Subhash Kak Many advanced artificial intelligence projects say they are working toward building a conscious machine, based on the idea that brain functions merely encode and process multisensory information. The assumption goes, then, that once brain functions are properly understood, it should be possible to program them into a computer. Microsoft recently announced that it would spend US$1 billion on a project to do just that. So far, though, attempts to build supercomputer brains have not even come close. A multi-billion-dollar European project that began in 2013 is now largely understood to have failed. That effort has shifted to look more like a similar but less ambitious project in the U.S., developing new software tools for researchers to study brain data, rather than simulating a brain. Some researchers continue to insist that simulating neuroscience with computers is the way to go. Others, like me, view these efforts as doomed to failure because we do not believe consciousness is computable. Our basic argument is that brains integrate and compress multiple components of an experience, including sight and smell – which simply can’t be handled in the way today’s computers sense, process and store data. Brains don’t operate like computers Living organisms store experiences in their brains by adapting neural connections in an active process between the subject and the environment. By contrast, a computer records data in short-term and long-term memory blocks. That difference means the brain’s information handling must also be different from how computers work. © 2010–2019, The Conversation US, Inc.

Keyword: Consciousness
Link ID: 26714 - Posted: 10.17.2019

By Laura Sanders Brainlike blobs made from chimpanzee cells mature faster than those grown from human cells. That finding, described October 16 in Nature along with other clues to human brain development, is one of the latest insights from studies of cerebral organoids — three-dimensional clumps of cells that can mimic aspects of early brain growth (SN: 2/20/18). The new study “draws interesting parallels, but also highlights important differences” in the way that the brains of humans and chimpanzees develop, says Paola Arlotta, a neurobiologist at Harvard University who was not involved in the study. While “it’s still early days in the organoid world,” the results represent an important step toward understanding the particulars of the human brain, she says. To make cerebral organoids from chimpanzees, researchers use cells in blood left over from veterinarians’ routine blood draws. In the vials were white blood cells that could be reprogrammed into stem cells, which themselves were then coaxed into blobs of brain cells. “From that, we get something that really looks a lot like the early brain,” says Gray Camp, a stem cell biologist at the Institute of Molecular and Clinical Ophthalmology Basel in Switzerland. There were no obvious differences in appearance between the chimpanzee organoids and the human organoids, Camp says. But a close look at how genes behaved in the two organoids — and how that behavior changed over time — turned up a big difference in pacing. Chimpanzee organoids seemed to grow up faster than their human counterparts. © Society for Science & the Public 2000–2019

Keyword: Development of the Brain; Evolution
Link ID: 26713 - Posted: 10.17.2019

Nicoletta Lanese Cell transplantation therapy offers a promising route to recovery after stroke, but the grafted cells face a harsh environment, with elevated levels of free radicals and proinflammatory cytokines, compromised blood supply, and degraded neural connectivity, says Shan Ping Yu, a neurology researcher at Emory University School of Medicine. He and his colleagues aimed to build a new tool to help stem cells integrate with host neural circuitry after implantation. Scientists have long known that stimulating transplanted neural stem cells encourages them to differentiate into neurons and connect with nearby host cells. Many researchers turn to optogenetics to excite grafted stem cells, but because light travels poorly through dense tissue, the technique requires researchers to stick a laser into their subjects’ brains. So Yu and his coauthors turned instead to a type of enzyme that grants fireflies and jellyfish their glow: luciferase. “These proteins carry their own light, so they do not need a light source,” says Yu. The researchers injected neural progenitor cells that had been derived from induced pluripotent stem cells (iPSCs) into the brains of mouse models of stroke. The cells were genetically engineered to express a fusion protein called luminopsin 3 (LMO3), crafted from the bioluminescent enzyme Gaussia luciferase and the light-sensitive protein VChR1. LMO3 activates in response to either physical light or a molecule called CTZ, which can be delivered noninvasively through the nose into the brain tissue. The fusion protein can be hooked up to either excitatory or inhibitory channels in the neurons to either stimulate or tamp down the cells’ function. Yu and his colleagues dubbed the new technique “optochemogenetics.” © 1986–2019 The Scientist.

Keyword: Stroke
Link ID: 26712 - Posted: 10.17.2019

National Institutes of Health scientists have developed an ultrasensitive new test to detect abnormal forms of the protein tau associated with uncommon types of neurodegenerative diseases called tauopathies. As they describe in Acta Neuropathologica, this advance gives them hope of using cerebrospinal fluid, or CSF—an accessible patient sample—to diagnose these and perhaps other, more common neurological diseases, such as Alzheimer’s disease. Scientists have linked the abnormal deposition of tau in the brain to at least 25 different neurodegenerative diseases. However, to accurately diagnose these diseases, brain tissue often must be analyzed after the patient has died. For their study, the researchers used the same test concept they developed when using post-mortem brain tissue samples to detect the abnormal tau types associated with Pick disease, Alzheimer’s disease and chronic traumatic encephalopathy (CTE). They adapted the test to use CSF for the detection of abnormal tau of progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and other less common tauopathies. They detected abnormal tau in CSF from both living and deceased patients. In one case, the test led to a corrected diagnosis in a patient who had died from CBD, but who was initially diagnosed with PSP. The new test is called 4R RT-QuIC—which stands for 4-repeat tau protein amplified in a real-time, quaking-induced conversion process.

Keyword: Alzheimers
Link ID: 26711 - Posted: 10.17.2019

By Karen Weintraub We all wish we could get by on less sleep, but one father and son actually can—without suffering any health consequences and while actually performing on memory tests as well as, or better than, most people. To understand this rare ability, researchers at the University of California, San Francisco, first identified a genetic mutation—in both individuals—that they thought might deserve the credit. Then the scientists intentionally made the same small genetic spelling mistake in mice. The mice also needed less sleep, remembered better and suffered no other ill effects, according to a study published today in Science Translational Medicine. Although a medication with the same benefits will not be available anytime soon—and might never materialize—the idea is incredibly appealing: take a pill that replicates whatever the father and son’s body does and sleep less, with no negative repercussions. “I find the concept of a gene product that might potentially provide protection against comorbid disorders of restricted sleep tantalizing,” says Patrick Fuller, an associate professor of neurology at Harvard Medical School and Beth Israel Deaconess Medical Center in Boston, who was not involved with the work. “If true, this would indeed have ‘potential therapeutic implications,’ as well as provide another point of entry for exploring and answering the question ‘Why do we sleep?’ which remains [one] of the greatest mysteries in neuroscience.” © 2019 Scientific American

Keyword: Sleep; Genes & Behavior
Link ID: 26710 - Posted: 10.17.2019

Diana Kwon There are approximately 5.6 million people over the age of 65 living with Alzheimer’s disease in the United States. With the population aging, that number is projected to grow to 7.1 million by 2025. Researchers know that age, a family history of the disease, and carrying a genetic variant known as APOE4 are all associated with a higher chance of developing the condition. But the biological mechanisms leading to Alzheimer’s are still largely a mystery. Over the last decade, scientists have amassed evidence for a hypothesis that, prior to developing full-blown Alzheimer’s disease, patients experience a period of hyperactivity and hyperconnectivity in the brain. Several functional magnetic resonance imaging studies have reported that people with mild cognitive impairment (MCI), a condition that often precedes Alzheimer’s, appear to have higher brain activity levels than their age-matched counterparts. Researchers have also found signs of such changes in healthy people carrying the APOE4 allele, as well as in presymptomatic stages of Alzheimer’s in rodent models of the disease. Krishna Singh, a physicist and imaging neuroscientist at the Cardiff University Brain Research Imaging Center (CUBRIC) in the UK, and his colleagues wanted to investigate this theory further. Previous studies of brain activity in young APOE4 carriers were mostly conducted using small sample sizes, according to Singh. But by the mid-2010s, his team had access to neuroimaging data from close to 200 participants studied at CUBRIC as part of an effort to build a massive dataset of healthy brains. So the researchers decided to use the data to search for signs of unusual brain activity and connectivity in people with the APOE4 allele. © 1986–2019 The Scientist

Keyword: Alzheimers
Link ID: 26709 - Posted: 10.16.2019

Mengying Zhang While many people love colorful photos of landscapes, flowers or rainbows, some biomedical researchers treasure vivid images on a much smaller scale – as tiny as one-thousandth the width of a human hair. To study the micro world and help advance medical knowledge and treatments, these scientists use fluorescent nano-sized particles. Quantum dots are one type of nanoparticle, more commonly known for their use in TV screens. They’re super tiny crystals that can transport electrons. When UV light hits these semiconducting particles, they can emit light of various colors. One nanometer is one-millionth of a millimeter. RNGS Reuters/Nanosys That fluorescence allows scientists to use them to study hidden or otherwise cryptic parts of cells, organs and other structures. I’m part of a group of nanotechnology and neuroscience researchers at the University of Washington investigating how quantum dots behave in the brain. Common brain diseases are estimated to cost the U.S. nearly US$800 billion annually. These diseases – including Alzheimer’s disease and neurodevelopmental disorders – are hard to diagnose or treat. Nanoscale tools, such as quantum dots, that can capture the nuance in complicated cell activities hold promise as brain-imaging tools or drug delivery carriers for the brain. But because there are many reasons to be concerned about their use in medicine, mainly related to health and safety, it’s important to figure out more about how they work in biological systems. © 2010–2019, The Conversation US, Inc.

Keyword: Brain imaging
Link ID: 26708 - Posted: 10.16.2019

By Dawn MacKeen The CBD industry is flourishing, conservatively projected to hit $16 billion in the United States by 2025. Already, the plant extract is being added to cheeseburgers, toothpicks and breath sprays. More than 60 percent of CBD users have taken it for anxiety, according to a survey of 5,000 people, conducted by the Brightfield Group, a cannabis market research firm. Chronic pain, insomnia and depression follow behind. Kim Kardashian West, for example, turned to the product when “freaking out” over the birth of her fourth baby. The professional golfer Bubba Watson drifts off to sleep with it. And Martha Stewart’s French bulldog partakes, too. What is CBD? Cannabidiol, or CBD, is the lesser-known child of the cannabis sativa plant; its more famous sibling, tetrahydrocannabinol, or THC, is the active ingredient in pot that catapults users’ “high.” With roots in Central Asia, the plant is believed to have been first used medicinally — or for rituals — around 750 B.C., though there are other estimates too. Cannabidiol and THC are just two of the plant’s more than 100 cannabinoids. THC is psychoactive, and CBD may or may not be, which is a matter of debate. THC can increase anxiety; it is not clear what effect CBD is having, if any, in reducing it. THC can lead to addiction and cravings; CBD is being studied to help those in recovery. Cannabis containing 0.3 percent or less of THC is hemp. Although last year’s Farm Bill legalized hemp under federal law, it also preserved the Food and Drug Administration’s oversight of products derived from cannabis. What are the claims? CBD is advertised as providing relief for anxiety, depression and post-traumatic stress disorder. It is also marketed to promote sleep. Part of CBD’s popularity is that it purports to be “nonpsychoactive,” and that consumers can reap health benefits from the plant without the high (or the midnight pizza munchies). © 2019 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 26707 - Posted: 10.16.2019

Hannah Devlin Science correspondent Boosting testosterone levels significantly improves female athletic performance, according to one of the first randomised controlled trials. The findings come as the International Association of Athletics Federations (IAAF) announced on Monday it would impose an upper limit for testosterone levels on trans female athletes competing in middle-distance events. Testosterone was assumed to be performance-enhancing and a factor in explaining differences in strength and endurance between men and women. However, there was a surprising lack of evidence on the impact of testosterone in women and the question had become mired in controversy following a series of rulings in professional sport. The latest research confirmed that testosterone significantly increases endurance and lean muscle mass among young women, even when given for a relatively short period. Angelica Hirschberg, a gynaecologist for the Swedish Olympic Committee based at Karolinska University Hospital and the study’s first author, said the results were the first to show a causal effect of testosterone on physical performance in women. “This has not been demonstrated previously because most studies have been performed in men,” she said. “Furthermore, the study shows the magnitude of performance enhancement by testosterone. Testosterone levels increased more than four times but were still much below the male range. The improvement in endurance performance by the increased testosterone levels was more than 8% – this is a huge effect in sports.” © 2019 Guardian News & Media Limited

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26706 - Posted: 10.16.2019

Using advanced imaging, researchers have uncovered new information regarding traumatic microbleeds, which appear as small, dark lesions on MRI scans after head injury but are typically too small to be detected on CT scans. The findings published in Brain suggest that traumatic microbleeds are a form of injury to brain blood vessels and may predict worse outcomes. The study was conducted in part by scientists at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Traumatic microbleeds may represent injury to blood vessels that occur following even minor head injury,” said Lawrence Latour, Ph.D., NINDS researcher and senior author of the study. “While we know that damage to brain cells can be devastating, the exact impact of this vascular injury following head trauma is uncertain and requires further study.” This study, which involved researchers from Cold Spring Harbor Laboratory in New York and the Uniformed Services University of the Health Sciences in Bethesda, Maryland, included 439 adults who experienced head injury and were treated in the emergency department. The subjects underwent MRI scans within 48 hours of injury, and again during four subsequent visits. Participants also completed behavioral and outcome questionnaires. The results showed that 31% of all study participants had evidence of microbleeds on their brain scans. More than half (58%) of participants with severe head injury showed microbleeds as did 27% of mild cases. The microbleeds appeared as either linear streaks or dotted, also referred to as punctate, lesions. The majority of patients who exhibited microbleeds had both types. The findings also revealed that the frontal lobes were the brain region most likely to show microbleeds.

Keyword: Brain Injury/Concussion; Stroke
Link ID: 26705 - Posted: 10.16.2019

Nicola Davis A cheap and widely available drug could reduce the risk of death from common head injuries and save tens of thousands of lives each year, researchers say. Tranexamic acid slows down the breakdown of blood clots, and is already used to control heavy bleeding in people who have experienced trauma elsewhere in the body – for example from being shot or stabbed. While some of these patients might also have head injuries, it has remained unclear whether tranexamic acid would help people with head injuries alone. Now scientists say it can – at least in those with mild to moderate traumatic brain injuries – suggesting the drug should be rapidly administered to such patients. “Previous to this research, patients with isolated head injuries were an exception in the policy of giving tranexamic acid to trauma patients as soon as possible,” said Prof Ian Roberts of the London School of Hygiene and Tropical Medicine, who co-led the study. “Now that exception can be removed.” Roberts says the study could have a dramatic impact. “Worldwide it has got the potential to save tens of thousands of lives – this is such a mass problem,” he said. It is estimated that there are about 70m new traumatic brain injuries worldwide every year – a situation commonly caused by motor vehicle crashes, assault or falls. The vast majority are mild or moderate injuries – but these can still prove deadly. The study, which was published in the Lancet medical journal, spanned 29 countries, with the analysis focusing on more than 9,000 patients who were treated within three hours of injury and were randomly allocated to receiving the drug, or a placebo, intravenously. The cost of the total dose of tranexamic acid used in the trial was about £6.20 per person. © 2019 Guardian News & Media Limited

Keyword: Brain Injury/Concussion; Stroke
Link ID: 26704 - Posted: 10.15.2019

Jyoti Madhusoodanan Douglas Storace still has the dollar bill that he triumphantly taped above his laboratory bench seven years ago, a trophy from a successful wager. His postdoctoral mentor, Larry Cohen at Yale University in New Haven, Connecticut, bet that Storace couldn’t express a protein sensor of voltage changes in mice back in September 2012. Storace won. The bill is a handy reminder that the experiments he aims to try in his new lab can work. And it’s a testament to just how tricky it is to correctly express these sensors and track their signals. Storace, now an assistant professor at Florida State University in Tallahassee, plans to use these sensors, known as genetically encoded voltage indicators (GEVIs), to study how neurons in the olfactory bulb sense and react to smells. GEVIs are voltage-sensitive, fluorescent proteins that change colour when a neuron fires or receives a signal. Because GEVIs can be targeted to individual cells and directly indicate a cell’s electrical signals, researchers consider them to be the ideal probes for studying neurons. But they have proved frustratingly difficult to use. “Being able to visualize voltage changes in a cell has always been the dream,” says neuroscientist Bradley Baker at the Korea Institute of Science and Technology in Seoul. “But probes that looked great often didn’t behave in ways that were useful.” Early GEVIs disappointed on several levels. They were bright when a cell was resting and dimmed when the cell fired an action potential, producing signals that were tough to distinguish from the background. And they failed to concentrate in the nerve-cell membranes, where they function. But researchers are beginning to solve these issues. Some are turning to advanced fluorescent proteins or chemical dyes for better signals; others are using directed evolution and high-throughput screens to make GEVIs more sensitive to voltage changes. Meanwhile, biologists are putting these molecules through their paces. GEVIs, says neuroscientist Katalin Toth at Laval University in Quebec City, Canada, are not yet widely used, but they’re getting there. “They are becoming brighter and faster — and growing in popularity,” she says. “I think this is the dawn of GEVIs.” © 2019 Springer Nature Limited

Keyword: Brain imaging
Link ID: 26703 - Posted: 10.15.2019

By Amanda Chicago Lewis In June of 2018, Mark Pennington received troubling news from his ex-girlfriend, with whom he shared custody of their 2-year-old son. She had taken a hair follicle from the boy, she said, and had it analyzed at a lab. A drug test had returned positive for THC, the intoxicating compound in marijuana; evidently their son had been exposed to it, presumably in Mr. Pennington’s presence. He was told that, from then on, he would be permitted to see the child only once a week, and under supervision. “I was mortified,” Mr. Pennington recalled recently. “My jaw hit the floor. I just knew from the bottom of my heart I hadn’t gotten any THC in my son’s system.” However, Mr. Pennington had been providing his son with honey infused with cannabidiol, or CBD, a nonintoxicating compound that, like THC, is found in varying amounts in the plant known as cannabis. THC is federally illegal, and until recently so was all cannabis. But last December, the Farm Bill legalized hemp — cannabis that contains less than 0.3 percent THC. With that, CBD became legal. It can now be found at stores across the country, in everything from tinctures and massage oils to coffee and makeup. Mr. Pennington, who lives in Colorado, where growing hemp for CBD has been legal since 2014, worked for Colorado Hemp Honey, a company that sells CBD-infused raw honey across the country. Mr. Pennington was despondent about possibly losing custody of his child, until he spoke with Frank Conrad, the chief technology officer and lab director at Colorado Green Lab, a scientific consultant to the cannabis industry. Mr. Conrad directed him to a little-known study published in 2012 in the Journal of Analytical Toxicology that showed that a common forensic drug testing method could easily mistake the presence of CBD for THC. In short, the drug testing lab may have erred; it was entirely possible that the CBD Mr. Pennington had given his child had caused the drug test to produce a false positive for THC. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26702 - Posted: 10.15.2019

Dean Burnett It’s a damp, midweek afternoon. Even so, Cardiff’s walk-in stress management course has pulled in more than 50 people. There are teenagers, white-haired older people with walking aids, people from Caucasian, Asian and Middle Eastern backgrounds. There is at least one pair who look like a parent and child – I’m unsure who is there to support whom. The course instructor makes it clear that she is not going to ask people to speak out about their own stress levels in this first class: “We know speaking in public is stressful in itself.” She tells us a bit about previous attendees: a police officer whose inexplicable and constant worrying prevented him from functioning; a retired 71-year-old unable to shake the incomprehensible but constant fatigue and sadness that blighted his life; a single mother unable to attend her daughter’s school concert, despite the disappointment it would cause. What is the common theme that links these people – and the varied group sitting there this afternoon and listening? Stress may once just have been a kind of executive trophy – “I’m so stressed!” – but recent research suggests it is a key element in developing mental health problems such as depression and anxiety. The constant, stress-induced stimulation of key brain regions seems to be a major contributor to anxiety. And, in turn, vital brain regions becoming unresponsive and inflexible is believed to be a fundamental element of depressive disorders. Why do these regions become unresponsive? Possibly because they’re overworked, exhausted, by the effects of stress. This would explain why anxiety and depression regularly occur together. © 2019 Guardian News & Media Limited

Keyword: Depression; Stress
Link ID: 26701 - Posted: 10.15.2019

Madeline K. Sofia Carine Chen-McLaughlin smoked for more than 40 years. She didn't want to be a smoker. She'd tried to stop literally dozens of times over the decades. But she always came back. Smoking was "one of my oldest, dearest friends," she said of her habit. "To not have that relationship was very, very scary." Then she heard about a clinical trial to treat nicotine addiction with something a little unusual: magic mushrooms. Well, not actual magic mushrooms, but a little pill of a drug called psilocybin. It's the ingredient in mushrooms that gives people hallucinogenic visions. New research shows that psilocybin may be an effective treatment for diseases like depression and addiction. While the work is still in its early stages, there are signs that psilocybin might help addicts shake the habit by causing the brain to talk with itself in different ways. "These brain changes lead to, often times, a sense of unity," says Matthew Johnson, an experimental psychologist at Johns Hopkins University. It all may sound a little "woo-woo," he admits, but it seems to be working. Early results suggest that psilocybin, coupled with therapy, may be far more effective than other treatments for smoking, such as the nicotine patch. Magic mushrooms have been used by indigenous communities for thousands of years, and research on psilocybin isn't all that new, either. Work began in the 1950s and 1960s. But studies involving it and other psychedelics dropped off following the passage of the Controlled Substance Act in 1970, which outlawed hallucinogens and other drugs. "The medical applications became, really, a casualty of a political war," Johnson says. © 2019 npr

Keyword: Drug Abuse
Link ID: 26700 - Posted: 10.15.2019

By Katie Thomas and Sheila Kaplan In 2009, not long after Dr. Margaret Hamburg became commissioner of the Food and Drug Administration, a package arrived at her home. Inside was a clunky device called an e-cigarette. “It was my first exposure to this emerging, new technology,” Dr. Hamburg recalled. The package was sent by an antismoking activist as a warning about a product that was taking off in the United States. But over the next decade, the federal government — across the span of two presidential administrations — allowed the rise of a largely unregulated industry that may be addicting a new generation to nicotine. E-cigarettes and vaping devices, with $7 billion in annual sales, have become a part of daily life for millions of Americans. Youth use has skyrocketed with the proliferation of flavors targeting teenagers, such as Bazooka Joe Bubble Gum and Zombie Blood. And nearly 1,300 people have been sickened by mysterious vaping-related lung injuries this year. Yet the agency has not vetted the vast majority of vaping devices or flavored liquids for safety. In dozens of interviews, federal officials and public health experts described a lost decade of inaction, blaming an intense lobbying effort by the e-cigarette and tobacco industries, fears of a political backlash in tobacco-friendly states, bureaucratic delays, and a late reprieve by an F.D.A. commissioner who had previously served on the board of a chain of vaping lounges. “The minute you saw cotton candy flavors — come on,” said Dr. Thomas R. Frieden, the former director of the Centers for Disease Control and Prevention, who had warned since 2013 of the harms to adolescents. “Everything that could have been done should have been done to get them off the market.” © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26699 - Posted: 10.14.2019

Heidi Ledford Until a few months ago, pulmonologist Sean Callahan didn’t typically ask his patients if they vaped. He thought that e-cigarettes might help smokers wean themselves off cigarettes, and that the risks of vaping would probably take years to become clear. The emergence of a mysterious, sometimes lethal, lung injury associated with vaping has changed his mind. Callahan works at the University of Utah Health in Salt Lake City, which has treated about 20 victims of the outbreak. “It was surprising: the overwhelming number of them — and how young they were,” he says. Researchers and physicians alike were caught unprepared by the illness, which has now sickened about 1,300 US vapers and killed 26. Scientists are scrambling to find out why, and to save other vapers from the same fate. “Everything is rapidly evolving,” says Brandon Larsen, a pulmonary pathologist at the Mayo Clinic in Phoenix, Arizona. “I could tell you something today and next week it could be totally wrong.” A paper1 published by Larsen and his colleagues in the New England Journal of Medicine on 2 October undercut a popular theory behind the outbreak — and underscored how far researchers still have to go to pinpoint its cause. Many of those sickened in the outbreak had vaped cartridges containing tetrahydrocannabinol (THC) — the active ingredient in marijuana — that was diluted with oily chemicals. Larsen’s study is the largest analysis to date of lung tissue taken from sickened vapers. The scientists searched for evidence of lipoid pneumonia, a condition that arises when oil enters the lungs. It is marked by lipid found in lung tissue and also in cells called macrophages, which normally sweep up debris in the lungs. But Larsen and his colleagues did not find substantial lipid droplets in any of their samples from 17 patients. Instead, their findings point to general lung damage and inflammation caused by exposure to toxic chemicals. © 2019 Springer Nature Limited

Keyword: Drug Abuse
Link ID: 26698 - Posted: 10.14.2019

Sandra G. Boodman The July day wasn’t too steamy — a rarity in Madison, Ala. — and her toddler’s physical therapy session wasn’t scheduled for another hour, so Jeannette Vega thought she’d take 26-month-old Tiana outside to play in their yard. Immediately, she was struck by her younger daughter’s difficulty climbing up the sturdy low-slung plastic slide, something Tiana had been able to do with ease only a week earlier. To distract her, Jeannette opened the door of the family’s truck. “Come on, let’s get in and buckle up,” she remembers saying. Tiana took particular delight in clambering into her car seat and fastening her seat belt. Not this time. The little girl seemed rooted to the ground, impervious to her mother's encouragement. "It wasn't that she wouldn't [comply]," Jeannette recalled of the 2015 incident. "I could tell she just couldn't." Later that afternoon, she mentioned Tiana's difficulties to the physical therapist who had been working with the little girl for more than a year to try to overcome her significant, unexplained developmental delays. “This isn’t normal, to regress after so many months of therapy,” Jeannette, now 37, remembers the therapist telling her. She mentioned a disorder Jeannette had never heard of and suggested it might be the cause. Jeannette did a quick search, dismissed the possibility and said she “forgot about it.” But the first anguished words she blurted out nearly a half-year later on that shattering day in the specialist’s office when she learned what was wrong, was that the therapist had been right.

Keyword: Autism
Link ID: 26697 - Posted: 10.14.2019

By Aaron E. Carroll There’s a decent chance you’ll be reading about diet soda studies until the day you die. (The odds are exceedingly good it won’t be the soda that kills you.) The latest batch of news reports came last month, based on another study linking diet soda to an increased risk of death. As usual, the study (and some of the articles) lacked some important context and caused more worry than was warranted. There are specific reasons that this cycle is unlikely to end. 1. If it’s artificial, it must be bad. People suspect, and not always incorrectly, that putting things created in a lab into their bodies cannot be good. People worry about genetically modified organisms, and monosodium glutamate and, yes, artificial sweeteners because they sound scary. But everything is a chemical, including dihydrogen monoxide (that’s another way of saying water). These are just words we use to describe ingredients. Some ingredients occur naturally, and some are coaxed into existence. That doesn’t inherently make one better than another. In fact, I’ve argued that research supports consuming artificial sweeteners over added sugars. (The latest study concludes the opposite.) 2. Soda is an easy target In a health-conscious era, soda has become almost stigmatized in some circles (and sales have fallen as a result). It’s true that no one “needs” soda. There are a million varieties, and almost none taste like anything in nature. Some, like Dr Pepper, defy description. But there are many things we eat and drink that we don’t “need.” We don’t need ice cream or pie, but for a lot of people, life would be less enjoyable without those things. None of this should be taken as a license to drink cases of soda a week. A lack of evidence of danger at normal amounts doesn’t mean that consuming any one thing is huge amounts is a good idea. Moderation still matters. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26696 - Posted: 10.14.2019

By Emily Willingham Most of us could use more sleep. We feel it in our urge for an extra cup of coffee and in a slipping cognitive grasp as a busy day grinds on. And sleep has been strongly tied to our thinking, sharpening it when we get enough and blunting it when we get too little. What produces these effects are familiar to neuroscientists: external light and dark signals that help set our daily, or circadian, rhythms, “clock” genes that act as internal timekeepers, and neurons that signal to one another through connections called synapses. But how these factors interact to freshen a brain once we do sleep has remained enigmatic. Findings published on October 10 in two papers in Science place synapses at center stage. These nodes of neuronal communication, researchers show, are where internal preparations for sleep and the effects of our sleep-related behaviors converge. Cellular timekeepers rhythmically prep areas around the synapses in anticipation of building synaptic proteins during slumber. But the new findings indicate neurons don’t end up building these critical proteins in the absence of sleep. Advertisement The results suggest the brain is “getting prepared for an event, but it doesn’t mean you actually follow through on doing it,” says Robert Greene, a neuroscientist at the University of Texas Southwestern Medical Center, who was not involved in the study. Greene calls the studies “fascinating,” saying they confirm a “long suspected” connection between internal timekeeping and sleep behaviors. © 2019 Scientific American

Keyword: Sleep
Link ID: 26695 - Posted: 10.11.2019