By Alejandro Portilla Navarro Dawn breaks in San Jose, the capital of Costa Rica. The city is still asleep, but the early risers are greeted by a beautiful symphony: Hummingbirds, corn-eaters, yigüirros (clay-colored thrushes), yellow-breasted grosbeaks, blue tanagers, house wrens, warblers and other birds announce that a new day has arrived. Soon the incessant noise of vehicles and their horns, construction, street vendors and more take over, shaping the soundscape of the frenetic routine of hundreds of thousands of people who travel and live in this city. Then, the birds’ songs will slip into the background. “The act of birdsong has two main functions in males: It is to attract females and also to defend their territory from other males,” says Luis Andrés Sandoval Vargas, an ornithologist at the University of Costa Rica. For females in the tropics, he adds, the primary role of their song is to defend territory. Thus, in order to communicate in cities, to keep their territory safe and find mates, birds must find ways to counteract the effects of anthropogenic noise — that is, the noise produced by humans. “The main effect of urban development on song is that many birds sing at higher frequencies,” says Sandoval Vargas. Studies over the past 15 years have found, for example, that blackbirds (Turdus merula), great tits (Parus major) and rufous-collared sparrows (Zonotrichia capensis) sing at higher pitches, with higher minimum frequencies, in urban environments than in rural ones. But the birds’ response to anthropogenic noise may be more complex than that, as Sandoval Vargas found when studying house wrens (Troglodytes aedon). House wrens are small, brown birds — about 10 centimeters tall and weighing 12 grams — that feed on insects and tend to live near humans. In Costa Rica, they are found almost everywhere, but are especially abundant in the cities. “Males sing almost year-round and sing for many hours during the day, and much of their behavior is mediated by vocalizations,” explains Sandoval Vargas. But what makes them ideal for studying adaptations to urban environments is that most of the components of their song are within the same frequency range as the noise that we humans produce. © 2022 Annual Reviews

Keyword: Animal Communication; Evolution
Link ID: 28553 - Posted: 11.16.2022

By Jim Davies Living for the moment gets a bad rap. If you’re smart, people say, you should work toward a good future, sacrificing fun and pleasure in the present. Yet there are good reasons to discount the future, which is why economists tend to do it when making predictions. Would you rather find $5 when you’re in elementary school, or in your second marriage? People tend to get richer as they age. Five dollars simply means more to you when you’re 9 than when you’re 49. Also, the future is uncertain. We can’t always trust there’ll be one. It’s likely some kids in Walter Mischel’s famous “marshmallow experiment”—which asked kids to wait to eat a marshmallow to get another one—didn’t actually believe that the experimenter would come through with the second marshmallow, and so ate the first marshmallow right away. Saving for retirement makes no sense if in five years a massive meteor cuts human civilization short. Economists call this the “catastrophe” or “hazard” rate. For Sangil “Arthur” Lee, a psychologist at the University of California, Berkeley, where he’s a postdoc, a hazard rate makes sense from an evolutionary perspective. “You might not survive until next winter, so there is some inherent trade off that you need to make, which is not only specific for humans, but also for animals,” he said. While an undergraduate, Lee experimented with delay-discounting tasks using pigeons. The pigeons would peck one button to get a small amount of pellets now, or peck a different button to get large amounts of pellets later. “What we know,” Lee said, “is that across pigeons, monkeys, rats, and various animals, they also discount future rewards in pretty much a similar way that humans do, which is this sort of hyperbolic fashion.” We discount future rewards by a lot very quickly, more so than we would be if discounting the future exponentially, but the hyperbolic discount rate eases after a bit. What makes us discount the future? Lee, in a new study with his colleagues, pins it at least partly on our powers of imagination.1 When we think about what hasn’t yet happened, it tends to be abstract. Things right now, on the other hand, we think of in more tangible terms. Several behavioral studies have supported the idea that what we cannot clearly imagine, we value less. © 2022 NautilusThink Inc, All rights reserved.

Keyword: Attention
Link ID: 28552 - Posted: 11.16.2022

By Christina Jewett By 2015, Philips Respironics knew its breathing devices had a problem: Foam inside the CPAP machines, which help people with sleep apnea breathe at night, was breaking off into black flecks and blowing into the mouths and noses of users. The company did nothing at the time. Years went by as complaints mounted, and the company made cursory efforts to examine the problem, according to an investigation conducted later by the Food and Drug Administration. But it was not until April of last year, the company has claimed, that it realized the flaking foam contained potentially cancer-causing particles, setting off the largest and most disruptive medical device recall in more than a decade. Nearly a year and a half after the recall that involved more than five million devices worldwide, millions of American have endured a long wait for a device. Many have been forced to find alternative methods to ensure they can breathe at night without becoming deprived of oxygen or risking a heart attack. Others have been outraged by unexpected illness, suspicious that a device meant to help them actually caused harm. The U.S. Justice Department is now negotiating the terms of a consent decree with Philips, underscoring the deep concern about what the company knew — or should have known — before millions of people received devices that many believe caused devastating illnesses. A decree would likely require the company to document the steps it would take to prevent such a failure in the future. Doug Shiffler, a retired tech executive in Utah, is one of hundreds of people suing the company. His wife began using the device in 2018, when there were no public warnings of possible problems with the machines, and developed a persistent cough. By mid-2020, Joleen Shiffler was diagnosed with an aggressive lung cancer that baffled her doctors, although a direct link between her disease and the Philips device had not been established. Ms. Shiffler, 60, died within the year. “Why weren’t we informed that there was an issue?” Mr. Shiffler asked. If they had known, “I might be standing right beside Joleen instead of mourning her loss.” © 2022 The New York Times Company

Keyword: Sleep
Link ID: 28551 - Posted: 11.16.2022

Linda Geddes Science correspondent Lead exposure during childhood may lead to reduced cognitive abilities in later life, meaning people experience symptoms of dementia sooner, data suggest. The study, one of the first to investigate the decades-long consequences of lead poisoning, suggests countries could face an explosion of people seeking support for dementia as individuals who were exposed to high lead levels during early life progress into old age. “In the US, and I would imagine the UK, the prime years when children were exposed to the most lead was in the 1960s and 70s. That’s when the most leaded gasoline was getting used, lead paint was still common, and municipal water systems hadn’t done much to clean up their lead,” said Prof John Robert Warren at the University of Minnesota in Minneapolis, who was involved in the research. “Those children who are now in their 40s, 50s and early 60s, will soon be entering the time of life when cognitive impairment and dementia are really common. So there’s this coming wave, potentially, of problems for the people who were most exposed.” Although scientists have long known that children and adults who are exposed to lead have poorer cognitive and educational outcomes, few studies have investigated the longer-term consequences. Warren and his colleagues combined data from the US-based longitudinal Health and Retirement Study (HRS), which has followed the brain health of thousands of adults over several decades, with census records to pinpoint where 1,089 of these individuals lived as children. They also mapped the locations of towns and cities that used lead pipes and had acidic or alkaline water – a proxy for high lead exposure. The research, published in Science Advances, revealed that people who lived in cities with lead-contaminated water as children had worse baseline cognitive functioning – a measure of their ability to learn, process information, and reason – at age 72, compared with those who did not. The difference was equivalent to being roughly eight years older. © 2022 Guardian News & Media Limited

Keyword: Neurotoxins; Alzheimers
Link ID: 28550 - Posted: 11.13.2022

Emma Marris For the first time, octopuses have been spotted throwing things — at each other1. Octopuses are known for their solitary nature, but in Jervis Bay, Australia, the gloomy octopus (Octopus tetricus) lives at very high densities. A team of cephalopod researchers decided to film the creatures with underwater cameras to see whether — and how — they interact. Once the researchers pulled the cameras out of the water, they sat down to watch more than 20 hours of footage. “I call it octopus TV,” laughs co-author David Scheel, a behavioural ecologist at Alaska Pacific University in Anchorage. One behaviour stood out: instances in which the eight-limbed creatures gathered shells, silt or algae with their arms — and then hurled them away, propelling them with water jetted from their siphon. And although some of the time it seemed that they were just throwing away debris or food leftovers, it did sometimes appear that they were throwing things at each other. The team found clues that the octopuses were deliberately targeting one another. Throws that made contact with another octopus were relatively strong and often occurred when the thrower was displaying a uniform dark or medium body colour. Another clue: sometimes the octopuses on the receiving end ducked. Throws that made octo-contact were also more likely to be accomplished with a specific set of arms, and the projectile was more likely to be silt. “We weren’t able to try and assess what the reasons might be,” Scheel cautions. But throwing, he says, “might help these animals deal with the fact that there are so many octopuses around”. In other words, it is probably social. © 2022 Springer Nature Limited

Keyword: Evolution; Learning & Memory
Link ID: 28549 - Posted: 11.13.2022

Laurel Wamsley Perhaps the real law of the jungle is that it's good to have friends — especially those who know where to find the the free food. Case in point: It turns out chimpanzees and gorillas can be pals, evidently with advantages for all. That finding is from a new paper in the journal iScience that analyzes social interactions between the primate species over two decades at the Nouabalé-Ndoki Park in the Republic of Congo. Over that 20-year period, researchers saw gorillas follow the sound of chimps to a canopy full of ripe figs, and then co-feed at the same tree. They witnessed young individuals of both species playing and wrestling with each other – interactions that can foster their development. And when bands of the two species encountered each other, researchers saw gorillas and chimps scan the others and then approach the ones they knew. They even saw chimpanzees beating their chests – a behavior associated with gorillas. Researchers had theorized that associations between the species could perhaps be to avoid predators such as leopards or snakes. But the apes' behavior didn't show that to be a major factor in their interactions. "Predation is certainly a threat in this region, as we have cases in which chimpanzees have been killed by leopards," Washington University primatologist Crickette Sanz, who led the research, said in a news release. "However, the number of chimpanzees in daily subgroups remains relatively small, and gorillas within groups venture far from the silverback who is thought to be a protector from predation." Instead, better foraging seemed to be a key upside for both species – sometimes eating at the same tree, sometimes dining nearby on different foods. Not every interaction was warm and friendly. "Interspecific aggression was bidirectional and most frequently consisted of threats," the study notes – but it never rose to the level of lethal aggression that has occurred between chimps and gorillas in Gabon. © 2022 npr

Keyword: Evolution; Learning & Memory
Link ID: 28548 - Posted: 11.13.2022

Hannah Devlin Science correspondent Music makes you lose control, Missy Elliott once sang on a hit that is almost impossible to hear without bopping along. Now scientists have discovered that rats also find rhythmic beats irresistible, showing how they instinctively move in time to music. This ability was previously thought to be uniquely human and scientists say the discovery provides insights into the animal mind and the origins of music and dance. “Rats displayed innate – that is, without any training or prior exposure to music – beat synchronisation,” said Dr Hirokazu Takahashi of the University of Tokyo. “Music exerts a strong appeal to the brain and has profound effects on emotion and cognition,” he added. While there have been previous demonstrations of animals dancing along to music – TikTok has a wealth of examples – the study is one of the first scientific investigations of the phenomenon. In the study, published in the journal Science Advances, 10 rats were fitted with wireless, miniature accelerometers to measure the slightest head movements. They were then played one-minute excerpts from Mozart’s Sonata for Two Pianos in D Major, at four different tempos: 75%, 100%, 200% and 400% of the original speed. Twenty human volunteers also participated. The scientists thought it possible that rats would prefer faster music as their bodies, including heartbeat, work at a faster pace. By contrast, the time constant of the brain is surprisingly similar across species. © 2022 Guardian News & Media Limited

Keyword: Hearing
Link ID: 28547 - Posted: 11.13.2022

Dyani Lewis Neuroscientists have identified the nerve cells responsible for helping paralysed people to walk again, opening up the possibility of targeted therapies that could benefit a wider range of people with spinal-cord injuries1. Severe spinal-cord injuries can disrupt the connection between the brain and the networks of nerve cells in the lower spine that control walking. In 2018, neuroscientist Grégoire Courtine at the Swiss Federal Institute of Technology in Lausanne and his colleagues showed that delivering electrical pulses to those lower-spine nerves — a technique known as epidural electrical stimulation (EES) — could, when combined with intensive training, get people with this kind of spinal-cord injury walking again2. All three participants in a trial went from having severe or complete motor paralysis and minimal sensation in their legs to being able to take steps on their own, or with a walker or crutches. Two other teams showed similar results that year3,4. Courtine’s team has now extended the work, showing that the system works in people who have lost all sensation in their legs. The group reports in Nature today that nine participants in the same trial — three of whom had complete paralysis and no sensation in their legs — regained the ability to walk after training paired with EES delivered by devices implanted in their spines. Five months into the trial, all participants could bear their own weight and take steps, using a walker for stability. Four no longer need the EES to be switched on to walk. This sustained recovery suggests that the stimulation triggers remodelling of the spinal neurons to bring the locomotion network back on line. “The amount of hope that it gives to people with spinal-cord injury is incredible,” says Marc Ruitenberg, a neurologist at the University of Queensland in Brisbane, Australia, who studies spinal-cord injury. © 2022 Springer Nature Limited

Keyword: Regeneration
Link ID: 28546 - Posted: 11.13.2022

By Gina Kolata What if an uncontrollable urge to rapidly eat large amounts of food is rooted in an impaired brain circuit? If that were the case, people who live with binge eating disorder — a psychiatric diagnosis — might be no more at fault for overeating than a patient with Parkinson’s disease is for their tremors. That question led doctors to try a new treatment different from anything ever attempted to help people with this common but underreported eating disorder. At least 3 percent of the population has it, said Dr. Casey Halpern, a neurosurgeon at the University of Pennsylvania. He and his colleagues decided to try deep brain stimulation, a method routinely used to quell tremors in patients with Parkinson’s. It involves placing electrodes in the brain to regulate aberrant signals. The wires, connected to the electrodes, are placed under the scalp, where they are invisible and unobtrusive. For the binge eating treatment, the device only stimulates neurons when the device detects a signal to start a binge. The pilot study, funded by the National Institutes of Health and published earlier this year in the journal Nature Medicine, involves two women and will be expanded in a few months to include four more people living with binge eating disorder who regained the weight they lost after bariatric surgery. Before the treatment can be approved by the Food and Drug Administration, researchers will need to rigorously test the method in at least 100 people in multiple medical centers. Such a study would take several years to complete. The two women whose devices were implanted a year ago will be followed for up to three years. They had the option to have their devices removed after 12 months, but both wanted to keep them because they no longer felt irresistible urges to binge. One of them, Robyn Baldwin, 58, of Citrus Heights, Calif., described herself as a “chunko child” who had “always been big.” She tried a wide range of diets. Once, she consumed only protein shakes for a month. In 2003 she had bariatric surgery, which usually involves altering the digestive system so that the stomach is smaller and food is more difficult to digest. It has enabled many people to lose weight when other methods failed. But for Ms. Baldwin, the weight she lost came back. © 2022 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28545 - Posted: 11.09.2022

by David Dobbs For 40 years, Leo Kanner and Hans Asperger have dominated virtually every story about the ‘pioneers of autism research.’ These two men published in 1943 and 1944, respectively, what were long accepted as the first descriptions of, as Kanner’s seminal paper claimed, ”children whose condition differs … markedly and uniquely from anything reported so far.” Both papers are absorbing, touching and authoritative. Both describe young people whose challenges defied the known diagnoses of the time but clearly fall into what we now call autism. And both offered a new diagnostic category for such people. Kanner’s 1943 paper, ”Autistic Disturbances of Affective Contact,” drew almost immediate attention. Within a year, he renamed the condition these children shared, dubbing it ‘early infantile autism,’ which soon became known as ‘autism’ or ‘Kanner’s syndrome.’ His articulation of the condition, based on observations of 11 children he and his associates treated in his Baltimore, Maryland, clinic, remained the standard well into the 1980s and involved three elements: Autism was a condition marked by: (1) emergence early in childhood, (2) deficits in communication and social interaction, and (3) restricted or repetitive behaviors and a desire for sameness. Even today, these three elements anchor the official diagnostic criteria in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, as well as the widely used International Classification of Diseases and Related Health Problems. Asperger’s 1944 paper, which presented case studies on four children he and his colleagues had seen in his clinic in Vienna, Austria, made its impact far more slowly. In fact, because Asperger published in German (and in a German journal in the middle of a war that had essentially halted transatlantic scholarly exchange), the paper went largely unnoticed outside Europe for decades. Asperger’s descriptions resembled Kanner’s in many ways, although he outlined a wider apparent range of intelligence and capabilities than Kanner did, with some of his study participants reaching prominence in their fields. Asperger coined the diagnostic term ‘autistic psychopathy.’ © 2022 Simons Foundation

Keyword: Autism
Link ID: 28544 - Posted: 11.09.2022

By Ken Belson AMSTERDAM — For the first time since 2016, one of the most influential groups guiding doctors, trainers and sports leagues on concussions met last month to decide, among other things, if it was time to recognize the causal relationship between repeated head hits and the degenerative brain disease known as C.T.E. Despite mounting evidence and a highly regarded U.S. government agency recently acknowledging the link, the group all but decided it was not. Leaders of the International Consensus Conference on Concussion in Sport, meeting in Amsterdam, signaled that it would continue its long practice of casting doubt on the connection between the ravages of head trauma and sports. C.T.E., or chronic traumatic encephalopathy, was first identified in boxers in 1928 and burst into prominence in 2005, when scientists published their posthumous diagnosis of the disease in the N.F.L. Hall of Fame center Mike Webster, creating an existential crisis for sports such as football and rugby that involve players hitting their heads thousands of times a year. Scientists have spent the past decade analyzing hundreds of brains from athletes and military veterans, and the variable evident in nearly every case of C.T.E. has been their exposure to repeated head trauma. Researchers have also established what they call a dose response between the severity of the C.T.E. and the number of years playing collision sports. After playing down an association between head injuries and brain damage for years, the N.F.L. in 2016 acknowledged that there was a link between football and degenerative brain disorders such as C.T.E. Just days before the conference in Amsterdam, the National Institutes of Health, the biggest funder of brain research in the United States, said that C.T.E. “is caused in part by repeated traumatic brain injuries.” But in one of the final sessions of the three-day conference, one of the leaders of the conference, a neuropsychologist who has received $1.5 million in research funding from the N.F.L., dismissed the work of scientists who have documented C.T.E. in hundreds of athletes and soldiers because he said their studies thus far did not account for other health variables, including heart disease, diabetes and substance abuse. © 2022 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 28543 - Posted: 11.09.2022

By Katherine Ellison News organizations were quick to trumpet the recent findings of a small study suggesting that “magic mushrooms” could be part of a breakthrough treatment for alcoholism. It’s no wonder. Every year, alcohol abuse kills more than 140,000 Americans and affects millions more, with a steep increase in deaths in recent years, according to data published by the Centers for Disease Control and Prevention on Nov. 4. But excitement about the psilocybin study also raises a question: Why aren’t there more medical treatments for such an obviously devastating problem? “There is a desperate need for new medications, and there are many good avenues that we’re pursuing,” said Dorit Ron, a neurology professor at the University of California at San Francisco Medical Center, who has been studying potential treatments that include rapamycin, a drug designed to help transplant patients tolerate new organs. But getting promising new medications into the hands of doctors and their patients has proved difficult, said George Koob, director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), adding “it doesn’t go for lack of trying.” Lack of awareness by doctors, funding decisions by the pharmaceutical industry and the stigma surrounding alcoholism have all held up progress, he said. Can pills help? Ron and other researchers say medication can play a vital role in combating alcohol use disorder, the medical condition commonly known as alcoholism. But fewer than 2 percent of people with an alcohol addiction take medication for the condition, national surveys show, compared with 13.4 percent of those dealing with opioid addiction.

Keyword: Drug Abuse
Link ID: 28542 - Posted: 11.09.2022

Hannah Devlin Science correspondent Scientists claim to have found the first direct evidence that people with depression have a reduced capacity for releasing serotonin in the brain. The findings from a brain-imaging study reignite a debate within psychiatry over the so-called serotonin hypothesis of depression and challenge the conclusions of an influential review published in July that found “no clear evidence” that low serotonin levels are responsible. The latest work, led by scientists at Imperial College London, suggested that people with depression have a decreased serotonin response. “This is the first direct evidence that the release of serotonin is blunted in the brains of people with depression,” said Prof Oliver Howes, a consultant psychiatrist based at Imperial College and King’s College London, and a co-author. “People have been debating this question for 60 years, but it’s all been based on indirect measures. So this is a really important step.” The serotonin hypothesis arose from evidence from postmortem brains and blood samples that suggested a serotonin deficit could be involved in depression. The theory provides a plausible biological mechanism for how the main class of antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs), are effective, and is why the brain chemical is sometimes referred to as a “happy hormone”. However, there is not yet conclusive evidence that serotonin abnormalities are the underlying cause of depression and resolving this question is seen as crucial to providing better treatments. The latest paper adds weight to the view that serotonin plays a role and demonstrates a new brain imaging technique that could pave the way to a better understanding of why SSRI drugs fail to help an estimated 10% to 30% of patients. “It’s the closest anyone has been able to get so far,” said Howes. “It’s hard to measure these transmitters in the brains of living people. We can’t put a pipette in there and take a sample. This is the closest we’re likely to come.” © 2022 Guardian News & Media Limited o

Keyword: Depression
Link ID: 28541 - Posted: 11.05.2022

By Leo Sands Psilocybin, the active hallucinogen found in psychedelic mushrooms — also known as “magic mushrooms” — can effectively alleviate a severe bout of depression when administered in a single dose and combined with talk therapy, a new clinical study found. Adults with depression who were administered a single 25-miligram dose of psilocybin were more likely to experience significant improvements in their mental health — both immediately and for up to three months — than others who were randomly assigned smaller doses of the same drug, said the peer-reviewed study, which was published Wednesday in the New England Journal of Medicine. “There’s something about the psychedelic experience that leads to a rapid resolution of depression symptoms,” said James Rucker, a consultant psychiatrist at King’s College London who worked on the trial. “We don’t really know what that is at the moment, but it’s very different to standard antidepressants.” The trial’s findings could be an encouraging sign for the 16 million Americans estimated each year by the Centers for Disease Control and Prevention to have depression, many of whom struggle to find treatments that work for them. Its authors hope the study — which was relatively small, with just 79 participants receiving the 25 mg dose — will pave the way for eventual regulatory approval of psilocybin by the Food and Drug Administration for use as a drug against depression. The new study randomly assigned 233 adults with depression three doses of psilocybin — 25 mg, 10 mg and 1 mg — across 22 sites in 10 countries. The authors found that the group given the largest dose recorded the most significant improvements in their depression, both immediately and for several weeks after.

Keyword: Depression; Drug Abuse
Link ID: 28540 - Posted: 11.05.2022

By Aimee Cunningham The death rate from alcohol use rose sharply in the United States in the first year of the pandemic. From 2019 to 2020, the rate of alcohol-induced deaths climbed 26 percent, from 10.4 per 100,000 people to 13.1 per 100,000, researchers report in a National Center for Health Statistics data brief published November 4. The rate of alcohol-induced deaths has generally increased yearly for the last two decades, but the annual uptick tended to be 7 percent or less. Deaths from alcoholic liver disease, which includes hepatitis and cirrhosis, were the most common driver of the increased rate. Deaths from mental and behavioral disorders due to alcohol use — mortality from dependence syndrome or withdrawal, for example — were the second most frequent contributor. The death rate from alcohol use jumped 26 percent overall from 2019 to 2020, a marked increase from previous years. Other researchers have reported that adults were drinking more frequently, and more heavily, early in the pandemic compared with the year before. There is also evidence of an increase in cases of alcoholic liver disease. A study at Johns Hopkins Hospital in Baltimore reported that 2.3 times as many patients with severe alcoholic liver disease and with recent unhealthy drinking were referred to their liver transplant center from July to December of 2020 compared with those months in 2019. © Society for Science & the Public 2000–2022.

Keyword: Drug Abuse; Stress
Link ID: 28539 - Posted: 11.05.2022

Vanessa Rom When put to the test, bees have proved over and over again that they've got a lot more to offer than pollinating, making honey and being fiercely loyal to a queen. The industrious insects can count and alter their behavior when things seem difficult, and now some scientists say there's proof they also like to play. A study recently published in Animal Behavior suggests that bumblebees, when given the chance, like to fool around with toys. Researchers from Queen Mary University of London conducted an experiment in which they set up a container that allowed bees to travel from their nest to a feeding area. But along the way, the bees could opt to pass through a separate section with a smattering of small wooden balls. Over 18 days, the scientists watched as the bees "went out of their way to roll wooden balls repeatedly, despite no apparent incentive to do so." The finding suggests that like humans, insects also interact with inanimate objects as a form of play. Also similar to people, younger bees seemed to be more playful than adult bees. In this experiment from researchers at Queen Mary University of London, bumblebees, especially young ones, appeared to show they liked to cling to wooden balls twice their size and roll them around just for the fun of it. "This research provides a strong indication that insect minds are far more sophisticated than we might imagine," Lars Chittka, a professor of sensory and behavioral ecology at Queen Mary University of London, who led the study, said in a statement. Earlier studies have shown that the black and yellow bugs are willing to learn new tricks in exchange for food or other rewards, so in this case Chittka and his team set out to create conditions that would eliminate external variables. They made sure that the bees had acclimated to their new home and that their environment was stress free. © 2022 npr

Keyword: Emotions; Evolution
Link ID: 28538 - Posted: 11.05.2022

By Veronique Greenwood Anyone who’s had a shady oyster or a mushroom soup that didn’t sit well remembers the ominous queasiness heralding impending bad times. Bacteria release toxins that start the body’s process of speedily evacuating the contents of the stomach. It’s a protective mechanism of sorts — getting rid of the invaders en masse is probably helpful in the long term, even if it’s unpleasant in the short. But it has remained something of a mystery how the brain gets the alarm signal, then sends another one to tell the stomach to initiate a technicolor yawn. Your next bout of food poisoning isn’t the only reason to understand this particular neural pathway. Figuring out how to counter it could be helpful for people who develop nausea caused by chemotherapy medication and other drugs. As if fighting cancer isn’t painful and scary enough, patients are often so turned off by food that keeping their weight up becomes a major struggle. In a new study, researchers report that both bacteria and chemotherapy drugs appear to trigger the same molecular pathways in the gut. The findings, which were based on experiments with mice and published Tuesday in the journal Cell, showed that a bacterial toxin and a chemo medication both set in motion a cascade of similar neural messages that cause queasiness. Choosing mice for the study was unusual. Mice, it turns out, can’t puke — a little foible that typically makes it difficult to use them to study nausea. Researchers have used cats and dogs in the past, but the biology of mice in general is so much better understood, with much better tools available to scientists to do so. Cao Peng, a professor at Tsinghua University in Beijing, and his colleagues wondered whether mice might still be capable of feeling ill in the way people do after ingesting a chemo drug or a bad salad — or close enough, anyway, that researchers could use the creatures to understand the origins of the sensation. © 2022 The New York Times Company

Keyword: Obesity; Stress
Link ID: 28537 - Posted: 11.02.2022

By Elena Renken The brain’s lifeline, its network of blood vessels, is like a tree, says Mathieu Pernot, deputy director of the Physics for Medicine Paris Lab. The trunk begins in the neck with the carotid arteries, a pair of broad channels that then split into branches that climb into the various lobes of the brain. These channels fork endlessly into a web of tiny vessels that form a kind of canopy. The narrowest of these vessels are only wide enough for a single red blood cell to pass through, and in one important sense these vessels are akin to the tree’s leaves. “When you want to look at pathology, usually you don’t see the sickness in the tree, but in the leaves,” Pernot says. (You can identify Dutch Elm Disease when the tree’s leaves yellow and wilt.) Just like leaves, the tiniest blood vessels in the brain often register changes in neuron and synapse activity first, including illness, such as new growth in a cancerous brain tumor.1, 2 But only in the past decade or so have we developed the technology to detect these microscopic changes in blood flow: It’s called ultrafast ultrasound. Standard ultrasound is already popular in clinical imaging given that it is minimally invasive, low-cost, portable, and can generate images in real time.3 But until now, it has rarely been used to image the brain. That’s partly because the skull gets in the way—bone tends to scatter ultrasound waves—and the technology is too slow to detect blood flow in the smaller arteries that support most brain function. Neurologists have mostly used it in niche applications: to examine newborns, whose skulls have gaps between the bone plates, or to guide surgeons in some brain surgeries, where part of the skull is typically removed. Neuroscience researchers have also used it to study functional differences between the two hemispheres of the brain, based on imaging of the major cerebral arteries, by positioning the device over the temporal bone window, the thinnest area of the skull. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Hearing
Link ID: 28536 - Posted: 11.02.2022

Jon Hamilton Computer games designed to boost self-esteem appear to prolong the antidepressant benefits of the mind-bending anesthetic ketamine. A recent study of 154 people found that those who played games featuring smiling faces and positive messages remained free of depression up to three months after a ketamine infusion, a team reports in the American Journal of Psychiatry. People who got ketamine alone tended to relapse after a week or two. The results are important because "we need new approaches that help people get feeling better faster and help them stay feeling better," says Rebecca Price, an author of the study and an associate professor of psychiatry and psychology at the University of Pittsburgh. Established drugs like Prozac and Zoloft can take weeks to ease depression, and don't work for every patient. Ketamine can offer immediate relief, but the effects often fade after a few days or weeks. "And then returning for infusions over and over to keep that relief going can end up being really burdensome and costly," Price says, "and just isn't accessible to all patients." So Price and a team of researchers wanted to find a way to make ketamine's antidepressant effects last longer. They decided to focus on a common symptom of depression: low self-esteem and self-loathing. The team drew on research suggesting that ketamine temporarily causes certain brain areas to enter a state in which they form lots of new connections. During this period, the brain seems to be more receptive to learning and change. "So we tried to use that window of opportunity just after ketamine to strengthen associations specifically between the idea of me, myself, and positive information and attributes," Price says. © 2022 npr

Keyword: Depression; Drug Abuse
Link ID: 28535 - Posted: 11.02.2022

Jon Hamilton An idea that has propelled Alzheimer's research for more than 30 years is approaching its day of reckoning. Scientists are launching a study designed to make or break the hypothesis that Alzheimer's is caused by a sticky substance called beta-amyloid. The study will give an experimental anti-amyloid drug to people as young as 18 who have gene mutations that often cause Alzheimer's to appear in their 30s or 40s. The study comes after several experimental drugs have failed to prevent declines in memory and thinking even though they succeeded in removing amyloid from the brains of patients in the early stages of Alzheimer's. Those failures have eroded support for the idea that amyloid is responsible for a cascade of events that eventually lead to the death of brain cells. "Many of us think of that as the ultimate test of the amyloid hypothesis," says Dr. Randall Bateman, a professor of neurology at Washington University School of Medicine in St. Louis."If that doesn't work, nothing will work." The new experiment, called the DIAN-TU primary Prevention Trial, is scheduled to begin enrolling patients by the end of the year. The amyloid hypothesis can be traced to Dr. Alois Alzheimer, a pathologist who first described the disease that would bear his name in 1906. Alzheimer was working at a psychiatric clinic in Munich, where he had the chance to conduct an autopsy on a woman who died at 50 after experiencing memory loss, disorientation, and hallucinations. He observed that the woman's brain had an "unusual disease of the cerebral cortex," including "senile plaque" usually seen in much older people. © 2022 npr

Keyword: Alzheimers
Link ID: 28534 - Posted: 11.02.2022