By Gretchen Reynolds For women with serious depression, a single session of exercise can change the body and mind in ways that might help to combat depression over time, according to a new study of workouts and moods. Interestingly, though, the beneficial effects of exercise may depend to a surprising extent on whether someone exercises at her own pace or gets coaching from someone else. Already, a wealth of recent research tells us that exercise buoys moods. Multiple studies show that physically active people are more apt to report being happy than sedentary people and are less likely to experience anxiety or depression. In a few experiments, regular exercise reduced the symptoms of depression as effectively as antidepressant medications. But science has yet to explain how exercise, a physical activity, alters people’s psychological health. Many exercise scientists speculate that working out causes the release of various proteins and other biochemical substances throughout our bodies. These substances can enter the bloodstream, travel to our brains and most likely jump-start neural processes there that affect how we feel emotionally. But it has not been clear which of the many substances released during exercise matter most for mental health and which kinds of exercise prompt the greatest gush in those biochemicals. Those open questions prompted Jacob Meyer, an assistant professor of kinesiology at Iowa State University in Ames, to start considering endocannabinoids and the runner’s high. As the name indicates, endocannabinoids are self-produced psychoactive substances, similar to the psychoactive compounds in cannabis, or marijuana. Created in many of our body’s tissues all the time, endocannabinoids bind to specialized receptors in our brains and nervous systems and help to increase calm and improve moods, among other effects. © 2019 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 26522 - Posted: 08.21.2019

By Ken Belson COLLEGE STATION, Tex. — On a steamy afternoon in June, Jim Poynter, the coach of the 7-on-7 touch football team at Lamar High School in Arlington, Tex., escorted one of his former players around the state tournament. In a game last spring, the player, Brett Green Jr., was knocked out after his head collided with a teammate’s shoulder as they jumped to intercept a pass. Green was airlifted to a hospital, where bleeding in his brain was discovered. He spent weeks in the hospital recovering from dizziness, headaches and blurred vision, and had eye surgery and physical therapy. He will never play football again. Poynter wanted Green to know that some good came of his misfortune. Spread across the fields, about 4,000 players on 128 teams from across Texas ran pass routes, defended receivers and celebrated with high fives. What mattered most to Poynter, though, was that every player wore a soft-shell helmet. For years, 7-on-7 touch football has been billed as a safe way for players to stay in shape until tackle football starts up in the late summer. Most injuries involve twisted ankles, sprained knees and pulled muscles. But Green’s injury prompted the Texas State 7on7 Organization, aware that parents are more concerned than ever about safety, to become the first statewide group in the country to require that all of its players wear soft-shell helmets, starting at this year’s state tournament. “I don’t want that to happen to anyone else,” Green said. “It felt good to see in person because you know for sure they are wearing protection. I wish the decision had been made earlier, but I try to look for the good in everything.” © 2019 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 26521 - Posted: 08.21.2019

By Anahad O’Connor Low-carbohydrate diets have fallen in and out of favor since before the days of Atkins. But now an even stricter version of low-carb eating called the ketogenic diet is gaining popular attention, igniting a fierce scientific debate about its potential risks and benefits. Both the Atkins and ketogenic diets encourage followers to cut carbs from their diets. But while the Atkins diet gradually increases carbs over time, keto places firm limits on carbs and protein. This way of eating depletes the body of glucose, forcing it to primarily burn fat and produce an alternate source of fuel called ketones. A typical ketogenic diet restricts carbs to less than 10 percent of calories and limits protein to 20 percent, while fat makes up the rest. The keto diet has been popularized in best-selling books, promoted by celebrities and touted on social media as an antidote to various ailments. Proponents say it causes substantial weight loss and can help those with Type 2 diabetes dramatically improve their blood sugar levels, which fall when people avoid carbs. There have been many studies of the ketogenic diet over the years, but most have been small and of fairly short duration. A federal registry of clinical research shows that more than 70 trials looking at the diet’s impact on brain, cardiovascular and metabolic health are either underway or in the beginning stages. Dr. Ethan Weiss, a researcher and preventive cardiologist at the University of California, San Francisco, had long been skeptical of low-carb diets but decided to experiment with the ketogenic diet a couple years ago. In a typical day he skips breakfast and eats mostly salads, nuts, cheese, roasted vegetables and grilled chicken, fish or tofu, as well as dark chocolate for dessert. The result, he says: He lost 20 pounds and had to buy a new wardrobe. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26520 - Posted: 08.20.2019

Nicola Davis People who struggle with sleep might be at greater risk of developing cardiovascular problems, research suggests. Scientists have found that people who are genetically predisposed to insomnia have a greater risk of heart failure, stroke and coronary artery disease. Researchers say the study backs previous work that has found links between poor sleep and cardiovascular problems, with the latest study supporting the idea that insomnia could play a role in causing such conditions. “If that really is the case, then if we can improve or reduce sleep disturbances, that might reduce the risk of stroke,” said Prof Hugh Markus, co-author of the research from the University of Cambridge. The new study relies on previous findings that there are about 250 genetic variants, each of which slightly increases the risk of someone having insomnia. “Most people don’t have all of them, people will have a number of them, a few or many of them,” said Markus. The crucial point is the way the genetic variants are inherited. Whether an individual carries them is random: their presence does not depend on the rest of that person’s genetic makeup or environmental factors, such as where they live, their wealth or how much they exercise. That means it is theoretically possible to look at whether an increased risk of insomnia could play a role in causing stroke, heart failure and coronary artery disease, while reducing the impact of other factors that can muddy the waters. This is a different approach to previous studies which could only show association, not causation. © 2019 Guardian News & Media Limited

Keyword: Sleep
Link ID: 26519 - Posted: 08.20.2019

By Robert C. Cantu and Mark Hyman If U.S. Surgeon General Jerome Adams asked for our advice (he hasn’t), we’d recommend that he issue the following statement: SURGEON GENERAL’S WARNING: Tackle football is dangerous for children. Children who play tackle football absorb repeated hits to the head. As adults, they’re at higher risk of suffering cognitive deficits as well as behavioral and mood problems. We’d suggest that, as the nation’s top doctor, the surgeon general put this warning on every youth football helmet and place it in bold type on all youth tackle football registration forms. A parent or guardian wouldn’t be able to sign up their child without seeing it. It’s hard to overstate the importance of these steps. It’s fair to say that millions of sports-playing kids would enter adulthood with healthier brains and better futures. Forty million children participate in organized sport each year. Protecting them from head injury is a big task. Youth sports organizations generally do an admirable job. In the past decade, the U.S. Soccer Federation has banned heading for players 10 years old and younger and limited heading for players 11 to 13. USA Hockey no longer allows body checking until players are 13. Even tackle football is safer — marginally. Pop Warner, the largest national youth football league, has eliminated kickoffs for the youngest players — 5- to 10-years-old — and limited full-contact practice time. Of late, we’re learning more about brain injury among youth players in rougher “collision” sports such as football. These young athletes are at greater risk than we knew and than many parents and coaches would find acceptable. Recent studies of youth football are particularly alarming. Since 2015, Boston University’s Chronic Traumatic Encephalopathy Center (which Robert C. Cantu co-founded) has published three studies all leading to a disquieting conclusion: Adults who played tackle football as children were more likely to deal with emotional and cognitive challenges in later life. © 1996-2019 The Washington Post

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 26518 - Posted: 08.20.2019

By Aaron E. Carroll In many areas of health policy, the best of intentions can lead to more harm than good. Such is the case with America’s approach to alcohol and pregnancy. The best evidence shows that punitive policies — such as equating drinking while pregnant as child abuse and threatening to involve child protective services — can dissuade women from getting prenatal care. Fetal alcohol spectrum disorders refer to a collection of problems in babies and children. These include low birth weight; impaired growth; and problems in the heart, kidneys and brain. Children can have developmental delays, communication difficulties, learning disabilities and lower I.Q. Some of these last a lifetime. It’s hard to know how many American children are affected. Studies done by the Centers for Disease Control and Prevention have estimated that between 2 and 15 infants per 10,000 born in the United States have fetal alcohol syndrome, the most severe form of the disorders. Some community-based studies that use the broader definition of the disorder have found more affected children, up to 5 percent. We know that infants of women who drink alcohol in pregnancy may develop these disorders. The problem is what we don’t know. We don’t know the level of alcohol exposure in utero that could cause a child to develop these disorders. We don’t know if the timing of the exposure matters. We don’t know why some women who drink little might have a child who is affected, while some can binge drink during pregnancy and have a child with no apparent problems. Because of this, most medical organizations, including the American Academy of Pediatrics and the C.D.C., recommend that women forgo alcohol during pregnancy. The only dose known to be “safe” is none, they say, and therefore women should not drink at all. © 2019 The New York Times Company

Keyword: Drug Abuse; Development of the Brain
Link ID: 26517 - Posted: 08.20.2019

By Michael Price First piloted as an experiment to reduce dental cavities in Grand Rapids, Michigan, in 1945, fluoridated drinking water has since been hailed by the U.S. Centers for Disease Control and Prevention in Atlanta as “one of public health’s greatest success stories.” Today, about two-thirds of people in the United States receive fluoridated tap water, as do many people in Australia, Brazil, Canada, New Zealand, Spain, and the United Kingdom. Now, a controversial new study links fluoridation to lower IQ in young children, especially boys whose mothers drank fluoridated water while pregnant. Longtime fluoridation critics are lauding the study, but other researchers say it suffers from numerous flaws that undercut its credibility. Either way, “It’s a potential bombshell,” says Philippe Grandjean, an environmental health researcher at Harvard University who wasn’t involved in the work. Fluoride is well-known for protecting teeth against cavities by strengthening tooth enamel. It’s found naturally in low concentrations in both freshwater and seawater, as well as in plant material, especially tea leaves. Throughout the 1940s and ’50s, public health researchers and government officials in cities around the world experimentally added fluoride to public drinking water; they found it reduced the prevalence of cavities by about 60%. Today, fluoridated water flows through the taps of about 5% of the world’s population, including 66% of Americans and 38% of Canadians. Yet skepticism has dogged the practice for as long as it has existed. Some have blamed fluoridated water for a wide range of illnesses including cancer, but most criticism has been dismissed as pseudoscience. Over the years, though, a small number of scientists have published meta-analyses casting doubt on the efficacy of water fluoridation in preventing cavities. More recently, scientists have published small-scale studies that appear to link prenatal fluoride exposure to lower IQ, although dental research groups were quick to challenge them. © 2019 American Association for the Advancement of Science.

Keyword: Development of the Brain; Intelligence
Link ID: 26516 - Posted: 08.19.2019

Ashley Yeager Drops of blood, filter paper, bacteria, a bacterial inhibitor, and a baking dish—that’s all it took for microbiologist Robert Guthrie to develop a basic test for phenylketonuria, a genetic metabolic disease that, if left untreated in infants, soon leads to neurological dysfunction and intellectual disability. The test would lay the foundation for screening newborns for diseases. In 1957, Guthrie met Robert Warner, a specialist who diagnosed individuals with mental disabilities. Warner told Guthrie about phenylketonuria (PKU), now known to affect roughly 1 in 10,000 children. The disease makes it impossible to break down the amino acid phenylalanine, so that it builds up to toxic levels in the body and disrupts neuronal communication. Once a child was diagnosed, a strict low-phenylalanine diet could prevent further damage, but Warner had no easy way to measure phenylalanine levels in his PKU patients’ blood to monitor the diet’s effects. He asked Guthrie for help. Guthrie reported back to Warner three days later with a solution. Guthrie knew from past work that the bacterial inhibitor β-2-thienylalanine blocked Bacillus subtilis from flourishing by substituting for phenylalanine in growing peptide chains, resulting in inactive proteins. He also knew that adding phenylalanine to the cell cultures restored normal protein function and spurred the bacterium’s growth. So his solution was simple: prick the skin, collect a few drops of blood on filter paper, and place the filter paper in a baking pan covered in β-2-thienylalanine. Add Bacillus subtilis to the filter paper and heat the pan overnight. If the bacterium grows exponentially, the level of phenylalanine is high. The assay worked well, so Guthrie used it as a model to develop tests for other metabolic diseases. © 1986–2019 The Scientist

Keyword: Development of the Brain; Genes & Behavior
Link ID: 26515 - Posted: 08.19.2019

Helena Blackstone The first study looking into the use of MDMA to treat alcohol addiction has shown the treatment is safe and early results show encouraging outcomes from the approach, scientists have said. Doctors in Bristol are testing whether a few doses of the drug, in conjunction with psychotherapy, could help patients overcome alcoholism more effectively than conventional treatments. Those who have completed the study have so far reported almost no relapse and no physical or psychological problems. In comparison, eight in 10 alcoholics in England relapse within three years after current treatment approaches. Dr Ben Sessa, an addiction psychiatrist and senior research fellow at Imperial College London, and who led the trial, said: “With the very best that medical science can work with, 80% of people are drinking within three years post alcohol detox.” Eleven people have so far completed the safety and tolerability study, which involves nine months of follow-ups. “We’ve got one person who has completely relapsed, back to previous drinking levels, we have five people who are completely dry and we have four or five who have had one or two drinks but wouldn’t reach the diagnosis of alcohol use disorder,” Sessa said. Most addiction is based on underlying trauma, often from childhood, explained Sessa. “MDMA selectively impairs the fear response,” he said. “It allows recall of painful memories without being overwhelmed. © 2019 Guardian News & Media Limited

Keyword: Drug Abuse
Link ID: 26514 - Posted: 08.19.2019

Researchers believe that stuttering — a potentially lifelong and debilitating speech disorder — stems from problems with the circuits in the brain that control speech, but precisely how and where these problems occur is unknown. Using a mouse model of stuttering, scientists report that a loss of cells in the brain called astrocytes are associated with stuttering. The mice had been engineered with a human gene mutation previously linked to stuttering. The study (link is external), which appeared online in the Proceedings of the National Academy of Sciences, offers insights into the neurological deficits associated with stuttering. The loss of astrocytes, a supporting cell in the brain, was most prominent in the corpus callosum, a part of the brain that bridges the two hemispheres. Previous imaging studies have identified differences in the brains of people who stutter compared to those who do not. Furthermore, some of these studies in people have revealed structural and functional problems in the same brain region as the new mouse study. The study was led by Dennis Drayna, Ph.D., of the Section on Genetics of Communication Disorders, at the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health. Researchers at the Washington University School of Medicine in St. Louis and from NIH’s National Institute of Biomedical Imaging and Bioengineering, and National Institute of Mental Health collaborated on the research. “The identification of genetic, molecular, and cellular changes that underlie stuttering has led us to understand persistent stuttering as a brain disorder,” said Andrew Griffith, M.D., Ph.D., NIDCD scientific director. “Perhaps even more importantly, pinpointing the brain region and cells that are involved opens opportunities for novel interventions for stuttering — and possibly other speech disorders.”

Keyword: Language; Glia
Link ID: 26513 - Posted: 08.19.2019

Laura Sanders Seconds before a memory pops up, certain nerve cells jolt into collective action. The discovery of this signal, described in the Aug. 16 Science, sheds light on the mysterious brain processes that store and recall information. Electrodes implanted in the brains of epilepsy patients picked up neural signals in the hippocampus, a key memory center, while the patients were shown images of familiar people and places, including former President Barack Obama and the Eiffel Tower in Paris. As the participants took in this new information, electrodes detected a kind of brain activity called sharp-wave ripples, created by the coordinated activity of many nerve cells in the hippocampus. Later blindfolded, the patients were asked to remember the pictures. One to two seconds before the participants began describing each picture, researchers noticed an uptick in sharp-wave ripples, echoing the ripples detected when the subjects had first seen the images. That echo suggests that these ripples are important for learning new information and for recalling it later, Yitzhak Norman of the Weizmann Institute of Science in Rehovot, Israel, and colleagues write in the study. Earlier studies suggested that these ripples in the hippocampus were important for forming memories. But it wasn’t clear if the ripples also had a role in bringing memories to mind. In another recent study, scientists also linked synchronized ripples in two parts of the brain to better memories of word pairs (SN Online: 3/5/19). |© Society for Science & the Public 2000 - 2019

Keyword: Learning & Memory
Link ID: 26512 - Posted: 08.19.2019

John Pappas A confidential government document containing evidence so critical it had the potential to change the course of an American tragedy was kept in the dark for more than a decade. The document, known as a “prosecution memo,” details how government lawyers believed that Purdue Pharma, the maker of the powerful opioid, OxyContin, knew early on that the drug was fueling a rise in abuse and addiction. They also gathered evidence indicating that the company’s executives had misled the public and Congress. “The Weekly” shines a light on that 2006 Justice Department memo and its consequences for today’s wave of lawsuits against opioid makers and members of the Sackler family, which owns Purdue Pharma. We go with Barry Meier, the New York Times reporter who for two decades has chronicled how opioid abuse has ravaged America, as he travels back to where the crisis began. Barry Meier covered business, public policy, health and safety for nearly 30 years for The New York Times. He began covering the marketing of the painkiller OxyContin and the resulting epidemic of opioid addiction as early as 2001. He is also the author of “Pain Killer: An Empire of Deceit and the Origin of America’s Opioid Epidemic,” first published in 2003 and recently reissued. The Confidential Memo Revealed Prosecutors cited evidence in their 2006 memo that Sackler family members who own Purdue were sent reports about problems with the company’s drugs. But that evidence never came to light because the recommended felony charges against Purdue executives never went forward. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26511 - Posted: 08.17.2019

By John Horgan At the beginning of my book Mind-Body Problems, I describe one of my earliest childhood memories: I am walking near a river on a hot summer day. My left hand grips a fishing rod, my right a can of worms. One friend walks in front of me, another behind. We’re headed to a spot on the river where we can catch perch, bullheads and large-mouth bass. Weeds bordering the path block my view of the river, but I can smell its dank breath and feel its chill on my skin. The seething of cicadas builds to a crescendo. I stop short. I’m me, I say. My friends don’t react, so I say, louder, I’m me. The friend before me glances over his shoulder and keeps walking, the friend behind pushes me. I resume walking, still thinking, I’m me, I’m me. I feel lonely, scared, exhilarated, bewildered. Advertisement That moment was when I first became self-conscious, aware of myself as something weird, distinct from the rest of the world, demanding explanation. Or so I came to believe when I recalled the incident in subsequent decades. I never really talked about it, because it was hard to describe. It meant a lot to me, but I doubted it would mean much to anyone else. Then I learned that others have had similar experiences. One is Rebecca Goldstein, the philosopher and novelist, whom I profiled in Mind-Body Problems. Before interviewing Goldstein, I read her novel 36 Arguments for the Existence of God, and I came upon a passage in which the hero, Cass, a psychologist, recalls a recurrent “metaphysical seizure” or “vertigo” that struck him in childhood. Lying in bed, he was overcome by the improbability that he was just himself and no one else. “The more he tried to get a fix on the fact of being Cass here,” Goldstein writes, “the more the whole idea of it just got away from him.” Even as an adult, Cass kept asking himself, “How can it be that, of all things, one is this thing, so that one can say, astonishingly, ‘Here I am’”? © 2019 Scientific American

Keyword: Consciousness; Development of the Brain
Link ID: 26510 - Posted: 08.17.2019

Laura Sanders Alzheimer’s disease destroys command centers in the brain that keep people awake. That finding could explain why the disease often brings daytime drowsiness. Sleep problems can precede dementias, including Alzheimer’s, sometimes by decades. But the new result, described online August 12 in Alzheimer’s & Dementia, suggests that disordered sleeping isn’t just an early harbinger of Alzheimer’s. Instead, sleep trouble is “part of the disease,” says Lea Grinberg, a neuropathologist at the University of California, San Francisco. Grinberg and colleagues focused on the brain stem and a structure perched above it called the hypothalamus. Together, these parts of the nervous system oversee crucial jobs such as keeping people awake and paying attention. Though important, the brain stem and its neighbors have been largely overlooked in studies of dementia, Grinberg says. In particular, the researchers searched for evidence of tau, a protein that can form tangles inside nerve cells, in postmortem brains of people who died with Alzheimer’s disease. Three small regions of the hypothalamus and brain stem, all of which usually contain nerve cells that keep people awake during the day, were packed with tau, the team found. And two of the three areas had lost over 70 percent of their nerve cells, or neurons. These areas “are hit hard, and they are hit by tau,” Grinberg says. That destruction could be part of the reason people with Alzheimer’s disease often feel tired during the day, even if they slept the night before. |© Society for Science & the Public 2000 - 2019.

Keyword: Alzheimers
Link ID: 26509 - Posted: 08.17.2019

By John Williams The first, startling epigraph in Nicci Gerrard’s new book, “The Last Ocean,” comes from Emily Dickinson: “Abyss has no Biographer.” Gerrard sets out to tell the story of dementia, a disease that can appear to consume those it afflicts. After her father, John, died in 2014, the author — who writes best-selling thrillers with her husband under the name Nicci French — embarked on learning more about the disease as both a journalist and an activist. The result is a tender, inquisitive tour of a subject that can be raw and painful. Below, Gerrard talks about loss, art that punches you in the solar plexus and the experience of writing a book that doesn’t answer questions. When did you first get the idea to write this book? I first had the idea when my father, who’d been living with dementia for over 10 years, went into hospital in February 2014. After four weeks without anyone to see him — we were allowed in for very limited times and then not at all, because of a norovirus outbreak — I barely recognized him. I will, for the rest of my life, feel terribly that I didn’t get him out earlier. Then he lived at home for nine months. He had become skeletal, immobile, inarticulate, and in a way he felt utterly lost, like a ghost in our lives and in his own life. He would lay downstairs in a hospital bed, looking outside at the garden he used to love. There was this clear sense that he’d already lost everything he had, everything he was, all his capacity, there was nothing left — and yet somehow that he didn’t lose himself. In the book I say that if I were religious, I would call that self he retained his soul. Something very indelible remained. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26508 - Posted: 08.17.2019

Nicola Davis A new organ involved in the sensation of pain has been discovered by scientists, raising hopes that it could lead to the development of new painkilling drugs. Researchers say they have discovered that the special cells that surround the pain-sensing nerve cells that extend into the outer layer of skin appear to be involved in sensing pain – a discovery that points to a new organ behind the feeling of “ouch!”. The scientists say the finding offers new insight into pain and could help answer longstanding conundrums. “The major question for us now is whether these cells are actually the cause for certain kinds of chronic pain disorders,” Prof Patrik Ernfors, a co-author of the research from the Karolinska Institute in Sweden, told the Guardian. Writing in the journal Science, the researchers reveal how they examined the nature of cells in the skin that, they say, have largely been overlooked. These are a type of Schwann cell, which wrap around and engulf nerve cells and help to keep them alive. The study has revealed these Schwann cells have an octopus-like shape. After examining tissues, the team found the body of the cells sits below the outer layer of the skin, but that the cells have long extensions that wrap around the ends of pain-sensing nerve cells that extend up into the epidermis, the outer layer of the skin. The scientists were surprised at the findings because it has long been believed that the endings of nerve cells in the epidermis were bare or unwrapped. “In the pain field, we talk about free nerve endings that are responsible for pain sensation. But actually they are not free,” Ernfors said. © 2019 Guardian News & Media Limited

Keyword: Pain & Touch; Glia
Link ID: 26507 - Posted: 08.16.2019

Statistics Canada says Canadian men are almost twice as likely to use cannabis as women. New data from the National Cannabis Survey today shows 16 per cent of Canadians over 15 years old report using pot in April, May or June. That's down slightly from 17.5 per cent in the first three months of the year. Almost five million Canadians consumed cannabis in some form during the three month period. One quarter of men, and 16 per cent of women, reported they plan to consume it in the next three months. The survey suggests men are more likely to use cannabis daily or weekly than women, and are also more likely to use it for non-medicinal purposes. About four in 10 marijuana users say they bought cannabis illegally. Smoking the drug remains the most common way of consuming it, with 68 per cent of men and 62 per cent of women consumers choosing this method. At 14 per cent, women were almost three times more likely than men (five per cent) to have consumed cannabis through "other methods," including edible and topical variants. Recreational marijuana became legal in Canada last October and Statistics Canada is tracking consumption habits every three months. ©2019 CBC/Radio-Canada.

Keyword: Drug Abuse; Sexual Behavior
Link ID: 26506 - Posted: 08.16.2019

By Dylan Loeb McClain Kary B. Mullis, a biochemist who won the 1993 Nobel Prize in Chemistry for discovering a way to analyze DNA easily and cheaply and thus pave the way for major advances in medical diagnostics, molecular biology and forensic science, died on Aug. 7 at his home in Newport Beach, Calif. He was 74. The cause was heart and respiratory failure brought on by pneumonia, his wife, Nancy Cosgrove Mullis, said. The process for analyzing DNA that Dr. Mullis invented is called polymerase chain reaction, or PCR. It replicates a single strand of DNA millions of times, enabling scientists to pinpoint a segment of the strand and amplify it for identification. Polymerase, an enzyme that synthesizes polymers and nucleic acids, is essential in creating DNA and RNA, the molecules that are responsible for coding DNA. Before PCR, amplifying DNA took weeks, because it had to be generated in bacteria. Once Dr. Mullis’s process was perfected, it took only hours, opening up a world of possibilities. We’ll bring you stories that capture the wonders of the human body, nature and the cosmos. Today, his method is used to detect genetic mutations that can lead to diagnoses of diseases, like sickle cell anemia; analyze ancient sources of DNA, like bones; assist in obtaining crime scene evidence; and determine paternity. It was used as well to decode and map the entire human DNA as part of the Human Genome Project, the landmark international research effort that ran from 1990 to 2003. As he told the story in his Nobel lecture, Dr. Mullis found his inspiration one night in 1983 while driving to his cabin in Mendocino, Calif. © 2019 The New York Times Company

Keyword: Genes & Behavior
Link ID: 26505 - Posted: 08.16.2019

By Bret Stetka Among the human body’s many maladies, few have stumped medical researchers like those that decimate the brain. After decades of effort, effectively treating—let alone curing—neurodegenerative disorders such as Huntington’s and Alzheimer's disease has been a source of frustration for many, as old theories are questioned and clinical trials fail. Basic scientists have achieved some progress. Over the past few decades, they have made serious headway in identifying single inherited genes responsible for genetic forms of various neurodegenerative diseases such as Alzheimer’s—and also the molecular and neural mechanisms behind nongenetic, or sporadic, forms of brain maladies. Yet translating these findings into working therapies has proved challenging. With genetic engineering technologies, such as CRISPR, that literally rewrite our DNA still a ways away from routine use, a number of clinical researchers have turned to a more immediate genome-based approach to treat disorders of the brain: manipulating RNA to modify levels of proteins associated with disease. DNA provides our genetic code, with its sister molecule RNA translating that code into the proteins that run our brains and myriad bodily functions. Scientists can now use molecules called antisense oligonucleotides (ASOs) to modify this process by binding to RNA and altering translation. ASOs are DNA-like molecules that greatly resemble the DNA that produced the RNA they correspond to in the first place. Depending on where they are designed to bind, these antisense molecules can prevent an RNA from being translated into a protein, which reduces levels of that protein in the body or brain. Alternatively, these same DNA-like molecules can be crafted to interfere with RNA machinery that normally inhibits or slows translation. In this case, more protein is made. © 2019 Scientific American

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 26504 - Posted: 08.15.2019

By Kate Murphy Maybe it was because when the waiter asked, “Still or sparkling?” you chose sparkling. It could have also been that you were ravenous and ate a little too much. Or, possibly, it was your ex, who happened to be dining at the same restaurant and stood a little too long over your table making awkward small talk. All of these things, hic, might cause spasms, hic, in your diaphragm, hic. Referred to in the medical literature as singultus (from the Latin singult, which means gasp or sob), hiccups are familiar to anyone who has ever taken a breath. In fact, you begin to hiccup while still in the womb. Most people hiccup the most during childhood, with the bouts becoming less frequent over time, but even in adulthood, hiccups are still a common, and annoying, occurrence. Just as we all have our own particular way of sneezing, we all have a unique way of hiccuping that can range from four to 60 hiccups per minute. Most hiccups are benign and last only a few minutes or hours. But sometimes hiccups are indicative of a more serious health issue, particularly when they recur or don’t go away for days, weeks or years. Beyond being embarrassing, the muscle contractions can be physically exhausting. They can interrupt sleep and make it hard to eat. Approximately 4,000 people in the United States are admitted to the hospital every year for hiccups. The patient with the longest recorded case, according to Guinness World Records, was Charles Osborne of Anthon, Iowa, who hiccuped for 68 years straight. He claimed it started while attempting to weigh a hog before slaughtering it. Doctors say there are as many causes for hiccups as there are crazy remedies, including tugging on your tongue, standing on your head and swallowing granulated sugar. Some actually work. Others are more likely just entertainment for friends and family who watch while you try to cure yourself. © 2019 The New York Times Company

Keyword: Miscellaneous
Link ID: 26503 - Posted: 08.15.2019