By Kim Tingley In the United States and other Western countries, diet and nutrition researchers face an urgent imperative: Figure out how to solve the crisis of obesity. About 40 percent of the adults and 19 percent of the children and adolescents in the United States have obesity, according to the Centers for Disease Control and Prevention. More and more of them face the increased risks of suffering from diabetes, cardiovascular disease and countless other negative health effects. This situation looks like a single problem from a population standpoint — one that simple guidelines for balancing calorie consumption and expenditure should be able to solve. Instead, a seeming infinitude of variables influence what each of us eats and how the body responds. That is: Obesity, like cancer, “is not one disease,” says Elizabeth Mayer-Davis, a professor of nutrition and medicine at the University of North Carolina at Chapel Hill. In order to treat it, “you really have to be thinking about biology and behavior and society and culture and policy all at the same time. Because if you miss any one of those pieces, your intervention or your diet — it’s less likely to actually work.” The same diet can affect even identical twins differently. “It’s also why there have been so many conflicting studies in nutrition,” Mayer-Davis says. “The public is very frustrated.” Indeed, just last month a paper in Annals of Internal Medicine created controversy when it argued that there’s not enough evidence to say whether red and processed meats are bad for us, despite years of guidance claiming just that. It also reignited a growing debate: How valuable can universal diet guidelines be for individuals? In recent decades, popular weight-loss plans have largely seesawed between low-fat strategies, which U.S. health agencies have also promoted, and low-carbohydrate ones. Many of them appear to work especially well for some people and not well for others; on average, however, in studies comparing the two kinds of regimens, participants lose the same moderate amount of weight. In those cases when opposing diets produce equivalent results, Kevin Hall, a researcher at the National Institutes of Health, wondered if there was, in fact, an explanation other than the nutrients. He noticed that many of those diets tended to have at least one rule in common: Avoid ultraprocessed food, the sort of packaged fare containing artificial flavorings and ingredients you wouldn’t find in your kitchen that make processed food cheap, convenient, tasty and shelf-stable — and popular. It currently accounts for 57 percent of the American diet (a proportion that is rising). Previous studies have found correlations between ultraprocessed-food consumption and obesity but no proof that it’s a cause. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26749 - Posted: 10.25.2019

By Gina Kolata Thousands of people have received brain scans, as well as cognitive and genetic tests, while participating in research studies. Though the data may be widely distributed among scientists, most participants assume their privacy is protected because researchers remove their names and other identifying information from their records. But could a curious family member identify one of them just from a brain scan? Could a company mining medical records to sell targeted ads do so, or someone who wants to embarrass a study participant? The answer is yes, investigators at the Mayo Clinic reported on Wednesday. A magnetic resonance imaging scan includes the entire head, including the subject’s face. And while the countenance is blurry, imaging technology has advanced to the point that the face can be reconstructed from the scan. Under some circumstances, that face can be matched to an individual with facial recognition software. In a letter published in the New England Journal of Medicine, researchers at the Mayo Clinic showed that the required steps are not complex. But privacy experts questioned whether the process could be replicated on a much larger scale with today’s technology. The subjects were 84 healthy participants in a long-term study of about 2,000 residents of Olmsted County, Minn. Participants get brain scans to look for signs of Alzheimer’s disease, as well as cognitive, blood and genetic tests. © 2019 The New York Times Company

Keyword: Brain imaging
Link ID: 26748 - Posted: 10.24.2019

By Elizabeth Pennisi The more researchers look, the more connections they find between the microbes in our intestines and those in our brain. Gut bacteria appear to influence everything from depression to autism. Now, a study on how mice overcome fear is starting to reveal more about the mysterious link between gut and mind. “This work is amazing,” says Peng Zheng, a neuroscientist at Chongqing Medical University in China who was not involved with the research. The study, he says, could provide new insight into several mental disorders. The research used a classic Pavlovian test: Shock a mouse on the foot while playing a tone and the rodent will quickly learn to associate the noise with pain, flinching whenever it hears the sound. But the association doesn’t last forever. After several sessions of hearing the tone but not getting the shock, the mouse will forget the association, and the sound will have no effect. This “forgetting” is important for people as well; it’s impaired, for example, in those with chronic anxiety and post-traumatic stress disorder. David Artis, an immunologist and microbiologist at Weill Cornell Medicine in New York City, wondered whether gut bacteria played any role in the learning and forgetting responses. He and colleagues treated mice with antibiotics to totally rid them of the bacteria in their gut, collectively known as the microbiome. They then played a tone and right after gave the mouse a mild shock, doing this multiple times. © 2019 American Association for the Advancement of Science.

Keyword: Obesity
Link ID: 26747 - Posted: 10.24.2019

People with long-term health problems such as arthritis are more likely to feel pain on humid days, a study has suggested. Folklore suggests the cold makes pain worse - but there is actually little research into the weather's effects. And this University of Manchester study of 2,500 people, which collected data via smartphones, found symptoms were actually worse on warmer, damper days. Researchers hope the findings will steer future research into why that is. Hearing someone say their knee is playing up because of the weather is pretty common - usually because of the cold, Some say they can even predict the weather based on how their joints feel. But carrying out scientific research into how different types of weather affect pain has been difficult. Previous studies have been small, or short-term. In this research, called Cloudy with a Chance of Pain, scientists recruited 2,500 people with arthritis, fibromyalgia, migraine and neuropathic pain from across the UK. They recorded pain symptoms each day, for between one and 15 months, while their phones recorded the weather where they were. Damp and windy days with low pressure increased the chances of experiencing more pain than normal by about 20%. So if someone's chances of a painful day with average weather were five in 100, they would increase to six in 100 on a damp and windy day. Cold, damp days also made pain worse. But there was no association with temperature alone, or rainfall. 'Pain forecast' Prof Will Dixon, of the Centre for Epidemiology Versus Arthritis, at the University of Manchester, who led the study said: "Weather has been thought to affect symptoms in patients with arthritis since [ancient Greek physician] Hippocrates. © 2019 BBC

Keyword: Pain & Touch
Link ID: 26746 - Posted: 10.24.2019

By Kelly Servick CHICAGO, ILLINOIS—By harnessing the power of imagination, researchers have nearly doubled the speed at which completely paralyzed patients may be able to communicate with the outside world. People who are “locked in”—fully paralyzed by stroke or neurological disease—have trouble trying to communicate even a single sentence. Electrodes implanted in a part of the brain involved in motion have allowed some paralyzed patients to move a cursor and select onscreen letters with their thoughts. Users have typed up to 39 characters per minute, but that’s still about three times slower than natural handwriting. In the new experiments, a volunteer paralyzed from the neck down instead imagined moving his arm to write each letter of the alphabet. That brain activity helped train a computer model known as a neural network to interpret the commands, tracing the intended trajectory of his imagined pen tip to create letters (above). Eventually, the computer could read out the volunteer’s imagined sentences with roughly 95% accuracy at a speed of about 66 characters per minute, the team reported here this week at the annual meeting of the Society for Neuroscience. The researchers expect the speed to increase with more practice. As they refine the technology, they will also use their neural recordings to better understand how the brain plans and orchestrates fine motor movements. © 2019 American Association for the Advancement of Science.

Keyword: Robotics; Brain imaging
Link ID: 26745 - Posted: 10.24.2019

By Nicholas Bakalar Trans fatty acids, known to increase the risk for heart disease, stroke and diabetes, have now been linked to an increased risk for dementia. Researchers measured blood levels of elaidic acid, the most common trans fats, in 1,628 men and women 60 and older and free of dementia. Over the following 10 years, 377 developed some type of dementia. Trans fats, which are added to processed food in the form of partially hydrogenated vegetable oils, increase levels of LDL, or “bad” cholesterol. Meat and dairy products naturally contain small amounts of trans fats, but whether these fats raise bad cholesterol is unknown. After controlling for other factors, the scientists found that compared with those in the lowest one-quarter in blood levels of elaidic acid, those in the highest were 50 percent more likely to develop any form of dementia and 39 percent more likely to develop Alzheimer’s disease in particular. Elaidic acid levels were not associated with vascular dementia considered alone. The study is in Neurology. The senior author, Dr. Toshiharu Ninomiya, a professor of public health at Kyushu University in Japan, said the study is observational so cannot prove cause and effect. “It is difficult to avoid trans fats completely, and the risk of a small amount of trans fats is unclear,” he said. “But it would be better to try to avoid them as much as possible.” © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26744 - Posted: 10.24.2019

By Meredith Wadman, Kelly Servick Biogen stunned investors and scientists alike today, announcing it will resurrect an Alzheimer’s drug it had declared a failure in March; the company plans in early 2020 to ask the U.S. Food and Drug Administration for marketing approval of aducanumab, an antibody designed to bind and eliminate the protein beta-amyloid in the brain. As STAT reports, Biogen says the about-face came after it assessed clinical trial data from a larger number of patients than it first analyzed. Whereas an initial “futility” analysis of data from two late-stage clinical trials found that the drug failed to meaningfully slow progression of early Alzheimer’s disease, the company now concludes that, due primarily to the responses of people on the higher of two doses of the antibody, the drug did significantly slow people’s cognitive decline and their functional decline, meaning their ability to cope with activities of daily living. Biogen’s first analysis used data from 1748 patients who had completed 18 months on a low dose or a high dose of the drug; the new analysis, whose underlying data are not yet publicly available nor described in a journal article, included 2066 such patients. Bart De Strooper, who directs the UK Dementia Research Institute at University College London, called the news “fantastic. … We currently have no effective treatments to slow or halt the progression of Alzheimer’s disease and I hope this signifies a turning point.” He also suggested the result could revive the once-dominant theory that the neurodegenerative condition is largely due to the brain’s accumulation of toxic amyloid. “We should now redouble our efforts to tackle this central problem in Alzheimer’s disease.” © 2019 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 26743 - Posted: 10.23.2019

By Gina Kolata Biogen, the drug company, said on Tuesday that it would ask the Food and Drug Administration to approve an experimental drug, aducanumab, to treat people with mild cognitive impairment and the earliest signs of Alzheimer’s disease. About 10 million Americans might qualify for treatment if the drug were approved, according to Michel Vounatsos, the company’s chief executive. Even so, it is not quite time for these patients to celebrate. The company has not published the most recent analyses, and experts are mostly in the dark as to how well the drug works. It neither prevents nor cures Alzheimer’s; the company claims only that aducanumab may slow cognitive decline in some patients. In fact, Biogen announced in March that it was halting two large studies of aducanumab for treatment of Alzheimer’s disease because data showed the effort was likely to be futile. The company resurrected the drug after additional analyses suggested it might have some effect at higher doses. (“Just in time for Halloween, aducanumab has risen from the dead,” one drug industry analyst said in an email.) Here are some takeaways from Tuesday’s announcement. What is this drug? Drug companies have spent billions of dollars on failed trials for Alzheimer’s drugs. So frustrating have the findings been that some have decided to abandon the search altogether. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26742 - Posted: 10.23.2019

Ian Sample Science editor Doctors in the US have launched a clinical trial to see whether exposure to flickering lights and low frequency sounds can slow the progression of Alzheimer’s disease. A dozen patients enrolled in the trial will have daily one-hour sessions of the radical therapy which researchers hope will induce brain activity that protects against the disorder. Animal tests have shown that exposure to light and sound waves at 40Hz reinforces so-called gamma waves in the brain, with knock-on effects across the organ. In mice used to model the disease, the therapy appears to boost the activity of the brain’s immune cells, making them clear the aberrant proteins that build up in Alzheimer’s. Li-Huei Tsai, a neuroscientist who is leading the trial at MIT, told the Society for Neuroscience meeting in Chicago on Tuesday that the therapy improved the survival and health of the animals’ neurons, boosted their connectivity, and dilated blood vessels, all of which may benefit patients. “We would like to see if our approach slows Alzheimer’s disease,” Tsai told the Guardian. The patients enrolled on the trial will have cognitive tests every three months to assess their brain function and regular scans to measure their brain activity and the connectivity of neurons across the organ. © 2019 Guardian News & Media Limited

Keyword: Alzheimers; Brain imaging
Link ID: 26741 - Posted: 10.23.2019

By Laura Sanders CHICAGO — Wide swings in blood sugar can mess with sleep. Food’s relationship with sleep gets even more muddled when signs of Alzheimer’s disease are present, a study of mice suggests. The results, presented in a news briefing October 20 at the annual meeting of the Society for Neuroscience, show that Alzheimer’s disease is not confined to the brain. “Your head is attached to your body,” says neuroscientist Shannon Macauley of Wake Forest School of Medicine in Winston-Salem, N.C. Metabolism, sleep and brain health “don’t happen in isolation,” she says. Along with Caitlin Carroll, also of Wake Forest, Macauley and coauthors rigged up a way to simultaneously measure how much sugar the brain consumes, the rate of nerve cell activity and how much time mice spend asleep. Injections of glucose into the blood led to changes in the brain: a burst of metabolism, a bump in nerve cell activity and more time spent awake. “It’s like giving a kid a lollipop,” Macauley says. “They’re going to run around in a circle.” But a dip in blood sugar, caused by insulin injections, also led to more nerve cell action and more wakefulness. “You can have it go up high or go down low, and it was just really bad either way,” Macauley says. Researchers did similar analyses in mice genetically engineered to have one of two key signs of Alzheimer’s. Some of these mice had clumps of amyloid-beta protein between nerve cells, while others had tangles of a protein called tau inside nerve cells. © Society for Science & the Public 2000–2019.

Keyword: Alzheimers; Sleep
Link ID: 26740 - Posted: 10.23.2019

Tara Boyle Some of Laurie Santos's most insightful research was sparked by an embarrassing incident. One day, monkeys — her research subjects — stole all the fruit she needed to run a study. She left the research site early for the day. On the boat ride home from Cayo Santiago, the island where the monkeys lived, Santos reflected on the monkeys' mischief. "It's not just that we're dumb researchers and they can outsmart us," she says. "They're specifically trying to steal from us when we're not aware of what they're doing." Santos, a professor of psychology at Yale University, decided to study the monkeys' theft. She found that they selectively stole from the person who couldn't see them. "In other words, they're rationally calculating whether or not someone could detect that they're about to do something dastardly," she says. It was behavior befitting a human. Over the years Santos has discovered other similarities in how humans and non-human primates act. She's also pinpointed important differences, helping us understand which capacities are unique to humans. This comparison between humans and other animals, Santos says, is essential for making any claims that humans are unique. "There's no way to study what makes humans special if you only study humans. You actually have to turn to all the other critters in the animal kingdom," she says. © 2019 npr

Keyword: Evolution
Link ID: 26739 - Posted: 10.23.2019

By Jonathan Lambert Prozac, a commonly prescribed medication for kids and teens with autism, is no more effective than a placebo at treating obsessive-compulsive behaviors, a small study finds. The results of the randomized clinical trial, published October 22 in JAMA, cast further doubt on the widespread practice of prescribing a class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs, to treat children with autism who have these behaviors, says pediatric neurologist Ann Neumeyer. “We really don’t have any good medications that have yet been studied in children with autism for these behaviors,” says Neumeyer, the medical director of the Massachusetts General Hospital Lurie Center for Autism in Lexington, who wasn’t involved in the study. “That’s a problem.” Autism spectrum disorders encompass a diversity of symptoms, but common among them are obsessive-compulsive behaviors (SN: 10/16/18). Individuals with autism can become hyperfocused on specific ideas or objects and can engage in ritualistic “tics,” such as rocking or hand-waving. For many individuals, these symptoms interfere with everyday functioning. SSRI antidepressants account for a quarter to a third of all prescriptions to children and teens with autism, according to pediatrician Dinah Reddihough at the Murdoch Children’s Research Institute in Melbourne, Australia. “Despite their widespread use, there is no evidence of effectiveness of SSRIs for autism spectrum disorders in children,” she says. © Society for Science & the Public 2000–2019.

Keyword: Autism
Link ID: 26738 - Posted: 10.23.2019

Alexander D. Reyes Information in the brain is thought to be encoded as complex patterns of electrical impulses generated by thousands of neuronal cells. Each impulse, known as an action potential, is mediated by currents of charged ions flowing through a neuron’s membrane. But how the ions pass through the insulated membrane of the neuron remained a puzzle for many years. In 1976, Erwin Neher and Bert Sakmann developed the patch-clamp technique, which showed definitively that currents result from the opening of many channel proteins in the membrane1. Although the technique was originally designed to record tiny currents, it has since become one of the most important tools in neuroscience for studying electrical signals — from those at the molecular scale to the level of networks of neurons. By the 1970s, current flowing through the cell was generally accepted to result from the opening of many channels in the membrane, although the underlying mechanism was unknown. At that time, current was commonly recorded by impaling tissue with a sharp electrode — a pipette with a very fine point. Unfortunately, however, the signal recorded in this way was excessively noisy, and so only the large, ‘macroscopic’ current — the collective current mediated by many different types of channel — that flows through the tissue could be resolved. In 1972, Bernard Katz and Ricardo Miledi2, pioneers of the biology of the synaptic connections between cells, managed to infer from the macroscopic current certain properties of the membrane channels, but only after a heroic effort to exclude all possible confounding factors. The problem was that the macroscopic current could be influenced by factors not directly related to channel activity, such as cell geometry and modulatory processes that regulate cell excitability. Also troublesome was that interpretations of macroscopic-current features were based on unverified assumptions about the statistics of individual channel activity2,3. Despite Katz and Miledi’s careful analyses, there was a lingering doubt about whether their conclusions were correct. The crucial data were obtained by Neher and Sakmann using patch clamp. © 2019 Springer Nature Limited

Keyword: Brain imaging
Link ID: 26737 - Posted: 10.23.2019

Anna Azvolinsky Nearly 30 years ago, Kamran Khodakhah, now a neuroscientist at Albert Einstein College of Medicine, signed up for a TV repair course that met several times a week at night at a local community college in London. While many of the other students were attending with the obvious goal of repairing TVs and other appliances, Khodakhah had a different aim. He reasoned that if he could understand how a television worked, he could design new tools to study the rat brain slices he had collected. Khodakhah was working as a PhD student in the lab of neuroscientist David Ogden at the National Institute for Medical Research, trying to determine whether a particular signaling pathway—the inositol trisphosphate (InsP3)/calcium signaling pathway—could be activated in nerve cells called Purkinje neurons. They are found in the cerebellum and have a high density of InsP3 receptors. By taking the TV repair class, Khodakhah wanted to learn to build an electronic circuit to enhance his camera images in order to better visualize the Purkinje cells within slices of the cerebellum and to study the InsP3/calcium ion signaling pathway. He used the new imaging setup, combined with existing lab tools such as flash photolysis, to introduce inert precursor molecules of InsP3—called caged InsP3—into Purkinje neurons in cerebellar slices prepared from rat brains. When stimulated with light, a caged InsP3 molecule is rapidly converted into an active form that binds to InsP3 receptors. Khodakhah then used a fluorescent calcium indicator and recorded the calcium channel activity to see if the binding of InsP3 receptors caused release of calcium from internal stores. At the time, researchers knew that in liver and other non-neuronal cells, InsP3 molecules act as messengers, stimulating the release of calcium ions, which then activates internal cellular pathways. Whether something similar happened in Purkinje neurons wasn’t clear, but if it did, the process might reveal something about how the cerebellum coordinates movement, Khodakhah thought. © 1986–2019 The Scientist.

Keyword: Movement Disorders
Link ID: 26736 - Posted: 10.23.2019

By Laura Sanders CHICAGO — Light pulses from outside a monkey’s brain can activate nerve cells deep within. This external control, described October 20 at the annual meeting of the Society for Neuroscience, might someday help scientists treat brain diseases such as epilepsy. Controlling nerve cell behavior with light, a method called optogenetics, often requires thin optical fibers to be implanted in the brain (SN: 1/15/10). That invasion can cause infections, inflammation and tissue damage, says study coauthor Diego Mendoza-Halliday of MIT. He and his colleagues created a new light-responsive molecule, called SOUL, that detects extra dim light. After injecting SOUL into macaque monkeys’ brains, researchers shined blue light through a hole in the skull. SOUL-containing nerve cells, which were as deep as 5.8 millimeters in the brain, became active. A dose of orange light stopped this activity. SOUL can’t sense light coming from outside of the macaques’ skulls. But in mice, the system works through the skull, the researchers reported. LEDs implanted just under people’s skulls might one day be used to treat brain diseases. Such a system might be able to temporarily turn off nerve cells that are about to cause an epileptic seizure, for instance. “This is basically scooping out a piece of brain and then putting it back in a few seconds later,” when the risk of a seizure has dropped, Mendoza-Halliday says. © Society for Science & the Public 2000–2019.

Keyword: Brain imaging
Link ID: 26735 - Posted: 10.23.2019

By Pam Belluck About 10 days after what seemed like a garden-variety cold, Luca Waugh, a healthy 4-year-old, developed troubling symptoms. Suddenly, his neck became so weak that he fell backward. Then his right arm couldn’t move. Within days, recalled his mother, Dr. Riley Bove, he developed “head-to-toe paralysis, where he could kind of move his eyes a little bit and one side of his face.” Doctors diagnosed Luca with acute flaccid myelitis or A.F.M., a mysterious neurological condition that can cause limb weakness and polio-like paralysis, mostly in young children. A.F.M. is rare, but in 2014, when Luca became afflicted, health authorities identified a burst of 120 cases. Since then, A.F.M. has made headlines as cases have spiked every two years, and nearly 600 have been confirmed across the country since 2014. What exactly causes A.F.M. has eluded experts, frustrating attempts to prevent or treat it. Now, a study by a team that includes Luca’s mother, Dr. Bove, who happens to be a neurologist, provides strong evidence of a likely cause. It involved dozens of children with A.F.M., including Luca, whose paralysis improved after weeks of hospitalization but who remains disabled five years later. The research, published Monday in the journal Nature Medicine, points to a long-suspected culprit: enteroviruses, a group of common viruses that usually produce mild effects, but can sometimes cause neurological symptoms. Using sophisticated laboratory techniques, researchers found antibodies to enteroviruses in the cerebrospinal fluid of nearly 70 percent of the children with A.F.M., a sign their bodies had mobilized to defend against enterovirus infection. © 2019 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26734 - Posted: 10.22.2019

By Sofie Bates Make some noise for the white bellbirds of the Brazilian Amazon, now the bird species with the loudest known mating call. The birds (Procnias albus) reach about 125 decibels on average at the loudest point in one of their songs, researchers report October 21 in Current Biology. Calls of the previous record-holder — another Amazonian bird called the screaming piha (Lipaugus vociferans) — maxed out around 116 decibels on average. This difference means that bellbirds can generate a soundwave with triple the pressure of that made by pihas, says Jeff Podos, a behavioral ecologist at the University of Massachusetts Amherst, who did the research along with ornithologist Mario Cohn-Haft, of the National Institute of Amazon Research in Manaus, Brazil. The team measured sound intensity from three pihas and eight bellbirds. Each sounded off at different distances from the scientists. So to make an accurate comparison, the researchers used rangefinder binoculars, with lasers to measure distance, to determine how far away each bird was. Then, they calculated how loud the sound would be a meter from each bird to crown a winner. The small white bellbird, which weighs less than 250 grams, appears to be built for creating loud sounds, with thick abdominal muscles and a beak that opens extra wide. “Having this really wide beak helps their anatomy be like a musical instrument,” Podos says. Being the loudest may come with a cost: White bellbirds can’t hold a note for long because they run out of air in their lungs. Their loudest call sounds like two staccato beats of an air horn while the calls of screaming pihas gradually build to the highest point. © Society for Science & the Public 2000–2019

Keyword: Sexual Behavior; Hearing
Link ID: 26733 - Posted: 10.22.2019

By Jon Cohen On a lightly snowing Sunday evening, a potential participant in Denis Rebrikov’s controversial plans to create gene-edited babies meets with me at a restaurant in a Moscow suburb. She does not want to be identified beyond her patronymic, Yevgenievna. We sit at a corner table in an empty upstairs section of the restaurant while live Georgian music plays downstairs. Yevgenievna, in her late 20s, cannot hear it—or any music. She has been deaf since birth. But with the help of a hearing aid that’s linked to a wireless microphone, which she places on the table, she can hear some sounds, and she is adept at reading lips. She speaks to me primarily in Russian, through a translator, but she is also conversant in English. Yevgenievna and her husband, who is partially deaf, want to have children who will not inherit hearing problems. There is nothing illicit about our discussion: Russia has no clear regulations prohibiting Rebrikov’s plan to correct the deafness mutation in an in vitro fertilization (IVF) embryo. But Yevgenievna is uneasy about publicity. “We were told if we become the first couple to do this experiment we’ll become famous, and HBO already tried to reach me,” Yevgenievna says. “I don’t want to be well known like an actor and have people bother me.” She is also deeply ambivalent about the procedure itself, a pioneering and potentially risky use of the CRISPR genome editor. The couple met on vk.com, a Russian Facebook of sorts, in a chat room for people who are hearing impaired. Her husband could hear until he was 15 years old, and still gets by with hearing aids. They have a daughter—Yevgenievna asks me not to reveal her age—who failed a hearing test at birth. Doctors initially believed it was likely a temporary problem produced by having a cesarean section, but 1 month later, her parents took her to a specialized hearing clinic. “We were told our daughter had zero hearing,” Yevgenievna says. “I was shocked, and we cried.” © 2019 American Association for the Advancement of Science.

Keyword: Hearing; Genes & Behavior
Link ID: 26732 - Posted: 10.22.2019

By Eric A. Taub Like clockwork, the sound of the freight train came roaring through our bedroom in the middle of each night. Or at least what sounded like a freight train. In reality, it was me, snoring. And according to my wife, that freight train had gotten considerably louder over the years. Unfortunately, snoring frequency and volume is exacerbated by age, among other factors. While there’s nothing I can do about getting older, there are products and procedures available that can eliminate or significantly reduce the annoyance to one’s bed partner caused by all that nighttime snorting and wheezing. Snoring and sleep apnea are not the same, although severe snoring can be an indication of apnea. If sleep apnea is not present, snoring is simply the benign result of an obstructed airway. As we age, the uvula — that soft, floppy, fingerlike projection in the back of the throat — gets softer and floppier. At the same time, muscles under the tongue get lax. And the condition is exacerbated if we are overweight or drink too much alcohol. “With age, the muscle tone of our airways decreases. That decreased tone allows the tissues to move more readily and become more prone to collapse and to vibrate,” said Dr. Michael D. Olson, an ear, nose and throat doctor and sleep surgeon in the Mayo Clinic’s department of head and neck surgery. In addition, if the size of the airway decreases, air pressure increases, allowing for tissue vibration and snoring. “Combine that with nasal congestion, a big tongue and body fat, and that leads to an excessive collapse of the airways,” Dr. Olson said. Another cause of snoring: teeth extraction, a particular issue for baby boomers who had braces in their youth. With the removal of four bicuspids as a common practice at the time, boomers may now be suffering snoring because of a larger tongue in a smaller mouth. © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26731 - Posted: 10.22.2019

Emma Yasinski Delta waves, patterns of slow, synchronized brain activity that occur during deep sleep, have long been considered “periods of silence,” in which neurons in the cortex stop firing. But these intervals may not be silent after all, researchers reported yesterday in Science. In rats, some cortical neurons remain active during delta waves, and their firing may even be involved in consolidating memories. “The paper is absolutely fascinating and will have a large impact on the field of memory and sleep,” says Björn Rasch, a biopsychologist at the University of Fribourg in Switzerland who was not involved in the study. He suggests it might even help explain surprising results in his own research in humans published earlier this year that indicated participants may better remember words from a foreign language if they are replayed during delta wave sleep than if they are never repeated during sleep. The latest study “challenges our views on the potential function of down states [when cortical neurons seem silent] in memory consolidation processes.” When humans (and rats) are awake, a brain structure called the hippocampus records the ongoing episodes of our lives. When we sleep, the hippocampus replays this activity, which is transmitted to the cortex where it forms long-term memories. Afterward, the cortex seems to go silent. This quiet delta wave period is known to be important for memory consolidation, but researchers have wondered how it helps the process. © 1986–2019 The Scientist.

Keyword: Sleep; Learning & Memory
Link ID: 26730 - Posted: 10.22.2019