By Smitha Mundasad Global Health Correspondent, BBC News Scientists say they have discovered the secret behind why some people are skinny while others pile on the pounds easily. Their work reveals newly discovered genetic regions linked to being very slim. The international team say this supports the idea that, for some people, being thin has more to do with inheriting a "lucky" set of genes than having a perfect diet or lifestyle. The study appears in PLOS Genetics. In the past few decades, researchers have found hundreds of genetic changes that increase the chance of a person being overweight - but there has been much less focus on the genes of people who are thin. In this investigation, scientists compared DNA samples from 1,600 healthy thin people in the UK - with a body mass index (BMI) of less than 18 - with those of 2,000 severely obese people and 10,400 people of normal weight. They also looked closely at lifestyle questionnaires - to rule out eating disorders, for example. Researchers found people who were obese were more likely to have a set of genes linked to being overweight. Meanwhile, people who were skinny not only had fewer genes linked to obesity but also had changes in gene regions newly associated with healthy thinness. Lead researcher Prof Sadaf Farooqi, from the University of Cambridge, called on people to be less judgemental about others' weight. "This research shows for the first time that healthy thin people are generally thin because they have a lower burden of genes that increase a person's chances of being overweight and not because they are morally superior, as some people like to suggest," she said. © 2019 BBC.

Keyword: Obesity; Genes & Behavior
Link ID: 25905 - Posted: 01.26.2019

Aimee Cunningham A sleep-deprived brain is awash in excess amounts of not one but two proteins whose bad behavior is implicated in Alzheimer’s disease. A new study finds excessive amounts of a protein called tau in the fluid that bathes the brain and spinal cord of extremely sleep-deprived adults. Tau, which is tied to nerve cell death, tangles and spreads throughout the brain during Alzheimer’s. An earlier report on these sleepy adults found that the protein amyloid-beta — globs of which dot the brains of Alzheimer’s patients — also increased. Samples of cerebrospinal fluid collected from eight adults, monitored during a night of normal sleep and over the course of 36 hours of sleep deprivation, revealed a 51.5 percent increase in tau in participants robbed of shut-eye. And sleep-deprived mice had twice the amount of tau as well-rested mice, researchers report online January 24 in Science. Earlier work by these researchers had suggested that the quality of sleep might affect tau levels; this time, it’s been linked to duration of sleep. With both A-beta and tau increasing with a lack of sleep, “it certainly argues that treating sleep disorders during mid-life as well as getting appropriate levels of sleep is likely to decrease risk for Alzheimer’s disease,” says coauthor David Holtzman, a neurologist and neuroscientist at Washington University School of Medicine in St. Louis. During sleep, the brain appears to flush out excess proteins and other debris (SN: 7/21/18, p. 22), so perhaps less sleep means that wash cycle is curtailed. |© Society for Science & the Public 2000 - 2019.

Keyword: Sleep; Alzheimers
Link ID: 25904 - Posted: 01.26.2019

Nicola Davis If you have trouble getting to sleep, it might be worth investing in a hammock: scientists say a gentle rocking motion not only helps people to fall asleep more rapidly but also improves the quality of sleep and the memory of the sleeper. While parents have long employed rocking as a way to calm babies and send them to sleep, some studies have suggested it helps adults too. Now researchers say they have found evidence to back this up and discovered further benefits to boot. “Rocking in people that do not have any sleep problems can still improve sleep quality, and the beneficial effects of sleep on – for instance – memory also seem to be enhanced,” said Dr Paul Franken, a co-author of the research, from the University of Lausanne in Switzerland. Writing in the journal Current Biology, he and colleagues in Lausanne and Geneva reveal that 18 young participants without sleep problems spent three nights in a laboratory: one night getting used to the environment, one night being monitored while sleeping in a stationary bed and one night being monitored with the bed gently rocking from side to side. Participants were asked to learn pairs of unrelated French words and were then tested on their ability to recall these pairs both before and after each of the test nights. Brain waves of the participants were monitored as they slept using EEG, and other metrics such as heart rate were also recorded. The brain wave data revealed that a gentle rocking did not affect the overall time participants spent asleep but did shorten their transition to “real” sleep. © 2019 Guardian News and Media Limited

Keyword: Sleep
Link ID: 25903 - Posted: 01.26.2019

By Teodora Stoica Try to explain to an alien why we sleep. Give it your best shot. “Well, we get tired. And our brain needs to rest.” “I see. So, you find another way to defend yourself during rest?” Advertisement “Well … no. Our body is paralyzed, and we lose consciousness.” There is an awkward pause. The alien tilts its head, feigning understanding. “But! We sometimes dream!” “Dream?” Blindly, unaware of how ridiculous you sound, you continue with unprecedented speed and cadence: “Yes! Dreams are fantastical stories projected from the mind into the mind, sometimes mixed with things that have already happened!” You catch your breath, and smile idiotically. “And … this helps with survival?” “Well … no. Sometimes the content confuses us in waking life,” you suddenly realize. newsletter promo Sign up for Scientific American’s free newsletters. The alien blinks silently a few times, furrowing his non-eyebrows: “Let me see if I understand. Your species spends one third of their lives paralyzed watching fantasy movies?” It is reasonable to assume the human race is doomed at this uncomfortable juncture in the conversation, and aliens will plan their stealthy attack during this incapacitated, seemingly futile stage of our existence.

Keyword: Sleep
Link ID: 25902 - Posted: 01.26.2019

Hannah Devlin Science correspondent People who stutter are being given electrical brain stimulation in a clinical trial aimed at improving fluency without the need for gruelling speech training. If shown to be effective, the technique – which involves passing an almost imperceptible current through the brain – could be routinely offered by speech therapists. “Stuttering can have serious effects on individuals in terms of their choice of career, what they can get out of education, their earning potential and personal life,” said Prof Kate Watkins, the trial’s principal investigator and a neuroscientist at the University of Oxford. About one in 20 young children go through a phase of stuttering, but most grow out of it. It is estimated that stuttering affects about one in 100 adults, with men about four times more likely to stutter than women. Advertisement In the film The King’s Speech, a speech therapist uses a barrage of techniques to help King George VI, played by Colin Firth, to overcome his stutter, including breathing exercises and speaking without hearing his own voice. The royal client also learns that he can sing without stuttering, a common occurrence in people with the impediment. Speech therapy has advanced since the 1930s, but some of the most effective programmes for improving fluency still require intensive training and involve lengthy periods of using unnatural-sounding speech. © 2019 Guardian News and Media Limited

Keyword: Language
Link ID: 25901 - Posted: 01.26.2019

Susan Milius After some 20 years of theorizing, a scientist is publicly renouncing the “beautiful hypothesis” that male birds’ sexy songs could indicate the quality of their brains. Behavioral ecologist Steve Nowicki of Duke University called birdsong “unreliable” as a clue for choosy females seeking a smart mate, in a paper published in the March 2018 Animal Behaviour. He will also soon publish another critique based on male songbirds that failed to score consistently on learning tests. And in what he calls a “public service announcement,” Nowicki summarized the negative results of those tests on January 4 at the annual meeting of the Society for Integrative and Comparative Biology in Tampa, Fla. “This was a beautiful hypothesis that got beaten up by data,” he says. Knowing that something about male singing matters to a female songbird, Nowicki and other researchers once proposed that the quality of singing might indicate a bird’s brainpower. The idea was that, because songbirds need to learn their songs, females could select males with the best brain development by selecting those singing the most precisely copied songs. A brainier male might be better at hunting baby food or spotting predators, thus helping more chicks to survive. Or braininess might signal an indirect benefit, such as contributing good genes to chicks. The first evidence for the notion that birdsong indicates bird smarts came from Neeltje Boogert at the University of Exeter in England, whose research suggested female zebra finches preferred smarter males with more complex songs. But subsequent studies have found evidence both supporting and contradicting the theory. To try to settle the matter, Nowicki and collaborators hand-raised 19 male song sparrows in the lab, controlling which songs the little birds heard as examples to copy so that it was clear how well each youngster learned each song. |© Society for Science & the Public 2000 - 2019

Keyword: Animal Communication; Sexual Behavior
Link ID: 25900 - Posted: 01.26.2019

By Jocelyn Kaiser Poor oral health is a risk factor for Alzheimer’s disease. What’s not clear is whether gum disease causes the disorder or is merely a result—many patients with dementia can’t take care of their teeth, for example. Now, a privately sponsored study has confirmed that the bacteria that cause gum disease are present in the brains of people with Alzheimer’s, not just in their mouths. The study also finds that in mice, the bacteria trigger brain changes typical of the disease. The provocative findings are the latest in a wave of research suggesting microbial infections may play a role in Alzheimer’s disease. But even some scientists who champion that once-fringy notion aren’t convinced that Porphyromonas gingivalis, the species fingered in the new study, is behind the disorder. “I'm fully on board with the idea that this microbe could be a contributing factor. I'm much less convinced that [it] causes Alzheimer’s disease,” says neurobiologist Robert Moir of the Harvard University–affiliated Massachusetts General Hospital (MGH) in Boston, whose work suggests the β-amyloid protein that forms plaques in the brains of Alzheimer’s patients is a protective response to microbial invaders. The new study, published today in Science Advances, was sponsored by the biotech startup Cortexyme Inc. of South San Francisco, California. Co-founder Stephen Dominy is a psychiatrist who in the 1990s became intrigued by the idea that Alzheimer’s could have an infectious cause. At the time, he was treating people with HIV at the University of California, San Francisco. Some had HIV-related dementia that resolved after they got antiviral drugs. Dominy began a side project looking for P. gingivalis in brain tissue from deceased patients with Alzheimer’s, and—after his work found hints—started the company with entrepreneur Casey Lynch, who had studied Alzheimer’s as a graduate student. © 2018 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 25899 - Posted: 01.24.2019

Andrew Scheyer We live in a medicated era. Recent data indicate that more than half of Americans are currently taking prescription drugs. Among pregnant women this number skyrockets to more than 80 percent. One of these women was a 24-year-old from California named Carol, whom I met and befriended through an online drug research forum. After weeks of debilitating morning sickness, persistent pain in her back and hips, and chronic anxiety about becoming a mother, Carol was taking a tranquilizer called alprazolam as needed, plus daily doses of acetaminophen and an anti-nausea drug called metoclopramide. Carol felt uneasy using the medications. Like many Americans and an even greater proportion of Europeans, Carol (who asked that I not use her surname) favors home remedies over pharmaceutical treatments. “I’ll always choose a tea over a pill,” she says. And so, as she sought relief during her pregnancy, she turned to marijuana. In the summer of 2007, Carol was surrounded by people touting the wonders of cannabis as a panacea for diseases from depression to glaucoma and myriad ailments in between—including nausea, pain, and anxiety. Worried that her suboptimal diet and poor sleep could be affecting the development of her child, she considered using small amounts of cannabis instead of the multiple prescription medications suggested by her doctor. Seventy percent of women in the United States believe that there is “slight or no risk of harm” in using can­nabis during pregnancy. © 1986 - 2019 The Scientist

Keyword: Development of the Brain; Drug Abuse
Link ID: 25898 - Posted: 01.24.2019

By Abdul-Kareem Ahmed, M.D. “He wouldn’t want to live like this.” The cardiology team consulted us that Sunday evening. A patient was getting sleepy, and weak on one side. The man was 68 years old, not a healthy man, but a strong man. He had suffered a heart attack, again, and had been transferred from another hospital. Because he’d been far from a major medical center, where a wire might have been used to clear the blockage in his coronary arteries, he was treated with the next best method, a blood-thinner, and then sent to us. The drug, tenecteplase, is an enzyme that works by digesting clots. It effectively reverses the problem and is lifesaving for a majority of patients. But in a small minority of patients, it can also cause bleeding. Titrating the thickness of blood is precarious. If your blood is too thick you can clot. If it’s too thin you can bleed. The team had performed a rapid head CT. “He’s not going to make it,” my senior whispered as I scrolled through the fresh images. Our patient was bleeding into his brain, suffering a hemorrhagic stroke. Tenecteplase thinned his blood to save his heart, but it most likely had resulted in injury to his brain. I ran downstairs to examine him. He was big, and bald, and lying peacefully in his bed. With some encouragement, he gave me a grin, though lopsided. His pupils were different sizes, and half his body was paralyzed. But he was completely “there.” I was only one month into residency. Though I knew he was critical, and I knew our next decision would be difficult, I remained optimistic. © 2019 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 25897 - Posted: 01.24.2019

David Cyranoski Japan has approved a stem-cell treatment for spinal-cord injuries. The event marks the first such therapy for this kind of injury to receive government approval for sale to patients. “This is an unprecedented revolution of science and medicine, which will open a new era of healthcare,” says oncologist Masanori Fukushima, head of the Translational Research Informatics Center, a Japanese government organization in Kobe that has been giving advice and support to the project for more than a decade. But independent researchers warn that the approval is premature. Ten specialists in stem-cell science or spinal-cord injuries, who were approached for comment by Nature and were not involved in the work or its commercialization, say that evidence that the treatment works is insufficient. Many of them say that the approval for the therapy, which is injected intravenously, was based on a small, poorly designed clinical trial. They say that the trial’s flaws — including that it was not double-blinded — make it difficult to assess the treatment’s long-term efficacy, because it is hard to rule out whether patients might have recovered naturally. And, although the cells used — known as mesenchymal stem cells (MSCs) — are thought to be safe, the infusion of stem cells into the blood has been connected with dangerous blood clots in the lungs. And all medical procedures carry risks, which makes them hard to justify unless they are proven to offer a benefit. © 2019 Springer Nature Publishing AG

Keyword: Regeneration; Stem Cells
Link ID: 25896 - Posted: 01.24.2019

/ By Courtenay Harris Bond When Anna Brennan was 15 years old, her mother abandoned her in the projects of northeast Philadelphia. Her aunt eventually took her in, but Brennan struggled with anxiety and depression. She also needed to support herself, so in ninth grade she dropped out of high school and went to work at an all-night diner downtown. At 20, she met her first husband, who also lived with mental illness and had substance use issues — and gave her a tooth-marked scar in her upper right shoulder. For years, Brennan waitressed seven days a week until she had her third child, Gemma, and her back pain started, forcing her to quit. “Our approach is: ‘Your urine is positive for substances. Let’s figure out how to make this work better for you.’” A physician prescribed painkillers, and Brennan became addicted. Her habit quickly turned from buying pills, which were expensive on the street, to snorting and then injecting heroin, which came cheap and pure. Twelve years into their marriage, Brennan’s husband committed suicide. Then she lost her house. Brennan’s two older kids went to stay with her sister, and Brennan hasn’t seen them in over a year. “I’m a drug addict,” Brennan says bluntly. “She won’t give them back.” Brennan started taking Suboxone, an opioid-replacement therapy that cut her cravings and kept her from experiencing withdrawal, two different times: in 2015 and then again from 2016 to 2018. During the second round, Brennan spent more than two years making trips to Prevention Point Philadelphia on Kensington Avenue. There, she met with her case manager and the doctor who prescribed her medication. Brennan seemed poised to be a success story. But she was weighed down by the stress of coping with a drug-addicted second husband, caring for her daughter Gemma, who is autistic; and despairing that she might never see her two older children again. Copyright 2019 Undark

Keyword: Drug Abuse
Link ID: 25895 - Posted: 01.24.2019

Jef Akst Levels of a protein called neurofilament light chain increase in the blood and spinal fluid of some Alzheimer’s patients 16 years before they develop symptoms, according to a study published today (January 21) in Nature Medicine. The results suggest that neurofilament light chain (NfL), which is part of the cytoskeleton of neurons and has previously been tied to brain damage in mice, could serve as a biomarker to noninvasively track the progression of the disease. “This is something that would be easy to incorporate into a screening test in a neurology clinic,” coauthor Brian Gordon, an assistant professor of radiology at Washington University, says in a press release. Gordon and his colleagues measured NfL in nearly 250 people carrying an Alzheimer’s-risk allele and more than 160 of their relatives who did not carry the variant. They found that those at risk of developing the disease had higher levels of the protein early on, and that NfL levels in both the blood and spinal fluid were on the rise well before the patients began to show signs of neurodegeneration, more than 16 years before disease onset. Examining a subset of the patients more closely, the team saw that the rate of increase in NfL correlated with the shrinkage of a brain region called the precuneus, and patients whose NfL levels were rising rapidly tested worse on cognitive tests. “It is not necessarily the absolute levels which tell you your neurodegeneration is ongoing, it is the rate of change,” coauthor Mathias Jucker, a professor of cellular neurology at the German Center for Neurodegenerative Diseases in Tübingen, tells The Guardian. © 1986 - 2019 The Scientist.

Keyword: Alzheimers
Link ID: 25894 - Posted: 01.24.2019

Bret Stetka As the story goes, nearly 80 years ago on the Faroe Islands - a stark North Atlantic archipelago 200 miles off the coast of Scotland — a neurologic epidemic may have washed, or rather convoyed, ashore. Before 1940 the incidence of multiple sclerosis on the Faroes was near, if not, zero, according to the tantalizing lore I recall from medical school. Yet in the years following British occupation of the islands during World War II, the rate of MS rose dramatically, leading many researchers to assume the outbreak was caused by some unknown germ transmitted by the foreign soldiers. We now know that MS is not infectious in the true sense of the word. It is not contagious in the way, say, the flu is. But infection does likely play a role in MS. As may be the case in Alzheimer's disease, it's looking more and more like MS strikes when infectious, genetic and immune factors gang up to eventually impair the function of neurons in the brain and spinal cord. Researchers are hoping to better understand this network of influences to develop more effective ways to treat MS, and perhaps prevent it in the first place. In the MS-free brain, electrical impulses zip down nerve fibers called axons causing the release of neurotransmitters. The wiring allows neurons to communicate with each other and generate biologic wonders like thought, sensation and movement. In many regions of the brain those axons are encased in an insulating jacket of protein and fat called myelin, which increases the speed that electrical nerve impulses travel. © 2019 npr

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 25893 - Posted: 01.22.2019

/ By Dave Levitan Scientific research on the effects of marijuana is rife with holes, thanks in large part to it still being categorized at the federal level alongside drugs such as heroin and LSD. Unfortunately, when research is scarce, it becomes easier to mislead people through cherry-picked data, sneaky word choice, and misinterpreted conclusions. On virtually every issue in his 272-page book, Adam Berenson commits one of the most common logical errors: He mixes up correlation and causation. Which brings us to Alex Berenson and Malcolm Gladwell, and what happens when tidy narratives outrun the science. Two weeks ago, Berenson, a former New York Times reporter and subsequent spy novelist, published a book with the ominous title “Tell Your Children: The Truth about Marijuana, Mental Illness, and Violence.” Gladwell, meanwhile, published a feature in the New Yorker, where he is a staff writer, drawing largely on Berenson’s book and questioning the supposed consensus that weed is among the safest drugs. Combined, these two works offer a master class in statistical malfeasance and a smorgasbord of logical fallacies and data-free fear-mongering that serve only to muddle an issue that, as experts point out, needs far more good-faith research. Berenson’s main argument is relatively simple. In his book, he claims, essentially, that the existing evidence really does contain solid answers, painting a truly alarming picture about marijuana: That it can and does cause psychosis and schizophrenia. He then makes the leap that since psychosis and schizophrenia can lead to violence, marijuana itself is causing violence to increase in the United States and elsewhere. Copyright 2019 Undark

Keyword: Drug Abuse; Schizophrenia
Link ID: 25892 - Posted: 01.22.2019

By James Gorman Carpenter ants follow trails. Just watch them wandering about on your wooden porch until they strike a trail of pheromones (chemicals ants use for communication) that another ant has laid down. Ants don’t have noses, so they wave their antennas around to pick up the trail, then off they go on the road to ruin. (Carpenter ants destroy houses.) Scientists know plenty about ants, including their ability to follow scent trails, but researchers at Harvard wanted to get a more detailed understanding of how exactly ants sniff, or taste, the pheromone-marked path. First, some basics: Ants use their antennas to pick up chemical cues left by other ants. And the chemical sense of ants, call it smell or taste or chemo-reception, enables them to follow straight trails, curved trails, even zigzags. To see how ants do it, the scientists mixed ink and ant pheromones and used the result to paint trails on paper. They set ants out on trails and recorded dozens of hours of ant movement. They analyzed the video and tried out different computer models of the ants’ behavior. What Ryan W. Dash and his adviser, Venkatesh N. Murthy, and other researchers found was that the ants had several strategies for path-following. The scientists published their results in the Journal of Experimental Biology. All the ants used their antennas to sweep the trail side to side. One strategy they used was probing. A probing ant moved slowly, keeping its antennas close together. The researchers termed another strategy exploratory: Ants still moved slowly, but they took winding paths moving away from and back to a trail. When they were locked into a pheromone trail, they moved along more quickly, keeping their antennas on either side of the path. They kept one antenna closer to the path, but which antenna varied from ant to ant. In other words, some were lefties and others were righties. © 2019 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 25891 - Posted: 01.22.2019

John Bergeron During the first weeks of the new year, resolutions are often accompanied by attempts to learn new behaviours that improve health. We hope that old bad habits will disappear and new healthy habits will become automatic. But how can our brain be reprogrammed to assure that a new health habit can be learned and retained? In 1949, Canadian psychologist Donald Hebb proposed the theory of Hebbian learning to explain how a learning task is transformed into a long-term memory. In this way, healthy habits become automatically retained after their continual repetition. Synapses transmit electrical signals. Svitlana Pavliuk Learning and memory are a consequence of how our brain cells (neurons) communicate with each other. When we learn, neurons communicate through molecular transmissions which hop across synapses producing a memory circuit. Known as long-term potentiation (LTP), the more often a learning task is repeated, the more often transmission continues and the stronger a memory circuit becomes. It is this unique ability of neurons to create and strengthen synaptic connections by repeated activation that leads to Hebbian learning. Understanding the brain requires investigation through different approaches and from a variety of specialities. The field of cognitive neuroscience initially developed through a small number of pioneers. Their experimental designs and observations led to the foundation for how we understand learning and memory today. © 2010–2019, The Conversation US, Inc.

Keyword: Learning & Memory
Link ID: 25890 - Posted: 01.22.2019

Alison Abbott Neuroscientists have for the first time discovered differences between the ‘software’ of humans and monkey brains, using a technique that tracks single neurons. They found that human brains trade off ‘robustness’ — a measure of how synchronized neuron signals are — for greater efficiency in information processing. The researchers hypothesize that the results might help to explain humans’ unique intelligence, as well as their susceptibility to psychiatric disorders. The findings were published in Cell1 on 17 January. Scientists say that this type of unusual study could help them to better translate research in animal models of psychiatric diseases into the clinic. The research exploited a rare set of data on the activity of single neurons collected deep in the brains of people with epilepsy who were undergoing neurosurgery to identify the origin of their condition. The technique is so difficult that only a handful of clinics around the world can participate in this type of research. The study also used similar, existing data from three monkeys and collected neuron information from two more. Over the decades, neuroscientists have discovered many subtle and significant differences in the anatomy — the hardware — of the brains of humans and other primates. But the latest study looked instead at differences in brain signals. © 2019 Springer Nature Publishing AG

Keyword: Schizophrenia; Epilepsy
Link ID: 25889 - Posted: 01.21.2019

By Scott Barry Kaufman Robert Plomin is a legend. For over 40 years he has been on the forefront of our understanding of the genetic and environmental influences on human behavior. Based on his groundbreaking work on twins, he showed that genes really do have a substantial influence on our psychological traits-- we are not born a lump of clay. Plomin coined the phrase "non-shared environment," and he was ranked as the 71st most "eminent psychologists of the 20th century." When I taught a course on human intelligence at NYU, I repeatedly cited his research and quoted his measured language and caution surrounding the interpretation of his findings. All of this makes it rather bewildering that, ever since his book Blueprint: How DNA Makes Us Who We Are came out, he has been spreading a lot of outdated misinformation in the media that is not supported by the latest science of genetics, including his own work. Also, many of his statements have been riddled with contradictions and logical non sequiturs, and some of his more exaggerated rhetoric is even potentially dangerous if actually applied to educational selection. Don't get me wrong: I am excited about the rapid progress scientists are making in using information about DNA to predict individual differences in intellectual functioning and personality. But I firmly believe we need to be more thoughtful in determining what relevance these rapidly emerging findings have for the actual individual human beings who are inhabited by the DNA.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 25888 - Posted: 01.21.2019

By Perri Klass, M.D. Acute pain that calls out to warn you — “Hey, don’t walk on this broken leg!” — may be unpleasant, but it’s also protective. That acute pain is letting you know that a part of your body needs to heal, or in some other way needs extra attention, said Dr. Neil Schechter, the director of the chronic pain clinic at Boston Children’s Hospital. That’s very different, he said, from chronic pain that goes on over the course of months, whether abdominal pain or headache or musculoskeletal — it may persist and be incapacitating, because “the pain has become the disease.” That doesn’t mean the pain is any less painful for the person experiencing it. “There is really strong evidence supporting the psychological treatment for chronic pain, and that doesn’t imply that the pain itself is a psychological problem,” said Rachael Coakley, a psychologist who is the director of clinical innovation and outreach in pain medicine at Boston Children’s Hospital. Her book, “When Your Child Hurts,” is an excellent resource for parents. “When you’re a kid and you’ve had pain for a really long time, a lot of that is an experience of not having control over what’s happening in your body,” said Anna C. Wilson, a pediatric pain psychologist at Oregon Health and Science University. “Relaxation and other biobehavioral techniques help kids gain a sense of control.” She tells patients, “Your pain is absolutely real, and chronic pain in particular is a neurologic problem.” She recommended TED Talks by Dr. Elliot Krane, an anesthesiologist, and Lorimer Moseley, a neuroscience professor, to help explain chronic pain. Chronic pain develops, Dr. Schechter said, when there is an underlying biological vulnerability, either inherited or resulting from stressors like infections or procedures or traumas, and then a triggering event, such as a gastrointestinal infection or an injury. © 2019 The New York Times Company

Keyword: Pain & Touch; Development of the Brain
Link ID: 25887 - Posted: 01.21.2019

By David Grossman The brain remains famously remains one of the most mysterious parts of the human body. The challenges of neuroscience are among the most daunting in the medical field. Expansion microscopy is a crucial element of that study, a chemical technique that expands a small specimen to make it more observable at the molecular level. A new technique allows scientists to expand microscopy so instead of focusing a single sell, it can explore full neural circuits, at a speed around 1,000 times faster than before. A struggle in studying live cells is watching them without altering their actions. Scientists work around this problem by using thin sheets of light to illuminate cells with a piece of complex technology called a lattice light sheet microscope. By combining this microscope with expansion microscopy, scientists at the Howard Hughes Medical Institute (HHMI) were able to expand the possibility of how they could study insect brains. “I thought they were full of it,” says Eric Betzig, now an HHMI investigator at the University of California, Berkeley, in a press statement. "They" refers to Ruixuan Gao and Shoh Asano of MIT, who wanted to use Betzig's lab to attempt their combining of the two practices. While a complex procedure involving high-end scientific equipment, at its heart “the idea does sound a bit crude,” Gao says. “We’re stretching tissues apart." When the experiment was over, Betzig says, “I couldn’t believe the quality of the data I was seeing. You could have knocked me over with a feather.” ©2019 Hearst Magazine Media, Inc

Keyword: Brain imaging
Link ID: 25886 - Posted: 01.21.2019