by Laura Sanders Amid a flurry of cabinet appointments and immigration policies, the Trump administration has announced one thing it will not do: pursue policies that protect transgender children in public schools. The Feb. 22 announcement rescinds Obama administration guidelines that, among other protections, allow transgender kids to use bathrooms and participate in sports that correspond with their genders, and to be called by their preferred names and pronouns. In a Feb. 23 news briefing, White House press secretary Sean Spicer said that this is a states’ rights issue. “States should enact laws that reflect the values, principles, and will of the people in their particular state,” he said. “That's it, plain and simple.” But this “plain and simple” move could be quite dangerous, even deadly, science suggests. Transgender children, who are born one biological sex but identify as the other, already face enormous challenges as they move through a society that often doesn’t understand or accept them. Consider this: Nearly half (46.5 percent) of young transgender adults have attempted suicide at some point in their lives, a recent survey of over 2,000 people found. Nearly half. For comparison, the attempted suicide rate among the general U.S. population is estimated to be about 4.6 percent. What’s more, a 2015 study in the Journal of Adolescent Health found that transgender youth are two to three times as likely as their peers to suffer from depression and anxiety disorders, or to attempt suicide or harm themselves. These troublesome stats, based on a sample of 180 transgender children and young adults in Boston ages 12 to 29, applied equally to those who underwent male-to-female transitions and those who underwent female-to-male transitions. © Society for Science & the Public 2000 - 2017.

Keyword: Sexual Behavior; Depression
Link ID: 23297 - Posted: 03.01.2017

By Drake Baer If you’re going to get any sort of science done, an experiment needs a control group: the unaffected, possibly placebo-ed population that didn’t take part in whatever intervention it is you’re trying to study. Back in the earlier days of cognitive neuroscience, the control condition was intuitive enough: Just let the person in the brain scanner lie in repose, awake yet quiet, contemplating the tube they’re inside of. But in 1997, 2001, and beyond, studies kept coming out saying that it wasn’t much of a control at all. When the brain is “at rest,” it’s doing anything but resting. When you don’t give its human anything to do, brain areas related to processing emotions, recalling memory, and thinking about what’s to come become quietly active. These self-referential streams of thought are so pervasive that in a formative paper Marcus Raichle, a Washington University neurologist who helped found the field, declared it to be the “the default mode of brain function,” and the constellation of brain areas that carry it out are the default mode network, or DMN. Because when given nothing else to do, the brain defaults to thinking about the person it’s embedded in. Since then, the DMN has been implicated in everything from depression to creativity. People who daydream more tend to have a more active DMN; relatedly, dreaming itself appears to be an amplified version of mind-wandering. In Buddhist traditions, this chattering described by neuroscientists as the default mode is a dragon to be tamed, if not slain. Chögyam Trungpa, who was instrumental in bringing Tibetan Buddhism to the U.S., said the meditation practice is “necessary generally because our thinking pattern, our conceptualized way of conducting our life in the world, is either too manipulative, imposing itself upon the world, or else runs completely wild and uncontrolled,” he wrote in Cutting Through Spiritual Materialism. “Therefore, our meditation practice must begin with ego’s outermost layer, the discursive thoughts which continually run through our minds, our mental gossip.” © 2017, New York Media LLC.

Keyword: Attention; Emotions
Link ID: 23296 - Posted: 03.01.2017

By Edward G. Barrett It’s no secret that fewer than 10 percent of investigational drugs achieve regulatory approval and reach the marketplace. But the chances of success for drugs developed to treat Alzheimer’s disease are even more grim. Despite researchers’ valiant efforts to stall, slow, or even beat this devastating neurodegenerative condition, there are still no effective drugs available to the estimated 5.4 million Americans with the disease. The scientific community has watched in dismay, time and again, as potential Alzheimer’s drugs that produced promising data in rodent models failed to work as expected in humans. For the most part, these drugs have pursued the promising “amyloid hypothesis,” which states that the disease may be caused by accumulation of beta-amyloid peptide in brain tissue resulting in neuron-killing plaques. But so far, no drug candidates targeting the beta-amyloid pathway have prevailed through late-stage clinical trials. Earlier this year, for example, Merck halted a Phase 2/3 trial of verubecestat, a small molecule inhibitor of a protein implicated in the buildup of beta-amyloid, called beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), due to a lack of efficacy. Another high-profile example occurred late last year, when Eli Lilly’s solanezumab, a monoclonal antibody active against the beta-amyloid peptide, failed to prevent cognitive decline in a Phase 3 trial. These accumulating failures call into question the promise of targeting the formation and occurrence of amyloid plaques as a viable approach for treating Alzheimer’s. So how do we break the chain? Are there other approaches we could be taking that could give us valuable insight before investing in human studies? © 1986-2017 The Scientist

Keyword: Alzheimers
Link ID: 23295 - Posted: 03.01.2017

By GRETCHEN REYNOLDS For some people with early-stage Alzheimer’s disease, frequent, brisk walks may help to bolster physical abilities and slow memory loss, according to one of the first studies of physical activity as an experimental treatment for dementia. But the study’s results, while encouraging, showed that improvements were modest and not universal, raising questions about just how and why exercise helps some people with dementia and not others. Alzheimer’s disease affects more than five million people in the United States and more than 35 million worldwide, a number that is expected to double within 20 years. There are currently no reliable treatments for the disease. But past studies of healthy elderly people have found relationships between regular exercise and improved memories. Physically active older people are, for instance, significantly less likely than those who are sedentary to develop mild cognitive impairment, a frequent precursor to Alzheimer’s disease. Physically fit older people also tend to have more volume in their brain’s hippocampus than do sedentary people of the same age, brain scans show. The hippocampus is the portion of the brain most intimately linked with memory function. But most of this research has examined whether exercise might prevent Alzheimer’s disease. Little has been known about whether it might change the trajectory of the disease in people who already have the condition. So for the new study, published in February in PLoS One, researchers at the University of Kansas decided to work directly with people who had previously been given a diagnosis of Alzheimer’s disease. Because the disease can affect coordination as it progresses, the researchers focused on men and women in its early stages, who were still living at home and could safely walk by themselves or perform other types of light exercise. © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 23294 - Posted: 03.01.2017

By Victoria Sayo Turner When you want to learn something new, you practice. Once you get the hang of it, you can hopefully do what you learned—whether it’s parallel parking or standing backflips—on the next day, and the next. If not, you fall back to stage one and practice some more. But your brain may have a shortcut that helps you lock in learning. Instead of practicing until you’re decent at something and then taking a siesta, practicing just a little longer could be the fast track to solidifying a skill. “Overlearning” is the process of rehearsing a skill even after you no longer improve. Even though you seem to have already learned the skill, you continue to practice at that same level of difficulty. A recent study suggests that this extra practice could be a handy way to lock in your hard-earned skills. In the experiment, participants were asked to look at a screen and say when they saw a stripe pattern. Then two images were flashed one after the other. The images were noisy, like static on an old TV, and only one contained a hard-to-see stripe pattern. It took about twenty minutes of practice for people to usually recognize the image with stripes in it. The participants then continued to practice for another twenty minutes for the overlearning portion. Next, the participants took a break before spending another twenty minutes learning a similar “competitor” task where the stripes were oriented at a new angle. Under normal circumstances, this second task would compete with the first and actually overwrite that skill, meaning people should now be able to detect the second pattern but no longer see the first. The researchers wanted to see if overlearning could prevent the first skill from disappearing. © 2017 Scientific American

Keyword: Learning & Memory
Link ID: 23293 - Posted: 03.01.2017

Ed Yong It’s a good time to be interested in the brain. Neuroscientists can now turn neurons on or off with just a flash of light, allowing them to manipulate the behavior of animals with exceptional precision. They can turn brains transparent and seed them with glowing molecules to divine their structure. They can record the activity of huge numbers of neurons at once. And those are just the tools that currently exist. In 2013, Barack Obama launched the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative—a $115 million plan to develop even better technologies for understanding the enigmatic gray blobs that sit inside our skulls. John Krakaeur, a neuroscientist at Johns Hopkins Hospital, has been asked to BRAIN Initiative meetings before, and describes it like “Maleficent being invited to Sleeping Beauty’s birthday.” That’s because he and four like-minded friends have become increasingly disenchanted by their colleagues’ obsession with their toys. And in a new paper that’s part philosophical treatise and part shot across the bow, they argue that this technological fetish is leading the field astray. “People think technology + big data + machine learning = science,” says Krakauer. “And it’s not.” He and his fellow curmudgeons argue that brains are special because of the behavior they create—everything from a predator’s pounce to a baby’s cry. But the study of such behavior is being de-prioritized, or studied “almost as an afterthought.” Instead, neuroscientists have been focusing on using their new tools to study individual neurons, or networks of neurons. According to Krakauer, the unspoken assumption is that if we collect enough data about the parts, the workings of the whole will become clear. If we fully understand the molecules that dance across a synapse, or the electrical pulses that zoom along a neuron, or the web of connections formed by many neurons, we will eventually solve the mysteries of learning, memory, emotion, and more. “The fallacy is that more of the same kind of work in the infinitely postponed future will transform into knowing why that mother’s crying or why I’m feeling this way,” says Krakauer. And, as he and his colleagues argue, it will not. © 2017 by The Atlantic Monthly Group

Keyword: Brain imaging
Link ID: 23292 - Posted: 02.28.2017

By Robert F. Service Scientists are chasing a new lead on a class of drugs that may one day fight both pain and opioid addiction. It’s still early days, but researchers report that they’ve discovered a new small molecule that binds selectively to a long-targeted enzyme, halting its role in pain and addiction while not interfering with enzymes critical to healthy cell function. The newly discovered compound isn’t likely to become a medicine any time soon. But it could jumpstart the search for other binders that could do the job. Pain and addiction have many biochemical roots, which makes it difficult to treat them without affecting other critical functions in cells. Today, the most potent painkillers are opioids, including heroin, oxycodone, and hydrocodone. In addition to interrupting pain, they inhibit enzymes known as adenylyl cyclases (ACs) that convert cells’ energy currency, ATP, into a molecule involved in intracellular chemical communication known as cyclic AMP (cAMP). Chronic opioid use can make cells increase the activity of ACs to compensate, causing cAMP levels to skyrocket. When opioid users try to stop using, their cAMP levels remain high, and drugs that reduce those levels—like buprenorphine—have unwanted side effects. A promising candidate for selectively reducing cAMP is one particular AC enzyme, known as AC1. Humans have 10 ACs, all of which convert ATP to cAMP. But they are expressed at different levels in different tissues, suggesting they serve disparate purposes. Over the last 15 years, experiments on mice without the gene for AC1 have shown they have reduced sensitivity to pain and fewer signs of opioid dependence. But the enzyme, along with its close relative AC8, also appears to be heavily involved in memory formation in a brain region known as the hippocampus. © 2017 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 23291 - Posted: 02.28.2017

By Daniel Barron On January 2, 1979, Dr. Rafael Osheroff was admitted to Chestnut Lodge, an inpatient psychiatric hospital in Maryland. Osheroff had a bustling nephrology practice. He was married with three children, two from a previous marriage. Everything had been going well except his mood. For the previous two years, Osheroff had suffered from bouts of anxiety and depression. Dr. Nathan Kline, a prominent psychopharmacologist in New York City, had begun Osheroff on a tricyclic antidepressant and, according to Kline’s notes—which were later revealed in court—he improved. But then Osheroff decided, against Kline’s advice, to change his dose. He got worse. So much worse that he was brought to Chestnut Lodge. For the next seven months, Osheroff was treated with intensive psychotherapy for narcissistic personality disorder and depression. It didn’t help. He lost 40 pounds, suffered from excruciating insomnia, and began pacing the floor so incessantly that his feet became swollen and blistered. Osheroff’s family, distressed by the progressive unraveling of his mind, hired a psychiatrist in Washington D.C. to intervene. In response, Chestnut Lodge held a clinical case conference yet decided to not change treatment. Importantly, they decided to not begin medications but to continue psychotherapy. They considered themselves “traditional psychiatrists”—practitioners of psychodynamic psychotherapy, the technique used by Sigmund Freud and other pioneers. © 2017 Scientific American

Keyword: Depression; Schizophrenia
Link ID: 23290 - Posted: 02.28.2017

By Melissa Pandika Groundbreaking research suggests that a treatment for autism may come in the form of a probiotic. Stress can send your stomach into a painful tailspin, causing cramps, spasms and grumbling. But trouble in the gut can also affect the brain. This two-way relationship may be an unlikely key to solving one of medicine’s most pressing — and perplexing — mysteries: autism. Nearly 60 years after the disorder was first identified, the number of cases has surged, and the United Nations estimates that up to 70 million people worldwide fall on the autism spectrum. Yet there is no known cause or cure. But scientists have found promising clues in the gut. Research has revealed striking differences in the trillions of bacteria — a.k.a., the microbiome — in the intestines of children with and without autism. But the gut bacteria in individuals with autism aren’t just different. Researchers at the California Institute of Technology have shown for the first time that they may actually contribute to the disorder. They reported in the journal Cell in December 2013 that an experimental probiotic therapy alleviated autism-like behaviors in mice and are already planning a clinical trial. Today autism is treated primarily through behavioral therapy. But the new study suggests that treatment may one day come in the form of a probiotic — live, beneficial bacteria like those found in yogurt. “If you block the gastrointestinal problem, you can treat the behavioral symptoms,” Paul Patterson, a professor of biology at Caltech who co-authored the study told SFARI.org. University of Colorado Boulder professor Rob Knight hailed the finding as “groundbreaking” in a commentary in Cell. © OZY 2017 Terms & Conditions

Keyword: Autism; Obesity
Link ID: 23289 - Posted: 02.28.2017

By Steve Mirsky To conserve water, members of my household abide by the old aphorism “If it's yellow, let it mellow.” You're in a state of ignorance about that wizened phrase? If so, it recommends that one not flush the toilet after each relatively innocent act of micturition. But there's one exception to the rule: after asparagus, it's one and done—because those delicious stalks make urine smell like hell. To me and mine, anyway. The digestion of asparagus produces methanethiol and S-methyl thioesters, chemical compounds containing stinky sulfur, also known as brimstone. Hey, when I said that postasparagus urine smells like hell, I meant it literally. Methanethiol is the major culprit in halitosis and flatus, which covers both ends of that discussion. And although thioesters can also grab your nostrils by the throat, they might have played a key role in the origin of life. So be glad they were there stinking up the abiotic Earth. But does a compound reek if nobody is there to sniff it? Less philosophically, does it reek if you personally can't smell it? For only some of us are genetically gifted enough to fully appreciate the distinctive scents of postasparagus urine. The rest wander around unaware of their own olfactory offenses. Recently researchers dove deep into our DNA to determine, although we've all dealt it, exactly who smelt it. Their findings can be found in a paper entitled “Sniffing Out Significant ‘Pee Values’: Genome Wide Association Study of Asparagus Anosmia.” Asparagus anosmia refers to the inability “to smell the metabolites of asparagus in urine,” the authors helpfully explain. They don't bother to note that their bathroom humor plays on the ubiquity in research papers of the p-value, a statistical evaluation of the data that assesses whether said data look robust or are more likely the stuff that should never be allowed to mellow. © 2017 Scientific American,

Keyword: Chemical Senses (Smell & Taste); Genes & Behavior
Link ID: 23288 - Posted: 02.28.2017

By Jessica Hamzelou Fancy a coffee after that cigarette? Smoking makes you drink more caffeinated drinks, possibly by changing your metabolism so that you break down caffeine quicker, pushing you to drink more to get the same hit. That’s according to Marcus Munafò at the University of Bristol, UK, and his colleagues who have looked into the smoking and drinking habits of about 250,000 people. It’s impossible to do a randomised controlled trial (the most rigorous kind of scientific trial) when it comes to smoking, because it would be unethical to ask a randomly selected group of people to smoke. The next best thing is to study huge biobanks of health data. These biobanks contain information about people’s genes, diets and lifestyles. To explore the relationship between smoking and caffeine, Munafo and his colleagues analysed data from biobanks in the UK, Norway and Denmark. They were particularly interested in people who had inherited a variant of a gene that has already been shown to increase cigarette smoking. The team found that people who had this gene variant also consumed more coffee – but only if they smoked. British people with the same variant also drank more tea, although their Danish and Norwegian counterparts didn’t. This is probably due to cultural differences, says Munafò. “People in Norway and Denmark don’t chain drink tea in the same way that people in the UK do,” he says. © Copyright Reed Business Information Ltd.

Keyword: Drug Abuse
Link ID: 23287 - Posted: 02.27.2017

Allison Aubrey If you drink more alcohol than you want to or should, you're not alone. A nationwide survey by the National Institutes of Health found that 28 percent of adults in the U.S. are heavy drinkers or drink more than is recommended. Yet, most heavy drinkers don't get the help they need. "The biggest problem we have in the field is that less than 10 percent of individuals with an alcohol use disorder get any treatment whatsoever," says George Koob, director of the National Institute on Alcohol Abuse and Alcoholism. Part of the challenge, researchers say, is that many drinkers don't realize that a medicine long used to help people addicted to opioids quit their drug habit can help alcoholics and other heavy drinkers cut back, too. "I thought my only option was AA," John tells NPR. We've agreed to use only his middle name; disclosing his trouble with alcohol publicly, he says, would jeopardize his business. He's a 47-year-old professional who says he started out as a social drinker — a few beers with his softball team after a game. But he sank into a deep depression after several deaths in his family, and sought "solace the bottle," he says. "I wanted to numb my thoughts," says John. He'd often start with hard liquor in the morning, John says, and it wasn't uncommon to have eight drinks or more before the end of the day. © 2017 npr

Keyword: Drug Abuse; Pain & Touch
Link ID: 23286 - Posted: 02.27.2017

By Christine Vestal NEW YORK — After a 12-year battle with debilitating abdominal conditions that forced her to stop working, marijuana has helped Lynn Sabulski feel well enough to look for a job. Sabulski is among nearly 14,000 patients in New York state who are certified to use medical marijuana for one of 10 ­conditions, including her ­primary diagnosis, inflammatory bowel disease. Marijuana doesn’t address her underlying disease, but it does relieve her painful symptoms. Nationwide, an estimated 1.4 million patients in 28 states and the District of Columbia use legal medical marijuana for a varying list of conditions. A much smaller number of patients in 16 states use limited extracts of the plant, primarily to treat seizure disorders. In the midst of an opioid crisis, some medical practitioners and researchers say they think that greater use of marijuana for pain relief could result in fewer people using the highly addictive prescription painkillers that led to the epidemic. A 2016 study by researchers at Johns Hopkins Bloomberg School of Public Health found that states with medical marijuana laws had 25 percent fewer opioid overdose deaths than states that do not have medical marijuana laws. And another study published in Health Affairs last year found that prescriptions for opioid painkillers such as OxyContin, Vicodin and Percocet paid for by Medicare dropped substantially in states that adopted medical marijuana laws. © 1996-2017 The Washington Post

Keyword: Drug Abuse; Pain & Touch
Link ID: 23285 - Posted: 02.27.2017

By JANE E. BRODY In letters to The Times, blind readers reacted with heartfelt reassurance and practical guidance to Edward Hoagland’s essay, “Feeling My Way Into Blindness,” published in November. Stanley F. Wainapel, clinical director of physical medicine and rehabilitation at Montefiore Medical Center in the Bronx, admitted that “adapting to vision loss is a major challenge.” But he disputed Mr. Hoagland’s allusion to “enforced passivity,” pointing out that many advances in technology — from screen-reading software for computers to portable devices that read menus or printed letters “with a delay of only seconds” — can keep productivity, creativity and pleasure very much alive for people who can no longer see. Rabbi Michael Levy, president of Yad HaChazakah, the Jewish Disability Empowerment Center, also acknowledged that “transition to a world without sight is far from easy.” But he insisted, “Blindness does not cut me off from the world.” He cited skillful use of a cane, travel devices that tell him where he is and what is around him and periodicals available in real time by telephone among myriad other gadgets that “see” for him. Annika Ariel, a blind student double-majoring in English and political science at Amherst College, wrote that her problems are not with her blindness but rather from people’s attitudes that depict the blind as helpless and dependent. She said she travels independently, uses assistive technologies to complete her work as efficiently as others who can see, and excels academically and socially. Equally inspiring was the response of Mark Riccobono, president of the National Federation of the Blind, who became legally blind at age 5 and lost all useful vision to glaucoma at 14. © 2017 The New York Times Company

Keyword: Vision
Link ID: 23284 - Posted: 02.27.2017

Sara Reardon Like ivy plants that send runners out searching for something to cling to, the brain’s neurons send out shoots that connect with other neurons throughout the organ. A new digital reconstruction method shows three neurons that branch extensively throughout the brain, including one that wraps around its entire outer layer. The finding may help to explain how the brain creates consciousness. Christof Koch, president of the Allen Institute for Brain Science in Seattle, Washington, explained his group’s new technique at a 15 February meeting of the Brain Research through Advancing Innovative Neurotechnologies initiative in Bethesda, Maryland. He showed how the team traced three neurons from a small, thin sheet of cells called the claustrum — an area that Koch believes acts as the seat of consciousness in mice and humans1. Tracing all the branches of a neuron using conventional methods is a massive task. Researchers inject individual cells with a dye, slice the brain into thin sections and then trace the dyed neuron’s path by hand. Very few have been able to trace a neuron through the entire organ. This new method is less invasive and scalable, saving time and effort. Koch and his colleagues engineered a line of mice so that a certain drug activated specific genes in claustrum neurons. When the researchers fed the mice a small amount of the drug, only a handful of neurons received enough of it to switch on these genes. That resulted in production of a green fluorescent protein that spread throughout the entire neuron. The team then took 10,000 cross-sectional images of the mouse brain and used a computer program to create a 3D reconstruction of just three glowing cells. © 2017 Macmillan Publishers Limited

Keyword: Consciousness; Brain imaging
Link ID: 23283 - Posted: 02.25.2017

Geoff Brumfiel When the half-brother of North Korean leader Kim Jong Un collapsed at a Malaysian airport last week, poisoning was instantly suspected. But on Friday, Malaysian authorities revealed that an autopsy had turned up not just any poison, but a rare nerve agent known as VX. VX is among the deadliest chemical weapons ever devised. A colorless, odorless liquid, similar in consistency to motor oil, it kills in tiny quantities that can be absorbed through the skin. A relative of the nerve agent Sarin, VX disrupts communications between nerves and muscles. Victims of VX initially experience nausea and dizziness. Without an antidote, the chemical eventually paralyzes the diaphragm, causing suffocation. That may have been the fate of Kim Jong Nam, the estranged half-brother of North Korea's leader. Security footage showed that Kim was approached by two women who appeared to cover his face with a cloth. Moments later, he fell ill and sought help. He died before reaching a hospital. If the Malaysian analysis is correct and VX was the culprit, that would seem to suggest that the North Korean state itself is behind the killing. "Hardly anybody has it," says Dan Kaszeta, a chemical weapons expert and consultant based in London. The U.S. has destroyed nearly all of its stocks of VX in recent years. North Korea is among the few states in the world that have an active chemical weapons program. It is not a signatory to the Chemical Weapons Convention, which bans the use of such weapons. © 2017 npr

Keyword: Neurotoxins
Link ID: 23282 - Posted: 02.25.2017

By James Gallagher Health and science reporter, Maps have revealed "hotspots" of schizophrenia and other psychotic illnesses in England, based on the amount of medication prescribed by GPs. The analysis by the University of East London showed North Kesteven, in Lincolnshire, had the highest rates. The lowest rate of schizophrenia prescriptions was in East Dorset. However, explaining the pattern across England is complicated and the research team says the maps pose a lot of questions. They were developed using anonymous prescription records that are collected from doctors' surgeries in England. They record only prescriptions given out by GPs - not the number of patients treated - so hospital treatment is missed in the analysis. Data between October 2015 and September 2016 showed the average number of schizophrenia prescriptions across England was 19 for every 1,000 people. Prof Allan Brimicombe, one of the researchers from UEL, said: "The pattern is not uniformly spread across the country." He suggests this could be due to "environmental effects" such as different rates of drink or drug abuse. Prof Brimicombe told the BBC: "The top one is in the Lincolnshire countryside and there are others in the countryside." © 2017 BBC

Keyword: Schizophrenia
Link ID: 23281 - Posted: 02.25.2017

By Joshua A. Krisch When Kathleen Gardiner first encountered female mice with Down syndrome, she was surprised to find that the rodents’ brains showed unexpected abnormalities. Gardiner, a neuroscientist at the University of Colorado School of Medicine in Aurora, knew that trisomic male mice typically had perturbed protein levels in their hippocampuses. But these trisomic female mice showed the most serious changes in their cerebellums. “Right away, there’s a brain region sex difference,” Gardiner said. “It’s very interesting to ponder the fact that this could lead to sex differences in the learning, memory, or behavioral abnormalities associated with [Down syndrome].” Although Gardiner recognized that differences between mouse sexes would not necessarily translate into sex differences in humans, she considered the potential implications for clinical studies on Down syndrome therapies. “If we find that males or females are differing not only in their baseline impairment, but in their response to drugs, we need to know that,” she said. “We could be missing a big piece of information that could lead to better or different clinical trials.” Indeed, sex differences in model organisms are becoming increasingly apparent. Studies have shown sex differences in mice can affect cardiovascular health, liver disease, and cancer risk. Many of these studies are now published in Biology of Sex Differences, where Gardiner’s own work on the trisomic female mice appeared. © 1986-2017 The Scientist

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 23280 - Posted: 02.25.2017

By Carolyn Gramling Trilobites—three-sectioned, crablike critters that dominated the early Paleozoic—are so abundant that they have become the gateway fossil for most collectors. But paleontologists have found little evidence of how the extinct arthropods reproduced—until now. Researchers studying a fossil specimen of the trilobite Triarthrus eatoni spotted something odd just next to the animal’s head: a collection of small (about 200 micrometers across), round objects (in light blue, above). Those, they determined, are actually eggs—the first time anyone had observed fossil trilobite eggs right next to the critters themselves. The structures were exceptionally well preserved, the eggs and exoskeletons of the trilobites replaced with an iron sulfide ore called pyrite. They came from the Lorraine Group, a rock formation that spans much of the northeastern United States and dates to the Ordovician period (about 485 million to 444 million years ago); it has long been a mecca for trilobite hunters because of the pyritization. The placement of the eggs is suggestive, the researchers report in the March issue of Geology: They hypothesize that trilobites released their eggs and sperm through a genital pore somewhere in the head—much like modern horseshoe crabs do today. One possible reason for the rarity of the find may be that the brooding behavior of T. eatoni was relatively unusual in the trilobite world: The species tended to prefer a harsh, low-oxygen environment, and may have kept a closer eye on their eggs than other trilobite species. But, the authors note, one idea this finding does lay to rest is that trilobites might reproduce via copulation—a titillating but little-regarded hypothesis based on the fact that trilobites are sometimes found clustered on top of one another. Instead, trilobites were most likely spawners—and, in fact, that clustering behavior may be another parallel to horseshoe crabs, which can climb on top of one another in competition to fertilize released eggs. © 2017 American Association for the Advancement of Science

Keyword: Sexual Behavior; Evolution
Link ID: 23279 - Posted: 02.25.2017

Rae Ellen Bichell Initially, Clint Perry wanted to make a vending machine for bumblebees. He wanted to understand how they solve problems. Perry, a cognitive biologist at Queen Mary University of London, is interested in testing the limits of animal intelligence. "I want to know: How does the brain do stuff? How does it make decisions? How does it keep memory?" says Perry. And how big does a brain need to be in order to do all of those things? He decided to test this on bumblebees by presenting the insects with a puzzle that they'd likely never encounter in the wild. He didn't end up building that vending machine, but he did put bees through a similar scenario. Perry and his colleagues wrote Thursday in the journal Science that, despite bees' miniature brains, they can solve new problems quickly just by observing a demonstration. This suggests that bees, which are important crop pollinators, could in time adapt to new food sources if their environment changed. As we have reported on The Salt before, bee populations around the world have declined in recent years. Scientists think a changing environment is at least partly responsible. Perry and colleagues built a platform with a porous ball sitting at the center of it. If a bee went up to the ball, it would find that it could access a reward, sugar water. One by one, bumblebees walked onto the platform, explored a bit, and then slurped up the sugar water in the middle. "Essentially, the first experiment was: Can bees learn to roll a ball?" says Perry. © 2017 npr

Keyword: Learning & Memory; Evolution
Link ID: 23278 - Posted: 02.24.2017