Maria Temming New artwork created by artificial intelligence does weird things to the primate brain. When shown to macaques, AI-generated images purposefully caused nerve cells in the monkeys’ brains to fire more than pictures of real-world objects. The AI could also design patterns that activated specific neurons while suppressing others, researchers report in the May 3 Science. This unprecedented control over neural activity using images may lead to new kinds of neuroscience experiments or treatments for mental disorders. The AI’s ability to play the primate brain like a fiddle also offers insight into how closely AIs can emulate brain function. The AI responsible for the new mind-bending images is an artificial neural network — a computer model composed of virtual neurons — modeled after the ventral stream. This is a neural pathway in the brain involved in vision (SN Online: 8/12/09). The AI learned to “see” by studying a library of about 1.3 million labeled images. Researchers then instructed the AI to design pictures that would affect specific ventral stream neurons in the brain. Viewing any image triggers some kind of neural activity in a brain. But neuroscientist Kohitij Kar of MIT and colleagues wanted to see whether the AI’s deliberately designed images could induce specific neural responses of the team’s choosing. The researchers showed these images to three macaques fitted with neuron-monitoring microelectrodes. |© Society for Science & the Public 2000 - 2019.

Keyword: Vision
Link ID: 26206 - Posted: 05.03.2019

Ruth Williams Showing monkeys a series of computer-generated images and simultaneously recording the animals’ brain cell activities enables deep machine learning systems to generate new images that ramp up the cells’ excitation, according to two papers published today (May 2) in Cell and Science. “It’s exciting because it’s bridging the fields of deep learning and neuroscience . . . to try and understand what is represented in different parts of the brain,” says neuroscientist Andreas Tolias of Baylor College of Medicine who was not involved with either of the studies, but has carried out similar experiments in mice. “I think these methods and their further development could provide a more systematic way for us to open the black box of the brain,” he says. It’s a goal of sensory neuroscience to understand exactly which stimuli activate which brain cells. In the primate visual system, certain neurons in the visual cortex and inferior temporal cortex (two key vision areas) are known to respond preferentially to certain stimuli—such as colors, specific directions of motion, curves, and even faces. But, says neuroscientist Carlos Ponce of Washington University School of Medicine in St. Louis, who co-authored the Cell paper, “the problem is, we’ve never quite known whether, in our selection of pictures, we have the secret true image that the cell really is encoding.” Maybe, he suggests, a cell isn’t responding to a face, but to an arrangement of features and shapes found in a face that may also be found in other images. And with countless available images, “it’s impossible to test all of them,” he says. In short, it has been impossible to determine the exact visual stimulus that would maximally activate a given neuron. © 1986–2019 The Scientist.

Keyword: Vision
Link ID: 26205 - Posted: 05.03.2019

By Jocelyn Kaiser WASHINGTON, D.C.—A new gene therapy treatment has had striking results in nine boys born with myotubular myopathy (MTM), a rare disease that causes extreme muscle weakness often from birth. All of the boys have better neuromuscular function, most can sit on their own, and four are now breathing without ventilators. As videos of their improvements were shown here on 1 May at the annual meeting of the American Society of Gene & Cell Therapy (ASGCT), the audience broke out in applause. The results, the first of their kind for this rare disease, cap a year of early signs of success in using gene therapy for inherited muscle diseases. As far as muscle function is concerned, the boys “have gone from nothing to something,” says principal investigator Perry Shieh, a neurologist at the University of California, Los Angeles. “Time will tell how much that something will be.” The patients in the new study have X-linked MTM, caused by a defect in a gene called MTM1 that encodes an enzyme, myotubularin. Skeletal muscles need the enzyme to develop and function. Boys with the disease have low muscle tone and, in many cases, can barely breathe or move on their own; most require a ventilator and feeding tube. Half of patients die by 18 months, and few live past age 10. In the trial, sponsored by Audentes Therapeutics, a gene therapy company in San Francisco, California, nine boys between 8 months and 6 years old with X-linked MTM received an intravenous (IV) infusion of many trillions of particles of a harmless virus, called an adeno-associated virus. The viruses were designed to carry a good copy of the MTM1 gene into the boys’ muscle cells. The gene, a free-floating piece of DNA, could then trigger the cell’s proteinmaking machinery to produce myotubularin. Three patients had serious side effects that may have been related to the therapy, such as heart inflammation, but all were treatable. © 2019 American Association for the Advancement of Science

Keyword: Movement Disorders; Muscles
Link ID: 26204 - Posted: 05.03.2019

By Heather Murphy The scent of lily of the valley cannot be easily bottled. For decades companies that make soap, lotions and perfumes have relied on a chemical called bourgeonal to imbue their products with the sweet smell of the little white flowers. A tiny drop can be extraordinarily intense. If you can smell it at all, that is. For a small percentage of people, it fails to register as anything. Similarly, the earthy compound 2-ethylfenchol, present in beets, is so powerful for some people that a small chunk of the root vegetable smells like a heap of dirt. For others, that same compound is as undetectable as the scent of bottled water. These — and dozens of other differences in scent perception — are detailed in a new study, published this week in the journal PNAS. The work provides new evidence of how extraordinarily different one person’s “smellscape” may be from another’s. It’s not that some people are generally better smellers, like someone else may have better eyesight, it’s that any one person might experience certain scents more intensely than their peers. “We’re all smelling things a little bit differently,” said Steven Munger, director of The Center for Smell and Taste at the University of Florida, who was not involved in the study. The scientists who conducted the study looked for patterns in subjects’ genetic code that could explain these olfactory differences. They were surprised to find that a single genetic mutation was linked to differences in perception of the lily of the valley scent, beet’s earthiness, the intensity of whiskey’s smokiness along with dozens of other scents. “I think it’s a very important finding,” said Stavros Lomvardas, a neuroscientist at Columbia University’s Zuckerman Institute, who was not involved in the research either. The study was conducted in a large room at Rockefeller University in New York City. Around 300 subjects were invited to sit in front of a computer screen surrounded by 150 jars of assorted odors. The screen alerted them to which jar sniff at any given time, and they then rated the intensity of each on a scale from 1 (extremely weak) to 7 (extremely strong) and pleasantness from 1 (extremely unpleasant) to 7 (extremely pleasant). © 2019 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Genes & Behavior
Link ID: 26203 - Posted: 05.03.2019

By Nicholette Zeliadt, Two drugs that alter the activity of the hormone vasopressin seem to improve social communication in people with autism. The findings come from two independent clinical trials published today in Science Translational Medicine. The results are encouraging, but some experts urge caution, saying the methods used to assess the drugs were not designed for that purpose. Vasopressin is related to oxytocin, a hormone thought to govern social bonding. But vasopressin’s link to autism is far from simple: There’s evidence implicating both too little and too much of the hormone in people with the condition. Advertisement The two drugs also target vasopressin in opposite ways. One of them, balovaptan, blocks a receptor for vasopressin in the brain and dampens the hormone’s activity. The other is a nasal spray containing vasopressin. Despite their opposing modes of action, both drugs appear to boost social function in autistic people; neither has serious side effects. The findings are noteworthy because no drugs are available to treat autism’s core traits, says Eric Hollander, professor of psychiatry and behavioral sciences at Albert Einstein College of Medicine in New York, who was not involved in either study. “These two studies provide important information that the vasopressin or vasopressin and oxytocin systems are important in social communication,” he says. “Different agents affecting these systems may ultimately be helpful in terms of new treatments for autism.” © 2019 Scientific American

Keyword: Autism; Hormones & Behavior
Link ID: 26202 - Posted: 05.03.2019

Sara Reardon The cannabis that’s used for research in the United States is genetically different to the stuff people are smoking, says a recent study1. The finding suggests that research investigating the plant’s biological effects might not completely replicate the experience of people using commercially available strains ― something researchers have long suspected. Scientists studying cannabis in the United States must source it from the National Center for Natural Products Research at the University of Mississippi in University. The facility holds the only licence from the US Drug Enforcement Administration (DEA) to grow and distribute cannabis for research purposes, and it has a contract with the National Institute on Drug Abuse (NIDA) to give researchers access to its products. Critics have long complained that NIDA’s pot is weaker than strains typically sold in dispensaries in states where the drug is now legal, or available on the street. The agency’s strongest variety contains more than 10% tetrahydrocannabinol (THC), the main psychoactive chemical responsible for marijuana’s ‘high’. Some street varieties contain more than 20% THC. The DEA, which licenses labs to buy and study illegal drugs, announced in 2016 that it would allow other institutions to apply for permission to grow marijuana for research. According to news reports, dozens of applications have since been submitted. But the DEA hasn’t yet approved any of them, leaving scientists to source research strains from NIDA. © 2019 Springer Nature Publishing AG

Keyword: Drug Abuse
Link ID: 26201 - Posted: 05.03.2019

By Kelly Servick For a hair-thin probe penetrating the brain to listen in on neurons' electrical chatter, finesse is key. It's easy to rip tissue on the way in. And once in place, a probe can do further damage that muffles the signals it aims to detect. But recent reports describe a generation of finer probes that should prove less damaging. Just a few micrometers thick—comparable to neurons themselves—these tools may soon capture unprecedented long-term recordings from hard-to-reach parts of animal brains. And they may lead to more sophisticated brain-computer interfaces for people. Improved material fabrication techniques have helped labs create the exquisitely fine probes, says neural engineer Timothy Hanson, who developed a system for inserting tiny electrodes while at the University of California, San Francisco (UCSF). And lab tests have shown that brain research using ultrasmall electrodes "can be done, and that it's worthwhile." Conventional brain probes are already vanishingly tiny. Stiff electrodes known as Michigan probes, commonly used in neuroscience research, are pointed, ribbonlike shafts that can be as thin as 15 micrometers and are usually 60 micrometers wide or more. In a standard grid known as the Utah array, each spike is roughly 200 micrometers thick at its base. But in the months after either device is implanted, its connection to neurons typically weakens and its signal fades. A key reason is that the probe provokes an immune reaction in the brain. Its initial plunge into the tissue can tear blood vessels. And even after that damage heals, the probe continues to push and pull on surrounding tissue. In response, nonneuronal cells called glia multiply and form scars that push neurons away from the electrode. © 2019 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 26200 - Posted: 05.02.2019

By Gretchen Reynolds A single, moderate workout may immediately change how our brains function and how well we recognize common names and similar information, according to a promising new study of exercise, memory and aging. The study adds to growing evidence that exercise can have rapid effects on brain function and also that these effects could accumulate and lead to long-term improvements in how our brains operate and we remember. Until recently, scientists thought that by adulthood, human brains were relatively fixed in their structure and function, especially compared to malleable tissues, like muscle, that continually grow and shrivel in direct response to how we live our lives. But multiple, newer experiments have shown that adult brains, in fact, can be quite plastic, rewiring and reshaping themselves in various ways, depending on our lifestyles. Exercise, for instance, is known to affect our brains. In animal experiments, exercise increases the production of neurochemicals and the numbers of newborn neurons in mature brains and improves the animals’ thinking abilities. Similarly, in people, studies show that regular exercise over time increases the volume of the hippocampus, a key part of the brain’s memory networks. It also improves many aspects of people’s thinking. But substantial questions remain about exercise and the brain, including the time course of any changes and whether they are short-term or, with continued training, become lasting. That particular issue intrigued scientists at the University of Maryland. They already had published a study in 2013 with older adults looking at the long-term effects of exercise on portions of the brain involved in semantic-memory processing. © 2019 The New York Times Company

Keyword: Learning & Memory
Link ID: 26199 - Posted: 05.02.2019

Matthew Warren Scientists have uncovered the most complete remains yet from the mysterious ancient-hominin group known as the Denisovans. The jawbone, discovered high on the Tibetan Plateau and dated to more than 160,000 years ago, is also the first Denisovan specimen found outside the Siberian cave in which the hominin was uncovered a decade ago — confirming suspicions that Denisovans were more widespread than the fossil record currently suggests. The research marks the first time an ancient human has been identified solely through the analysis of proteins. With no usable DNA, scientists examined proteins in the specimen’s teeth, raising hopes that more fossils could be identified even when DNA is not preserved. “This is fantastic work,” says Katerina Douka, an archaeologist at the Max Planck Institute for the Science of Human History in Jena, Germany, who runs a separate project aiming to uncover Denisovan fossils in Asia. “It tells us that we are looking at the right area.” Until now, everything scientists have learnt about Denisovans has come from a handful of teeth and bone fragments from Denisova Cave in Russia’s Altai Mountains. DNA from these remains revealed that the Denisovans were a sister group to Neanderthals, both descending from a population that split away from modern humans about 550,00–765,000 years ago. And at Denisova Cave, the two groups seem to have met and interbred: a bone fragment described last year belonged an ancient-human hybrid individual who had a Denisovan father and Neanderthal mother.

Keyword: Evolution
Link ID: 26198 - Posted: 05.02.2019

By Kelly Servick Many people with autism have trouble making eye contact, reading the emotions in other faces, and sharing affection. And no drugs are approved to treat such social impairments. Now, results from a small academic clinical trial suggest boosting levels of vasopressin—a hormone active in the brain that’s known to promote bonding in many animals—can improve social deficits in children with autism. But in a confusing twist, a larger, company-sponsored trial that took the reverse approach, tamping down vasopressin’s effects, also found some improvements in adults with autism. “I’ve never seen this before,” Kevin Pelphrey, a neuroscientist who studies autism at the University of Virginia in Charlottesville, says of the conflicting results. He and others say the vasopressin-blocking approach doesn’t have much support from previous animal research. The new study showed some benefits but failed to meet the main endpoint set out by investigators. Still, he says, both studies suggest vasopressin’s signaling in the brain plays a key role in autism and “give me a lot of renewed excitement” for treating the condition. Though vasopressin seems to stimulate social bonding in animals, the hormone’s activity in the brain isn’t fully understood, and its effects vary by species and context. Blocking its activity in the brains of some rodents prevents them from forming an attraction to a mate. But in a species of asocial hamster, injecting it into a male’s brain seems to stimulate aggression. © 2019 American Association for the Advancement of Science.

Keyword: Autism; Hormones & Behavior
Link ID: 26197 - Posted: 05.02.2019

By Gina Kolata The Court of Arbitration for Sport in Zurich has ruled that women with very high testosterone levels — far above the normal range — cannot compete against other women in races from 400 meters to one mile unless they take drugs to suppress production of the hormone. The ruling prevents Caster Semenya, 28, an elite runner and Olympic champion from South Africa, from competing in those races because her testosterone levels are naturally very high. She had challenged attempts to disqualify her from racing as a woman. The science underpinning that decision is complicated, raising difficult questions about biology, fairness and gender identity. What is testosterone? Where does it come from in women? It’s a hormone, an androgen, that has a variety of effects on the body. Women and men produce testosterone, but women don’t make nearly as much In men, high levels of testosterone are made by the testes. Much lower levels are produced in the adrenal glands, which rest above the kidneys. Women also make testosterone in their adrenal glands, and in their ovaries. But testes produce much more: Testosterone levels in men are 295 to 1,150 nanograms per deciliter of blood, while the levels in the women are 12 to 61 nanograms per deciliter of blood. Testosterone “builds muscle,” said Dr. Benjamin D. Levine, who studies sex differences in athletic performance at the University of Texas Southwestern Medical Center. “It builds skeletal muscle, it builds cardiac muscle. It increases the number of red blood cells.” The effects are seen whether the hormone is naturally present or introduced with drugs. In one of the most infamous examples, women who represented East Germany at the Olympic Games in the ’70s and ’80s achieved astounding success after they were unknowingly doped with anabolic steroids including testosterone. “The science is quite clear,” said Dr. Aaron Baggish of Massachusetts General Hospital, who is an expert on testosterone’s effects. “An androgenized body has a performance advantage.” © 2019 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 26196 - Posted: 05.02.2019

By R. Douglas Fields From his sniper’s perch on the 32nd floor of the Mandalay Bay hotel in Las Vegas, a lone gunman fired 1,000 bullets from high-powered rifles into a crowd of concertgoers in 2017, murdering 58 innocent people and injuring 869 others. After he committed suicide at the crime scene, the mass murderer’s brain was shipped to Stanford University to seek a possible biological explanation for this depraved incident. What could the scientists possibly find during such an inspection? Quite a lot, in fact. No genetic test for homicidal behavior is in the offing. But this type of investigation can add insight into how violence is controlled by the brain. Using the same experimental methods that have enabled the tracing of brain circuits responsible for other complex human activities—including walking, speech and reading—neuroscientists now can pinpoint pathways that underlie aggressive behaviors. These new findings help to expose the underlying mechanisms at work in acts of extreme violence, such as the Las Vegas atrocity, but they also help to explain the more commonplace road rage and even a mother’s instantaneous response to any threat to her child. Physical, sometimes deadly violence is the hub of nature’s survival-of-the fittest struggle, and all animals have evolved specialized neural circuitry to execute—and control—aggressive behavior. In pioneering experiments on cats beginning in the late 1920s, Walter Hess discovered a locus deep within the hypothalamus, a brain area that unleashes violent aggression. It turns out that this is the same spot where other powerful compulsive urges and behaviors are activated, including sex, eating and drinking. When Hess stimulated this knot of neurons using a wire electrode inserted into the brain of a docile cat, the feline instantly launched into a hissing rage, attacking and killing another animal in its cage. The human brain has this same neural structure, labeled the hypothalamic attack area.

Keyword: Aggression; Hormones & Behavior
Link ID: 26195 - Posted: 05.02.2019

By Nicholas Bakalar Girls who have serious or repeated infections in childhood are at higher risk for developing eating disorders in adolescence, a new study has found. The study, in JAMA Psychiatry, tracked 525,643 girls — every girl born in Denmark from 1989 through 2006. The researchers recorded all prescriptions that were filled for antibiotics and other anti-infective medications, as well as hospitalizations for infection, through 2012. There were 4,240 diagnoses of eating disorders during that time. Compared with girls who had never been hospitalized for infection, those who had been hospitalized were at a 22 percent increased risk for anorexia, a 35 percent increased risk for bulimia and a 39 percent increased risk for other eating disorders. Filling three or more prescriptions for anti-infective drugs was associated with similar increases in the risk, and the more infections or hospitalizations a girl had, the more likely she was to develop an eating disorder. This is an observational study so it cannot determine cause and effect, and the authors acknowledge that other mechanisms — genetic factors, or stress and anxiety, for example — could increase the risk of both eating disorders and infection. The lead author, Lauren Breithaupt, a research fellow at Harvard, said that the reasons for the link are unknown, but “it could be that the anti-infective agents are upsetting the microbes in the gut. Changing the microbiome could affect behaviors through the connection of the gut to the brain through the vagus nerve.” © 2019 The New York Times Company

Keyword: Anorexia & Bulimia; Neuroimmunology
Link ID: 26194 - Posted: 05.02.2019

By Benedict Carey Federal health regulators announced on Tuesday that they would require manufacturers of sleeping pills such as Ambien and related drugs to post strongly worded warnings in boxes on labels and patient guides. The Food and Drug Administration, in what it called a safety announcement, noted that the drugs’ side effects included risky behaviors, such as sleepwalking and sleep driving, that can lead to injury and even death. The F.D.A. singled out Ambien and two other popular sleep aids, Lunesta and Sonata, as well as three formulations of zolpidem, the generic name for Ambien. The boxed warnings — the most prominent form of warning required by the agency — must list side effects such as sleepwalking and sleep driving, in which people using the drugs take risks without being fully awake. The agency said such reactions were rare but could lead to injuries or death; it advised doctors not to prescribe the drugs to people who have had such side effects in the past. “Patients, stop taking your insomnia medicine and contact your health care professional right away if you experience a complex sleep behavior where you engage in activities while you are not fully awake,” the agency’s safety alert said, “or if you do not remember activities you have done while taking the medicine.” Prescriptions for sleeping pills grew to more than 20 million in 2010 from 5.3 million in 1999, according to national estimates. About one in eight people with sleeping difficulty report using the drugs; among people of retirement age, more than a third report taking a sleeping aid. The F.D.A. warned about such effects in 2007, after doctors reported that some patients were having strange nighttime experiences, mostly while taking zolpidem (Ambien), the first of the so-called z-drugs. © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26193 - Posted: 05.01.2019

Laura Sanders A newly described dementia strikes people in their last decades of life. The disease, aptly named LATE, comes with symptoms that resemble Alzheimer’s disease, but is thought to be caused by something completely different. An international team of scientists and clinicians describe the disease and officially christen it LATE, which stands for the more technical description, “limbic-predominant age-related TDP-43 encephalopathy,” online April 30 in Brain. Study coauthor Peter Nelson, a neuropathologist at the University of Kentucky in Lexington, helped organize a meeting last year that addressed a growing realization among doctors and scientists: “There’s this disease, and it doesn’t have a name,” he says. Estimates vary, but it’s possible that about a quarter of people age 85 and older have LATE, Nelson says. “This is a disease that really attacks the very latest portion of the human aging spectrum,” he says. LATE comes with memory trouble and dementia — symptoms that mirror Alzheimer’s, Nelson says. But instead of the plaques and tangles that mark the brains of people with Alzheimer’s disease, LATE is characterized by a lesser-known protein called TDP-43. In LATE, that protein accumulates and spreads through parts of the brain that are key to thinking and memory, including the amygdala and hippocampus. In Brain, Nelson and his colleagues describe the signs of LATE in the brain in a series of stages, from less severe to most severe. But the trouble is that these signs, which include the spread of TDP-43 and occasionally signs of damage to the hippocampus, can be found only after a person has died. There are currently no surefire clinical tests that identify LATE in a living person. |© Society for Science & the Public 2000 - 2019.

Keyword: Alzheimers
Link ID: 26192 - Posted: 05.01.2019

By Lisa Sanders, M.D. “I don’t know where I am,” said a terrified voice on the phone. It was the woman’s husband, and he was scared. “I’m lost,” he said in a panicked tone. It’s O.K., she told him, sounding as calm and reassuring as she could. Her husband, a former high school English teacher in his 60s, left his mother-in-law’s that morning to return to their home several hours away in Pinon Hills, just north of San Bernardino, Calif. It was a route he drove often enough to know well. But after making his way through towns that seemed familiar, he lost his sense of how to get home. With her voice on the speakerphone, she guided him. His voice shook, and she knew he was crying. She wanted to cry, too, but forced herself to be the strength he needed. She still loved her husband, but he’d changed so much. Where was the man she married over 30 years ago? Twenty years earlier, he found out he had multiple sclerosis. It started with numbness in his arms and hands. Sometimes his vision would darken on the periphery, as if he were in a tunnel. And then, after a couple of hours or so, he’d be fine. He was referred to a local neurologist, who did some testing. An M.R.I. of his brain showed patchy white clouds among the normal gray swirls of brain. That finding was suggestive of multiple sclerosis. In M.S., the immune system goes awry and attacks the fatty sleeves that surround the nerves in the brain and spine; that’s what causes the characteristic M.R.I. findings. But it wasn’t a perfect fit. The fluid taken from his spine did not show the proteins that are usually seen in M.S. Moreover, while M.S. is characterized by episodes of unusual neurological symptoms that come and go, they usually last days or weeks rather than hours. Still, there are different forms of the disorder, and they can vary widely in symptom intensity and rate of progression. And there are few diseases that result in the M.R.I. findings and intermittent symptoms that this man had. Subsequent neurologists confirmed the diagnosis of M.S. © 2019 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 26191 - Posted: 05.01.2019

By Sayuri Hayakawa, Viorica Marian As Emperor Akihito steps down from the Chrysanthemum Throne in Japan’s first abdication in 200 years, Naruhito officially becomes the new Emperor on May 1, 2019, ushering in a new era called Reiwa (令和; “harmony”). Japan’s tradition of naming eras reflects the ancient belief in the divine spirit of language. Kotodama (言霊; “word spirit”) is the idea that words have an almost magical power to alter physical reality. Through its pervasive impact on society, including its influence on superstitions and social etiquette, traditional poetry and modern pop songs, the word kotodama has, in a way, provided proof of its own concept. For centuries, many cultures have believed in the spiritual force of language. Over time, these ideas have extended from the realm of magic and mythology to become a topic of scientific investigation—ultimately leading to the discovery that language can indeed affect the physical world, for example, by altering our physiology. Our bodies evolve to adapt to our environments, not only over millions of years but also over the days and years of an individual’s life. For instance, off the coast of Thailand, there are children who can “see like dolphins.” Cultural and environmental factors have shaped how these sea nomads of the Moken tribe conduct their daily lives, allowing them to adjust their pupils underwater in a way that most of us cannot. © 2019 Scientific American

Keyword: Language
Link ID: 26190 - Posted: 05.01.2019

By Sheila Kaplan WASHINGTON — The Food and Drug Administration said Tuesday that it would permit the sale of IQOS, a “heat not burn” tobacco device made by Philip Morris International, in the United States. While the agency stopped short of declaring that the device was safer than traditional cigarettes, the F.D.A. did say the heated tobacco-stick system could help people to quit smoking. Philip Morris has waited two years for the agency to clear IQOS (pronounced EYE-kose), a penlike electronic device that comes with a sleek battery pack resembling a cigarette case. The product includes an electronically controlled heating blade that warms a tobacco stick and releases a vapor with the taste of tobacco but fewer harmful chemicals than cigarette smoke. It differs from e-cigarettes already on the market because it contains tobacco rather than liquid nicotine. But IQOS still delivers an amount of nicotine that’s similar to traditional cigarettes. “The F.D.A.’s decision to authorize IQOS in the U.S. is an important step forward for the approximately 40 million American men and women who smoke,” said André Calantzopoulos, the chief executive of Philip Morris International. “Some will quit. Most won’t, and for them IQOS offers a smoke-free alternative to continued smoking.” Howard A. Willard III, chief executive of Altria, which will distribute the product in this country, said the company planned to begin sales of IQOS in Atlanta. A few years ago, the F.D.A.’s decision would have been a clear win for both Philip Morris and Altria. But IQOS products will now have to compete with the extremely popular devices sold by the vaping giant Juul Labs, in which Altria has a 35 percent stake. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26189 - Posted: 05.01.2019

April Dembosky Amelia and her roommate had been awake for two days straight. They decided to spray-paint the bathroom hot pink. After that, they laid into building and rebuilding the pens for the nine pit bull puppies they were raising in their two-bedroom apartment. Then the itching started. It felt like pin pricks under the skin of her hands. Amelia was convinced she had scabies, skin lice. She spent hours in front of the mirror checking her skin, picking at her face. She even got a health team to come test the apartment. All they found were a few dust mites. "At first, with meth, I remember thinking, 'What's the big deal?' " says Amelia, who asked that we not reveal her last name to protect her family's privacy. "But when you look at how crazy things got, everything was so out of control. Clearly, it is a big deal." While public health officials have focused on the opioid epidemic in recent years, another epidemic has been brewing quietly, but vigorously, behind the scenes. Methamphetamine use is surging in parts of the U.S., particularly the West, leaving first responders and addiction treatment providers struggling to handle a rising need. Across the country, overdose deaths involving methamphetamine doubled from 2010 to 2014. Admissions to treatment facilities for meth are up 17%. Hospitalizations related to meth jumped by about 245% from 2008 to 2015. And throughout the West and Midwest, 70% of local law enforcement agencies say meth is their biggest drug threat. © 2019 npr

Keyword: Drug Abuse
Link ID: 26188 - Posted: 05.01.2019

By Shubham Saharan Thomas Jessell, renowned neurologist and former director of and key contributor to the founding of Columbia’s Mortimer B. Zuckerman Mind Brain Behavior Institute, has died. He was 67. In a statement to MBBI affiliates, Institute co-directors Rui Costa, Eric Kandel, and Richard Axel attributed Jessell’s death to a rapidly-progressing neurodegenerative disorder. Jessell was endowed under the Claire Tow Professorship in Motor Neuron Disorders in the neuroscience and biochemistry and molecular biophysics departments. He was well known for his research on chemical signals and neurological circuits. Originally an assistant professor in the department of neurobiology at Harvard Medical School, Jessell moved to Columbia in 1985 to work as an investigator for the Howard Hughes Medical Institute, a philanthropic organization that provides funding for biological and medical research as well as scientific education. Jessell, along with Axel and Kandel from the department of neuroscience, played a significant role in founding the MBBI, a center dedicated to neuroscience research, which is located at the Jerome L. Greene Science Center on the Manhattanville campus. In March 2018, HHMI stripped Jessell of all titles and grants and announced that it would stop funding his lab starting May 31. Columbia began investigating Jessell’s misconduct in December 2017, after which he was removed from all administrative positions, including his co-directorship of the MBBI, for engaging in a years-long relationship that violated the University policy on consensual romantic and sexual relationships between faculty and students. Copyright Spectator Publishing Company

Keyword: Development of the Brain
Link ID: 26187 - Posted: 05.01.2019