By Rachel Bluth The number of children diagnosed with attention-deficit/hyper­activity disorder (ADHD) has reached more than 10 percent, a significant increase during the past 20 years, according to a new study. The rise was most pronounced in minority groups, suggesting that better access to health insurance and mental-health treatment through the Affordable Care Act (ACA) may have played some role in the increase. The rate of diagnosis doubled in girls, although it was still much lower than in boys. But the researchers say they found no evidence confirming frequent complaints that the condition is overdiagnosed or misdiagnosed. The United States has significantly more instances of ADHD than other developed countries, which researchers said has led some to think Americans are overdiagnosing children. Wei Bao, the lead author of the study, said in an interview that a review of studies around the world doesn’t support that. “I don’t think overdiagnosis is the main issue,” he said. Nonetheless, those doubts persist. Stephen Hinshaw, who co-authored a 2014 book called “The ADHD Explosion: Myths, Medication, Money, and Today’s Push for Performance,” compared ADHD to depression. He said in an interview that neither condition has unequivocal biological markers, which makes it hard to determine whether a person has the condition. Symptoms of ADHD can include inattention, fidgety behavior and impulsivity. © 1996-2018 The Washington Post

Keyword: ADHD; Development of the Brain
Link ID: 25434 - Posted: 09.11.2018

By Jan Hoffman BOSTON — To the medical students, the patient was a conundrum. According to his chart, he had residual pain from a leg injury sustained while working on a train track. Now he wanted an opioid stronger than the Percocet he’d been prescribed. So why did his urine test positive for two other drugs — cocaine and hydromorphone, a powerful opioid that doctors had not ordered? It was up to Clark Yin, 29, to figure out what was really going on with Chris McQ, 58 — as seven other third-year medical students and two instructors watched. “How are you going to have a conversation around the patient’s positive tox screen results?” asked Dr. Lidya H. Wlasiuk, who teaches addiction awareness and interventions here at Boston University School of Medicine. Mr. Yin threw up his hands. “I have no idea,” he admitted. Chris McQ is a fictional case study created by Dr. Wlasiuk, brought to life for this class by Ric Mauré, a keyboard player who also works as a standardized patient — trained to represent a real patient, to help medical students practice diagnostic and communication skills. The assignment today: grappling with the delicate art and science of managing a chronic pain patient who might be tipping into a substance use disorder. How can a doctor win over a patient who fears being judged? How to determine whether the patient’s demand for opioids is a response to dependence or pain? Addressing these quandaries might seem fundamental in medical training — such patients appear in just about every field, from internal medicine to orthopedics to cardiology. The need for front-line intervention is dire: primary care providers like Dr. Wlasiuk, who practices family medicine in a Boston community clinic, routinely encounter these patients but often lack the expertise to prevent, diagnose and treat addiction. © 2018 The New York Times Company

Keyword: Drug Abuse
Link ID: 25433 - Posted: 09.11.2018

Diana Kwon In the early 2000s, Stefano Schiaffino, a muscle physiologist at the University of Padova in Italy, was faced with puzzling results: two seemingly identical experiments involving hind leg muscles in rats had yielded different findings. Schiaffino and his team were investigating nuclear factor of activated T cells (NFAT), a transcription factor that responds to the level of muscle activity. Despite using similar procedures, the researchers found that in the tissues from one set of animals, NFAT had moved from the cytoplasm into the nucleus in a large proportion of cells, while in tissues from another experiment, this change had not occurred. The explanation for this difference turned out to be simple: timing. The researcher responsible for one trial had sacrificed the nocturnal animals in the evening, while another had conducted the same procedure for the second trial in the morning. This meant that the first group of animals was more active at the time of measurement than the second. When the scientists repeated the second experiment late in the day, when the animals were more likely to be awake, they observed high levels of NFAT in the nuclei of the muscle cells, essentially replicating the first experiment. “At that time, I’d been working for many years on muscle, but had never thought about the circadian rhythms,” recalls Schiaffino, whose research now focuses on this aspect of muscle biology. © 1986 - 2018 The Scientist

Keyword: Biological Rhythms; Obesity
Link ID: 25432 - Posted: 09.11.2018

Laura Sanders Obesity can affect brainpower, and a study in mice may help explain how. In the brains of obese mice, rogue immune cells chomp nerve cell connections that are important for learning and memory, scientists report September 10 in the Journal of Neuroscience. Drugs that stop this synapse destruction may ultimately prove useful for protecting the brain against the immune cell assault. Like people, mice that eat lots of fat quickly pack on pounds. After 12 weeks of a high-fat diet, mice weighed almost 40 percent more than mice fed standard chow. These obese mice showed signs of diminished brainpower, neuroscientist Elizabeth Gould of Princeton University and colleagues found. Obese mice were worse at escaping mazes and remembering an object’s location than mice of a normal weight. On nerve cells, microscopic knobs called dendritic spines receive signals. Compared with normal-sized mice, obese mice had fewer dendritic spines in several parts of the mice’s hippocampi, brain structures important for learning and memory. The dendritic spine destruction comes from immune cells called microglia, the results suggest. In obese mice, higher numbers of active microglia lurked among these sparser nerve cell connections compared with mice of normal weights. When the researchers interfered with microglia in obese mice, dendritic spines were protected and the mice’s performance on thinking tests improved. |© Society for Science & the Public 2000 - 2018.

Keyword: Obesity; Learning & Memory
Link ID: 25431 - Posted: 09.11.2018

By Susana Martinez-Conde Last month, for the first time in over a year, I had lucid dreams for two nights in a row. A lucid dream, or realizing that you’re dreaming while still inside of the dream, is not an unusual experience: most people will have at least one lucid dream in their lives. An occasional lucid dreamer myself, I’ve never developed the degree of control that some master lucid dreamers have, who can bend, Matrix-like, the fabric of their dreams to their will, night after night. Instead, my own version of lucid dreaming tends to consist on being in the midst of some horrifying nightmare, then having the thought that “this is just too awful to be real, so I must be dreaming,” and eventually grasping that that’s indeed the case. When that happens, I typically use my newfound awareness to wake myself up at once and be done with the whole thing. But in these two recent instances, I had an altogether different experience. Critically, I figured out that I was dreaming while having a neutral sort of dream, so I wasn’t compelled to seek an immediate exit. So my understanding of my unusual situation was a lot more matter-of-fact than in the majority of my prior lucid dreaming episodes. On each consecutive occasion, I immediately decided on flying. I had had dreams of flight before, but never intentionally. Now I could soar with purpose. I ascended at vertiginous speeds over the Manhattan skyline, and as soon as the clouds enveloped me I dove down, superhero-style, unafraid of gravity. Rising up again, I darted around buildings and billboards with ballistic accuracy. I briefly joined a flock of birds, then left them behind. © 2018 Scientific American

Keyword: Sleep
Link ID: 25430 - Posted: 09.10.2018

By Richard A. Friedman We hear a lot these days that modern digital technology is rewiring the brains of our teenagers, making them anxious, worried and unable to focus. Don’t panic; things are really not this dire. Despite news reports to the contrary, there is little evidence of an epidemic of anxiety disorders in teenagers. This is for the simple reason that the last comprehensive and representative survey of psychiatric disorders among American youth was conducted more than a decade ago, according to Kathleen Ries Merikangas, chief of the Genetic Epidemiology Research Branch at the National Institute of Mental Health. There are a few surveys reporting increased anxiety in adolescents, but these are based on self-reported measures — from kids or their parents — which tend to overestimate the rates of disorders because they detect mild symptoms, not clinically significant syndromes. So what’s behind the idea that teenagers are increasingly worried and nervous? One possibility is that these stories are the leading edge of a wave of anxiety disorders that has yet to be captured in epidemiological surveys. Or maybe anxiety rates have risen, but only in the select demographic groups — the privileged ones — that receive a lot of media attention. But it’s more likely that the epidemic is simply a myth. The more interesting question is why it has been so widely accepted as fact. One reason, I believe, is that parents have bought into the idea that digital technology — smartphones, video games and the like — are neurobiologically and psychologically toxic. If you believe this, it seems intuitive that the generations growing up with these ubiquitous technologies are destined to suffer from psychological problems. But this dubious notion comes from a handful of studies with serious limitations. © 2018 The New York Times Company

Keyword: Development of the Brain
Link ID: 25429 - Posted: 09.10.2018

Mandy McKnight's son Liam has Dravet syndrome, a form of epilepsy that causes him to have up to 70 seizures a day. McKnight began giving the 10-year-old cannabis products about five years ago. "He'll always have Dravet syndrome, but it has definitely provided him with a quality of life that other medication failed to do," said McKnight, who is originally from Torbay but lives in Ottawa. Since that time, Liam's seizures have nearly stopped — his mother estimates they've been reduced by 90 per cent. Doctors have said they're hearing from more and more parents who have purchased cannabinoid products online and believe they are helping their children, but still have questions about appropriate dosage and formulas, said Lauren Kelly, a clinical researcher with a PhD in pharmacology working at the University of Manitoba. Parents are self-prescribing for a variety of conditions in children including epilepsy, migraines, autism and brain cancer, said Kelly, who co-authored a commentary for the Canadian Medical Association Journal titled "Clinical trials needed to study cannabinoid use in Canadian children." There are different types of cannabinoids, she said, and they have different effects. But because many of the products are unregulated, it's often not known exactly what dosage a child might be getting. ©2018 CBC/Radio-Canada

Keyword: Epilepsy; Drug Abuse
Link ID: 25428 - Posted: 09.10.2018

By Nicholas Bakalar Yet another reason to stop smoking: It may reduce your risk for dementia. Korean researchers studied 46,140 men, 60 and older, following them for an average of eight years with periodic health examinations. Over the course of the study, 1,644 people were given a diagnosis of Alzheimer’s disease or another form of dementia. After controlling for age, body mass index, blood pressure, physical activity and other health and behavioral characteristics, they found that the less time men smoked, the less likely they were to have dementia. Compared with continual smokers, men who had quit for up to four years had a 13 percent lower risk, those who had quit for four years or more a 14 percent lower risk, and never-smokers a 19 percent lower risk. The study is in the Annals of Clinical and Translational Neurology. The authors acknowledge that they had no data on education level, which is a risk factor for dementia, and that the eight-year follow-up may not have been long enough to pick up all cases of dementia, a disease that develops slowly. “Smoking has not been well known as a risk factor for dementia,” said the lead author, Dr. Daein Choi, a researcher at the Seoul University College of Medicine. “Our findings suggest that smoking cessation, or reduced smoking, might be helpful in reducing the risk.” © 2018 The New York Times Company

Keyword: Alzheimers; Drug Abuse
Link ID: 25427 - Posted: 09.10.2018

By: Helene Benveniste, M.D., Ph.D. The brain, like other parts of the body, needs to maintain “homeostasis” (a constant state) to function, and that requires continuous removal of metabolic waste. For decades, the brain’s waste-removal system remained a mystery to scientists. A few years ago, a team of researchers—with the help of our author—finally found the answer. This discovery—dubbed the glymphatic system— will help us understand how toxic waste accumulates in devastating disorders such as Alzheimer’s disease and point to possible strategies to prevent it. In early February 2012, I received a note from Maiken Nedergaard, a renowned neuroscientist at the University of Rochester whom I knew from our time as medical students at the University of Copenhagen. She explained that her team had discovered important features of a new system that transports the fluid that surrounds the brain—a substance called cerebrospinal fluid (CSF). The discovery of how this fluid was transported in the brain, she believed, was the key to understanding how waste is cleared from the brain. Nedergaard’s work with the non-neuronal brain cells called “astroglia” had led her to suspect that these cells might play a role in CSF transport and brain cleansing. She was inspired by an older study' which showed that CSF could rapidly penetrate into channels along the brain vasculature, and astroglial cells structurally help create these channels. Now she needed help with visualizing the system in the whole brain to confirm her suspicions. Her team needed imaging scientists like myself who might be able to visualize the unique CSF flow patterns in a rodent brain and shed light on the new system. Because I had experience and expertise in imaging CSF in the small rodent brain and spinal cord, I was equipped to take on this new challenge. © 2018 The Dana Foundation.

Keyword: Brain imaging
Link ID: 25426 - Posted: 09.08.2018

Elana Gordon As drug-related deaths rise to record numbers, at least a dozen U.S. cities are considering opening supervised injection sites, where people can use illicit drugs with trained staff present, ready to respond in case of an overdose. The future of such proposals in the U.S. is uncertain. A California bill that would greenlight a pilot injection site in San Francisco awaits the governor's signature, but a representative of the Justice Department vowed to crack down on any such site in recent public statements. Critics say supervised injection sites encourage drug use and bring crime to surrounding communities. Proponents argue that they save lives and can help people in addiction reconnect with society and get health services. Out with the dark alley, fear and shame, they say, in with a safe space, clean injection supplies, care and compassion. It's an approach that falls under the umbrella of harm reduction, a public health philosophy that emphasizes lessening the harms of drug use. But what does evidence say? If the policy goal is to save lives and eventually curb opioid addiction, do these sites work? It's a tricky question to answer, although many of these sites have been studied for years. At least 100 supervised injection sites operate around the world, mainly in Europe, Canada and Australia. Typically, drug users come in with their own drugs and are given clean needles and a clean, safe space to consume them. Staff are on hand with breathing masks and naloxone, the overdose antidote, and to provide safer injection advice and information about drug treatment and other health services. Cities Planning Supervised Drug Injection Sites Fear Justice Department Reaction July 12, 2018 © 2018 npr

Keyword: Drug Abuse
Link ID: 25425 - Posted: 09.08.2018

By Sarah Kaplan and Joel Achenbach A series of attacks with a microwave weapon is the latest theory for what could have sickened or distressed roughly two dozen people associated with the U.S. Embassy in Cuba over the past two years. The alleged attacks dominated a House Foreign Affairs subcommittee hearing on Cuba policy Thursday afternoon. But a panel of State Department officials said there is still no explanation for the reported injuries. “We’re seeing a unique syndrome. I can’t even call it a syndrome. It’s a unique constellation of symptoms and findings, but with no obvious cause,” testified Charles Rosenfarb, the State Department’s medical director. Despite the buzz over microwaves, advanced in news reports in recent days, experts warn that caution is in order. There’s an old scientific aphorism that extraordinary claims require extraordinary evidence. “And they’re not giving the extraordinary evidence. They’re not giving any evidence,” said physicist Peter Zimmerman, an arms control expert and former scientific adviser to the State Department and Senate Foreign Relations Committee. No microwave weapon that affects the brain is known to exist. The FBI has investigated the Cuba cases and found no evidence of a plot. Searches of the U.S. Embassy and other locations in Havana have turned up no sign of a weapon. © 1996-2018 The Washington Post

Keyword: Brain Injury/Concussion
Link ID: 25424 - Posted: 09.08.2018

By Kelly Servick Stay active; age gracefully. Behind this truism, there’s a pile of unanswered scientific questions. Researchers are still sorting out what it is about physical activity that seems to lower the risk of dementia later in life. Even more uncertain is whether the effects of exercise can alter the course of diseases that cause dementia—chief among them, Alzheimer’s disease—once they’ve already taken root. A study published today in Science offers some new clues. In mice that mimic a severe, genetic form of Alzheimer’s disease, a combination of treatments that prompt the growth of new brain cells and protect them from damage can mimic the beneficial effects of exercise in preventing memory decline. So could we someday bottle the effects of exercise to treat Alzheimer’s? And if so, what exactly would we need to bottle? Here’s a rundown of what we know, and what’s still controversial. What’s the link between exercise and brain aging? Many large studies suggest staying active and fit throughout life lowers the risk of memory problems later on. For example, a recent project tracked more than 1000 Swedish women over 4 decades and found that for those judged to have “high” cardiovascular fitness on entering the study—as measured by the maximum workload they could handle on a stationary cycle machine before exhaustion—the onset of dementia was delayed, on average, by 9.5 years compared to those with “medium” fitness. But such studies can’t rule out all other confounding factors that might influence dementia risk—from genes to other aspects of a healthy lifestyle common in regular exercisers. And they don’t explain what exercise actually does to the brain. Does exercise fight the effects of Alzheimer’s disease once someone has it? © 2018 American Association for the Advancement of Scienc

Keyword: Alzheimers; Neurogenesis
Link ID: 25423 - Posted: 09.07.2018

By Stephani Sutherland With nearly 50,000 drug overdose deaths from opioids last year and an estimated two million Americans addicted, the opioid crisis continues to rage throughout the U.S. This statistic must be contrasted with another: 25 million Americans live with daily chronic pain, for which few treatment options are available apart from opioid medications. Opioid drugs like morphine and Oxycontin are still held as the gold standard when it comes to relieving pain. But it has become brutally obvious that opioids have dangerous side effects, including physical dependence, addiction and the impaired breathing that too often leads to death from an overdose. Researchers have long been searching for a drug that would relieve pain without such a heavy toll, with few results so far. Now a study in monkeys published in Science Translational Medicine shows a new type of opioid drug met all the criteria on drug developers’ wish list. The findings even suggest that instead of causing addiction, the new compound might be used to curb addiction and pain all at once. The study was led by Mei-Chuan (Holden) Ko, a researcher at Wake Forest University, and medical chemist Nurulain Zaveri, founder of California-based Astraea Therapeutics. “They’ve got something here that’s really important,” says William Schmidt, a pharmaceutical consultantbased in Davis, Calif., who was not involved in the work. “I think the chances of a compound with these properties moving forward are high, and simultaneously pretty exciting.” © 2018 Scientific American

Keyword: Drug Abuse; Pain & Touch
Link ID: 25422 - Posted: 09.07.2018

Increasing time between meals made male mice healthier overall and live longer compared to mice who ate more frequently, according to a new study published in the Sept. 6, 2018 issue of Cell Metabolism. Scientists from the National Institute on Aging (NIA) at the National Institutes of Health, the University of Wisconsin-Madison, and the Pennington Biomedical Research Center, Baton Rouge, Louisiana, reported that health and longevity improved with increased fasting time, regardless of what the mice ate or how many calories they consumed. “This study showed that mice who ate one meal per day, and thus had the longest fasting period, seemed to have a longer lifespan and better outcomes for common age-related liver disease and metabolic disorders,” said NIA Director Richard J. Hodes, M.D. “These intriguing results in an animal model show that the interplay of total caloric intake and the length of feeding and fasting periods deserves a closer look.” The scientists randomly divided 292 male mice into two diet groups. One group received a naturally sourced diet that was lower in purified sugars and fat, and higher in protein and fiber than the other diet. The mice in each diet group were then divided into three sub-groups based on how often they had access to food. The first group of mice had access to food around the clock. A second group of mice was fed 30 percent less calories per day than the first group. The third group was meal fed, getting a single meal that added up to the exact number of calories as the round-the-clock group. Both the meal-fed and calorie-restricted mice learned to eat quickly when food was available, resulting in longer daily fasting periods for both groups.

Keyword: Obesity
Link ID: 25421 - Posted: 09.07.2018

By: Richard Restak, M.D. Editor’s Note: Unthinkable’s author, a British neuroscientist, tracked down nine people with rare brain disorders to tell their stories. From the man who thinks he's a tiger to the doctor who feels the pain of others just by looking at them to a woman who hears music that’s not there, their experiences illustrate how the brain can shape our lives in unexpected and, in some cases, brilliant and alarming ways. Several years ago, science writer Helen Thomson, consultant to New Scientist and contributor to the Washington Post and Nature, decided to travel around the world to interview people with "the most extraordinary brains." In the process, as described in Unthinkable: An Extraordinary Journey Through the World's Strangest Brains (Ecco/Harper Collins 2018), Thomas discovered that "by putting their lives side-by-side, I was able to create a picture of how the brain functions in us all. Through their stories, I uncovered the mysterious manner in which the brain can shape our lives in unexpected—and, some cases, brilliant and alarming ways." Thomson wasn't just learning about the most extraordinary brains in the world, but in the process was "uncovering the secrets of my own." During her journey Thomson encounters Bob, who can remember days from 40 years ago with as much clarity and detail as yesterday; Sharon, who has lost her navigational abilities and on occasion becomes lost in her own home; Tommy who, after a ruptured aneurysm that damaged his left temporal lobe, underwent a total personality change; Sylvia, an otherwise normal retired school teacher who experiences near constant musical hallucinations; and Louise, who is afflicted with a permanent sense of detachment from herself and everyone around her. Beyond skillfully portraying each of these and other fascinating individuals, Thomson places them in historical and scientific context: when neuroscientists first encountered similar patients, along with past and current explanations of what has gone amiss in their brains. © 2018 The Dana Foundation

Keyword: Attention
Link ID: 25420 - Posted: 09.07.2018

By Carl Zimmer In a study carried out over the summer, a group of volunteers drank a white, peppermint-ish concoction laced with billions of bacteria. The microbes had been engineered to break down a naturally occurring toxin in the blood. The vast majority of us can do this without any help. But for those who cannot, these microbes may someday become a living medicine. The trial marks an important milestone in a promising scientific field known as synthetic biology. Two decades ago, researchers started to tinker with living things the way engineers tinker with electronics. They took advantage of the fact that genes typically don’t work in isolation. Instead, many genes work together, activating and deactivating one another. Synthetic biologists manipulated these communications, creating cells that respond to new signals or respond in new ways. Until now, the biggest impact has been industrial. Companies are using engineered bacteria as miniature factories, assembling complex molecules like antibiotics or compounds used to make clothing. In recent years, though, a number of research teams have turned their attention inward. They want to use synthetic biology to fashion microbes that enter our bodies and treat us from the inside. The bacterial concoction that volunteers drank this summer — tested by the company Synlogic — may become the first synthetic biology-based medical treatment to gain approval by the Food and Drug Administration. The bacteria are designed to treat a rare inherited disease called phenylketonuria, or PKU. People with the condition must avoid dietary protein in foods such as meat and cheese, because their bodies cannot break down a byproduct, an amino acid called phenylalanine. As phenylalanine builds up in the blood, it can damage neurons in the brain, leading to delayed development, intellectual disability and psychiatric disorders. The traditional treatment for PKU is a strict low-protein diet, accompanied by shakes loaded with nutritional supplements. © 2018 The New York Times Company

Keyword: Development of the Brain
Link ID: 25419 - Posted: 09.05.2018

By Rebecca Nebel Growing older may be inevitable, but getting Alzheimer’s disease is not. Although we can’t stop the aging process, which is the biggest risk factor for Alzheimer’s, there are many other factors that can be modified to lower the risk of dementia. Yet our ability to reduce Alzheimer’s risk and devise new strategies for prevention and treatment is impeded by a lack of knowledge about how and why the disease differs between women and men. There are tantalizing hints in the literature about factors that act differently between the sexes, including hormones and specific genes, and these differences could be important avenues of research. Unfortunately, in my experience, most studies of Alzheimer’s risk combine data for women and men. For that reason, researchers at the Society for Women’s Health Research Interdisciplinary Network on Alzheimer’s Disease recently published a review paper in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association that calls for greater analysis of research data by sex to stimulate new approaches that will improve prevention, diagnosis and treatment of Alzheimer’s. We have some evidence, for example, that sex hormones such as estrogen influence the course of the disease, but we do not understand enough about why and how. Ovaries are the primary source of estrogen for premenopausal women, and surgical removal of a woman’s ovaries before menopause is associated with a higher risk of dementia. But using estrogen therapy after surgery until age 50 negates that risk. This fact suggests that estrogen may be protective in premenopausal women. © 2018 Scientific American

Keyword: Alzheimers; Sexual Behavior
Link ID: 25418 - Posted: 09.05.2018

By Frankie Schembri For animals unlucky enough to run into a carnivorous songbird known as the shrike, a quiet scurry through the woods can quickly morph into a dance with death. Loggerhead shrikes (Lanius ludovicianus), aka butcherbirds, impale their prey on spiky plants or barbed wire before delivering a death blow to the neck with their hooked beaks. Now, a new study shows how the birds can take down lizards and mice with body masses more than twice their own. Scientists used a high-speed video camera to film 28 shrikes attacking large vertebrate prey at a zoological research center on San Clemente Island in California. When the researchers examined the slowed-down footage, they found that in nearly all fatal attacks, the shrikes would first latch onto the necks of their prey, vigorously shaking them up and down. By using their prey’s neck as a pivot to whip them in wavelike motion, the shrikes could cause fatal damage to cervical vertebrae and spinal cords, the researchers report today in Biology Letters. When the team analyzed the shaking motions, they found that the shrikes could exert up to 6 gs of accelerative force. By comparison, humans in low-speed, rear-end car crashes can experience head accelerations of 2 to 12 gs, enough to cause whiplash. On a mouse’s smaller spine, these forces can be fatal. © 2018 American Association for the Advancement of Science

Keyword: Aggression
Link ID: 25417 - Posted: 09.05.2018

Marcy Cuttler · CBC News Janaya Chekowski-McKenzie was born with the odds against her. On the day she arrived in 2009, she was non-responsive, and she spent a month in hospital with a lung infection. At three months, she had a seizure. Janaya needed hormone replacements to grow and doctors determined she had underdeveloped optic nerves. In spite of these early difficulties, the Beaumont, Alta., youngster has grown up to be a sassy, funny, bright girl with a lion's mane of curly-brown hair. When Janaya started complaining of worsening headaches last January, her mother, Amanda Chekowski, thought it was yet another medical hurdle to overcome. Instead, doctors told her Janaya had a rare, incurable form of brain cancer called diffuse intrinsic pontine glioma, or DIPG. Hearing the news, Chekowski and her family were stunned. They had to figure out how to explain this to an eight-year-old in terms she would understand. Initially, they made a bit of a joke of it. Janaya was told that "we found a booger in your brain that's not supposed to be there and we're going to try to shrink it," said Chekowski. The truth is very different. DIPG is a cancer that targets kids, and thus far, none have survived. But doctors around the world are trying to change that. ©2018 CBC/Radio-Canada.

Keyword: Movement Disorders
Link ID: 25416 - Posted: 09.05.2018

By Jane E. Brody “Use it or lose it.” I’m sure you’re familiar with this advice. And I hope you’ve been following it. I certainly thought I was. I usually do two physical activities a day, alternating among walking, cycling and swimming. I do floor exercises for my back daily, walk up and down many stairs and tackle myriad physical tasks in and around my home. My young friends at the Y say I’m in great shape, and I suppose I am compared to most 77-year-old women in America today. But I’ve noticed in recent years that I’m not as strong as I used to be. Loads I once carried rather easily are now difficult, and some are impossible. Thanks to an admonition from a savvy physical therapist, Marilyn Moffat, a professor at New York University, I now know why. I, like many people past 50, have a condition called sarcopenia — a decline in skeletal muscle with age. It begins as early as age 40 and, without intervention, gets increasingly worse, with as much as half of muscle mass lost by age 70. (If you’re wondering, it’s replaced by fat and fibrous tissue, making muscles resemble a well-marbled steak.) “Sarcopenia can be considered for muscle what osteoporosis is to bone,” Dr. John E. Morley, geriatrician at Saint Louis University School of Medicine, wrote in the journal Family Practice. He pointed out that up to 13 percent of people in their 60s and as many as half of those in their 80s have sarcopenia. As Dr. Jeremy D. Walston, geriatrician at Johns Hopkins University School of Medicine, put it, “Sarcopenia is one of the most important causes of functional decline and loss of independence in older adults.” Yet few practicing physicians alert their older patients to this condition and tell them how to slow or reverse what is otherwise an inevitable decline that can seriously impair their physical and emotional well-being and ability to carry out the tasks of daily life. Sarcopenia is also associated with a number of chronic diseases, increasingly worse insulin resistance, fatigue, falls and, alas, death. © 2018 The New York Times Company

Keyword: Muscles; Development of the Brain
Link ID: 25415 - Posted: 09.05.2018