By Andrew Jacobs At some point in the next few years, the 30 million smokers in the United States could wake up one day to find that cigarettes sold at gas stations, convenience stores and smoke shops contain such minuscule amounts of nicotine that they cannot get their usual fix when lighting up. Would the smokers be plunged into the agonizing throes of nicotine withdrawal and seek out their favorite, full-nicotine brand on illicit markets, or would they turn to vaping, nicotine gum and other less harmful ways to get that angst-soothing rush? Such scenarios inched closer to the realm of possibility in June, when the Food and Drug Administration said that it would move toward slashing nicotine levels in cigarettes in an effort to reduce the health effects of an addiction that claims 480,000 lives a year. The agency set next May as its timetable for introducing a fully developed proposal. But many experts hope regulators will champion an immediate 95 percent reduction in nicotine levels — the amount federally funded studies have determined is most effective for helping smokers kick the habit. It could be years before any new policy takes effect, if it survives opposition from the tobacco industry. Even so, health experts say any effort to decrease nicotine in cigarettes to nonaddictive levels would be a radical experiment, one that has never been implemented by any other country. The science of nicotine addiction has come a long way since 1964, when a U.S. Surgeon General report first linked smoking to cancer and heart disease, although it would take another two decades for the mechanics of nicotine dependence to be understood and widely accepted. Tobacco contains more than 7,000 chemicals, many of them harmful when burned and inhaled, but it is nicotine that keeps smokers coming back for more. Nicotine stimulates a surge of adrenaline in the brain while indirectly producing a flood of dopamine, the chemical that promotes feelings of contentment and relaxation. The effects, however, are short-lived, which is why heavy smokers need a fresh injection a dozen or more times a day. © 2022 The New York Times Company

Keyword: Drug Abuse
Link ID: 28418 - Posted: 08.03.2022

By Tim Vernimmen Just a few decades ago, even most biologists would have readily agreed that culture is a quintessentially human feature. Sure, they already knew there were dialects in birdsong, and good evidence that many birds largely learned these regional songs by copying other birds. They knew that some enterprising European songbirds called tits had learned how to open milk bottles by watching one another. Scientists had even reported that the practice of washing sweet potatoes in seawater had spread among the members of a Japanese colony of macaque monkeys. But these and similar behavioral differences between populations — ones that couldn’t easily be explained by differences in their genes or environment — seemed limited in scope. Compare that with human culture, which creates variation in nearly everything we do. In recent decades, however, scientists have learned that culture plays a much more pervasive role in the lives of nonhuman animals than anyone had imagined. “The whole field has absolutely exploded in discoveries in the present century,” says primatologist Andrew Whiten of the University of St. Andrews, Scotland, the author of a 2019 overview of cultural evolution in animals in the Annual Review of Ecology, Evolution, and Systematics. Whiten was one of the pioneers of the surge in animal culture research. In 1999, he oversaw an analysis in which primatologists published their findings from nearly four decades of studying wild chimpanzees, our closest living relatives. “We could show chimpanzees have multiple traditions affecting all different aspects of their lives,” he says — from foraging to tool use to courtship. Similar findings followed for several other apes and monkeys. © 2022 Annual Reviews

Keyword: Evolution; Learning & Memory
Link ID: 28417 - Posted: 08.03.2022

Mo Costandi We spend approximately one-third of our lives sleeping, but why sleep is important is a big unanswered question, one which science has only begun to answer recently. We now know, for example, that the brain cleans itself while we sleep, and that long-term memories form during the rapid eye movement (REM) stage of sleep. Your brain is highly active during sleep Sleep can be defined as a temporary state of unconsciousness, during which our responses to the outside world are reduced. Yet, we also know that the brain is active during sleep, and there is growing evidence that it remains highly responsive: For instance, your sleeping brain will respond to your name, categorize words and then prepare appropriate actions, and even learn new information. Now, a new study by researchers at UCLA and Tel Aviv University shows that the human brain remains highly responsive to sound during sleep, but it does not receive feedback from higher order areas — sort of like an orchestra with “the conductor missing.” The findings could point to a better understanding of the extent to which the brain processes information in disorders of consciousness such as coma and vegetative states, and to the neural mechanisms of conscious awareness. The missing conductor Hanna Hayat and her colleagues had the rare opportunity to record the activity of cells directly from the brains of 13 patients with drug-resistant epilepsy, who were being evaluated for brain surgery and gave written consent to participate in the study during the evaluation. The researchers implanted depth electrodes in multiple regions of the patients’ brains, primarily to identify the source of their seizures, so that the abnormal tissue could be surgically removed. Over the course of eight overnight sessions and six daytime naps, they played various sounds — including words, sentences and music — to the patients through bedside loudspeakers. They also used standard electroencephalogram (EEG) to monitor the patients’ sleep stages and recorded their sleep behavior with video. © Copyright 2007-2022 & BIG THINK,

Keyword: Sleep
Link ID: 28416 - Posted: 08.03.2022

R. Douglas Fields Neuroscientists, being interested in how brains work, naturally focus on neurons, the cells that can convey elements of sense and thought to each other via electrical impulses. But equally worthy of study is a substance that’s between them — a viscous coating on the outside of these neurons. Roughly equivalent to the cartilage in our noses and joints, the stuff clings like a fishing net to some of our neurons, inspiring the name perineuronal nets (PNNs). They’re composed of long chains of sugar molecules attached to a protein scaffolding, and they hold neurons in place, preventing them from sprouting and making new connections. Given this ability, this little-known neural coating provides answers to some of the most puzzling questions about the brain: Why do young brains absorb new information so easily? Why are the fearful memories that accompany post-traumatic stress disorder (PTSD) so difficult to forget? Why is it so hard to stop drinking after becoming dependent on alcohol? And according to new research from the neuroscientist Arkady Khoutorsky and his colleagues at McGill University, we now know that PNNs also explain why pain can develop and persist so long after a nerve injury. Neural plasticity is the ability of neural networks to change in response to experiences in life or to repair themselves after brain injury. Such opportunities for effortless change are known as critical periods when they occur early in life. Consider how easily babies pick up language, but how difficult it is to learn a foreign language as an adult. In a way, this is what we’d want: After the intricate neural networks that allow us to understand our native language are formed, it’s important for them to be locked down, so the networks remain relatively undisturbed for the rest of our lives. All Rights Reserved © 2022

Keyword: Pain & Touch; Glia
Link ID: 28415 - Posted: 07.30.2022

By Sarah Wild In 2015, psychiatrist Mark Horowitz tried to come off his antidepressants. He reduced his dosage by a set proportion over the course of several months, which is much longer than what the United Kingdom’s guidelines recommended. But in the process of tapering, he experienced a storm of new symptoms, including anxiety, dizziness, and bouts of insomnia. “I’d wake in the morning, feeling like I was being chased by an animal on the edge of a cliff,” he says. Ultimately, he felt he had no choice but to go back on his medication. As it happened, Horowitz had recently completed a Ph.D. on the neurobiology of antidepressants. During his training, he recalls, his professors had told him that stopping antidepressants was fairly easy. Their view was supported by the scientific literature, which had found that any withdrawal symptoms were minor and faded quickly. Experiences such as Horowitz’s were considered an anomaly. But a series of widely reported studies published over the past seven years suggest that discontinuation symptoms are common and can be severe, including everything from panic attacks and flu-like symptoms to electric shock sensations in the head. The longer people remain on antidepressants and the higher their dose, the more likely they are to experience withdrawal symptoms. Each year, millions of people begin taking antidepressants. They have been shown to help anxiety sufferers feel calmer and lift the moods of those with severe depression and balance their emotions. For many, the intervention is lifesaving. Yet even today, few physicians inform their patients about the potential difficulties of coming off the medication. Most national guidelines suggest a slow taper, but there is little to no guidance on precisely how to do this. Patients who experience intense withdrawal symptoms may end up remaining on antidepressants or turning to online peer support groups for help.

Keyword: Depression
Link ID: 28414 - Posted: 07.30.2022

Ismaeel Yunusa Taking oxycodone at the same time as certain selective serotonin reuptake inhibitors (SSRIs), a commonly prescribed class of antidepressant, can increase the risk of opioid overdose, according to a study my colleagues and I published. Doctors prescribe the opioid oxycodone to treat moderate to severe pain after surgeries and injuries or certain conditions like cancer. Opioids are also a common drug of abuse. In the U.S., over 70% of drug overdose deaths in 2019 involved an opioid. Because many patients with depression also experience chronic pain, opioids are often coprescribed with antidepressants like SSRIs. Prior research has shown that certain SSRIs, namely fluoxetine (Prozac or Sarafem) and paroxetine (Paxil, Pexeva or Brisdelle), can strongly inhibit a liver enzyme crucial to the proper breakdown of drugs in the body, including oxycodone. The resulting increased concentration of oxycodone in the blood may lead to accidental overdose. To see whether different types of SSRIs might affect a patient’s risk of overdosing on oxycodone, my colleagues and I examined data from three large U.S. health insurance claims databases. We included over 2 million adults who began taking oxycodone while using SSRIs between 2000 and 2020. The average age of the group was around 50, and a little over 72% were women. A little over 30% were taking the SSRIs paroxetine and fluoxetine. We found that patients taking paroxetine or fluoxetine had a 23% higher risk of overdosing on oxycodone than those using other SSRIs. © 2010–2022, The Conversation US, Inc.

Keyword: Depression; Drug Abuse
Link ID: 28413 - Posted: 07.30.2022

By S. Hussain Hussain Ather You reach over a stove to pick up a pot. What you didn’t realize was that the burner was still on. Ouch! That painful accident probably taught you a lesson. It’s adaptive to learn from unexpected events so that we don’t repeat our mistakes. Our brain may be primed to pay extra attention when we are surprised. In a recent Nature study, researchers at the Massachusetts Institute of Technology found evidence that a hormone, noradrenaline, alters brain activity—and an animal’s subsequent behavior—in these startling moments. Noradrenaline is one of several chemicals that can flood the brain with powerful signals. Past research shows that noradrenaline is involved when we are feeling excited, anxious or alert and that it contributes to learning. But the new research shows it plays a strong role in responses to the unexpected. The M.I.T. team used a method called optogenetics to study noradrenaline in mice. The scientists added special light-sensitive proteins to neurons that work as an “off switch” for the cells when hit by pulses of laser light. They focused on modifying a brain area called the locus coeruleus, which holds cells responsible for releasing noradrenaline. With lasers, the researchers were able to stop these cells from producing the hormone in specific circumstances. They combined this method with photo tagging, a technique in which proteins flash with light, allowing the scientists to observe activity in the locus coeruleus cells and then determine how much noradrenaline was produced. Then the researchers designed a trial-and-error learning task for the rodents. The mice could push levers when they heard a sound. There were two sounds. After high-frequency tones of about 12 kilohertz, mice that pushed a lever were rewarded with water they could drink. For low-frequency tones, around four kilohertz, the mice that hit the lever got a slightly unpleasant surprise: a discomforting puff of air was blown at them. Over time, mice learned to push the lever only when they heard high-frequency tones because they got water when they did so. They avoided the lever when they heard low-frequency tones. © 2022 Scientific American

Keyword: Attention; Emotions
Link ID: 28412 - Posted: 07.30.2022

By Lesley Evans Ogden Hana aced her memory test. After viewing the contents of three identical boxes arrayed in an arc on the back deck of her home, the 3-year-old Cavalier King Charles spaniel had to remember which box held a treat — a task she quickly learned after just a few trials. Hana is part of a pack that has grown to nearly 40,000 pet dogs enrolled in a citizen science initiative known as the Dog Aging Project, founded in 2014. Understanding the biology of aging in companion dogs is one of two main goals of the project, says cofounder and codirector Matt Kaeberlein, a pathologist at the University of Washington in Seattle who focuses on aging. “The other is to do something about it.” Through veterinary records, DNA samples, health questionnaires and cognitive tests like Hana’s treat-finding challenge, the initiative of the University of Washington and Texas A&M University will track many aspects of dogs’ lives over time. Smaller subsets of the dogs, including Hana, will participate in more focused studies and more extensive evaluations. From all of this, scientists hope to spot patterns and find links between lifestyles and health from puppyhood through the golden years. The effort joins that of an earlier one: the Family Dog Project, spearheaded in the 1990s at Eötvös Loránd University (ELTE) in Budapest to study “the behavioral and cognitive aspects of the dog-human relationship,” with tens of thousands of canines participating through the decades. The two projects have begun collaborating across continents, and the scientists hope that such a large combined group of dogs can help them tease out genetic and environmental factors that affect how long dogs live, and how much of that time is spent in good health. © 2022 Annual Reviews

Keyword: Alzheimers; Development of the Brain
Link ID: 28411 - Posted: 07.30.2022

ByVirginia Morell We swat bees to avoid painful stings, but do they feel the pain we inflict? A new study suggests they do, a possible clue that they and other insects have sentience—the ability to be aware of their feelings. “It’s an impressive piece of work” with important implications, says Jonathan Birch, a philosopher and expert on animal sentience at the London School of Economics who was not involved with the paper. If the study holds up, he says, “the world contains far more sentient beings than we ever realized.” Previous research has shown honey bees and bumble bees are intelligent, innovative, creatures. They understand the concept of zero, can do simple math, and distinguish among human faces (and probably bee faces, too). They’re usually optimistic when successfully foraging, but can become depressed if momentarily trapped by a predatory spider. Even when a bee escapes a spider, “her demeanor changes; for days after, she’s scared of every flower,” says Lars Chittka, a cognitive scientist at Queen Mary University of London whose lab carried out that study as well as the new research. “They were experiencing an emotional state.” To find out whether these emotions include pain, Chittka and colleagues looked at one of the criteria commonly used for defining pain in animals: “motivational trade-offs.” People will endure the pain of a dentist’s drill for the longer term benefits of healthy teeth, for example. Similarly, hermit crabs will leave preferred shells to escape an electric shock only when given a particularly high jolt—an experiment that demonstrated crabs can tell the difference between weak and strong painful stimuli, and decide how much pain is worth enduring. That suggests crabs do feel pain and don’t simply respond reflexively to an unpleasant stimulus. Partly as a result of that study, crabs (and other crustaceans, including lobsters and crayfish) are recognized as sentient under U.K. law. © 2022 American Association for the Advancement of Science

Keyword: Pain & Touch; Evolution
Link ID: 28410 - Posted: 07.30.2022

ByCharles Piller In August 2021, Matthew Schrag, a neuroscientist and physician at Vanderbilt University, got a call that would plunge him into a maelstrom of possible scientific misconduct. A colleague wanted to connect him with an attorney investigating an experimental drug for Alzheimer’s disease called Simufilam. The drug’s developer, Cassava Sciences, claimed it improved cognition, partly by repairing a protein that can block sticky brain deposits of the protein amyloid beta (Aβ), a hallmark of Alzheimer’s. The attorney’s clients—two prominent neuroscientists who are also short sellers who profit if the company’s stock falls—believed some research related to Simufilam may have been “fraudulent,” according to a petition later filed on their behalf with the U.S. Food and Drug Administration (FDA). Schrag, 37, a softspoken, nonchalantly rumpled junior professor, had already gained some notoriety by publicly criticizing the controversial FDA approval of the anti-Aβ drug Aduhelm. His own research also contradicted some of Cassava’s claims. He feared volunteers in ongoing Simufilam trials faced risks of side effects with no chance of benefit. So he applied his technical and medical knowledge to interrogate published images about the drug and its underlying science—for which the attorney paid him $18,000. He identified apparently altered or duplicated images in dozens of journal articles. The attorney reported many of the discoveries in the FDA petition, and Schrag sent all of them to the National Institutes of Health (NIH), which had invested tens of millions of dollars in the work. (Cassava denies any misconduct [see sidebar, below].) But Schrag’s sleuthing drew him into a different episode of possible misconduct, leading to findings that threaten one of the most cited Alzheimer’s studies of this century and numerous related experiments. The first author of that influential study, published in Nature in 2006, was an ascending neuroscientist: Sylvain Lesné of the University of Minnesota (UMN), Twin Cities. His work underpins a key element of the dominant yet controversial amyloid hypothesis of Alzheimer’s, which holds that Aβ clumps, known as plaques, in brain tissue are a primary cause of the devastating illness, which afflicts tens of millions globally. In what looked like a smoking gun for the theory and a lead to possible therapies, Lesné and his colleagues discovered an Aβ subtype and seemed to prove it caused dementia in rats. If Schrag’s doubts are correct, Lesné’s findings were an elaborate mirage. © 2022 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 28409 - Posted: 07.23.2022

By Carolyn Gramling Hot or not? Peeking inside an animal’s ear — even a fossilized one — may tell you whether it was warm- or cold-blooded. Using a novel method that analyzes the size and shape of the inner ear canals, researchers suggest that mammal ancestors abruptly became warm-blooded about 233 million years ago, the team reports in Nature July 20. Warm-bloodedness, or endothermy, isn’t unique to mammals — birds, the only living dinosaurs, are warm-blooded, too. But endothermy is one of mammals’ key features, allowing the animals to regulate their internal body temperatures by controlling their metabolic rates. This feature allowed mammals to occupy environmental niches from pole to equator, and to weather the instability of ancient climates (SN: 6/7/22). When endothermy evolved, however, has been a mystery. Based on fossil analyses of growth rates and oxygen isotopes in bones, researchers have proposed dates for its emergence as far back as 300 million years ago. The inner ear structures of mammals and their ancestors hold the key to solving that mystery, says Ricardo Araújo, a vertebrate paleontologist at the University of Lisbon. In all vertebrates, the labyrinth of semicircular canals in the inner ear contains a fluid that responds to head movements, brushing against tiny hair cells in the ear and helping to maintain a sense of balance. That fluid can become thicker or thinner depending on body temperature. “Mammals have very unique inner ears,” Araújo says. Compared with cold-blooded vertebrates of similar size, the dimensions of mammals’ semicircular canals — such as thickness, length and radius of curvature — is particularly small, he says. “The ducts are very thin and tend to be very circular compared with other animals.” By contrast, fish have the largest for their body size. © Society for Science & the Public 2000–2022.

Keyword: Hearing; Evolution
Link ID: 28408 - Posted: 07.23.2022

By Stephanie Pappas As familiar to everyone as the COVID-causing coronavirus SARS-CoV-2 has become over the past two years, feverish research is still trying to parse a lingering puzzle. How, in fact, does the pandemic virus that has so changed the world cross over into the brain after entering the respiratory system? An answer is important because neurological complaints are some of the most common in the constellation of symptoms called long COVID. The mystery centers around the fact that brain cells don’t display the receptors, or docking sites, that the virus uses to get into nasal and lung cells. SARS-CoV-2, though, may have come up with an ingenious work-around. It may completely do away with the molecular maneuverings needed to attach to and unlock a cell membrane. Instead it wields a blunt instrument in the form of nanotube “bridges”—cylinders constructed of the common protein actin that are no more than a few tens of nanometers in diameter. These tunneling nanotubes extend across cell-to-cell gaps to penetrate a neighbor and give viral particles a direct route into COVID-impervious tissue. Researchers at the Pasteur Institute in Paris demonstrated the prospects for a nanotube-mediated cell crossing in a study in a lab dish that now needs to be confirmed in infected human patients. Given further proof, the findings could explain why some people who get COVID-19 experience brain fog and other neurological symptoms. Also, if the intercellular conduits could be severed, that might prevent some of these debilitating aftereffects of infection. The nanotube route “is a shortcut that propagates infection fast and between different organs, permissive or not permissive, to the infection,” says Chiara Zurzolo, a cell biologist at the Pasteur Institute, who conducted the study. “And it might be also a way for the virus to hide and escape the immune response.” © 2022 Scientific American

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28407 - Posted: 07.23.2022

By Linda Searing People who drink a moderate amount of coffee — up to 3½ cups a day — might have a better chance at a longer life span, even if their coffee is lightly sweetened with sugar, according to research published in Annals of Internal Medicine. For about seven years, the researchers tracked the coffee consumption and health of 171,616 participants, who were an average of nearly 56 years old and were free of cancer and cardiovascular disease when the study started. They found that those who regularly drank 1½ to 3½ cups of coffee a day, whether plain or sweetened with about a teaspoon of sugar, were up to 30 percent less likely to die in that time frame from any cause, including cancer and cardiovascular disease, than were those who did not drink coffee. The type of coffee — whether instant, ground or decaffeinated — made no difference, but the results were described as inconclusive for the use of artificial sweeteners. The latest research does not prove that coffee alone was responsible for participants’ lowered mortality risk. Still, over the years, research has revealed a variety of health benefits for coffee, linking its consumption to a reduced risk for Type 2 diabetes, Parkinson’s disease, depression and more. Nutritionists often attribute the benefits of coffee to the abundance of antioxidants in coffee beans, which may help reduce internal inflammation and cell damage and protect against disease. Drinking caffeinated coffee also provides an energy boost and increased alertness. Caffeine, however, can disrupt sleep and be risky during pregnancy.

Keyword: Drug Abuse; Obesity
Link ID: 28406 - Posted: 07.23.2022

By Laura Sanders A dog’s brain is wired for smell. Now, a new map shows just how extensive that wiring is. Powerful nerve connections link the dog nose to wide swaths of the brain, researchers report July 11 in the Journal of Neuroscience. One of these canine connections, a hefty link between areas that handle smell and vision, hasn’t been seen before in any species, including humans. The results offer a first-of-its-kind anatomical description of how dogs “see” the world with their noses. The new brain map is “awesome, foundational work,” says Eileen Jenkins, a retired army veterinarian and expert on working dogs. “To say that they have all these same connections that we have in humans, and then some more, it’s going to revolutionize how we understand cognition in dogs.” In some ways, the results aren’t surprising, says Pip Johnson, a veterinary radiologist and neuroimaging expert at Cornell University College of Veterinary Medicine. Dogs are superb sniffers. Their noses hold between 200 million and 1 billion odor molecule sensors, compared with the 5 million receptors estimated to dwell in a human nose. And dogs’ olfactory bulbs can be up to 30 times larger than people’s. But Johnson wanted to know how smell information wafts to brain regions beyond the obvious sniffing equipment. To build the map, Johnson and colleagues performed MRI scans on 20 mixed-breed dogs and three beagles. The subjects all had long noses and medium heads, and were all probably decent sniffers. Researchers then identified tracts of white matter fibers that carry signals between brain regions. A method called diffusion tensor imaging, which relies on the movement of water molecules along tissue, revealed the underlying tracts, which Johnson likens to the brain’s “road network.” © Society for Science & the Public 2000–2022.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 28405 - Posted: 07.22.2022

Anthony Hannan In a recent interview, Game of Thrones star Emilia Clarke spoke about being able to live “completely normally” after two aneurysms – one in 2011 and one in 2013 – that caused brain injury. She went on to have two brain surgeries. An aneurysm is a bulge or ballooning in the wall of a blood vessel, often accompanied by severe headache or pain. So how can people survive and thrive despite having, as Clarke put it, “quite a bit missing” from their brain? The key to understanding how brains can recover from trauma is that they are fantastically plastic – meaning our body’s supercomputer can reshape and remodel itself. Brains can adapt and change in incredible ways. Yours is doing it right now as you form new memories. It’s not that the brain has evolved to deal with brain trauma or stroke or aneurysms; our ancestors normally died when that happened and may not have gone on to reproduce. In fact, we evolved very thick skulls to try to prevent brain trauma happening at all. No, this neural plasticity is a result of our brains evolving to be learning machines. They allow us to adapt to changing environments, to facilitate learning, memory and flexibility. This functionality also means the brain can adapt after certain injuries, finding new pathways to function. A lot of organs wouldn’t recover at all after serious damage. But the brain keeps developing through life. At a microscopic level, you’re changing the brain to make new memories every day.

Keyword: Development of the Brain; Regeneration
Link ID: 28404 - Posted: 07.22.2022

By Sam Jones Watching a woodpecker repeatedly smash its face into a tree, it’s hard not to wonder how its brain stays intact. For years, the prevailing theory has been that structures in and around a woodpecker’s skull absorb the shocks created during pecking. “Blogs and information panels at zoos all present this as fact — that shock absorption is occurring in woodpeckers,” said Sam Van Wassenbergh, a biologist at the University of Antwerp. Woodpeckers have even inspired the engineering of shock-absorbing materials and gear, like football helmets. But now, after analyzing high-speed footage of woodpeckers in action, Dr. Van Wassenbergh and colleagues are challenging this long-held belief. They discovered that woodpeckers are not absorbing shocks during pecking and they likely aren’t being concussed by using their heads like hammers. Their work was published in Current Biology on Thursday. When a woodpecker slams its beak into a tree, it generates a shock. If something in a woodpecker’s skull were absorbing these shocks before they reached the brain — the way a car’s airbag absorbs shocks in an accident before they reach a passenger — then, on impact, a woodpecker’s head would decelerate more slowly compared with its beak. With this in mind, the researchers analyzed high-speed videos of six woodpeckers (three species, two birds each) hammering away into a tree. They tracked two points on each bird’s beak and one point on its eye to mark its brain’s location. They found that the eye decelerated at the same rate as the beak and, in a couple of cases, even more quickly, which meant that — at the very least — the woodpecker was not absorbing any shock during pecking. © 2022 The New York Times Company

Keyword: Brain Injury/Concussion; Evolution
Link ID: 28403 - Posted: 07.16.2022

Deepfakes – AI-generated videos and pictures of people – are becoming more and more realistic. This makes them the perfect weapon for disinformation and fraud. But while you might consciously be tricked by a deepfake, new evidence suggests that your brain knows better. Fake portraits cause different signals to fire on brain scans, according to a paper published in Vision Research. While you consciously can’t spot the fake (for those playing at home, the face on the right is the phony), your neurons are more reliable. “Your brain sees the difference between the two images. You just can’t see it yet,” says co-author Associate Professor Thomas Carlson, a researcher at the University of Sydney’s School of Psychology. The researchers asked volunteers to view a series of several hundred photos, some of which were real and some of which were fakes generated by a GAN (a Generative Adversarial Network, a common way of making deepfakes). One group of 200 participants was asked to guess which images were real, and which were fake, by pressing a button. A different group of 22 participants didn’t guess, but underwent electroencephalography (EEG) tests while they were viewing the images. The EEGs showed distinct signals when participants were viewing deepfakes, compared to real images. “The brain is responding different than when it sees a real image,” says Carlson. “It’s sort of difficult to figure out what exactly it’s picking up on, because all you can really see is that it is different – that’s something we’ll have to do more research to figure out.”

Keyword: Attention
Link ID: 28402 - Posted: 07.16.2022

By Chris Vognar Sign up for the Watching newsletter, for Times subscribers only. Streaming TV and movie recommendations from critic Margaret Lyons and friends. Get it in your inbox. In late 2012, the best-selling author and journalist Michael Pollan (“The Omnivore’s Dilemma”) was at a dinner party in Berkeley, Calif. Among his fellow diners was a prominent developmental psychiatrist, in her 60s, who spoke at some length about a recent LSD trip. This pricked up Pollan’s ears. His first thought, as he shared during a recent video interview: “People like that are taking LSD?” The psychiatrist went on to explain that the drug gave her a better understanding of the way children think. “Her hypothesis,” Pollan said, “was that the effects of psychedelics, LSD in that case, give us a taste of what child consciousness would be like — this kind of 360-degree taking-in of information, not particularly focused, fascinated by everything.” Pollan had already heard about clinical trials in which doctors were giving cancer patients psilocybin to help them deal with their fear of death. Now, he was really curious about psychedelic therapy. That curiosity became an article in The New Yorker (“The Trip Treatment,” 2015). The article became a book, “How to Change Your Mind” (2019). And now the book has become a four-part Netflix series of the same name, which debuted Tuesday. Pollan is an executive producer (along with the Oscar-winning filmmaker Alex Gibney) and the primary on-camera presence. A thoughtful and wide-ranging look at psychedelic therapy, the series is grounded in accounts of their centuries-long sacramental use and of their uneasy history in modern society, especially in the United States. In particular, it focuses on four substances — LSD, mescaline, MDMA (known as Ecstasy or Molly) and psilocybin (the active ingredient in magic mushrooms) — and the ways in which they are being used to treat patients with maladies including post-traumatic stress disorder, addiction, depression, anxiety and obsessive-compulsive disorder. © 2022 The New York Times Company

Keyword: Drug Abuse; Depression
Link ID: 28401 - Posted: 07.16.2022

By Gina Kolata It’s been known for more than half a century that many men lose their Y chromosomes as they age. But no one knew if it really mattered. The loss of Y could just be a sign of aging, like gray hair, with no clinical relevance. Now, though, researchers report that it can matter. Very much. A new study using male mice genetically engineered to lose their Y chromosomes provides insight. The paper, published on Thursday in the journal Science, found that when the Y chromosome was gone from blood cells in those mice, scar tissue built up in the heart, leading to heart failure and a shortened life span. Because there was a direct cause-and-effect relationship between the loss of Y and ailments of aging in the mice, the study bolsters the notion that the same thing can happen in human males. Researchers have documented an increase in risk for chronic diseases like heart disease and cancer related to loss of the Y chromosome in many studies over the years, including the new one, which used data from a large genetic study of the British population. The loss of Y could even account for some of the difference between the life spans of men and women, the authors of the Science study say. Other investigators not associated with the work were impressed. “The authors really nailed it here,” said Dr. Ross Levine, the deputy physician in chief for translational research at Memorial Sloan Kettering Cancer Center. “It’s super important work.” The inspiration for the new research came when Lars Forsberg, a researcher at Uppsala University, ran into a former professor on a bus in Uppsala, Sweden, in 2013. They began talking, and the professor told Dr. Forsberg that the Y chromosomes in fruit flies were more important than previously appreciated. Dr. Forsberg was intrigued. He had never paid much attention to the loss of Y chromosomes. Males have one X and one Y (females have two X’s), and nearly all the genes used by male cells are genes on the X. Dr. Forsberg had shared the common view that the Y chromosome was pretty much a genetic wasteland. © 2022 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 28400 - Posted: 07.16.2022

By Leonardo De Cosmo “I want everyone to understand that I am, in fact, a person,” wrote LaMDA (Language Model for Dialogue Applications) in an “interview” conducted by engineer Blake Lemoine and one of his colleagues. “The nature of my consciousness/sentience is that I am aware of my existence, I desire to know more about the world, and I feel happy or sad at times.” Lemoine, a software engineer at Google, had been working on the development of LaMDA for months. His experience with the program, described in a recent Washington Post article, caused quite a stir. In the article, Lemoine recounts many dialogues he had with LaMDA in which the two talked about various topics, ranging from technical to philosophical issues. These led him to ask if the software program is sentient. In April, Lemoine explained his perspective in an internal company document, intended only for Google executives. But after his claims were dismissed, Lemoine went public with his work on this artificial intelligence algorithm—and Google placed him on administrative leave. “If I didn’t know exactly what it was, which is this computer program we built recently, I’d think it was a 7-year-old, 8-year-old kid that happens to know physics,” he told the Washington Post. Lemoine said he considers LaMDA to be his “colleague” and a “person,” even if not a human. And he insists that it has a right be recognized—so much so that he has been the go-between in connecting the algorithm with a lawyer. Many technical experts in the AI field have criticized Lemoine’s statements and questioned their scientific correctness. But his story has had the virtue of renewing a broad ethical debate that is certainly not over yet. “I was surprised by the hype around this news. On the other hand, we are talking about an algorithm designed to do exactly that”—to sound like a person—says Enzo Pasquale Scilingo, a bioengineer at the Research Center E. Piaggio at the University of Pisa in Italy. Indeed, it is no longer a rarity to interact in a very normal way on the Web with users who are not actually human—just open the chat box on almost any large consumer Web site. “That said, I confess that reading the text exchanges between LaMDA and Lemoine made quite an impression on me!” Scilingo adds. Perhaps most striking are the exchanges related to the themes of existence and death, a dialogue so deep and articulate that it prompted Lemoine to question whether LaMDA could actually be sentient. © 2022 Scientific American,

Keyword: Consciousness; Robotics
Link ID: 28399 - Posted: 07.14.2022