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Video Gamers Really Do See More: Gamers Capture More Information Faster for Visual Decision-Making

— Hours spent at the video gaming console not only train a player’s hands to work the buttons on the controller, they probably also train the brain to make better and faster use of visual input, according to Duke University researchers.

“Gamers see the world differently,” said Greg Appelbaum, an assistant professor of psychiatry in the Duke School of Medicine. “They are able to extract more information from a visual scene.”

It can be difficult to find non-gamers among college students these days, but from among a pool of subjects participating in a much larger study in Stephen Mitroff’s Visual Cognition Lab at Duke, the researchers found 125 participants who were either non-gamers or very intensive gamers.

Each participant was run though a visual sensory memory task that flashed a circular arrangement of eight letters for just one-tenth of a second. After a delay ranging from 13 milliseconds to 2.5 seconds, an arrow appeared, pointing to one spot on the circle where a letter had been. Participants were asked to identify which letter had been in that spot.

At every time interval, intensive players of action video games outperformed non-gamers in recalling the letter.

Earlier research by others has found that gamers are quicker at responding to visual stimuli and can track more items than non-gamers. When playing a game, especially one of the “first-person shooters,” a gamer makes “probabilistic inferences” about what he’s seeing — good guy or bad guy, moving left or moving right — as rapidly as he can.

Appelbaum said that with time and experience, the gamer apparently gets better at doing this. “They need less information to arrive at a probabilistic conclusion, and they do it faster.”

Both groups experienced a rapid decay in memory of what the letters had been, but the gamers outperformed the non-gamers at every time interval.

The visual system sifts information out from what the eyes are seeing, and data that isn’t used decays quite rapidly, Appelbaum said. Gamers discard the unused stuff just about as fast as everyone else, but they appear to be starting with more information to begin with.

The researchers examined three possible reasons for the gamers’ apparently superior ability to make probabilistic inferences. Either they see better, they retain visual memory longer or they’ve improved their decision-making.

Looking at these results, Applebaum said, it appears that prolonged memory retention isn’t the reason. But the other two factors might both be in play — it is possible that the gamers see more immediately, and they are better able make better correct decisions from the information they have available.

To get at this question, the researchers will need more data from brainwaves and MRI imagery to see where the brains of gamers have been trained to perform differently on visual tasks.

This study, which appears in the June edition of the journal Attention, Perception and Psychophysics, was supported by grants from the Army Research Office (54528LS), the Department of Homeland Security (HSHQDC-08-C-00100), DARPA (D12AP00025-002) and Nike Inc.

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The evolution of human intelligence

The nature and origins of hominid intelligence is a much-studied and much-debated topic, of natural interest to humans as the most successful and intelligent hominid species.

There is no universally accepted definition of intelligence, one definition is “the ability to reason, plan, solve problems, think abstractly, comprehend ideas and language, and learn.” The evolution of hominid intelligence can be traced over its course for the past 10 million years, and attributed to specific environmental challenges.

It is a misunderstanding of evolutionary theory, however, to see this as a necessary process, and an even greater misunderstanding to see it as one directed to a particular outcome.

There are primate species which have not evolved any greater degree of intelligence than they had 10 million years ago: this is because their particular environment has not demanded this particular adaptation of them.

Intelligence as an adaptation to the challenge of natural selection is no better or worse than any other adaptation, such as the speed of the cheetah or the venomous bite of the cobra.

It is, however, the only adaptation which has allowed a species to establish complete domination over the rest of the natural world.

Whether our species has yet acquired sufficient intelligence to manage this responsibility is a matter for debate.

For more information about the topic The evolution of human intelligence, read the full article at Wikipedia.org, or see the following related articles:

Note: This page refers to an article that is licensed under the GNU Free Documentation License. It uses material from the article The evolution of human intelligence at Wikipedia.org. See the Wikipedia copyright page for more details.

 

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Researchers Announce Discovery of Oldest-Known Fossil Primate Skeleton

— An international team of researchers has announced the discovery of the world’s oldest known fossil primate skeleton representing a previously unknown genus and species named Archicebus achilles. The fossil was unearthed from an ancient lake bed in central China’s Hubei Province, near the course of the modern Yangtze River. In addition to being the oldest known example of an early primate skeleton, the new fossil is crucial for illuminating a pivotal event in primate and human evolution — the evolutionary divergence between the lineage leading to modern monkeys, apes and humans (collectively known as anthropoids) on the one hand and that leading to living tarsiers on the other.

The scientific paper describing the discovery appears today in the journal Nature.

The international team of scientists who studied the skeleton of Archicebus was led by Dr. Xijun Ni of the Institute of Vertebrate Paleontology and Paleoanthropology (IVPP) at the Chinese Academy of Sciences in Beijing. Ni’s collaborators include Dr. Christopher Beard of the Carnegie Museum of Natural History in Pittsburgh; Dr. Daniel Gebo of Northern Illinois University; Dr. Marian Dagosto of Northwestern University in Chicago; Dr. Jin Meng and Dr. John Flynn of the American Museum of Natural History in New York; and Dr. Paul Tafforeau of the European Synchrotron Radiation Facility in Grenoble, France. According to Dr. Ni, “Archicebus marks the first time that we have a reasonably complete picture of a primate close to the divergence between tarsiers and anthropoids. It represents a big step forward in our efforts to chart the course of the earliest phases of primate and human evolution.”

Archicebus achilles

The skeleton of Archicebus is about 7 million years older than the oldest fossil primate skeletons known previously, which include Darwinius from Messel in Germany and Notharctus from the Bridger Basin in Wyoming. Furthermore, Archicebus belongs to an entirely separate branch of the primate evolutionary tree that lies much closer to the lineage leading to modern monkeys, apes and humans. Darwinius and Notharctus, on the other hand, are adapiform primates that are early relatives of living lemurs, the most distant branch of the primate family tree with respect to humans and other anthropoids.

Dr. Christopher Beard, whose earlier work on Eosimias and other fossil primates from China and Myanmar has placed Asia at the center of early primate evolution, said that, “Archicebus differs radically from any other primate, living or fossil, known to science. It looks like an odd hybrid with the feet of a small monkey, the arms, legs and teeth of a very primitive primate, and a primitive skull bearing surprisingly small eyes. It will force us to rewrite how the anthropoid lineage evolved.”

Statistical analyses aimed at reconstructing how much an adult Archicebus would have weighed in life show that it was slightly smaller than the smallest living primates, which are pygmy mouse lemurs from Madagascar. Archicebus would have weighed about 20-30 grams (~ 1 ounce). Dr. Daniel Gebo, an expert on the evolution of body anatomy in primates, said that, “The tiny size and very basal evolutionary position of Archicebus support the idea that the earliest primates, as well as the common ancestor of tarsiers and anthropoids, were miniscule. This overturns earlier ideas suggesting that the earliest members of the anthropoid lineage were quite large, the size of modern monkeys.”

Dr. Marian Dagosto notes that, “Even though Archicebus appears to be a very basal member of the tarsier lineage, it resembles early anthropoids in several features, including its small eyes and monkey-like feet. It suggests that the common ancestor of tarsiers and anthropoids was in some ways more similar than most scientists have thought.”

The evolutionary relationships among primates and their potential relatives, and among the major lineages within the Primate order have been debated intensively for many years. “To test these different hypotheses and determine the phylogenetic position of the new primate, we developed a massive data matrix including more than 1000 anatomical characters and scored for 157 mammals,” said Dr. Jin Meng.

The new fossil takes its name from the Greek arche (meaning beginning or first; the same root as archaeology) and the Greek kebos (meaning long-tailed monkey). The species name achilles (derived from the mythological Greek warrior achilles) highlights the new fossil’s unusual ankle anatomy.

Archicebus: exhumed and digitally resurrected

The fossil was recovered from sedimentary rock strata that were deposited in an ancient lake roughly 55 million years ago, during the early part of the Eocene epoch. This was an interval of global “greenhouse” conditions, when much of the world was shrouded in tropical rainforests and palm trees grew as far north as Alaska. Like most other fossils recovered from ancient lake strata, the skeleton of Archicebus was found by splitting apart the thin layers of rock containing the fossil. As a result, the skeleton of Archicebus is now preserved in two complementary pieces called a “part” and a “counterpart,” each of which contain elements of the actual skeleton as well as impressions of bones from the other side.

In order to study the entire fossil, the scientific team first had to scan the specimen at ultra high resolution using the state-of-the-art facilities of the European Synchrotron Radiation Facility in Grenoble, France. Three-dimensional digital reconstruction of the fossil using the synchrotron scans allowed the team of scientists to study the tiny, fragile skeleton of Archicebus in intricate detail. “During the past few years, we at the ESRF have developed the technology to look at those parts of the fossil that are still buried in the rock at a level of detail that is unique in the world. Speaking virtually, we made the skeleton stand up,” said Dr. Paul Tafforeau, a leading expert in developing paleontological applications of highly sophisticated Synchrotron CT scanning.

“People may see this simply as another discovery of a well preserved fossil, but to reveal the remarkable secrets that have been hidden in the rock for millions of years, we undertook extensive work, applied state-of-the-art technology, and intensive international cooperation took place behind the scenes at several museums. It took us ten years,” added Dr. John Flynn, dean of the Richard Gilder Graduate School and curator of the American Museum of Natural History

 

This is an artist impression of Archicebus achilles in its natural habitat of trees. (Credit: CAS/Xijun Ni)

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Menopause May Be an Unintended Outcome of Men’s Preference for Younger Mates

— After decades of laboring under other theories that never seemed to add up, a team led by biologist Rama Singh has concluded that what causes menopause in women is men.

Singh, an evolutionary geneticist, backed by computer models developed by colleagues Jonathan Stone and Richard Morton, has determined that menopause is actually an unintended outcome of natural selection — the result of its effects having become relaxed in older women.

Over time, human males have shown a preference for younger women in selecting mates, stacking the Darwinian deck against continued fertility in older women, the researchers have found.

“In a sense it is like aging, but it is different because it is an all-or-nothing process that has been accelerated because of preferential mating,” says Singh, a professor in McMaster’s Department of Biology whose research specialties include the evolution of human diversity.

Stone is an associate professor in the Department of Biology and associate director of McMaster’s Origins Institute, whose themes include the origins of humanity, while Morton is a professor emeritus in Biology.

While conventional thinking has held that menopause prevents older women from continuing to reproduce, in fact, the researchers’ new theory says it is the lack of reproduction that has given rise to menopause.

Their work appears in the online, open-access journal PLOS Computational Biology.

Menopause is believed to be unique to humans, but no one had yet been able to offer a satisfactory explanation for why it occurs, Singh says.

The prevailing “grandmother theory” holds that women have evolved to become infertile after a certain age to allow them to assist with rearing grandchildren, thus improving the survival of kin. Singh says that does not add up from an evolutionary perspective.

“How do you evolve infertility? It is contrary to the whole notion of natural selection. Natural selection selects for fertility, for reproduction — not for stopping it,” he says.

The new theory holds that, over time, competition among men of all ages for younger mates has left older females with much less chance of reproducing. The forces of natural selection, Singh says, are concerned only with the survival of the species through individual fitness, so they protect fertility in women while they are most likely to reproduce.

After that period, natural selection ceases to quell the genetic mutations that ultimately bring on menopause, leaving women not only infertile, but also vulnerable to a host of health problems.

“This theory says that natural selection doesn’t have to do anything,” Singh says. “If women were reproducing all along, and there were no preference against older women, women would be reproducing like men are for their whole lives.”

The development of menopause, then, was not a change that improved the survival of the species, but one that merely recognized that fertility did not serve any ongoing purpose beyond a certain age.

For the vast majority of other animals, fertility continues until death, Singh explains, but women continue to live past their fertility because men remain fertile throughout their lives, and longevity is not inherited by gender.

Singh points out that if women had historically been the ones to select younger mates, the situation would have been reversed, with men losing fertility.

The consequence of menopause, however, is not only lost fertility for women, but an increased risk of illness and death that arises with hormonal changes that occur with menopause. Singh says a benefit of the new research could be to suggest that if menopause developed over time, that ultimately it could also be reversed.

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A Turbocharger for Nerve Cells: Key Mechanism Boosts the Signaling Function of Neurons in Brain

— Locating a car that’s blowing its horn in heavy traffic, channel-hopping between football and a thriller on TV without losing the plot, and not forgetting the start of a sentence by the time we have read to the end — we consider all of these to be normal everyday functions. They enable us to react to fast-changing circumstances and to carry out even complex activities correctly. For this to work, the neuron circuits in our brain have to be very flexible. Scientists working under the leadership of neurobiologists Nils Brose and Erwin Neher at the Max Planck Institutes of Experimental Medicine and Biophysical Chemistry in Göttingen have now discovered an important molecular mechanism that turns neurons into true masters of adaptation.

Neurons communicate with each other by means of specialised cell-to-cell contacts called synapses. First, an emitting neuron is excited and discharges chemical messengers known as neurotransmitters. These signal molecules then reach the receiving cell and influence its activation state. The transmitter discharge process is highly complex and strongly regulated. Its protagonists are synaptic vesicles, small blisters surrounded by a membrane, which are loaded with neurotransmitters and release them by fusing with the cell membrane. In order to be able to respond to stimulation at any time by releasing transmitters, a neuron must have a certain amount of vesicles ready to go at each of its synapses. Brose has been studying the molecular foundations of this stockpiling for years.

The problem is not merely academic. “The number of immediately releasable vesicles at a synapse determines its reliability,” explains Brose. “If there are too few and they are replenished too slowly, the corresponding synapse becomes tired very quickly in conditions of repeated activation. The opposite applies when a synapse can quickly top up its immediately available vesicles under pressure. In fact, such a synapse may even improve with constant activation.”

This synaptic adaptability can be observed in practically all neurons. It is known as short-term plasticity and is indispensable for a large number of extremely important brain processes. Without it, we would not be able to localise sounds, mental maths would be impossible, and the speed and flexibility with which we can alter our behaviour and turn our attention to new goals would be lost.

Some years ago, Brose and his team discovered a protein with the cryptic name of Munc13. Not only is this protein indispensable for the replenishment of vesicles for immediate release at synapses; neuron activity regulates it in such a way that the fresh supply of vesicles can be adjusted in line with demand. This regulation occurs by means of a complex consisting of the signal protein calmodulin and calcium ions that build up in the synapses during intense neuron activity.

“Our earlier work on individual neurons in culture dishes showed that the calcium-calmodulin complex activates Munc13 and consequently ensures that immediately releasable vesicles are replenished faster,” says Noa Lipstein, an Israeli guest scientist in Brose’s lab. “But many colleagues were not convinced that this process also played a role in neurons in the intact brain.”

So Lipstein and her Japanese colleague Takeshi Sakaba created a mutant mouse with genetically altered Munc13 proteins that could not be activated by calcium-calmodulin complexes. The two neurophysiologists first studied the effects of this genetic manipulation on synapses involved in the localisation of sound, which are typically activated several hundred times every second. “Our study shows that the sustained efficiency of synapses in intact neuron networks is critically dependent on the activation of Munc13 by calcium-calmodulin complexes,” explains Lipstein.

The Göttingen-based scientists are convinced of the significance of their study. After all, leading neuroscientists of the past described the calcium sensor responsible for synaptic short-term plasticity and its target protein as the Holy Grail. “I am confident that we have discovered a key molecular mechanism of short-term plasticity that plays a role in all synapses in the brain, and not only in cultivated neurons, as many colleagues believed,” affirms Lipstein. And if she is, in fact, proved right about the interpretation of her findings, Munc13 could even be an ideal pharmacological target for drugs that influence brain function.

 

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Gustatory Tug-Of-War Key to Whether Salty Foods Taste Good

As anyone who’s ever mixed up the sugar and salt while baking knows, too much of a good thing can be inedible. What hasn’t been clear, though, is how our tongues and brains can tell when the saltiness of our food has crossed the line from yummy to yucky — or, worse, something dangerous.

 

Now researchers at the Johns Hopkins University School of Medicine and the University of California, Santa Barbara report that in fruit flies, at least, that process is controlled by competing input from two different types of taste-sensing cells: one that attracts flies to salty foods, and one that repels them. Results of their research are described in the June 14 issue of Science.

“The body needs sodium for crucial tasks like putting our muscles into action and letting brain cells communicate with each other, but too much sodium will cause heart problems and other health concerns,” explains Yali Zhang, Ph.D., who led the recent study as part of his graduate work at Johns Hopkins. To maintain health, Zhang says, humans and other animals perceive foods with relatively low salt concentrations as tasty, but avoid eating things with very high salt content.

To find out how the body pulls off this balancing act, Zhang worked with his adviser, Craig Montell, Ph.D., a leading scientist in the field of sensory biology and now a professor at UC Santa Barbara, and graduate student Jinfei Ni to get an up-close view of the fly equivalent of a tongue: its long, curly proboscis. They zoomed in on the proboscis’ so-called sensilla, hair-like structures that serve as the fly’s taste buds.

Previous research had identified several distinct types of sensilla, one of which attracts flies to a taste, while another repels them. Zhang loaded an electrode with a mixture of water and different concentrations of salt, and touched it to each type of sensilla, using the same electrode to detect the electrical signals fired by the sensilla in response to the salt. He found that up to a point, increasing salt concentrations would produce increasingly strong electrical signals in the attractive sensilla, but after that point, the electrical signals dropped off as the concentration continued to rise. In contrast, the repellant sensilla gave off stronger and stronger electrical signals as the salt concentration rose.

Zhang said the team realized that the taste receptor cells in the attractive and repellant sensilla were likely locked in a tug-of-war over whether the fly would continue eating or go off in search of better food. At lower concentrations, the attractive signal would dominate the repellant signal, sending a cumulative message of “yum!” But at high concentrations, the repellant signal would overwhelm the attractive signal, sending the signal “yuck!”

To further test this conclusion, the team mutated a gene called Ir76b that codes for a protein they suspected was involved in the action of the attractive sensilla. To their great surprise, Zhang found that loss of Ir76b function caused flies to avoid the otherwise attractive low-salt food. The reason for this, he found, was that mutating Ir76b only impaired the responses of the attractive sensilla, leaving the repellant sensilla to win the day. Looking further into the action of the protein produced by Ir76b, the team found that it is a channel with a pore that lets sodium pass into the taste cells of the sensilla. Unlike most pores of this type, which have gates that must be opened by certain key chemical or voltage changes in their environment, this gate is always open, meaning that at any time, sodium can flood into the cell and spark an electrical signal. “It’s an unusual setup, but it makes sense because the local sodium concentration outside taste receptor cells appears to be a lot lower than that surrounding most cells. The taste receptor cells don’t need to keep the gate closed to protect themselves from that excess sodium,” Zhang says.

Long before we humans started worrying about regulating our sodium intake, it was a problem all animals had to deal with, Zhang says, and thus his research has implications for other animals, including humans. Although animal taste buds and insect sensilla have different makeups, he suspects that the tug-of-war principle may apply to salt-tasting throughout the animal kingdom, given that different species behave similarly when it comes to salty foods. Identifying the low-salt sensor in humans could be particularly useful, he says, as it could lead to the development of better salt substitutes to help people control their sodium intake.

This study was funded by the National Institute on Deafness and Other Communication Disorders (DC007864).

An illustration shows how flies taste salt via channels made up of the protein IR76b, which let sodium ions into the cells that sense taste. (Credit: Tim Phelps/Johns Hopkins University School of Medicine)

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Memory-Boosting Chemical Identified in Mice: Cell Biologists Find Molecule Targets a Key Biological Pathway

— Memory improved in mice injected with a small, drug-like molecule discovered by UCSF San Francisco researchers studying how cells respond to biological stress

The same biochemical pathway the molecule acts on might one day be targeted in humans to improve memory, according to the senior author of the study, Peter Walter, PhD, UCSF professor of biochemistry and biophysics and a Howard Hughes Investigator.

The discovery of the molecule and the results of the subsequent memory tests in mice were published in eLife, an online scientific open-access journal, on May 28, 2013.

In one memory test included in the study, normal mice were able to relocate a submerged platform about three times faster after receiving injections of the potent chemical than mice that received sham injections.

The mice that received the chemical also better remembered cues associated with unpleasant stimuli — the sort of fear conditioning that could help a mouse avoid being preyed upon.

Notably, the findings suggest that despite what would seem to be the importance of having the best biochemical mechanisms to maximize the power of memory, evolution does not seem to have provided them, Walter said.

“It appears that the process of evolution has not optimized memory consolidation; otherwise I don’t think we could have improved upon it the way we did in our study with normal, healthy mice,” Walter said.

The memory-boosting chemical was singled out from among 100,000 chemicals screened at the Small Molecule Discovery Center at UCSF for their potential to perturb a protective biochemical pathway within cells that is activated when cells are unable to keep up with the need to fold proteins into their working forms.

However, UCSF postdoctoral fellow Carmela Sidrauski, PhD, discovered that the chemical acts within the cell beyond the biochemical pathway that activates this unfolded protein response, to more broadly impact what’s known as the integrated stress response. In this response, several biochemical pathways converge on a single molecular lynchpin, a protein called eIF2 alpha.

Scientists have known that in organisms ranging in complexity from yeast to humans different kinds of cellular stress — a backlog of unfolded proteins, DNA-damaging UV light, a shortage of the amino acid building blocks needed to make protein, viral infection, iron deficiency — trigger different enzymes to act downstream to switch off eIF2 alpha.

“Among other things, the inactivation of eIF2 alpha is a brake on memory consolidation,” Walter said, perhaps an evolutionary consequence of a cell or organism becoming better able to adapt in other ways.

Turning off eIF2 alpha dials down production of most proteins, some of which may be needed for memory formation, Walter said. But eIF2 alpha inactivation also ramps up production of a few key proteins that help cells cope with stress.

Study co-author Nahum Sonenberg, PhD, of McGill University previously linked memory and eIF2 alpha in genetic studies of mice, and his lab group also conducted the memory tests for the current study.

The chemical identified by the UCSF researchers is called ISRIB, which stands for integrated stress response inhibitor. ISRIB counters the effects of eIF2 alpha inactivation inside cells, the researchers found.

“ISRIB shows good pharmacokinetic properties [how a drug is absorbed, distributed and eliminated], readily crosses the blood-brain barrier, and exhibits no overt toxicity in mice, which makes it very useful for studies in mice,” Walter said. These properties also indicate that ISRIB might serve as a good starting point for human drug development, according to Walter.

Walter said he is looking for scientists to collaborate with in new studies of cognition and memory in mouse models of neurodegenerative diseases and aging, using ISRIB or related molecules.

In addition, chemicals such as ISRIB could play a role in fighting cancers, which take advantage of stress responses to fuel their own growth, Walter said. Walter already is exploring ways to manipulate the unfolded protein response to inhibit tumor growth, based on his earlier discoveries.

At a more basic level, Walter said, he and other scientists can now use ISRIB to learn more about the role of the unfolded protein response and the integrated stress response in disease and normal physiology.

Additional UCSF study authors are Diego Acosta-Alvear, PhD, Punitha Vedantham, PhD, Brian Hearn, PhD, Ciara Gallagher, PhD, Kenny Ang, PhD, Chris Wilson, PhD, Voytek Okreglak, PhD, Byron Hann, MD, PhD, Michelle Arkin, PhD, and Adam Renslo, PhD. Other authors are Han Li, PhD, and Avi Ashkenazi, PhD, from Genentech; and, Karim Nader, PhD, Karine Gamache, and Arkady Khoutorsky, PhD, from McGill University. The study was funded by the Howard Hughes Medical Institute.

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