By Gretchen Reynolds People hoping to lose weight with exercise often wind up being their own worst enemies, according to the latest, large-scale study of workouts, weight loss and their frustrating interaction. The study, which carefully tracked how much people ate and moved after starting to exercise, found that many of them failed to lose or even gained weight while exercising, because they also reflexively changed their lives in other, subtle ways. But a few people in the study did drop pounds, and their success could have lessons for the rest of us. In a just and cogent universe, of course, exercise would make us thin. Physical activity consumes calories, and if we burn calories without replacing them or reducing our overall energy expenditure, we enter negative energy balance. In that condition, we utilize our internal energy stores, which most of us would call our flab, and shed weight. But human metabolisms are not always just and cogent, and multiple past studies have shown that most men and women who begin new exercise routines drop only about 30 percent or 40 percent as much weight as would be expected, given how many additional calories they are expending with exercise. Why exercise underwhelms for weight reduction remains an open question, though. Scientists studying the issue agree that most of us compensate for the calories lost to exercise by eating more, moving less, or both. Our resting metabolic rates may also decline if we start to lose pounds. All of this shifts us back toward positive energy balance, otherwise known as weight gain. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26382 - Posted: 07.03.2019

By Bret Stetka The pathology of a stroke is deceptively complicated. In the simplest sense, strokes occur when the blood supply to a particular region of the brain is interrupted, cutting off the area to oxygen and nutrients. This deprivation results in injury and death to the local brain cells. But for days after the breach in blood flow, the immune system also does its own fair share of damage to the already injured brain through an inflammatory response. New research by a group at Stanford University has identified a subset of immune cells that drive brain injury following a stroke, raising the possibility that immune-system inhibition might be a promising treatment for a blood-deprived brain. More surprising is that much of the immune reaction to a stroke appears to begin in the gut, shedding new light on our ever evolving understanding of the gut-brain axis. The research was published on July 1 in Nature Immunology. Strokes manifest in two ways: either an artery in the brain bursts—causing a hemorrhagic stroke—or it becomes clogged, typically by a blood clot, causing the far more common ischemic stroke. In the new study, the authors used positron-emission tomography to scan immune system activity in mice that had the blood in a single cerebral artery interrupted for 45 minutes, mimicking an ischemic stroke. © 2019 Scientific American

Keyword: Stroke; Neuroimmunology
Link ID: 26381 - Posted: 07.03.2019

By Matthew Shaer A few years ago, a scientist named Nenad Sestan began throwing around an idea for an experiment so obviously insane, so “wild” and “totally out there,” as he put it to me recently, that at first he told almost no one about it: not his wife or kids, not his bosses in Yale’s neuroscience department, not the dean of the university’s medical school. Like everything Sestan studies, the idea centered on the mammalian brain. More specific, it centered on the tree-shaped neurons that govern speech, motor function and thought — the cells, in short, that make us who we are. In the course of his research, Sestan, an expert in developmental neurobiology, regularly ordered slices of animal and human brain tissue from various brain banks, which shipped the specimens to Yale in coolers full of ice. Sometimes the tissue arrived within three or four hours of the donor’s death. Sometimes it took more than a day. Still, Sestan and his team were able to culture, or grow, active cells from that tissue — tissue that was, for all practical purposes, entirely dead. In the right circumstances, they could actually keep the cells alive for several weeks at a stretch. When I met with Sestan this spring, at his lab in New Haven, he took great care to stress that he was far from the only scientist to have noticed the phenomenon. “Lots of people knew this,” he said. “Lots and lots.” And yet he seems to have been one of the few to take these findings and push them forward: If you could restore activity to individual post-mortem brain cells, he reasoned to himself, what was to stop you from restoring activity to entire slices of post-mortem brain? © 2019 The New York Times Company

Keyword: Consciousness
Link ID: 26380 - Posted: 07.02.2019

By Max Bertolero, Danielle S. Bassett | Networks pervade our lives. Every day we use intricate networks of roads, railways, maritime routes and skyways traversed by commercial flights. They exist even beyond our immediate experience. Think of the World Wide Web, the power grid and the universe, of which the Milky Way is an infinitesimal node in a seemingly boundless network of galaxies. Few such systems of interacting connections, however, match the complexity of the one underneath our skull. Neuroscience has gained a higher profile in recent years, as many people have grown familiar with splashily colored images that show brain regions “lighting up” during a mental task. There is, for instance, the temporal lobe, the area by your ear, which is involved with memory, and the occipital lobe at the back of your head, which dedicates itself to vision. What has been missing from this account of human brain function is how all these distinct regions interact to give rise to who we are. Our laboratory and others have borrowed a language from a branch of mathematics called graph theory that allows us to parse, probe and predict complex interactions of the brain that bridge the seemingly vast gap between frenzied neural electrical activity and an array of cognitive tasks—sensing, remembering, making decisions, learning a new skill and initiating movement. This new field of network neuroscience builds on and reinforces the idea that certain regions of the brain carry out defined activities. In the most fundamental sense, what the brain is—and thus who we are as conscious beings—is, in fact, defined by a sprawling network of 100 billion neurons with at least 100 trillion connecting points, or synapses. © 2019 Scientific American

Keyword: Consciousness
Link ID: 26379 - Posted: 07.02.2019

Tam Hunt How can you know that any animal, other human beings, or anything that seems conscious, isn’t just faking it? Does it enjoy an internal subjective experience, complete with sensations and emotions like hunger, joy, or sadness? After all, the only consciousness you can know with certainty is your own. Everything else is inference. The nature of consciousness makes it by necessity a wholly private affair. These questions are more than philosophical. As intelligent digital assistants, self-driving cars and other robots start to proliferate, are these AIs actually conscious or just seem like it? Or what about patients in comas – how can doctors know with any certainty what kind of consciousness is or is not present, and prescribe treatment accordingly? In my work, often with with psychologist Jonathan Schooler at the University of California, Santa Barbara, we’re developing a framework for thinking about the many different ways to possibly test for the presence of consciousness. There is a small but growing field looking at how to assess the presence and even quantity of consciousness in various entities. I’ve divided possible tests into three broad categories that I call the measurable correlates of consciousness. There are three types of ways to gauge consciousness. You can look for brain activity that occurs at the same time as reported subjective states. Or you can look for physical actions that seem to be accompanied by subjective states. Finally, you can look for the products of consciousness, like artwork or music, or this article I’ve written, that can be separated from the entity that created them to infer the presence – or not – of consciousness. © 2010–2019, The Conversation US, Inc.

Keyword: Consciousness
Link ID: 26378 - Posted: 07.02.2019

By Ken Garber The idea that chemical tags on genes can affect their expression without altering the DNA sequence, once surprising, is the stuff of textbooks. The phenomenon, epigenetics, has now come to messenger RNA (mRNA), the molecule that carries genetic information from DNA to a cell’s proteinmaking factories. At a conference here last month, researchers discussed evidence that RNA epigenetics is also critical for gene expression and disease, and they described a new chemical modification linked to leukemia. Research has found that epigenetic marks decorate mRNAs like Christmas lights on a fence. The cell uses the marks “to determine where, when, and how much of the [associated] protein should be generated,” RNA biologist Pedro Batista of the National Cancer Institute (NCI) in Bethesda, Maryland, said at the conference. What’s more, says Michael Kharas of Memorial Sloan Kettering Cancer Center in New York City, mRNA modifications “can affect the viability of cells, whether cells divide, cancer, neurologic diseases.” They are providing promising leads for drug developers. And, he adds, “There’s so many [more] diseases these things could be important in, ones people aren’t even looking at.” Modified mRNAs had been reported in the 1970s, but by 2008 they were largely forgotten. Then, Chuan He at the University of Chicago, Samie Jaffrey at Cornell University, and Gideon Rechavi at Tel Aviv University in Israel took a fresh look. Their teams focused on one mRNA modification called m6A: a methyl group—a simple chemical unit—attached to some of an RNA molecule’s adenine bases. He’s group showed that a well-known enzyme removes this mRNA modification, indicating that m6A has an important biological role, and Jaffrey’s and Rechavi’s groups developed mapping tools that showed it is widespread. Before the work, researchers knew mRNA epigenetic marks were there, but “they just didn’t know how to actually look for them,” says NCI researcher Shalini Oberdoerffer. © 2019 American Association for the Advancement of Science

Keyword: Epigenetics; Development of the Brain
Link ID: 26377 - Posted: 07.02.2019

By Chris Woolston When Sylvia Groth steps through the doors of the Vanderbilt Eye Institute in Nashville, she knows she has a tough day ahead. Before she goes home, she’ll likely have at least one hard talk with a person whose sight has been ravaged by glaucoma. “When I make a diagnosis of advanced glaucoma, I do it with a heavy heart,” the ophthalmologist says. “It’s such an empty feeling to not be able to do anything.” An incurable eye disease that kills vital nerve cells at the back of the retina, glaucoma is a leading cause of irreversible blindness in the world. More than 70 million people have it, and 3 million of them already are blind. Nothing can be done to restore vision once it’s lost, and even the best treatments can’t always slow disease progression. But researchers foresee a time when they can offer therapies to protect nerve cells in the eye and perhaps even restore lost sight. “We’re making advances with every different type of treatment,” ophthalmologist Leonard Levin of McGill University in Montreal says. Researchers have long understood the basics of the most common form of glaucoma, called open-angle glaucoma. The eye is nourished by a clear fluid called the aqueous humor that keeps the eyeball inflated, plump and healthy. But just like a tire, the eye can become overinflated. If the aqueous humor can’t drain properly, pressure inside the eye grows too high and can crush cells within the optic nerve — the sensory cable that carries images from the retina to the optical centers of the brain. Pressure probably hurts nerve cells in other ways too, ophthalmologist Harry Quigley of Johns Hopkins University says. © 1996-2019 The Washington Post

Keyword: Vision
Link ID: 26376 - Posted: 07.02.2019

Millions of people in the UK are putting their sight at risk by continuing to smoke, warn specialists. Despite the clear connection, only one in five people recognise that smoking can lead to blindness, a poll for the Association of Optometrists (AOP) finds. Smokers are twice as likely to lose their sight compared with non-smokers, says the RNIB. That is because tobacco smoke can cause and worsen a number of eye conditions. How smoking can harm your eyes Cigarette smoke contains toxic chemicals that can irritate and harm the eyes. For example, heavy metals, such as lead and copper, can collect in the lens - the transparent bit that sits behind the pupil and brings rays of light into focus - and lead to cataracts, where the lens becomes cloudy. Smoking can make diabetes-related sight problems worse by damaging blood vessels at the back of the eye (the retina). Smokers are around three times more likely to get age-related macular degeneration - a condition affecting a person's central vision, meaning that they lose their ability to see fine details. And they are 16 times more likely than non-smokers to develop sudden loss of vision caused by optic neuropathy, where the blood supply to the eye becomes blocked. In the poll of 2,006 adults, 18% correctly said that smoking increased the risk of blindness or sight loss, while three-quarters (76%) knew smoking was linked to cancer. © 2019 BBC

Keyword: Drug Abuse; Vision
Link ID: 26375 - Posted: 07.02.2019

Laura Sanders Some nerve cells in the brain are multitaskers, responding to both color and shape, a survey of over 4,000 neurons in the visual systems of macaque monkeys finds. The finding, described in the June 28 Science, counters earlier ideas that vision cells nestled in the back of the brain each handle information about only one aspect of sight: an object’s color or its orientation, an element of shape. Some scientists had thought that those aspects were then put together by other brain cells in later stages of visual processing to form a more complete picture of the world. In the new experiment, four macaques looked at a series of sights made of moving lines on a screen. Each time, the lines were one of 12 possible colors and moved at particular angles, creating an effect similar to a spinning candy cane in two dimensions. Using genetic tricks that made nerve cells glow when active, the researchers watched for action among the monkeys’ cells in an area of the brain that handles vision. Called V1, this stretch at the back of the brain is one of the first areas to interpret sight signals. Most of the cells that had a favorite color, indicated by their activity, also had a favorite orientation of lines, the researchers found. “Thus, textbook models of primate V1 must be updated,” the team writes. PUTTING IT TOGETHER This video captures nerve cells in a monkey’s visual system firing off signals. Some of these cells respond both to a favorite color and favorite shape. The discovery counters previous ideas that information about color is processed separately from information about shape in the brain. |© Society for Science & the Public 2000 - 2019.

Keyword: Vision
Link ID: 26374 - Posted: 07.02.2019

By Nicholas Bakalar People with obesity-related disorders may benefit from supplements of a common gut bacterium, a small pilot study suggests. Researchers tested the bacterium, Akkermansia muciniphila, in 32 men and women who met the criteria for metabolic syndrome by having at least three of five conditions: high fasting blood sugar, high blood pressure, high triglycerides, low HDL (the “good” cholesterol) or excessive waist circumference. A. muciniphila is a normal inhabitant of the human gut that is less prevalent in people with metabolic syndrome. In a three-month trial, volunteers were randomized to one of three groups: daily tablets containing live bacteria, pasteurized bacteria or a placebo. Compared with the placebo group, those who took pasteurized A. muciniphila had significantly improved insulin sensitivity and total cholesterol, and decreases in several blood markers of inflammation and liver dysfunction. They also had decreased body weight, fat mass and waist circumference, though those differences were not statistically significant. From the team at NYT Parenting: Get the latest news and guidance for parents. We'll celebrate the little parenting moments that mean a lot — and share stories that matter to families. The live bacteria were largely ineffective. The study is in Nature Medicine. “I hope people will not see this as a miracle cure,” said the senior author, Patrice D. Cani, a professor at the Catholic University of Louvain in Brussels. “The finding is significant, but it has to be confirmed in a larger cohort. Keep in mind that the first treatment for cardiometabolic disorders is healthy diet and sufficient exercise.” © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26373 - Posted: 07.02.2019

By Nathan Dunne I would stare at my hands and think, “I’m not me.” No matter where I was, in the middle of a busy street or at my dining table at home, the condition would be the same. It was like looking at my hands through a plate of glass. Although I could feel the skin on my palms, it did not feel like my own. Half of myself would move through the day while the other half watched. I was split in two. Nothing I did would relieve the condition. I went to see an ophthalmologist, convinced I had cataracts. The verdict was near-perfect vision. I tried taking time off work, talking with family and writing notes about how my life had become a simulation. Each morning I would stare at the mirror in an attempt to recognize myself, but the distance between my body and this new, outer eye only grew larger. I began to believe I was becoming psychotic and would soon be in a psychiatric ward. I was a 28-year-old, working as a copywriter while pursuing a PhD in art history, and I felt my life was nearing its end. One evening in April 2008, as I contemplated another helpless night trapped beyond my body, full blown panic set in. I took up the phone, ready to dial for emergency, when suddenly music began to play from downstairs. It was a nauseating pop song that my neighbor played incessantly, but something about the melody gave me pause. The next day I began a series of frustrating doctor’s visits. First with my physician, then a neurologist, gastroenterologist and chiropractor. I said that I had never taken drugs or drank alcohol excessively. While I was fatigued from my doctoral study, I didn’t think this qualified me for the split in the self that had occurred. © 1996-2019 The Washington Post

Keyword: Attention
Link ID: 26372 - Posted: 07.01.2019

By Jane E. Brody Strange as it may seem, the massive stroke Ted Baxter suffered in 2005 at age 41, leaving him speechless and paralyzed on his right side, was a blessing in more ways than one. Had the clot, which started in his leg, lodged in his lungs instead of his brain, the doctors told him he would have died from a pulmonary embolism. And as difficult as it was for him to leave his high-powered professional life behind and replace it with a decade of painstaking recovery, the stroke gave his life a whole new and, in many ways, more rewarding purpose. Before the stroke, Mr. Baxter’s intense work-focused life as a globe-trotting executive in international finance had eroded his marriage and deprived him of fulfilling relationships with family and friends. Unable to relax even on vacation, he rarely took time to smell the roses. Now, he told me, he leads a richer, calmer, happier life as a volunteer educator for stroke victims and their caregivers and for the therapists who treat them. The stroke began with a cramping pain in his leg after a long international flight during which he wore compression hose to support his varicose veins. He didn’t take the pain seriously until suddenly he couldn’t talk or move the right side of his body. The clot that caused his leg pain had broken loose and cut off blood flow to the left side of his brain. From the team at NYT Parenting: Get the latest news and guidance for parents. We'll celebrate the little parenting moments that mean a lot — and share stories that matter to families. © 2019 The New York Times Company

Keyword: Stroke
Link ID: 26371 - Posted: 07.01.2019

Maanvi Singh The notion that you can smile your way to happiness is an enduring one. Back in the 1800s, Charles Darwin was among the first to come up with what modern scientists further developed into the "facial feedback hypothesis." That's the idea that smiling can make you happier and frowning can make you sadder or angrier — that changing your facial expression can intensify or even transform your mood. Dick Van Dyke sang about the phenomenon — and so did Nat King Cole. And it is still taught in psychology classes today. But researchers are now finding that this phenomenon may be more complicated than they once thought. A recent study that reviewed around 50 years of data, including the results of nearly 300 experiments testing the facial feedback theory, has found that if smiling boosts happiness, it's only by a tiny bit. "I know when I'm sad and people tell me to smile, it just makes me more angry." Nick Coles, social psychology researcher, University of Tennessee, Knoxville After crunching all the numbers, the researchers say their results suggest that if 100 people smiled — all else equal among them — only about seven might expect to feel happier than if they hadn't smiled. The study also looked at the effects of a number of other facial expressions, including scowling and frowning, and tried to more generally understand the extent to which positive facial expressions create positive emotions and negative facial expressions create negative emotions. In each case, "the effects were extremely tiny," says Nick Coles, a social psychology Ph.D. candidate at the University of Tennessee, Knoxville, who led the study. The results, published in the June issue of Psychological Bulletin, add to a debate that has been ongoing "for at least 100 years — since the dawn of psychology," Coles says. © 2019 npr

Keyword: Emotions
Link ID: 26370 - Posted: 07.01.2019

Mike Power Roll up, roll up, ladies and gentleman, and gather around. Do you, your loved one – or family pet – suffer from any of the following conditions? Cancer, epilepsy, diabetes, arthritis, anxiety, menstrual cramps, insomnia, dry skin, psychosis, Alzheimer’s, dementia, anger, depression, ADHD, Crohn’s and IBS, PTSD, opiate addiction, Parkinson’s, pain of any kind, migraine, or canine uptightness? Then it’s your lucky day. All can be treated, claim the snake oil salesmen of the modern wild west, with the miracle cure-all: CBD, or cannabidiol. It’s one of the 119 cannabinoids contained in cannabis sativa, indica and ruderalis, and all hybrids thereof; aka weed. CBD is legal and doesn’t get you high – still-illegal cannabinoid THC does that job very efficiently – but it’s fair to say business is blazing. What a giddy array of products there are: from CBD water (sold in clear bottles that mean the sensitive compound swiftly degrades), to cooking or massage oils, pills, chewing gum, transdermal patches, pessaries, gin, beer and lube. The crown for silliest CBD product of the year, however, belongs indisputably to the CBD-infused pillowcases sold by one hopeful firm of US fabric-makers. Yoga classes offering CBD-assisted asanas and guided meditation have sprung up, with devotees claiming greater flexibility and elevated mood. Sellers in the UK are careful not to claim any specific medical benefits for the products because of a lack of clinical evidence, so they are instead marketed as food supplements. In this, they are supported by breathless, uncritical media reports on CBD use for airily unspecified “wellbeing” purposes. © 2019 Guardian News & Media Limited

Keyword: Drug Abuse; Sleep
Link ID: 26369 - Posted: 07.01.2019

Laura Sanders A gut-busting diet may set the brain up for more of the same. After mice ate fatty food for just two weeks, cells in their brains that send a “stop eating” signal were quieter than those in mice that didn’t eat high-fat chow, researchers report in the June 28 Science. The result helps untangle the complex relationship between food and appetite, one that can become muddled when people overeat. Because food is crucial to survival, the brain has built-in redundancy — a multitude of overlapping pro-food systems to make sure animals eat enough. Neuroscientist Garret Stuber of the University of Washington in Seattle took aim at one brain area known to be involved in eating behavior. Called the lateral hypothalamus, this brain structure contains a large number of diverse cells. Stuber and his colleagues looked at gene behavior in single cells there, and found that one group, called glutamatergic nerve cells, showed particularly big changes in which genes were active when the team compared lean mice with obese mice. Earlier work suggested that these glutamatergic cells acted like a brake on feeding: When the cells were artificially blocked from firing signals, mice ate more food and gained more weight. But it wasn’t clear how these cells actually behaved over a more natural shift from leanness to obesity. |© Society for Science & the Public 2000 - 2019

Keyword: Obesity
Link ID: 26368 - Posted: 06.28.2019

By Bret Stetka The hippocampus is a small curl of brain, which nests beneath each temple. It plays a crucial role in memory formation, taking our experiences and interactions and setting them in the proverbial stone by creating new connections among neurons. A report published on June 27in Science reveals how the hippocampus learns and hard wires certain experiences into memory. The authors show that following a particular behavior, the hippocampus replays that behavior repeatedly until it is internalized. They also report on how the hippocampus tracks our brain’s decision-making centers to remember our past choices. Previous research has shown that the rodent hippocampus replays or revisits past experiences during sleep or periods of rest. While a rat navigates a maze, for example, so-called place cells are activated and help the animal track its position. Following their journey through the maze, those same cells are reactivated in the exact same pattern. What previously happened is mentally replayed again. The authors of the new study were curious whether this phenomenon only applies to previous encounters with a particular location or if perhaps this hippocampal replay also applies to memory more generally, including mental and nonspatial memories. It turns out it does. In the study, 33 participants were presented with a series of images containing both a face and a house. They had to judge the age of either one or the other. If during the second trial, the age of the selected option remained the same, the judged category also did not change in the subsequent trial. If the ages differed, the judged category flipped to the other option in the next round. © 2019 Scientific American

Keyword: Attention; Learning & Memory
Link ID: 26367 - Posted: 06.28.2019

Allison Aubrey At 8 p.m. on a Saturday night, people are starting to pack into a popular bar called Harvard & Stone in a hip Los Angeles neighborhood. The chatter gets louder as the booze begins to flow. In the far corner, about a dozen women in a group are clearly enjoying themselves too, but they are not drinking alcohol. They're sipping handcrafted mocktails, with names like Baby's First Bourbon and Honey Dew Collins, featuring nonalcoholic distilled spirits. They're part of a sober social club, made up mostly of women in their 30s who want to have fun and make friends without alcohol. The members of this club work out, have demanding jobs and simply don't want to feel foggy or hungover anymore. Without alcohol, they say, they just feel better. "Oh my gosh. Well, one thing that was noticeable to pretty much everybody was my overall health and, like, my skin, my eyes. ... I lost weight," says Stephanie Forte, who works in sales in the beauty industry. Another social club member, Kathy Kuzniar, says she used to obsess over whether there was enough wine in the house. She says she feels calmer since she became sober, and she has lost 30 pounds. Not too long ago, a group of women in a bar who were not drinking alcohol would have seemed kind of strange. According to the National Institute on Alcohol Abuse and Alcoholism, 86 percent of adults over 18 report having had an alcoholic drink or drinks at some point in their lifetime, and 56 percent say they've had alcohol in the past month. Still, abstaining from alcohol — on a short-term basis or longer term — is becoming more common. © 2019 npr

Keyword: Drug Abuse
Link ID: 26366 - Posted: 06.28.2019

By Richard Klasco, M.D. Q. Please explain positional vertigo. Two of my siblings have woken up in the morning with it. What do you do if you experience it? A. Positional vertigo is a common type of dizziness that can be treated with a simple maneuver. Vertigo is an illusory sensation of motion that is often accompanied by intense nausea. Benign paroxysmal positional vertigo, or B.P.P.V., is the medical term for positional vertigo. It is important to use this term, as there are other types of vertigo with different causes and treatments. B.P.P.V. is caused by microscopic “stones” that are present on the ends of hair follicles in the ear canal and that help you maintain your balance. Vertigo occurs when these stones break off and move from the body of the inner ear into its semicircular canals, which determine our perception of three-dimensional space. This usually occurs as a result of aging or head trauma. Free-floating stones cause the inner ear to give faulty information to the brain about our position in space, creating a false sensation of motion. The mechanism of B.P.P.V. was discovered almost a century ago by the Viennese physician Dr. Robert Bárány, who won a Nobel Prize for his work. In 1979, Dr. John Epley, an ear, nose and throat specialist in Portland, Ore., found that a simple maneuver could treat most cases of B.P.P.V. without the need for drugs or surgery. The Epley maneuver is a series of rapid changes in position of the head that are performed in a doctor’s office. The maneuver repositions stones so they do not cause symptoms. Incidentally, B.P.P.V. has been reported to be cured in some people after they have ridden on roller coasters. © 2019 The New York Times Company

Keyword: Miscellaneous
Link ID: 26365 - Posted: 06.28.2019

/ By Dan Falk Suppose I give you the name of a body part, and ask you to list its main uses: I say legs, you say walking and running; I say ears, you say hearing. And if I say the brain? Well, that’s a no-brainer (so to speak); obviously the brain is for thinking. Of course, it does a bunch of other things, too; after all, when the brain ceases to function, we die — but clearly it’s where cognition happens. Tversky argues that gesturing is more than just a by-product of speech: it literally helps us think. Or is it? No one would argue that the brain isn’t vital for thinking — but quite a few 21st-century psychologists and cognitive scientists believe that the body, as well as the brain, is needed for thinking to actually happen. And it’s not just that the brain needs a body to keep it alive (that much is obvious), but rather, that the brain and the body somehow work together: it’s the combination of brain-plus-body that creates the mental world. The latest version of this proposition comes from Barbara Tversky, a professor emerita of psychology at Stanford University who also teaches at Columbia. Her new book, “Mind in Motion: How Action Shapes Thought,” is an extended argument for the interplay of mind and body in enabling cognition. She draws on many different lines of evidence, including the way we talk about movement and space, the way we use maps, the way we talk about and use numbers, and the way we gesture. Copyright 2019 Undark

Keyword: Language; Attention
Link ID: 26364 - Posted: 06.28.2019

By Benedict Carey Doctors have known for years that some patients who become unresponsive after a severe brain injury nonetheless retain a “covert consciousness,” a degree of cognitive function that is important to recovery but is not detectable by standard bedside exams. As a result, a profound uncertainty often haunts the wrenching decisions that families must make when an unresponsive loved one needs life support, an uncertainty that also amplifies national debates over how to determine when a patient in this condition can be declared beyond help. Now, scientists report the first large-scale demonstration of an approach that can identify this hidden brain function right after injury, using specialized computer analysis of routine EEG recordings from the skull. The new study, published Wednesday in the New England Journal of Medicine, found that 15 percent of otherwise unresponsive patients in one intensive care unit had covert brain activity in the days after injury. Moreover, these patients were nearly four times more likely to achieve partial independence over the next year with rehabilitation, compared to patients with no activity. The EEG approach will not be widely available for some time, due in part to the technical expertise required, which most I.C.U.’s don’t yet have. And doctors said the test would not likely resolve the kind of high-profile cases that have taken on religious and political dimensions, like that of Terri Schiavo, the Florida woman whose condition touched off an ethical debate in the mid-2000s, or Karen Ann Quinlan, a New Jersey woman whose case stirred similar sentiments in the 1970s. Those debates centered less on recovery than on the definition of life and the right to die; the new analysis presumes some resting level of EEG, and that signal in both women was virtually flat. © 2019 The New York Times Company

Keyword: Consciousness; Brain imaging
Link ID: 26363 - Posted: 06.27.2019