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By Joel Achenbach Friends often look alike. The tendency of people to forge friendships with people of a similar appearance has been noted since the time of Plato. But now there is research suggesting that, to a striking degree, we tend to pick friends who are genetically similar to us in ways that go beyond superficial features. For example, you and your friends are likely to share certain genes associated with the sense of smell. Our friends are as similar to us genetically as you’d expect fourth cousins to be, according to the study published Monday in the Proceedings of the National Academy of Sciences. This means that the number of genetic markers shared by two friends is akin to what would be expected if they had the same great-great-great-grandparents. “Your friends don’t just resemble you superficially, they resemble you genetically,” said Nicholas A. Christakis, a physician and social scientist at Yale University and a co-author of the study. The resemblance is slight, just about 1 percent of the genetic markers, but that has huge implications for evolutionary theory, said James Fowler, a professor of medical genetics and political science at the University of California at San Diego. “We can do better than chance at predicting if two people are going to be friends if all we have is their genetic data,” Fowler said. This is a data-driven study that covers hundreds of friendship pairs and stranger pairs, plus hundreds of thousands of genetic markers. There’s no single “friendship” gene driving people together. There’s no way to say that a person befriended someone else because of any one genetic trait.
By Lizzie Wade It probably won’t come as a surprise that smoking a joint now and then will leave you feeling … pretty good, man. But smoking a lot of marijuana over a long time might do just the opposite. Scientists have found that the brains of pot abusers react less strongly to the chemical dopamine, which is responsible for creating feelings of pleasure and reward. Their blunted dopamine responses could leave heavy marijuana users living in a fog—and not the good kind. After high-profile legalizations in Colorado, Washington, and Uruguay, marijuana is becoming more and more available in many parts of the world. Still, scientific research on the drug has lagged. Pot contains lots of different chemicals, and scientists don’t fully understand how those components interact to produce the unique effects of different strains. Its illicit status in most of the world has also thrown up barriers to research. In the United States, for example, any study involving marijuana requires approval from four different federal agencies, including the Drug Enforcement Administration. One of the unanswered questions about the drug is what, exactly, it does to our brains, both during the high and afterward. Of particular interest to scientists is marijuana’s effect on dopamine, a main ingredient in the brain’s reward system. Pleasurable activities such as eating, sex, and some drugs all trigger bursts of dopamine, essentially telling the brain, “Hey, that was great—let’s do it again soon.” Scientists know that drug abuse can wreak havoc on the dopamine system. Cocaine and alcohol abusers, for example, are known to produce far less dopamine in their brains than people who aren’t addicted to those drugs. But past studies had hinted that the same might not be true for those who abuse marijuana. © 2014 American Association for the Advancement of Science
Keyword: Drug Abuse
Link ID: 19832 - Posted: 07.15.2014
By ALEX STONE Last summer, in a failed attempt at humor, Clorox ran an online ad that declared, “Like dogs or other house pets, new dads are filled with good intentions but lacking the judgment and fine motor skills to execute well.” Although the company pulled the ad amid a flurry of scorn from the online commentariat, it nevertheless played to a remarkably widespread stereotype — that fathers are somehow unfit to raise children. In “Do Fathers Matter?” — spoiler alert: they do — the veteran science writer Paul Raeburn jumps to Dad’s defense, drawing on several decades of research and his own experience as a five-time father. What emerges is a thought-provoking field piece on the science of fatherhood, studded with insights on how to apply it in the real world. Historically, developmental psychologists have largely dismissed fathers as irrelevant. Nearly half the articles on child and adolescent psychology published in leading journals from 1997 to 2005, for example, make no mention of fathers; before 1970, when fathers weren’t even allowed in delivery rooms, less than a fifth of the research on parental bonding took them into account. This bias reflects a deeply ingrained assumption that fathers play a marginal role in how their children turn out, a belief enshrined in the theory of infant attachment, which grew out of the work of the British psychiatrist John Bowlby in the second half of the 20th century. “It focused exclusively on mothers,” Mr. Raeburn writes. “The role of the father, Bowlby believed, was to provide support for the mother. In the drama of childhood, he was merely a supporting actor.” This was more or less the established view until a few decades ago, when psychologists, motivated in part by the growing number of women entering the work force, finally started paying attention to fathers. © 2014 The New York Times Company
by Azeen Ghorayshi Food could be a new weapon in shaking off the effects of jet lag after research in mice showed that the insulin released as a result of eating can be a key factor in restoring a disrupted body clock. Miho Sato and her colleagues at The Research Institute for Time Studies at Yamaguchi University in Japan did experiments in mice and tissue cultures to show, for the first time, that increases in insulin affect circadian rhythms. These daily rhythms affect alertness, sleep patterns, and mediate many other physiological processes. Your biological clock is regulated by two broad factors: first, the central rhythm is reset daily by light, as sensory input from the eyes is processed by a small part of the brain called the suprachiasmatic nucleus. The rise and fall of hormones linked to sleep, for example, match this rhythm. But circadian rhythms are also present in peripheral "clocks" in a wide range of cell types in the body. Some of these can be influenced by food. Sato demonstrated the role of insulin by shifting the peripheral body clock in the livers of mice by feeding them only at night. They then split the mice into two groups, supressed insulin levels in one group, and returned all the mice to daytime feeding. Four days later, the livers of the non-supressed mice had readjusted to a normal daily rhythm, as revealed by the daily rise and fall of liver-gene expression. The livers of the insulin-suppressed mice had still not returned to normal. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 19830 - Posted: 07.15.2014
By Neuroskeptic An entertaining paper just out in Frontiers in Systems Neuroscience offers a panoramic view of the whole of neuroscience: Enlarging the scope: grasping brain complexity The paper is remarkable not just for its content but also for its style. Some examples: How does the brain work? This nagging question is an habitué from the top ten lists of enduring problems in Science’s grand challenges. Grasp this paradox: how is one human brain – a chef d’oeuvre of complexity honed by Nature – ever to reach such a feast as to understand itself? Where one brain may fail at this notorious philosophical riddle, may be a strong and diversely-skilled army of brains may come closer. Or It remains an uneasy feeling that so much of Brain Science is built upon the foundation of a pair of neurons, outside the context of their networks, and with two open-ended areas of darkness at either of their extremities that must be thought of as the entire remainder of the organism’s brain (and body). And my favorite: As humans tend to agree, increased size makes up for smarter brains (disclosure: both authors are human) I love it. I’m not sure I understand it, though. The authors, Tognoli and Kelso, begin by framing a fundamental tension between directed information transfer and neural synchrony, pointing out that neurons firing perfectly in synch with each other could not transfer information between themselves.
Link ID: 19829 - Posted: 07.15.2014
|By Maria Burke and ChemistryWorld The world needs to tackle head-on the market failures undermining dementia research and drug development, UK Prime Minister David Cameron told a summit of world health and finance leaders in London in June. He announced an investigation into how to get medicines to patients earlier, extend patents and facilitate research collaborations, to report this autumn. But just how much difference will these sorts of measures make when scientists are still grappling with exactly what causes different types of dementia? Added to these problems is that dementia has become a graveyard for a large number of promising drugs. A recent study looked at how 244 compounds in 413 clinical trials fared for Alzheimer's disease between 2002 and 2012. The researchers findings paint a gloomy picture. Of those 244 compounds, only one was approved. The researchers report that this gives Alzheimer's disease drug candidates one of the highest failures rates of any disease area – 99.6%, compared with 81% for cancer. ‘Dementia is a ticking bomb costing the global economy £350 billion and yet progress with research is achingly slow,’ warned the World Dementia Envoy, Dennis Gillings. Businesses need incentives to invest in research and bring in faster, cheaper clinical trials, or the world won’t meet the ambition to find a cure or disease-modifying therapy by 2025, he added. ‘We need to free up regulation so that we can test ground-breaking new drugs, and examine whether the period for market exclusivity could be extended.’ © 2014 Scientific American
Link ID: 19828 - Posted: 07.15.2014
By Sharon Oosthoek, CBC News Mounting evidence that gut bacteria affect mood and behaviour has researchers investigating just how much power these tiny microbes wield over our mental health. "Many people with chronic intestinal conditions also have psychological disturbances and we never understood why," says McMaster University gastroenterologist Dr. Stephen Collins. Now, scientists such as Dr. Collins are starting to come up with answers. Our lower gastrointestinal tract is home to almost 100 trillion microorganisms, most of which are bacteria. They are, by and large, "good" bacteria that help us digest food and release the energy and nutrients we need. They also crowd out bacteria that can trigger disease. But when things go awry in our guts, they can also go awry in our brains. Up to 80 per cent of people with irritable bowel syndrome experience increased anxiety and depression. And those with autism — a syndrome associated with problems interacting with others — are more likely to have abnormal levels of gut bacteria. Dr. Collins and fellow McMaster gastroenterologist Premysl Bercik have done some of the seminal research into the bacteria-brain-behaviour connection. In a study published last year, they changed the behaviour of mice by giving them fecal transplants of intestinal bacteria. It involved giving adventurous mice bacteria from timid ones, thereby inducing timid behaviour. Before the transplant, adventurous mice placed in a dark, protected enclosure spent much of their time exploring an attached bright, wide-open area. After the transplant, they rarely ventured beyond their enclosure. © CBC 2014
|By William Skaggs Jet lag is a pain. Besides the inconvenience and frustration of traveling more than a few time zones, jet lag likely causes billions of dollars in economic losses. The most effective treatment, according to much research, is structured exposure to light, although the drug melatonin may also sometimes be helpful at bedtime. Both approaches have been used for more than 20 years, and during that time no viable new interventions have appeared. Recently, however, research into the molecular biology of circadian rhythms has raised the prospect of developing new drugs that might produce better results. Jet lag occurs when the “biological clock” in the brain becomes misaligned with the local rhythm of daily activity. The ultimate goal of circadian medicine is a treatment that instantly resets the brain's clock. Failing that, it would be helpful to have treatments that speed the rate of adjustment. Four recent discoveries suggest new possibilities. The first involves vasopressin, which is the main chemical signal used to synchronize cellular rhythms of activity in the brain area that is responsible for our biological clock. Blocking vasopressin makes it much easier to reset this clock. Potentially, a drug that interferes with vasopressin could work as a fast-acting treatment for jet lag. The second and third possibilities involve a pair of brain chemicals called salt-inducible kinase 1 (SIK1) and casein kinase 1ε (CK1ε), both of which limit the ability of light to reset the brain's clock. Drugs already exist that interfere with their action and greatly increase the effectiveness of light exposure. The existing drugs are not viable jet-lag treatments, because they are hard to administer and have unpleasant side effects, but researchers hope better drugs can be developed that work in a similar way. © 2014 Scientific American,
By Fredrick Kunkle Sleep disturbances such as apnea may increase the risk of Alzheimer’s disease, while moderate exercise in middle age and mentally stimulating games, such as crossword puzzles, may prevent the onset of the dementia-causing disease, according to new research to be presented Monday. The findings — which are to be introduced during the six-day Alzheimer’s Association International Conference in Copenhagen — bolster previous studies that suggest sleep plays a critical role in the aging brain’s health, perhaps by allowing the body to cleanse itself of Alzheimer's-related compounds during down time. The studies also add to a growing body of literature that suggests keeping the brain busy keeps it healthy. The battle against Alzheimer’s disease has become more urgent for the United States and other developing nations as their populations turn increasingly gray. The disease is the leading cause of dementia in older people and afflicts more than 5 million Americans. At its current pace, the number is expected to soar to 16 million people by 2050. In 2012, the United States adopted a national plan to combat the disease and the G-8 nations last year adopted a goal of providing better treatment and prevention by 2025. Erin Heintz, a spokeswoman for the Alzheimer’s Association, said U.S. government funding to combat the disease now stands at about $500 million a year. To reach its 2025 goal, the United States should be spending $2 billion a year, she said.
One in three cases of Alzheimer's disease worldwide is preventable, according to research from the University of Cambridge. The main risk factors for the disease are a lack of exercise, smoking, depression and poor education, it says. Previous research from 2011 put the estimate at one in two cases, but this new study takes into account overlapping risk factors. Alzheimer's Research UK said age was still the biggest risk factor. Writing in The Lancet Neurology, the Cambridge team analysed population-based data to work out the main seven risk factors for Alzheimer's disease. These are: Diabetes Mid-life hypertension Mid-life obesity Physical inactivity Depression Smoking Low educational attainment They worked out that a third of Alzheimer's cases could be linked to lifestyle factors that could be modified, such as lack of exercise and smoking. The researchers then looked at how reducing these factors could affect the number of future Alzheimer's cases. They found that by reducing each risk factor by 10%, nearly nine million cases of the disease could be prevented by 2050. In the UK, a 10% reduction in risk factors would reduce cases by 8.8%, or 200,000, by 2050, they calculated. BBC © 2014
Link ID: 19824 - Posted: 07.14.2014
By Fredrick Kunkle A simple test of a person’s ability to identify odors and noninvasive eye exams might someday help doctors learn whether their patients are at risk of Alzheimer’s disease, according to research to be presented Sunday. With Alzheimer’s disease growing fast among the world’s aging population, researchers are increasingly focused on the search for new ways to detect and treat the brain-killing disease in its earliest stages. In two separate studies on the connection between dementia and sense of smell, teams of researchers found that a decreased ability to detect odors in older people, as determined by a common scratch-and-sniff test, could point to brain cell loss and the onset of dementia. In two other studies, researchers showed that noninvasive eye exams also might offer a way to identify Alzheimer’s in its early stages. The findings — which are to be presented at the Alzheimer’s Association International Conference in Copenhagen on Sunday — raise hopes that doctors could develop simple, inexpensive diagnostic tools that would hunt down reliable biomarkers of a disease that affects more than 5 million people in the United States. Alzheimer’s is a progressive and incurable disease that begins in areas of the brain associated with memory. It is the leading cause of dementia in older people, usually striking after the age of 65. It robs people of their cognitive abilities, speech and, ultimately, their identities. Eventually, it shuts down the most basic body functions, resulting in death.
Link ID: 19823 - Posted: 07.14.2014
|By Roni Jacobson Prozac, Paxil, Celexa, Zoloft, Lexapro. These so-called selective serotonin reuptake inhibitors (SSRIs) are among the most widely prescribed drugs in the U.S. Although they are typically used to treat depression and anxiety disorders, they are also prescribed off-label for conditions such as chronic pain, premature ejaculation, bulimia, irritable bowel syndrome, premenstrual syndrome and hot flashes. Even if you have never taken an SSRI, chances are you know someone who has. About one in every 10 American adults is being prescribed one now. For women aged 40 to 59 years old, the proportion increases to one in four. SSRIs block the body from reabsorbing serotonin, a neurotransmitter mostly found in the brain, spinal cord and digestive tract whose roles include regulation of mood, appetite, sexual function and sleep. Specifically, SSRIs bind to the protein that carries serotonin between nerve cells—called SERT, for serotonin transporter—intercepting it before it can escort the released neurotransmitter back into the cell. This action leaves more active serotonin in the body, a chemical effect that is supposed to spur feelings of happiness and well-being. But there are hints that SSRIs are doing something other than simply boosting serotonin levels. First, people vary in their response to SSRIs: Studies have shown that the drugs are not very effective for mild to moderate depression, but work well when the disorder is severe. If low serotonin were the only culprit in depression, SSRIs would be more uniformly helpful in alleviating symptoms. Second, it takes weeks after starting an SSRI for depression and anxiety to lift even though changes in serotonin ought to happen pretty much right away. © 2014 Scientific American
Posted by alison abbott Cautious efforts to restore unity to the billion-euro Human Brain Project have begun. Both the European Commission and the project’s leaders have now responded to a scorching open letter in which angry neuroscientists condemn the flagship project, and pledge to boycott it. Signed by 156 top neuroscientists, including many research institute directors in Europe, the letter was sent on 7 July to the European Commission, which is funding the project’s first phase. It expresses concern about both the scientific approach in the neuroscience arm of the project, which aims to simulate brain function in supercomputers, and the general project management. The letter makes a series of demands for changes that it claims are needed to make the management and governance of the Human Brain Project more transparent and representative of the scientific views of the whole community. Since it was sent, a further 408 neuroscientists have added their signatures. On 10 July, the European Commission sent a bland statement to Nature, stating that “it is too early to draw conclusions on the success or failure of the project”, given that it has only been running for nine months. The Commission’s response also says that a “divergence of views” is not unusual in large-scale projects, particularly at their beginnings and that the Commission will “continue to engage with all partners in this ambitious project”. © 2014 Macmillan Publishers Limited
Keyword: Brain imaging
Link ID: 19821 - Posted: 07.14.2014
Sara Reardon For chimps, nature and nurture appear to contribute equally to intelligence. Smart chimpanzees often have smart offspring, researchers suggest in one of the first analyses of the genetic contribution to intelligence in apes. The findings, published online today in Current Biology1, could shed light on how human intelligence evolved, and might even lead to discoveries of genes associated with mental capacity. A team led by William Hopkins, a psychologist at Georgia State University in Atlanta, tested the intelligence of 99 chimpanzees aged 9 to 54 years old, most of them descended from the same group of animals housed at the Yerkes National Primate Research Center in Atlanta. The chimps faced cognitive challenges such as remembering where food was hidden in a rotating object, following a human’s gaze and using tools to solve problems. A subsequent statistical analysis revealed a correlation between the animals' performance on these tests and their relatedness to other chimpanzees participating in the study. About half of the difference in performance between individual apes was genetic, the researchers found. In humans, about 30% of intelligence in children can be explained by genetics; for adults, who are less vulnerable to environmental influences, that figure rises to 70%. Those numbers are comparable to the new estimate of the heritability of intelligence across a wide age range of chimps, says Danielle Posthuma, a behavioural geneticist at VU University in Amsterdam, who was not involved in the research. “This study is much overdue,” says Rasmus Nielsen, a computational biologist at the University of California, Berkeley. “There has been enormous focus on understanding heritability of intelligence in humans, but very little on our closest relatives.” © 2014 Nature Publishing Group
By Jules Wellinghoff A simple change in electric charge may make the difference between someone getting the medicine they need and a trip to the emergency room—at least if a new study bears out. Researchers investigating the toxicity of particles designed to ferry drugs inside the body have found that carriers with a positive charge on their surface appear to cause damage if they reach the brain. These particles, called micelles, are one type of a class of materials known as nanoparticles. By varying properties such as charge, composition, and attached surface molecules, researchers can design nanoparticles to deliver medicine to specific body regions and cell types—and even to carry medicine into cells. This ability allows drugs to directly target locations they would otherwise be unable to, such as the heart of tumors. Researchers are also looking at nanoparticles as a way to transport drugs across the blood-brain barrier, a wall of tightly connected cells that keeps most medication out of the brain. Just how safe nanoparticles in the brain are, however, remains unclear. So Kristina Bram Knudsen, a toxicologist at the National Research Centre for the Working Environment in Copenhagen, and colleagues tested two types of micelles, which were made from different polymers that gave the micelles either a positive or negative surface charge. They injected both versions, empty of drugs, into the brains of rats, and 1 week later they checked for damage. Three out of the five rats injected with the positively charged micelles developed brain lesions. The rats injected with the negatively charged micelles or a saline control solution did not suffer any observable harm from the injections, the team will report in an upcoming issue of Nanotoxicology. © 2014 American Association for the Advancement of Science
Link ID: 19819 - Posted: 07.12.2014
By GARY MARCUS ARE we ever going to figure out how the brain works? After decades of research, diseases like schizophrenia and Alzheimer’s still resist treatment. Despite countless investigations into serotonin and other neurotransmitters, there is still no method to cure clinical depression. And for all the excitement about brain-imaging techniques, the limitations of fMRI studies are, as evidenced by popular books like “Brainwashed” and “Neuromania,” by now well known. In spite of the many remarkable advances in neuroscience, you might get the sinking feeling that we are not always going about brain science in the best possible way. This feeling was given prominent public expression on Monday, when hundreds of neuroscientists from all over the world issued an indignant open letter to the European Commission, which is funding the Human Brain Project, an approximately $1.6 billion effort that aims to build a complete computer simulation of the human brain. The letter charges that the project is “overly narrow” in approach and not “well conceived.” While no neuroscientist doubts that a faithful-to-life brain simulation would ultimately be tremendously useful, some have called the project “radically premature.” The controversy serves as a reminder that we scientists are not only far from a comprehensive explanation of how the brain works; we’re also not even in agreement about the best way to study it, or what questions we should be asking. The European Commission, like the Obama administration, which is promoting a large-scale research enterprise called the Brain Initiative, is investing heavily in neuroscience, and rightly so. (A set of new tools such as optogenetics, which allows neuroscientists to control the activity of individual neurons, gives considerable reason for optimism.) But neither project has grappled sufficiently with a critical question that is too often ignored in the field: What would a good theory of the brain actually look like? Different kinds of sciences call for different kinds of theories. Physicists, for example, are searching for a “grand unified theory” that integrates gravity, electromagnetism and the strong and weak nuclear forces into a neat package of equations. Whether or not they will get there, they have made considerable progress, in part because they know what they are looking for. © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19818 - Posted: 07.12.2014
By Dominic Basulto It turns out that the human brain may not be as mysterious as it has always seemed to be. Researchers at George Washington University, led by Mohamad Koubeissi, may have found a way to turn human consciousness on and off by targeting a specific region of the brain with electrical currents. For brain researchers, unlocking the mystery of human consciousness has always been viewed as one of the keys for eventually building an artificial brain, and so this could be a big win for the future of brain research. What the researchers did was deliver a serious of high frequency electrical impulses to the claustrum region of the brain in a woman suffering from epilepsy. Before the electric shocks, the woman was capable of writing and talking. During the electric shocks, the woman faded out of consciousness, and started staring blankly into space, incapable of even the most basic sensory functions. Even her breathing slowed. As soon as the electrical shocks stopped, the woman immediately regained her sensory skills with no memory of the event. The researchers claim that this test case is evidence of being able to turn consciousness on and off. Granted, there’s a lot still to be done. That George Washington test, for example, has only been successfully performed on one person. And that woman had already had part of her hippocampus removed, so at least one researcher says the whole experiment must be interpreted carefully. There have been plenty of scientific experiments that have been “one and done,” so it remains to be seen whether these results can be replicated again.
Link ID: 19817 - Posted: 07.12.2014
by Helen Thomson You are what your grandmother ate, potentially, but maybe not what your great grandmother consumed. A study in mice shows that undernourishment during pregnancy increases the chances that the next two generations will develop obesity and diabetes. But by then the slate is wiped clean. If the same holds true for humans, it may mean that stressful events in our lives affect our grandchildren's health, but not great-grandchildren. Environmental stresses cause chemical changes to DNA that turn genes on and off. Many researchers believe that these changes can be passed down through sperm and eggs – a mechanism known as epigenetic inheritance. Low-calorie diet For example, studies have linked pregnant mothers that were undernourished during the second world war with gene changes in their children that put them at higher risk of becoming obese or getting cancer. But what happens to later generations is not clear. To model this effect, Anne Ferguson-Smith at the University of Cambridge and her colleagues fed pregnant mice a diet containing 50 per cent fewer calories than usual from the 12th day of gestation until the birth, which is normally after about 20 days. Offspring were smaller than average and developed diabetes when fed a healthy diet. When the male pups had offspring, they were also at higher risk of becoming diabetic. The team analysed the sperm of the offspring from the undernourished mothers to see how many genes had had their expression altered by the addition or removal of a methyl group – an epigenetic change. The team found a decrease in methylation in 111 regions of the DNA compared with sperm from mice born to mothers fed a healthy diet. © Copyright Reed Business Information Ltd
Erika Check Hayden Nearly 750,000 babies born each year in the United Kingdom are at risk of brain damage because of low oxygen during birth. Cooling babies who are at risk of brain damage provides long-lasting prevention of such injuries, researchers report today in the New England Journal of Medicine1. A team led by Denis Azzopardi, a neonatologist at King’s College London, lowered the body temperature of 145 full-term babies who were born after at least 36 weeks of gestation. All were at risk of brain damage because they had been deprived of oxygen during birth — a problem that is often caused by troubles with the placenta or umbilical cord, and affects nearly 750,000 babies a year in the United Kingdom. The researchers cooled the infants to between 33°C and 34°C for 72 hours, starting within 6 hours of birth. The technique is known to boost the chances that children avoid brain damage until they become toddlers2, but any longer-term benefits have remained unclear. The study finds treated babies had better mental and physical health than untreated infants through to ages 6 or 7: they were 60% more likely to have normal intelligence, hearing and vision. Those who survived to childhood also had fewer disabilities such as difficulty walking and seeing. "The bottom line is that this doubles a child’s chance of normal survival," says David Edwards, a neonatologist at King’s College London and an author of the study. Neonatologist David Rowitch from the University of California, San Francisco, who studies treatments for paediatric brain damage, says the new findings are important because they show sustained improvements. "This study is encouraging, adding to the weight of evidence showing both positive early indicators and also school-age benefits to hypothermia," Rowitch adds. © 2014 Nature Publishing Group,
Keyword: Development of the Brain
Link ID: 19814 - Posted: 07.10.2014
Thomas B. Edsall It’s been a key question of American politics since at least 1968: Why do so many poor, working-class and lower-middle-class whites — many of them dependent for survival on government programs — vote for Republicans? The debate over the motives of conservative low-income white voters remains unresolved, but two recent research papers suggest that the hurdles facing Democrats in carrying this segment of the electorate may prove difficult to overcome. In “Obedience to Traditional Authority: A heritable factor underlying authoritarianism, conservatism and religiousness,” published by the journal Personality and Individual Differences in 2013, three psychologists write that “authoritarianism, religiousness and conservatism,” which they call the “traditional moral values triad,” are “substantially influenced by genetic factors.” According to the authors — Steven Ludeke of Colgate, Thomas J. Bouchard of the University of Minnesota, and Wendy Johnson of the University of Edinburgh — all three traits are reflections of “a single, underlying tendency,” previously described in one word by Bouchard in a 2006 paper as “traditionalism.” Traditionalists in this sense are defined as “having strict moral standards and child-rearing practices, valuing conventional propriety and reputation, opposing rebelliousness and selfish disregard of others, and valuing religious institutions and practices.” Working along a parallel path, Amanda Friesen, a political scientist at Indiana University, and Aleksander Ksiazkiewicz, a graduate student in political science at Rice University, concluded from their study comparing identical and fraternal twins that “the correlation between religious importance and conservatism” is “driven primarily, but usually not exclusively, by genetic factors.” The substantial “genetic component in these relationships suggests that there may be a common underlying predisposition that leads individuals to adopt conservative bedrock social principles and political ideologies while simultaneously feeling the need for religious experiences.” © 2014 The New York Times Company