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By ERICA GOODE Horses snooze in their stalls. Fish take their 40 winks floating in place. Dogs can doze anywhere, anytime. And even the lowly worm nods off now and then. All animals, most scientists agree, engage in some form of sleep. But the stages of sleep that characterize human slumber had until now been documented only in mammals and birds. A team of researchers in Germany announced in a report published on Thursday, however, that they had found evidence of similar sleep stages in a lizard: specifically, the bearded dragon, or Pogona vitticeps, a reptile native to Australia and popular with pet owners. Recordings from electrodes implanted in the lizards’ brains showed patterns of electrical activity that resembled what is known as slow-wave sleep and another pattern resembling rapid eye movement, or REM, sleep, a stage of deep slumber associated with brain activity similar to that of waking. Some researchers had argued that these stages were of relatively recent origin in evolutionary terms because they had not been found in more primitive animals like amphibians, fish, reptiles other than birds, and other creatures with backbones. But the new finding, said Gilles Laurent, director of the department of neural systems at the Max Planck Institute for Brain Research and the principal author of the study, “increases the probability that sleep evolved in all these animals from a common ancestor.” He added that it also raised the possibility that staged sleep evolved even earlier and that some version of it might exist in animals like amphibians or fish. The report appeared in Thursday’s issue of the journal Science. Other researchers said the study could help scientists understand more about the purpose and mechanisms of sleep. But the finding, they added, is bound to generate more controversy about whether the resting state of primitive animals is really the same as sleep, and whether the brain activity seen in a lizard can be compared to that in mammals. © 2016 The New York Times Company
Tina Hesman Saey To rewrite an Alanis Morissette song, the brain has a funny way of waking you up (and putting you to sleep). Isn’t it ionic? Some scientists think so. Changes in ion concentrations, not nerve cell activity, switch the brain from asleep to awake and back again, researchers report in the April 29 Science. Scientists knew that levels of potassium, calcium and magnesium ions bathing brain cells changed during sleep and wakefulness. But they thought neurons — electrically active cells responsible for most of the brain’s processing power — drove those changes. Instead, the study suggests, neurons aren’t the only sandmen or roosters in the brain. “Neuromodulator” brain chemicals, which pace neuron activity, can bypass neurons altogether to directly wake the brain or lull it to sleep by changing ion concentrations. Scientists hadn’t found this direct connection between ions and sleep and wake before because they were mostly focused on what neurons were doing, says neuroscientist Maiken Nedergaard, who led the study. She got interested in sleep after her lab at the University of Rochester in New York found a drainage system that washes the brain during sleep (SN: 11/16/13, p. 7).When measuring changes in the fluid between brain cells, Nedergaard and colleagues realized that ion changes followed predictable patterns: Potassium ion levels are high when mice (and presumably people) are awake, and drop during sleep. Calcium and magnesium ions follow the opposite pattern; they are higher during sleep and lower when mice are awake. © Society for Science & the Public 2000 - 2016
Link ID: 22163 - Posted: 04.30.2016
By BENEDICT CAREY Listening to music may make the daily commute tolerable, but streaming a story through the headphones can make it disappear. You were home; now you’re at your desk: What happened? Storytelling happened, and now scientists have mapped the experience of listening to podcasts, specifically “The Moth Radio Hour,” using a scanner to track brain activity. In a paper published Wednesday by the journal Nature, a research team from the University of California, Berkeley, laid out a detailed map of the brain as it absorbed and responded to a story. Widely dispersed sensory, emotional and memory networks were humming, across both hemispheres of the brain; no story was “contained” in any one part of the brain, as some textbooks have suggested. The team, led by Alexander Huth, a postdoctoral researcher in neuroscience, and Jack Gallant, a professor of psychology, had seven volunteers listen to episodes of “The Moth” — first-person stories of love, loss, betrayal, flight from an abusive husband, and more — while recording brain activity with an M.R.I. machine. Sign Up for the Science Times Newsletter Every week, we'll bring you stories that capture the wonders of the human body, nature and the cosmos. Using novel computational methods, the group broke down the stories into units of meaning: social elements, for example, like friends and parties, as well as locations and emotions . They found that these concepts fell into 12 categories that tended to cause activation in the same parts of people’s brains at the same points throughout the stories. They then retested that model by seeing how it predicted M.R.I. activity while the volunteers listened to another Moth story. Would related words like mother and father, or times, dates and numbers trigger the same parts of people’s brains? The answer was yes. © 2016 The New York Times Company
By Andy Coghlan “I’ve become resigned to speaking like this,” he says. The 17-year old boy’s mother tongue is Dutch, but for his whole life he has spoken with what sounds like a French accent. “This is who I am and it’s part of my personality,” says the boy, who lives in Belgium – where Dutch is an official language – and prefers to remain anonymous. “It has made me stand out as a person.” No matter how hard he tries, his speech sounds French. About 140 cases of foreign accent syndrome (FAS) have been described in scientific studies, but most of these people developed the condition after having a stroke. In the UK, for example, a woman in Newcastle who’d had a stroke in 2006 woke up with a Jamaican accent. Other British cases include a woman who developed a Chinese accent, and another who acquired a pronounced French-like accent overnight following a bout of cerebral vasculitis. But the teenager has had the condition from birth, sparking the interest of Jo Verhoeven of City University London and his team. Scans revealed that, compared with controls, the flow of blood to two parts of the boy’s brain were significantly reduced. One of these was the prefrontal cortex of the left hemisphere – a finding unsurprising to the team, as it is known to be associated with planning actions including speech. © Copyright Reed Business Information Ltd.
Link ID: 22161 - Posted: 04.30.2016
By n. r. kleinfield IT BEGAN WITH what she saw in the bathroom mirror. On a dull morning, Geri Taylor padded into the shiny bathroom of her Manhattan apartment. She casually checked her reflection in the mirror, doing her daily inventory. Immediately, she stiffened with fright. Huh? What? She didn’t recognize herself. She gazed saucer-eyed at her image, thinking: Oh, is this what I look like? No, that’s not me. Who’s that in my mirror? This was in late 2012. She was 69, in her early months getting familiar with retirement. For some time she had experienced the sensation of clouds coming over her, mantling thought. There had been a few hiccups at her job. She had been a nurse who climbed the rungs to health care executive. Once, she was leading a staff meeting when she had no idea what she was talking about, her mind like a stalled engine that wouldn’t turn over. “Fortunately I was the boss and I just said, ‘Enough of that; Sally, tell me what you’re up to,’” she would say of the episode. Certain mundane tasks stumped her. She told her husband, Jim Taylor, that the blind in the bedroom was broken. He showed her she was pulling the wrong cord. Kept happening. Finally, nothing else working, he scribbled on the adjacent wall which cord was which. Then there was the day she got off the subway at 14th Street and Seventh Avenue unable to figure out why she was there. So, yes, she had had inklings that something was going wrong with her mind. She held tight to these thoughts. She even hid her suspicions from Mr. Taylor, who chalked up her thinning memory to the infirmities of age. “I thought she was getting like me,” he said. “I had been forgetful for 10 years.”
Link ID: 22160 - Posted: 04.30.2016
By PAM BELLUCK Alzheimer’s disease can seem frightening, mysterious and daunting. There are still a lot of unknowns about the disease, which afflicts more than five million Americans. Here are answers to some common questions: Sometimes I forget what day it is or where I put my glasses. Is this normal aging, or am I developing Alzheimer’s? Just because you forgot an item on your grocery list doesn’t mean you are developing dementia. Most people have occasional memory lapses, which increase with age. The memory problems that characterize warning signs of Alzheimer’s are usually more frequent, and they begin to interfere with safe or competent daily functioning: forgetting to turn off the stove, leaving home without being properly dressed or forgetting important appointments. Beyond that, the disease usually involves a decline in other cognitive abilities: planning a schedule, following multistep directions, carrying out familiar logistical tasks like balancing a checkbook or cooking a meal. It can also involve mood changes, agitation, social withdrawal and feelings of confusion, and can even affect or slow a person’s gait. How is Alzheimer’s diagnosed? Diagnosing Alzheimer’s usually involves a series of assessments, including memory and cognitive tests. Clinicians will also do a thorough medical work-up to determine whether the thinking and memory problems can be explained by other diagnoses, such as another type of dementia, a physical illness or side effects from a medication. Brain scans and spinal taps may also be conducted to check for corroborating evidence like the accumulation of amyloid, the hallmark protein of Alzheimer’s, in the brain or spinal fluid. The cause is unknown for most cases. Fewer than 5 percent of cases are linked to specific, rare gene mutations. Those are usually early-onset cases that develop in middle age. © 2016 The New York Times Company
Link ID: 22159 - Posted: 04.30.2016
By Adam Bear It happens hundreds of times a day: We press snooze on the alarm clock, we pick a shirt out of the closet, we reach for a beer in the fridge. In each case, we conceive of ourselves as free agents, consciously guiding our bodies in purposeful ways. But what does science have to say about the true source of this experience? In a classic paper published almost 20 years ago, the psychologists Dan Wegner and Thalia Wheatley made a revolutionary proposal: The experience of intentionally willing an action, they suggested, is often nothing more than a post hoc causal inference that our thoughts caused some behavior. The feeling itself, however, plays no causal role in producing that behavior. This could sometimes lead us to think we made a choice when we actually didn’t or think we made a different choice than we actually did. But there’s a mystery here. Suppose, as Wegner and Wheatley propose, that we observe ourselves (unconsciously) perform some action, like picking out a box of cereal in the grocery store, and then only afterwards come to infer that we did this intentionally. If this is the true sequence of events, how could we be deceived into believing that we had intentionally made our choice before the consequences of this action were observed? This explanation for how we think of our agency would seem to require supernatural backwards causation, with our experience of conscious will being both a product and an apparent cause of behavior. In a study just published in Psychological Science, Paul Bloom and I explore a radical—but non-magical—solution to this puzzle. © 2016 Scientific America
Link ID: 22158 - Posted: 04.30.2016
Ian Sample Science editor Scientists have created an “atlas of the brain” that reveals how the meanings of words are arranged across different regions of the organ. Like a colourful quilt laid over the cortex, the atlas displays in rainbow hues how individual words and the concepts they convey can be grouped together in clumps of white matter. “Our goal was to build a giant atlas that shows how one specific aspect of language is represented in the brain, in this case semantics, or the meanings of words,” said Jack Gallant, a neuroscientist at the University of California, Berkeley. No single brain region holds one word or concept. A single brain spot is associated with a number of related words. And each single word lights up many different brain spots. Together they make up networks that represent the meanings of each word we use: life and love; death and taxes; clouds, Florida and bra. All light up their own networks. Described as a “tour de force” by one researcher who was not involved in the study, the atlas demonstrates how modern imaging can transform our knowledge of how the brain performs some of its most important tasks. With further advances, the technology could have a profound impact on medicine and other fields. “It is possible that this approach could be used to decode information about what words a person is hearing, reading, or possibly even thinking,” said Alexander Huth, the first author on the study. One potential use would be a language decoder that could allow people silenced by motor neurone disease or locked-in syndrome to speak through a computer. © 2016 Guardian News and Media Limited
Nicola Davis People with a larger circle of friends are better able to tolerate pain, according to research into the pain thresholds and social networks of volunteers. The link is thought to be down a system in the brain that involves endorphins: potent pain-killing chemicals produced by the body that also trigger a sense of wellbeing. “At an equivalent dose, endorphins have been shown to be stronger than morphine,” said Katerina Johnson, a doctoral student at the University of Oxford, who co-authored the research. Writing in the journal Scientific Reports, Johnson and Robin Dunbar, professor of evolutionary psychology at the University of Oxford, sought to probe the theory that the brain’s endorphin system might have evolved to not only handle our response to physical discomfort, but influence our experience of pleasure from social interactions too. “Social behaviour and being attached to other individuals is really important for our survival - whether that is staying close to our parents, or our offspring or cooperating with others to find food or to help defend ourselves,” said Johnson. To test the link, the authors examined both the social networks and pain thresholds of 101 adults aged between 18 and 34. Each participant was asked to complete a questionnaire, designed to quiz them on friends they contacted once a week and those they got in touch with once a month. The personality of each participant was probed, looking at traits such as “agreeableness”; they were also asked to rate their fitness and stress levels. © 2016 Guardian News and Media Limited
Keyword: Pain & Touch
Link ID: 22156 - Posted: 04.28.2016
Jon Hamilton People who sustain a concussion or a more severe traumatic brain injury are likely to have sleep problems that continue for at least a year and a half. A study of 31 patients with this sort of brain injury found that 18 months afterward, they were still getting, on average, an hour more sleep each night than similar healthy people were getting. And despite the extra sleep, 67 percent showed signs of excessive daytime sleepiness. Only 19 percent of healthy people had that problem. Surprisingly, most of these concussed patients had no idea that their sleep patterns had changed. "If you ask them, they say they are fine," says Dr. Lukas Imbach, the study's first author and a senior physician at the University Hospital Zurich in Zurich. When Imbach confronts patients with their test results, "they are surprised," he says. The results, published Thursday in the online edition of the journal Neurology, suggest there could be a quiet epidemic of sleep disorders among people with traumatic brain injuries. The injuries are diagnosed in more than 2 million people a year in the United States. Common causes include falls, motor vehicle incidents and assaults. Previous studies have found that about half of all people who sustain sudden trauma to the brain experience sleep problems. But it has been unclear how long those problems persist. "Nobody actually had looked into that in detail," Imbach says. A sleep disorder detected 18 months after an injury will linger for at least two years, and probably much longer, the researchers say. © 2016 npr
People who've recovered from depression stave off relapses with mindfulness therapy as well as with antidepressants, a new review finds. Mindfulness-based cognitive therapy (MBCT) is an eight-week group program that helps people become better observers of their own thoughts and emotions and to learn to distance themselves before ruminations spiral downwards. An international team of psychiatry researchers combined data from nine randomized trials of 1,258 patients total with recurrent depression to compare the mindfulness therapy to placebo, treatment as usual and other active treatments including antidepressants. People suffering from depression who received the mindfulness therapy were 31 per cent less likely to suffer a relapse during the next 60 weeks compared with those who did not receive it, Willem Kuyken of the University of Oxford, in England and his co-authors reported in a meta-analysis review in Wednesday's issue of the journal JAMA Psychiatry. "If you compare MBCT against antidepressant medication it basically holds its own, which means it provides protection on par with what people would get from continuing to take to take medications for one, two or three years after they've recovered from depression," said co-author Dr. Zindel Segal, a professor of psychology at the University of Toronto Scarborough. No one reported side-effects associated with participating in the therapy. ©2016 CBC/Radio-Canada.
By SABRINA TAVERNISE Taking a stance sharply at odds with most American public health officials, a major British medical organization urged smokers to switch to electronic cigarettes, saying they are the best hope in generations for people addicted to tobacco cigarettes to quit. The recommendation, laid out in a report published Thursday by the Royal College of Physicians, summarizes the growing body of science on e-cigarettes and finds that their benefits far outweigh the potential harms. It concludes resoundingly that, at least so far, the devices are helping people more than harming them, and that the worries about them — including that using them will lead young people to eventually start smoking traditional cigarettes — have not come to pass. “This is the first genuinely new way of helping people stop smoking that has come along in decades,” said John Britton, director of the U.K. Center for Tobacco and Alcohol Studies at the University of Nottingham, who led the committee that produced the report. E-cigarettes, he said, “have the potential to help half or more of all smokers get off cigarettes. That’s a huge health benefit, bigger than just about any medical intervention.” That conclusion is likely to be controversial in the United States, where arguments about e-cigarettes have jolted the traditionally low-key public health community. E-cigarettes deliver nicotine without the harmful tar and chemicals that cause cancer. Some public health experts see e-cigarettes as the first real chance in years for 40 million addicted Americans to quit. But others, including the federal Centers for Disease Control and Prevention, have focused on the potential dangers of e-cigarettes, for example that they could extend smoking habits, that they could be a gateway to traditional cigarettes for children, or that their vapor could to turn out to have long-term health effects. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22153 - Posted: 04.28.2016
Nicola Davis Benedict Cumberbatch’s deep and booming voice might have made him a hit among women, but a low pitch is more likely to have evolved to intimidate other men, new research suggests. When both heterosexual men and women were played recordings of male voices, the deeper tones were hailed by men as sounding more dominant. While the deeper voices were judged to be more attractive by female listeners, the effect was weaker, the researchers report. “If you look at what men’s traits look like they are designed for, they look much better designed for intimidating other males than for attracting females,” said David Puts of Pennsylvania State University, who led the study. Published in Proceedings of the Royal Society B: Biological Sciences, the three-part study by an international team of scientists explored the links between voice pitch and mating systems, attractiveness and, for males only, perceived dominance. A formula for the perfect voice? Read more In the first leg of the research, the scientists turned their attention to primates encompassing Old and New World monkeys, as well as humans and other apes, to explore differences in “fundamental frequency” between males and females of each species - the aspect of the voice that is perceived as pitch. After selecting 1721 recordings, they found large differences were more common in polygynous species - where males mate with more than one female - than monogamous ones. That, they say, could be because in polygynous species, competition between males is greater - hence a male with a lower-pitched voice deemed to be intimidating could have the edge in securing a mate. Intriguingly, the researchers found that among the apes humans showed the greatest difference in pitch between the sexes, suggesting our ancestors were not searching for “the one” but were polygynous - a situation Puts still believes to be the case. © 2016 Guardian News and Media Limited
by Bethany Brookshire Interviewing for a new job is filled with uncertainty, and that uncertainty fuels stress. There’s the uncertainty associated with preparing for the interview — what questions will they ask me? What should I put in my portfolio? And then there’s the ambiguity when you’re left to stew. Did I get the job? Or did someone else? Scientists have recently shown that these two types of uncertainty — the kind we can prepare for, and the kind we’re just stuck with — are not created equal. The uncertainty we can’t do anything about is more stressful than the one we can. The results help show exactly what in our lives freaks us out — and why. But the findings also show a positive side to the stress we feel when not knowing what’s ahead — the closer our stress levels reflect the real ambiguity in the world, the better we perform in it. “There is a bias in the public perception” against stress, says Claus Lamm, a cognitive neuroscientist at the University of Vienna in Austria. But stress “prepares us to deal with environmental challenges,” he notes, preparing us to fight or flee, and it keeps us paying attention to our surroundings. For decades, scientists have been trying to figure out just what makes us stressed and why. It turns out that unpredictability is a great stressor. Studies in the 1960s and 1970s showed that rats and humans who can’t predict a negative effect (such as a small shock) end up more frazzled than those who can predict when a zap is coming. In a 2006 study, people zapped with unpredictable electric shocks to the hand rated the pain as more unpleasant than when they knew what to expect. © Society for Science & the Public 2000 - 2016.
Link ID: 22151 - Posted: 04.27.2016
By ERICA GOODE PORTLAND, Ore. — The 911 caller had reported a man with a samurai sword, lunging at people on the waterfront. It was evening, and when the police arrived, they saw the man pacing the beach and called to him. He responded by throwing a rock at the embankment where they stood. They shouted to him from a sheriff’s boat; he threw another rock. They told him to drop the sword; he said he would kill them. He started to leave the beach, and after warning him, they shot him in the leg with a beanbag gun. He turned back, still carrying the four-foot blade. In another city — or in Portland itself not that long ago — the next step would almost certainly have been a direct confrontation and, had the man not put down the weapon, the use of lethal force. But the Portland Police Bureau, prodded in part by the 2012 findings of a Justice Department investigation, has spent years putting in place an intensive training program and protocols for how officers deal with people with mental illness. At a time when police behavior is under intense scrutiny — a series of fatal shootings by police officers have focused national attention on issues of race and mental illness — Portland’s approach has served as a model for other law enforcement agencies around the country. And on that Sunday last summer, the police here chose a different course. At 2:30 a.m., after spending hours trying to engage the man, the officers decided to “disengage,” and they withdrew, leaving the man on the beach. A search at daylight found no signs of him. People with mental illnesses are overrepresented among civilians involved in police shootings: Twenty-five percent or more of people fatally shot by the police have had a mental disorder, according to various analyses. © 2016 The New York Times Company
Link ID: 22150 - Posted: 04.27.2016
By Bret Stetka The multibillion-dollar supplement industry spews many dubious claims, but a new study suggests that some nutritional supplements, including omega-3 fatty acids and vitamin D, may boost the effectiveness of antidepressants. If so, the supplements might help relieve symptoms for the millions of people who don’t immediately respond to these drugs. The meta-analysis—published Tuesday in the American Journal of Psychiatry—reviewed the results of 40 clinical trials that evaluated the effects of taking nutritional supplements in conjunction with several major classes of antidepressants, including selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants. It revealed that four supplements in particular upped the potency of the medications, compared with a placebo. The researchers, based at Harvard University and the University of Melbourne, found the strongest evidence for an omega-3 fish oil called eicosapentaenoic acid, or EPA. In general, people with depression who took an antidepressant drug and an omega-3 sourced from fish oil experienced a significant reduction in their symptoms as assessed by a the Hamilton Depression Rating Scale, a common measure used by most of the studies in the review. The same was true, although to a lesser extent, for S-adenosylmethionine, methylfolate (a form of the B vitamin folic acid) and Vitamin D. A few isolated studies found some benefit from augmenting treatment with creatine, while adding zinc, vitamin C, the amino acid tryptophan and folic acid produced mixed results. The authors deemed all of these supplements relatively safe. © 2016 Scientific American,
Link ID: 22149 - Posted: 04.27.2016
By Nicholas Bakalar Treating pregnant women for depression may benefit not just themselves but their babies as well. A study, in the May issue of Obstetrics & Gynecology, included 7,267 pregnant women, of whom 831 had symptoms of depression. After controlling for maternal age, race, income, body mass index and other health and behavioral characteristics, the researchers found that depressive symptoms were associated with a 27 percent increased relative risk of preterm birth (less than 37 weeks of gestation), an 82 percent increased risk of very preterm birth (less than 32 weeks of gestation), and a 28 percent increased risk of having a baby small for gestational age. They also found that among those who were treated with antidepressants for depression — about a fifth of those with the diagnosis — there was no association with increased risk for any of these problems. But they acknowledge that this group was quite small, which limits the power to draw conclusions. Still, the lead author, Dr. Kartik K. Venkatesh, a clinical fellow in obstetrics and gynecology at Harvard, said that it was important to screen mothers for depression, not only for their health but for that of their babies. “By screening early in pregnancy, you could identify those at higher risk and counsel them about the importance of treatment,” he said. “Treating these women for depression may have real benefits.” © 2016 The New York Times Company
Anna Nowogrodzki Prions, the misfolded proteins that are known for causing degenerative illnesses in animals and humans, may have been spotted for the first time in plants. Researchers led by Susan Lindquist, a biologist at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, report that they have found a section of protein in thale cress (Arabidopsis) that behaves like a prion when it is inserted into yeast. In plants, the protein is called Luminidependens (LD), and it is normally involved in responding to daylight and controlling flowering time. When a part of the LD gene is inserted into yeast, it produces a protein that does not fold up normally, and which spreads this misfolded state to proteins around it in a domino effect that causes aggregates or clumps. Later generations of yeast cells inherit the effect: their versions of the protein also misfold. This does not mean that plants definitely have prion-like proteins, adds Lindquist — but she thinks that it is likely. “I’d be surprised if they weren’t there,” she says. To prove it, researchers would need to grind up a plant and see whether they could find a protein such as LD in several different folded states, as well as show that any potential prion caused a misfolding cascade when added to a test-tube of protein. Lindquist adds that because she's not a plant scientist — her focus is on using yeast to investigate prions — she hasn't tried these experiments. The study is reported on 25 April in the Proceedings of the National Academy of Sciences1. © 2016 Nature Publishing Group
By Jordana Cepelewicz Everyone is familiar with the complaints of a hungry stomach. For years, scientists attributed the gnawing increase in appetite before a meal to ghrelin, a hormone which is secreted in the gut and circulates in the blood, playing a role in food intake and storage. Researchers have found that levels of ghrelin, dubbed the “hunger hormone,” peak before meals and recede after eating. Given its association with appetite, ghrelin is a tempting drug target for potential obesity treatments—but findings thus far have not lived up to expectations. Experiments that knock out the genes coding for ghrelin and its single receptor, GHSR (growth hormone secretagogue receptor), have been inconclusive: Remove the hormone or receptor, and rodents used in the experiments do not necessarily lose their drive to eat. Now a team of researchers at the French Institute of Health and Medical Research (INSERM) in Paris believe that scientists have had it wrong all along. In a study published this week in Science Signaling, they report that ghrelin does not enhance appetite in rats but rather increases weight gain and fat buildup. Unlike in earlier work, in the new study the researchers used a novel genetic method that kept the ghrelin receptor functional but modified it to have greater signaling in response to ghrelin—in other words, the receptor would enhance the hormone’s effects. The team then performed a series of experiments, first in isolated cells and then in rats. As expected, exposing ghrelin to modified receptors prompted a more potent response compared with the unaltered GHSR. © 2016 Scientific American
By Clare Wilson One day, you might be seeing in blue for 24 hours before you have an operation – to prevent organ damage. A study in mice suggests that exposure to blue light reduces a form of organ damage that is common during surgery. Reperfusion injury can happen when blood vessels are temporarily tied off during surgery, or when blocked arteries are surgically widened after a heart attack or stroke. Some damage is caused by a lack of oxygen, and further harm results when oxygen levels rebound, causing cells to become overactive, and triggering an attack by the immune system. But blue light seems to reduce this, in mice at least. Matthew Rosengart of the University of Pittsburgh, Pennsylvania, and his team have found that when mice are exposed to blue light for 24 hours before the blood supply to their liver or kidney is temporarily tied off, there is less reperfusion injury than if the mice are exposed to other types of light. “That’s pretty remarkable,” says Jack Pickard, a reperfusion researcher at University College London. Further tests showed that blue light seems to dampen down the sympathetic nervous system, which is involved in mammal stress responses. In turn, this reduced the activity of immune cells called neutrophils, which are involved in inflicting the damage of a reperfusion injury. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 22145 - Posted: 04.26.2016