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By Benedict Carey Scott Lilienfeld, an expert in personality disorders who repeatedly disturbed the order in his own field, questioning the science behind many of psychology’s conceits, popular therapies and prized tools, died on Sept. 30 at his home in Atlanta. He was 59. The cause was pancreatic cancer, his wife, Candice Basterfield, said. Dr. Lilienfeld’s career, most of it spent at Emory University in Atlanta, proceeded on two tracks: one that sought to deepen the understanding of so-called psychopathic behavior, the other to expose the many faces of pseudoscience in psychology. Psychopathy is characterized by superficial charm, grandiosity, pathological lying and a lack of empathy. Descriptions of the syndrome were rooted in research in the criminal justice system, where psychopaths often end up. In the early 1990s, Dr. Lilienfeld worked to deepen and clarify the definition. In a series of papers, he anchored a team of psychologists who identified three underlying personality features that psychopaths share, whether they commit illegal acts or not: fearless dominance, meanness and impulsivity. The psychopath does what he or she wants, without anxiety, regret or regard for the suffering of others. “When you have these three systems interacting, it’s a bad brew, and it creates the substrate for what can become psychopathy,” said Mark F. Lenzenweger, a professor of psychology at the State University of New York at Binghamton. “This was Scott’s great contribution: He helped change the thinking about psychopathy, in a profound way, by focusing on aspects of personality, rather than on a list of bad behaviors.” Dr. Lilienfeld’s parallel career encompassed clinical psychology and aimed to shake it free of empty theorizing, softheadedness and bad practice. In the late 1990s and early 2000s, he led a loose group of researchers who began to question the validity of some of the field’s favored constructs, like repressed memories of abuse and multiple personality disorder. The Rorschach inkblot test took a direct hit as largely unreliable. The group also attacked treatments including psychological debriefing and eye movement desensitization and reprocessing, or E.M.D.R., both of which are used for trauma victims. © 2020 The New York Times Company
Keyword: Aggression; Learning & Memory
Link ID: 27529 - Posted: 10.19.2020
By Lydia Denworth, Spectrum, Brendan Borrell, Allyson Berent is a specialty veterinarian in New York City. She treats animals that other doctors cannot help. When no good therapies are available, she invents one. Cats and dogs consumed almost all of her time—until 6 years ago, when her second daughter was born. As a baby, Quincy appeared healthy and happy, smiling at an early age and giggling frequently. But during her first few months of life, she missed many developmental milestones: At 10 weeks, she was not making eye contact. When her parents waved toys in front of her, she stared blankly. She had trouble feeding. And when she was lying on her stomach, she could not lift her head. Doctors kept telling Berent and her husband to give it time, but the couple insisted on genetic testing: At 7 months old, their daughter was diagnosed with Angelman syndrome, a neurodevelopmental condition that affects as many as one in 12,000 people. Most people with Angelman syndrome have severe intellectual disability. They never talk or live an independent life. They experience seizures, gut issues, and sleeping and feeding difficulties. Due to balance and motor problems, they are usually unable or barely able to walk. Many also meet the diagnostic criteria for autism. Within days of learning her daughter’s diagnosis, Berent set herself a new goal: curing Quincy. With her medical background, she had no trouble parsing the scientific research on Angelman syndrome. She learned that it stems from a missing or mutated copy of a gene called UBE3A, which generates a protein essential for healthy brain activity. People inherit two copies of UBE3A, one from each parent, but the paternal copy is typically silent. In about 70% of people with Angelman, the maternal copy is absent, and they produce none of the protein. Many others with the syndrome have a small mutation in the mother’s copy, rendering it ineffective. © 2020 American Association for the Advancement of Science.
Keyword: Autism; Development of the Brain
Link ID: 27528 - Posted: 10.16.2020
Jon Hamilton Researchers appear to have shown how the brain creates two different kinds of thirst. The process involves two types of brain cells, one that responds to a decline in fluid in our bodies, while the other monitors levels of salt and other minerals, a team reports in the journal Nature. Together, these specialized thirst cells seem to determine whether animals and people crave pure water or something like a sports drink, which contains salt and other minerals. "Our brain can detect these two distinct stimuli with different cell types," says Yuki Oka, a professor of biology at Caltech and the study's lead author. The finding appears to help answer "this question that we've been trying to ask for decades and decades and decades," says Sean Stocker, a professor at the University of Pittsburgh who studies water and salt balance in the body. Stocker was not involved in the study. Oka's research is part of an effort to understand the brain biology underlying behavior that's seen in people and many animals. Article continues after sponsor message For example, people who've just finished a long, sweaty workout often experience a special kind of thirst. "Pure water doesn't do it, right? It's not enough," Oka says. "You need water and salt to recover. And we can easily imagine that under such condition, we crave [a] sport drink." Sports drinks like Gatorade generally include a mix of salt and sugar, as well as water. To understand what triggers this type of thirst, Oka's team studied cells in two regions of mouse brains. Both regions are known to contain neurons involved in the sensation of thirst. © 2020 npr
Keyword: Miscellaneous
Link ID: 27527 - Posted: 10.16.2020
by Angie Voyles Askham Autism is a neurodevelopmental condition. Although it is diagnosed based on the presence of two core behaviors — restricted interests and repetitive behaviors, as well as difficulties with social interactions and communication — those traits are thought to arise because of alterations in how different parts of the brain form and connect to one another. No research has uncovered a ‘characteristic’ brain structure for autism, meaning that no single pattern of changes appears in every autistic person. Studies of brain structure often turn up dissimilar results — there is great variety across individuals in general. But some trends have begun to emerge for subsets of autistic people. These differences might one day provide some insight into how some autistic people’s brains function. They may also point to bespoke treatments for particular subtypes of autism. Here is what we know about how brain structure differs between people with and without autism. Which brain regions are known to be structurally different between autistic and non-autistic people? Children and adolescents with autism often have an enlarged hippocampus, the area of the brain responsible for forming and storing memories, several studies suggest, but it is unclear if that difference persists into adolescence and adulthood1,2. © 2020 Simons Foundation
Keyword: Autism
Link ID: 27526 - Posted: 10.16.2020
Frank R. Lin, M.D., Ph.D. When I was going through my otolaryngology residency at Johns Hopkins in the early 2000s, I was struck by the disparity between how hearing loss was managed in children and in older adults. In the case of the child, it was a medical priority to ensure access to a hearing aid so he or she could communicate optimally at home and in school, and such devices were covered by insurance. This approach was justified based on extensive research demonstrating that hearing loss could have a substantial impact on a child’s cognitive and brain development, with lifetime consequences for educational and vocational achievement. For the older adult, the approach was radically different, even if the degree of hearing impairment was the same as in the child. The adult would be reassured that the deficit was to be expected, based on his or her age, and told that a hearing aid, if desired, would represent an out-of-pocket expense averaging about $4,000. Medicare provided no coverage for hearing aids. There was no robust research demonstrating meaningful consequences of hearing loss for older adults, as there was for children, and the clinical approach was typically guided by the notion that it was a very common, and hence inconsequential, aspect of aging. But this approach didn’t make sense, given what I had observed clinically. Older adults with hearing loss recounted to me their sense of isolation and loneliness, and the mental fatigue of constantly concentrating in trying to follow conversations. Family members would often describe a decline in patients’ general well-being and mental acuity as they struggled to hear. For those who obtained effective treatment for their hearing loss with hearing aids or a cochlear implant, the effects were often equally dramatic. Patients spoke of reengaging with family, no longer getting fatigued from straining to listen, and becoming their “old selves” again. If hearing was fundamentally important for children and represented a critical sensory input that could affect brain function, wouldn’t loss of hearing have corresponding implications for the aging brain and its function? © 2020 The Dana Foundation.
Keyword: Hearing; Alzheimers
Link ID: 27525 - Posted: 10.16.2020
By Nicholas Bakalar Weighted blankets, which have long been popular aids to induce calm, could help reduce insomnia, a new study suggests. Swedish researchers studied 121 patients with depression, bipolar disorder and other psychiatric diagnoses, all of whom had sleep problems. They randomly assigned them to two groups. The first slept with an 18-pound blanket weighted with metal chains, and the second with an identical looking three-pound plastic chain blanket. The study, in the Journal of Clinical Sleep Medicine, used the Insomnia Severity Index, a 28-point questionnaire that measures sleep quality, and participants wore activity sensors on their wrists to measure sleep time, awakenings and daytime activity. More than 42 percent of those using the heavy blanket scored low enough on the Insomnia Severity Index to be considered in remission from their sleep troubles, compared with 3.6 percent of the controls. The likelihood of having a 50 percent reduction on the scale was nearly 26 times greater in the weighted blanket group. The weighted blankets did not have a significant effect on total sleep time, but compared with the controls, the users had a significant decrease in wakenings after sleep onset, less daytime sleepiness and fewer symptoms of depression and anxiety. The senior author, Dr. Mats Adler of the Karolinska Institute in Stockholm, acknowledged that this is only one study and doesn’t provide scientific proof that the blankets work. “I have colleagues using it, and they love it,” he said, “but that’s not proof. This study is an indication that they may work, but more studies should be done.” © 2020 The New York Times Company
Keyword: Sleep
Link ID: 27524 - Posted: 10.16.2020
Keith A. Trujillo1, Alfredo Quiñones-Hinojosa2, Kenira J. Thompson3 Joe Louis Martinez Jr. died on 29 August at the age of 76. In addition to making extraordinary contributions to the fields of neurobiology and Chicano psychology, Joe was a tireless advocate of diversity, equity, and inclusion in the sciences. He established professional development programs for individuals from underrepresented groups and provided lifelong mentoring as they pursued careers in science and academia. Joe was passionately devoted to expanding opportunities in the sciences well before diversity became a visible goal for scientific organizations and academic institutions. Born in Albuquerque, New Mexico, on 1 August 1944, Joe received his bachelor's degree in psychology from the University of San Diego in 1966; his master's in experimental psychology from New Mexico Highlands University in 1968; and his Ph.D. in physiological psychology from the University of Delaware in 1971. His faculty career began in 1972 at California State University, San Bernardino (CSUSB), shortly after the campus was established. He later completed postdocs in the laboratory of neurobiologist James McGaugh at the University of California, Irvine, and with neurobiologist Floyd Bloom at the Salk Institute for Biological Studies in San Diego, California. The University of California, Berkeley, recruited Joe in 1982, and he served as a professor as well as the area head of biopsychology and faculty assistant to the vice chancellor for affirmative action. As the highest-ranking Hispanic faculty member in the University of California system, Joe used his voice to help others from underrepresented groups. However, he felt that he could have a greater impact on diversity in the sciences by helping to build a university with a high concentration of Hispanic students, so in 1995 he moved to the University of Texas, San Antonio (UTSA). He began as a professor of biology and went on to assume a range of leadership roles, including director of the Cajal Neuroscience Institute. At UTSA, he worked with colleagues to obtain nearly $18 million in funding for neuroscience research and education. In 2012, he moved to the University of Illinois at Chicago where he served as professor and psychology department head until his retirement in 2016. At each institution, he embraced the opportunity to provide guidance and mentoring to innumerable students, faculty, and staff. © 2020 American Association for the Advancement of Science.
Keyword: Learning & Memory
Link ID: 27523 - Posted: 10.16.2020
By Pam Belluck After contracting the coronavirus in March, Michael Reagan lost all memory of his 12-day vacation in Paris, even though the trip was just a few weeks earlier. Several weeks after Erica Taylor recovered from her Covid-19 symptoms of nausea and cough, she became confused and forgetful, failing to even recognize her own car, the only Toyota Prius in her apartment complex’s parking lot. Lisa Mizelle, a veteran nurse practitioner at an urgent care clinic who fell ill with the virus in July, finds herself forgetting routine treatments and lab tests, and has to ask colleagues about terminology she used to know automatically. “I leave the room and I can’t remember what the patient just said,” she said, adding that if she hadn’t exhausted her medical leave she’d take more time off. “It scares me to think I’m working,” Ms. Mizelle, 53, said. “I feel like I have dementia.” It’s becoming known as Covid brain fog: troubling cognitive symptoms that can include memory loss, confusion, difficulty focusing, dizziness and grasping for everyday words. Increasingly, Covid survivors say brain fog is impairing their ability to work and function normally. “There are thousands of people who have that,” said Dr. Igor Koralnik, chief of neuro-infectious disease at Northwestern Medicine in Chicago, who has already seen hundreds of survivors at a post-Covid clinic he leads. “The impact on the work force that’s affected is going to be significant. Scientists aren’t sure what causes brain fog, which varies widely and affects even people who became only mildly physically ill from Covid-19 and had no previous medical conditions. Leading theories are that it arises when the body’s immune response to the virus doesn’t shut down or from inflammation in blood vessels leading to the brain. © 2020 The New York Times Company
Keyword: Alzheimers; Learning & Memory
Link ID: 27522 - Posted: 10.12.2020
By Eddie Jacobs How would you feel about a new therapy for your chronic pain, which—although far more effective than any available alternative—might also change your religious beliefs? Or a treatment for lymphoma that brings one in three patients into remission, but also made them more likely to vote for your least preferred political party? These seem like idle hypothetical questions about impossible side effects. After all, this is not how medicine works. But a new mental health treatment, set to be licensed next year, poses just this sort of problem. Psychotherapy assisted by psilocybin, the psychedelic compound in “magic mushrooms,” seems to be remarkably effective in treating a wide range of psychopathologies, but also causes a raft of unusual nonclinical changes not seen elsewhere in medicine. Although its precise therapeutic mechanisms remain unclear, clinically relevant doses of psilocybin can induce powerful mystical experiences more commonly associated with extended periods of fasting, prayer or meditation. Arguably, then, it is unsurprising that it can generate long-lasting changes in patients: studies report increased prosociality and aesthetic appreciation, plus robust shifts in personality, values and attitudes to life, even leading some atheists to find God. What’s more, these experiences appear to be a feature, rather than a bug, of psilocybin-assisted psychotherapy, with the intensity of the mystical experience correlating with the extent of clinical benefit. © 2020 Scientific American,
Keyword: Drug Abuse; Emotions
Link ID: 27521 - Posted: 10.12.2020
By Linda Searing U.S. deaths from overdoses of cocaine, a powerfully addictive stimulant, numbered 14,666 in 2018, the most recent year tallied, according to a new report from the Centers for Disease Control and Prevention. The rate of overdose deaths remained stable from 2009 through 2013, the report found, but then headed upward at about 27 percent each year from 2013 through 2018. That rate increase represents about 2½ times more cocaine-related deaths in 2018 than in 2014. Although the report does not address potential causes of the increase in cocaine overdose deaths, the Drug Enforcement Administration has said increased availability of the drug, “in large part due to record levels of coca cultivation and cocaine production in Colombia,” has led to increased usage in the United States. The CDC report says that the rate of overdose deaths from cocaine was higher among men than women and more common among middle-aged people (35 to 44 years old), those living in urban rather than rural areas, and people residing in the Northeast region. In addition, the rate of overdose deaths attributed to cocaine laced with a synthetic opioid such as fentanyl increased faster in recent years than did overdose deaths from purely cocaine. Cocaine overdoses can cause breathing problems, high blood pressure, hallucinations and extreme agitation, as well as seizures, heart attacks and strokes.
Keyword: Drug Abuse
Link ID: 27520 - Posted: 10.12.2020
By Katherine J. Wu Researchers in Iceland have identified a new mutant superpower — but the genetic trait probably won’t be granting anyone admission to the X-Men. A small contingent of the world’s population carries a mutation that makes them immune to the odious funk that wafts off fish, according to a study of some 11,000 people published Thursday in the journal Current Biology. The trait is rare, but potent: When faced with a synthetic odor that would put many people off their lunch, some test subjects smelled only the pleasant aroma of caramel, potato or rose. The vast majority of people aren’t so lucky. Nearly 98 percent of Icelanders, the research said, are probably as put off by the scent as you’d expect. The mutation is thought to be even rarer in populations in other countries. “I can assure you I do not have this mutation,” said Dr. Kári Stefánsson, a neurologist and the study’s senior author. “I tend to get nauseated when I get close to fish that is not completely fresh.” Dr. Stefánsson is the founder and chief executive of deCODE genetics, a biopharmaceutical company in Iceland’s capital, Reykjavik, which has been parsing the human genome for several decades. The team’s latest caper involved a deep dive into the underappreciated sense of olfaction. Study participants were asked to take a whiff of six Sniffin’ Sticks — pens imbued with synthetic odors resembling the recognizable scents of cinnamon, peppermint, banana, licorice, lemon and fish. They were asked to identify the smell, then rate its intensity and pleasantness. The older the study subjects were, the more they struggled to accurately pinpoint the scents. That’s unsurprising, given that sensory functions tend to decline later in life, said Rósa Gísladóttir, the study’s lead author. But even younger people didn’t always hit the mark, she said. The lemon and banana sticks, for instance, prompted descriptions of gummy bears and other candy-sweet smells. © 2020 The New York Times Company
Keyword: Chemical Senses (Smell & Taste); Genes & Behavior
Link ID: 27519 - Posted: 10.10.2020
By Bret Stetka The human brain is hardwired to map our surroundings. This trait is called spatial memory—our ability to remember certain locations and where objects are in relation to one another. New findings published today in Scientific Reports suggest that one major feature of our spatial recall is efficiently locating high-calorie, energy-rich food. The study’s authors believe human spatial memory ensured that our hunter-gatherer ancestors could prioritize the location of reliable nutrition, giving them an evolutionary leg up. In the study, researchers at Wageningen University & Research in the Netherlands observed 512 participants follow a fixed path through a room where either eight food samples or eight food-scented cotton pads were placed in different locations. When they arrived at a sample, the participants would taste the food or smell the cotton and rate how much they liked it. Four of the food samples were high-calorie, including brownies and potato chips, and the other four, including cherry tomatoes and apples, were low in calories—diet foods, you might call them. After the taste test, the participants were asked to identify the location of each sample on a map of the room. They were nearly 30 percent more accurate at mapping the high-calorie samples versus the low-calorie ones, regardless of how much they liked those foods or odors. They were also 243 percent more accurate when presented with actual foods, as opposed to the food scents. “Our main takeaway message is that human minds seem to be designed for efficiently locating high-calorie foods in our environment,” says Rachelle de Vries, a Ph.D. candidate in human nutrition and health at Wageningen University and lead author of the new paper. De Vries feels her team’s findings support the idea that locating valuable caloric resources was an important and regularly occurring problem for early humans weathering the climate shifts of the Pleistocene epoch. “Those with a better memory for where and when high-calorie food resources would be available were likely to have a survival—or fitness—advantage,” she explains. © 2020 Scientific American
Keyword: Learning & Memory; Obesity
Link ID: 27518 - Posted: 10.10.2020
By Cathleen O’Grady Tinnitus—a constant ringing or buzzing in the ears that affects about 15% of people—is difficult to understand and even harder to treat. Now, scientists have shown shocking the tongue—combined with a carefully designed sound program—can reduce symptoms of the disorder, not just while patients are being treated, but up to 1 year later. It’s “really important” work, says Christopher Cederroth, a neurobiologist at the University of Nottingham, University Park, who was not involved with the study. The finding, he says, joins other research that has shown “bimodal” stimulation—which uses sound alongside some kind of gentle electrical shock—can help the brain discipline misbehaving neurons. Hubert Lim, a biomedical engineer at the University of Minnesota, Twin Cities, hit on the role of the tongue in tinnitus by accident. A few years ago, he experimented with using a technique called deep brain stimulation to restore his patients’ hearing. When he inserted a pencil-size rod covered in electrodes directly into the brains of five patients, some of those electrodes landed slightly outside the target zone—a common problem with deep brain stimulation, Lim says. Later, when he started up the device to map out its effects on the brain, a patient who had been bothered by ringing ears for many years, said, “Oh, my tinnitus! I can’t hear my tinnitus,” Lim recalls. With certain kinds of tinnitus, people hear real sounds. For instance, there might be repeated muscular contractions in the ear, Lim says. But for many people, it’s the brain that’s to blame, perceiving sounds that aren’t there. One potential explanation for the effect is that hearing loss causes the brain to overcompensate for the frequencies it can no longer hear. © 2020 American Association for the Advancement of Science.
Keyword: Hearing; Attention
Link ID: 27517 - Posted: 10.10.2020
By Matt Richtel VALLEJO, Calif. — The adolescent patient turned sullen and withdrawn. He hadn’t eaten in 13 days. Treatment with steroids, phenobarbital and Valium failed to curb the symptoms of his epilepsy. Then, on Sept. 18, he had a terrible seizure — violently jerking his flippers and turning unconscious in the water. Cronutt, a 7-year-old sea lion, had to be rescued so he didn’t drown. His veterinarian and the caretakers at Six Flags Discovery Kingdom began discussing whether it was time for palliative care. “We’d tried everything,” said Dr. Claire Simeone, Cronutt’s longtime vet. “We needed more extreme measures.” On Tuesday morning, Cronutt underwent groundbreaking brain surgery aimed at reversing the epilepsy. If successful, the treatment could save increasing numbers of sea lions and sea otters from succumbing to a new plague of epilepsy. The cause is climate change. As oceans warm, algae blooms have become more widespread, creating toxins that get ingested by sardines and anchovies, which in turn get ingested by sea lions, causing damage to the brain that results in epilepsy. Sea otters also face risk when they consume toxin-laden shellfish. The animals who get stranded on land have been given supportive care, but often die. Cronutt may change that. “If this works, it’s going to be big,” said Mariana Casalia, a neuroscientist at the University of California, San Francisco, who helped pioneer the techniques that led to a procedure that took place a vet surgery center in Redwood City, Ca. © 2020 The New York Times Company
Keyword: Epilepsy; Neurotoxins
Link ID: 27516 - Posted: 10.10.2020
By Elizabeth Svoboda After a 3-year-old named Matthew started having one seizure after another, his worried parents learned he had a chronic brain condition that was causing the convulsions. They faced an impossible decision: allow the damaging seizures to continue indefinitely, or allow surgeons to remove half of their son’s brain. They chose the latter. When Matthew emerged from surgery, he couldn’t walk or speak. But bit by bit, he remastered speech and recaptured his lost milestones. The moment one side of his brain was removed, the remainder set itself to the colossal task of re-forging lost neural connections. This gut-level renovation was so successful that no one who meets Matthew today would guess that half his brain is gone. Stanford neuroscientist David Eagleman is obsessed with probing the outer limits of this kind of neural transformation — and harnessing it to useful ends. We’ve all heard that our brains are more plastic than we think, that they can adapt ingeniously to changed conditions, but in “Livewired: The Inside Story of the Ever-Changing Brain,” Eagleman tackles this topic with fresh élan and rigor. He shows not just how we can direct our own neural remodeling on a cellular level, but how such remodeling — a process he calls “livewiring” — alters the core of who we are. “Our machinery isn’t fully preprogrammed, but instead shapes itself by interacting with the world,” Eagleman writes. “You are a different person than you were at this time last year, because the gargantuan tapestry of your brain has woven itself into something new.”
Keyword: Development of the Brain; Language
Link ID: 27515 - Posted: 10.10.2020
By Benedict Carey The swarm of insects — sometimes gnats, sometimes wasps or flying ants — arrived early in this year of nightmares. With summer came equally unsettling dreams: of being caught in a crowd, naked and mask-less; of meeting men in white lab coats who declared, “We dispose of the elders.” Autumn has brought still other haunted-house dramas, particularly for women caring for a vulnerable relative or trying to manage virtual home-schooling. “I am home-schooling my 10-year-old,” one mother told researchers in a recent study of pandemic dreams. “I dreamed that the school contacted me to say it had been decided that his whole class would come to my home and I was supposed to teach all of them for however long the school remained closed.” Deirdre Barrett, a psychologist at Harvard Medical School and the author of “Pandemic Dreams,” has administered dream surveys to thousands of people in the last year, including the one with the home-schooling mother. “At least qualitatively, you see some shifts in content of dreams from the beginning of the pandemic into the later months,” Dr. Barrett said. “It’s an indication of what is worrying people most at various points during the year.” Dr. Barrett is the editor in chief of the journal Dreaming, which in its September issue posted four new reports on how the sleeping brain has incorporated the threat of Covid-19. The findings reinforce current thinking about the way that waking anxiety plays out during REM sleep: in images or metaphors representing the most urgent worries, whether these involve catching the coronavirus (those clouds of insects) or violating mask-wearing protocols. Taken together, the papers also hint at an answer to a larger question: What is the purpose of dreaming, if any? The answers that science has on offer can seem mutually exclusive, or near so. Freud understood dreams as wish fulfillment; the Finnish psychologist Antti Revonsuo saw them as simulations of pending threats. In recent years, brain scientists have argued that REM sleep — the period of sleep during which most dreaming occurs — bolsters creative thinking, learning and emotional health, providing a kind of unconscious psychotherapy. Then again, there is some evidence that dreaming serves little or no psychological purpose — that it is no more than a “tuning of the mind in preparation for awareness,” as Dr. J. Allan Hobson, a Harvard psychiatrist, has said. © 2020 The New York Times Company
Adrian Owen DR. ADRIAN OWEN: Imagine this scenario. You've unfortunately had a terrible accident. You're lying in a hospital bed and you're aware—you're aware but you're unable to respond, but the doctors and your relatives don't know that. You have to lie there, listening to them deciding whether to let you live or die. I can think of nothing more terrifying. Communication is at the very heart of what makes us human. It's the basis of everything. What we're doing is we're returning the ability to communicate to some patients who seem to have lost that forever. The vegetative state is often referred to as a state of wakefulness without awareness. Patients open their eyes, they'll just gaze around the room. They'll have sleeping and waking cycles, but they never show any evidence of having any awareness. So, typically, the way that we assess consciousness is through command following. We ask somebody to do something, say, squeeze our hand, and if they do it, you know that they're conscious. The problem in the vegetative state is that these patients by definition can produce no movements. And the question I asked is, well, could somebody command follow with their brain? It was that idea that pushed us into a new realm of understanding this patient population. When a part of your brain is involved in generating a thought or performing an action, it burns energy in the form of glucose, and it's replenished through blood flow. As blood flows to that part of the brain, we're able to see that with the FMRI scanner. I think one of the key insights was the realization that we could simply get somebody to lie in the scanner and imagine something and, based on the pattern of brain activity, we will be able to work out what it is they were thinking. We had to find something that produces really a quite distinct pattern of activity that was more or less the same for everybody. So, we came up with two tasks. One task, imagine playing tennis, produces activity in the premotor cortex in almost every healthy person we tried this in. A different task, thinking about moving from room to room in your house, produces an entirely different pattern of brain activity; particularly, it involves a part of the brain known as the parahippocampal gyrus. And again, it's very consistent across different people.
Keyword: Consciousness; Brain imaging
Link ID: 27513 - Posted: 10.07.2020
R. Stanley Williams For the first time, my colleagues and I have built a single electronic device that is capable of copying the functions of neuron cells in a brain. We then connected 20 of them together to perform a complicated calculation. This work shows that it is scientifically possible to make an advanced computer that does not rely on transistors to calculate and that uses much less electrical power than today’s data centers. Our research, which I began in 2004, was motivated by two questions. Can we build a single electronic element – the equivalent of a transistor or switch – that performs most of the known functions of neurons in a brain? If so, can we use it as a building block to build useful computers? Neurons are very finely tuned, and so are electronic elements that emulate them. I co-authored a research paper in 2013 that laid out in principle what needed to be done. It took my colleague Suhas Kumar and others five years of careful exploration to get exactly the right material composition and structure to produce the necessary property predicted from theory. Kumar then went a major step further and built a circuit with 20 of these elements connected to one another through a network of devices that can be programmed to have particular capacitances, or abilities to store electric charge. He then mapped a mathematical problem to the capacitances in the network, which allowed him to use the device to find the solution to a small version of a problem that is important in a wide range of modern analytics. © 2010–2020, The Conversation US, Inc.
Keyword: Learning & Memory; Robotics
Link ID: 27512 - Posted: 10.07.2020
By Bill Hathaway Our brains respond differently when talking to a person from a different socioeconomic group than during a conversation with someone of a similar background, a novel new imaging study shows. While neuroscientists have used brain imaging scans to track in great detail neural responses of individuals to a host of factors such as stress, fear, addiction, and even love and lust, new research shows what happens in the brains of two individuals engaged in a simple social interaction. The study, published in the journal Social Cognitive and Affective Neuroscience, reveals the distinct neurobiology of a conversation between two people of different backgrounds. “When a Yale professor talks to a homeless person, his or her frontal lobe activates a different neural network than if they were chatting with another colleague,” said senior author Joy Hirsch, the Elizabeth Mears and House Jameson Professor of Psychiatry and professor of comparative medicine and of neuroscience. “Our brain has apparently designed a frontal lobe system that helps us deal with our diversity.” Hirsch has a joint appointment in neuroscience at the University College of London. The study is the brainchild of recent Yale graduate Olivia Descorbeth, who first proposed the research idea as a high school student. Hirsch and Descorbeth wanted to know if a person’s brain responds differently when speaking with individuals from different socioeconomic backgrounds. Copyright © 2020 Yale University
Keyword: Emotions; Brain imaging
Link ID: 27511 - Posted: 10.07.2020
By Ian Randall It’s one of life’s little ironies: Sweet foods get sweeter when you add a little salt. Now, scientists may have provided connoisseurs of salted caramel and grapefruit with the reason this culinary trick is worth its salt. Your ability to savor food comes from the receptor cells in your tongue’s taste buds. Sweet tastes are detected by a family of receptors called T1R, which pick up both natural sugars and artificial sweeteners. Scientists originally thought disabling the T1R family would stop any responses to sweet stimuli. But in 2003, researchers showed that mice whose T1R genes had been genetically “knocked out” still liked the sugar glucose. The finding suggested there must be another way that mice—and possibly humans—sense sweetness. Seeking an explanation, physiologist Keiko Yasumatsu of Tokyo Dental Junior College and colleagues turned to a protein that works with glucose elsewhere in the body: sodium-glucose cotransporter 1 (SGLT1). In the kidneys and intestine, SGLT1 uses sodium to carry glucose into cells to provide them with energy. Curiously, the protein is also found in sweet-responsive taste cells. The researchers rubbed the tongues of unconscious T1R mice with a solution of glucose and salt—which contains the sodium SGLT1 needs to work—and recorded the responses of nerves connected to their taste cells. The salt seemed to make all the difference: It caused the rodents’ nerves to fire more rapidly, compared with mutated mice given only glucose. Conscious mice also seemed to show a preference for the sugar-salt solution. But this only worked with glucose; sweeteners like saccharin didn’t trigger a response. © 2020 American Association for the Advancement of Science.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 27510 - Posted: 10.07.2020


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