By David Grimm It started in May with a web post by People for the Ethical Treatment of Animals (PETA). “Tell Yale University to Stop Tormenting Birds!” the headline read, followed by text accusing postdoc Christine Lattin of wasteful experiments and animal abuse in her research on stress in wild house sparrows. Then the emails from PETA supporters began flooding Lattin’s inbox: “You should kill yourself, you sick bitch!” Then the messages on Facebook and Twitter: “What you’re doing is so sick and evil.” “I hope someone throws you into the fire …” By the end of August, PETA—based in Norfolk, Virginia—had organized three protests against Lattin, and she says she was getting 40 to 50 messages a day. “Every time I went to check my email or Twitter, my heart started racing. I worried there might be another message. I worried about the safety of my family.” In some ways, Lattin’s story is nothing new. PETA and other animal rights groups have hounded researchers for decades in hopes of shutting down animal experiments in the United States and elsewhere. But Lattin is an unusual target. She’s a self-professed animal lover with a background in bird rescue; her studies are far less invasive than the research PETA has traditionally gone after; and she’s only a postdoc, much younger and less established than any scientist the group has singled out before. That has prompted critics to accuse PETA of trying to destroy Lattin’s career. “She’s at the most vulnerable point in the academic spectrum,” says Kevin Folta, a molecular biologist at the University of Florida in Gainesville. (Folta was targeted by activists opposed to genetically engineered crops after reports that he did not disclose funding from agriculture giant Monsanto; Folta say he did nothing wrong.) PETA’s campaign, he says, “is a warning shot for anyone even thinking about doing animal research.” © 2017 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 24052 - Posted: 09.09.2017

Nicola Davis A pioneering approach to tackling a host of diseases using an electrical implant could eventually reduce or even end pill-taking for some patients, researchers have claimed. The technology relies on electrical stimulation of the vagus nerve – a bundle of nerve fibres that runs from the brain to the abdomen, branching off to organs including the heart, spleen, lungs and gut, and which relays signals from the body’s organs to the brain and vice versa. The pacemaker-like device is typically implanted below the left collarbone with wires running to the vagus nerve in the neck and is already used to tackle treatment-resistant epilepsy and depression. But a growing body of researchers say that such “hacking” of the body’s neural circuits could alleviate the symptoms of diseases including rheumatoid arthritis and Crohn’s disease by tapping into a recently discovered link between the brain and the immune system. That, they say, could bring hope for those with currently untreatable conditions while raising the possibility for others of dramatically reducing medication, or even cutting it out altogether. “In your lifetime and mine we are going to see millions of people with devices so they don’t have to take drugs,” said Kevin Tracey, president of the Feinstein Institute for Medical Research and co-founder of bioelectronics company, SetPoint Medical.

Keyword: Stress; Depression
Link ID: 24051 - Posted: 09.09.2017

By NICHOLAS BAKALAR High carbohydrate intake is associated with a higher risk of mortality, and high fat intake with a lower risk, researchers report. An international team of scientists studied diet and mortality in 135,335 people between 35 and 70 years old in 18 countries, following them for an average of more than seven years. Diet information depended on self-reports, and the scientists controlled for factors including age, sex, smoking, physical activity and body mass index. The study is in The Lancet. Compared with people who ate the lowest 20 percent of carbohydrates, those who ate the highest 20 percent had a 28 percent increased risk of death. But high carbohydrate intake was not associated with cardiovascular death. People with the highest 20 percent in total fat intake — an average of 35.3 percent of calories from fat — had about a 23 percent reduced risk of death compared with the lowest 20 percent (an average of 10.6 percent of calories from fat). Consuming higher saturated fat, polyunsaturated fat and monounsaturated fat were all associated with lower mortality. Higher fat diets were also associated with a lower risk of stroke. “Guidelines recommend low saturated fat, and some recommend really low amounts,” said a co-author, Andrew Mente, an epidemiologist at McMaster University in Ontario. “Our study, which captures intake at the lowest levels, shows that this may be harmful.” Current federal guidelines recommend a diet that provides no more than 35 percent of calories from fat. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 24050 - Posted: 09.09.2017

Laura Sanders The brain chemical missing in Parkinson’s disease may have a hand in its own death. Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic chain reaction that ultimately kills the nerve cells that make it, a new study suggests. By studying lab dishes of human nerve cells, or neurons, derived from Parkinson’s patients, researchers found that a harmful form of dopamine can inflict damage on cells in multiple ways. The result, published online September 7 in Science, “brings multiple pieces of the puzzle together,” says neuroscientist Teresa Hastings of the University of Pittsburgh School of Medicine. The finding also hints at a potential treatment for the estimated 10 million people worldwide with Parkinson’s: Less cellular damage occurred when some of the neurons were treated early on with antioxidants, molecules that can scoop up harmful chemicals inside cells. Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy people and people with one of two types of Parkinson’s disease, inherited or spontaneously arising. The researchers then coaxed these skin cells into becoming dopamine-producing neurons. These cells were similar to those found in the substantia nigra, the movement-related region of the brain that degenerates in Parkinson’s. |© Society for Science & the Public 2000 - 2017.

Keyword: Parkinsons
Link ID: 24049 - Posted: 09.08.2017

Bruno Martin “I heard a thud behind me,” says zoologist Stefan Greif, recalling the first time he noticed a bat crash into a metal plate propped up against a wall in his lab’s flight chamber. Now, in a study published on 7 September in Science1, a team led by Greif — of the Max Planck Institute for Ornithology in Seewiesen, Germany — explains why bats often slam into vertical panes, such as glass windows.These smooth surfaces interfere with bats’ echolocation by reflecting sound away from the creatures. Bats rely on echolocation to navigate in the dark. They locate and identify objects by sending out shrill calls and listening to the echoes that bounce back. Greif and his colleagues tested the echolocation of 21 wild-caught greater mouse-eared bats (Myotis myotis) in the lab. The researchers placed a featureless metal plate on a side wall at the end of a flight tunnel. The bats interpreted the smooth surface — but not the adjacent, felt-covered walls — as a clear flight path. Over an an average of around 20 trials for each bat, 19 of them crashed into the panel at least once. The researchers also put up smooth, vertical plates near wild bat colonies, and saw similar results. The animals became confused owing to a property of smooth surfaces called ‘acoustic mirroring’. Whereas rough objects bounce some echoes back towards the bat, says Greif, a smooth surface reflects all echolocation calls away from the source. This makes a smooth wall appear as empty space to the bats, until they are directly in front of it. Only once a bat is facing the surface are their perpendicular echoes reflected back, which alerts the bat to its mistake. This explains why some bats attempted to swerve out of harm’s way at the last second — but often too late. © 2017 Macmillan Publishers Limited

Keyword: Hearing
Link ID: 24048 - Posted: 09.08.2017

Claudia Dreifus Dr. Gregory Berns, 53, a neuroscientist at Emory University in Atlanta, spends his days scanning the brains of dogs, trying to figure out what they’re thinking. The research is detailed in a new book, “What It’s Like to Be a Dog.” Among the findings: Your dog may really love you for you — not for your food. We spoke during his recent visit to New York City and later by telephone. The conversation below has been edited and condensed for space and clarity. How did your canine studies begin? It really started with the mission that killed bin Laden. There had been this dog, Cairo, who’d leapt out of the helicopter with the Navy SEALs. Watching the news coverage gave me an idea. Helicopters are incredibly noisy. Dogs have extremely sensitive hearing. I thought, “Gee, if the military can train dogs to get into noisy helicopters, it might be possible to get them into noisy M.R.I.s.” Why? To find out what dogs think and feel. A year earlier, my favorite dog, a pug named Newton, had died. I thought about him a lot. I wondered if he’d loved me, or if our relationship had been more about the food I’d provided. As a neuroscientist, I’d seen how M.R.I. studies helped us understand which parts of the human brain were involved in emotional processes. Perhaps M.R.I. testing could teach us similar things about dogs. I wondered if dogs had analogous functions in their brains to what we humans have. The big impediment doing this type of testing was to find some way to get dogs into an M.R.I. and get them to hold still for long enough to obtain useful images. © 2017 The New York Times Company

Keyword: Brain imaging; Emotions
Link ID: 24047 - Posted: 09.08.2017

Devin Coldewey We count on machine learning systems for everything from creating playlists to driving cars, but like any tool, they can be bent towards dangerous and unethical purposes as well. Today's illustration of this fact is a new paper from Stanford researchers, who have created a machine learning system that they claim can tell from a few pictures whether a person is gay or straight. The research is as surprising as it is disconcerting. In addition to exposing an already vulnerable population to a new form of systematized abuse, it strikes directly at the egalitarian notion that we can't (and shouldn't) judge a person by their appearance, nor guess at something as private as sexual orientation from something as simple as a snapshot or two. But the accuracy of the system reported in the paper seems to leave no room for mistake: this is not only possible, it has been achieved. It relies on cues apparently more subtle than most can perceive — cues many would suggest do not exist. And it demonstrates, as it is intended to, a class of threat to privacy that is entirely unique to the imminent era of ubiquitous computer vision. Before discussing the system itself, it should be made clear that this research was by all indications done with good intentions. In an extensive set of authors' notes that anyone commenting on the topic ought to read, Michal Kosinski and Yilun Wang address a variety of objections and questions. Most relevant are perhaps their remarks as to why the paper was released at all: We were really disturbed by these results and spent much time considering whether they should be made public at all. We did not want to enable the very risks that we are warning against. The ability to control when and to whom to reveal one’s sexual orientation is crucial not only for one’s well-being, but also for one’s safety.

Keyword: Sexual Behavior
Link ID: 24046 - Posted: 09.08.2017

James Gorman African wild dogs sneeze. And that’s a first. No other social animal has been reported to cast a vote, of sorts, by sneezing, although in humans sneezing may once have expressed a negative opinion, as in, “nothing to sneeze at.” Wild dog sneezing is different. For one thing it seems to indicate a positive reaction to a proposal before a group of dogs. When a pack of these dogs is getting ready to hunt, scientists reported Tuesday, the more sneezes, the more likely they are to actually get moving. Just about all social organisms make group decisions that require reaching a consensus. If monkeys or meerkats are looking for a better place to forage, they need to reach a consensus about moving on among a minimum number of animals — called a quorum, just like in Congress. Even some bacteria do this before releasing toxins or lighting up with bioluminescence. Bacteria use chemical signals but larger animals often use sounds as a way of saying, I’m in. However, among grunts, huffs, piping signals and others, the sneeze had not been reported as one of those signals until a group of American, British and Australian researchers published their observations of African dogs in the Proceedings of the Royal Society B. They were studying the dogs where they live in Botswana to see how they decide to go on a hunt. Like most carnivores, the wild dogs sleep a lot. But at some point one of the pack will start what is called a rally, getting all the other members excited and milling around as if they want to play. Sometimes the rallies are successful, and off the pack goes. Sometimes the pack members lie down and go back to sleep. Neil R. Jordan of the University of New South Wales in Sydney, the senior author of the report, noticed that the successful rallies there seemed to have more sneezing. © 2017 The New York Times Company

Keyword: Aggression
Link ID: 24045 - Posted: 09.07.2017

By Andy Coghlan A type of therapy originally designed for insomnia has been found to also help a range of mental health issues, including negative thoughts, anxiety, depression and psychosis. Daniel Freeman, at the University of Oxford, and his colleagues have been testing Sleepio, a type of cognitive behavioural therapy available online. The ten-week course is intended to restore healthy sleep patterns in people with insomnia, and Freeman wanted to see if it could also relieve other problems. Learn more about the science of sleep: In our expert talk at New Scientist Live in London His team asked nearly 1900 students who have difficulty sleeping to try using Sleepio, and nearly 1870 others to try following standard advice for insomnia. Both groups filled in questionnaires beforehand that assessed their sleep patterns, as well as tendencies to experience paranoia and hallucinations. They repeated these questionnaires at three, ten and 22 weeks into the experiment. Overall, those using Sleepio slept 50 per cent better than the control group, says Freeman. Compared to this group, the Sleepio users also had a 30 per cent reduction in hallucinations, 25 per cent reduction in paranoia, and their anxiety and depression levels were 20 per cent lower. © Copyright New Scientist Ltd.

Keyword: Sleep; Depression
Link ID: 24044 - Posted: 09.07.2017

By Bob Grant Eating a diet high in fat and low in carbohydrates keeps mice living longer, healthier lives, according to two separate studies published in Cell Metabolism today (September 5). One of the studies, conducted by researchers at the University of California, San Francisco, and the Buck Institute for Research on Aging in California, cycled mice on and off a ketogenic diet, which forces the body to produce fatty acids called ketone bodies to fuel metabolism through the severe limiting of carbohydrates. Those mice, which were given non-ketogenic diets one week and ketogenic diets the next, avoided obesity and memory decline and displayed reductions in midlife mortality, compared to mice on a control diet. The other study, performed by scientists at the Buck Institute in collaboration with researchers at the University of California, Davis, kept mice on a ketogenic diet for 14 months and showed similar results, with the addition of improvements in motor function, grip strength, and other indicators of muscle mass. “The fact that we had such an effect on memory and preservation of brain function is really exciting,” Eric Verdin, CEO of the Buck Institute and coauthor of the study that alternated ketogenic and non-ketogenic diets, says in a statement. “The older mice on the ketogenic diet had a better memory than the younger mice. That’s really remarkable.” © 1986-2017 The Scientist

Keyword: Obesity
Link ID: 24043 - Posted: 09.07.2017

A test that involves drawing a spiral on a sheet of paper could be used to diagnose early Parkinson's disease. Australian researchers have trialled software that measures writing speed and pen pressure on the page. Both are useful for detecting the disease, which causes shaking and muscle rigidity. The Melbourne team said the test could be used by GPs to screen their patients after middle age and to monitor the effect of treatments. The study, published in Frontiers of Neurology, involved 55 people - 27 had Parkinson's and 28 did not. Speed of writing and pen pressure while sketching are lower among Parkinson's patients, particularly those with a severe form of the disease. Image copyright RMIT University Image caption Treatment options are effective only when the disease is diagnosed early In the trial, a tablet computer with special software took measurements during the drawing test and was able to distinguish those with the disease, and how severe it was. Poonam Zham, study researcher from RMIT University, said: "Our aim was to develop an affordable and automated electronic system for early-stage diagnosis of Parkinson's disease, which could be easily used by a community doctor or nursing staff." The system combines pen speed and pressure into one measurement, which can be used to tell how severe the disease is. David Dexter, deputy research director at Parkinson's UK, said current tests for the disease were not able to accurately measure how advanced someone's condition was. "This can impact on the ability to select the right people for clinical research, which is essential to develop new and better treatments for Parkinson's. "This new test could provide a more accurate assessment by measuring a wider range of features that may be affected by Parkinson's, such as co-ordination, pressure, speed and cognitive function." He added that the test could be a "stepping stone" to better clinical trials for Parkinson's. © 2017 BBC.

Keyword: Parkinsons
Link ID: 24042 - Posted: 09.07.2017

Laura Sanders Peer inside the brain of someone learning. You might be lucky enough to spy a synapse pop into existence. That physical bridge between two nerve cells seals new knowledge into the brain. As new information arrives, synapses form and strengthen, while others weaken, making way for new connections. You might see more subtle changes, too, like fluctuations in the levels of signaling molecules, or even slight boosts in nerve cell activity. Over the last few decades, scientists have zoomed in on these microscopic changes that happen as the brain learns. And while that detailed scrutiny has revealed a lot about the synapses that wire our brains, it isn’t enough. Neuroscientists still lack a complete picture of how the brain learns. They may have been looking too closely. When it comes to the neuroscience of learning, zeroing in on synapse action misses the forest for the trees. A new, zoomed-out approach attempts to make sense of the large-scale changes that enable learning. By studying the shifting interactions between many different brain regions over time, scientists are beginning to grasp how the brain takes in new information and holds onto it. These kinds of studies rely on powerful math. Brain scientists are co-opting approaches developed in other network-based sciences, borrowing tools that reveal in precise, numerical terms the shape and function of the neural pathways that shift as human brains learn. © Society for Science & the Public 2000 - 2017.

Keyword: Learning & Memory
Link ID: 24041 - Posted: 09.06.2017

Ian Sample Science editor A drug that mimics a zero-carbohydrate diet could help people live longer, healthier lives and have better memories in old age, US researchers claim. Scientists hope to develop a medication after two independent studies showed that mice fed on a diet stripped of all carbohydrate lived longer and performed better on a range of physical and mental tasks than those that had regular meals. Because the diet is hard to stick to, the researchers are working on a compound that aims to deliver the same benefits for humans. If they are successful, it would amount to an extra seven to ten years of life on average, and protection against the weakening muscles and faltering memories that are defining aspects of human ageing. “I’m excited about this, and it’s hard not to be after what we’ve seen that it does. These are pretty profound effects,” said Eric Verdin, a physician who led one of the studies at the Buck Institute for Research on Aging in California. The zero carb diet was designed to induce a dramatic change in metabolism, by fooling the mice into thinking they were fasting. When deprived of carbohydrate, the body shifts from using glucose as its main energy source to burning fat and producing chemicals in the liver known as ketone bodies. In 2013, Verdin showed that a ketone body called BHB served as fuel in the body and might also protect animals against the microscopic damage that builds up in cells as part of the natural ageing process. © 2017 Guardian News and Media Limited

Keyword: Obesity
Link ID: 24040 - Posted: 09.06.2017

Laurel Hamers Zika’s damaging neurological effects might someday be enlisted for good — to treat brain cancer. In human cells and in mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alone. Jeremy Rich, a regenerative medicine scientist at the University of California, San Diego, and colleagues report the findings online September 5 in the Journal of Experimental Medicine. Previous studies had shown that Zika kills stem cells that generate nerve cells in developing brains (SN: 4/2/16, p. 26). Because of similarities between those neural precursor cells and stem cells that turn into glioblastomas, Rich’s team suspected the virus might also target the cells that cause the notoriously deadly type of cancer. In the United States, about 12,000 people are expected to be diagnosed with glioblastoma in 2017. (It’s the type of cancer U.S. Senator John McCain was found to have in July.) Even with treatment, most patients live only about a year after diagnosis, and tumors frequently recur. In cultures of human cells, Zika infected glioblastoma stem cells and halted their growth, Rich and colleagues report. The virus also infected full-blown glioblastoma cells but at a lower rate, and didn’t infect normal brain tissues. Zika-infected mice with glioblastoma either saw their tumors shrink or their tumor growth slow compared with uninfected mice. The virus-infected mice lived longer, too. In one trial, almost half of the mice survived more than six weeks after being infected with Zika, while all of the uninfected mice died within two weeks of receiving a placebo. |© Society for Science & the Public 2000 - 2017. A

Keyword: Glia
Link ID: 24039 - Posted: 09.06.2017

By Michael Le Page We are still evolving – very slowly. In the 20th century, people in the UK evolved to be less likely to smoke heavily, but the effect was tiny. So claims a study of 200,000 genomes. A population can be described as evolving when the frequency of gene variants changes over time. Because most people in rich countries now live well beyond reproductive age, some argue that we have stopped evolving because natural selection has been weakened. But several recent studies claim we are still evolving, albeit slowly. Now Joseph Pickrell at Columbia University in New York and his team have analysed human genome sequences to spot gene variants that are becoming rarer. One variant, of a gene called CHRNA3, is associated with heavier smoking in those that smoke, raising their risk of a smoking-related death. Comparing people over the age of 80 with people over the age of 60, Pickrell estimates that the variant has declined by 1 per cent between generations. However, his team was not able to prove this, as they did not have any genomic data from people under the age of 40. A variant of the ApoE4 gene that is known to increase the risk of late-onset Alzheimer’s disease, as well as cardiovascular disease, may also be getting rarer. © Copyright New Scientist Ltd.

Keyword: Alzheimers; Genes & Behavior
Link ID: 24038 - Posted: 09.06.2017

By NATALIE ANGIER A normal human baby, according to psychologists, will cry about two hours over the course of a day. A notorious human crybaby, according to her older siblings, parents and the building superintendent, will cry for two hours every two hours, refusing to acknowledge any distinction between crying and other basic infant activities, like “being awake” or “breathing.” Current and former whine enthusiasts, take heart. It turns out that infant crying is not only as natural and justifiable as breathing: The two acts are physically, neurologically, primally intertwined. Scientists have discovered that the small cluster of brain cells in charge of fast, active respiration also grant a baby animal the power to cry. Reporting in the Proceedings of the National Academy of Sciences, Carmen Birchmeier and Luis Hernandez-Miranda, of the Max Delbruck Center for Molecular Medicine in Berlin, and their colleagues showed that infant mice stripped of this key node — a mere 17,000 neurons, located in the evolutionarily ancient hindbrain — can breathe slowly and passively, but not vigorously or animatedly. When they open their mouths to cry, nothing comes out. As a result, their mothers ignore them, and the poorly breathing pups quickly die. “This was an astonishing finding,” Dr. Birchmeier said. “The mother could see the pups and smell the pups, but if they didn’t vocalize, it was as though they didn’t exist.” The new study is just one in a series of recent reports that reveal the centrality of crying to infant survival, and how a baby’s bawl punches through a cluttered acoustic landscape to demand immediate adult attention. The sound of an infant’s cry arouses a far quicker and stronger response in action-oriented parts of the adult brain than do similarly loud or emotionally laden noises, like a dog barking or a neighbor weeping. © 2017 The New York Times Company

Keyword: Sexual Behavior; Animal Communication
Link ID: 24037 - Posted: 09.05.2017

By Susan Noakes, CBC News Researchers studying fish from the Niagara River have found that human antidepressants and remnants of these drugs are building up in their brains. The concentration of human drugs was discovered by scientists from University at Buffalo, Buffalo State and two Thai universities, Ramkhamhaeng University and Khon Kaen University. Active ingredients and metabolized remnants of Zoloft, Celexa, Prozac and Sarafem — drugs that have seen a sharp spike in prescriptions in North America — were found in 10 fish species. Diana Aga, professor of chemistry at University at Buffalo, says these drugs are found in human urine and are not stripped out by wastewater treatment. Could affect fish behaviour "It is a threat to biodiversity, and we should be very concerned," Aga said in a release from the university. Fish in the Niagara River show concentrations of antidepressants in their brains higher than levels in the river itself. (David Duprey/The Associated Press) "These drugs could affect fish behaviour. We didn't look at behaviour in our study, but other research teams have shown that antidepressants can affect the feeding behaviour of fish or their survival instincts. Some fish won't acknowledge the presence of predators as much." The Niagara River, which carries water from Lake Erie to Lake Ontario, is already under stress, with reports this summer of untreated wastewater released into the river. The research, published in the journal Environmental Science & Technology, found levels of antidepressants in fish brains that were several times higher than levels in the river itself, indicating that the chemicals are accumulating over time. ©2017 CBC/Radio-Canada.

Keyword: Depression
Link ID: 24036 - Posted: 09.05.2017

Lauren Silverman In health care, you could say radiologists have typically had a pretty sweet deal. They make, on average, around $400,000 a year — nearly double what a family doctor makes — and often have less grueling hours. But if you talk with radiologists in training at the University of California, San Francisco, it quickly becomes clear that the once-certain golden path is no longer so secure. "The biggest concern is that we could be replaced by machines," says Phelps Kelley, a fourth-year radiology fellow. He's sitting inside a dimly lit reading room, looking at digital images from the CT scan of a patient's chest, trying to figure out why he's short of breath. Because MRI and CT scans are now routine procedures and all the data can be stored digitally, the number of images radiologists have to assess has risen dramatically. These days, a radiologist at UCSF will go through anywhere from 20 to 100 scans a day, and each scan can have thousands of images to review. "Radiology has become commoditized over the years," Kelley says. "People don't want interaction with a radiologist, they just want a piece of paper that says what the CT shows." 'Computers are awfully good at seeing patterns' That basic analysis is something he predicts computers will be able to do. Dr. Bob Wachter, an internist at UCSF and author of The Digital Doctor, says radiology is particularly amenable to takeover by artificial intelligence like machine learning. "Radiology, at its core, is now a human being, based on learning and his or her own experience, looking at a collection of digital dots and a digital pattern and saying 'That pattern looks like cancer or looks like tuberculosis or looks like pneumonia,' " he says. "Computers are awfully good at seeing patterns." © 2017 npr

Keyword: Brain imaging; Robotics
Link ID: 24035 - Posted: 09.05.2017

By TARA PARKER-POPE It started as a simple conversation about a child’s birthday party. But it quickly escalated into a full-blown marital rift. She accused him of neglecting the family. He said she was yelling. “Whatever,” she said. “Go. Go.” “Go where?” he replied. “I don’t know,” she told him. “I don’t want to talk to you anymore.” The bickering parents were among 43 couples taking part in an Ohio State University study exploring how marital interactions influence a person’s health. Every couple in the study — just like couples in the real world — had experienced some form of routine marital conflict. Hot-button topics included managing money, spending time together as a family or an in-law intruding on the relationship. But while marital spats were universal among the couples, how they handled them was not. Some couples argued constructively and even with kindness, while others — like the couple fighting about the birthday party — were hostile and negative. What made the difference? The hostile couples were most likely to be those who weren’t getting much sleep. “When people have slept less, it’s a little like looking at the world through dark glasses,” said Janice Kiecolt-Glaser, a longtime relationship scientist and director of the Ohio State Institute for Behavioral Medicine Research. “Their moods are poorer. We’re grumpier. Lack of sleep hurts the relationship.” The men and women in the study had been married from three to 27 years. They reported varying amounts of sleep — anywhere from three and a half to nine hours a night. Each couple made two visits to the lab, where the partners were prodded to talk about the issues that caused the most conflict in their relationship. Then the researchers analyzed videos of their exchanges using well-established scoring techniques to assess positive and negative interactions and hostile and constructive responses. After all the data were parsed, a clear pattern emerged. © 2017 The New York Times Company

Keyword: Sleep; Emotions
Link ID: 24034 - Posted: 09.05.2017

Anna VlasitsAnna Vlasits A sheen is starting to appear on Rocky Blumhagen’s forehead, just below his gray hair. He’s marching in place in a starkly lit room decked out with two large flatscreens. On both of the TVs, a volcano lets off steam through wide cracks glowing with lava, their roar muffling the Andean percussion and flutes on the soundtrack. Golden coins slide across the screen. Rocky reaches out his left hand, as if to grasp a coin from midair, and one of them disappears with a brrring. “I don’t know if I can do it,” he says to a guy named Josh sitting nearby in a felt-covered lounge chair. He looks up from his iPad, watching Rocky, age 66, grab, jog, kick, and reach his way through the videogame. “Keep it up,” Josh says as the heart monitor in the corner of the screen reads 129. Rocky and research assistant Josh Volponi are technically in a lab clinic at the University of California, San Francisco, but aside from the mannequin heads studded with electrodes, the room looks more like a man cave. But here, the videogames could halt the mental decay of aging. This is the premise that the university’s new research institute, named Neuroscape, was built to test. This is Rocky’s 18th training session at Neuroscape, founded by neuroscientist Adam Gazzaley. Rocky is fit for his age—he works as a substitute yoga instructor, after retiring from careers producing radio and performing Cole Porter songs—but as he makes it to the end of the level, he looks exhausted. The game cuts to an animation of a jungle, birds chirping and light playing through the canopy as a list of his past scores pops up. This round wasn’t his best. “I haven’t been here for a week,” he says. Volponi asks him to rate his physical exertion level. Rocky gives it a 15 out of 20; Volponi marks it on the iPad. “I feel rusty,” he says, wiping his hands on his orange exercise shorts.

Keyword: Alzheimers; Learning & Memory
Link ID: 24033 - Posted: 09.04.2017