “Usually if you give people a hard perceptual choice, they take longer, because the brain needs to integrate information until it has enough to make a decision. “This is the first time in an animal as low as a fruit fly we have been able to show that similar processes occur.” To study how flies make up their minds, Oxford researchers placed the animals in bifurcated chambers filled on both sides with an odor they had been taught to avoid. When the odor was clearly more potent on one side of the chamber than the other, the flies were quick to choose which chamber to inhabit (and nearly always chose the less odorous one). But when the difference between chambers was subtle, the flies took longer to make a decision, and were more apt to make the wrong choice. “We were surprised,” Dr. Miesenböck said. “The original thought was that the flies would just act impulsively, they won’t take time to deliberate. We found that’s not true.” The process so closely mimics decision-making in humans, the researchers said, that the same mathematical models used to describe the actions of deliberating people can be used to predict a fly’s behavior. © 2014 The New York Times Company

Keyword: Attention
Link ID: 19653 - Posted: 05.24.2014

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: 05.24.2014

By BRUCE WEBER Dr. Gerald M. Edelman at Rockefeller University in 1972, in front of a gamma globulin model. Credit Don Hogan Charles/The New York Times Dr. Gerald M. Edelman, who shared a 1972 Nobel Prize for a breakthrough in immunology and went on to contribute key findings in neuroscience and other fields, becoming a leading if contentious theorist on the workings of the brain, died on Saturday at his home in the La Jolla section of San Diego. He was 84. The precise cause was uncertain, but Dr. Edelman had Parkinson’s disease and prostate cancer, his son David said. Dr. Edelman was known as a problem solver, a man of relentless intellectual energy who asked big questions and attacked big projects. What interested him, he said, were “dark areas” where mystery reigned. “Anybody in science, if there are enough anybodies, can find the answer,” he said in a 1994 interview in The New Yorker. “It’s an Easter egg hunt. That isn’t the idea. The idea is: Can you ask the question in such a way as to facilitate the answer? And I think the great scientists do that.” His Nobel Prize in Physiology or Medicine came in 1972 after more than a decade of work on the process by which antibodies, the foot soldiers of the immune system, mount their defense against infection and disease. He shared the prize with Rodney R. Porter, a British scientist who worked independent of Dr. Edelman. The Nobel committee cited them for their separate approaches in deciphering the chemical structure of antibodies, also known as immunoglobulins. Dr. Edelman discovered that antibodies were not constructed in the shape of one long peptide chain, as thought, but of two different ones — one light, one heavy — that were linked. © 2014 The New York Times Company

Keyword: Development of the Brain; Trophic Factors
Link ID: 19651 - Posted: 05.24.2014

By John Horgan Biologist Gerald Edelman–one of the truly great scientific characters I’ve encountered, whose work raised profound questions about the limits of science—has died. I interviewed Edelman in June 1992 at Rockefeller University in New York. Edelman subsequently left Rockefeller to head a center for neuroscience at the Scripps Institute in California. Edelman, 84, died in his home in La Jolla. The following is an edited version of my profile of Edelman in my 1996 book The End of Science. Gerald Edelman, who sought to solve the riddle of consciousness, had "the brain of an empiricist and the heart of a romantic." Gerald Edelman’s career, like that of his rival Francis Crick, has been eclectic, and highly successful. While still a graduate student, Edelman helped to determine the structure of a protein molecule crucial to the body’s immune response. In 1972 he shared a Nobel Prize for that work. Edelman moved on to developmental biology, the study of how a single fertilized cell becomes a full-fledged organism. He found a class of proteins, called cell adhesion molecules, thought to play an important role in embryonic development. All this was merely prelude, however, to Edelman’s grand project of creating a theory of mind. Edelman has set forth his theory in three books: Neural Darwinism, The Remembered Present and Bright Air, Brilliant Fire. The gist of the theory is that just as environmental stresses select the fittest members of a species, so do inputs to the brain select groups of neurons–corresponding to useful memories, for example–by strengthening the connections between them. © 2014 Scientific American

Keyword: Development of the Brain; Trophic Factors
Link ID: 19650 - Posted: 05.24.2014

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

Keyword: Robotics
Link ID: 19649 - Posted: 05.24.2014

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

Keyword: Muscles; Movement Disorders
Link ID: 19648 - Posted: 05.24.2014

By JENEEN INTERLANDI Bessel van der Kolk sat cross-legged on an oversize pillow in the center of a smallish room overlooking the Pacific Ocean in Big Sur. He wore khaki pants, a blue fleece zip-up and square wire-rimmed glasses. His feet were bare. It was the third day of his workshop, “Trauma Memory and Recovery of the Self,” and 30 or so workshop participants — all of them trauma victims or trauma therapists — lined the room’s perimeter. They, too, sat barefoot on cushy pillows, eyeing van der Kolk, notebooks in hand. For two days, they had listened to his lectures on the social history, neurobiology and clinical realities of post-traumatic stress disorder and its lesser-known sibling, complex trauma. Now, finally, he was about to demonstrate an actual therapeutic technique, and his gaze was fixed on the subject of his experiment: a 36-year-old Iraq war veteran named Eugene, who sat directly across from van der Kolk, looking mournful and expectant. Van der Kolk began as he often does, with a personal anecdote. “My mother was very unnurturing and unloving,” he said. “But I have a full memory and a complete sense of what it is like to be loved and nurtured by her.” That’s because, he explained, he had done the very exercise that we were about to try on Eugene. Here’s how it would work: Eugene would recreate the trauma that haunted him most by calling on people in the room to play certain roles. He would confront those people — with his anger, sorrow, remorse and confusion — and they would respond in character, apologizing, forgiving or validating his feelings as needed. By projecting his “inner world” into three-dimensional space, Eugene would be able to rewrite his troubled history more thoroughly than other forms of role-play therapy might allow. If the experiment succeeded, the bad memories would be supplemented with an alternative narrative — one that provided feelings of acceptance or forgiveness or love. The exercise, which van der Kolk calls a “structure” but which is also known as psychomotor therapy, was developed by Albert Pesso, a dancer who studied with Martha Graham. He taught it to van der Kolk about two decades ago. Though it has never been tested in a controlled study, van der Kolk says he has had some success with it in workshops like this one. He likes to try it whenever he has a small group and a willing volunteer. © 2014 The New York Times Company

Keyword: Stress
Link ID: 19647 - Posted: 05.24.2014