By Jim Robbins TUCSON, Ariz. — In a small room in a building at the Arizona-Sonora Desert Museum, the invertebrate keeper, Emma Califf, lifts up a rock in a plastic box. “This is one of our desert hairies,” she said, exposing a three-inch-long scorpion, its tail arced over its back. “The largest scorpion in North America.” This captive hairy, along with a swarm of inch-long bark scorpions in another box, and two dozen rattlesnakes of varying species and sub- species across the hall, are kept here for the coin of the realm: their venom. Efforts to tease apart the vast swarm of proteins in venom — a field called venomics — have burgeoned in recent years, and the growing catalog of compounds has led to a number of drug discoveries. As the components of these natural toxins continue to be assayed by evolving technologies, the number of promising molecules is also growing. “A century ago we thought venom had three or four components, and now we know just one type of venom can have thousands,” said Leslie V. Boyer, a professor emeritus of pathology at the University of Arizona. “Things are accelerating because a small number of very good laboratories have been pumping out information that everyone else can now use to make discoveries.” She added, “There’s a pharmacopoeia out there waiting to be explored.” It is a striking case of modern-day scientific alchemy: The most highly evolved of natural poisons on the planet are creating a number of effective medicines with the potential for many more. One of the most promising venom-derived drugs to date comes from the deadly Fraser Island funnel web spider of Australia, which halts cell death after a heart attack. Blood flow to the heart is reduced after a heart attack, which makes the cell environment more acidic and leads to cell death. The drug, a protein called Hi1A, is scheduled for clinical trials next year. In the lab, it was tested on the cells of beating human hearts. It was found to block their ability to sense acid, “so the death message is blocked, cell death is reduced, and we see improved heart cell survival,” said Nathan Palpant, a researcher at the University of Queensland in Australia who helped make the discovery. © 2022 The New York Times Company

Keyword: Pain & Touch; Neurotoxins
Link ID: 28315 - Posted: 05.04.2022

Ellen Phiddian Tricyclic antidepressants have long been known to have more than one purpose: among other things, they can alleviate pain – particularly nerve pain. Recent research has finally established why these tricyclic antidepressants (TCAs) can help with nerve pain. The discovery could lead to the rapid development of pain relief medications that don’t include the side effects of TCAs. Nerve pain comes from a variety of sources – including cancer, diabetes, trauma, multiple sclerosis, and infections. These treatments could address a range of different types of nerve pain. It turns out the drugs inhibit a key protein in our nerves, called an N-type calcium channel. These N-type calcium channels are shaped like tiny gates, allowing positively charged calcium ions, or Ca2+, through them. This helps with the transmission of pain signals in the body. Researchers have long been keen to find things that “close” the gate of these calcium channels because that’s likely to have analgesic effects. Adjunct Professor Peter Duggan, a researcher with the CSIRO and senior collaborator on the project, says that he and his colleagues initially stumbled across TCAs from a very different direction: they were investigating the toxins of venomous marine cone snails. “A few of the components in that toxin are actually painkillers and they block these calcium ion channels very, very effectively,” says Duggan. The cone snail toxin has the potential to be very dangerous to people, as well as needing to be administered in an impractical way, so the researchers started looking at similar compounds that might have some of the same properties.

Keyword: Pain & Touch; Depression
Link ID: 28312 - Posted: 05.04.2022

By Helen Ouyang After an hour-and-a-half bus ride last November, Julia Monterroso arrived at a white Art Deco building in West Hollywood, just opposite a Chanel store and the Ivy, a restaurant famous for its celebrity sightings. Monterroso was there to see Brennan Spiegel, a gastroenterologist and researcher at Cedars-Sinai who runs one of the largest academic medical initiatives studying virtual reality as a health therapy. He started the program in 2015 after the hospital received a million-dollar donation from an investment banker on its board. Spiegel saw Monterroso in his clinic the week before and thought he might be able to help alleviate her symptoms. Monterroso is 55 and petite, with youthful bangs and hair clipped back by tiny jeweled barrettes. Eighteen months earlier, pain seized her lower abdomen and never went away. After undergoing back surgery in September to treat a herniated disc — and after the constant ache in her abdomen worsened — she had to stop working as a housecleaner. Eventually, following a series of tests that failed to reveal any clear cause, she landed in Spiegel’s office. She rated her pain an 8 on a 10-point scale, with 10 being the most severe. Chronic pain is generally defined as pain that has lasted three months or longer. It is one of the leading causes of long-term disability in the world. By some measures, 50 million Americans live with chronic pain, in part because the power of medicine to relieve pain remains woefully inadequate. As Daniel Clauw, who runs the Chronic Pain and Fatigue Research Center at the University of Michigan, put it in a 2019 lecture, there isn’t “any drug in any chronic-pain state that works in better than one out of three people.” He went on to say that nonpharmacological therapy should instead be “front and center in managing chronic pain — rather than opioids, or for that matter, any of our drugs.” Virtual reality is emerging as an unlikely tool for solving this intractable problem. The V.R. segment in health care alone, which according to some estimates is already valued at billions of dollars, is expected to grow by multiples of that in the next few years, with researchers seeing potential for it to help with everything from anxiety and depression to rehabilitation after strokes to surgeons strategizing where they will cut and stitch. In November, the Food and Drug Administration gave authorization for the first V.R. product to be marketed for the treatment of chronic pain. © 2022 The New York Times Company

Keyword: Pain & Touch; Vision
Link ID: 28304 - Posted: 04.27.2022

By Brittany Shammas and Timothy Bella William Husel, an Ohio doctor who was accused of killing 14 patients with what prosecutors described as “wildly excessive” doses of fentanyl between 2015 and 2018, was acquitted on all counts of murder Wednesday, concluding one of the most significant murder cases of its kind against a health-care professional. Husel, a onetime physician of the year trained at the Cleveland Clinic, faced one count of murder for each of the 14 critically ill patients he was accused of killing. The jury deliberated for seven days before finding him not guilty on all 14 counts in what was one of the largest murder trials in Ohio history. He had been charged with causing or hastening their deaths amid a period of lax oversight of fentanyl at Mount Carmel West, a Catholic hospital in Columbus. Husel would have faced life in prison with just one guilty verdict. While the synthetic opioid is significantly more powerful than morphine and has wreaked havoc on American streets, it can provide pain relief in medical settings that is crucial to end-of-life care. The alleged victims in the Ohio case suffered critical medical conditions including overdoses, cancer, strokes and internal bleeding. Prosecutors acknowledged that all were being kept alive on ventilators and that many of them were dying. “In truth, William Husel was an innocent man, and thank goodness the justice system prevailed,” Jose Baez, one of Husel’s defense attorneys, told reporters. The 46-year-old’s acquittal came after a two-month trial that triggered a debate on end-of-life medical care. Husel and Baez argued in the trial that the doctor offered comfort care for dying patients and was not trying to kill them. They pointed out that the doctor’s actions did not occur in secret — nurses were the ones to administer the doses — and alleged that hospital officials made Husel the villain after realizing the systemic failures at play. The fallout over the allegations at Mount Carmel West had repercussions: the firing of 23 employees; the resignation of the hospital’s chief executive, chief clinical officer and chief pharmacy officer; and Medicare and Medicaid funding for the institution was put in jeopardy. © 1996-2022 The Washington Post

Keyword: Pain & Touch; Drug Abuse
Link ID: 28297 - Posted: 04.23.2022

ByKelly Servick An experimental pain drug that may offer an alternative to opioids has shown promise in two small clinical trials for acute pain, its developer announced today. Vertex Pharmaceuticals’s compound, called VX-548, outperformed a placebo in phase 2 trials for two types of postsurgical pain, the company said in a press release. The results pave the way for larger trials that could lead to regulatory approval. “This is a major advance in the effort to supersede opioids,” says John Wood, a neurobiologist at University College London who has studied the cellular channel that VX-548 targets. “These results are terrific, and the side effect profile is very good.” Opioids are powerful pain relievers, but they can cause side effects including slowed breathing, and they come with the potential for addiction. An epidemic of overdose deaths has prompted a hunt for safer alternatives. The new trials grew out of research into sodium channels on the surface of pain-sensing neurons, which let them fire electrical signals. One such channel, called Nav1.8, is crucial to relaying pain signals to the spinal cord from nerves throughout the body. People with genetic mutations that make Nav1.8 hyperactive can suffer pain even in the absence of injury. But relieving pain by blocking either Nav1.8 or another channel, Nav1.7, has proved difficult. One issue is their structure closely resembles those of other sodium channels, which regulate vital functions in the heart, muscles, and brain. To be safe, a compound needs to target the channel of interest and not accidentally target these other, critical channels. Vertex has spent years developing highly specific Nav1.8-blocking drugs, but it has abandoned previous candidates before they reached pivotal phase 3 trials. One drug, known as VX-150, succeeded in three phase 2 clinical studies but never advanced to larger ones, in part because its high dose might be impractical for clinical use. “We wanted to have higher potency,” explains Vertex Chief Scientific Officer David Altshuler. © 2022 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 28265 - Posted: 04.02.2022

By Lisa Sanders, M.D. The 51-year-old man sat at his desk preparing for his next online meeting when he suddenly became aware of a familiar stiffness and exhaustion. Had he slept badly? Or was this the beginning of one of his strange episodes? As the symptoms worsened, he had his answer. He knew that when he started to feel this way, the only recourse was to get into bed before he got any weaker. As he made his way slowly down the hall, his legs felt heavy, as if he were wearing ankle weights. Just lifting them was real work. He passed his wife’s home office without a word. She knew just from looking at him that he would probably have to spend the rest of the day in bed. For much of their 30-year marriage, he had these strange spells; he would suddenly feel exhausted and weak and have to lie down. He couldn’t work. He was a software engineer, and any mental exertion was too much for him. Once the fatigue fully set in — maybe after the first hour or so — he couldn’t walk, couldn’t stand, couldn’t even sit up. It was as if his body was totally out of gas, worse than how it felt when he ran a marathon. He would lie in a dark room, too weak to even hold up a book and too tired to think. But by the next morning, he would usually be fine, brimming with energy and enthusiasm, like normal. It was so strange. After more than 20 years, they both had come to expect these episodes. For most of that time, the spells were infrequent, maybe once a month. But recently they became more frequent. The monthly episodes became weekly, then a couple of times a week. They often came, as they did that morning, out of nowhere. Just before leaving his office, he sent an email to the woman he was to meet online. Sorry, he wrote, I’m not feeling well. Could we reschedule? Seeing a Psychiatrist Over the years the man saw many doctors. They had their theories, but so far none panned out. A few were convinced that he had periodic paralysis, a disorder sometimes linked to thyroid disease, where patients become temporarily paralyzed by too much or too little potassium in the bloodstream. But his potassium was always normal, even during these episodes. © 2022 The New York Times Company

Keyword: Pain & Touch
Link ID: 28263 - Posted: 04.02.2022

Gabino Iglesias The Man Who Tasted Words is a deep dive into the world of our senses — one that explores the way they shape our reality and what happens when something malfunctions or functions differently. Despite the complicated science permeating the narrative and the plethora of medical explanations, the book is also part memoir. And because of the way the author, Dr. Guy Leschziner, treats his patients — and how he presents the ways their conditions affect their lives and those of the people around them — it is also a very humane, heartfelt book. We rely on vision, hearing, taste, smell, and touch to not only perceive the reality around us but also to help us navigate it by constantly processing stimuli, predicting what will happen based on previous experiences, and filling the gaps of everything we miss as we construct it. However, that truth, the "reality" we see, taste, hear, touch, and smell, isn't actually there; our brains, with the help of our nervous system continuously build it for us. But sometimes our brains or nervous system have a glitch, and that has affects reality. The Man Who Tasted Words carefully looks at — and tries to explain — some of the most bizarre glitches. Sponsor Message "What we believe to be a precise representation of the world around us is nothing more than an illusion, layer upon layer of processing of sensory information, and the interpretation of that information according to our expectations," states Leschziner. When one of those senses doesn't work correctly, that illusion morphs in ways that significantly impact the lives of those whose nervous systems or brain work differently. Paul, for example, is a man who feels no pain. While this sounds like a great "flaw" to have, Leschziner shows it's the opposite. Pain helps humans learn "to avoid sharp or hot objects." It teaches that certain things in our environment are potentially harmful, tells us when we've had an injury and makes us protect it, and even lets us know there's an infection in our body so we can go to the doctor. © 2022 npr

Keyword: Consciousness
Link ID: 28233 - Posted: 03.11.2022

By Jan Hoffman For years, Dr. Xiulu Ruan was one of the nation’s top prescribers of quick-release fentanyl drugs. The medicines were approved only for severe breakthrough pain in cancer patients, but Dr. Ruan dispensed them almost exclusively for more common ailments: neck aches, back and joint pain. According to the Department of Justice, he and his partner wrote almost 300,000 prescriptions for controlled substances from 2011 to 2015, filled through the doctors’ own pharmacy in Mobile, Ala. Dr. Ruan often signed prescriptions without seeing patients, prosecutors said. Dr. Ruan has been serving a 21-year sentence in federal prison, convicted in 2017 for illegally prescribing opioids and related financial crimes. To collect millions of dollars in fines, the government seized houses, beach condos and bank accounts belonging to him and his business partner, as well as 23 luxury cars, such as Bentleys, Lamborghinis and Ferraris. On Tuesday, lawyers both for Dr. Ruan and for Dr. Shakeel Kahn, who is serving 25 years on charges related to pill mill clinics in Arizona and Wyoming will argue before the Supreme Court of the United States that the criminal standard the physicians faced is applied inconsistently among the federal circuits. In asking that the doctors’ convictions be overturned, they want the court to establish a uniform standard that permits doctors to raise a “good faith” defense. Juries could then consider whether doctors subjectively believed they were using their best medical judgment. The likelihood of these two doctors being set free is small, legal experts believe, but the court’s decision on the broader legal questions could have significant implications for the latitude doctors can take in prescribing potentially addictive painkillers and other restricted medications. The cases confront an uneasy relationship between law and medicine. In an era when overdose deaths are soaring, how should the law balance letting physicians exercise their best judgment with stopping egregious outliers? © 2022 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 28226 - Posted: 03.02.2022

By Jan Hoffman The federal government on Thursday proposed new guidelines for prescribing opioid painkillers that remove its previous recommended ceilings on doses for chronic pain patients and instead encourage doctors to use their best judgment. But the overall thrust of the recommendations was that doctors should first turn to “nonopioid therapies” for both chronic and acute pain, including prescription medications like gabapentin and over-the-counter ones like ibuprofen, as well as physical therapy, massage and acupuncture. Though still in draft form, the 12 recommendations, issued by the Centers for Disease Control and Prevention, are the first comprehensive revisions of the agency’s opioid prescribing guidelines since 2016. They walk a fine line between embracing the need for doctors to prescribe opioids to alleviate some cases of severe pain while guarding against exposing patients to the well-documented perils of opioids. Dr. Samer Narouze, president of the American Society of Regional Anesthesia and Pain Medicine, an association of clinicians, praised the tone, level of detail and focus of the project. “It’s a total change in the culture from the 2016 guidelines,” he said, characterizing the earlier edition as ordering doctors to “just cut down on opioids — period.” By contrast, the new proposal “has a much more caring voice than a policing one, and it’s left room to preserve the physician-patient relationship,” added Dr. Narouze, chairman of the Center for Pain Medicine at Western Reserve Hospital in Cuyahoga Falls, OH. The 229-page document warns of addiction, depressed breathing, altered mental status and other dangers associated with opioids, but it also notes that the drugs serve an important medical purpose, especially for easing the immediate agony from traumatic injuries such as burns and crushed bones. In those instances when opioids seem the way to go, the recommendations said, doctors should start with the lowest effective dose and prescribe immediate-release pills rather than long-acting ones. © 2022 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 28207 - Posted: 02.16.2022

Chloe Tenn On October 4, physiologist David Julius and neurobiologist Arden Patapoutian were awarded the Nobel Prize in Physiology or Medicine for their work on temperature, pain, and touch perception. Julius researched the burning sensation people experience from chilies, and identified an ion channel, TRPV1 that is activated by heat. Julius and Patapoutian then separately reported on the TRPM8 ion channel that senses menthol’s cold in 2002. Patapoutian’s group went on to discover the PIEZO1 and PIEZO2 ion channels that are involved in sensing mechanical pressure. The Nobel Committee wrote that the pair’s work inspired further research into understanding how the nervous system senses temperature and mechanical stimuli and that the laureates “identified critical missing links in our understanding of the complex interplay between our senses and the environment.” This year saw innovations in augmenting the brain’s capabilities by plugging it in to advanced computing technology. For example, a biology teacher who lost her vision 16 years ago was able to distinguish shapes and letters with the help of special glasses that interfaced with electrodes implanted in her brain. Along a similar vein, a computer connected to a brain-implant system discerned brain signals for handwriting in a paralyzed man, enabling him to type up to 90 characters per minute with an accuracy above 90 percent. Such studies are a step forward for technologies that marry cutting-edge neuroscience and computational innovation in an attempt to improve people’s lives. © 1986–2021 The Scientist.

Keyword: Pain & Touch; Language
Link ID: 28134 - Posted: 12.31.2021

By Cara Giaimo Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. It’s tough out there for a mouse. Outdoors, its enemies lurk on all sides: owls above, snakes below, weasels around the bend. Indoors, a mouse may find itself targeted by broom-wielding humans or bored cats. Mice compensate with sharp senses of sight, hearing and smell. But they may have another set of tools we’ve overlooked. A paper published last week in Royal Society Open Science details striking similarities between the internal structures of certain small mammal and marsupial hairs and those of man-made optical instruments. In this paper as well as other unpublished experiments, the author, Ian Baker, a physicist who works in private industry, posits that these hairs may act as heat-sensing “infrared antennae” — further cluing the animals into the presence of warm-blooded predators. Although much more work is necessary to connect the structure of these hairs to this potential function, the study paints an “intriguing picture,” said Tim Caro, a professor of evolutionary ecology at the University of Bristol in England who was not involved. Dr. Baker has spent decades working with thermal imaging cameras, which visualize infrared radiation produced by heat. For his employer, the British defense company Leonardo UK Ltd., he researches and designs infrared sensors. But in his spare time he often takes the cameras to fields and forests near his home in Southampton, England, to film wildlife. Over the years, he has developed an appreciation for “how comfortable animals are in complete darkness,” he said. That led him to wonder about the extent of their sensory powers. © 2021 The New York Times Company

Keyword: Pain & Touch; Evolution
Link ID: 28120 - Posted: 12.18.2021

Jon Hamilton Scientists may have learned why opioids depress breathing while relieving pain. The finding could lead to pain drugs that don't cause respiratory failure, the usual cause of death in opioid overdoses. When people feel pain, they tend to breathe faster. When they take an opioid to kill that pain, their breathing slows down. Now scientists think they know how pain and respiration are connected in the brain. NPR's Jon Hamilton reports that the discovery could eventually lead to safer pain drugs. JON HAMILTON, BYLINE: Sung Han has been studying the link between pain and breathing in his lab at the Salk Institute in San Diego. But he got a real-world demonstration recently while taking a shower. SUNG HAN: I forgot to change the temperature, and the cold water just suddenly came out and covered my entire body. And then I just - I was breathing really fast. HAMILTON: A typical reaction to what Han calls aversive sensory information - and he thinks he knows the cause. Han's lab has identified a brain circuit in mice that appears to link the emotional experience of pain to breathing rhythm. Han says the circuit involves two populations of brain cells both found in the same small area of the brain stem. HAN: One population regulate pain and the other population regulate breathing, and that's the reason why pain and breathing are interacting each other. HAMILTON: They're linked together. If that's also true in people, it would help explain the mysterious connection between breathing and emotion, which has puzzled scientists for centuries. And the finding, which appears in the journal Neuron, could also have practical applications. That's because both groups of brain cells - the ones for breathing and the ones for pain - respond to opioids. Han says this is why an overdose can be fatal. © 2021 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 28117 - Posted: 12.18.2021

By Lisa Sanders, M.D. The 66-year-old man had just started his third lap at the community swimming pool outside Poughkeepsie, N.Y., when it struck. As he was turning his head to take a breath, an octopus of pain wrapped around the right side of his skull, starting at the joint where the jaw connects and slamming across his face and head with tentacles of squeezing agony. For a moment he was paralyzed — first with pain, then with fear. He couldn’t breathe; he could barely move. He struggled to the side of the pool and hung on, his breath ragged through involuntarily clenched teeth. His wife hurried over. He was a good swimmer; what was wrong? She saw his lips move and leaned closer. His jaw was clenched. “I can’t speak,” he mumbled. She helped him out of the pool. “We’re going to go to urgent care,” she said as she handed him a towel. These strange pains had been tormenting the man for nearly three weeks. It started as a headache that woke him from a dead sleep, a squeezing pressure deep inside his brain. He got up and took some acetaminophen. When he awoke the next morning, the headache was gone, but the regions around his head and face where the pressure had been strongest felt strangely tender. He couldn’t even brush his hair on the right side of his head. Bizarre as this was, he most likely would have soon forgotten about it except that it happened again the next night — and just about every night since. The pain in his jaw started a couple of days later. Opening and closing his mouth, and especially chewing, made his jaw throb. Eating anything more solid than mashed potatoes triggered excruciating pain. He went to his dentist, who poked and prodded. The only tenderness was in the joint where the jaw attached to the skull. It’s most likely TMJ, the dentist concluded — temporomandibular joint pain. That joint and the many attached muscles make speech and facial expressions possible. Lots of people have pain there, the dentist added. Bad habits like jaw-clenching and tooth-grinding aggravate the joint. The treatment is behavior modification to unlearn these habits, and sometimes a bite block, a custom-made piece of acrylic worn at night to protect teeth from injury. © 2021 The New York Times Company

Keyword: Pain & Touch; Neuroimmunology
Link ID: 28113 - Posted: 12.15.2021

By David Dobbs Chronic pain is both one of the world’s most costly medical problems, affecting one in every five people, and one of the most mysterious. In the past two decades, however, discoveries about the crucial role played by glia — a set of nervous system cells once thought to be mere supports for neurons — have rewritten chronic pain science. These findings have given patients and doctors a hard-science explanation that chronic pain previously lacked. By doing so, this emerging science of chronic pain is beginning to influence care — not by creating new treatments, but by legitimizing chronic pain so that doctors take it more seriously. Although glia are scattered throughout the nervous system and take up almost half its space, they long received far less scientific attention than neurons, which do the majority of signaling in the brain and body. Some types of glia resemble neurons, with roughly starfish-like bodies, while others look like structures built with Erector sets, their long, straight structural parts joined at nodes. When first discovered in the mid-1800s, glia — from the Greek word for glue — were thought to be just connective tissue holding neurons together. Later they were rebranded as the nervous system’s janitorial staff, as they were found to feed neurons, clean up their waste and take out their dead. In the 1990s they were likened to secretarial staff when it was discovered they also help neurons communicate. Research over the past 20 years, however, has shown that glia don’t just support and respond to neuronal activity like pain signals — they often direct it, with enormous consequences for chronic pain. If you’re hearing this for the first time and you’re one of the billion-plus people on Earth who suffer from chronic pain (meaning pain lasting beyond three to six months that has no apparent cause or has become independent of the injury or illness that caused it), you might be tempted to say that your glia are botching their pain-management job. © 2021 The New York Times Company

Keyword: Pain & Touch; Glia
Link ID: 28075 - Posted: 11.13.2021

By James Gallagher An innovative type of medicine - called gene silencing - is set to be used on the NHS for people who live in crippling pain. The drug treats acute intermittent porphyria, which runs in families and can leave people unable to work or have a normal life. Clinical trials have shown severe symptoms were cut by 74% with the drug. While porphyria is rare, experts say the field of gene silencing has the potential to revolutionise medicine. Sisters Liz Gill and Sue Burrell have both had their lives turned around by gene silencing. Before treatment, Liz, from County Durham, remembers the trauma of living in "total pain" and, at its worst, she spent two years paralysed in hospital. Younger sister Sue says she "lost it all overnight" when she was suddenly in and out of hospital, made redundant and did know whether her partner would stick with her (he did). "It was scary," she tells me. Both became used to taking potent opioid painkillers on a daily basis. But even morphine could not block the pain during a severe attack that needed hospital treatment. Gene silencing gets to the root-cause of the sisters' disease rather than just managing their symptoms. Their porphyria leads to a build-up of toxic proteins in the body, that cause the physical pain. Gene silencing "mutes" a set of genetic instructions to block that protein production. Both had been taking the therapy as part of a clinical trial and are still getting monthly injections. © 2021 BBC.

Keyword: Pain & Touch
Link ID: 28046 - Posted: 10.23.2021

Brenda Patoine Science likes to package its successes in neat stories that show a clear progression from this to that. The “bench-to-bedside” story—when biological insights yield targeted treatments—is a long-time favorite. Reality, however, doesn’t always cooperate, and history is littered with basic-science discoveries that seemed important but failed to yield viable treatments. When they do succeed, it’s cause for celebration—and awards. Migraine research is an example. Although it is the second most disabling condition in the world, affecting one billion people, migraine had long been relegated to the backwaters of scientific research. Only recently has research bloomed—scientific papers sharply increased from the 1990s onward, with discoveries in basic science driving a new class of drugs that some in the field are calling game changers. This year, the recognition of four migraine researchers with a major neuroscience award has pushed the field into the limelight of science. The 2021 Brain Prize recognizes science that embodies the so-called bench-to-bedside research described above. That’s a jargony term scientists seem to love that denotes the rare and wonderful occurrence when laboratory research aimed at illuminating fundamental mechanisms (the “bench”) yields insights that lead to drugs that ultimately help millions of sick people (the “bedside”). In the case of migraine research, the leading character is a neuropeptide called calcitonin gene-related peptide (CGRP). © 2021 The Dana Foundation.

Keyword: Pain & Touch
Link ID: 28040 - Posted: 10.16.2021

Jordana Cepelewicz We often appreciate the world around us in terms of its glorious sights, stirring sounds and evocative smells, all of which mark important stimuli and changes in our environment. But senses that are no less crucial to our survival are often taken for granted, including our abilities to register heat, cold and touch, a form of perception called somatosensation. Because of them, we can feel the warmth of the sun or the gentle caress of a breeze against our skin, as well as the positions and movement of our own bodies. In fact, the somatosensory neurons that make all these sensations possible constitute the largest sensory system in mammals. Scientists knew that for somatosensation to occur, there must be molecular receptors on some cells that could detect temperature and touch, and could convert those stimuli into electrical and chemical signals for the nervous system to process. For the discovery of some of those receptors David Julius, a physiologist at the University of California, San Francisco, and Ardem Patapoutian, a molecular biologist and neuroscientist at Scripps Research in La Jolla, have now been awarded the 2021 Nobel Prize in Physiology or Medicine. Julius and his colleagues started with questions about receptors for heat and pain. To find answers, they turned to capsaicin, the compound that causes us to experience a burning and sometimes painful sensation when we eat chili peppers or other spicy food. Based on our physiological response to the chemical, which includes sweating, capsaicin seemed to be inducing the nervous system to register a change in body temperature. To figure out how, Julius and his team screened millions of DNA fragments for a gene that could induce a response to the compound in cells that typically don’t react to it at all. After an arduous search, and what the Nobel Prize committee called “a high-risk project,” the researchers identified a gene that allowed cells to sense capsaicin. It encoded a novel ion channel protein, later called TRPV1, that Julius and his team discovered could be activated by hot temperatures perceived as painful. All Rights Reserved © 2021

Keyword: Pain & Touch
Link ID: 28025 - Posted: 10.06.2021

Amanda Heidt Qin Liu studies sneezing for a personal reason: her entire family suffers from seasonal allergies. “Until you experience something chronically, it is really hard to appreciate how disruptive it can be,” says Liu, a neuroscientist at Washington University in St. Louis. And given the role of sneezing in pathogen transmission, a better understanding of the molecular underpinnings of the phenomenon could one day help scientists mitigate or treat infectious diseases. When Liu first started looking into the mechanisms governing sneezing, she found that scientists know surprisingly little about how this process works. While prior research had identified a region in the brains of cats and humans that is active during sneezing, the exact pathways involved in turning a stimulus like pollen or spicy food into a sneeze remained unknown. To study sneezing in more detail, Liu and her team developed a new model by exposing mice to irritants such as histamine and capsaicin—a chemical in spicy peppers—and characterizing the physical properties of their resulting sneezes. Then, focusing on that previously discovered sneeze center, located in the brain’s ventromedial spinal trigeminal nucleus (SpV), Liu attempted to map the neural pathway. SNEEZE TRIGGER: When exposed to allergens such as histamine or chemical irritants such as capsaicin (1), sensory neurons in the noses of mice produce a peptide called neuromedin B (NMB). This signaling molecule binds to neurons in a region of the brainstem known as the ventromedial spinal trigeminal nucleus (SpV), which is known to be active during sneezing (2). These neurons send electrical signals (3) to neurons in another brainstem region called the caudal ventral respiratory group (cVRG), which controls exhalation, thus driving the initiation and propagation of sneezing (4). Ablating the nasal neurons or disrupting NMB signaling led to a significantly reduced sneezing reflex in the mice. WEB | PDF © 1986–2021 The Scientist.

Keyword: Brain imaging; Pain & Touch
Link ID: 28014 - Posted: 10.02.2021

By Baland Jalal Obsessive-compulsive disorder (OCD) has puzzled artists and scientists for centuries. Afflicting one in 50 people, OCD can take several forms, such as compulsively putting things in just the right order or checking if the stove is turned off 10 times in a row. One type of OCD that affects nearly half of those with the condition entails irresistible washing urges. People with this type can spend hours scrubbing their hands in agitation after touching something as trivial as a doorknob even though they know this makes no sense. There is currently a shortage of effective therapies for OCD: 40 percent of patients do not benefit from existing treatments. A major issue is that today’s treatments are often too stressful. First-line “nonpharmacological therapies” involve telling patients to repeatedly touch things such as toilet seats and then refrain from washing their hands. But recent work by my colleagues and me has found something surprising: people diagnosed with OCD appear to have a more malleable “sense of self,” or brain-based “self-representation” or “body image”—the feeling of being anchored here and now in one’s body—than those without the disorder. This finding suggests new ways to treat OCD and perhaps unexpected insights into how our brain creates a distinction between “self” and “other.” In our recent experiments, for example, we showed that people with and without OCD responded differently to a well-known illusion. In our first study, a person without OCD watched as an experimenter used a paintbrush to stroke a rubber hand and the subject’s hidden real hand in precise synchrony. This induces the so-called rubber hand illusion: the feeling that a fake hand is your hand. When the experimenter stroked the rubber hand and the real one out of sync, the effect was not induced (or was greatly diminished). This compelling illusion illustrates how your brain creates your body image based on statistical correlations. It’s extremely unlikely for such stroking to be seen on a rubber hand and simultaneously felt on a hidden real one by chance. So your brain concludes, however illogically, that the rubber hand is part of your body. © 2021 Scientific American

Keyword: OCD - Obsessive Compulsive Disorder; Pain & Touch
Link ID: 27980 - Posted: 09.08.2021

Allison Whitten Our mushy brains seem a far cry from the solid silicon chips in computer processors, but scientists have a long history of comparing the two. As Alan Turing put it in 1952: “We are not interested in the fact that the brain has the consistency of cold porridge.” In other words, the medium doesn’t matter, only the computational ability. Today, the most powerful artificial intelligence systems employ a type of machine learning called deep learning. Their algorithms learn by processing massive amounts of data through hidden layers of interconnected nodes, referred to as deep neural networks. As their name suggests, deep neural networks were inspired by the real neural networks in the brain, with the nodes modeled after real neurons — or, at least, after what neuroscientists knew about neurons back in the 1950s, when an influential neuron model called the perceptron was born. Since then, our understanding of the computational complexity of single neurons has dramatically expanded, so biological neurons are known to be more complex than artificial ones. But by how much? To find out, David Beniaguev, Idan Segev and Michael London, all at the Hebrew University of Jerusalem, trained an artificial deep neural network to mimic the computations of a simulated biological neuron. They showed that a deep neural network requires between five and eight layers of interconnected “neurons” to represent the complexity of one single biological neuron. All Rights Reserved © 2021

Keyword: Brain imaging; Vision
Link ID: 27978 - Posted: 09.04.2021