By Keith Doucette, In what her mother calls a "Christmas miracle," a Nova Scotia woman who suffered a catastrophic brain injury in a 1996 car accident communicated one-on-one with her mother for the first time in 21 years. Louise Misner said her 37-year-old daughter Joellan Huntley used eye-motion cameras and software on an iPad to respond to a comment from Misner about her clothes. Huntley has been severely disabled since she was 15, unable to walk or talk and is fed through a tube. She has always responded to family members' presence by making sounds, but was unable to communicate any thoughts. The breakthrough occurred during a Christmas Day visit at the Kings Regional Rehabilitation Centre in Waterville, N.S. "I said, 'Joellan, I like your new Christmas outfit you got on,"' Misner said in a telephone interview on Friday. Misner said her daughter then used the technology to find an icon for a short-sleeved shirt. "And then she said no, and went to a long-sleeve shirt because she was trying to tell me what she had on." Misner said her reaction to the long-hoped-for communication was immediate. "Christmas miracle," she said. "It was God's way of telling me that she's finally achieved what she needed to since the accident." Settlement helped buy technology Huntley was thrown from a car that had swerved to avoid a dog running loose along a road in Centreville, N.S., on April 18, 1996. The accident claimed the life of her boyfriend and a young girl who was the sister of the driver. ©2017 CBC/Radio-Canada.

Keyword: Movement Disorders; Robotics
Link ID: 24469 - Posted: 12.30.2017

By Sharon Begley Technologies to detect brain activity — fine, we’ll come right out and call it mind reading — as well as to change it are moving along so quickly that “a bit of a gold rush is happening, both on the academic side and the corporate side,” Michel Maharbiz of the University of California, Berkeley, told a recent conference at the Massachusetts Institute of Technology. Here are three fast-moving areas of neuroscience we’ll be watching in 2018: Neural dust/neurograins Whatever you call these electronics, they’re really, really tiny. We’re eagerly awaiting results from DARPA’s $65 million neural engineering program, which aims to develop a brain implant that can communicate digitally with the outside world. The first step is detecting neurons’ electrochemical signaling (DARPA, the Pentagon’s Defense Advanced Research Projects Agency, says 1 million neurons at a time would be nice). To do that, scientists at Brown University are developing salt-grain-sized “neurograins” containing an electrode to detect neural firing as well as to zap neurons to fire, all via a radio frequency antenna. Advertisement Maharbiz’s “neural dust” is already able to do the first part. The tiny wireless devices can detect what neurons are doing, he and his colleagues reported in a 2016 rat study. (The study’s lead scientist recently moved to Elon Musk’s startup Neuralink, one of a growing number of brain-tech companies.) Now Maharbiz and team are also working on making neural dust receive outside signals and cause neurons to fire in certain ways. Such “stimdust” would be “the smallest [nerve] stimulator ever built,” Maharbiz said. Eventually, scientists hope, they’ll know the neural code for, say, walking, letting them transmit the precise code needed to let a paralyzed patient walk. They’re also deciphering the neural code for understanding spoken language, which raises the specter of outside signals making people hear voices — raising ethical issues that, experts said, neurotech will generate in abundance. © 2017 Scientific American

Keyword: Brain imaging; Robotics
Link ID: 24468 - Posted: 12.29.2017

Shankar Vedantam Decades ago, Randy Gardner stayed awake for 11 days. He broke a record in the process, but the teenage stunt has come back to haunt him. At 71, he offers wisdom about staying up past your bedtime. NOEL KING, HOST: And this next story is about something we think about a lot at MORNING EDITION. It's about sleep. It's actually about the lack of sleep. Decades ago, a teenage boy named Randy Gardner stopped sleeping for 11 nights. And because of that, scientists were able to learn something about the price we pay when we don't get enough rest. NPR's Shankar Vedantam has the story. SHANKAR VEDANTAM, BYLINE: Our story begins in 1963, when Randy Gardner moved to San Diego. He was 17. It was the last in a long line of childhood moves. RANDY GARDNER: I'm the oldest of four siblings in a military family. VEDANTAM: In every town he lived in, Randy entered the science fair. GARDNER: I was a kind of a science nerd when I was young. When we came to this town, San Diego, I thought, boy, this is a big city. VEDANTAM: If he wanted to win the science fair here, he'd have to pull out all the stops. The idea he came up with? Going without sleep for 264 hours, exactly 11 days - long enough to break a world record. He recruited two of his friends... GARDNER: Bruce McAllister, and Joe Marciano. VEDANTAM: ...And asked them to stay awake on rotations around the clock to help him stay awake. GARDNER: If you're on your own, you're going to succumb. You're going to fall asleep. © 2017 npr

Keyword: Sleep
Link ID: 24467 - Posted: 12.29.2017

/ By Michael Schulson Late last month, Senate Minority Leader Chuck Schumer took a break from the tax bill debate to talk with reporters about genetics. It takes just a few minutes to put some spit into a vial, but that little bit of spit can yield volumes of deeply intimate data. In a press conference, the New York senator criticized how direct-to-consumer genetic testing companies — outfits like 23andMe and AncestryDNA — discuss and handle users’ genetic information. “What those companies can do with all that data — your most sensitive and deepest info, your genetics — is not clear, and in some cases not fair and not right,” said Schumer. Schumer called on the Federal Trade Commission to launch an investigation into genetic testing companies’ privacy and disclosure practices, though the commercial and regulatory tides seem — at least for now — to be going in the other direction. Discounted prices for 23andMe dropped below $50 earlier this year, and sales of AncestryDNA kits are breaking records: In the weekend after Thanksgiving, the company said it had sold around 1.5 million genetic tests. That’s more units than 23andMe sold in its first eight years on the market. Last spring, for the first time, the Food and Drug Administration approved an over-the-counter test that tells consumers their genetic risk for a variety of conditions, from Parkinson’s and Alzheimer’s to Celiac disease and numerous blood diseases. And a new FDA policy announced at the beginning of November is likely to allow a wave of new, health-oriented genetic screening products to enter the market. Copyright 2017 Undark

Keyword: Genes & Behavior
Link ID: 24466 - Posted: 12.29.2017

John Daley Seven years ago, Robert Kerley, who makes his living as a truck driver, was loading drywall onto his trailer when a gust of wind knocked him off. He fell 14 feet and hurt his back. For pain, a series of doctors prescribed him a variety of opioids: Vicodin, Percocet and Oxycontin. In less than a year, the 45-year-old from Federal Heights, Colo., says he was hooked. "I spent most of my time high, laying on the couch, not doing nothing, sleeping, dozing off, falling asleep everywhere," he says. Kerley lost weight. He lost his job. His relationships with his wife and kids suffered. He remembers when he hit rock bottom. One night hanging out in a friend's basement, he drank three beers and the alcohol reacted with an opioid in his system. "I was taking so much morphine that I respiratory arrested because of it," Kerley says. "I stopped breathing." An ambulance arrived, and EMTs administered the overdose reversal drug naloxone. Kerley was later hospitalized. As the father of a 12-year-old son, he knew he needed to turn things around. That's when he signed up for Kaiser Permanente's Integrated Pain Service. "After seven years of being on narcotics and in a spiral downhill, the only thing that pulled me out of it was going to this class," he says. "The only thing that pulled me out of it was doing and working the program that they ask you to work." © 2017 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 24465 - Posted: 12.29.2017

By JOANNA KLEIN Most rodents are just rodents. And the ones with exceptional abilities are usually cartoon rats or mice. But here in the real world of flesh, bones, brains and nerves that we mammals use each second to survive, some woodland rodents really do have a superpower that helps them tolerate cold and endure harsh winters. In grasslands from central Canada to Texas, a species known as thirteen-lined ground squirrels can adjust their body temperature to match the air around them. This is especially important during hibernation: They don’t have to fatten up like bears or find warm hide-outs like conventional mice and rats. They slumber, surviving in bodies just above freezing. Another species, the Syrian hamster, does it too. “They combine warm and cold blooded animals in one,” said Elena Gracheva, a neurophysiologist at Yale University. This uncanny ability to withstand prolonged cold (and even hypothermia) results in part from an adaptation these rodents have developed in molecules they share with other mammals, including us, Dr. Gracheva and her colleagues found in a study published last week in the journal Cell Reports. Unique properties of TRPM8, a cold-sensing protein found in their peripheral nervous systems, shields these rodents from harsh weather. It’s really important because if they’re too cold, they can’t hibernate — just like if you’re too cold, you might have trouble sleeping. The new research brings scientists closer to understanding enigmas of hibernation and solving a mystery of how this molecular sensor works. The work also may lead to therapies for allodynia, a nerve condition that causes some people to misperceive something normally not-so-cold as painful. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 24464 - Posted: 12.28.2017

Girls who go through puberty early could be more likely to experience depression and behaviour problems that last into their 20s compared to peers who start menstruation later, a U.S. study suggests. Researchers studied data on nearly 7,800 women who had their first menstrual cycle at an average age of 12. The women were interviewed four times, starting around age 16 and continuing until about age 28. Girls who went through puberty earlier than most were more likely to become depressed, and their symptoms were also more severe in adolescence, the study found. The younger the age at the first period, the stronger the association between early puberty and mental health problems; It was stronger for girls who started menstruation at age 8 than at age 10, for example. With earlier puberty, girls were also more likely to have behaviour issues that led to things like stealing, lying, breaking into buildings and selling drugs. The link lasted into young adulthood. Interestingly, the magnitude of the association between puberty and these psychological difficulties remains stable, meaning that puberty is as strongly associated with depressive symptoms and antisocial behaviour during adulthood as it is during adolescence, said lead study author Jane Mendle, a researcher at Cornell University in Ithaca, New York. ©2017 CBC/Radio-Canada.

Keyword: Depression; Hormones & Behavior
Link ID: 24463 - Posted: 12.28.2017

By Helen Shen Brain-controlled prosthetic devices have the potential to dramatically improve the lives of people with limited mobility resulting from injury or disease. To drive such brain-computer interfaces, neuroscientists have developed a variety of algorithms to decode movement-related thoughts with increasing accuracy and precision. Now researchers are expanding their tool chest by borrowing from the world of cryptography to decode neural signals into movements. During World War II, codebreakers cracked the German Enigma cipher by exploiting known language patterns in the encrypted messages. These included the typical frequencies and distributions of certain letters and words. Knowing something about what they expected to read helped British computer scientist Alan Turing and his colleagues find the key to translate gibberish into plain language. Many human movements, such as walking or reaching, follow predictable patterns, too. Limb position, speed and several other movement features tend to play out in an orderly way. With this regularity in mind, Eva Dyer, a neuroscientist at the Georgia Institute of Technology, decided to try a cryptography-inspired strategy for neural decoding. She and her colleagues published their results in a recent study in Nature Biomedical Engineering. “I’ve heard of this approach before, but this is one of the first studies that’s come out and been published,” says Nicholas Hatsopoulos, a neuroscientist at the University of Chicago, who was not involved in the work. “It’s pretty novel.” © 2017 Scientific American,

Keyword: Movement Disorders; Robotics
Link ID: 24462 - Posted: 12.28.2017

Acclaimed Stanford neuroscientist Ben Barres, MD, PhD, died on Dec. 27, 20 months after being diagnosed with pancreatic cancer. He was 63. Barres’ path-breaking discoveries of the crucial roles played by glial cells — the unsung majority of brain cells, which aren’t nerve cells — revolutionized the field of neuroscience. Barres was incontestably visionary yet, ironically, face-blind — he suffered from prosopagnosia, an inability to distinguish faces, and relied on voices or visual cues such as hats and hairstyles to identify even people he knew well. And there were many of them. A professor of neurobiology, of developmental biology and of neurology, Barres was widely praised as a stellar and passionate scientist whose methodologic rigor was matched only by his energy and enthusiasm. He was devoted to his scholarly pursuits and to his trainees, advocating unrelentingly on their behalf. He especially championed the cause of women in academia, with whom he empathized; he was transgender. “Ben was a remarkable person. He will be remembered as a brilliant scientist who transformed our understanding of glial cells and as a tireless advocate who promoted equity and diversity at every turn,” said Marc Tessier-Lavigne, PhD, president of Stanford University. “He was also a beloved mentor to students and trainees, a dear friend to many in our community and a champion for the fundamental dignity of us all.”

Keyword: Glia
Link ID: 24461 - Posted: 12.28.2017

By Katherine Sellgren BBC News Kids seem to spend endless hours on smartphones, games consoles, computers and tablets these days. Playing on electronic devices certainly doesn't help their waistlines, but do you ever wonder what regular device use is doing to their eyesight? While there isn't much research out there yet about the impact of screens on eyesight - after all the iPhone was first unveiled by Apple in only 2007 - experts are concerned about growing levels of short-sightedness in children. And they suggest the best thing parents can do to prevent it is to encourage youngsters to spend more time outdoors in the sunlight. How short-sightedness is on the rise There has been a massive rise around the globe in short-sightedness - or myopia as it's officially known - over recent decades. "We know that myopia or short-sightedness is becoming more common," says Chris Hammond, professor of ophthalmology at King's College London and consultant ophthalmic surgeon at St Thomas' Hospital. "It has reached epidemic levels in East Asia, Singapore, Taiwan, South Korea, where approaching 90% of 18-year-olds are now short-sighted. "In Europe, it's potentially getting up to 40% to 50% of young adults in their mid-20s who are short-sighted now in Western Europe. It's been gradually rising over the decades of the 20th Century from around 20-30%." Why has it become so much more common? Annegret Dahlmann-Noor, consultant ophthalmologist at Moorfields Eye Hospital in London says lack of natural light seems to be the key issue. "The main factor seems to be a lack of exposure to direct sunlight, because children who study a lot and who use computers or smartphones or tablet computers a lot have less opportunity to run around outside and are less exposed to sunshine and because of that seem to be at more risk of developing short-sightedness." Prof Hammond says: "It may be that there's no coincidence that in East Asian countries, the most myopic ones all correlate with the maths league tables. "These kids are being pushed with very intensive education from a very young age and spend a lot of time indoors studying everything close up and very little time outdoors. © 2017 BBC.

Keyword: Vision
Link ID: 24460 - Posted: 12.28.2017

By Emily Anthes Men with autism respond differently to human odors — and the social signals that they contain — than do their neurotypical peers, according to a new study. The results suggest that men with autism misread social signals present in human odors — causing them to misinterpret others’ emotions. Human sweat contains chemicals believed to convey social and emotional information. For instance, when women smell sweat collected from men watching scary movies, they are more likely to describe faces with ambiguous expressions as fearful. Advertisement In the new study, researchers exposed men to sweat collected from people who were skydiving. Unlike controls, men with autism do not show increased skin conductance, a measure of physiological arousal, to this ‘fear sweat.’ They are also more likely than controls to trust a mannequin that emits this scent. “I think this could be a meaningful aspect of impaired social interaction,” says lead investigator Noam Sobel, professor of neurobiology at the Weizmann Institute of Science in Rehovot, Israel. “Humans constantly engage in social chemo-signaling; we do this all the time, and it shapes our interactions,” he says. “And somehow these mechanisms work differently in autism.” Several studies have examined olfaction in people with autism. Researchers have found, for example, that children with autism inhale odors differently than their typical peers do, and some children with the condition may be particularly sensitive to smells. © 2017 Scientific American

Keyword: Autism; Chemical Senses (Smell & Taste)
Link ID: 24459 - Posted: 12.26.2017

Haroon Siddique Researchers are developing an internet-based tool they hope will predict the effectiveness of antidepressants for individual patients, ending the current prescription lottery. Patients with depression often try many different drugs before settling on one that works, but a study aims to help clinicians make an informed choice as to which is likely to work best for a particular person. Dr Claire Gillan, at Trinity College Dublin, likened deciding which antidepressant to prescribe to a “flip of a coin” at present. But she hopes to create an algorithm that will take away the need for trial and error, potentially transforming treatment for millions of people. Guardian Today: the headlines, the analysis, the debate - sent direct to you Read more “There’s an awful lot of time and money wasted in people going through a 12-week treatment that doesn’t work, then another 12-week treatment that doesn’t work ad nauseam,” she said. “There will never be a point where algorithms are making these decisions in isolation; side effects have to be taken into account, for example. But this is a process of identifying treatment the clinician can use when debating a bunch of drugs – when they have no idea which will work through no fault of their own – for a particular patient.” © 2017 Guardian News and Media Limited

Keyword: Depression
Link ID: 24458 - Posted: 12.26.2017

By Sally Abrahams BBC News For years, Mary Rose struggled to get off to sleep or to stay asleep, because she felt like she was being attacked by insects. "Imagine having a swarm of bees buzzing inside the skin of your legs, biting you," she says, describing the sensation that overwhelmed her. "It's really very, very painful." Now in her 80s, the art historian has a condition called restless legs syndrome (RLS), which tortures her at night. "It makes you want to scratch your legs and get up and walk about - it was just impossible to lie down and sleep because one's legs were twitching in this uncontrollable way," she explained. The symptoms were so severe, she didn't want to go to bed at night. 'No sleep at all' Mary Rose can't remember when the problem began, but the condition went undiagnosed for years. "People would say 'oh you've got cramp; you must take quinine or sleep with corks in your bed'. And I did all these things." Of course, they had no effect. She also tried rubbing ointment into her legs to ease the stinging sensation, but that never lasted long enough to let her sleep through the night. Visits to her GP also failed to bring relief. Eventually, she was referred to the sleep clinic at Guy's and St Thomas's hospitals in London, where she's now being treated by neurologist Dr Guy Leschziner. "Restless legs syndrome is a common neurological disorder that causes an irresistible urge to move, particularly at night, and is often linked with unpleasant sensations in the legs," Dr Leschziner explains. "It affects up to one in 20 adults," he continues, "and can cause severe sleep deprivation." At its worst, Mary Rose was surviving on only a few hours' sleep at night, sometimes even less. "I have had complete nights without any sleep at all," she says. © 2017 BBC

Keyword: Sleep; Movement Disorders
Link ID: 24457 - Posted: 12.26.2017

Michael May Carl Luepker suffers from a nerve disorder which causes involuntary muscle spasms. He lived with the symptoms for 30 years until he discovered he'd passed the genetic disorder on to his son. NOEL KING, HOST: Parents make all kinds of sacrifices for their children, but what do you do when you want to save your child from experiencing the same kind of suffering you have experienced? NPR's Michael May brings us the story of one father who's searching for a way to ease his son's discomfort that's caused by a shared genetic disorder. MICHAEL MAY, BYLINE: Carl Luepker suffers from dystonia, a disorder that causes involuntary muscle spasms. When I met him 30 years ago, Carl's spasms were in his right hand. Then they spread to the muscles of his face until they garbled his speech. Last December, Carl sat down in the office of his neurologist, Dr. Jerrold Vitek, to discuss a surgery called deep brain stimulation. CARL LUEPKER: My fears are - obviously, first is death. MAY: It's not an easy decision to let a doctor drill a hole in your skull and put electrodes deep in your brain. LUEPKER: Those are sort of my three biggest fears, are death, loss of cognition and any behavioral changes I might incur from the procedure. JERROLD VITEK: Well, Carl, what I would say is that the potential risk is about a 1 to 2 percent chance that there'd be a significant bleed. That's the greatest risk. The chance of benefit is marked. The vast majority of people will benefit. MAY: Deep brain stimulation has been called a pacemaker for the brain. It regulates the neurons that are misfiring. It's used for everything from Parkinson's disease to major depression. Scientists still don't understand exactly why DBS works. But for some patients, it dramatically reduces symptoms. At first, scientists literally destroyed the part of the brain that was malfunctioning. Vitek says there's a reason doctors would be willing to try something so brutal. VITEK: One word will answer that - desperation. © 2017 npr

Keyword: Movement Disorders; Genes & Behavior
Link ID: 24456 - Posted: 12.26.2017

By Judith Graham, Ask Edith Smith, a proud 103-year-old, about her friends, and she’ll give you an earful. There’s Johnetta, 101, whom she’s known for 70 years and who has Alzheimer’s disease. “I call her every day and just say ‘Hi, how are you doing?’ She never knows, but she says hi back, and I tease her,” Smith said. There’s Katie, 93, whom Smith met during a long teaching career with the Chicago Public Schools. “Every day we have a good conversation. She’s still driving and lives in her own house, and she tells me what’s going on.” Then there’s Rhea, 90, whom Smith visits regularly at a retirement facility. And Mary, 95, who doesn’t leave her house anymore, “so I fix her a basket about once a month of jelly and little things I make and send it over by cab.” And fellow residents at Smith’s Chicago senior community, whom she recognizes with a card and a treat on their birthdays. “I’m a very friendly person,” Smith said, when asked to describe herself. That may be one reason why this lively centenarian has an extraordinary memory for someone her age, suggests a recent study by researchers at Northwestern University highlighting a notable link between brain health and positive relationships. For nine years, these experts have been examining “SuperAgers”—men and women over age 80 whose memories are as good—or better—than people 20 to 30 years younger. Every couple of years, the group fills out surveys about their lives and gets a battery of neuropsychological tests, brain scans and a neurological examination, among other evaluations. © 2017 Scientific American,

Keyword: Stress
Link ID: 24455 - Posted: 12.26.2017

By Katarina Zimmer | CRISPR-Cas9 gene editing can extend survival in a mouse model of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease, according to a study published yesterday (December 20) in Science Advances. “The treatment did not make the ALS mice normal and it is not yet a cure,” study coauthor David Schaffer, a professor of chemical and biomolecular engineering at the University of California, Berkeley, says in a press release. “But based upon what I think is a really strong proof of concept, CRISPR-Cas9 could be a therapeutic molecule for ALS.” ALS, or Lou Gehrig’s disease, affects some 20,000 Americans and is characterized by the premature death of motor neurons in the brain stem and spinal cord. The disease causes progressive muscle deterioration and eventually results in paralysis and death. There are no available treatments to delay the muscle wasting and currently approved drugs can extend survival by a few months at most. Schaffer and his colleagues suspected that ALS could be treated through genome editing because some forms of the disease (around 20 percent of inherited forms and 2 percent of all cases) are caused by dominant mutations in a gene that encodes superoxide dismutase 1 (SOD1), an enzyme that helps protect cells against toxic free radicals. © 1986-2017 The Scientist

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 24454 - Posted: 12.22.2017

Michaeleen Doucleff It's not every day that surgeons develop a new brain surgery that could save tens of thousands of babies, even a hundred thousand, each year. And it's definitely not every day that the surgery is developed in one of the world's poorest countries. But that's exactly what neurosurgeons from Boston and Mbale, Uganda, report Wednesday in the New England Journal of Medicine. The treatment is for a scary condition in which a baby's head swells up, almost like balloon. It's called hydrocephalus, or "water on the brain." But a more accurate description is "spinal fluid inside the brain." Inside our brains, there are four chambers that continually fill up and release spinal fluid. So their volume stays constant. In babies with hydrocephalus, the chambers don't drain properly. They swell up, putting pressure on the brain. If left untreated about half the children will die, and the others will be badly disabled. Traditionally doctors treat hydrocelphalus in the U.S. with what's called a shunt: They place a long tube in the baby's brain, which allows the liquid to drain into the child's stomach. © 2017 npr

Keyword: Development of the Brain
Link ID: 24453 - Posted: 12.22.2017

By Rebecca Keogh Imagine you are at Ikea to pick up a sofa for your new flat. You see one you like, a wine-coloured two-seater with big soft cushions. You imagine what it would look like with your current furniture, and decide that’s the sofa you want. As you continue meandering through the store you find a nice industrial-style lamp and coffee table, so you try to imagine what they might look like with the sofa. But imagining all three items together is more difficult than just imagining the sofa alone. How many pieces of furniture do you think you could rearrange in your mind? Is there a limit to how much we can imagine at once, or is our imagination truly unlimited? viewpoints Limitations to our imagery can constrain what we are able to achieve, both in daily life and in therapeutic interventions. This is the question that my supervisor and I tried to answer in our lab at the University of New South Wales recently. Instead of furniture, we used simple shapes known as Gabor patches, which are essentially circles with lines through them. We also used a visual illusion known as binocular rivalry. Binocular rivalry occurs when two different images are shown, one to each eye, and instead of seeing a mix of the two images you see only one of them, either the image that was presented to the left eye or the image presented to the right eye. Previous work by Joel Pearson (my supervisor) has shown that simply imagining a Gabor patch, or seeing a very weak Gabor patch, will make you more likely to see that image in a subsequent binocular rivalry display. Copyright 2017 Undark

Keyword: Vision; Attention
Link ID: 24452 - Posted: 12.22.2017

A promising approach to post-operative incision-site pain control uses a naturally occurring plant molecule called resiniferatoxin (RTX). RTX is found in Euphorbia resinifera, a cactus-like plant native to Morocco, which is 500 times more potent than the chemical that produces heat in hot peppers, and may help limit the use of opioid medication while in the hospital and during home recovery. In a paper published online in Anesthesiology, the peer-reviewed medical journal of the American Society of Anesthesiologists, researchers found that RTX could be used to block postoperative incisional pain in an animal model. Many medical providers turn to opioids, such as morphine or fentanyl, for moderate to severe post-operative pain relief, but these often come with side effects that can interfere with recovery, including respiratory depression, inhibition of gut motility and constipation, nausea and vomiting. Prolonged use of opioids can produce tolerance and introduces the risk of misuse. RTX is not an opioid and does not act in the brain but rather on the nerve endings in the skin. Scientists found that it can be used to block pain from the surgical incision selectively for approximately 10 days. In the study, researchers pre-treated the skin incision site with RTX to render the nerve endings in the skin and subcutaneous tissue along the incision path selectively insensitive to pain. Unlike local anesthetics, which block all nerve activity including motor axons, RTX allows many sensations, like touch and vibration, as well as muscle function, to be preserved. Long after the surgery, and towards the end of healing of an incision wound, the nerve endings eventually grow back. Thus, pain from the skin incision is reduced during the recovery period.

Keyword: Pain & Touch
Link ID: 24451 - Posted: 12.22.2017

By Catherine Offord Jerrold Olefsky has spent much of the last decade trying to decipher the connection between obesity and the risk for type 2 diabetes. It’s now known that “in obesity, the adipose tissue becomes highly inflamed and fills up with macrophages and other immune cells,” Olefsky, an endocrinologist at the University of California, San Diego, explains. “This inflammation is very important for causing insulin resistance,” in which cells fail to respond to hormonal signals to take up glucose. But a crucial piece of the puzzle has been missing. “Insulin resistance is a systemic thing,” Olefsky says. For inflamed fat tissue to trigger it, “somehow, all the tissues must talk to each other. We just didn’t know how.” Research has not supported a major role for early suspects such as cytokines. But reading a paper a few years ago on the role of tiny vesicles called exosomes in intercellular communication in cancer, Olefsky was struck by the fact that, “Well, gee, all these cells make exosomes.” Known to carry microRNAs (miRNAs)—small nucleic acids that influence gene expression—exosomes seemed like plausible candidates for an inter-tissue communication system in obesity. Olefsky’s group isolated macrophages from adipose tissue in obese and lean mice and harvested exosomes produced by the cells in vitro. Then, the researchers added these vesicles to cultured muscle, liver, and fat cells—major insulin targets in the body. While lean-type exosomes made recipient cells “super insulin-sensitive,” Olefsky says, obese-type exosomes induced insulin resistance. In vivo work showed a similar effect: lean mice injected with obese-type exosomes became insulin resistant without gaining weight, while obese mice treated with lean-type exosomes stayed obese, but developed normalized insulin sensitivity. © 1986-2017 The Scientist

Keyword: Obesity
Link ID: 24450 - Posted: 12.22.2017