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By David Grimm “Painful, bizarre, and wasteful experiments.” Buying dogs “just to cut them apart … and kill them.” These statements might sound like the rhetoric used by extreme animal rights groups, but they come from White Coat Waste—a new, unlikely coalition of fiscal conservatives and liberal activists that aims to end federal funding for research involving dogs and other animals by targeting people’s pocketbooks in addition to their heartstrings. Last week, the group made its first foray into the political arena, holding a briefing on Capitol Hill in Washington, D.C., for reporters and congressional staff. Speakers called on policymakers to launch an audit of the agencies that fund animal research, and depicted animal studies as another example of big government spending run amok. “I can’t think of any right-wing groups that have taken on animal research before,” says Tom Holder, the director of Speaking of Research, an international organization that supports the use of animals in scientific labs. “It’s a new way to crowbar off policymakers who might not otherwise support” efforts to end the use of animals in research. White Coat Waste, based in Washington, D.C., is the brainchild of Anthony Bellotti, a former Republican strategist who has consulted for campaigns against Obamacare and Planned Parenthood. His opposition to animal research began in 1995, when, in the summer between high school and college, he worked in a hospital laboratory that was conducting heart studies on pigs and witnessed experiments he saw as cruel. After he became a political consultant, he hit upon the idea of framing such research as a waste of taxpayer money. “That story was being told in the Planned Parenthood and Obamacare debates, but not in the anti–animal research movement,” he says. “I wanted to unite the animal lovers and the liberty lovers.” © 2016 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 22891 - Posted: 11.21.2016
Ian Sample Science editor A leading psychologist whose research on human memory exposed her to death threats, lawsuits, personal abuse and a campaign to have her sacked has won a prestigious prize for her courage in standing up for science. Professor Elizabeth Loftus endured a torrent of abuse from critics who objected to her work on the unreliable nature of eyewitness testimonies, and her defining research on how people can develop rich memories for events that never happened. The work propelled Loftus into the heart of the 1990 “memory wars”, when scores of people who had gone into therapy with depression, eating disorders and other common psychological problems, came out believing they had recovered repressed memories for traumatic events, often involving childhood abuse. Loftus, now a professor of law and cognitive science at the University of California, Irvine, performed a series of experiments that showed how exposure to inaccurate information and leading questions could corrupt eyewitness testimonies. More controversially, she demonstrated how therapy and hypnosis could plant completely false childhood memories in patients. She went on to become an expert witness or consultant for hundreds of court cases. In the 1990s, thousands of repressed memory cases came to light, with affected patients taking legal action against family members, former neighbours, doctors, dentists and teachers. The accusations tore many families apart. As an expert witness in such cases, Loftus came under sustained attack from therapists and patients who were convinced the new-found memories were accurate. The abuse marked a distinct shift away from the good-natured debates she was used to having in academic journals. © 2016 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 22890 - Posted: 11.19.2016
By Jessica Wright, A laboratory mouse has a modest home: a small, smelly cage lined with soft bedding, which it shares with up to four other animals. But it is home nonetheless—a place of comfort. That is, until the massive hand of a researcher reaches in to pluck it out for an experiment. The experiment might gauge whether a mouse feels anxious or social, or tap the activity in its brain. But does the intrusion of the researcher’s hand influence the very behavior under study? Yes, says Timothy Murphy, professor of cellular and physiological sciences at the University of British Columbia in Vancouver, Canada. Murphy’s team has developed a high-tech cage that allows a mouse to go about its business uninterrupted^1. The cage records the mouse’s every move. Whenever the animal is thirsty, it enters a corridor, attaches its head to an apparatus, and takes a drink while a microscope takes a picture of its brain activity. Murphy and his colleagues have used the cages to measure synchrony between mouse brain regions. In one experiment, the researchers captured more than 7,000 snapshots of brain activity in less than two months—all of them after the mice voluntarily ‘posed’ for the camera. We asked Murphy how he trains mice to participate, and how this approach could help autism research. © 2016 Scientific American
Keyword: Brain imaging
Link ID: 22889 - Posted: 11.19.2016
Ramin Skibba Bats sing just as birds and humans do. But how they learn their melodies is a mystery — one that scientists will try to solve by sequencing the genomes of more than 1,000 bat species. The project, called Bat 1K, was announced on 14 November at the annual meeting of the Society for Neuroscience in San Diego, California. Its organizers also hope to learn more about the flying mammals’ ability to navigate in the dark through echolocation, their strong immune systems that can shrug off Ebola and their relatively long lifespans. “The genomes of all these other species, like birds and mice, are well-understood,” says Sonja Vernes, a neurogeneticist at the Max Planck Institute for Psycholinguistics in Nijmegen, Netherlands, and co-director of the project. “But we don’t know anything about bat genes yet.” Some bats show babbling behaviour, including barks, chatter, screeches, whistles and trills, says Mirjam Knörnschild, a behavioural ecologist at Free University Berlin, Germany. Young bats learn the songs and sounds from older male tutors. They use these sounds during courtship and mating, when they retrieve food and as they defend their territory against rivals. Scientists have studied the songs of only about 50 bat species so far, Knörnschild says, and they know much less about bat communication than about birds’. Four species of bats have so far been found to learn songs from each other, their fathers and other adult males, just as a child gradually learns how to speak from its parents1. © 2016 Macmillan Publishers Limited,
Nicola Davis Smart bottles that dispense the correct dose of medication at the correct time, digital assistants, and chairs that know how long you’ve sat in them are among the devices set to change the face of care for those living with dementia. Dementia is now the leading cause of death in England and Wales, and is thought to affect more than 850,000 people in the UK. But a new wave of connected devices, dubbed “the internet of things”, could offer new ways to help people live independently for longer. “We have got an elderly population, and children in their 40s and 50s are looking after their elderly parents – and they may not have the capabilities to coordinate that care effectively,” said Idris Jahn, head of health and data at IoTUK, a programme within the government-backed Digital Catapult. While phone calls and text messages help to keep people in touch, says Jahn, problems can still arise, from missed appointments to difficulties in taking medication correctly. But he adds, connected sensors and devices that collect and process data in real time could help solve the problem. “For [people living with dementia] the sensors would be more in the environment itself, so embedded into the plug sockets, into the lights – so it is effectively invisible. You carry on living your life but in the background things will monitor you and provide feedback to people who need to know,” he said. “That might be your carer, it might be your family, it might be your clinician.” The approach, he added, has the potential to change the way care is given. “It is having that cohesive mechanism to put everyone into the loop, which I think hasn’t existed in the past and it is something that people need.” © 2016 Guardian News and Media Limited
Link ID: 22887 - Posted: 11.19.2016
By Jef Akst WIKIMEDIA COMMONS, GERRYSHAWThe deeper scientists probe into the complexity of the human brain, the more questions seem to arise. One of the most fundamental questions is how many different types of brain cells there are, and how to categorize individual cell types. That dilemma was discussed during a session yesterday (November 11) at the ongoing Society for Neuroscience (SfN) conference in San Diego, California. As Evan Macosko of the Broad Institute said, the human brain comprises billions of brain cells—about 170 billion, according to one recent estimate—and there is a “tremendous amount of diversity in their function.” Now, new tools are supporting the study of single-cell transcriptomes, and the number of brain cell subtypes is skyrocketing. “We saw even greater degrees of heterogeneity in these cell populations than had been appreciated before,” Macosko said of his own single-cell interrogations of the mouse brain. He and others continue to characterize more brain regions, clustering cell types based on differences in gene expression, and then creating subclusters to look for diversity within each cell population. Following Macosko’s talk, Bosiljka Tasic of the Allen Institute for Brain Science emphasized that categorizing cell types into subgroups based on gene expression is not enough. Researchers will need to combine such data with traditional metrics, such as morphology and electrophysiology to “ultimately come up with an integrative taxonomy of cell types,” Tasic said. “Multimodal data acquisition—it’s a big deal and I think it’s going to be a big focus of our future endeavors.” © 1986-2016 The Scientist
Keyword: Brain imaging
Link ID: 22886 - Posted: 11.19.2016
By R. Douglas Fields SAN DIEGO—A wireless device that decodes brain waves has enabled a woman paralyzed by locked-in syndrome to communicate from the comfort of her home, researchers announced this week at the annual meeting of the Society for Neuroscience. The 59-year-old patient, who prefers to remain anonymous but goes by the initials HB, is “trapped” inside her own body, with full mental acuity but completely paralyzed by a disease that struck in 2008 and attacked the neurons that make her muscles move. Unable to breathe on her own, a tube in her neck pumps air into her lungs and she requires round-the-clock assistance from caretakers. Thanks to the latest advance in brain–computer interfaces, however, HB has at least regained some ability to communicate. The new wireless device enables her to select letters on a computer screen using her mind alone, spelling out words at a rate of one letter every 56 seconds, to share her thoughts. “This is a significant achievement. Other attempts on such an advanced case have failed,” says neuroscientist Andrew Schwartz of the University of Pittsburgh, who was not involved in the study, published in The New England Journal of Medicine. HB’s mind is intact and the part of her brain that controls her bodily movements operates perfectly, but the signals from her brain no longer reach her muscles because the motor neurons that relay them have been damaged by amyotrophic lateral sclerosis (ALS), says neuroscientist Erick Aarnoutse, who designed the new device and was responsible for the technical aspects of the research. He is part of a team of physicians and scientists led by neuroscientist Nick Ramsey at Utrecht University in the Netherlands. Previously, the only way HB could communicate was via a system that uses an infrared camera to track her eye movements. But the device is awkward to set up and use for someone who cannot move, and it does not function well in many situations, such as in bright sunlight. © 2016 Scientific American,
Sara Reardon Lasers shone into the brains of mice can now activate individual neurons — and change the animals behaviour. Scientists have used the technique to increase how fast mice drink a milkshake, but it could also help researchers to map brain functions at a much finer scale than is currently possible. Neuroscientists at Stanford University in California conducted their experiments on mice that were genetically engineered to have light-sensitive neurons in a brain region called the orbitofrontal cortex. That area is involved in perceiving, and reacting to, rewards. By shining a laser at specific neurons, the researchers increased the pace at which the mice consumed a high-calorie milkshake. The results, reported on 12 November at the annual meeting of the Society for Neuroscience in San Diego, California, illustrate for the first time that the technique, known as optogenetics, can control behaviour by activating a sequence of individual cells. One goal of optogenetics is to create automated systems that manipulate the brain on the fly using only light, says Michael Häusser, a neuroscientist at University College London, UK. This might be done by engineering neurons to contain one protein that makes the cell fire when activated by a flash of coloured light, and another that causes the cell to flash in a different colour when it fires. A device that detected this second colour could quickly determine sites of activity associated with certain behaviours and customize which cells the first light would stimulate in response. Such a system might be able to alter the neural processes that link alcohol with reward in addiction, or a visual trigger with flashbacks in post-traumatic stress disorder. © 2016 Macmillan Publishers Limited,
By Alice Klein Alzheimer’s disease can be prevented by stopping a crucial brain protein from turning rogue, a study in mice suggests. Tau protein has long been suspected to play a role in causing the condition. In healthy brains, tau is essential for normal cell functioning. But during Alzheimer’s disease, the protein goes haywire, clumping together to form twisted tangles and, it is thought, releasing toxic chemicals that harm the brain. Now Lars Ittner at the University of New South Wales, Australia, and his colleagues have pinpointed a crucial enzyme that controls how tau proteins behave in the brain. The enzyme, called p38γ kinase, helps keep tau in a healthy, tangle-free state, preventing the onset of memory loss and other symptoms in mice that have been bred to develop Alzheimer’s disease. The enzyme seems to block Alzheimer’s by interfering with the action of another problem protein, called beta-amyloid. Like tau, clumps of this protein accumulate in the brains of people with Alzheimer’s, making it another suspected cause of the disease. When beta-amyloid forms these sticky plaques, it can also modify the structure of tau proteins, causing them to form tangles and release toxic chemicals. But Ittner’s team found that p38γ kinase makes a different kind of structural change to tau. If this change is made first, it prevents beta-amyloid from being able to turn tau bad, and mice do not develop the disease. © Copyright Reed Business Information Ltd.
Link ID: 22883 - Posted: 11.18.2016
Hannah Devlin Science Correspondent Blind animals have had their vision partially restored using a revolutionary DNA editing technique that scientists say could in future be applied to a range of devastating genetic diseases. The study is the first to demonstrate that a gene editing tool, called Crispr, can be used to replace faulty genes with working versions in the cells of adults - in this case adult rats. Previously, the powerful procedure, in which strands of DNA are snipped out and replaced, had been used only in dividing cells - such as those in an embryo - and scientists had struggled to apply it to non-dividing cells that make up most adult tissue, including the brain, heart, kidneys and liver. The latest advance paves the way for Crispr to be used to treat a range of incurable illnesses, such as muscular dystrophy, haemophilia and cystic fibrosis, by overwriting aberrant genes with a healthy working version. Professor Juan Carlos Izpisua Belmonte, who led the work at the Salk Institute in California, said: “For the first time, we can enter into cells that do not divide and modify the DNA at will. The possible applications of this discovery are vast.” The technique could be trialled in humans in as little as one or two years, he predicted, adding that the team were already working on developing therapies for muscular dystrophy. Crispr, a tool sometimes referred to as “molecular scissors”, has already been hailed as a game-changer in genetics because it allows scientists to cut precise sections of DNA and replace them with synthetic, healthy replacements. © 2016 Guardian News and Media Limited
Link ID: 22882 - Posted: 11.17.2016
Laura Sanders SAN DIEGO — Over the course of months, clumps of a protein implicated in Parkinson’s disease can travel from the gut into the brains of mice, scientists have found. The results, reported November 14 at the annual meeting of the Society for Neuroscience, suggest that in some cases, Parkinson’s may get its start in the gut. That’s an intriguing concept, says neuroscientist John Cryan of the University College Cork in Ireland. The new study “shows how important gut health can be for brain health and behavior.” Collin Challis of Caltech and colleagues injected clumps of synthetic alpha-synuclein, a protein known to accumulate in the brains of people with Parkinson’s, into mice’s stomachs and intestines. The researchers then tracked alpha-synuclein with a technique called CLARITY, which makes parts of the mice’s bodies transparent. Seven days after the injections, researchers saw alpha-synuclein clumps in the gut. Levels there peaked 21 days after the injections. These weren’t the same alpha-synuclein aggregates that were injected, though. These were new clumps, formed from naturally occurring alpha-synuclein, that researchers believe were coaxed into forming by the synthetic versions in their midst. Also 21 days after the injections, alpha-synuclein clumps seemed to have spread to a part of the brain stem containing nerve cells that make up the vagus nerve, a neural highway that connects the gut to the brain. Sixty days after the injections, alpha-synuclein had accumulated in the midbrain, a region packed with nerve cells that make the chemical messenger dopamine. These are the nerve cells that die in people with Parkinson’s, a progressive brain disorder that affects movement. © Society for Science & the Public 2000 - 2016
Link ID: 22881 - Posted: 11.17.2016
By ARNAUD COLINART, AMAURY LA BURTHE, PETER MIDDLETON and JAMES SPINNEY “What is the world of sound?” So begins a diary entry from April 1984, recorded on audiocassette, about the nature of acoustic experience. The voice on the tape is that of the writer and theologian John Hull, who at the time of the recording had been totally blind for almost two years. After losing his sight in his mid-40s, Dr. Hull, a newlywed with a young family, had decided that blindness would destroy him if he didn’t learn to understand it. For three years he recorded his experiences of sight loss, documenting “a world beyond sight.” We first met Dr. Hull in 2011, having read his acclaimed 1991 book “Touching The Rock: An Experience of Blindness,” which was transcribed from his audio diaries. We began collaborating with him on a series of films using his original recordings. These included an Emmy-winning Op-Doc in 2014 and culminated in the feature-length documentary “Notes on Blindness.” But we were also interested in how interactive forms of storytelling might further explore Dr. Hull’s vast and detailed account — in particular how new mediums like virtual reality could illuminate his investigations into auditory experience. The diaries describe his evolving appreciation of “the breadth and depth of three-dimensional world that is revealed by sound,” the awakening of an acoustic perception of space. The sound of falling rain, he said, “brings out the contours of what is around you”; wind brings leaves and trees to life; thunder “puts a roof over your head.” This interactive experience is narrated by Dr. Hull, using extracts from his diary recordings to consider the nature of acoustic space. Binaural techniques map the myriad details of everyday life (in this case, the noises that surround Dr. Hull in a park) within a 3-D sound environment, a “panorama of music and information,” rich in color and texture. The real-time animation visualizes this multilayered soundscape in which, Dr. Hull says, “every sound is a point of activity.” © 2016 The New York Times Company
Laurence O'Dwyer Until as late as 2013 a joint (or comorbid) diagnosis of autism and attention deficit hyperactivity disorder (ADHD) was not permitted by the most influential psychiatric handbook, the Diagnostic and Statistical Manual of Mental Disorders (DSM). The DSM is an essential tool in psychiatry as it allows clinicians and researchers to use a standard framework for classifying mental disorders. Health insurance companies and drug regulation agencies also use the DSM, so its definition of what does or doesn’t constitute a particular disorder can have far-reaching consequences. One of the reasons for the prohibition of a comorbid diagnosis of autism and ADHD was that the severity of autism placed it above ADHD in the diagnostic hierarchy, so the inattention that is normally present in autism did not seem to merit an additional diagnosis. Nevertheless, that was an odd state of affairs, as any clinician working in the field would be able to quote studies that point to anything from 30% to 80% of patients with autism also having ADHD. More problematic still is the fact that patients with both sets of symptoms may respond poorly to standard ADHD treatments or have increased side effects. The fifth edition of the DSM opened the way for a more detailed look at this overlap, and just a year after the new guidelines were adopted, a consortium (which I am a part of) at the Radboud University in Nijmegen (Netherlands) called NeuroIMAGE published a paper which showed that autistic traits in ADHD participants could be predicted by complex interactions between grey and white matter volumes in the brain. © 2016 Guardian News and Media Limited
Amir Kheradmand, When we spin—on an amusement park ride or the dance floor—we often become disoriented, even dizzy. So how do professional athletes, particularly figure skaters who spin at incredible speeds, avoid losing their balance? The short answer is training, but to really grasp why figure skaters can twirl without getting dizzy requires an understanding of the vestibular system, the apparatus in our inner ear that helps to keep us upright. This system contains special sensory nerve cells that can detect the speed and direction at which our head moves. These sensors are tightly coupled with our eye movements and with our perception of our body's position and motion through space. For instance, if we rotate our head to the right while our eyes remain focused on an object straight ahead, our eyes naturally move to the left at the same speed. This involuntary response allows us to stay focused on a stationary object. Spinning is more complicated. When we move our head during a spin, our eyes start to move in the opposite direction but reach their limit before our head completes a full 360-degree turn. So our eyes flick back to a new starting position midspin, and the motion repeats as we rotate. When our head rotation triggers this automatic, repetitive eye movement, called nystagmus, we get dizzy. © 2016 Scientific American
Link ID: 22878 - Posted: 11.17.2016
Laura Beil NEW ORLEANS — Popular heartburn drugs — already under investigation for possible links to dementia, kidney and heart problems (SN: 6/11/16, p. 8) — have a new health concern to add to the list. An analysis of almost 250,000 medical records in Denmark has found an association with stroke. Researchers from the Danish Heart Foundation in Copenhagen studied patients undergoing gastric endoscopy from 1997 to 2012. About 9,500 of all patients studied suffered from ischemic strokes, which occur when a blood clot blocks a blood vessel in the brain. Overall, the risk of stroke was 21 percent higher in patients taking a proton pump inhibitor, a drug that relieves heartburn, the researchers reported November 15 during the American Heart Association’s annual meeting. While those patients also tended to be older and sicker to start with, the level of risk was associated with dose, the researchers found. People taking the lowest drug doses (between 10 and 20 milligrams a day, depending on the drug) did not have a higher risk. At the highest doses, though, Prevacid (more than 60 mg/day) carried a 30 percent higher risk and Protonix (more than 80 mg/day) a 94 percent higher risk. For Prilosec and Nexium, stroke risk fell within that range. Introduced in the 1980s, proton pump inhibitors are available in both prescription and over-the-counter forms. While they are valuable drugs, “their use has been increasing rapidly,” says lead author Thomas Sehested, adding that people often take them for too long, or without a clear reason. Before taking them, he says, “patients need a conversation with their doctor to see if they really need these drugs.” |© Society for Science & the Public 2000 - 2016
Link ID: 22877 - Posted: 11.17.2016
Laura Sanders SAN DIEGO — Mice raised in cages bombarded with glowing lights and sounds have profound brain abnormalities and behavioral trouble. Hours of daily stimulation led to behaviors reminiscent of attention-deficit/hyperactivity disorder, scientists reported November 14 at the annual meeting of the Society for Neuroscience. Certain kinds of sensory stimulation, such as sights and sounds, are known to help the brain develop correctly. But scientists from Seattle Children’s Research Institute wondered whether too much stimulation or stimulation of the wrong sort could have negative effects on the growing brain. To mimic extreme screen exposure, mice were blasted with flashing lights and TV audio for six hours a day. The cacophony began when the mice were 10 days old and lasted for six weeks. After the end of the ordeal, scientists examined the mice’s brains. “We found dramatic changes everywhere in the brain,” said study coauthor Jan-Marino Ramirez. Mice that had been stimulated had fewer newborn nerve cells in the hippocampus, a brain structure important for learning and memory, than unstimulated mice, Ramirez said. The stimulation also made certain nerve cells more active in general. Stimulated mice also displayed behaviors similar to some associated with ADHD in children. These mice were noticeably more active and had trouble remembering whether they had encountered an object. The mice also seemed more inclined to take risks, venturing into open areas that mice normally shy away from, for instance. |© Society for Science & the Public 2000 - 2016.
By Clare Wilson It’s one of the boldest treatments in medicine: delivering an electrical current deep into the brain by implanting a long thin electrode through a hole in the skull. Such “deep brain stimulation” (DBS) works miracles on people with otherwise untreatable epilepsy or Parkinson’s disease – but drilling into someone’s head is an extreme step. In future, we may be able to get the same effects by using stimulators placed outside the head, an advance that could see DBS used to treat a much wider range of conditions. DBS is being investigated for depression, obesity and obsessive compulsive disorder, but this research is going slowly. Implanting an electrode requires brain surgery, and carries a risk of infection, so the approach is only considered for severe cases. But Nir Grossman of Imperial College London and his team have found a safer way to experiment with DBS – by stimulating the brain externally, with no need for surgery. The technique, unveiled at the Society for Neuroscience conference in San Diego, California, this week, places two electrical fields of different frequencies outside the head. The brain tissue where the fields overlap is stimulated, while the tissue under just one field is unaffected because the frequencies are too high. For instance, they may use one field at 10,000 hertz and another at 10,010 hertz. The affected nerve cells are stimulated at 10 hertz – the difference between the two frequencies. © Copyright Reed Business Information Ltd.
Link ID: 22875 - Posted: 11.16.2016
By GRETCHEN REYNOLDS Exercise may be an effective treatment for depression and might even help prevent us from becoming depressed in the first place, according to three timely new studies. The studies pool outcomes from past research involving more than a million men and women and, taken together, strongly suggest that regular exercise alters our bodies and brains in ways that make us resistant to despair. Scientists have long questioned whether and how physical activity affects mental health. While we know that exercise alters the body, how physical activity affects moods and emotions is less well understood. Past studies have sometimes muddied rather than clarified the body and mind connections. Some randomized controlled trials have found that exercise programs, often involving walking, ease symptoms in people with major depression. But many of these studies have been relatively small in scale or had other scientific deficiencies. A major 2013 review of studies related to exercise and depression concluded that, based on the evidence then available, it was impossible to say whether exercise improved the condition. Other past reviews similarly have questioned whether the evidence was strong enough to say that exercise could stave off depression. A group of global public-health researchers, however, suspected that newer studies and a more rigorous review of the statistical evidence might bolster the case for exercise as a treatment of and block against depression. So for the new analyses, they first gathered all of the most recent and best-designed studies about depression and exercise. © 2016 The New York Times Company
Link ID: 22874 - Posted: 11.16.2016
By Daniel Barron Neurobiology was the first class I shuffled into as a dopey freshman undergraduate student. Dr. Brown’s class began at 8AM. I wore that bowling jacket I bought from the Orem Deseret Industries, Utah’s version of Goodwill. I’d spent much of my childhood in lower-middle class neighborhoods of small towns: Middle and Junior High School in the Texas Hill Country; High School in rural Utah. In High School, I would jog through the countryside—down by the River Bottom’s road—and rehearse conversations and ideas that troubled me. I hadn’t learned the language of social justice or of science. I felt uneasy with many of the ideas I’d been taught but lacked the vocabulary to pinpoint why. Dr. Brown’s first lecture covered visual perception, ocular dominance columns, and the idea that brain structure and function were intertwined. To use my parlance at that age, this was a Revelation. The lecture outlined a completely novel way of thinking: the notion that between my ears, behind my forehead and nose was a collection of cells—of neurons, an organ—responsible for how I saw and perceived the world. I was young, I was a drug-free virgin, and this was without question the greatest catharsis I had ever experienced. Here wasn’t simply a foundation for my behavior, but for others’ as well. My theological leanings faded as I began to learn why I was Me. In response, I worked my ass off. © 2016 Scientific American,
Link ID: 22873 - Posted: 11.16.2016
Laura Beil NEW ORLEANS — Chronic sleep problems are associated with atrial fibrillation — a temporary but dangerous disruption of heart rhythm — even among people who don’t suffer from sleep apnea. An analysis of almost 14 million patient records has found that people suffering from insomnia, frequent waking and other sleep issues are more likely than sound sleepers to experience a condition in which the upper chambers of the heart quiver instead of rhythmically beating, allowing blood to briefly stagnate. “Even if you don’t have sleep apnea, is there something about sleep disruption that puts you at a higher risk of fibrillation,” said Gregory Marcus, a cardiologist at the University of California, San Francisco. “We should put a higher priority on studying sleep itself.” Marcus and Matthew Christensen, from the University of Michigan, presented their results November 14 at the annual meeting of the American Heart Association. People with atrial fibrillation have double the risk of having a heart attack, and up to five times the risk of stroke. Although the heart condition can be a consequence of aging, its prevalence is rising at about 4 percent per year for reasons that aren’t totally explained. In the United States, about 5 million people currently have the condition, and that number is expected to rise to 12 million by 2030. A large body of studies has found that sleep apnea, which occurs when a person stops breathing during the night, can lead to atrial fibrillation and a host of other health concerns. Identifying a risk of atrial fibrillation among people with no sleep apnea is unexpected, says Richard Becker, director of the University of Cincinnati Heart, Lung & Vascular Institute, who was not part of the study. |© Society for Science & the Public 2000 - 2016.
Link ID: 22872 - Posted: 11.16.2016