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Thursday, November 24, 2011

Qualcomm challenges LCDs through new e-reader




A new electronic display is poised to challenge power-hungry LCDs after U.S. mobile chip maker Qualcomm Inc. teamed up with a South Korean bookseller to introduce a new e-reader.
The "Kyobo eReader"

A new electronic display is poised to challenge power-hungry LCDs after US mobile chip maker Qualcomm Inc. teamed up with a South Korean bookseller to introduce a new e-reader. The "Kyobo eReader" was unveiled this week in Seoul and will reach South Korean consumers as early as December 1, Kyobo Book Centre officials said Thursday. The e-reader features Qualcomm's 1.0 GHz "Snapdragon" processor, a custom Kyobo application based on Android and a 5.7 inch "XGA" mirasol display.

The mirasol display uses ambient light instead of its own in much the same way that a peacock's plumage gets its scintillating hues. Qualcomm's mirasols have already been used in a few Chinese and South Korean phones, and in an MP3 player on the US market. The display contains tiny mirrors that consume power only when they're moving, easing battery drain. Mirasol displays also quickly change from one image to the next and show video.

The global market for e-readers is dominated by bright LCDs and grayscale "e-ink" screens. LCDs consume relatively more battery power while e-ink screens are slow to refresh. The introduction of the e-reader jointly developed by Qualcomm and Kyobo signals increasing competition in the global market for tablets.

US online retailer Amazon.com Inc. and bookseller Barnes & Noble Inc. have recently released tablets of their own, Kindle Fire and Nook Tablet, and are challenging Apple's iPad in pricing.



Qualcomm CEO Paul Jacobs noted South Koreans' near-100 percent literacy rate and digital reading skills during a launching ceremony in Seoul on Tuesday, according to the San Diego-based company. Fifteen-year-old South Koreans scored highest in their ability to absorb information from digital devices, according to a 2009 study by the Organization for Economic Cooperation and Development. Over 80 percent of households in South Korea have broadband Internet access. The e-reader featuring the mirasol display will be priced at 349,000 won, or $302, said Seoul-based Kyobo, South Korea's largest bookseller.


Tuesday, November 22, 2011

How brains benefit from meditation




Experienced meditators seem to be able switch off areas of the brain associated with daydreaming as well as psychiatric disorders such as autism and schizophrenia, according to a new brain imaging study by Yale researchers.


Experienced meditators seem to switch off areas of the brain
associated with wandering thoughts, anxiety and some
psychiatric disorders such as schizophrenia. Researchers
used fMRI scans to determine how the brains of meditators
differed from subjects who were not meditating. The areas
shaded in blue highlight areas of decreased activity in the
brains of meditators. Credit: courtesy of yale

Meditation's ability to help people stay focused on the moment has been associated with increased happiness levels, said Judson A. Brewer, assistant professor of psychiatry and lead author of the study published the week of Nov. 21 in the Proceedings of the National Academy of Sciences. Understanding how meditation works will aid investigation into a host of diseases, he said.

"Meditation has been shown to help in variety of health problems, such as helping people quit smoking, cope with cancer, and even prevent psoriasis," Brewer said.

The Yale team conducted functional magnetic resonance imaging scans on both experienced and novice meditators as they practiced three different meditation techniques.

They found that experienced meditators had decreased activity in areas of the brain called the default mode network, which has been implicated in lapses of attention and disorders such as anxiety, attention deficit and hyperactivity disorder, and even the buildup of beta amyloid plaques in Alzheimer's disease. The decrease in activity in this network, consisting of the medial prefrontal and posterior cingulate cortex, was seen in experienced meditators regardless of the type of meditation they were doing.

The scans also showed that when the default mode network was active, brain regions associated with self-monitoring and cognitive control were co-activated in experienced meditators but not novices. This may indicate that meditators are constantly monitoring and suppressing the emergence of "me" thoughts, or mind-wandering. In pathological forms, these states are associated with diseases such as autism and schizophrenia.

The meditators did this both during meditation, and also when just resting — not being told to do anything in particular. This may indicate that meditators have developed a "new" default mode in which there is more present-centered awareness, and less "self"-centered, say the researchers. "Meditation's ability to help people stay in the moment has been part of philosophical and contemplative practices for thousands of years," Brewer said. "Conversely, the hallmarks of many forms of mental illness is a preoccupation with one's own thoughts, a condition meditation seems to affect. This gives us some nice cues as to the neural mechanisms of how it might be working clinically."


Thursday, November 17, 2011

Better Batteries: New Technology Improves Both Energy Capacity and Charge Rate in Rechargeable Batteries



Imagine a cellphone battery that stayed charged for more than a week and recharged in just 15 minutes. That dream battery could be closer to reality thanks to Northwestern University research.
New research could lead to rechargeable lithium-ion
batteries that hold a charge up to 10 times greater than
current technology and that charge 10 times faster than
current batteries. (Credit: © janaka Dharmasena / Fotolia)

A team of engineers has created an electrode for lithium-ion batteries -- rechargeable batteries such as those found in cellphones and iPods -- that allows the batteries to hold a charge up to 10 times greater than current technology. Batteries with the new electrode also can charge 10 times faster than current batteries.

The researchers combined two chemical engineering approaches to address two major battery limitations -- energy capacity and charge rate -- in one fell swoop. In addition to better batteries for cellphones and iPods, the technology could pave the way for more efficient, smaller batteries for electric cars.

The technology could be seen in the marketplace in the next three to five years, the researchers said.

A paper describing the research is published by the journal Advanced Energy Materials.

"We have found a way to extend a new lithium-ion battery's charge life by 10 times," said Harold H. Kung, lead author of the paper. "Even after 150 charges, which would be one year or more of operation, the battery is still five times more effective than lithium-ion batteries on the market today."

Kung is professor of chemical and biological engineering in the McCormick School of Engineering and Applied Science. He also is a Dorothy Ann and Clarence L. Ver Steeg Distinguished Research Fellow.

Lithium-ion batteries charge through a chemical reaction in which lithium ions are sent between two ends of the battery, the anode and the cathode. As energy in the battery is used, the lithium ions travel from the anode, through the electrolyte, and to the cathode; as the battery is recharged, they travel in the reverse direction.

With current technology, the performance of a lithium-ion battery is limited in two ways. Its energy capacity -- how long a battery can maintain its charge -- is limited by the charge density, or how many lithium ions can be packed into the anode or cathode. Meanwhile, a battery's charge rate -- the speed at which it recharges -- is limited by another factor: the speed at which the lithium ions can make their way from the electrolyte into the anode.

In current rechargeable batteries, the anode -- made of layer upon layer of carbon-based graphene sheets -- can only accommodate one lithium atom for every six carbon atoms. To increase energy capacity, scientists have previously experimented with replacing the carbon with silicon, as silicon can accommodate much more lithium: four lithium atoms for every silicon atom. However, silicon expands and contracts dramatically in the charging process, causing fragmentation and losing its charge capacity rapidly.

Currently, the speed of a battery's charge rate is hindered by the shape of the graphene sheets: they are extremely thin -- just one carbon atom thick -- but by comparison, very long. During the charging process, a lithium ion must travel all the way to the outer edges of the graphene sheet before entering and coming to rest between the sheets. And because it takes so long for lithium to travel to the middle of the graphene sheet, a sort of ionic traffic jam occurs around the edges of the material.

Now, Kung's research team has combined two techniques to combat both these problems. First, to stabilize the silicon in order to maintain maximum charge capacity, they sandwiched clusters of silicon between the graphene sheets. This allowed for a greater number of lithium atoms in the electrode while utilizing the flexibility of graphene sheets to accommodate the volume changes of silicon during use.

"Now we almost have the best of both worlds," Kung said. "We have much higher energy density because of the silicon, and the sandwiching reduces the capacity loss caused by the silicon expanding and contracting. Even if the silicon clusters break up, the silicon won't be lost."

Kung's team also used a chemical oxidation process to create miniscule holes (10 to 20 nanometers) in the graphene sheets -- termed "in-plane defects" -- so the lithium ions would have a "shortcut" into the anode and be stored there by reaction with silicon. This reduced the time it takes the battery to recharge by up to 10 times.

This research was all focused on the anode; next, the researchers will begin studying changes in the cathode that could further increase effectiveness of the batteries. They also will look into developing an electrolyte system that will allow the battery to automatically and reversibly shut off at high temperatures -- a safety mechanism that could prove vital in electric car applications.

The Energy Frontier Research Center program of the U.S. Department of Energy, Basic Energy Sciences, supported the research.

The paper is titled "In-Plane Vacancy-Enabled High-Power Si-Graphene Composite Electrode for Lithium-Ion Batteries." Other authors of the paper are Xin Zhao, Cary M. Hayner and Mayfair C. Kung, all from Northwestern.

Wednesday, November 16, 2011

Mimicking the Brain -- In Silicon: New Computer Chip Models How Neurons Communicate With Each Other at Synapses




For decades, scientists have dreamed of building computer systems that could replicate the human BRAIN's talent for learning new tasks.


Researchers have taken a major step toward that goal by designing a computer chip that mimics how the brain's neurons adapt in response to new information. (Credit: MIT)

MIT researchers have now taken a major step toward that goal by designing a computer chip that mimics how the brain's neurons adapt in response to new information. This phenomenon, known as plasticity, is believed to underlie many brain functions, including learning and memory.

With about 400 transistors, the silicon chip can simulate the activity of a single brain synapse -- a connection between two neurons that allows information to flow from one to the other. The researchers anticipate this chip will help neuroscientists learn much more about how the brain works, and could also be used in neural prosthetic devices such as artificial retinas, says Chi-Sang Poon, a principal research scientist in the Harvard-MIT Division of Health Sciences and Technology.

Poon is the senior author of a paper describing the chip in the Proceedings of the National Academy of Sciences the week of Nov. 14. Guy Rachmuth, a former postdoc in Poon's lab, is lead author of the paper. Other authors are Mark Bear, the Picower Professor of Neuroscience at MIT, and Harel Shouval of the University of Texas Medical School.

Modeling synapses

There are about 100 billion neurons in the brain, each of which forms synapses with many other neurons. A synapse is the gap between two neurons (known as the presynaptic and postsynaptic neurons). The presynaptic neuron releases neurotransmitters, such as glutamate and GABA, which bind to receptors on the postsynaptic cell membrane, activating ion channels. Opening and closing those channels changes the cell's electrical potential. If the potential changes dramatically enough, the cell fires an electrical impulse called an action potential.

All of this synaptic activity depends on the ion channels, which control the flow of charged atoms such as sodium, potassium and calcium. Those channels are also key to two processes known as long-term potentiation (LTP) and long-term depression (LTD), which strengthen and weaken synapses, respectively.

The MIT researchers designed their computer chip so that the transistors could mimic the activity of different ion channels. While most chips operate in a binary, on/off mode, current flows through the transistors on the new brain chip in analog, not digital, fashion. A gradient of electrical potential drives current to flow through the transistors just as ions flow through ion channels in a cell.

"We can tweak the parameters of the circuit to match specific ion channels," Poon says. "We now have a way to capture each and every ionic process that's going on in a neuron."

Previously, researchers had built circuits that could simulate the firing of an action potential, but not all of the circumstances that produce the potentials. "If you really want to mimic brain function realistically, you have to do more than just spiking. You have to capture the intracellular processes that are ion channel-based," Poon says.

The new chip represents a "significant advance in the efforts to incorporate what we know about the biology of neurons and synaptic plasticity onto CMOS [complementary metal-oxide-semiconductor] chips," says Dean Buonomano, a professor of neurobiology at the University of California at Los Angeles, adding that "the level of biological realism is impressive.

The MIT researchers plan to use their chip to build systems to model specific neural functions, such as the visual processing system. Such systems could be much faster than digital computers. Even on high-capacity computer systems, it takes hours or days to simulate a simple brain circuit. With the analog chip system, the simulation is even faster than the biological system itself.

Another potential application is building chips that can interface with biological systems. This could be useful in enabling communication between neural prosthetic devices such as artificial retinas and the brain. Further down the road, these chips could also become building blocks for artificial intelligence devices, Poon says.

Debate resolved

The MIT researchers have already used their chip to propose a resolution to a longstanding debate over how LTD occurs.

One theory holds that LTD and LTP depend on the frequency of action potentials stimulated in the postsynaptic cell, while a more recent theory suggests that they depend on the timing of the action potentials' arrival at the synapse.

Both require the involvement of ion channels known as NMDA receptors, which detect postsynaptic activation. Recently, it has been theorized that both models could be unified if there were a second type of receptor involved in detecting that activity. One candidate for that second receptor is the endo-cannabinoid receptor.

Endo-cannabinoids, similar in structure to marijuana, are produced in the brain and are involved in many functions, including appetite, pain sensation and memory. Some neuroscientists had theorized that endo-cannabinoids produced in the postsynaptic cell are released into the synapse, where they activate presynaptic endo-cannabinoid receptors. If NMDA receptors are active at the same time, LTD occurs.

When the researchers included on their chip transistors that model endo-cannabinoid receptors, they were able to accurately simulate both LTD and LTP. Although previous experiments supported this theory, until now, "nobody had put all this together and demonstrated computationally that indeed this works, and this is how it works," Poon says.

Monday, November 14, 2011

GPS-Enabled Shoes to Help Track Down Grandpa



The next frontier for GPS? Footwear for those suffering from Alzheimer's.
New GPS-enabled shoes are meant to provide safety and security for all walks of life.

Shoes with built-in GPS could be coming to a store near you this month. AFP reports that 3,000 of the shoes, a collaboration between GTX Corp and Aetrex Worldwide, have shipped and will retail at about $300 per pair.

What, exactly, you may wonder, is a possible use case for a GPS-enabled shoe? There are several, apparently.

MSNBC reports that another effort, from something called "The Aphrodite Project" (URL: SexyGpsShoes.com) involves GPS-equipped sandals intended to keep prostitutes safe. "Our first shoe...was inspired by the prostitutes of ancient Greece and Rome, who enticed clients with their flutes and sandals that left 'follow me' footprints in the earth," write the founders of The Aphrodite Project.

Another use case could be for missing children: GTX Corp first got the idea for the shoes, reportedly, in the wake of the 2002 Elizabeth Smart case. The idea was that if a child were kidnapped or wandered off while wearing the GPS shoes, you could easily track him or her down. Call it a digitally enabled AMBER alert.

Eventually, GTX Corp and Aetrex came to settle on another "use case" entirely: the Alzheimer's patient. Those suffering from early-stage Alzheimer's will often wander off and become lost or confused. "They go for a walk and they can get lost for days," Andrew Carle, a professor of Health and Human Services at George Mason College (and an adviser on the GPS shoe project), told AFP. It is, sadly, a growth market. Five million Americans have Alzheimer's; as many as 20 million may come to suffer from it in the near future. The majority of Alzheimer's patients exhibit wandering behavior at some point; if not found within a few days, these sufferers can become severely injured or even die from dehydration.

Much like with similar technologies that allow you to essentially helicopter parent your pet, the GTX/Aetrex shoe allows caretakers or family members to set up a geofence for safe wandering; if the wearer strays beyond the geofence, an alert will go out. But aren't there easier ways to get a GPS unit on a senior? Carle claimed that paranoia often prevents Alzheimer's patients from wearing, say, a wristwatch with a GPS unit. "If it's a wristwatch and it's not their wristwatch," he said, "they will take it off. So you have to hide it."

It isn't the first time caretakers have resorted to a bit of ingenuity to aid in caring for those with Alzheimer's. Listen, for example, to this amazing story care of Radiolab about a German nursing home that built a fake bus stop to convince its wandering Alzheimer's sufferers to simply sit and wait.

Sunday, November 13, 2011

A revolution in knot theory


In the 19th century, Lord Kelvin made the inspired guess that elements are knots in the "ether". Hydrogen would be one kind of knot, oxygen a different kind of knot---and so forth throughout the periodic table of elements. This idea led Peter Guthrie Tait to prepare meticulous and quite beautiful tables of knots, in an effort to elucidate when two knots are truly different. From the point of view of physics, Kelvin and Tait were on the wrong track: the atomic viewpoint soon made the theory of ether obsolete. But from the mathematical viewpoint, a gold mine had been discovered: The branch of mathematics now known as "knot theory" has been burgeoning ever since.
This knot has Gauss code O1U2O3U1O2U3.
Credit: Graphic by Sam Nelson.

In his article "The Combinatorial Revolution in Knot Theory", to appear in the December 2011 issue of the Notices of the AMS, Sam Nelson describes a novel approach to knot theory that has gained currency in the past several years and the mysterious new knot-like objects discovered in the process.

As sailors have long known, many different kinds of knots are possible; in fact, the variety is infinite. A *mathematical* knot can be imagined as a knotted circle: Think of a pretzel, which is a knotted circle of dough, or a rubber band, which is the "un-knot" because it is not knotted. Mathematicians study the patterns, symmetries, and asymmetries in knots and develop methods for distinguishing when two knots are truly different.

Mathematically, one thinks of the string out of which a knot is formed as being a one-dimensional object, and the knot itself lives in three-dimensional space. Drawings of knots, like the ones done by Tait, are projections of the knot onto a two-dimensional plane. In such drawings, it is customary to draw over-and-under crossings of the string as broken and unbroken lines. If three or more strands of the knot are on top of each other at single point, we can move the strands slightly without changing the knot so that every point on the plane sits below at most two strands of the knot. A planar knot diagram is a picture of a knot, drawn in a two-dimensional plane, in which every point of the diagram represents at most two points in the knot. Planar knot diagrams have long been used in mathematics as a way to represent and study knots.

As Nelson reports in his article, mathematicians have devised various ways to represent the information contained in knot diagrams. One example is the Gauss code, which is a sequence of letters and numbers wherein each crossing in the knot is assigned a number and the letter O or U, depending on whether the crossing goes over or under. The Gauss code for a simple knot might look like this: O1U2O3U1O2U3.

In the mid-1990s, mathematicians discovered something strange. There are Gauss codes for which it is impossible to draw planar knot diagrams but which nevertheless behave like knots in certain ways. In particular, those codes, which Nelson calls *nonplanar Gauss codes*, work perfectly well in certain formulas that are used to investigate properties of knots. Nelson writes: "A planar Gauss code always describes a [knot] in three-space; what kind of thing could a nonplanar Gauss code be describing?" As it turns out, there are "virtual knots" that have legitimate Gauss codes but do not correspond to knots in three-dimensional space. These virtual knots can be investigated by applying combinatorial techniques to knot diagrams.

Just as new horizons opened when people dared to consider what would happen if -1 had a square root---and thereby discovered complex numbers, which have since been thoroughly explored by mathematicians and have become ubiquitous in physics and engineering---mathematicians are finding that the equations they used to investigate regular knots give rise to a whole universe of "generalized knots" that have their own peculiar qualities. Although they seem esoteric at first, these generalized knots turn out to have interpretations as familiar objects in mathematics. "Moreover," Nelson writes, "classical knot theory emerges as a special case of the new generalized knot theory."

More information: Related to this subject are an upcoming issue of the Journal of Knot Theory and its Ramifications, devoted to virtual knot theory, and the upcoming Knots in Washington conference at George Washington University, December 2-4, 2011, which will focus on on "Categorification of Knots, Algebras, and Quandles; Quantum Computing".

Provided by American Mathematical Society

Saturday, November 12, 2011

Diseased hearts to heal themselves in future




Cellular reversion processes arise in diseases of the heart muscle, for example myocardial infarction and cardiomyopathy, which limit the fatal consequences for the organ. Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim and the Schüchtermann Klinik in Bad Rothenfelde have identified a protein which fulfils a central task in this reversion process by stimulating the regression of individual heart muscle cells into their precursor cells. It is now planned to improve the self-healing powers of the heart with the help of this protein.

Cellular regression in diseased heart tissue with the help
of oncostatin M: The image shows heart muscles under
the fluorescence microscope. The myofibrils are stained
red, the cell nuclei blue.
Credit: MPI for Heart and Lung Research

In order to regenerate damaged heart muscle as caused by a heart attack, for example, the damaged muscle cells must be replaced by new ones. The number of cells to be replaced may be considerable, depending on the extent of the damage caused. Simpler vertebrates like the salamander adopt a strategy whereby surviving healthy heart muscle cells regress into an embryonic state. This process, which is known as dedifferentiation, produces cells which contain a series of stem cell markers and re-attain their cell division activity. Thus, new cells are produced which convert, in turn, into heart muscle cells. The cardiac function is then restored through the remodelling of the muscle tissue.

An optimised repair mechanism of this kind does not exist in humans. Although heart stem cells were discovered some time ago, exactly how and to what extent they play a role in cardiac repair is a matter of dispute. It has only been known for a few years that processes comparable to those found in the salamander even exist in mammals.

Thomas Braun's research group at the Max Planck Institute for Heart and Lung Research in Bad Nauheim has now discovered the molecule responsible for controlling this dedifferentiation of heart muscle cells in mammals. The scientists initially noticed the high concentration of oncostatin M in tissue samples from the hearts of patients suffering from myocardial infarction. It was already known that this protein is responsible for the dedifferentiation of different cell types, among other things. The researchers therefore treated cultivated heart muscle cells with oncostatin M in the laboratory and were then able to trace the regression of the cells live under the microscope: "Based on certain changes in the cells, we were able to see that almost all heart muscle cells had been dedifferentiated within six days of treatment with oncostatin M," explains Braun. "We were also able to demonstrate the presence of various stem cell markers in the cells. This should be understood as an indicator that these cells had been switched to a repair mode."

Using a mouse infarct model, the Max Planck researchers succeeded in demonstrating that oncostatin M actually does stimulate the repair of damaged heart muscle tissue as presumed. One of the two test groups had been modified genetically in advance to ensure that the oncostatin M could not have any effect in these animals. "The difference between the two groups was astonishing. Whereas in the group in which oncostatin M could take effect almost all animals were still alive after four weeks, 40 percent of the genetically modified mice had died from the effects of the infarction," says Braun. The reason for this was that oncostatin M ensured clearly quantifiable better cardiac function in the unmodified animals.

The scientists in Bad Nauheim would now like to find a way of using oncostatin M in treatment. The aim is to strengthen the self-healing powers of the damaged heart muscle and to enable the restoration of cardiac function for the first time. The downside, however, is that oncostatin M was also observed to be counterproductive and exacerbated the damage in an experiment on a chronically diseased heart. "We believe that oncostatin M has considerable potential for efficiently healing damaged heart muscle tissue. What we now need is to be able to pinpoint the precise window of application to prevent any possible negative effects," says Braun.
More information: Thomas Kubin, Jochen Pöling, Sawa Kostin, Praveen Gajawada, Stefan Hein, Wolfgang Rees, Astrid Wietelmann, Minoru Tanaka, Holger Lörchner, Silvia Schimanski, Marten Szibor, Henning Warnecke, Thomas Braun: Oncostatin M Is a Major Mediator of Cardiomyocyte Dedifferentiation and Remodeling. Cell Stem Cell 9, 420, 2011

Tuesday, November 8, 2011

City Lights Could Reveal E.T. Civilization



In the search for extraterrestrial intelligence, astronomers have hunted for radio signals and ultra-short laser pulses. In a new paper, Avi Loeb (Harvard-Smithsonian Center for Astrophysics) and Edwin Turner (Princeton University) suggest a new technique for finding aliens: look for their city lights. "Looking for alien cities would be a long shot, but wouldn't require extra resources. And if we succeed, it would change our perception of our place in the universe," said Loeb.
If an alien civilization builds brightly-lit cities like those shown in this artist's conception, future generations of telescopes might allow us to detect them. This would offer a new method of searching for extraterrestrial intelligence elsewhere in our Galaxy. (Credit: David A. Aguilar (CfA))

As with other SETI methods, they rely on the assumption that aliens would use Earth-like technologies. This is reasonable because any intelligent life that evolved in the light from its nearest star is likely to have artificial illumination that switches on during the hours of darkness.

How easy would it be to spot a city on a distant planet? Clearly, this light will have to be distinguished from the glare from the parent star. Loeb and Turner suggest looking at the change in light from an exoplanet as it moves around its star.

As the planet orbits, it goes through phases similar to those of the Moon. When it's in a dark phase, more artificial light from the night side would be visible from Earth than reflected light from the day side. So the total flux from a planet with city lighting will vary in a way that is measurably different from a planet that has no artificial lights.

Spotting this tiny signal would require future generations of telescopes. However, the technique could be tested closer to home, using objects at the edge of our solar system.

Loeb and Turner calculate that today's best telescopes ought to be able to see the light generated by a Tokyo-sized metropolis at the distance of the Kuiper Belt -- the region occupied by Pluto, Eris, and thousands of smaller icy bodies. So if there are any cities out there, we ought to be able to see them now. By looking, astronomers can hone the technique and be ready to apply it when the first Earth-sized worlds are found around distant stars in our galaxy.

"It's very unlikely that there are alien cities on the edge of our solar system, but the principle of science is to find a method to check," Turner said. "Before Galileo, it was conventional wisdom that heavier objects fall faster than light objects, but he tested the belief and found they actually fall at the same rate."

As our technology has moved from radio and TV broadcasts to cable and fiber optics, we have become less detectable to aliens. If the same is true of extraterrestrial civilizations, then artificial lights might be the best way to spot them from afar.

Loeb and Turner's work has been submitted to the journal Astrobiology.

Friday, November 4, 2011

Brain Cells Responsible for Keeping Us Awake


Bright light arouses us. Bright light makes it easier to stay awake. Very bright light not only arouses us but is known to have antidepressant effects. Conversely, dark rooms can make us sleepy. It's the reason some people use masks to make sure light doesn't wake them while they sleep.
Researchers have identified the group of neurons
that mediates whether light arouses us and keeps
us awake, or not. (Credit: iStockphoto/Osman Safi)

Now researchers at UCLA have identified the group of neurons that mediates whether light arouses us -- or not. Jerome Siegel, a professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA, and colleagues report in the current online edition of the Journal of Neuroscience that the cells necessary for a light-induced arousal response are located in the hypothalamus, an area at the base of the brain responsible for, among other things, control of the autonomic nervous system, body temperature, hunger, thirst, fatigue -- and sleep.

These cells release a neurotransmitter called hypocretin, Siegel said. The researchers compared mice with and without hypocretin and found that those who didn't have it were unable to stay awake in the light, while those who had it showed intense activation of these cells in the light but not while they were awake in the dark.

This same UCLA research group earlier determined that the loss of hypocretin was responsible for narcolepsy and the sleepiness associated with Parkinson's disease. But the neurotransmitter's role in normal behavior was, until now, unclear.

"This current finding explains prior work in humans that found that narcoleptics lack the arousing response to light, unlike other equally sleepy individuals, and that both narcoleptics and Parkinson's patients have an increased tendency to be depressed compared to others with chronic illnesses," said Siegel, who is also a member of the UCLA Brain Research Institute and chief of neurobiology research at the Sepulveda Veterans Affairs Medical Center in Mission Hills, Calif.



Prior studies of the behavioral role of hypocretin in rodents had examined the neurotransmitter's function during only light phases (normal sleep time for mice) or dark phases (their normal wake time), but not both. And the studies only examined the rodents when they were performing a single task.

In the current study, researchers examined the behavioral capabilities of mice that had their hypocretin genetically "knocked-out" (KO mice) and compared them with the activities of normal, wild-type mice (WT) that still had their hypocretin neurons. The researchers tested the two groups while they performed a variety of tasks during both light and dark phases.

Surprisingly, they found that the KO mice were only deficient at working for positive rewards during the light phase. During the dark phase, however, these mice learned at the same rate as their WT littermates and were completely unimpaired in working for the same rewards.

Consistent with the data in the KO mice, the activity of hypocretin neurons in their WT littermates was maximized when working for positive rewards during the light phase, but the cells were not activated when performing the same tasks in the dark phase.

"The findings suggest that administering hypocretin and boosting the function of hypocretin cells will increase the light-induced arousal response," Siegel said. "Conversely, blocking their function by administering hypocretin receptor blockers will reduce this response and thereby induce sleep."

Further, Siegel noted, "The administration of hypocretin may also have antidepressant properties, and blocking it may increase tendencies toward depression. So we feel this work has implications for treating sleep disorders as well as depression."

Other authors on the study included Ronald McGregor (first author), Ming-Fung Wu, Grace Barber and Lalini Ramanathan, all of UCLA, the Veterans Affairs Greater Los Angeles Healthcare System and the UCLA Brain Research Institute.

The research was supported by the National Institutes of Health and the Medical Research Service of the Department of Veterans Affairs. The authors report no conflict of interest.