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By Neuroskeptic In a thought-provoking new paper called What are neural correlates neural correlates of?, NYU sociologist Gabriel Abend argues that neuroscientists need to pay more attention to philosophy, social science, and the humanities. Abend’s main argument is that if we are to study the neural correlates or neural basis of a certain phenomenon, we must first define that phenomenon and know how to identify instances of it. Sometimes, this identification is straightforward: in a study of brain responses to the taste of sugar, say, there is little room for confusion because we all agree what sugar is. However, if a neuroscientist wants to study the neural correlates of, say, love, they will need to decide what love is, and this is something that philosophers and others have been debating for a long time. Abend argues that cognitive neuroscientists “cannot avoid taking sides in philosophical and social science controversies” in studying phenomena, such as love or morality, which have no neutral, universally accepted definition. In choosing a particular set of stimuli in order to experimentally evoke something, neuroscientists are aligning themselves with a certain theory of what that thing is. For example, the field of “moral neuroscience” makes heavy use of a family of hypothetical dilemmas called trolley problems. The classic trolley problem asks us to choose between allowing a runaway trolley to hit and kill five people, or throwing one person in front of the trolley, killing them but saving the other five.

Keyword: Consciousness
Link ID: 23501 - Posted: 04.18.2017

By Ryan Cross Microscopes reveal miniscule wonders by making things seem bigger. Just imagine what scientists could see if they could also make things bigger. A new strategy to blow brains up does just that. Researchers previously invented a method for injecting a polyacrylate mesh into brain tissue, the same water-absorbing and expanding molecule that makes dirty diapers swell up. Just add water, and the tissue enlarges to 4.5 times its original size. But it wasn’t good enough to see everything. The brain is full of diminutive protrusions called dendritic spines lining the signal receiving end of a neuron. Hundreds to thousands of these nubs help strengthen or weaken an individual dendrite’s connection to other neurons in the brain. The nanoscale size of these spines makes studying them with light microscopes impossible or blurry at best, however. Now, the same group has overcome this barrier in an improved method called iterative expansion microscopy, described today in Nature Methods. Here, the tissue is expanded once, the crosslinked mesh is cleaved, and then the tissue is expanded again, resulting in roughly 20-fold enlargement. Neurons are then visualized by light-emitting molecules linked to antibodies which latch onto specified proteins. The technique has yielded detailed images showing the formation of proteins along synapses in mice, as well as detailed renderings of dendritic spines (seen in the image above) in the mouse hippocampus—a center or learning and memory in the brain. The advance could enable neuroscientists to map the many individual connections between neurons across the brain and the unique arrangement of receptors that turn brain circuits on and off. © 2017 American Association for the Advancement of Science

Keyword: Brain imaging
Link ID: 23500 - Posted: 04.18.2017

By John Horgan I’m writing a book on the mind-body problem, and one theme is that mind-theorists’ views are shaped by emotionally traumatic experiences, like mental illness, the death of a child and the breakup of a marriage. David Chalmers is a striking counter-example. He seems remarkably well adjusted and rational, especially for a philosopher. I’ve tracked his career since I heard him call consciousness “the hard problem” in 1994. Although I often disagree with him—about, for example, whether information theory can help solve consciousness—I’ve always found him an admirably clear thinker, who doesn’t oversell his ideas (unlike Daniel Dennett when he insists that consciousness is an “illusion”). Just in the last couple of years, Chalmers's writings, talks and meetings have helped me understand integrated information theory, Bayesian brains, ethical implications of artificial intelligence and philosophy’s lack of progress, among other topics. Last year I interviewed Chalmers at his home in a woody suburb of New York City. My major takeaway: Although he has faith that consciousness can be scientifically solved, Chalmers doesn’t think we’re close to a final theory, and if we find such a theory, consciousness might remain as philosophically confusing as, say, quantum mechanics. In other words, Chalmers is a philosophical hybrid, who fuses optimism with mysterianism, the position that consciousness is intractable. Below are edited excerpts from our conversation. Chalmers, now 50, was born and raised in Australia. His parents split up when he was five. “My father is a medical researcher, a pretty successful scientist and administrator in medicine in Australia… My mother is I would say a spiritual thinker.” “So if you want an historical story, I guess I end up halfway between my father and mother… My father is a reductionist, and my mother is very much a non-reductionist. I’m a non-reductionist with a tolerance for ideas that might look a bit crazy to some people, like the idea that there’s consciousness everywhere, consciousness is not reducible to something physical. That said, the tradition I’m working in is very much in the western scientific and analytic tradition.” © 2017 Scientific American

Keyword: Consciousness
Link ID: 23499 - Posted: 04.17.2017

Richard A. Friedman I was doing KenKen, a math puzzle, on a plane recently when a fellow passenger asked why I bothered. I said I did it for the beauty. O.K., I’ll admit it’s a silly game: You have to make the numbers within the grid obey certain mathematical constraints, and when they do, all the pieces fit nicely together and you get this rush of harmony and order. Still, it makes me wonder what it is about mathematical thinking that is so elegant and aesthetically appealing. Is it the internal logic? The unique mix of simplicity and explanatory power? Or perhaps just its pure intellectual beauty? I’ve loved math since I was a kid because it felt like a big game and because it seemed like the laziest thing you could do mentally. After all, how many facts do you need to remember to do math? Later in college, I got excited by physics, which I guess you could say is just a grand exercise in applying math to understand the universe. My roommate, a brainy math major, used to bait me, saying that I never really understood the math I was using. I would counter that he never understood what on Earth the math he studied was good for. We were both right, but he’d be happy to know that I’ve come around to his side: Math is beautiful on a purely abstract level, quite apart from its ability to explain the world. We all know that art, music and nature are beautiful. They command the senses and incite emotion. Their impact is swift and visceral. How can a mathematical idea inspire the same feelings? Well, for one thing, there is something very appealing about the notion of universal truth — especially at a time when people entertain the absurd idea of alternative facts. The Pythagorean theorem still holds, and pi is a transcendental number that will describe all perfect circles for all time. © 2017 The New York Times Company

Keyword: Brain imaging
Link ID: 23498 - Posted: 04.17.2017

Emily Corwin Michael Treadwell sat at the back of a courtroom in New Hampshire. He wore a windbreaker and khaki pants and leaned over his work boots with his elbows on his knees. At first it looked like he was chewing gum — a bold choice in a courtroom. But when he spoke it was clear: He wasn't chewing gum, he was chewing his own gums. Michael doesn't have any teeth. Taxpayers in Hillsborough County, N.H., have spent $63,000 over the last six years keeping Treadwell in jail for little more than trespassing. Law Investigation Into Private Prisons Reveals Crowding, Under-Staffing And Inmate Deaths For years now, his life has looked like this: Trespass in an apartment building, spend 30 days in jail; bother restaurant customers, spend 42 days in jail; panhandle aggressively, spend 30 days in jail. "When you live in a town like Nashua, there's not a lot of homelessness there, and it kinda like focuses, puts you in the spotlight," Treadwell says. "Especially if you drink alcohol and stuff." His charges all come from some combination of being homeless and getting drunk. Still, he says, jail is no worse than the streets. "People kill homeless people, violence and everything else," Treadwell says. "It can be a very dangerous life to live in. I don't suggest jail as an alternative. Ain't no kinda life." © 2017 npr

Keyword: Schizophrenia
Link ID: 23497 - Posted: 04.17.2017

By Jia Naqvi The rate of stroke among young people has apparently been rising steadily since 1995, according to a study published this week. Hospitalization rates for stroke increased for women between the ages of 18 and 44, and nearly doubled for men in that age range from 1995 through 2012. Using more-detailed data for 2003 through 2012, the researchers found that rates of hospitalizations for acute ischemic stroke increased by nearly 42 percent for men 35 to 44, while rates for women of the same age group increased by 30 percent over the same time, the study published in the JAMA, the Journal of the American Medical Association. Across all adults, including those in older age ranges, stroke was the fifth leading cause of death in 2013. Overall mortality rates from strokes have significantly decreased over the past 50 years due to multiple factors, including better treatment for hypertension and increased use of aspirin, even as incidence of acute ischemic stroke among young adults has been on the rise. The study also looked at stroke risk factors and whether there were any changes in their prevalence from 2003 to 2012. The likelihood of having three or more of five common risk factors — diabetes, hypertension, lipid disorders, obesity and tobacco use — doubled in men and women hospitalized for acute ischemic strokes. © 1996-2017 The Washington Post=

Keyword: Stroke; Development of the Brain
Link ID: 23496 - Posted: 04.17.2017

By David Noonan Like many people with epilepsy, Richard Shane, 56, has some problems with memory. But he can easily recall his first seizure, 34 years ago. “I was on the phone with my father, and I noticed that I started moaning, and I lost some level of consciousness,” Shane says. After experiencing a similar episode three weeks later, he went to a doctor and learned he had epilepsy, a neurological disorder caused by abnormal electrical activity in the brain. The first medication he was prescribed, Dilantin (phenytoin), failed to stop or even reduce his seizures. So did the second and the third. His epilepsy, it turned out, was drug-resistant. Over the next 22 years Shane suffered two to five or more seizures a week. He and his doctors tried every new antiseizure drug that came along, but none worked. Finally, in 2004, as a last resort, a neurosurgeon removed a small part of Shane's brain where his seizures originated. “It was a matter of what sucks less,” Shane says, “having brain surgery or having epilepsy.” Shane has been seizure-free ever since. As many as three million people in the U.S. live with epilepsy, and more than 30 percent of them receive inadequate relief from medication, a number that persists despite the introduction of more than a dozen new antiepileptic drugs since 1990. Although surgery has helped some patients such as Shane, uncontrollable epilepsy remains a living nightmare for patients and an intractable foe for clinicians and researchers. “I hate to say it, but we do not know why” some people respond to medications and others do not, says neurologist Michael Rogawski, who studies epilepsy treatments at the University of California, Davis. And yet if the central conundrum continues, so does the determined quest for new and different approaches to treating the toughest cases. © 2017 Scientific American

Keyword: Epilepsy
Link ID: 23495 - Posted: 04.15.2017

By Andy Coghlan It tastes foul and makes people vomit. But ayahuasca, a hallucinogenic concoction that has been drunk in South America for centuries in religious rituals, may help people with depression that is resistant to antidepressants. Tourists are increasingly trying ayahuasca during holidays to countries such as Brazil and Peru, where the psychedelic drug is legal. Now the world’s first randomised clinical trial of ayahuasca for treating depression has found that it can rapidly improve mood. The trial, which took place in Brazil, involved administering a single dose to 14 people with treatment-resistant depression, while 15 people with the same condition received a placebo drink. A week later, those given ayahuasca showed dramatic improvements, with their mood shifting from severe to mild on a standard scale of depression. “The main evidence is that the antidepressant effect of ayahuasca is superior to the placebo effect,” says Dráulio de Araújo of the Brain Institute at the Federal University of Rio Grande do Norte in Natal, who led the trial. Shamans traditionally prepare the bitter, deep-brown brew of ayahuasca using two plants native to South America. The first, Psychotria viridis, is packed with the mind-altering compound dimetheyltryptamine (DMT). The second, the ayahuasca vine (Banisteriopsis caapi), contains substances that stop DMT from being broken down before it crosses the gut and reaches the brain. © Copyright Reed Business Information Ltd.

Keyword: Depression; Drug Abuse
Link ID: 23494 - Posted: 04.15.2017

Sarah Boseley in Amsterdam The city of Amsterdam is leading the world in ending the obesity epidemic, thanks to a radical and wide-reaching programme which is getting results even among the poorest communities that are hardest to reach. Better known for tulips and bicycles, Amsterdam has the highest rate of obesity in the Netherlands, with a fifth of its children overweight and at risk of future health problems. The programme appears to be succeeding by hitting multiple targets at the same time – from promoting tap water to after-school activities to the city refusing sponsorship to events that take money from Coca Cola or McDonalds. It is led by a dynamic deputy mayor with the unanimous backing of the city’s politicians. From 2012 to 2015, the number of overweight and obese children has dropped by 12%. Even more impressive, Amsterdam has done what nobody else has managed, because the biggest fall has been amongst the lowest socio-economic groups. It is in neighbourhoods like the Bijlmer in the south-east that the programme is changing lives. The Bijlmer is notorious, says Wilbert Sawat, coordinator and PE teacher at De Achtsprong primary school, and that’s why he wanted to work there. Other teachers do too, he says. “Here we can make a difference.

Keyword: Obesity
Link ID: 23493 - Posted: 04.15.2017

Laurel Hamers Earth’s magnetic field helps eels go with the flow. The Gulf Stream fast-tracks young European eels from their birthplace in the Sargasso Sea to the European rivers where they grow up. Eels can sense changes in Earth’s magnetic field to find those highways in a featureless expanse of ocean — even if it means swimming away from their ultimate destination at first, researchers report in the April 13 Current Biology. European eels (Anguilla anguilla) mate and lay eggs in the salty waters of the Sargasso Sea, a seaweed-rich region in the North Atlantic Ocean. But the fish spend most of their adult lives living in freshwater rivers and estuaries in Europe and North Africa. Exactly how eels make their journey from seawater to freshwater has baffled scientists for more than a century, says Nathan Putman, a biologist with the National Oceanic and Atmospheric Administration in Miami. The critters are hard to track. “They’re elusive,” says study coauthor Lewis Naisbett-Jones, a biologist now at the University of North Carolina at Chapel Hill. “They migrate at night and at depth. The only reason we know they spawn in the Sargasso Sea is because that’s where the smallest larvae have been collected.” |© Society for Science & the Public 2000 - 2017.

Keyword: Animal Migration
Link ID: 23492 - Posted: 04.14.2017

By James Gallagher Health and science reporter, BBC News website Toddlers who spend time playing on smartphones and tablets seem to get slightly less sleep than those who do not, say researchers. The study in Scientific Reports suggests every hour spent using a touchscreen each day was linked to 15 minutes less sleep. However, those playing with touchscreens do develop their fine motor skills more quickly. Experts said the study was "timely" but parents should not lose sleep over it. There has been an explosion in touchscreens in the home, but understanding their impact on early childhood development has been lacking. The study by Birkbeck, University of London, questioned 715 parents of children under three years old. It asked how often their child played with a smartphone or tablet and about the child's sleep patterns. It showed that 75% of the toddlers used a touchscreen on a daily basis, with 51% of those between six and 11 months using one, and 92% of those between 25 and 36 months doing so as well. But children who did play with touchscreens slept less at night and more in the day. Overall they had around 15 minutes less sleep for every hour of touchscreen use. Not before bedtime? Dr Tim Smith, one of the researchers, told the BBC News website: "It isn't a massive amount when you're sleeping 10-12 hours a day in total, but every minute matters in young development because of the benefits of sleep." © 2017 BBC.

Keyword: Sleep
Link ID: 23491 - Posted: 04.14.2017

By CATHERINE SAINT LOUIS Halfway through February, I could no longer sleep through the night. At 2 a.m., I’d find myself chugging milk from the carton to extinguish a fire at the top of my rib cage. The gnawing feeling high in my stomach alternated with nausea so arresting I kept a bucket next to my laptop and considered taking a pregnancy test, even though I was 99 percent sure I wasn’t expecting. One day on the subway platform, I doubled over and let out a groan so pathetic it prompted a complete stranger to ask, “Are you all right?” Then I knew it was time to seek medical attention. New Yorkers don’t address strangers on the subway, I told myself. It’s like breaking the fourth wall. The next day, my primary care doctor told me I probably had an ulcer, a raw spot or sore in the lining of the stomach or small intestine. Here are some of the things I learned about ulcers during the odyssey that followed. ■ Anyone Can Get an Ulcer. Back in the 1980s, when doctors and most everyone else thought psychological stress or spicy foods led to ulcers, two Australian scientists discovered that the main culprit was actually a bacterium called Helicobacter pylori. That discovery eventually won them a Nobel Prize in 2005, and ushered in an era of using antibiotics to cure ulcers. But that didn’t wipe out ulcers altogether. Far from it. Indeed, my tribe of fellow sufferers are legion. Nearly 16 million adults nationwide reported having an ulcer in 2014,according to the Centers for Disease Control and Prevention’s National Center for Health Statistics. The largest group, roughly 6.2 million, were 45 to 64 years old. Those 18 to 44 accounted for 4.6 million, 65- to 74-year-olds for 2.6 million, and those 75 and older for 2.4 million. I got a blood test to see if I was infected with H. pylori; the test came back negative, so I didn’t need antibiotics. Regular use of nonsteroidal anti-inflammatory drugs, like ibuprofen or aspirin, can also lead to an ulcer, but I wasn’t taking those medicines. My ulcer turned out to be “idiopathic,” which is a fancy way of saying that doctors have no idea why it happened. © 2017 The New York Times Company

Keyword: Stress
Link ID: 23490 - Posted: 04.14.2017

By Pascal Wallisch One of psychologist Robert Zajonc’s lasting contributions to science is the “mere exposure effect,” or the observation that people tend to like things if they are exposed to them more often. Much of advertising is based on this notion. But it was sorely tested in late February 2015, when “the dress” broke the internet. Within days, most people were utterly sick of seeing or talking about it. I can only assume that now, two years later, you have very limited interest in being here. (Thank you for being here.) But the phenomenon continues to be utterly fascinating to vision scientists like me, and for good reason. The very existence of “the dress” challenged our entire understanding of color vision. Up until early 2015, a close reading of the literature could suggest that the entire field had gone somewhat stale—we thought we basically knew how color vision worked, more or less. The dress upended that idea. No one had any idea why some people see “the dress” differently than others—we arguably still don’t fully understand it. It was like discovering a new continent. Plus, the stimulus first arose in the wild (in England, no less), making it all the more impressive. (Most other stimuli used by vision science are generally created in labs.) Even outside of vision scientists, most people just assume everyone sees the world in the same way. Which is why it’s awkward when disagreements arise—it suggests one party either is ignorant, is malicious, has an agenda, or is crazy. We believe what we see with our own eyes more than almost anything else, which may explain the feuds that occurred when “the dress” first struck and science lacked a clear explanation for what was happening.

Keyword: Vision
Link ID: 23489 - Posted: 04.14.2017

By Andy Coghlan Using a virus to reprogram cells in the brain could be a radical way to treat Parkinson’s disease. People with Parkinson’s have difficulty controlling their movements due to the death of neurons that make dopamine, a brain signalling chemical. Transplants of fetal cells have shown promise for replacing these dead neurons in people with the disease, and a trial is currently under way. But the transplant tissue comes from aborted pregnancies, meaning it is in short supply, and some people may find this ethically difficult. Recipients of these cells have to take immunosuppressant drugs too. Ernest Arenas, at the Karolinska Institute in Stockholm, Sweden, and his team have found a new way to replace lost dopamine-making neurons. They injected a virus into the brains of mice whose dopamine neurons had been destroyed. This virus had been engineered to carry four genes for reprogramming astrocytes – the brain’s support cells – into dopamine neurons. Five weeks later, the team saw improvements in how the mice moved. “They walked better and their gait showed less asymmetry than controls,” says Arenas. This is the first study to show that reprogramming cells in the living brain can lead to such improvements, he says. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 23488 - Posted: 04.14.2017

Tina Hesman Saey Some Pakistani people are real knockouts, a new DNA study finds. Knockouts in this sense doesn’t refer to boxing or a stunning appearance, but to natural mutations that inactivate, or “knock out” certain genes. The study suggests that human knockouts could prove valuable evidence for understanding how genes work and for developing drugs. Among 10,503 adults participating in a heart disease study in Pakistan, 1,843 people have at least one gene of which both copies have been knocked out, researchers report online April 12 in Nature. Researchers also drew blood from many of the participants and used medical records to study more than 200 traits, such as heart rate, blood pressure and blood levels of sugar, cholesterol, hormones or other substances. Studying how the knockout mutations affect those traits and health could point to genes that are potentially safe and effective targets for new drugs. Combining genetic data with medical information will provide “a rich dataset for many applications,” says Robert Plenge, a human geneticist formerly with the pharmaceutical company Merck. Scientists have traditionally learned about genes’ roles by deleting the genes from mice and then cataloging abnormalities in how those mice developed and behaved. Such animal research will always be needed, but studies of people naturally lacking certain genes “will change the nature of the scientific investigation of the genetic basis of human disease,” Plenge wrote in a commentary in the same issue of Nature. Often, a person will inherit a broken copy of a gene from one parent and a healthy copy from the other. But 39 percent of the people in this study had parents who were closely related — often first cousins — increasing the odds of inheriting two mutant copies of a gene. Of this study’s 1,843 participants, 1,504 had both copies of a single gene knocked out. The rest had more than one gene knocked out, including one person in whom six genes were predicted to be completely nonfunctional. |© Society for Science & the Public 2000 - 2017.

Keyword: Genes & Behavior; Obesity
Link ID: 23487 - Posted: 04.13.2017

In two studies of mice, researchers showed that a drug, engineered to combat the gene that causes spinocerebellar ataxia type 2 (SCA2), might also be used to treat amyotrophic lateral sclerosis (ALS). Both studies were published in the journal Nature with funding from National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our results provide hope that we may one day be able to treat these devastating disorders,” said Stefan M. Pulst, M.D., Dr. Med., University of Utah, professor and chair of neurology and a senior author of one the studies. In 1996, Dr. Pulst and other researchers discovered that mutations in the ataxin 2 gene cause spinocerebellar ataxia type 2, a fatal inherited disorder that primarily damages a part of the brain called the cerebellum, causing patients to have problems with balance, coordination, walking and eye movements. For this study his team found that they could reduce problems associated with SCA2 by injecting mouse brains with a drug programmed to silence the ataxin 2 gene. In the accompanying study, researchers showed that injections of the same type of drug into the brains of mice prevented early death and neurological problems associated with ALS, a paralyzing and often fatal disorder. “Surprisingly, the ataxin 2 gene may act as a master key to unlocking treatments for ALS and other neurological disorders,” said Aaron Gitler, Ph.D., Stanford University, associate professor and senior author of the second study. In 2010, Dr. Gitler and colleagues discovered a link between ataxin 2 mutations and ALS.

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 23486 - Posted: 04.13.2017

By Simon Makin When the now-famous neurological patient Henry Molaison had his brain’s hippocampus surgically sectioned to treat seizures in 1953, science’s understanding of memory inadvertently received perhaps its biggest boost ever. Molaison lost the ability to form new memories of events, and his recollection of anything that had happened during the preceding year was severely impaired. Other types of memory such as learning physical skills were unaffected, suggesting the hippocampus specifically handles the recall of events—known as “episodic” memories. Further research on other patients with hippocampal damage confirmed recent memories are more impaired than distant ones. It appears the hippocampus provides temporary storage for new information whereas other areas may handle long-term memory. Events that we are later able to remember appear to be channeled for more permanent storage in the cortex (the outer layers of the brain responsible for higher functions such as planning and problem-solving). In the cortex these memories form gradually, becoming integrated with related information to build lasting knowledge about ourselves and the world. Episodic memories that are intended for long-term storage accumulate to form the “autobiographical” memory that is so essential for our sense of identity. Neuroscientists know a lot about how short-term memories are formed in the brain but the processes underlying long-term storage are still not well understood. © 2017 Scientific American,

Keyword: Learning & Memory
Link ID: 23485 - Posted: 04.13.2017

By Jyoti Madhusoodanan For three consecutive winters, starting in 2011, researchers at the University of Birmingham asked healthy men and women over the age of 65 to come in to clinics across the western Midlands in the U.K. for a seasonal influenza vaccination at specific times of day—either between 9 and 11 a.m., or between 3 and 5 p.m. Blood drawn a month later revealed that participants, who totaled nearly 300 over the three years, had higher levels of anti-flu antibodies if they’d received their vaccinations in the morning.1 The results suggested that daily rhythms of people’s bodies tweaked the vaccine’s effectiveness. Lead author Anna Phillips Whittaker had suspected as much, after observing similar trends in her studies on behavioral factors such as exercise that affect vaccination responses, and in the wake of a growing body of literature suggesting that a little timing can go a long way when it comes to health. Many hormones and immune signals are produced rhythmically in 24-hour cycles. Cortisol, for example, which is known to suppress inflammation and regulate certain T cell–mediated immune responses, peaks early in the morning and ebbs as the day progresses. Other facets of the immune system undergo similar cycles that could underlie the differences in antibody responses Phillips observed among people receiving the flu vaccine. Much more work is required to nail down the immune mechanisms responsible for such variation and exploit them appropriately, she says. But timing flu vaccine delivery would be straightforward to implement. “It’s such a simple, low-risk intervention that’s free to do, and could have massive implications for vulnerable populations.” © 1986-2017 The Scientist

Keyword: Biological Rhythms
Link ID: 23484 - Posted: 04.13.2017

By Niall Firth The firing of every neuron in an animal’s body has been recorded, live. The breakthrough in imaging the nervous system of a hydra – a tiny, transparent creature related to jellyfish – as it twitches and moves has provided insights into how such simple animals control their behaviour. Similar techniques might one day help us get a deeper understanding of how our own brains work. “This could be important not just for the human brain but for neuroscience in general,” says Rafael Yuste at Columbia University in New York City. Instead of a brain, hydra have the most basic nervous system in nature, a nerve net in which neurons spread throughout its body. Even so, researchers still know almost nothing about how the hydra’s few thousand neurons interact to create behaviour. To find out, Yuste and colleague Christophe Dupre genetically modified hydra so that their neurons glowed in the presence of calcium. Since calcium ions rise in concentration when neurons are active and fire a signal, Yuste and Dupre were able to relate behaviour to activity in glowing circuits of neurons. For example, a circuit that seems to be involved in digestion in the hydra’s stomach-like cavity became active whenever the animal opened its mouth to feed. This circuit may be an ancestor of our gut nervous system, the pair suggest. © Copyright Reed Business Information Ltd.

Keyword: Brain imaging; Evolution
Link ID: 23483 - Posted: 04.12.2017

By Partha Mitra Intricate, symmetric patterns, in tiles and stucco, cover the walls and ceilings of Alhambra, the “red fort,” the dreamlike castle of the medieval Moorish kings of Andalusia. Seemingly endless in variety, the two dimensionally periodic patterns are nevertheless governed by the mathematical principles of group theory and can be classified into a finite number of types: precisely seventeen, as shown by Russian crystallographer Evgraf Federov. The artists of medieval Andalusia are unlikely to have been aware of the mathematics of space groups, and Federov was unaware of the art of Alhambra. The two worlds met in the 1943 PhD thesis of Swiss astronomer Edith Alice Muller, who counted eleven of the seventeen planar groups in the adornments of the palace (more have been counted since). All seventeen space groups can also be found in the periodic patterns of Japanese wallpaper. Without conscious intent or explicit knowledge, the creations of artists across cultures at different times nevertheless had to conform to the constraints of periodicity in two dimensional Euclidean space, and were thus subject to mathematically precise theory. Does the same apply to the “endless forms most beautiful,” created by the biological evolutionary process? Are there theoretical principles, ideally ones which may be formulated in mathematical terms, underlying the bewildering complexity of biological phenomema? Without the guidance of such principles, we are only generating ever larger digital butterfly collections with ever better tools. In a recent article, Krakauer and colleagues argue that by marginalizing ethology, the study of adaptive behaviors of animals in their natural settings, modern neuroscience has lost a key theoretical framework. The conceptual framework of ethology contains in it the seeds of a future mathematical theory that might unify neurobiological complexity as Fedorov’s theory of wallpaper groups unified the patterns of the Alhambra. © 2017 Scientific American

Keyword: Miscellaneous
Link ID: 23482 - Posted: 04.12.2017