By Knvul Sheikh The tiny, transparent roundworm known as Caenorhabditis elegans is roughly the size of a comma. Its entire body is made up of just about 1,000 cells. A third are brain cells, or neurons, that govern how the worm wriggles and when it searches for food — or abandons a meal to mate. It is one of the simplest organisms with a nervous system. The circuitry of C. elegans has made it a common test subject among scientists wanting to understand how the nervous system works in other animals. Now, a team of researchers has completed a map of all the neurons, as well as all 7,000 or so connections between those neurons, in both sexes of the worm. “It’s a major step toward understanding how neurons interact with each other to give rise to different behaviors,” said Scott Emmons, a developmental biologist at the Albert Einstein College of Medicine in New York who led the research. Structure dictates function in several areas of biology, Dr. Emmons said. The shape of wings provided insight into flight, the helical form of DNA revealed how genes are coded, and the structure of proteins suggested how enzymes bind to targets in the body. It was this concept that led biologist Sydney Brenner to start cataloging the neural wiring of worms in the 1970s. He and his colleagues preserved C. elegans in agar and osmium fixative, sliced up their bodies like salami and photographed their cells with a powerful electron microscope. © 2019 The New York Times Company

Keyword: Brain imaging; Development of the Brain
Link ID: 26389 - Posted: 07.04.2019

By Sabine Galvis Scientists looking for a link between repeated brain trauma and lasting neurological damage typically study the brains of soldiers or football players. But it’s unclear whether this damage—known as chronic traumatic encephalopathy (CTE)—is prevalent in the general population. Now, a new study reports those rates for the first time. To conduct the research, neuropathologist Kevin Bieniek, then at the Mayo Clinic in Rochester, Minnesota, and colleagues sorted through nearly 3000 brains donated to the clinic's tissue registry between 2005 and 2016. Then, by scanning obituaries and old yearbooks, the researchers narrowed the group to 300 athletes who played contact sports and 450 nonathletes. The scientists removed all infants under age 1, brain samples with insufficient tissue, and brain donors without biographical data attached to their samples. Finally, they collected medical records and looked under a microscope at tissue from up to three sections of each brain for signs of CTE. Those signs include lesions and buildup of tau, a protein associated with neurodegenerative disorders such as Alzheimer’s disease. Six percent of the brains showed some or all signs of CTE, Bieniek and his colleagues report in Brain Pathology. Not all the people experienced symptoms associated with CTE, at least according to their medical records. Those symptoms include anxiety, depression, and drug use. However, people with CTE were about 31% more likely to develop dementia and 27% more likely to develop Alzheimer’s disease than those without CTE. © 2019 American Association for the Advancement of Science

Keyword: Brain Injury/Concussion
Link ID: 26388 - Posted: 07.04.2019

Maria Temming A new analysis of brain scans may explain why hyperrealistic androids and animated characters can be creepy. By measuring people’s neural activity as they viewed pictures of humans and robots, researchers identified a region of the brain that seems to underlie the “uncanny valley” effect — the unsettling sensation sometimes caused by robots or animations that look almost, but not quite, human (SN Online: 11/22/13). Better understanding the neural circuitry that causes this feeling may help designers create less unnerving androids. In research described online July 1 in the Journal of Neuroscience, neuroscientist Fabian Grabenhorst and colleagues took functional MRI scans of 21 volunteers during two activities. In each activity, participants viewed pictures of humans, humanoid robots of varying realism and — to simulate the appearance of hyperrealistic robots — “artificial humans,” pictures of people whose features were slightly distorted through plastic surgery and photo editing. In the first activity, participants rated each picture on likability and how humanlike the figures appeared. Next, participants chose between pairs of these pictures, based on which subject they would rather receive a gift from. In line with the uncanny valley effect, participants generally rated more humanlike candidates as more likable, but this trend broke down for artificial humans — the most humanlike of the nonhuman options. A similar uncanny valley trend emerged in participants’ judgments about which figures were more trustworthy gift-givers. |© Society for Science & the Public 2000 - 2019.

Keyword: Attention; Emotions
Link ID: 26387 - Posted: 07.04.2019

Two nationally renowned neurosurgeons at Washington University School of Medicine in St. Louis will present “BrainWorks,” a live theatrical performance that explores the wonders of the human brain by dramatizing real-life neurological cases. The performance, comprised of four one-act plays, will debut July 19-21 at the Loretto-Hilton Center for the Performing Arts at Webster University. Albert Kim, PhD, MD, associate professor of neurological surgery, and Eric C. Leuthardt, MD, professor of neurological surgery, will guide the audience through each scene as they explain the mysteries of the human brain and the neuroscience of diseases such as Alzheimer’s disease, epilepsy, brain tumors and stroke. Kim and Leuthardt teamed up with playwrights from the New Dramatists to write each one-act play; the scenarios are based on patients the doctors have treated. “We have involved conversations about what’s going to happen – the course of treatment, the risks and benefits,” Kim said. “We also ensure the families become involved in those conversations. Together, the patient and family members become a part of the process that transforms and heals them. It’s this kind of conversation we want to bring to others through ‘BrainWorks.’” ©2019 Washington University in St. Louis

Keyword: Alzheimers; Epilepsy
Link ID: 26386 - Posted: 07.04.2019

Laura Sanders Immune cells can storm into the brains of older mice, where these normally helpful cells seem to be up to no good. The result, described July 3 in Nature, raises the possibility that immune cells may have a role in aging. Anne Brunet of Stanford University School of Medicine and colleagues studied gene activity to identify all sorts of cells in a particular spot in mice brains — the subventricular zone, where new nerve cells are born. Compared with young mice, old mice had many more killer T cells in that area. These immune system fighters take out damaged or infected cells in the rest of the body, but aren’t usually expected to show up in the brain. Experiments on postmortem human brain tissue suggest that a similar thing happens in old people. T cells were more abundant in tissue from people ages 79 to 93 than in tissue from people ages 20 to 44, the researchers found. In the brains of mice, killer T cells churn out a compound called interferon-gamma. This molecule might be responsible for the falling birthrate of new nerve cells that comes with old age, experiments on mice’s stem cells in dishes suggest. The results come amid a debate over whether human brains continue to make new nerve cells as adults (SN Online: 3/8/2018). If so, then therapies that shut T cells out of the brain might help keep nerve cell production rates high, even into old age — a renewal that might stave off some of the mental decline that comes with aging. |© Society for Science & the Public 2000 - 2019

Keyword: Alzheimers; Neuroimmunology
Link ID: 26385 - Posted: 07.04.2019

By Nicholas Bakalar Hormone therapy for prostate cancer is associated with an increased risk for dementia, a new study has found. Androgen deprivation therapy, or A.D.T., is used to treat prostate cancer of varying degrees of severity. It can significantly reduce the risk for cancer progression and death. The study, in JAMA Network Open, included 154,089 men whose average age was 74 and who had diagnoses of prostate cancer. Of these, 62,330 received A.D.T. and the rest did not. In an average follow-up of eight years, the scientists found that compared with men who had no hormone therapy, one to four doses of A.D.T. was associated with a 19 percent increased risk for both Alzheimer’s disease and other forms of dementia, and the risk increased with the number of doses. At five to eight doses the increased risk was 28 percent for Alzheimer’s and 24 percent for other dementias. The lead author, Ravishankar Jayadevappa, an associate professor at the University of Pennsylvania Perelman School of Medicine, said that for advanced cancer, A.D.T. can be a lifesaving treatment and should not be avoided because of any increased risk for dementia. But, he said, “Patients with localized cancer should be looking at the risks of dementia, and possibly avoiding A.D.T.” © 2019 The New York Times Company

Keyword: Alzheimers; Hormones & Behavior
Link ID: 26384 - Posted: 07.04.2019

By Ryan Dalton In the dystopian world of George Orwell’s Nineteen Eighty-Four, the government of Oceania aims to achieve thought control through the restriction of language. As explained by the character ‘Syme’, a lexicologist who is working to replace the English language with the greatly-simplified ‘Newspeak’: “Don’t you see that the whole aim of Newspeak is to narrow the range of thought?” While Syme’s own reflections were short-lived, the merits of his argument were not: the words and structure of a language can influence the thoughts and decisions of its speakers. This holds for English and Greek, Inuktitut and Newspeak. It also may hold for the ‘neural code’, the basic electrical vocabulary of the neurons in the brain. Neural codes, like spoken languages, are tasked with conveying all manner of information. Some of this information is immediately required for survival; other information has a less acute use. To accommodate these different needs, a balance is struck between the richness of information being transferred and the speed or reliability with which it is transferred. Where the balance is set depends on context. In the example of language, the mention of the movie Jaws at a dinner party might result in a ranging and patient—if disconcerting—discussion around the emotional impact of the film. In contrast, the observation of a dorsal fin breaking through the surf at the beach would probably elicit a single word, screamed by many beachgoers at once: “shark!” In one context, the language used has been optimized for richness; in the other, for speed and reliability. © 2019 Scientific American

Keyword: Language
Link ID: 26383 - Posted: 07.03.2019

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