By Darby Saxbe Perinatal depression—depression that occurs during pregnancy or after the birth of a child—is surprisingly common, affecting about 1 in 7 women. And, although depression is debilitating at any time, it may carry a particularly heavy public health burden during the transition to parenthood. Women with depression are less likely to obtain medical care for themselves and their babies, and may struggle to bond with their infants. It’s no wonder that the children of depressed mothers experience heightened long-term risk of emotional and behavioral problems. Despite this grim picture, a new report from the US Preventive Services Task Force offers some hope. The USPSTF, a nonpartisan body of experts, reviews scientific research and makes recommendations for preventing disease. In the past, they’ve issued guidelines for lung cancer detection, aspirin use to prevent heart disease, and blood pressure screening. In a review recently published in the Journal of the American Medical Association (JAMA), the task force shared what they deemed “convincing evidence” that counseling (talk therapy) interventions can not just treat, but actually prevent, perinatal depression. This is exciting news given the high cost of depression during this time and the fact that, unlike other potential treatments for perinatal depression (like the new drug Zulresso), talk therapy is low-tech, relatively low-cost, and brings few side effects. In their report, the USPSTF reviewed 50 studies that they deemed to be at least “good or fair quality.” Almost all were randomized clinical trials, the gold standard for treatment research, in which a treatment is directly compared to a control group condition. About half of the studies focused on pregnant women, and the rest on postpartum women. Some studies targeted women who already had elevated risk for depression, based on risk factors like a personal or family history of depression, low socioeconomic status, and exposure to life stress or intimate partner violence. © 2019 Scientific American

Keyword: Depression; Hormones & Behavior
Link ID: 26109 - Posted: 04.03.2019

By Jeffrey Mervis A fledgling, small-scale approach to dealing with the state’s opioid crisis paid off big last week for Oklahoma State University (OSU) when it became the surprise beneficiary of a $270 million legal settlement with Purdue Pharma. It’s the first agreement in some 1700 pending cases around the United States against Purdue, which makes the painkiller OxyContin, and other manufacturers of prescription opioids. On 26 March, the state of Oklahoma agreed to drop its suit alleging deceptive marketing practices by Purdue in exchange for a National Center for Addiction Studies and Treatment at OSU’s medical complex in Tulsa. Purdue and the Sackler family, which owns the Stamford, Connecticut–based company, will provide a $177 million endowment for the national center, along with $20 million over 5 years for naloxone and other drugs to treat opioid addiction. The state is continuing its suit against several other companies, with opening arguments set for 28 May. The windfall for the new entity, which aspires “to become the premier addiction research center in the nation,” rewards OSU’s ambition. In October 2017, it opened a modest Center for Wellness and Recovery within its medical school to train future addiction medicine physicians, study the underlying causes of addiction and pain, provide treatment to those suffering from opioid use disorder, and educate the public about the burgeoning epidemic, which claims 130 lives a day in the United States and in 2017 killed nearly 800 Oklahomans. The center now has a staff of eight and a $2.4 million budget. © 2019 American Association for the Advancement of Science

Keyword: Drug Abuse
Link ID: 26108 - Posted: 04.03.2019

/ By Richard Kemeny Northern Ethiopia was once home to a vast, ancient lake. Saber-toothed cats prowled around it, giant crocodiles swam within. The streams and rivers that fed it — over 3 million years ago, during the Pliocene — left behind trails of sediment that have now hardened into sandstone. Deposited within these layers are fossils: some of early hominins, along with the bones of hippos, antelope, and elephants. Anthropologist Jessica Thompson encountered two of these specimens, from an area named Dikika, in 2010. At the time, she was a visiting researcher at the Institute of Human Origins at Arizona State University. Given no explanation as to their history, she analyzed the bones and found signs of butchery. Percussion marks suggested someone may have accessed the marrow; cut marks hinted that flesh was stripped from bone. To her surprise, the specimens were 3.4 million years old, putting the butcher’s behaviors back 800,000 years earlier than conventional estimates would suggest. That fact got Thompson, now an assistant professor in the Department of Anthropology at Yale University, thinking there might be more traces of tool use from those early times. In a wide-ranging review published in February’s issue of Current Anthropology, Thompson joins a team of researchers to weave together several strands of recent evidence and propose a new theory about the transition to large animal consumption by our ancestors. The prevailing view, supported by a confluence of fossil evidence from sites in Ethiopia, is that the emergence of flaked tool use and meat consumption led to the cerebral expansion that kickstarted human evolution more than 2 million years ago. Thompson and her colleagues disagree: Rather than using sharpened stones to hunt and scrape meat from animals, they suggest, earlier hominins may have first bashed bones to harvest fatty nutrients from marrow and brains. Copyright 2019 Undark

Keyword: Evolution
Link ID: 26107 - Posted: 04.03.2019

“What we didn’t know before was some individuals seem to be able to choose whether they lay eggs or give birth to live babies,” Whittington said on Wednesday. “That was pretty staggering. We had no idea that could be the case. So I think it just makes this lizard even weirder.” Previous research has shown that if a Sydney skink was taken north it would still lay eggs, while live bearers transferred south would also continue to reproduce as they previously did. “I’m curious to know what happens if you breed an egg layer with a live bearer – what do their sons and daughters do?” Whittington said. Another skink in South Australia has also been shown to be bimodal. Bougainville’s skinks give birth to babies on Kangaroo Island, while on the mainland they lay eggs. Only a handful of species in the world do this. The University of Sydney study into the three-toed skink will be published in Biology Letters this week. Whittington hopes to map where they lay eggs and where they give birth in further research. The three-toed skink, which looks like a baby snake with tiny legs, is widespread along Australia’s east coast and is often seen in gardens or compost heaps. © 2019 Guardian News & Media Limited

Keyword: Sexual Behavior
Link ID: 26106 - Posted: 04.03.2019

By Carl Zimmer In 2011, Dr. Dena Dubal was hired by the University of California, San Francisco, as an assistant professor of neurology. She set up a new lab with one chief goal: to understand a mysterious hormone called Klotho. Dr. Dubal wondered if it might be the key to finding effective treatments for dementia and other disorders of the aging brain. At the time, scientists only knew enough about Klotho to be fascinated by it. Mice bred to make extra Klotho lived 30 percent longer, for instance. But scientists also had found Klotho in the brain, and so Dr. Dubal launched experiments to see whether it had any effect on how mice learn and remember. The results were startling. In one study, she and her colleagues found that extra Klotho protects mice with symptoms of Alzheimer’s disease from cognitive decline. “Their thinking, in every way that we could measure them, was preserved,” said Dr. Dubal. She and her colleagues also bred healthy mice to make extra Klotho. They did better than their fellow rodents on learning mazes and other cognitive tests. Klotho didn’t just protect their brains, the researchers concluded — it enhanced them. Experiments on more mice turned up similar results. “I just couldn’t believe it — was it true, or was it just a false positive?” Dr. Dubal recalled. “But here it is. It enhances of cognition even in a young mouse. It makes them smarter.” Five years have passed since Dr. Dubal and her colleagues began publishing these extraordinary results. Other researchers have discovered tantalizing findings of their own, suggesting that Klotho may protect against other neurological disorders, including multiple sclerosis and Parkinson’s disease. © 2019 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 26105 - Posted: 04.02.2019

By Rachel Aviv Laura Delano recognized that she was “excellent at everything, but it didn’t mean anything,” her doctor wrote. She grew up in Greenwich, Connecticut, one of the wealthiest communities in the country. Her father is related to Franklin Delano Roosevelt, and her mother was introduced to society at a débutante ball at the Waldorf-Astoria. In eighth grade, in 1996, Laura was the class president—she ran on a platform of planting daffodils on the school’s grounds—and among the best squash players in the country. She was one of those rare proportional adolescents with a thriving social life. But she doubted whether she had a “real self underneath.” The oldest of three sisters, Laura felt as if she were living two separate lives, one onstage and the other in the audience, reacting to an exhausting performance. She snapped at her mother, locked herself in her room, and talked about wanting to die. She had friends at school who cut themselves with razors, and she was intrigued by what seemed to be an act of defiance. She tried it, too. “The pain felt so real and raw and mine,” she said. Her parents took her to a family therapist, who, after several months, referred her to a psychiatrist. Laura was given a diagnosis of bipolar disorder, and prescribed Depakote, a mood stabilizer that, the previous year, had been approved for treating bipolar patients. She hid the pills in a jewelry box in her closet and then washed them down the sink. © 2019 Condé Nast

Keyword: Depression
Link ID: 26104 - Posted: 04.02.2019

Almost 71m prescriptions for antidepressants were given out in England last year – not including drugs dispensed in hospitals outside the NHS. This is a vast number of pills – more than twice the number of prescriptions given for antibiotics; 20m more than for cholesterol-lowering statins. In a decade, the number of antidepressant prescriptions has doubled; it has risen by 3m in a year. Around 7 million adults (16% of the English adult population) are now taking this medicine, and around 330,000 children. The new data can’t say whether more people are depressed than previously – only that more are being medicated. The most recent official survey, in 2016, revealed an increase in rates of the most common mental health conditions among women, particularly teenage girls. Recent reports from a commission assembled by the Lancet medical journal, and the World Health Organization, have warned of a growing global mental health crisis, and called on policymakers and professionals worldwide to make this a priority. While people being ill is bad news, reports of people being treated for illness should, so long as the treatment is appropriate, be welcomed. Some researchers believe mental disorders remain under-treated because they are poorly understood, because doctors and patients share doubts about the remedies, and because of the social stigma that makes people reluctant to report symptoms or seek a diagnosis. But even granting that some people may be taking antidepressants who previously went untreated, there is a debate about whether pills are being overprescribed. © 2019 Guardian News & Media Limited

Keyword: Depression
Link ID: 26103 - Posted: 04.02.2019

By C. Claiborne Ray Q. How do bees find the flowers in the container garden on the fourth-floor deck of my city apartment? A. Foraging bees use the same methods to find nectar and pollen four floors up that they use at ground level. Honeybees routinely fly two miles from their hives in their search for raw material for honey; it doesn’t require much extra energy to fly several stories up. It takes only one scout to report a promising garden to the rest of the hive with a famous waggle dance. The scout relies on its sophisticated eyes, which are tuned to a variety of wavelengths, including ultraviolet color patterns in flowers that are invisible to people. We’re taking you on a journey to help you understand how bees, while hunting for pollen, use all of their senses — taste, touch, smell and more — to decide what to pick up and bring home. When the bees get closer to flowers, smell receptors begin transmitting information. And it has recently been discovered that both bumblebees and honeybees can detect and discriminate among weak electrostatic fields emanating from flowers. The bees accumulate a positive charge, while the flowers have a negative charge. The interaction between the fields is detected by antennae or sensitive hairs on the body. The electrical field helps bees to recognize pollen-rich blooms and perhaps even to transfer the pollen. © 2019 The New York Times Company

Keyword: Animal Migration; Animal Communication
Link ID: 26102 - Posted: 04.02.2019

By Jane E. Brody Attention all consumers seeking to protect brain health: You can save hundreds of dollars a year and enhance the health of your brain and body by ignoring the myriad unproven claims for anti-dementia supplements and instead focusing on a lifestyle long linked to better mental and physical well-being. How many of these purported brain boosters have you already tried — Ginkgo biloba, coenzyme Q10, huperzine A, caprylic acid and coconut oil, coral calcium, among others? The Alzheimer’s Association says that, with the possible exception of omega-3 fatty acids, all that were properly tested thus far have been found wanting. I admit it’s very appealing to think you can maintain your cognitive powers by swallowing a few pills a day instead of adopting a brain-healthy diet, getting regular exercise and adequate sleep, among other health-preserving measures like not smoking. But you’d only be fooling yourself and wasting precious dollars that could be better spent on nutritious foods and a good pair of walking shoes. “No known dietary supplement prevents cognitive decline or dementia,” Dr. Joanna Hellmuth stated emphatically in JAMA in January. “Yet,” she added, “supplements advertised as such are widely available and appear to gain legitimacy when sold by major U.S. retailers.” Dr. Hellmuth, a neurologist at the University of California, San Francisco, Memory and Aging Center, reminds consumers that supplement manufacturers do not have to test their products for effectiveness or safety. Lacking sound scientific backing, most are promoted by testimonials that appeal to people worried about developing dementia. © 2019 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 26101 - Posted: 04.01.2019

By Heather Murphy An article this week about Jo Cameron, who has lived for 71 years without experiencing pain or anxiety because she has a rare genetic mutation, prompted questions from New York Times readers. The notion that the same gene could be responsible for the way a person processes physical and psychological pain left many perplexed: Aren’t they totally different? Or does her story hint that sensitivity to one type of pain might be intertwined with sensitivity to another? Childbirth, Ms. Cameron said, felt like “a tickle.” She often relies on her husband to alert her when she is bleeding, bruised or burned because nothing hurts. When someone close to her has died, she said, she has felt sad but “I don’t go to pieces.” She cannot recall ever having been riled by anything — even a recent car crash. On an anxiety disorder questionnaire, she scored zero out of 21. “I drive people mad by being cheerful,” she said. Here’s a bit about what’s known: Do those who live without pain also live without anxiety? No. Before encountering Ms. Cameron, the scientists who studied her case worked with other patients who did not experience pain. “Reduced anxiety has not really been noted before in the other pain insensitivity disorders we work on,” said Dr. James Cox, a senior lecturer from the Molecular Nociception Group at University College London. He also said that given Ms. Cameron had gone more than six decades without realizing just how unusual she was, there could be others like her. A number of such individuals contacted The Times after the article was published. © 2019 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 26100 - Posted: 04.01.2019

By Ilana Marcus Grit alone got Linda Greene through her husband’s muscular dystrophy, her daughter’s traumatic brain injury, and her own mysterious illness that lasted for three years and left her vomiting daily before doctors identified the cause. But eventually, after too many days sitting at her desk at work crying, she went to see her doctor for help. He prescribed an antidepressant and referred her to a psychiatrist. When the first medication didn’t help, the psychiatrist tried another — and another and another — hoping to find one that made her feel better. Instead, Greene felt like a zombie and sometimes she hallucinated and couldn’t sleep. In the worst moment, she found herself contemplating suicide. “It was horrible,” she said. She never had suicidal thoughts before and was terrified. She went back her primary care doctor. In the past, when Jeremy Bruce, Greene’s physician in Cincinnati, treated patients for depression, he followed the same steps for almost everyone: start the patient on one antidepressant and switch to another until something helped. Sometimes, before they found the right treatment, the patient would leave his practice to find a new doctor. “They would usually be very angry,” Bruce said. But about three years ago, Bruce tried a new approach. Linda Greene and her husband. She tried many antidepressants before her doctor suggested genetic testing to find a medicine that worked for her. Doctors increasingly use information about genes to evaluate potential risk for some diseases and to determine the best drug treatment. But using pharmacogenetics to help treat depression remains controversial. (Family Photo) © 1996-2019 The Washington Post

Keyword: Depression; Genes & Behavior
Link ID: 26099 - Posted: 04.01.2019

By Michael C. Reichert Early in my first go at being a father, I was hijacked by ancient impulses. Our family lived in a rowhouse neighborhood in Philadelphia, and right down the street was a small playground where gangs of boys gathered for games of stickball and basketball. My son loved playing sports. But he was unprepared for what developed as his friends grew older. After years together laughing and riding their tricycles and then bikes up and down the block, several of the boys grew angry and mean. Ultimately, they turned on my son, taunting him, leaving him out of their games. He began to trudge home, tail between his legs. And I felt called to action. At first, I tried to bolster his confidence so he would give the playground another go. But one Saturday morning I met him at the front steps and told him he could not come into the house. “You have to figure this out,” I said. “I’ll stay with you as long as you need, but I cannot let you just give up.” He tried to push past me, his humiliation becoming frantic. He melted down, screaming and crying. I kept saying: “You can do it. You don’t have to give up.” A neighbor poked her head out, concerned about what must have sounded like child abuse. Did I do the right thing? Even now I’m not sure. He did go back to the playground, and eventually managed some kind of truce with the other kids. He grew up into a fine man, a teacher, and understands I was trying to help, in my clumsy way. But while teaching him to stand up for himself, was I also passing along the prejudice that a boy should override his pain and never back down from a fight? What happened in my son’s peer group was perfectly predictable. Boyhood immerses boys in violence and the bullying that leads to it. High school boys are more likely than girls to have been in a physical fight in the past year and male children are more likely to have been victims of violence. Three types of male violence — violence against women, violence against other men and violence against themselves — are deeply interwoven. © 2019 The New York Times Company

Keyword: Sexual Behavior; Aggression
Link ID: 26098 - Posted: 04.01.2019

Maria Temming Synthetic opioids outlast current antidotes. A nanoparticle-based alternative could fix that. A newly developed single-dose opioid antidote lasts several days, a study in mice shows. If the results can be duplicated in humans, the treatment may one day help prevent overdoses from deadly drugs like fentanyl. Normally, a dose of the opioid antidote naloxone passes through a person’s body in about 30 minutes — far too quickly to fully counteract the effects of such synthetic opioids as fentanyl and carfentanil (SN Online: 5/1/18). These drugs, tens to thousands of times stronger than morphine, can linger in a person’s system for hours or even days (SN: 6/10/17, p. 22). That requires multiple doses of an antidote to prevent someone from overdosing. So researchers developed a new naloxone-based antidote to outlast synthetic opioids by creating nanoparticles in which naloxone molecules are tangled up with a biodegradable polymer called polylactic acid. Water and enzymes in the body slowly break down these nanosized tangles, gradually releasing naloxone. In mice, the new nanoparticle delivery system counteracted the pain-relieving effects of morphine for up to 96 hours after administering a single dose of the antidote, according to research being presented March 31 at the American Chemical Society meeting in Orlando, Fla. |© Society for Science & the Public 2000 - 2019

Keyword: Drug Abuse
Link ID: 26097 - Posted: 04.01.2019

Alix Spiegel Our thoughts and fears, movements and sensations all arise from the electrical blips of billions of neurons in our brain. Streams of electricity flow through neural circuits to govern these actions of the brain and body, and some scientists think that many neurological and psychiatric disorders may result from dysfunctional circuits. As this understanding has grown, some scientists have asked whether we could locate these faulty circuits, reach deep into the brain and nudge the flow to a more functional state, treating the underlying neurobiological cause of ailments like tremors or depression. The idea of changing the brain for the better with electricity is not new, but deep brain stimulation takes a more targeted approach than the electroconvulsive therapy introduced in the 1930s. DBS seeks to correct a specific dysfunction in the brain by introducing precisely timed electric pulses to specific regions. It works by the action of a very precise electrode that is surgically inserted deep in the brain and typically controlled by a device implanted under the collarbone. Once in place, doctors can externally tailor the pulses to a frequency that they hope will fix the faulty circuit. This week's Invisibilia podcast features the story of a woman with obsessive-compulsive disorder and depression who signed up for a deep brain stimulation trial. The story describes what it's like to be able to adjust her mood by adjusting the settings on her device. Listen to that story here. © 2019 npr

Keyword: Depression; Emotions
Link ID: 26096 - Posted: 03.30.2019

Alix Spiegel We have the story of one woman who is taking part in an experiment on deep brain stimulation. RACHEL MARTIN, HOST: We are about to go deep - deep into your brain. STEVE INSKEEP, HOST: With a story about deep brain stimulation, or DBS, which sounds like a kind of massage, actually. But it means that patients get an implant that delivers small pulses of electricity to their brains. MARTIN: It's often used to treat Parkinson's disease. But for years, researchers have been trying to figure out how to use it to treat psychiatric disorders. INSKEEP: Results and experiments so far have been mixed. Many patients see no benefit. But some with obsessive-compulsive disorder have seen big changes. MARTIN: Like the next woman you're going to meet. For privacy, we are withholding her last name. Alix Spiegel from NPR's INVISIBILIA has her story. ALIX SPIEGEL, BYLINE: During the appointment, Megan didn't have to do that much, just sit in a chair while one of the doctors from the experiment used what looked like an oversized remote control to reprogram her electricity levels. Even after five years of having the implant, getting her electricity adjusted was unpredictable. Sometimes it went fine. But having electrodes in your brain is really complicated. And occasionally, the adjustments didn't go well. UNIDENTIFIED DOCTOR: While you were talking, I slowly ramped it up again. Anything different now? MEGAN: Slightly more aware. UNIDENTIFIED DOCTOR: OK. MEGAN: It's not like in the past, where it was like, oh, I feel good. But it's, like, a different feeling. SPIEGEL: After the doctor turned her up higher, Megan said she felt better. But then he decided to dial it back just a notch. He was worried that too much electricity might make her manic. UNIDENTIFIED DOCTOR: Now, if you notice me turning it down, then maybe I'll change my mind on that. MEGAN: (Crying) I'm sorry; don't do it. UNIDENTIFIED DOCTOR: Did you just feel it? MEGAN: (Crying) I don't feel very good at all right now. © 2019 npr

Keyword: Depression
Link ID: 26095 - Posted: 03.30.2019

Emma Yasinski In the 1970s, scientists discovered that certain neurons in the hippocampus—an area of the brain involved in learned and memory—would fire in response to particular locations. They were called “place cells,” explains Charlotte Boccara, a researcher at the University of Oslo. “They were deemed important for spatial representation . . . a bit like the ‘You Are Here’ signal’ on a map.” But it wasn’t until 2005 that researchers discovered the brain’s grid cells, which they believed function as that map. These cells, found adjacent to the hippocampus in the medial entorhinal cortex (MEC), self-organize into a pattern of hexagons that serve as coordinates to help animals make sense of their surroundings and the signals from our place cells. A pair of studies published today (March 28) in Science suggests that this map may not be as rigid as once thought. The experiments demonstrated that, in rats at least, the cellular activity within these grids changes as the animals learn and remember where they can find food rewards. “These are wonderful studies,” says György Buzsáki, a neuroscientist at New York University who was not involved in either of them. “When ideas converge from multiple, different directions, and they converge and come to the same conclusion, the result is always stronger.” In the first study, Boccara, then a researcher at the Institute of Science and Technology Austria, and her team placed rats one by one in a cheeseboard maze, a flat board drilled full of holes. They hid three food rewards in different holes then scattered food dust over the entire surface so the rats would not be able to sniff their ways to the reward. The rats explored the maze until they found the prizes and repeated the task until they learned to go straight to the food instead of foraging. The next day, the researchers conducted the same experiment but changed the locations of the rewards. © 1986 - 2019 The Scientist.

Keyword: Learning & Memory
Link ID: 26094 - Posted: 03.30.2019

By Simon Makin Neurodegenerative diseases all involve the accumulation of toxic versions of naturally produced proteins in the brain. Multiple proteins are often abnormal in a patient, and the same aberrant protein can be involved in several different conditions. One common culprit is tau, which is abnormal in various conditions: chronic traumatic encephalopathy, a neurodegenerative disorder caused by repeated head trauma; a group of conditions known collectively as frontotemporal dementia; and, most famously, Alzheimer’s disease (AD). Normally, tau stabilizes structures inside neural connections, called microtubules, which facilitate chemical communication between cells. In disease states, tau is chemically altered, becoming misshapen and breaking away from microtubules. These toxic versions accumulate into structures called “neurofibrillary tangles,” which disrupt cells’ ability to communicate and may trigger other forms of damage, such as inflammation. Tau is involved in AD, but abnormalities in a different protein, amyloid-beta, are thought to be the initial trigger for a chain of biological events (including tau pathology) that underlies neurodegeneration. This is why most AD drugs developed to date have targeted amyloid, although tau has received increasing attention as multiple drugs intended to remove amyloid have failed. A new study, published Wednesday in Science Translational Medicine, suggests that an existing drug, lonafarnib, could be repurposed to treat neurodegenerative diseases that involve tau. A team of researchers, led by neuroscientist Kenneth Kosik of the University of California, Santa Barbara, found the drug had beneficial effects on tau-related pathology in mice, if administered early over an extended period. They also found evidence suggesting it works via a previously unknown biological mechanism. “This opens up a previously completely unsuspected pathway for tau degradation,” says Kosik, a longtime tau researcher. “We don’t have all the molecular details, but as a place to look, this is full of new opportunities.” © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26093 - Posted: 03.29.2019

Nell Greenfieldboyce Mosquitoes searching for a meal of blood use a variety of clues to track down humans, including our body heat and the carbon dioxide in our breath. Now, research shows that a certain olfactory receptor in their antennae also serves as a detector of humans, responding to smelly chemicals in our sweat. Targeting this receptor might offer a new way to foil blood-seeking mosquitoes and prevent the transmission of diseases including malaria, Zika virus and dengue, according to the study published Thursday in the journal Current Biology. "We found a receptor for human sweat, and we found that acidic volatiles that come off of us are really key for mosquitoes to find us," says Matthew DeGennaro, a neurogeneticist at Florida International University in Miami. "I think what's exciting about it is that finally we have evidence that there is some sort of pathway, in the sense of smell, that is required for mosquitoes to like us," says Lindy McBride, a scientist at Princeton University who studies mosquito behavior and was not part of the research team. It's long been known that mosquitoes rely on multiple clues to target humans. First, a mosquito will sense exhaled carbon dioxide from a distance that can be more than 30 feet. "After the carbon dioxide," DeGennaro explains, "then it begins to sense human odor." © 2019 npr

Keyword: Chemical Senses (Smell & Taste)
Link ID: 26092 - Posted: 03.29.2019

By James Gallagher Health and science correspondent, BBC News French scientists say they have proof that dogs can pick up the smell of an epileptic seizure. The University of Rennes team hope the findings could lead to ways to predict when people will have a seizure. These could include dogs or "electronic noses" that pick up the precise odour being given off during a seizure. Dogs have previously been shown to be able to sniff out diseases including cancers, Parkinson's, malaria and diabetes. Some people with epilepsy already rely on the animals. One sleeping in a child's bedroom can alert family members of a seizure in the middle of the night. The latest study, in the journal Scientific Reports, trained five dogs from Medical Mutts, in the US, to recognise the smell of sweat taken from a patient having a seizure. They were then given a choice of seven sweat samples taken from other patients while they were either relaxing, exercising or having a seizure. Two of the dogs found the seizure sample about two-thirds of the time and the other three were 100% accurate The report says: "The results are extremely clear and constitute a first step towards identifying a seizure-specific odour." © 2019 BBC

Keyword: Chemical Senses (Smell & Taste); Epilepsy
Link ID: 26091 - Posted: 03.29.2019

Ian Sample Science editor Doctors have identified a new mutation in a woman who is barely able to feel pain or stress after a surgeon who was baffled by her recovery from an operation referred her for genetic testing. Jo Cameron, 71, has a mutation in a previously unknown gene which scientists believe must play a major role in pain signalling, mood and memory. The discovery has boosted hopes of new treatments for chronic pain which affects millions of people globally. Cameron, a former teacher who lives in Inverness, has experienced broken limbs, cuts and burns, childbirth and numerous surgical operations with little or no need for pain relief. She sometimes leans on the Aga and knows about it not from the pain, but the smell. “I’m vegan, so the smell is pretty obvious,” she says. “There’s no other burning flesh going on in the house.” But it is not only an inability to sense pain that makes Cameron stand out: she also never panics. When a van driver ran her off the road two years ago, she climbed out of her car, which was on its roof in a ditch, and went to comfort the shaking young driver who cut across her. She only noticed her bruises later. She is relentlessly upbeat, and in stress and depression tests she scored zero. “I knew that I was happy-go-lucky, but it didn’t dawn on me that I was different,” she says. “I thought it was just me. I didn’t know anything strange was going on until I was 65.” © 2019 Guardian News & Media Limited

Keyword: Pain & Touch; Genes & Behavior
Link ID: 26090 - Posted: 03.28.2019