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By Carl Zimmer SAN DIEGO — Two hundred and fifty miles over Alysson Muotri’s head, a thousand tiny spheres of brain cells were sailing through space. The clusters, called brain organoids, had been grown a few weeks earlier in the biologist’s lab here at the University of California, San Diego. He and his colleagues altered human skin cells into stem cells, then coaxed them to develop as brain cells do in an embryo. The organoids grew into balls about the size of a pinhead, each containing hundreds of thousands of cells in a variety of types, each type producing the same chemicals and electrical signals as those cells do in our own brains. In July, NASA packed the organoids aboard a rocket and sent them to the International Space Station to see how they develop in zero gravity. Now the organoids were stowed inside a metal box, fed by bags of nutritious broth. “I think they are replicating like crazy at this stage, and so we’re going to have bigger organoids,” Dr. Muotri said in a recent interview in his office overlooking the Pacific. What, exactly, are they growing into? That’s a question that has scientists and philosophers alike scratching their heads. On Thursday, Dr. Muotri and his colleagues reported that they have recorded simple brain waves in these organoids. In mature human brains, such waves are produced by widespread networks of neurons firing in synchrony. Particular wave patterns are linked to particular forms of brain activity, like retrieving memories and dreaming. As the organoids mature, the researchers also found, the waves change in ways that resemble the changes in the developing brains of premature babies. “It’s pretty amazing,” said Giorgia Quadrato, a neurobiologist at the University of Southern California who was not involved in the new study. “No one really knew if that was possible.” © 2019 The New York Times Company
Keyword: Development of the Brain
Link ID: 26569 - Posted: 09.04.2019
Nicoletta Lanese Federal health officials issued a warning yesterday (August 29), advising pregnant mothers and teens not to use marijuana. The surgeon general cautioned that marijuana use has adverse effects on brain development in teens and fetuses and has also been linked to later alcohol and opioid addiction, according to STAT News. At a press conference, officials reported that President Donald Trump has donated $100,000 toward a digital campaign to raise awareness of the risks of marijuana use in pregnancy and adolescence, according to the Associated Press. “No amount of marijuana use during pregnancy or adolescence is safe,” says Surgeon General Jerome Adams at a press conference, reports STAT News. “As I like to say, this ain’t your mother’s marijuana,” adds Department of Health and Human Services (HHS) Secretary Alex Azar. Between 1995 and 2014, the concentration of the psychoactive compound THC in marijuana plants tripled, according to the government advisory. “The higher the THC delivery, the higher the risk,” says Adams to NPR. Meanwhile, new delivery products such as vapes, waxes, and liquids make the drug easier to consume. See “Prenatal Exposure to Cannabis Affects the Developing Brain” Medicinal marijuana has been legalized in 33 states and the District of Columbia, and 11 states have legalized the drug’s recreational use, according to STAT News. However, no states allow recreational marijuana use by teens, and minors can only use medical marijuana with consent from a legal guardian and certification from a doctor, the AP reports. © 1986–2019 The Scientist.
Keyword: Drug Abuse; Development of the Brain
Link ID: 26568 - Posted: 09.04.2019
By James Gorman When the moon hits your eye like a big pizza pie, it may not be amore at all, but a ghostly white barn owl about to kill and eat you. If you’re a vole, that is. Voles are a favorite meal for barn owls, which come in two shades, reddish brown and white. When the moon is new, both have equal success hunting for their young, snagging about five voles in a night. But when the moon is full and bright, the reddish owls do poorly, dropping to three a night. Barn owls with white faces and breasts do as well as ever, however, even though they should be more easily spotted than their reddish relatives when the lunar light reflects off their feathers. They may well be more easily seen, but it doesn’t matter because of the behavior of their prey. Voles have two responses to owl sightings. They freeze, and hope the owl doesn’t see them. Or they run. But when they see a white owl in bright moonlight, the terrified rodents act like deer caught in headlights and freeze up to five seconds longer than they do for a reddish brown barn owl. This is not what Luis M. San-Jose and Alexandre Roulin, both of the University of Lausanne in Switzerland, expected. They and other scientists reported in Nature Ecology and Evolution on Monday that they expected the white owls to do worse. “The study is a fascinating new look at an old question: How does moonlight affect the plumage of nocturnal predators?” said Richard Prum, an evolutionary biologist and ornithologist at Yale University, who has studied how coloration evolved in birds. He added that authors used “a remarkable array of technologies and methods” to investigate the effect of the variation. Dr. San-Jose, who researches animal coloration, said that there has been little study of color in nocturnal animals in the past, but that has begun to change, producing many surprises in recent years. “Many nocturnal species actually see color at night,” he said. Voles probably don’t. For them, the owls probably appear in shades of gray. Still, the lighter the shade, the more visible the owl. © 2019 The New York Times Company
Keyword: Vision; Biological Rhythms
Link ID: 26567 - Posted: 09.03.2019
By Laura Sanders Dog breeders have been shaping the way the animals look and behave for centuries. That meddling in canine evolution has sculpted dogs’ brains, too. A brain-scanning study of 62 purebred dogs representing 33 breeds reveals that dog brains are not all alike — offering a starting point for understanding how brain anatomy relates to behavior. Different breeds had different shapes of various brain regions, distinctions that were not simply the result of head shape or the size of the dogs’ brains or bodies, researchers report September 2 in the Journal of Neuroscience. Through selective breeding, “we have been systematically shaping the brains of another species,” Erin Hecht, an evolutionary neuroscientist at Harvard University, and colleagues conclude. The MRI scans were taken of dogs with normal brain anatomy at the Veterinary Teaching Hospital at the University of Georgia at Athens. While the study wasn’t designed to directly link brain shape to behavior, the results offer some hints. Researchers identified groups of brain areas, such as smell and taste regions, that showed the most variability between breeds. Those groups are involved in specialized behaviors that often serve humans, such as hunting by smell, guarding and providing companionship to people, earlier studies have suggested. © Society for Science & the Public 2000–2019
Keyword: Evolution
Link ID: 26566 - Posted: 09.03.2019
By Joanna Broder It had been two agonizing years of not knowing what was wrong with their baby who, since birth, had frequent spells of eye flickering, uncontrollable muscle contractions, pain and temporary paralysis. Simon and Nina Frost had spared no expense, taking Annabel to all the best neurologists around the country. Finally a potential diagnosis emerged: alternating hemiplegia of childhood, an ultrarare genetic disorder. The Frosts’ initial excitement at having answers quickly waned, however. They learned that, for many of the 900 or so children in the world affected by AHC, mutations in one of the genes that code for a subunit of the body’s critical sodium potassium pump interferes with the body’s ability to repeatedly fire nerve cells. In addition to Annabel’s other symptoms, difficulty breathing, choking and falling are common. They also learned that there is no effective treatment or cure, that any one of Annabel’s episodes has the potential to lead to permanent brain damage or death, and that it is hard to get information about the disease. Foundations dedicated to AHC informally recommend only four physicians in the United States as knowledgeable enough about the disorder to see patients. Of those who are closest to the Frosts, who live in Northwest D.C., one was too busy to see Annabel. There was a two-month wait to see the other one. The foundations themselves didn’t have many answers to the Frosts’ initial questions about life expectancy or what course Annabel’s disease might take. The Frosts discovered that relatively few scientists and clinicians study AHC, and their focus seemed to be basic research and not developing a therapy. © 1996-2019 The Washington Post
Keyword: Movement Disorders
Link ID: 26565 - Posted: 09.03.2019
David Cyranoski A Japanese woman in her forties has become the first person in the world to have her cornea repaired using reprogrammed stem cells. At a press conference on 29 August, ophthalmologist Kohji Nishida from Osaka University, Japan, said the woman has a disease in which the stem cells that repair the cornea, a transparent layer that covers and protects the eye, are lost. The condition makes vision blurry and can lead to blindness. How iPS cells changed the world To treat the woman, Nishida says his team created sheets of corneal cells from induced pluripotent stem (iPS) cells. These are made by reprogramming adult skin cells from a donor into an embryonic-like state from which they can transform into other cell types, such as corneal cells. Nishida said that the woman’s cornea remained clear and her vision had improved since the transplant a month ago. Currently people with damaged or diseased corneas are generally treated using tissue from donors who have died, but there is a long waiting list for such tissue in Japan. Japan has been ahead of the curve in approving the clinical use of iPS cells, which were discovered by stem-cell biologist Shinya Yamanaka at Kyoto University, who won a Nobel prize for the work. Japanese physicians have also used iPS cells to treat spinal cord injury, Parkinson’s disease and another eye disease. © 2019 Springer Nature Publishing AG
Keyword: Vision; Stem Cells
Link ID: 26564 - Posted: 09.03.2019
By Michelle Roberts Health editor, BBC News online Experts are warning about the risks of extreme fussy eating after a teenager developed permanent sight loss after living on a diet of chips and crisps. Eye doctors in Bristol cared for the 17-year-old after his vision had deteriorated to the point of blindness. Since leaving primary school, the teen had been eating only French fries, Pringles and white bread, as well as an occasional slice of ham or a sausage. Tests revealed he had severe vitamin deficiencies and malnutrition damage. Extreme picky eater The adolescent, who cannot be named, had seen his GP at the age of 14 because he had been feeling tired and unwell. At that time he was diagnosed with vitamin B12 deficiency and put on supplements, but he did not stick with the treatment or improve his poor diet. Three years later, he was taken to the Bristol Eye Hospital because of progressive sight loss, Annals of Internal Medicine journal reports. Dr Denize Atan, who treated him at the hospital, said: "His diet was essentially a portion of chips from the local fish and chip shop every day. He also used to snack on crisps - Pringles - and sometimes slices of white bread and occasional slices of ham, and not really any fruit and vegetables. "He explained this as an aversion to certain textures of food that he really could not tolerate, and so chips and crisps were really the only types of food that he wanted and felt that he could eat." Dr Atan and her colleagues rechecked the young man's vitamin levels and found he was low in B12 as well as some other important vitamins and minerals - copper, selenium and vitamin D. He was not over or underweight, but was severely malnourished from his eating disorder - avoidant-restrictive food intake disorder. "He had lost minerals from his bone, which was really quite shocking for a boy of his age." He was put on vitamin supplements and referred to a dietitian and a specialist mental health team. In terms of his sight loss, he met the criteria for being registered blind. "He had blind spots right in the middle of his vision," said Dr Atan. "That means he can't drive and would find it really difficult to read, watch TV or discern faces. © 2019 BBC.
Keyword: Vision
Link ID: 26563 - Posted: 09.03.2019
By Jane E. Brody Tiffany Martinez was a 17-year-old college freshman when she began hearing voices, seeing shadowy figures and experiencing troubling, intrusive thoughts. Her friends at the University of Southern Maine, where she was majoring in psychology, noticed that she was acting strangely and urged her to get help. They most likely saved her from a crippling mental health crisis, prevented the derailment of her education and ultimately enabled her to become a psychiatric nurse practitioner who can help other young people avert a psychiatric crisis. Tiffany’s friends convinced her to go to the university’s health center, where she met with a nurse who had just attended an educational seminar about identifying the early signs of mental illness in young adults. The nurse suspected that Tiffany was at risk of developing a psychotic episode and referred her to the Portland Identification and Early Referral, or PIER, program at the Maine Health Center. The program was developed in 2001 by Dr. William R. McFarlane, a psychiatrist who suspected that if early intervention could reverse the course of diseases like cancer and heart disease, it should do likewise for psychosis. Despite conventional wisdom suggesting otherwise, he persevered in the belief that an impending psychotic break could be identified and prevented if it was recognized early and appropriate steps taken to head it off. Tiffany, who said her father had schizophrenia, was an early beneficiary of his vision and has become a poster child for what can be done to prevent a devastating, costly illness that afflicts up to 3 percent of the population. After the PIER program was extended to 25 school districts in and around Portland, there was a 35 percent decline in new hospital admissions for psychotic symptoms, Dr. McFarlane said. © 2019 The New York Times Company
Keyword: Schizophrenia
Link ID: 26562 - Posted: 09.02.2019
By Sheila Kaplan and Matt Richtel An 18-year-old showed up in a Long Island emergency room, gasping for breath, vomiting and dizzy. When a doctor asked if the teenager had been vaping, he said no. The patient’s older brother, a police officer, was suspicious. He rummaged through the youth’s room and found hidden vials of marijuana for vaping. “I don’t know where he purchased it. He doesn’t know,” said Dr. Melodi Pirzada, chief pediatric pulmonologist at NYU Winthrop Hospital in Mineola, N.Y., who treated the young man. “Luckily, he survived.” Dr. Pirzada is one of the many physicians across the country treating patients — now totaling more than 215 — with mysterious and life-threatening vaping-related illnesses this summer. The outbreak is “becoming an epidemic,” she said. “Something is very wrong.” Patients, mostly otherwise healthy and in their late teens and 20s, are showing up with severe shortness of breath, often after suffering for several days with vomiting, fever and fatigue. Some have wound up in the intensive care unit or on a ventilator for weeks. Treatment has been complicated by patients’ lack of knowledge — and sometimes outright denial — about the actual substances they might have used or inhaled. Health investigators are now trying to determine whether a particular toxin or substance has sneaked into the supply of vaping products, whether some people reused cartridges containing contaminants, or whether the risk stems from a broader behavior, like heavy e-cigarette use, vaping marijuana or a combination. On Friday, the Centers for Disease Control and Prevention issued a warning to teenagers and other consumers, telling them to stop buying bootleg and street cannabis and e-cigarette products, and to stop modifying devices to vape adulterated substances. © 2019 The New York Times Company
Keyword: Drug Abuse
Link ID: 26561 - Posted: 09.02.2019
By Roni Caryn Rabin Every year, hundreds of thousands of obese Americans undergo weight-loss surgery in a last-ditch effort to shed pounds and control their Type 2 diabetes. Now a new study suggests that bariatric surgery may also have other significant health benefits, cutting the overall risk of serious cardiovascular events and premature death by almost half. The study, published in the medical journal JAMA on Monday, is not definitive. Though it compared the long-term outcomes of about 2,300 bariatric surgery patients with some 11,500 closely matched patients who had not undergone surgery, it was an observational study, not a randomized controlled trial of the kind considered the gold standard in medicine. But the findings were so striking that an editorial accompanying the paper suggested that weight-loss surgery, rather than medications, should be the preferred treatment for Type 2 diabetes in certain patients with obesity. “The new information here is the ability of bariatric surgery to control macrovascular events like strokes, heart attacks, heart failure and kidney disease,” not just improve weight and diabetes control, said Dr. Edward H. Livingston, the editorial’s author. “That’s a big deal.” A bariatric surgeon himself, Dr. Livingston said he had long been known as a “curmudgeon” who was reluctant to make claims about the long-term health benefits of weight-loss surgery. “This is the first time I’ve come out publicly saying, ‘You know what, this may be a better way to go,’” he said, adding that insurers should cover the procedure more liberally. © 2019 The New York Times Company
Keyword: Obesity
Link ID: 26560 - Posted: 09.02.2019
By Francie Diep For as long as Brad Johnson can remember, he has never been able to sleep more than six hours a night. Most nights, he sleeps even less. Mr. Johnson, 63, always wakes without an alarm clock, feeling rested and ready for the day. “If you paid me $100,000 to sleep eight hours tonight, I couldn’t do it,” he said. He’s not the only one in his family like this. Two of his seven siblings also are natural short sleepers. He suspects that their father was one, too. At least 15 years ago, he said, one of his brothers reached out to a sleep doctor at the University of Utah, who took an interest in the family, collecting blood samples and conducting interviews at a reunion. Ultimately, researchers identified six members of Mr. Johnson’s extended family, men and women, who get by on an average of less than six hours of sleep a night, much less than the eight and a half hours that people typically need to function at their best. Researchers wondered whether there was something about their genetics that might help explain how sleep works for the rest of us. “The problem is, we know so little about what sleep really is and what it’s for,” said Dr. Louis Ptacek, a neurologist at the University of California, San Francisco. “As we identify more and more genes, hopefully this will outline a system, or systems, that are critically important to sleep.” Dr. Ptacek and his colleagues identified a gene mutation that shows up in every naturally short-sleeping member of Mr. Johnson’s family. When the scientists took the mutated version of the gene and put it in lab mice, they found that the mice needed about an hour less sleep a day than their siblings that did not have the gene. The researchers, who published their findings in the journal Neuron on Wednesday, determined that the gene, ADRB1, has a direct bearing on how much sleep people need. Their findings, they said, could be used to design therapies to help people with sleep problems. © 2019 The New York Times Company
Keyword: Sleep; Genes & Behavior
Link ID: 26559 - Posted: 08.31.2019
By Joanne Chen The only thing worse than feeling completely wired at 11 p.m. when you’re ready for sleep is being stark awake at 3 a.m. Blissfully passing out at an appropriate bedtime is cold comfort when the brain wakes up too soon and refuses to take advantage of those eight full hours. I toss and turn and scrunch up my pillow every which way, exasperated and fixated on the impending doom of the alarm clock set to go off at 6 a.m. About half of all insomnia sufferers experience this middle-of-the-night “sleep-maintenance” insomnia, either by itself or along with the “sleep-onset” sort, trouble falling asleep in the first place, said Jennifer Martin, Ph.D., a professor of medicine at the University of California at Los Angeles. If, after 20 minutes, you’re still up, the American Academy of Sleep Medicine recommends stepping out of the bedroom and doing some reading or other quiet activity. But I didn’t realize that it’s actually a last-resort tactic. “Get up only when you’re so upset you can’t fall asleep anyway,” said Dr. Martin, an insomnia specialist. In fact, some of the best first-line strategies are pursued (more or less) lying down. The next time you find yourself staring at the ceiling at 3 a.m., try these six things: Remain in bed For you to fall asleep, your heart rate needs to slow down, said Michael Breus, Ph.D., a Los Angeles area clinical sleep psychologist. But when you get up, you elevate it. So my impulse to use the bathroom just because I’m awake only makes matters worse. “Do that only if you need to,” said Breus, who is also the author of “The Power of When.” © 2019 The New York Times Company
Keyword: Sleep
Link ID: 26558 - Posted: 08.31.2019
By Tam Hunt How do you know your dog is conscious? Well, she wags her tail when she’s happy, bounces around like a young human child when excited, and yawns when sleepy— among many other examples of behaviors that convince us (most of us, at least) that dogs are quite conscious in ways that are similar to, but not the same as, human consciousness. Most of us are okay attributing emotions, desires, pain and pleasure—which is what I mean by consciousness in this context—to dogs and many other pets. What about further down the chain. Is a mouse conscious? We can apply similar tests for “behavioral correlates of consciousness” like those I’ve just mentioned, but, for some of us, the mice behaviors observed will be considerably less convincing than for dogs in terms of there being an inner life for the average mouse. Advertisement What about an ant? What behaviors do ants engage in that might make us think an individual ant is at least a little bit conscious? Or is it not conscious at all? Let me now turn the questions around: how do I know you, my dear reader, are conscious? If we met, I’d probably introduce myself and hear you say your name and respond to my questions and various small talk. You might be happy to meet me and smile or shake my hand vigorously. Or you might get a little anxious at meeting someone new and behave awkwardly. All of these behaviors would convince me that you are in fact conscious much like I am, and not just faking it! Now here’s the broader question? How can we know anybody or any animal or any thing is actually conscious and not just faking it? The nature of consciousness makes it by necessity a wholly private affair. The only consciousness I can know with certainty is my own. Everything else is inference. © 2019 Scientific American
Keyword: Consciousness
Link ID: 26557 - Posted: 08.31.2019
By Laura Sanders It’s baby’s first brain wave, sort of. As lentil-sized clusters of nerve cells grow in a lab dish, they begin to fire off rhythmic electrical signals. These oscillations share some features with those found in the brains of developing human babies, researchers report October 3 in Cell Stem Cell. Three-dimensional spheres of human brain cells, called cerebral organoids, are extremely simplistic models of the human brain. Still, these easy-to-obtain organoids may offer a better way to study how a brain is made, and how that process can go wrong (SN: 2/20/18). “The field is white-hot,” with fast progress in both making and understanding brain organoids, says John Huguenard, a neuroscientist at Stanford University not involved in the study. Finding this sort of coordinated electrical activity in organoids’ nerve cells, or neurons, is a first, he says. “The neurons are growing up and becoming mature enough where they can not only start to behave like neurons and fire individually, but now they can be coordinated.” For the study, researchers coaxed stem cells into forming some of the neurons that make up the outer layer of the brain. These cortical organoids grew in lab dishes that held arrays of electrodes printed along the bottom, allowing the scientists to monitor electrical activity as the organoids developed. © Society for Science & the Public 2000–2019
Keyword: Development of the Brain
Link ID: 26556 - Posted: 08.30.2019
By Pam Belluck How do genes influence our sexuality? The question has long been fraught with controversy. An ambitious new study — the largest ever to analyze the genetics of same-sex sexual behavior — found that genetics does play a role, responsible for perhaps a third of the influence on whether someone has same-sex sex. The influence comes not from one gene but many, each with a tiny effect — and the rest of the explanation includes social or environmental factors — making it impossible to use genes to predict someone’s sexuality. “I hope that the science can be used to educate people a little bit more about how natural and normal same-sex behavior is,” said Benjamin Neale, a geneticist at the Broad Institute of M.I.T. and Harvard and one of the lead researchers on the international team. “It’s written into our genes and it’s part of our environment. This is part of our species and it’s part of who we are.” The study of nearly half a million people, funded by the National Institutes of Health and other agencies, found differences in the genetic details of same-sex behavior in men and women. The research also suggests the genetics of same-sex sexual behavior shares some correlation with genes involved in some mental health issues and personality traits — although the authors said that overlap could simply reflect the stress of enduring societal prejudice. Even before its publication Thursday in the journal Science, the study has generated debate and concern, including within the renowned Broad Institute itself. Several scientists who are part of the L.G.B.T.Q. community there said they were worried the findings could give ammunition to people who seek to use science to bolster biases and discrimination against gay people. One concern is that evidence that genes influence same-sex behavior could cause anti-gay activists to call for gene editing or embryo selection, even if that would be technically impossible. Another fear is that evidence that genes play only a partial role could embolden people who insist being gay is a choice and who advocate tactics like conversion therapy. © 2019 The New York Times Company
Keyword: Sexual Behavior; Genes & Behavior
Link ID: 26555 - Posted: 08.30.2019
By Lindsey Bever There is no one gene that determines a person’s sexual orientation, but genetics — along with environment — play a part in shaping sexuality, a massive new study shows. Researchers analyzed DNA from hundreds of thousands of people and found that there are a handful of genes clearly connected with same-sex sexual behavior. The researchers say that, although variations in these genes cannot predict whether a person is gay, these variants may partly influence sexual behavior. Andrea Ganna, lead author and European Molecular Biology Laboratory group leader at the Institute of Molecular Medicine in Finland, said the research reinforces the understanding that same-sex sexual behavior is simply “a natural part of our diversity as a species.” The new study, published Thursday in the journal Science, is not the first to explore the link between genetics and same-sex behavior, but it is the largest of its kind, and experts say it provides one of the clearest pictures of genes and sexuality. Ganna, who is also an instructor at Massachusetts General and Harvard, and an international team of scientists examined data from more than 470,000 people in the United States and the United Kingdom to see whether certain genetic markers in their DNA were linked to their sexual behavior. Specifically, the researchers used data from the UK Biobank study and from the private genomics company 23andMe, which included their DNA data and responses to questions about sexual behaviors, sexual attraction and sexual identity. More than 26,000 participants reported at least one sexual encounter with someone of the same sex. Earlier studies, the researchers said, weren’t large enough to reveal the subtle effects of individual genes. © 1996-2019 The Washington Post
Keyword: Sexual Behavior; Genes & Behavior
Link ID: 26554 - Posted: 08.30.2019
By Stephen L. Macknik In normal vision, light falls on the retinas inside the eyes, and is immediately transduced into electrochemical signals before being uploaded to the brain through the optic nerves. So you do not see light itself, but the brain's interpretation of electrochemical signals in the visual parts of the brain. It follows that, if your eyes do not work, but your brain is stimulated just so, your visual neurons will activate (and you will be able to see) just the same as if your eyes were in perfect condition. Sounds easy, but can we do that? Building on decades of research in visual neuroscience, my lab, in collaboration with Susana Martinez-Conde’s, has now conducted some of the studies that validate this idea, completing some of the most important preliminary steps towards a new kind of visual prosthetic. Francis Collins, the Director of the National Institutes of Health, has just posted a blog that highlights our approach. He took notice of our work when we first presented it at this year's meeting for the Principal Investigators of the BRAIN Initiative—the NIH led government funding initiative meant to spur research along on topics like brain implants. The BRAIN Initiative funds several agencies including the NIH, including the National Science Foundation, who kindly funded the grant driving our research thus far. Our starting premise is that vision is fundamentally a thumbnail sketch. Even if 99.9% of your retina works fine, but the central 1/1000th of your visual field is broken, you will be legally blind. That central 0.1% of your visual field is about the same size as your thumbnail held up at arm's length. Because that central 0.1% of the retina is the visual sweet spot, it is the place where the visual magic happens. In fact, much of the remaining 99.9% of the retina’s main job is to help you detect where to move your eyes next. This means that we need to restore central vision in the blind, or we are not really restoring functional vision at all. © 2019 Scientific American
Keyword: Vision; Robotics
Link ID: 26553 - Posted: 08.29.2019
By Annie Roth Kalutas live fast and die young — or, at least, the males do. Male kalutas, small mouselike marsupials found in the arid regions of Northwestern Australia, are semelparous, meaning that shortly after they mate, they drop dead. This extreme reproductive strategy is rare in the animal kingdom. Only a few dozen species are known to reproduce in this fashion, and most of them are invertebrates. Kalutas are dasyurids, the only group of mammals known to contain semelparous species. Only around a fifth of the species in this group of carnivorous marsupials — which includes Tasmanian devils, quolls and pouched mice — are semelparous and, until recently, scientists were not sure if kalutas were among them. Now there is no doubt that, for male kalutas, sex is suicide. In a study, published in April in the Journal of Zoology, researchers from the University of Western Australia and the University of Queensland confirmed that kalutas exhibit what is known as obligate male semelparity. “We found that males only mate during one highly synchronized breeding season and then they all die,” said Genevieve Hayes, a vertebrate ecologist and the lead author of the study. Dr. Hayes and her colleagues monitored the breeding habits of a population of kalutas in Millstream Chichester National Park in Western Australia during the 2013 and 2014 breeding seasons. In both seasons, the researchers observed a complete die-off of males. Although male kalutas have exhibited semelparity in captivity, this was the first time it had been seen in the wild. Kalutas evolved independently of other semelparous dasyurids, so the confirmation that male kalutas die after mating suggests that this unorthodox reproductive strategy has evolved not once, but twice in dasyurids.
Keyword: Sexual Behavior
Link ID: 26552 - Posted: 08.29.2019
Colin Barras An ancient face is shedding new light on our earliest ancestors. Archaeologists have discovered a 3.8-million-year-old hominin skull in Ethiopia — a rare and remarkably complete specimen that could change what we know about the origins of one of humanity’s most famous ancestors, Lucy. The researchers who discovered the skull say it belongs to a species called Australopithecus anamensis, and it gives scientists their first good look at the face of this hominin. This species was thought to precede Lucy’s species, Australopithecus afarensis. But features of the latest find now suggest that A. anamensis shared the prehistoric Ethiopian landscape with Lucy’s species for at least 100,000 years, the researchers say. This hints that the early hominin evolutionary tree was more complicated than scientists had thought — but other researchers say the evidence isn’t yet conclusive. “Fossil hominin crania are exceptionally rare treasures,” says Carol Ward, a palaeoanthropologist at the University of Missouri in Columbia who wasn’t involved in the analysis. “This to me is the specimen we have been waiting for.” An analysis of the skull is published in Nature1 . Exceptionally preserved A. afarensis lived in East Africa between about 4 million and 3 million years ago. It is important to the understanding of human evolution because it might have been the ape-like species from which the ‘true’ human genus, Homo, evolved about 2.8 million years ago. Over the past few decades, researchers have discovered dozens of fragments of australopithecine fossils in Ethiopia and Kenya that date back more than 4 million years. Most researchers think these older fossils belong to the earlier species, A. anamensis. It’s generally thought that A. anamensis gradually morphed into A. afarensis, implying that the two species never coexisted.
Keyword: Evolution
Link ID: 26551 - Posted: 08.29.2019
By Kelly Servick Try to cheat your body out of a full night’s sleep and you’ll suffer the consequences … unless you happen to carry a rare genetic mutation. According to a new study, some people who function normally on just 6 hours of sleep harbor an altered version of a particular gene, the second gene so far linked to short sleep. In 2009, researchers described a mother and daughter with a mutation in a gene called DEC2 who felt well rested after with about 6 hours of sleep per night. (Many experts recommend that adults get at least 7 hours.) DEC2 codes for a protein that helps turn off the expression of other genes, including the gene for the hormone orexin, known to regulate wakefulness. Now, by studying another family containing naturally short sleepers, the scientists have identified another mutation, which they estimate is present in roughly four of every 100,000 people. Mice genetically engineered to have this mutation slept, on average, 1 hour less per day than controls, the researchers report online today in Neuron. The mutation affects a gene called ADRB1, which encodes a receptor for the common neural signaling molecule noradrenaline. In a part of the mouse brainstem, cells studded with this receptor were active during wakefulness and quiet during deep (non–rapid eye movement) sleep, the researchers found. And stimulating these ADRB1-bearing brainstem neurons could immediately awaken them from deep sleep. They propose that the mutation renders these wake-promoting brainstem neurons more active, which could explain why its human carriers are content to sleep less. © 2019 American Association for the Advancement of Science.
Keyword: Sleep; Genes & Behavior
Link ID: 26550 - Posted: 08.29.2019


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