Gabino Iglesias The Man Who Tasted Words is a deep dive into the world of our senses — one that explores the way they shape our reality and what happens when something malfunctions or functions differently. Despite the complicated science permeating the narrative and the plethora of medical explanations, the book is also part memoir. And because of the way the author, Dr. Guy Leschziner, treats his patients — and how he presents the ways their conditions affect their lives and those of the people around them — it is also a very humane, heartfelt book. We rely on vision, hearing, taste, smell, and touch to not only perceive the reality around us but also to help us navigate it by constantly processing stimuli, predicting what will happen based on previous experiences, and filling the gaps of everything we miss as we construct it. However, that truth, the "reality" we see, taste, hear, touch, and smell, isn't actually there; our brains, with the help of our nervous system continuously build it for us. But sometimes our brains or nervous system have a glitch, and that has affects reality. The Man Who Tasted Words carefully looks at — and tries to explain — some of the most bizarre glitches. Sponsor Message "What we believe to be a precise representation of the world around us is nothing more than an illusion, layer upon layer of processing of sensory information, and the interpretation of that information according to our expectations," states Leschziner. When one of those senses doesn't work correctly, that illusion morphs in ways that significantly impact the lives of those whose nervous systems or brain work differently. Paul, for example, is a man who feels no pain. While this sounds like a great "flaw" to have, Leschziner shows it's the opposite. Pain helps humans learn "to avoid sharp or hot objects." It teaches that certain things in our environment are potentially harmful, tells us when we've had an injury and makes us protect it, and even lets us know there's an infection in our body so we can go to the doctor. © 2022 npr

Keyword: Consciousness
Link ID: 28233 - Posted: 03.11.2022

By Roni Caryn Rabin Few of Covid-19’s peculiarities have piqued as much interest as anosmia, the abrupt loss of smell that has become a well-known hallmark of the disease. Covid patients lose this sense even without a stuffy nose; the loss can make food taste like cardboard and coffee smell noxious, occasionally persisting after other symptoms have resolved. Scientists are now beginning to unravel the biological mechanisms, which have been something of a mystery: The neurons that detect odors lack the receptors that the coronavirus uses to enter cells, prompting a long debate about whether they can be infected at all. Insights gleaned from new research could shed new light on how the coronavirus might affect other types of brain cells, leading to conditions like “brain fog,” and possibly help explain the biological mechanisms behind long Covid — symptoms that linger for weeks or months after the initial infection. The new work, along with earlier studies, settles the debate over whether the coronavirus infects the nerve cells that detect odors: It does not. But the virus does attack other supporting cells that line the nasal cavity, the researchers found. The infected cells shed virus and die, while immune cells flood the region to fight the virus. The subsequent inflammation wreaks havoc on smell receptors, proteins on the surface of the nerve cells in the nose that detect and transmit information about odors. The process alters the sophisticated organization of genes in those neurons, essentially short-circuiting them, the researchers reported. Their paper significantly advances the understanding of how cells critical to the sense of smell are affected by the virus, despite the fact that they are not directly infected, said Dr. Sandeep Robert Datta, an associate professor of neurobiology at Harvard Medical School, who was not involved in the study. © 2022 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28232 - Posted: 03.05.2022

Linda Geddes Setting daily meat reduction goals and keeping an online diary of intake helped frequent meat eaters to halve their consumption in just over nine weeks, a trial has found. The trial, by researchers at the University of Oxford’s Livestock, Environment and People (Leap) programme, also found the routine was popular with participants, who felt it supported them to change their diet. Many people wish to reduce their meat consumption, whether for health or environmental reasons, or animal welfare concerns. Leap researchers wondered whether tapping into psychological principles employed by weight-loss apps, such as Noom, could help boost participants’ resolve. They developed an online platform called the Optimise meat tracker (standing for online programme to tackle individuals’ meat intake through self-regulation). Users log on and pick one meat reduction strategy from a list to focus on for that day, such as “try a new vegetarian recipe”, or “eat no processed meat”. The next morning they report whether they achieved this and record how much fish, poultry, red and processed meat they consumed. They receive weekly feedback on how they have done. The approach is based on self-regulation theory: the idea that people monitor and contextualise their own behaviour, reflect on it in relation to their goals, and try to modify it in response to feedback. “We know that people tend to underestimate the amount of meat they eat, the health and environmental impacts of their meat consumption; we also know that our meat-eating habits are strongly engrained. This process of self-regulation tries to tap into all of that,” said Dr Cristina Stewart at the University of Oxford, who led the research. © 2022 Guardian News & Media Limited

Keyword: Obesity
Link ID: 28231 - Posted: 03.05.2022

Brian Mann Nine state attorneys general have agreed to drop their objection to a deal granting immunity from opioid lawsuits to members of the Sackler family who own Purdue Pharma, the maker of OxyContin. In exchange, the family has agreed to increase the amount it pays from personal holdings from roughly $4.5 billion under a previous settlement to $6 billion. Washington state Attorney General Robert Ferguson described the terms of the new settlement as a victory. "Rather than join the majority of states in settlement, Washington chose to lead the fight against the Sacklers and Purdue," Ferguson said in a statement. "As a result, we won more than $100 million for Washington state to address the opioid epidemic, and more than $1 billion for states, cities and tribes across the country." The prior deal was overturned by a federal judge in Manhattan last December after some states and the Justice Department filed an appeal. States demanding more money from the Sacklers — California, Connecticut, Delaware, Maryland, New Hampshire, Oregon, Vermont and Washington — have among the highest overdose death rates in the country. In a statement, members of various branches of the Sackler family again denied any wrongdoing and described the settlement as one that will "allow very substantial additional resources to reach people and communities in need." "While the families have acted lawfully in all respects, they sincerely regret that OxyContin, a prescription medicine that continues to help people suffering from chronic pain, unexpectedly became part of an opioid crisis that has brought grief and loss to far too many families and communities." Critics, including many of the state attorneys general who approved this deal, have long accused members of the Sackler family of aggressively marketing opioids in ways that contributed to soaring rates of addiction and overdoses. © 2022 npr

Keyword: Drug Abuse
Link ID: 28230 - Posted: 03.05.2022

By Christa Hillstrom To hear more audio stories from publications like The New York Times, download Audm for iPhone or Android. In 2017, when Becky was about to turn 40, she woke up in the middle of the night and was startled by her reflection in the bathroom mirror. Her face, gaunt from weight loss, looked pale. A scar snaked under her chin from when her boyfriend punched her. Her nostrils were now asymmetrical from when he broke her nose. Smaller scars marked her eyebrows and her bottom lip, where a tooth once cut through. She always wore her hair in a bun to mask a bald spot; he had slammed her head against a door frame, and she had needed staples there. She could barely hear from one ear. Her chipped front tooth was harder to hide than the broken molars knocked loose during two decades of beatings. When she went shopping, she would hold items in her hands, assessing how much damage they would do to her body. She had stopped buying leather belts, the braided kind. She remembered getting some of her injuries. With others, the memories hung fuzzy and distant. They met in 1996, when she was a teenager with a new baby. She had already spent years raising her younger siblings when her own mother, who suffered from mental illness and was a survivor of domestic abuse, could not. The first time Becky remembers her boyfriend hurting her, about six months into their relationship, was when he was joking around: a tug on her hair that was surprisingly forceful. Underneath the laughing, something felt mean. And then the meanness got darker. From the beginning of their relationship, Becky’s boyfriend drew the reins tightly around their lives. She could never predict what would set him off. Some days, he attacked her for sleeping too late; others, for waking him up too early. He hit her when the house was too messy or if he wasn’t in the mood for the breakfast she made. Becky, who asked to be identified by a nickname for her safety, often showed up to work with bruises on her face, caked over with foundation, but her co-workers never said anything. © 2022 The New York Times Company

Keyword: Brain Injury/Concussion; Aggression
Link ID: 28229 - Posted: 03.02.2022

Researchers at the National Eye Institute (NEI) have discovered that power-producing organelles in the eye’s photoreceptor cells, called mitochondria, function as microlenses that help channel light to these cells’ outer segments where it’s converted into nerve signals. The discovery in ground squirrels provides a more precise picture of the retina’s optical properties and could help detect eye disease earlier. The findings, published today in Science Advances, also shed light on the evolution of vision. NEI is part of the National Institutes of Health. “We were surprised by this fascinating phenomenon that mitochondria appear to have a dual purpose: their well-established metabolic role producing energy, as well as this optical effect,” said the study’s lead investigator, Wei Li, Ph.D./B.M., who leads the NEI Retinal Neurophysiology Section. Using a modified confocal microscope, the researchers observed the optical properties of living cone mitochondria exposed to light. The path of light became concentrated with transmission from the inner to the outer segments of cone photoreceptors. Credit: John Ball, Ph.D., NEI The findings also address a long-standing mystery about the mammalian retina. Despite evolutionary pressure for light to be translated into signals and pass instantly from the retina to the brain, the trip is hardly direct. Once light reaches the retina, it must pass through multiple neural layers before reaching the outer segment of photoreceptors, where phototransduction (the conversion of light’s physical energy into cellular signals) occurs. Photoreceptors are long, tube-like structures divided into inner and outer segments. The last obstacle a photon must traverse before moving from the inner to the outer segment is an unusually dense bundle of mitochondria. Those bundles of mitochondria would seem to work against the process of vision either by scattering light or absorbing it. So, Li’s team set out to investigate their purpose by studying cone photoreceptors from the 13-lined ground squirrel.

Keyword: Vision
Link ID: 28228 - Posted: 03.02.2022

by Niko McCarty The ‘opto’ in optogenetics — the powerful method some autism researchers use to control neurons in mice and other animals — comes from the Greek optós, meaning visible. It’s a nod to the blue light used to switch on select neurons. A new technique can do the same, albeit with something invisible: sound. In a study published in Nature Communications this month, researchers engineered neurons in the motor cortex of mice to express an ultrasound-sensitive ion channel protein called hsTRPA1. They placed an ultrasound transducer near the animal’s skull and switched it on. The response? A flex of a muscle, a perceptible twitch. The approach, called sonogenetics, enables noninvasive control over any neural circuit that can be manipulated with optogenetics, an invasive method, says lead investigator Sreekanth Chalasani, associate professor in the Molecular Neurobiology Laboratory at the Salk Institute for Biological Studies in La Jolla, California. Spectrum spoke to Chalasani about his early experiments in Caenorhabditis elegans, lucky number 63 and how sonogenetics could one day have clinical applications. Spectrum: Our readers might be familiar with optogenetics, but I’m assuming sonogenetics is new for most people. Sreekanth Chalasani: Yeah. Well, the idea in sonogenetics is that we want to manipulate things noninvasively. Ultrasound can travel through bone and skin, into the body. We’ve been using it for decades. It’s safe. The question is: Can we leverage it to get in the body and control cells, like with optogenetics? S: Literally controlling cells with sound. SC: Right. In optogenetics, light triggers action potentials in cells that have a channelrhodopsin, or opsin, protein. In sonogenetics, we wanted a protein that would let us have that same level of cellular control. But finding that protein has been difficult. Lots of groups have been looking for these proteins, and we were fortunate to find one. © 2022 Simons Foundation

Keyword: Brain imaging
Link ID: 28227 - Posted: 03.02.2022

By Jan Hoffman For years, Dr. Xiulu Ruan was one of the nation’s top prescribers of quick-release fentanyl drugs. The medicines were approved only for severe breakthrough pain in cancer patients, but Dr. Ruan dispensed them almost exclusively for more common ailments: neck aches, back and joint pain. According to the Department of Justice, he and his partner wrote almost 300,000 prescriptions for controlled substances from 2011 to 2015, filled through the doctors’ own pharmacy in Mobile, Ala. Dr. Ruan often signed prescriptions without seeing patients, prosecutors said. Dr. Ruan has been serving a 21-year sentence in federal prison, convicted in 2017 for illegally prescribing opioids and related financial crimes. To collect millions of dollars in fines, the government seized houses, beach condos and bank accounts belonging to him and his business partner, as well as 23 luxury cars, such as Bentleys, Lamborghinis and Ferraris. On Tuesday, lawyers both for Dr. Ruan and for Dr. Shakeel Kahn, who is serving 25 years on charges related to pill mill clinics in Arizona and Wyoming will argue before the Supreme Court of the United States that the criminal standard the physicians faced is applied inconsistently among the federal circuits. In asking that the doctors’ convictions be overturned, they want the court to establish a uniform standard that permits doctors to raise a “good faith” defense. Juries could then consider whether doctors subjectively believed they were using their best medical judgment. The likelihood of these two doctors being set free is small, legal experts believe, but the court’s decision on the broader legal questions could have significant implications for the latitude doctors can take in prescribing potentially addictive painkillers and other restricted medications. The cases confront an uneasy relationship between law and medicine. In an era when overdose deaths are soaring, how should the law balance letting physicians exercise their best judgment with stopping egregious outliers? © 2022 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 28226 - Posted: 03.02.2022

By Gina Kolata Dr. John Q. Trojanowski, a neuropathologist whose work was at the forefront of research on Alzheimer’s and other neurodegenerative diseases, died on Feb. 8 in a hospital in Philadelphia. He was 75. His wife and longtime collaborator, Virginia M.-Y. Lee, said the cause was complications of chronic spinal cord injuries. Dr. Trojanowski “was a giant in the field,” said Leslie Shaw, a professor with Dr. Trojanowski in the department of pathology and laboratory medicine at the University of Pennsylvania — adding that he meant that in two ways. At 6 feet 4 inches, Dr. Trojanowski towered over his colleagues. And, Dr. Shaw said, he was also a towering figure in his field, whose scientific contributions were “phenomenal” because they combined pathology and biochemistry to figure out what goes wrong, and why, when people get diseases as disparate as Alzheimer’s, Parkinson’s and A.L.S. The results can lead to improved diagnosis and potential treatments. Key to the work Dr. Trojanowski did with Dr. Lee was their establishment of a brain bank: stored brains from patients with diseases like Alzheimer’s and Parkinson’s, as well as from people without degenerative brain diseases. It allowed them to compare the brains of people with and without the conditions and ask what proteins were involved in the diseases and what brain regions were affected. Among their first quests was an attempt to solve the mystery of strange areas in the brains of people with Alzheimer’s. Known as tangles and first described by Alois Alzheimer himself at the turn of the 20th century, they look like twisted strands of spaghetti in dying nerve cells. In 1991, Dr. Trojanowski and Dr. Lee determined that the regions are made up of a malformed protein called tau, which causes the structure of nerve cells to collapse. At a time when most Alzheimer’s researchers and drug companies were focused on a different protein, amyloid, Dr. Trojanowski and Dr. Lee insisted that tau was equally important. They then discovered that it also played a central role in a rare group of degenerative dementias known as frontotemporal lobar degeneration. © 2022 The New York Times Company

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 28225 - Posted: 03.02.2022

By Linda Searing Depression affects about 280 million people worldwide, including about 5 percent of all adults, according to data from the World Health Organization and a report from the World Psychiatric Association Commission, an international research group. The commission describes depression as “one of the leading causes of avoidable suffering and premature mortality in the world” and labels it a neglected global health crisis. FAQ: What to know about the omicron variant of the coronavirus In the United States, an estimated 21 million adults, or about 8 percent of those 18 and older, are living with depression, according to the National Institute of Mental Health. In addition, the Centers for Disease Control and Prevention note that roughly 11 percent of all physician office visits and emergency department visits are related to depression. Though most everyone feels sad or gloomy from time to time, depression — what the medical world refers to as depressive disorder or major depression — goes beyond simple mood fluctuations. Rather, such feelings as sadness, hopelessness or low self-worth, loss of interest in usual activities, sleep problems and lack of energy persist for two weeks or more, interfering with a person’s everyday life. Genetics, chemical changes in the brain and stressful events are among factors believed to be responsible for depressive episodes. Left untreated, depression can have devastating effects. But treatment — which may include such approaches as talk therapy, medication, exercise, light therapy or acupuncture — can ease symptoms and help prevent a recurrence. However, the World Psychiatric Association Commission report, published in the Lancet, notes that about half of people suffering from depression in high-income countries are not diagnosed or treated, a number that increases to as much as 90 percent of those with depression who live in low- and middle-income countries. © 1996-2022 The Washington Post

Keyword: Depression
Link ID: 28224 - Posted: 03.02.2022

By Kim Tingley Denis Burkitt, an Irish surgeon, traveled to Africa during World War II as a member of the Royal Army Medical Corps, and afterward he settled in Uganda to practice medicine. There he observed that a surprising number of children developed strange jaw tumors, a cancer that would come to be known as Burkitt lymphoma. Eventually, Burkitt sent samples of the tumor cells to Middlesex Hospital Medical School in London, where Michael Anthony Epstein, a pathologist, and his colleagues Yvonne Barr and Bert Achong examined them through an electron microscope. Their findings — they noticed particles shaped like a herpesvirus, only smaller — were published in a landmark paper in The Lancet in 1964 and spurred the realization that this newly identified member of the Herpes​viridae family, subsequently named Epstein-Barr virus, was a cause of Burkitt lymphoma. It was the first evidence that a viral infection could lead to cancer. The virus has since been shown to increase the risk of Hodgkin lymphoma, as well as nasopharyngeal and stomach cancer. It is also the virus most often responsible for infectious mononucleosis, a disease usually characterized by extreme fatigue, sore throat, fever and swollen lymph nodes in the neck. These symptoms can last for weeks and, in chronic cases, recur for years. We now know that upward of 90 percent of adults have the Epstein-Barr virus. As happens with other herpes​viruses, once you have been infected, the virus stays with you forever — it deposits its DNA alongside yours in the nucleus of many of your cells. (RNA viruses, like SARS-CoV-2, can be cleared from your body.) Most people contract Epstein-Barr in childhood: It is spread through body fluids, usually saliva; kissing is a frequent route of transmission (as may be the sharing of utensils). Young children, if they get sick at all, typically develop symptoms indistinguishable from those of a cold or flu; mono is more common when the first infection happens after puberty. “Most people never know they’re infected,” says Jeffrey Cohen, the chief of the Laboratory of Infectious Diseases at the National Institute of Allergy and Infectious Diseases. © 2022 The New York Times Company

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28223 - Posted: 02.26.2022

By Amanda Coletta Health officials in New Brunswick released a long-awaited report Thursday into a mysterious and debilitating neurological disorder that has struck dozens of people with bizarre symptoms — including a belief that family members have been replaced by impostors — stumped doctors and stoked fears across the province. The conclusion? There is no new disorder. “The oversight committee has unanimously agreed that these 48 people should never have been identified as having a neurological syndrome of unknown cause, and that based on the evidence reviewed, no such syndrome exists,” said Jennifer Russell, chief medical officer of health for the Canadian province. “Public Health concurs with these findings. But I stress again, this does not mean that these people aren’t seriously ill. It means they are ill with a known neurological condition.” The report’s authors say the 48 cases in what was thought to be a cluster were randomly allocated to pairs of neurologists who reviewed them and presented their findings to an oversight committee of six New Brunswick neurologists and other officials. The committee said none of the cases met the full criteria of the case definition. But that finding, coming at the end of an investigation marred by accusations of opacity from the start and allegations that Canada’s top scientists and experts from around the world had been abruptly shut out of the process, appeared unlikely to assuage alarm in the province and more likely to deepen mistrust. Patients and their family members questioned the committee’s findings Thursday, saying the province has not carried out the relevant testing and opted to “abandon scientific rigor in exchange for political expediency.” © 1996-2022 The Washington Post

Keyword: Stress; Prions
Link ID: 28222 - Posted: 02.26.2022

By Maryam Clark, science writer Neuroscientists have recorded the activity of a dying human brain and discovered rhythmic brain wave patterns around the time of death that are similar to those occurring during dreaming, memory recall, and meditation. Now, a study published to Frontiers brings new insight into a possible organizational role of the brain during death and suggests an explanation for vivid life recall in near-death experiences. Imagine reliving your entire life in the space of seconds. Like a flash of lightning, you are outside of your body, watching memorable moments you lived through. This process, known as ‘life recall’, can be similar to what it’s like to have a near-death experience. What happens inside your brain during these experiences and after death are questions that have puzzled neuroscientists for centuries. However, a new study published to Frontiers in Aging Neuroscience suggests that your brain may remain active and coordinated during and even after the transition to death, and be programmed to orchestrate the whole ordeal. When an 87-year-old patient developed epilepsy, Dr Raul Vicente of the University of Tartu, Estonia and colleagues used continuous electroencephalography (EEG) to detect the seizures and treat the patient. During these recordings, the patient had a heart attack and passed away. This unexpected event allowed the scientists to record the activity of a dying human brain for the first time ever.

Keyword: Consciousness; Attention
Link ID: 28221 - Posted: 02.26.2022

By David A. Kaplan Our cross-country drive last winter from New York to Lake Tahoe was going to be eventful enough, with a pandemic, blizzards and the cancellation of salads at McDonald’s. But by Omaha, when the lanes on Interstate 80 seemed to be bouncing around before my very eyes, we entered unexpected territory. “Are you practicing your slalom turns at 80 miles an hour?” my wife asked. Road conditions were normal. Our S.U.V. had new tires. But the lanes often seemed to blur together. Sometimes the melding of lanes occurred late in the day, sometimes early. Sometimes in blinding sun, sometimes in fog. If I closed one eye, the lanes became separate again. What was happening? I’d worn glasses for nearsightedness since fifth grade; I’d seen my eye doctor within the year; my prescription was current. When we reached Tahoe, I went to an optometrist before even unpacking my skis. She said my eyes were fine, but advised an M.R.I. to rule out a brain bleed or a tumor. Days later, it did. She also told me to see a neuro-ophthalmologist, an increasingly rare subspecialty. Nationally, there are only about 600 of them, and because many do academic research or have general ophthalmic practices, just 250 of them are full-time clinicians. In six states, there are none practicing, according to a paper in the Journal of Neuro-Ophthalmology last year. The Tahoe optometrist warned it could take months to obtain an appointment with one of the few practitioners in the area. But my brother, a surgeon at Stanford, helped me get an appointment at Stanford Medical Center, four hours away, in Palo Alto, Ca., the following week. Dr. Heather Moss conducted the 90-minute examination, taking measurements that included the degree to which my eyes were properly centered. © 2022 The New York Times Company

Keyword: Vision
Link ID: 28220 - Posted: 02.26.2022

By Diana Kwon People with a rare genetic disorder known as Prader-Willi syndrome never feel full, and this insatiable hunger can lead to life-threatening obesity. Scientists studying the problem have now found that the fist-shaped structure known as the cerebellum—which had not previously been linked to hunger—is key to regulating satiation in those with this condition. This finding is the latest in a series of discoveries revealing that the cerebellum, long thought to be primarily involved in motor coordination, also plays a broad role in cognition, emotion and behavior. “We’ve opened up a whole field of cerebellar control of food intake,” says Albert Chen, a neuroscientist at the Scintillon Institute in California. The project began with a serendipitous observation: Chen and his team noticed they could make mice stop eating by activating small pockets of neurons in regions known as the anterior deep cerebellar nuclei (aDCN), within the cerebellum. Intrigued, the researchers contacted collaborators at Harvard Medical School. Scientists there had gathered data using functional MRI to compare brain activity in 14 people who had Prader-Willi syndrome with activity in 14 unaffected people while each subject viewed images of food—either immediately following a meal or after fasting for at least four hours. New analysis of these scans revealed that activity in the same regions Chen’s group had pinpointed in mice, the aDCN, appeared to be significantly disrupted in humans with Prader-Willi syndrome. In healthy individuals, the aDCN were more active in response to food images while fasting than just after a meal, but no such difference was identifiable in participants with the disorder. The result suggested that the aDCN were involved in controlling hunger. Further experiments on mice, conducted by researchers from several different institutions, demonstrated that activating the animals’ aDCN neurons dramatically reduced food intake by blunting how the brain’s pleasure center responds to food. The findings were recently detailed in Nature. © 2022 Scientific American,

Keyword: Obesity
Link ID: 28219 - Posted: 02.26.2022

Dominique Potvin When we attached tiny, backpack-like tracking devices to five Australian magpies for a pilot study, we didn’t expect to discover an entirely new social behaviour rarely seen in birds. Our goal was to learn more about the movement and social dynamics of these highly intelligent birds, and to test these new, durable and reusable devices. Instead, the birds outsmarted us. As our new research paper explains, the magpies began showing evidence of cooperative “rescue” behaviour to help each other remove the tracker. While we’re familiar with magpies being intelligent and social creatures, this was the first instance we knew of that showed this type of seemingly altruistic behaviour: helping another member of the group without getting an immediate, tangible reward. As academic scientists, we’re accustomed to experiments going awry in one way or another. Expired substances, failing equipment, contaminated samples, an unplanned power outage—these can all set back months (or even years) of carefully planned research. For those of us who study animals, and especially behaviour, unpredictability is part of the job description. This is the reason we often require pilot studies. Our pilot study was one of the first of its kind—most trackers are too big to fit on medium to small birds, and those that do tend to have very limited capacity for data storage or battery life. They also tend to be single-use only. A novel aspect of our research was the design of the harness that held the tracker. We devised a method that didn’t require birds to be caught again to download precious data or reuse the small devices. © 1986–2022 The Scientist.

Keyword: Evolution; Learning & Memory
Link ID: 28218 - Posted: 02.26.2022

Nicola Davis Science correspondent It may not yet feature in a West End musical but scientists say they have found an unexpected response to singin’ in the brain. Researchers say they have found particular groups of neurons that appear to respond selectively to the sound of singing. Writing in the journal Current Biology, a team of scientists in the US report how they made their discovery by recording electrical activity in the brains of 15 participants, each of whom had electrodes inserted inside their skulls to monitor epileptic seizures before undergoing surgery. The team recorded electrical activity in response to 165 different sounds, from pieces of instrumental music to speech and sounds such as dogs barking, and then processed them using an algorithm. They combined the results with data from fMRI brain scans previously collected from 30 different individuals to map the location of the patterns in the brain. Dr Samuel Norman-Haignere, a co-author of the study based at the University of Rochester, said the team decided to combine the data from the different approaches to overcome their respective weaknesses and combine their strengths. “fMRI is one of the workhorses of human cognitive neuroscience, but it is very coarse. Intracranial data is much more precise but has very poor spatial coverage,” he said. The results confirmed previous findings from fMRI scans that some neurons respond only to speech or respond more strongly to music. However, they also revealed populations of neurons that appear to respond selectively to the sound of singing, showing only very weak responses to other types of music or speech alone. © 2022 Guardian News & Media Limited

Keyword: Hearing; Attention
Link ID: 28217 - Posted: 02.23.2022

Brian Mann Over the next two weeks, some of the biggest U.S. corporations accused of "turbocharging" the opioid epidemic could finalize payouts to victims and governments worth roughly $32 billion. "We've lost more than a million Americans to this epidemic, and sadly, it's at an all-time high as overdose deaths continue to rise," said Texas Attorney General Ken Paxton last week, in a statement announcing his state is now in line to receive roughly $1.1 billion. Paxton said pharmaceutical companies that made, distributed and sold opioids were "at the root of the problem." Their payments will help fund "treatment for those currently still struggling with opioid addiction," he added. This comes as communities across the U.S. are scrambling for resources to combat an opioid crisis that keeps getting worse. Drug overdoses killed more than 104,000 Americans in the most recent 12-month period for which data is available, according to the Centers for Disease Control and Prevention. That's a tragic new record for the U.S. There are two major negotiations nearing completion. The largest involves major drug distributors and wholesalers AmerisourceBergen, Cardinal Health and McKesson, along with health products giant Johnson & Johnson. Article continues after sponsor message The four firms, which maintain they did nothing wrong, have tentatively agreed to payouts totaling $26 billion. The Texas money would come from that deal, as would roughly $590 million that would go to Native American tribes. © 2022 npr

Keyword: Drug Abuse
Link ID: 28216 - Posted: 02.23.2022

by Laura Dattaro Some genomic areas that help determine cerebellar size are associated with autism, schizophrenia and bipolar disorder, according to a new study. But heritable genetic variants across the genome that also influence cerebellar size are not. The cerebellum sits at the base of the skull, below and behind the much larger cerebrum. It coordinates movement and may also play roles in social cognition and autism, according to previous research. The new work analyzed genetic information and structural brain scans from more than 33,000 people in the UK Biobank, a biomedical and genetic database of adults aged 40 to 69 living in the United Kingdom. A total of 33 genetic sequence variants, known as single nucleotide polymorphisms (SNPs), were associated with differences in cerebellar volume. Only one SNP overlapped with those linked to autism, but the association should be explored further in other cohorts, says lead investigator Richard Anney, senior lecturer in bioinformatics at Cardiff University in Wales. “There’s lots of caveats to say why it might be worth following up on,” Anney says. “But from this data alone, it’s not telling us there’s a major link between [autism] and cerebellar volume.” So far, cognitive neuroscientists have largely ignored the cerebellum, says Jesse Gomez, assistant professor of neuroscience at Princeton University, who was not involved in the work. The new study represents a first step in better understanding genetic influences on the brain region and its role in neurodevelopmental conditions, he says. “It’s a fun paper,” Gomez says. “It’s the beginning of what’s an exciting revolution in the field.” Of the 33 inherited variants Anney’s team found, 5 had not previously been significantly associated with cerebellar volume. They estimated that the 33 variants account for about 50 percent of the differences in cerebellar volume seen across participants. © 2022 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28215 - Posted: 02.23.2022

By Ellen Barry A new book by Dr. Thomas P. Insel, who for 13 years ran the United States’ foremost mental health research institution, begins with a sort of confession. During his tenure as the “nation’s psychiatrist,” he helped allocate $20 billion in federal funds and sharply shifted the focus of the National Institute of Mental Health away from behavioral research and toward neuroscience and genetics. “I should have been able to help us bend the curves for death and disability,” Dr. Insel writes. “But I didn’t.” Dr. Insel, 70, who left N.I.M.H. in 2015, calls the advances in neuroscience of the last 20 years “spectacular” — but in the very first pages of his new book, he says that, for the most part, they haven’t yet benefited patients. His book, “Healing: Our Path From Mental Illness to Mental Health,” is not an indictment of the science to which he devoted much of his adult life. Instead, it chronicles failures in virtually every other element of our mental health system, including the ineffective delivery of care, the gutting of community health services and the reliance on police and jails for crisis services. It also calls out a paradox: that the United States, a country that leads the world in spending on medical research, also stands out for its dismal outcomes in people with mental illnesses. Indeed, over the last three decades, even as the government invested billions of dollars in better understanding the brain, by some measures, those outcomes have deteriorated. The country’s long spell without breakthrough treatments can be attributed, in part, to the complexity of the brain. Dr. Insel rose through the ranks at a time of optimism that advances in neurobiology would lead to new treatments, and as head of N.I.M.H., as he put it, he “bet big on genomics.” But 20 years later, he said the role that genes play in schizophrenia and bipolar disorder has proven to be extraordinarily complex. “Each of those variants that have been discovered just account for a tiny, tiny amount of risk, so in aggregate, they’re probably significant, but you have to put a hundred of them together,” he said. “So we started doing bigger and bigger studies to find smaller and smaller effects.” © 2022 The New York Times Company

Keyword: Depression; Schizophrenia
Link ID: 28214 - Posted: 02.23.2022