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Philip Ball Some problems in science are so hard, we don’t really know what meaningful questions to ask about them — or whether they are even truly solvable by science. Consciousness is one of those: Some researchers think it is an illusion; others say it pervades everything. Some hope to see it reduced to the underlying biology of neurons firing; others say that it is an irreducibly holistic phenomenon. The question of what kinds of physical systems are conscious “is one of the deepest, most fascinating problems in all of science,” wrote the computer scientist Scott Aaronson of the University of Texas at Austin. “I don’t know of any philosophical reason why [it] should be inherently unsolvable” — but “humans seem nowhere close to solving it.” Now a new project currently under review hopes to close in on some answers. It proposes to draw up a suite of experiments that will expose theories of consciousness to a merciless spotlight, in the hope of ruling out at least some of them. If all is approved and goes according to plan, the experiments could start this autumn. The initial aim is for the advocates of two leading theories to agree on a protocol that would put predictions of their ideas to the test. Similar scrutiny of other theories will then follow. Whether or not this project, funded by the Templeton World Charity Foundation, narrows the options for how consciousness arises, it hopes to establish a new way to do science for difficult, contentious problems. Instead of each camp championing its own view and demolishing others, researchers will collaborate and agree to publish in advance how discriminating experiments might be conducted — and then respect the outcomes. © 2019 Quanta Magazine
Keyword: Consciousness
Link ID: 26017 - Posted: 03.07.2019
By Jan Hoffman and Abby Goodnough Three years ago this month, as alarms about the over-prescription of opioid painkillers were sounding across the country, the federal government issued course-correcting guidelines for primary care doctors. Prescriptions have fallen notably since then, and the Trump administration is pushing for them to drop by another third by 2021. But in a letter to be sent to the Centers for Disease Control and Prevention on Wednesday, more than 300 medical experts, including three former White House drug czars, contend that the guidelines are harming one group of vulnerable patients: those with severe chronic pain, who may have been taking high doses of opioids for years without becoming addicted. They say the guidelines are being used as cover by insurers to deny reimbursement and by doctors to turn patients away. As a result, they say, patients who could benefit from the medications are being thrown into withdrawal and suffering renewed pain and a diminished quality of life, even to the point of suicide. The letter writers form an uneasy alliance spanning differing positions on opioids — professors of addiction medicine as well as pain specialists, some patient representatives who have taken money from the pharmaceutical industry, and the former drug czars, from the Obama, Clinton and Nixon administrations. Michael Botticelli, who served as the drug czar under President Obama and now leads the Grayken Center for Addiction at Boston Medical Center, said he signed the letter because “there has been enough anecdotal evidence to raise the alarm bells” about the misuse of the guidelines leading to pain patients losing effective treatment. “The C.D.C. really does need a rigorous evaluation of this because we don’t know how big the problem is,” he said. “Minimally, we need some level of clarification on appropriate use of the guidelines.” © 2019 The New York Times Company
Keyword: Pain & Touch; Drug Abuse
Link ID: 26016 - Posted: 03.07.2019
GPs are urging women not to be alarmed by research linking long-term hormone replacement therapy (HRT) use with a small increased risk of Alzheimer's. They say HRT is an effective and safe treatment for most women with menopause symptoms and the risk is "extremely low". The BMJ research looked at data on 170,000 women in Finland over 14 years. It found a 9%-17% increased risk for Alzheimer's, particularly in women taking HRT for more than 10 years. This equates to between nine and 18 extra cases of the disease per year in every 10,000 women aged between 70 and 80, the researchers said. But the study was observational and, as a result, it cannot be said for certain that other factors had not affected the results. Other studies have found that HRT actually improves brain function. The Royal College of GPs said the research does not prove that HRT causes Alzheimer's disease, and women currently taking it should continue to do so. Prof Helen Stokes-Lampard, chairwoman of the College, said: "Hormone replacement therapy can be of greatest benefit to many women who are suffering from some of the unpleasant side-effects of the menopause, such as hot flushes and night sweats - and there is a large body of evidence that shows it is an effective and safe treatment for most women. "We would urge patients not to be alarmed by this research - as the researchers state, any risk is extremely low - and if they are currently taking HRT, to continue doing so as prescribed by their doctor. " However, she said there were risks with any medication and it was important that women were aware of them. "To minimise any risk, best practice for most women is to prescribe the lowest possible dose of hormones for the shortest possible time in order to achieve satisfactory relief of symptoms," Prof Stokes-Lampard said. © 2019 BBC
Keyword: Alzheimers; Hormones & Behavior
Link ID: 26015 - Posted: 03.07.2019
By Elizabeth Pennisi Cowbirds are the quintessential deadbeat parents. They, and about 90 other bird species, abandon their eggs in other birds’ nests, leaving the burden of chick care to others. An arms race is the result: Cuckolded foster parents keep evolving ways to fight back, and deadbeats evolve countermeasures. Now, researchers have discovered how spots on an egg play a crucial role in a parent’s decision to keep an egg—or boot it from the nest. One of the shiny cowbird’s (Molothrus bonariensis) most common victims is the chalk-browed mockingbird (Mimus saturninus). The mockingbird’s eggs are blue-green and spotted, whereas the cowbird’s eggs vary from pure white to brown and spotted. Researchers had assumed mockingbirds reject cowbird eggs that don't look like their own, in pattern and color. But the new study finds it’s not that simple. To get a better sense of how mockingbirds decide which eggs to boot, evolutionary ecologist Daniel Hanley at Long Island University in Brookville, New York, and colleagues painted 70 3D-printed eggs a range of colors and put spots on half of them. They distributed these eggs among 85 mockingbird nests and checked several days later to see which eggs were still there. Spots tended to make the mockingbirds hedge their bets and keep an egg, even if the color wasn’t “right,” Hanley and his colleagues report in the April issue of the Philosophical Transactions of the Royal Society B. For example, the mockingbirds removed unspotted brown eggs—a “wrong” color and pattern—90% of the time. But the birds were less sure when the egg had spots. They removed brown eggs with spots just 60% of the time, for example. In general, mockingbirds were more accepting of very blue eggs, even those that were much bluer than their own eggs. And when these blue eggs had spots, parents kept them more than 90% of the time. © 2019 American Association for the Advancement of Science
Keyword: Sexual Behavior; Evolution
Link ID: 26014 - Posted: 03.07.2019
By Carolyn Y. Johnson and Laurie McGinley The Food and Drug Administration approved a novel antidepressant late Tuesday for people with depression that does not respond to other treatments — the first in decades to work in a completely new way in the brain. The drug, a nasal spray called esketamine, has been eagerly anticipated by psychiatrists and patient groups as a powerful new tool to fight intractable depression. The spray acts within hours, rather than weeks or months as is typical for current antidepressants, and could offer a lifeline to about 5 million people in the United States with major depressive disorder who haven’t been helped by current treatments. That accounts for about one in three people with depression. “This is undeniably a major advance,” said Jeffrey Lieberman, a Columbia University psychiatrist. But he cautioned much is still unknown about the drug, particularly regarding its long-term use. “Doctors will have to be very judicious and feel their way along,” he said. The label for the drug will carry a black box warning – the most serious safety warning issued by the FDA. It will caution users they could experience sedation and problems with attention, judgment and thinking, and that there’s potential for abuse and suicidal thoughts. People who take esketamine will have to be monitored for at least two hours after receiving a dose to guard against some of these side effects. The medicine has a complex legacy because it is a component of ketamine, which was approved years ago as an anesthetic and was once popular as a party drug called Special K. Esketamine must be administered under medical supervision and can only be used in a certified doctor’s office or clinic, according to the conditions of the FDA approval. It is to be taken with an oral antidepressant. © 1996-2019 The Washington Post
Keyword: Depression; Drug Abuse
Link ID: 26013 - Posted: 03.06.2019
By Benedict Carey Thousands, perhaps millions, of people who try to quit antidepressant drugs experience stinging withdrawal symptoms that last for months to years: insomnia, surges of anxiety, even so-called brain zaps, sensations of electric shock in the brain. But doctors have dismissed or downplayed such symptoms, often attributing them to the recurrence of underlying mood problems. The striking contrast between the patients’ experience and their doctors’ judgment has stirred heated debate in Britain, where last year the president of the Royal College of Psychiatrists publicly denied claims of lasting withdrawal in “the vast majority of patients.” Patient-advocacy groups demanded a public retraction; psychiatrists, in the United States and abroad, came to the defense of the Royal College. Now, a pair of prominent British psychiatrists has broken ranks, calling the establishment’s position badly mistaken and the standard advice on withdrawal woefully inadequate. In a paper published Tuesday in the Lancet, the authors argued that any responsible withdrawal regimen should have the patient tapering off medication over months or even years, depending on the individual, and not over four weeks, the boilerplate advice. The paper is by far the strongest research-backed denunciation of standard tapering practice by members of the profession. “I know people who stop suddenly and get no side effects,” said Dr. Mark Horowitz, a clinical research fellow at Britain’s National Health Service and King’s College London, and one of the paper’s authors. But many people, he said, “have to pull apart their capsules and reduce the dosage bead by bead. We provided the science to back up what they’re already doing.” © 2019 The New York Times Company
Keyword: Depression
Link ID: 26012 - Posted: 03.06.2019
By Max Evans BBC News A stranger once waved at Boo James on a bus. She did not think any more of it - until it later emerged it was her mother. She has a relatively rare condition called face blindness, which means she cannot recognise the faces of her family, friends, or even herself. Scientists have now launched a study they hope could help train people like Boo to recognise people better. Boo said for many years she thought she was "from another planet". "It is immensely stressful and very emotionally upsetting to sit and dwell upon so I try not to do that," she said. "It's very hard work. It can be physically and emotionally exhausting to spend a day out in public constantly wondering whether you should have spoken to someone." For most of her life, she didn't know she had the condition - also known as prosopagnosia - and blamed herself for the "social awkwardness" caused when she failed to recognise people. "I had to try and find a way to explain that. I really couldn't very well, except to think that I was just the one to blame for not being bothered to remember who people were. "[Like it was] some sort of laziness: I didn't want to know them, obviously I wasn't interested enough to remember them, so that was some kind of deficiency, perhaps, in me." But the penny dropped in her early 40s when she saw a news item about the condition on television. "I then knew that the only reason I wasn't recognising that person was because my brain physically wasn't able to do it," she said. "I could immediately engage more self-understanding and forgive myself and try to approach things from a different angle." Image caption Boo has developed techniques to try to help her cope, including remembering what people wear She said her childhood was punctuated by "traumatic experiences" with fellow children, childminders and teachers she could not recognise. © 2019 BBC
Keyword: Attention
Link ID: 26011 - Posted: 03.06.2019
Carolyn Wilke Over the course of human evolution, our brains expanded massively. One of the areas that ballooned over the past few million years is the cerebral cortex, the wrinkly outer layer of the brain. It processes sensory information, coordinates our motion, and is in charge of our higher order functions, such as language processing and problem solving. Scientists are scrutinizing the structure of the cortex for clues about its development throughout our lives and our evolution as a species and to understand where heredity intersects with intelligence. A new study of hundreds of developing brains reveals a trifecta of overlap in regions of the cortical surface that develop from childhood to adulthood, expanded during evolution, and are connected to genetics. The scientists also found genetically mediated links between IQ test scores and surface area in regions related to intelligence, they report today (March 4) in the Journal of Neuroscience. “I think it’s a very, very strong work,” says Rachel Brouwer, a neuroscientist at University Medical Center Utrecht in the Netherlands who was not part of the study. The authors pick up which regions of the brain where variability is most explained by genes, but by looking for connections with evolutionary expansion and neurodevelopment, “it is an attempt to link [heritability] to what it actually means in a broader picture,” she says. © 1986 - 2019 The Scientist
Keyword: Intelligence; Evolution
Link ID: 26010 - Posted: 03.06.2019
Rob Stein There's strong new evidence that a common childhood vaccine is safe. A large study released Monday finds no evidence that the vaccine that protects against measles, mumps and rubella increases the risk of autism. The study of children born in Denmark is one of the largest ever of the MMR vaccine. "The study strongly supports that MMR vaccination does not increase the risk for autism," the authors write in the Annals of Internal Medicine. "We believe our results offer reassurance and provide reliable data." The study's first author, epidemiologist Anders Hviid of the Staten Serum Institute in Copenhagen, added in an email: "MMR does not cause autism." In the study, researchers analyzed data collected from all children born in Denmark to Danish-born mothers between 1999 and 2010. Among the 657,461 children included in the analysis, 6,517 were diagnosed with autism over the next decade. But there was no overall increased risk for the developmental disorder among those who received the MMR vaccine when compared with those who had not gotten the vaccine, the researchers found. The researchers also found no increased risk among subgroups of children who might be unusually susceptible to autism, such as those with a brother or sister with the disorder. © 2019 npr
Keyword: Autism
Link ID: 26009 - Posted: 03.06.2019
Robin McKie Matt Ellison was seven when his father was diagnosed with Huntington’s disease. The condition – which is progressive, incurable and invariably fatal – took 15 years to kill John Ellison. The impact on Matt’s life was profound. His father, who had inherited the disease from his mother, found he could no longer concentrate enough to hold down his job as an engineer at Jaguar. Later he began to lose the power of movement and, eventually, lost his ability to speak. At his local school Matt was mocked because of his father’s odd, uncoordinated gait. The taunting got so bad that Matt stopped attending. “I stayed at home and helped Mum look after Dad,” he recalls. Then in 2007, when Matt reached 18, he decided to find out whether he faced a similar fate. He was tested and told: yes, he had the Huntington’s gene. A few years later his father died, aged 55. “I had had time to prepare myself, but it still hits you hard when you are told you are positive,” says Matt. “I had wanted to be negative as much for my mum, who had gone through enough pain.” For Matt, and thousands of others who have been told they have inherited this affliction, the future would appear bleak, a prospect of inexor able physical and mental decline. The Huntington’s gene is remorseless in its impact. But recently this dark outlook has brightened. Scientists believe they are closing in on a treatment to control Huntington’s worst effects. © 2019 Guardian News & Media Limited
Keyword: Huntingtons
Link ID: 26008 - Posted: 03.05.2019
By Karen Weintraub For decades researchers have focused their attacks against Alzheimer’s on two proteins, amyloid beta and tau. Their buildup in the brain often serves as a defining indicator of the disease. Get rid of the amyloid and tau, and patients should do better, the thinking goes. But drug trial after drug trial has failed to improve patients’ memory, agitation and anxiety. One trial of a drug that removes amyloid even seemed to make some patients worse. The failures suggest researchers were missing something. A series of observations and recently published research findings have hinted at a somewhat different path for progression of Alzheimer’s, offering new ways to attack a disease that robs memories and devastates the lives of 5.7 million Americans and their families. One clue hinting at the need to look further afield was a close inspection of the 1918 worldwide flu pandemic, which left survivors with a higher chance of later developing Alzheimer’s or Parkinson’s. A second inkling came from the discovery that the amyloid of Alzheimer’s and the alpha-synuclein protein that characterizes Parkinson’s are antimicrobials, which help the immune system fight off invaders. The third piece of evidence was the finding in recent years, as more genes involved in Alzheimer’s have been identified, that traces nearly all of them to the immune system. Finally, neuroscientists have paid attention to cells that had been seen as ancillary—“helper” or “nursemaid” cells. They have come to recognize these brain cells, called microglia and astrocytes, play a central role in brain function—and one intimately related to the immune system. © 2019 Scientific American
Keyword: Alzheimers; Neuroimmunology
Link ID: 26007 - Posted: 03.05.2019
By Andrew Jacobs CAMBRIDGE, Mass. — There’s a new war raging in health care, with hundreds of millions of dollars at stake and thousands of lives in the balance. The battle, pitting drug companies against doctors and patient advocates, is being fought over the unlikeliest of substances: human excrement. The clash is over the future of fecal microbiota transplants, or F.M.T., a revolutionary treatment that has proved remarkably effective in treating Clostridioides difficile, a debilitating bacterial infection that strikes 500,000 Americans a year and kills 30,000. The therapy transfers fecal matter from healthy donors into the bowels of ailing patients, restoring the beneficial works of the community of gut microbes that have been decimated by antibiotics. Scientists see potential for using these organisms to treat diseases from diabetes to cancer. At the heart of the controversy is a question of classification: Are the fecal microbiota that cure C. diff a drug, or are they more akin to organs, tissues and blood products that are transferred from the healthy to treat the sick? The answer will determine how the Food and Drug Administration regulates the procedure, how much it costs and who gets to profit. In 2013, the F.D.A. announced a draft decision to regulate the therapy as a new drug but said it would continue to study the matter before reaching a final decision — which is expected to happen soon. Critics say that approach is based on outdated science and could lead to increased costs for patients, most of whom currently rely on a nonprofit stool bank in Cambridge. At stake, some researchers say, is the future of pioneering therapies that harness the human microbiome — the trillions of organisms that colonize the body and are increasingly seen as critical for healthy brain development and immune function. © 2019 The New York Times Company
Keyword: Obesity
Link ID: 26006 - Posted: 03.05.2019
/ By Jonathan S. Jones Newly unsealed documents from a lawsuit by the state of Massachusetts allege that Purdue Pharma, maker of OxyContin and other addictive opioids, actively sniffed out new, sinister ways to cash in on the opioid crisis. Despite years of negative press coverage, unwanted attention from regulators, multimillion dollar fines and several major lawsuits, Purdue staff and owners sought to expand the company’s sights beyond its usual array of opioid painkillers. Purdue planned to become an “end-to-end pain provider,” by branching into the market for opioid addiction and overdose medicines, looking to peddle these medicines even while the company continued to aggressively market its addictive opioids. Internal research materials coldly explained the rationale behind this plan: “Pain treatment and addiction are naturally linked.” As thousands of Americans continue to overdose on opioids annually, Purdue’s secret marketing research predicted that sales of naloxone, the overdose reversal drug, and buprenorphine, a medicine used to treat opioid addiction, would increase exponentially. Addiction to Purdue’s opioids would thus drive the sale of the company’s opioid addiction and overdose medicines. Purdue even planned to target as customers patients already taking the company’s opioids and doctors who prescribed opioids excessively, according to the Massachusetts lawsuit filing. To keep the plan quiet, Purdue staff dubbed the scheme “Project Tango.” Copyright 2019 Undark
Keyword: Drug Abuse
Link ID: 26005 - Posted: 03.05.2019
Assessing the patterns of energy use and neuronal activity simultaneously in the human brain improves our understanding of how alcohol affects the brain, according to new research by scientists at the National Institutes of Health. The new approach for characterizing brain energetic patterns could also be useful for studying other neuropsychiatric diseases. A report of the findings is now online in Nature Communications. “The brain uses a lot of energy compared to other body organs, and the association between brain activity and energy utilization is an important marker of brain health,” said George F. Koob, Ph.D., director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of NIH, which funded the study. “This study introduces a new way of characterizing how brain activity is related to its consumption of glucose, which could be very useful in understanding how the brain uses energy in health and disease.” The research was led by Dr. Ehsan Shokri-Kojori and Dr. Nora D. Volkow of the NIAAA Laboratory of Neuroimaging. Dr. Volkow is also the director of the National Institute on Drug Abuse at NIH. In previous studies they and their colleagues have shown that alcohol significantly affects brain glucose metabolism, a measure of energy use, as well as regional brain activity, which is assessed through changes in blood oxygenation. “The findings from this study highlight the relevance of energetics for ensuring normal brain function and reveal how it is disrupted by excessive alcohol consumption,” says Dr. Volkow.
Keyword: Drug Abuse; Brain imaging
Link ID: 26004 - Posted: 03.05.2019
Laura Sanders Fast waves of activity ripple in the brain a half second before a person calls up a memory. The finding, published in the March 1 Science, hint that these brain waves might be a key part of a person’s ability to remember. The results come from a study of 14 people with epilepsy who had electrodes placed on their brains as part of their treatment. Those electrodes also allowed scientists to monitor neural activity while the people learned pairs of words. One to three minutes after learning the pairs, people were given one word and asked to name its partner. As participants remembered the missing word, neuroscientist and neurosurgeon Kareem Zaghloul and his colleagues caught glimpses of fast brain waves rippling across parts of the brain at a rate of around 100 per second. These ripples appeared nearly simultaneously in two brain regions — the medial temporal lobe, which is known to be important for memory, and the temporal association cortex, which has a role in language. When a person got the answer wrong, or didn’t answer at all, these coordinated ripples were less likely to be present, the researchers found. “We see this happening, and then we see people remember,” says Zaghloul, of the National Institutes of Health in Bethesda, Md. While recalling a memory, “you mentally jump back in time and re-experience it,” Zaghloul says. Just after the ripples, the researchers saw telltale signs of that mental time travel — an echo of brain activity similar to the brain activity when the memory of the word pair was first formed. |© Society for Science & the Public 2000 - 201
Keyword: Learning & Memory
Link ID: 26003 - Posted: 03.05.2019
By Paula Span Donna Kaye Hill realized that her 80-year-old mother was faltering cognitively when her phone suddenly stopped working. When Ms. Hill called the phone company, “they told me she hadn’t paid her bill in three months.” Finding other alarming evidence of memory gaps, she took her mother, Katie, to a memory clinic. A geriatrician there diagnosed dementia and recommended two prescription drugs and a dietary supplement, a form of vitamin E. Katie Hill dutifully took vitamin E capsules, along with a host of other medications, until she died four years later. As she declined, her daughter didn’t think the vitamin, or the two prescription medications, was making much difference. “But if it doesn’t hurt, if there’s a chance it helps even a tiny bit, why not?” she reasoned. Ms. Hill, 62, a retired public employee in Danville, Va., takes fish oil capsules daily herself, hoping they’ll help ward off the disease that killed her mother. The elder Ms. Hill was unusual only in that a doctor had recommended the supplement; most older Americans are taking them without medical guidance. The Food and Drug Administration estimates that 80 percent of older adults rely on dietary supplements, many purporting to prevent or treat Alzheimer’s and other forms of dementia. Last month, the F.D.A. cracked down on this burgeoning market, sending warning letters or advisories to 17 companies selling about 60 supplements with names like Cogni-Flex and Mind Ignite. The warnings pointed out that the companies had touted these products as working like Alzheimer’s drugs, “but naturally and without side effects.” Or as “clinically shown to help diseases of the brain, such as Alzheimer’s.” The pills, oils and capsules were said to treat other diseases, too, from stroke to erectile dysfunction. © 2019 The New York Times Company
Keyword: Alzheimers
Link ID: 26002 - Posted: 03.02.2019
Analysis of genetic data from more than 94,000 individuals has revealed five new risk genes for Alzheimer’s disease, and confirmed 20 known others. An international team of researchers also reports for the first time that mutations in genes specific to tau, a hallmark protein of Alzheimer’s disease, may play an earlier role in the development of the disease than originally thought. These new findings support developing evidence that groups of genes associated with specific biological processes, such as cell trafficking, lipid transport, inflammation and the immune response, are “genetic hubs” that are an important part of the disease process. The study, which was funded in part by the National Institute on Aging (NIA) and other components of the National Institutes of Health, follows results from 2013. It will be published online February 28, 2019 in the journal Nature Genetics . “This continuing collaborative research into the genetic underpinnings of Alzheimer’s is allowing us to dig deeper into the complexities of this devastating disease,” said Richard J. Hodes, M.D., director of the NIA. “The size of this study provides additional clarity on the genes to prioritize as we continue to better understand and target ways to treat and prevent Alzheimer’s.” The researchers, members of the International Genomic Alzheimer’s Project (IGAP), analyzed both rare and common gene variants in 94,437 individuals with late onset Alzheimer’s disease, the most common form of dementia in older adults. IGAP is made up of four consortia in the United States and Europe that have been working together since 2011 on genome-wide association studies (GWAS) involving thousands of DNA samples and shared datasets. GWAS are aimed at detecting variations in the genome that are associated with Alzheimer’s. Understanding genetic variants is helping researchers define the molecular mechanisms that influence disease onset and progression.
Keyword: Alzheimers; Genes & Behavior
Link ID: 26001 - Posted: 03.02.2019
Laura Sanders People often fret about television time for children. A new study examines the habit at the other end of life. The more television older people watched, the worse they recalled a list of words, researchers report online February 28 in Scientific Reports. But the study describes only a correlation; it can’t say that lots of TV time actually causes the memory slips. Researchers examined data on 3,590 people collected as part of the English Longitudinal Study of Aging, a long-running study of English people aged 50 and older. In 2008 and 2009, participants reported how many hours a day, on average, they spent watching television. In addition to the surveys, participants listened to a recording of 10 common words, one word every two seconds. Then, people tried to remember as many words as they could, both immediately after hearing the words and after a short delay. Six years later, people took the same tests. People who watched more than 3.5 hours of TV daily back in 2008 or 2009 were more likely to have worse verbal memory scores six years later, the researchers found. Television “dose” seemed to matter: Beyond that 3.5-hour threshold, the more TV people watched, the bigger their later verbal memory scores declined. It’s not known whether television time actually causes verbal memory problems. The reverse could be true: People who have worse memories might be more likely to watch more television. Still, the researchers suggest that TV might cause a certain kind of mental stress that might contribute to memory trouble. |© Society for Science & the Public 2000 - 2019
Keyword: Learning & Memory
Link ID: 26000 - Posted: 03.02.2019
Matthew Warren Cue the super-mouse. Scientists have engineered mice that can see infrared light normally invisible to mammals — including humans. To do so, they injected into the rodents’ eyes nanoparticles that convert infrared light into visible wavelengths1. Humans and mice, like other mammals, cannot see infrared light, which has wavelengths slightly longer than red light — between 700 nanometres and 1 millimetre. But Tian Xue, a neuroscientist at the University of Science and Technology of China in Hefei, and his colleagues developed nanoparticles that convert infrared wavelengths into visible light. The nanoparticles absorb photons at wavelengths of around 980 nanometres and emit them at shorter wavelengths, around 535 nanometres, corresponding to green light. Xue’s team attached the nanoparticles to proteins that bind to photoreceptors — the cells in the eye that convert light into electrical impulses — and then injected them into mice. The researchers showed that the nanoparticles successfully attached to the photoreceptors, which in turn responded to infrared light by producing electrical signals and activating the visual-processing areas of the brain. The team conducted experiments to show that the mice did actually detect and respond to infrared light.
Keyword: Vision
Link ID: 25999 - Posted: 03.01.2019
Laura Sanders In the understory of Central American cloud forests, musical mice trill songs to one another. Now a study of the charismatic creatures reveals how their brains orchestrate these rapid-fire duets. The results, published in the March 1 Science, show that the brains of singing mice split up the musical work. One brain system directs the patterns of notes that make up songs, while another coordinates duets with another mouse, which are carried out with split-second precision. The study suggests that “a quirky animal from the cloud forest of Costa Rica could give us a brand new insight,” into the rapid give-and-take in people’s conversations, says study coauthor Michael Long, a neuroscientist at New York University’s School of Medicine. Quirks abound in these mice, known as Alston’s singing mice (Scotinomys teguina). Like famous singers with extreme green room demands, these mice are “kind of divas,” Long says, requiring larger terrariums, exercise equipment and a very special diet. In the lab, standard mouse chow doesn’t cut it; instead, singing mice feast on fresh meal worm, dry cat food and fresh fruits and berries, says Bret Pasch. The biologist at Northern Arizona University in Flagstaff has studied these singing mice for years but wasn’t involved in this study. The mice are also, of course, loud. “They’re very vocal,” particularly in the confines of a lab, Pasch says. “Once an animal calls, it’s like a symphony that goes off,” with repeating calls. In the wild, these duets are thought to attract mates and stake out territory. |© Society for Science & the Public 2000 - 2019.
Keyword: Animal Communication; Sexual Behavior
Link ID: 25998 - Posted: 03.01.2019


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