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Leonard Mlodinow Charles Darwin created the most successful theory in the history of biology: the theory of evolution. He was also responsible for another grand theory: the theory of emotion, which dominated his field for more than a century. That theory was dead wrong. The most important tenet of his theory was that the mind consists of two competing forces, the rational and the emotional. He believed emotions played a constructive role in the lives of non-human animals, but in humans emotions were a vestige whose usefulness had been largely superseded by the evolution of reason. We now know that, on the contrary, emotions enhance our process of reasoning and aid our decision-making. In fact, we can’t make decisions, or even think, without being influenced by our emotions. Consider a pioneering 2010 study in which researchers analysed the work of 118 professional traders in stocks, bonds and derivatives at four investment banks. Some were highly successful, but many were not. The researchers’ goal was to understand what differentiated the two groups. Their conclusion? They had different attitudes toward the role of emotion in their job. The relatively less successful traders for the most part denied that emotion played a significant role. They tried to suppress their emotions, while at the same time denying that emotions had an effect on their decision-making. The most successful traders, in contrast, had a different attitude. They showed a great willingness to reflect on their emotion-driven behaviour. They recognised that emotion and good decision-making were inextricably linked. Accepting that emotions were necessary for high performance, they “tended to reflect critically about the origin of their intuitions and the role of emotion”. © 2021 Guardian News & Media Limited

Keyword: Emotions; Learning & Memory
Link ID: 28136 - Posted: 01.05.2022

By Jane E. Brody You’re probably familiar with these major risk factors for heart disease: high blood pressure, high cholesterol, smoking, diabetes, obesity and physical inactivity. And chances are your doctor has checked you more than once for these risks and, I would hope, offered advice or treatment to help ward off a heart attack or stroke. But has your doctor also asked about the level of stress in your life? Chronic psychological stress, recent studies indicate, may be as important — and possibly more important — to the health of your heart than the traditional cardiac risk factors. In fact, in people with less-than-healthy hearts, mental stress trumps physical stress as a potential precipitant of fatal and nonfatal heart attacks and other cardiovascular events, according to the latest report. The new study, published in November in JAMA, assessed the fates of 918 patients known to have underlying, but stable, heart disease to see how their bodies reacted to physical and mental stress. The participants underwent standardized physical and mental stress tests to see if their hearts developed myocardial ischemia — a significantly reduced blood flow to the muscles of the heart, which can be a trigger for cardiovascular events — during either or both forms of stress. Then the researchers followed them for four to nine years. Among the study participants who experienced ischemia during one or both tests, this adverse reaction to mental stress took a significantly greater toll on the hearts and lives of the patients than did physical stress. They were more likely to suffer a nonfatal heart attack or die of cardiovascular disease in the years that followed. I wish I had known that in 1982, when my father had a heart attack that nearly killed him. Upon leaving the hospital, he was warned about overdoing physical stresses, like not lifting anything heavier than 30 pounds. But he was never cautioned about undue emotional stress or the risks of overreacting to frustrating circumstances, like when the driver ahead of him drove too slowly in a no-passing zone. © 2022 The New York Times Company

Keyword: Stress
Link ID: 28135 - Posted: 01.05.2022

Chloe Tenn On October 4, physiologist David Julius and neurobiologist Arden Patapoutian were awarded the Nobel Prize in Physiology or Medicine for their work on temperature, pain, and touch perception. Julius researched the burning sensation people experience from chilies, and identified an ion channel, TRPV1 that is activated by heat. Julius and Patapoutian then separately reported on the TRPM8 ion channel that senses menthol’s cold in 2002. Patapoutian’s group went on to discover the PIEZO1 and PIEZO2 ion channels that are involved in sensing mechanical pressure. The Nobel Committee wrote that the pair’s work inspired further research into understanding how the nervous system senses temperature and mechanical stimuli and that the laureates “identified critical missing links in our understanding of the complex interplay between our senses and the environment.” This year saw innovations in augmenting the brain’s capabilities by plugging it in to advanced computing technology. For example, a biology teacher who lost her vision 16 years ago was able to distinguish shapes and letters with the help of special glasses that interfaced with electrodes implanted in her brain. Along a similar vein, a computer connected to a brain-implant system discerned brain signals for handwriting in a paralyzed man, enabling him to type up to 90 characters per minute with an accuracy above 90 percent. Such studies are a step forward for technologies that marry cutting-edge neuroscience and computational innovation in an attempt to improve people’s lives. © 1986–2021 The Scientist.

Keyword: Pain & Touch; Language
Link ID: 28134 - Posted: 12.31.2021

By Abdulrahman Olagunju How does our brain know that “this” follows “that”? Two people meet, fall in love and live happily ever after—or sometimes not. The sequencing of events that takes place in our head—with one thing coming after another—may have something to do with so-called time cells recently discovered in the human hippocampus. The research provides evidence for how our brain knows the start and end of memories despite time gaps in the middle. As these studies continue, the work could lead to strategies for memory restoration or enhancement. The research has focused on “episodic memory,” the ability to remember the “what, where and when” of a past experience, such as the recollection of what you did when you woke up today. It is part of an ongoing effort to identify how the organ creates such memories. A team led by Leila Reddy, a neuroscience researcher at the French National Center for Scientific Research, sought to understand how human neurons in the hippocampus represent temporal information during a sequence of learning steps to demystify the functioning of time cells in the brain. In a study published this summer in the Journal of Neuroscience, Reddy and her colleagues found that, to organize distinct moments of experience, human time cells fire at successive moments during each task. The study provided further confirmation that time cells reside in the hippocampus, a key memory processing center. They switch on as events unfold, providing a record of the flow of time in an experience. “These neurons could play an important role in how memories are represented in the brain,” Reddy says. “Understanding the mechanisms for encoding time and memory will be an important area of research.” © 2021 Scientific American

Keyword: Learning & Memory; Attention
Link ID: 28133 - Posted: 12.31.2021

By Emily Witt In the fall of 1972, a psychiatrist named Salvador Roquet travelled from his home in Mexico City to the Maryland Psychiatric Research Center, an institution largely funded by the United States government, to give a presentation on an ongoing experiment. For several years, Roquet had been running a series of group-therapy sessions: over the course of eight or nine hours, his staff would administer psilocybin mushrooms, morning-glory seeds, peyote cacti, and the herb datura to small groups of patients. He would then orchestrate what he called a “sensory overload show,” with lights, sounds, and images from violent or erotic movies. The idea was to push the patients through an extreme experience to a psycho-spiritual rebirth. One of the participants, an American psychology professor, described the session as a “descent into hell.” But Roquet wanted to give his patients smooth landings, and so, eventually, he added a common hospital anesthetic called ketamine hydrochloride. He found that, given as the other drugs were wearing off, it alleviated the anxiety brought on by these punishing ordeals. Clinicians at the Maryland Psychiatric Research Center had been studying LSD and other psychedelics since the early nineteen-fifties, beginning at a related institution, the Spring Grove Hospital Center. But ketamine was new: it was first synthesized in 1962, by a researcher named Calvin Stevens, who did consulting work for the pharmaceutical company Parke-Davis. (Stevens had been looking for a less volatile alternative to phencyclidine, better known as PCP.) Two years later, a doctor named Edward Domino conducted the first human trials of ketamine, with men incarcerated at Jackson State Prison, in Michigan, serving as his subjects. At higher doses, Domino noticed, ketamine knocked people out, but at lower ones it produced odd psychoactive effects on otherwise lucid patients. Parke-Davis wanted to avoid characterizing the drug as psychedelic, and Domino’s wife suggested the term “dissociative anesthetic” to describe the way it seemed to separate the mind from the body even as the mind retained consciousness. The F.D.A. approved ketamine as an anesthetic in 1970, and Parke-Davis began marketing it under the brand name Ketalar. It was widely used by the U.S. military during the Vietnam War, and remains a standard anesthetic in emergency rooms around the world. © 2021 Condé Nast.

Keyword: Depression; Drug Abuse
Link ID: 28132 - Posted: 12.31.2021

By Christina Caron Q: Sometimes my eyelid twitches on and off for days — weeks, even. It’s distracting and irritating. How do I get it to stop? And should I be concerned? Eyelid spasms, while annoying, are “rarely a sign of something serious,” said Stephanie Erwin, an optometrist at Cleveland Clinic’s Cole Eye Institute. The most common type of eye twitch is a series of muscle contractions called eyelid myokymia, which produces involuntary and intermittent contractions of the eyelid, typically the lower one. Only one eye is affected at a time because the twitch originates in the muscle surrounding the eye, and not the nerve that controls the blink reflex, which sends the same message to both eyes simultaneously, Dr. Erwin added. The spasms can last from hours to days to months. “If the twitching persists for a long period of time, or is accompanied by additional symptoms, it is a good idea to be checked by an eye doctor to make sure nothing else is going on,” she said. If the twitching spreads to other muscles in the face or if you notice both eyes are twitching at the same time, those are indications of a more serious problem. Other red flags include a drooping eyelid or a red eye. But if just one eyelid is twitching on and off, it is usually a harmless (and often exasperating) case of eyelid myokymia. As for why it happens: “Nobody knows exactly why,” said Dr. Alice Lorch, an ophthalmologist at Massachusetts Eye and Ear in Boston. But more commonly, it is stress, lack of sleep or excessive caffeine intake that brings on eyelid twitching, the experts said. Dry eye, a common affliction among those who stare at screens most of the day, is another culprit. Studies have indicated that we blink less when looking at digital devices, which makes our eyes feel dry. © 2021 The New York Times Company

Keyword: Vision; Stress
Link ID: 28131 - Posted: 12.31.2021

By Vanessa Barbara JUIZ DE FORA, Brazil — My first encounter with ketamine did not go well. A lifelong depressive — I picked up the habit of despairing sadness in early adulthood, and it remained faithfully with me — I’d turned to a more experimental form of treatment: ketamine infusions, in which a kindly anesthesiologist funnels the drug into a sad person’s veins for around 50 minutes and hopes it perks her up. Forty-five minutes into my first session, I rather anxiously asked my partner, who was in the room with me, if our 3-year-old daughter was fine. He decided it was the perfect time for a joke. Our daughter, he answered, was safe at home — and as a matter of fact, he added, she was already a very independent 15-year-old. I panicked. While under the strong, dissociative effect of the drug, patients sometimes enter what’s called a k-hole, in which their sense of time and space is distorted or eliminated. In that state of oblivion, I found it entirely plausible that my daughter was not a toddler anymore, but a strong-willed teenager. I became very distressed. My heartbeat accelerated. The anesthesiologist hurriedly ended the session as my partner said: “I’m kidding! Sorry! She’s still 3!” It was an inauspicious start, but I was determined to make the best of it. Ketamine, long used as an anesthetic but better known as an illegal party drug and, of course, a horse tranquilizer, has in recent years been gaining traction as an antidepressant. People have written enthusiastic accounts of their experiences, and researchers and psychiatrists, in a cascade of studies, have pointed to its possible benefits, not least the speed with which it can alleviate symptoms. Today, hundreds of clinics around the world provide infusions to people who have found little, if any, improvement with other treatments. That’s where I come in. Over the years, apart from the good old psychotropic medications, I have tried several types of talk therapy, meditation, acupuncture, singing lessons, bungee jumping and transcranial magnetic stimulation. (I still have sweet memories of the woodpecker sounds tapped into my brain.) © 2021 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 28130 - Posted: 12.29.2021

By Molly Young Two distinguished academics walk into a restaurant in Manhattan. It is their first meeting — their first date, in fact — and the year is 2015. The man wears a down jacket against the icy winter evening. The woman has a shock of glossy white hair. The restaurant is on a cozy corner of the West Village and has foie gras on the menu. What the man doesn’t know is that the interior of his down jacket has suffered a structural failure, and the filling has massed along the bottom hem, forming a conspicuous bulge at his waist. As they greet each other, the woman perceives the bulge and asks herself: Is my date wearing a colostomy bag? They sit down to eat, but the woman is distracted. As they chat about their lives — former spouses, work, interests — the woman has “colostomy bag” on her mind. Is it or isn’t it? The two academics are of an age where such an intervention is, well, not exactly common, but not out of the realm of possibility. At the end of their dinner, the man takes the train back to Philadelphia, where he lives, and the woman returns to her apartment on the Upper West Side. Despite the enigma of the man’s midsection, the date is a success. It wasn’t until their third date that the question got resolved: no colostomy bag. “I was testing her,” Paul Rozin, one of the academics, later joked, “to see if she would put up with me.” (He wasn’t testing her. He was unaware of the bulge.) “I was worried,” said Virginia Valian, the other academic. It was fitting that an imaginary colostomy bag played a starring role in the couple’s first encounter. Paul Rozin is known for many things — he is an eminent psychologist who taught at the University of Pennsylvania for 52 years, and he has gathered honors and fellowships and published hundreds of influential papers and served on editorial boards and as chairman of the university’s department of psychology — but he is best known for his work on the topic of disgust. In the early 1980s, Rozin noticed that there was surprisingly little data available on this universal aspect of life. Odd, he thought, that of the six so-called basic emotions — anger, surprise, fear, enjoyment, sadness, disgust — the last had hardly been studied. © 2021 The New York Times Company

Keyword: Emotions
Link ID: 28129 - Posted: 12.29.2021

Robert Martone We are all time travelers. Each day, we experience new things as we travel forward through time. In the process, the countless connections between the nerve cells in our brain recalibrate to accommodate these experiences. It’s as if we reassemble ourselves daily, maintaining a mental construct of ourselves in physical time, and the glue that holds together our core identity is memory. Not only do we travel in physical time; we also experience mental time travel. We visit the past through our memories and then journey into the future by imagining what tomorrow or next year might bring. When we do so, we think of ourselves as we are now, remember who we once were and imagine how we will be. A new study, published in the journal Social Cognitive and Affective Neuroscience(SCAN), explores how a specific brain region helps knit together memories of the present and future self. Injury to that area leads to an impaired sense of identity. The region—called the ventral medial prefrontal cortex (vmPFC)—may produce a fundamental model of our self and place it in mental time. In doing so, this study suggests, it may be the source of our sense of self. Psychologists have long noticed that our mind handles information about one’s self differently from other details. Memories that reference the self are easier to recall than other forms of memory. They benefit from what researchers have called a self-reference effect (SRE), in which information related to one’s self is privileged and more salient in our thoughts. Self-related memories are distinct from both episodic memory, the category of recollections that pertains to specific events and experiences, and semantic memory, which connects to more general knowledge, such as the color of grass and the characteristics of the seasons. © 2021 Scientific American,

Keyword: Consciousness; Attention
Link ID: 28128 - Posted: 12.29.2021

By Nicholas Bakalar Need more incentive to get a flu shot, or to keep taking extra precautions this flu season? A new study suggests there may be a link between influenza infection and an increased risk for Parkinson’s disease. For decades, neurologists have suspected there may be a link between the flu and Parkinson’s disease, a chronic and progressive disorder of the nervous system marked by problems with movement, cognitive changes and a range of other symptoms. Several earlier studies, for example, reported a sharp increase in Parkinson’s cases following the 1918 influenza pandemic. Some cases of Parkinson’s have been linked to environmental exposures to pesticides and other toxic chemicals, and genetics may also play a role, but most cases of Parkinson’s have no known cause. Treatments for Parkinson’s can help delay its progression, but there is no known cure. The new study, using Danish health care databases, included 10,231 men and women who had been diagnosed with Parkinson’s between 2000 and 2016. Researchers compared them with 51,196 controls who were matched for age and sex. The researchers tracked influenza infections beginning in 1977 using hospital and outpatient discharge records. The report appeared in JAMA Neurology. Parkinson’s takes years, if not decades, to develop, and initially may produce only subtle symptoms like a hand tremor. It may take years for doctors to diagnose the condition, so any connection between a flu infection and the disease would be evident only many years later. The researchers found that compared with people who had not had a flu infection, those who had the flu had a 70 percent higher risk of Parkinson’s 10 years later, and a 90 percent higher risk 15 years after. © 2021 The New York Times Company

Keyword: Parkinsons
Link ID: 28127 - Posted: 12.29.2021

By Linda Searing Among people who have covid-19, those who have certain sleep disorders (including sleep apnea) face a 31 percent greater chance of developing a severe case that requires hospitalization, or dying from the disease, than do people who have covid-19 and who do not have sleep-disturbed breathing, according to research published in The study links the increase in risk to breathing disorders that can cause oxygen levels to drop during sleep, creating a low oxygen level called hypoxia. The researchers found that having such a sleep-related breathing disorder did not make people more likely to contract the coronavirus. They wrote, however, that having low oxygen levels “may play a role in worse outcomes once the viral illness evolves,” describing hypoxia as an “amplifier” of covid effects. The findings were based on data from 5,402 adults (average age 56) who had undergone sleep studies and coronavirus testing in 2020 through the Cleveland Clinic Health System. For someone with sleep apnea, which is one of the most common sleep disorders, breathing repeatedly stops and starts during sleep, sometimes 30 times or more an hour and often is accompanied by gasping or snorting sounds. This causes hypoxia. Treatment often involves using what is called positive airway pressure (PAP) while sleeping. The person wears a mask, which has a tube connected to a small PAP machine that sits bedside. It pumps pressurized air into the upper airway, keeping it open and allowing normal breathing. The researchers suggested further studies to determine whether such treatment would improve covid-19 outcomes for people with a sleep disorder. © 1996-2021 The Washington Post

Keyword: Sleep
Link ID: 28126 - Posted: 12.29.2021

By Carl Zimmer Edward O. Wilson, a biologist and author who conducted pioneering work on biodiversity, insects and human nature — and won two Pulitzer Prizes along the way — died on Sunday in Burlington, Mass. He was 92. His death was announced on Monday by the E.O. Wilson Biodiversity Foundation. When Dr. Wilson began his career in evolutionary biology in the 1950s, the study of animals and plants seemed to many scientists like a quaint, obsolete hobby. Molecular biologists were getting their first glimpses of DNA, proteins and other invisible foundations of life. Dr. Wilson made it his life’s work to put evolution on an equal footing. “How could our seemingly old-fashioned subjects achieve new intellectual rigor and originality compared to molecular biology?” he recalled in 2009. He answered his own question by pioneering new fields of research. As an expert on insects, Dr. Wilson studied the evolution of behavior, exploring how natural selection and other forces could produce something as extraordinarily complex as an ant colony. He then championed this kind of research as a way of making sense of all behavior — including our own. As part of his campaign, Dr. Wilson wrote a string of books that influenced his fellow scientists while also gaining a broad public audience. “On Human Nature” won the Pulitzer Prize for general nonfiction in 1979; “The Ants,” which Dr. Wilson wrote with his longtime colleague Bert Hölldobler, won him his second Pulitzer, in 1991. © 2021 The New York Times Company

Keyword: Evolution
Link ID: 28125 - Posted: 12.29.2021

By Karen Brown For decades, Linda Larson has been trying to distance herself from the diagnosis she was given as a teenager: schizophrenia. She accepts that she has the mental disorder but deeply resents the term’s stigma. People hear it and think, “violent, amoral, unhygienic,” she said. Ms. Larson, 74, is part of a group trying to remove that association — by changing the name of the illness. The idea is that replacing the term “schizophrenia” with something less frightening and more descriptive will not only change how the public perceives people with the diagnosis, but also how these people see themselves. Ms. Larson is a member of the Consumer Advisory Board of the Massachusetts Mental Health Center, which is associated with Beth Israel Deaconess Medical Center in Boston. The group has been working with psychiatrists at Harvard to build momentum for a name change, most recently through a national survey published in the journal Schizophrenia Research. “That term over time has become so associated with hopelessness, with dangerousness, with volatile and erratic behavior, that doctors are afraid to use that term with people and their family members,” said Dr. Raquelle Mesholam-Gately, a Harvard psychologist and the lead author of the new paper. “And people who have the condition don’t want to be associated with that name.” As a result, she said, clinicians often avoid making such a devastating diagnosis and many patients and their families don’t seek treatment until after the illness has wreaked considerable damage. Dr. Mesholam-Gately and her team asked about 1,200 people connected to schizophrenia — including those with the disorder, their family members, mental health providers, researchers and government officials — whether it should be called something else. The survey proposed nine alternative names, based partly on the experience of people diagnosed with schizophrenia. Among them: altered perception disorder, attunement disorder, disconnectivity syndrome, integration disorder and psychosis spectrum disorder. © 2021 The New York Times Company

Keyword: Schizophrenia
Link ID: 28124 - Posted: 12.22.2021

By Christof Koch A young Ernest Hemingway, badly injured by an exploding shell on a World War I battlefield, wrote in a letter home that “dying is a very simple thing. I’ve looked at death, and really I know. If I should have died it would have been very easy for me. Quite the easiest thing I ever did.” Years later Hemingway adapted his own experience—that of the soul leaving the body, taking flight and then returning—for his famous short story “The Snows of Kilimanjaro,” about an African safari gone disastrously wrong. The protagonist, stricken by gangrene, knows he is dying. Suddenly, his pain vanishes, and Compie, a bush pilot, arrives to rescue him. The two take off and fly together through a storm with rain so thick “it seemed like flying through a waterfall” until the plane emerges into the light: before them, “unbelievably white in the sun, was the square top of Kilimanjaro. And then he knew that there was where he was going.” The description embraces elements of a classic near-death experience: the darkness, the cessation of pain, the emerging into the light and then a feeling of peacefulness. Peace Beyond Understanding Near-death experiences, or NDEs, are triggered during singular life-threatening episodes when the body is injured by blunt trauma, a heart attack, asphyxia, shock, and so on. About one in 10 patients with cardiac arrest in a hospital setting undergoes such an episode. Thousands of survivors of these harrowing touch-and-go situations tell of leaving their damaged bodies behind and encountering a realm beyond everyday existence, unconstrained by the usual boundaries of space and time. These powerful, mystical experiences can lead to permanent transformation of their lives. © 2021 Scientific American,

Keyword: Consciousness; Stress
Link ID: 28123 - Posted: 12.22.2021

by Anna Goshua A variety of traits, including developmental delay and intellectual disability, characterize people with mutations in the autism-linked gene MYT1L, according to a new study. The gene encodes a transcription factor important for cells that make myelin, which insulates nerve cells and is deficient in some forms of autism. The work, published 8 November in Human Genetics, represents the most detailed study of the traits associated with MYT1L mutations to date. “We wanted to gather more cases to bring a clearer clinical and molecular picture of the condition for lab scientists, clinicians and also for patients and families,” says study investigator Juliette Coursimault, a physician-researcher in the genetics department at Rouen University Hospital in France. She and her co-researchers described 62 people, whereas previous literature included only 12 cases. The new characterization will “benefit clinicians’ diagnosis and treatment strategies when a patient with MYT1L mutation arrives in their clinic,” says Brady Maher, a lead investigator at the Lieber Institute for Brain Development at Johns Hopkins University in Baltimore, Maryland, who was not part of the study. The researchers identified and reviewed data for 22 people with MYT1L mutations who had been described in the academic literature, and collected clinical and molecular data from an additional 40 people, aged 1 to 34 years old, with likely or confirmed pathogenic variants of MYT1L. They recruited the participants through Rouen University Hospital and data-sharing networks such as GeneMatcher, which connects clinicians and researchers. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28122 - Posted: 12.22.2021

By Gretchen Reynolds People who work out regularly and are aerobically fit tend to guzzle a surprising amount of alcohol, according to a new study, well timed for the holidays, of the interplay between fitness, exercise and imbibing. The study, which involved more than 40,000 American adults, finds that active, physically fit men and women are more than twice as likely to be moderate or heavy drinkers as people who are out of shape. The results add to mounting evidence from previous studies — and many of our bar tabs — that exercise and alcohol frequently go hand in hand, with implications for the health effects of each. Many people, and some researchers, might be surprised to learn how much physically active people tend to drink. In general, people who take up one healthy habit, such as working out, tend to practice other salubrious habits, a phenomenon known as habit clustering. Fit, active people seldom smoke, for instance, and tend to eat healthful diets. So, it might seem logical that people who often exercise would drink alcohol sparingly. But multiple studies in recent years have found close ties between working out and tippling. In one of the earliest, from 2001, researchers used survey answers from American men and women to conclude that moderate drinkers, defined in that study as people who finished off about a drink a day, were twice as likely as those who didn’t drink at all to exercise regularly. Later studies found similar patterns among college athletes, who drank substantially more than other collegians, a population not famous for its temperance. © 2021 The New York Times Company

Keyword: Drug Abuse; Obesity
Link ID: 28121 - Posted: 12.22.2021

By Cara Giaimo Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. It’s tough out there for a mouse. Outdoors, its enemies lurk on all sides: owls above, snakes below, weasels around the bend. Indoors, a mouse may find itself targeted by broom-wielding humans or bored cats. Mice compensate with sharp senses of sight, hearing and smell. But they may have another set of tools we’ve overlooked. A paper published last week in Royal Society Open Science details striking similarities between the internal structures of certain small mammal and marsupial hairs and those of man-made optical instruments. In this paper as well as other unpublished experiments, the author, Ian Baker, a physicist who works in private industry, posits that these hairs may act as heat-sensing “infrared antennae” — further cluing the animals into the presence of warm-blooded predators. Although much more work is necessary to connect the structure of these hairs to this potential function, the study paints an “intriguing picture,” said Tim Caro, a professor of evolutionary ecology at the University of Bristol in England who was not involved. Dr. Baker has spent decades working with thermal imaging cameras, which visualize infrared radiation produced by heat. For his employer, the British defense company Leonardo UK Ltd., he researches and designs infrared sensors. But in his spare time he often takes the cameras to fields and forests near his home in Southampton, England, to film wildlife. Over the years, he has developed an appreciation for “how comfortable animals are in complete darkness,” he said. That led him to wonder about the extent of their sensory powers. © 2021 The New York Times Company

Keyword: Pain & Touch; Evolution
Link ID: 28120 - Posted: 12.18.2021

Mir Jalil Razavi Weiying Dai The human brain has been called the most complex object in the known universe. And with good reason: It has around 86 billion neurons and several hundred thousand miles of axon fibers connecting them. Unsurprisingly, the process of brain folding that results in the brain’s characteristic bumps and grooves is also highly complex. Despite decades of speculation and research, the underlying mechanism behind this process remains poorly understood. As biomechanics and computer science researchers, we have spent several years studying the mechanics of brain folding and ways to visualize and map the brain, respectively. Figuring out this complexity may help researchers better diagnose and treat developmental brain disorders such as lissencephaly, or smooth brain, and epilepsy. Because many neurological disorders emerge at the early stages of development, understanding how brain folding works can provide useful insights into normal and pathological brain function. The mechanics of brain folding The brain is made of two layers. The outer layer, called the cerebral cortex, is composed of folded gray matter made up of small blood vessels and the spherical cell bodies of billions of neurons. The inner layer is composed of white matter, consisting mostly of the neurons’ elongated tails, called myelinated axons. When a story fascinates you, remember: Your donations make it possible Illustration of cross section of brain showing axonal pathways transitioning from gray matter into white matter. In recent years, researchers have shown that mechanics, or the forces that objects exert on one another, play an important role in the growth and folding of the brain. © 2010–2021, The Conversation US, Inc.

Keyword: Development of the Brain
Link ID: 28119 - Posted: 12.18.2021

Rafael Yuste Michael Levin In the middle of his landmark book On the Origin of Species, Darwin had a crisis of faith. In a bout of honesty, he wrote, “To suppose that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I confess, absurd in the highest degree.” While scientists are still working out the details of how the eye evolved, we are also still stuck on the question of how intelligence emerges in biology. How can a biological system ever generate coherent and goal-oriented behavior from the bottom up when there is no external designer? In fact, intelligence—a purposeful response to available information, often anticipating the future—is not restricted to the minds of some privileged species. It is distributed throughout biology, at many different spatial and temporal scales. There are not just intelligent people, mammals, birds and cephalopods. Intelligent, purposeful problem-solving behavior can be found in parts of all living things: single cells and tissues, individual neurons and networks of neurons, viruses, ribosomes and RNA fragments, down to motor proteins and molecular networks. Arguably, understanding the origin of intelligence is the central problem in biology—one that is still wide open. In this piece, we argue that progress in developmental biology and neuroscience is now providing a promising path to show how the architecture of modular systems underlies evolutionary and organismal intelligence. © 2021 Scientific American

Keyword: Evolution; Development of the Brain
Link ID: 28118 - Posted: 12.18.2021

Jon Hamilton Scientists may have learned why opioids depress breathing while relieving pain. The finding could lead to pain drugs that don't cause respiratory failure, the usual cause of death in opioid overdoses. When people feel pain, they tend to breathe faster. When they take an opioid to kill that pain, their breathing slows down. Now scientists think they know how pain and respiration are connected in the brain. NPR's Jon Hamilton reports that the discovery could eventually lead to safer pain drugs. JON HAMILTON, BYLINE: Sung Han has been studying the link between pain and breathing in his lab at the Salk Institute in San Diego. But he got a real-world demonstration recently while taking a shower. SUNG HAN: I forgot to change the temperature, and the cold water just suddenly came out and covered my entire body. And then I just - I was breathing really fast. HAMILTON: A typical reaction to what Han calls aversive sensory information - and he thinks he knows the cause. Han's lab has identified a brain circuit in mice that appears to link the emotional experience of pain to breathing rhythm. Han says the circuit involves two populations of brain cells both found in the same small area of the brain stem. HAN: One population regulate pain and the other population regulate breathing, and that's the reason why pain and breathing are interacting each other. HAMILTON: They're linked together. If that's also true in people, it would help explain the mysterious connection between breathing and emotion, which has puzzled scientists for centuries. And the finding, which appears in the journal Neuron, could also have practical applications. That's because both groups of brain cells - the ones for breathing and the ones for pain - respond to opioids. Han says this is why an overdose can be fatal. © 2021 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 28117 - Posted: 12.18.2021