Thursday, April 30, 2015

Walking an extra two minutes each hour may offset hazards of sitting too long -- ScienceDaily

Walking an extra two minutes each hour may offset hazards of sitting too long -- ScienceDaily

Numerous studies have shown that sitting for extended periods of time each day leads to increased risk for early death, as well as heart disease, diabetes and other health conditions. Considering that 80 percent of Americans fall short of completing the recommended amount of exercise, 2.5 hours of moderate activity each week, it seems unrealistic to expect that people will replace sitting with even more exercise.

With this in mind, scientists at the University of Utah School of Medicine investigated the health benefits of a more achievable goal, trading sitting for lighter activities for short periods of time. They used observational data from National Health and Nutrition Examination Survey (NHANES) to examine whether longer durations of low intensity activities (e.g. standing), and light intensity activities (e.g. casual walking, light gardening, cleaning) extends the life span of people who are sedentary for more than half of their waking hours.

They found that there is no benefit to decreasing sitting by two minutes each hour, and adding a corresponding two minutes more of low intensity activities. However, a "trade-off" of sitting for light intensity activities for two minutes each hour was associated with a 33 percent lower risk of dying.

"It was fascinating to see the results because the current national focus is on moderate or vigorous activity. To see that light activity had an association with lower mortality is intriguing," says lead author Srinivasan Beddhu, M.D., professor of internal medicine.

Beddhu explains that while it's obvious that it takes energy to exercise, strolling and other light activities use energy, too. Even short walks add up to a lot when repeated many times over the course of a week. Assuming 16 awake hours each day, two minutes of strolling each hour expends 400 kcal each week. That number approaches the 600 kcal it takes to accomplish the recommended weekly goal of moderate exercise. It is also substantially larger than the 50 kcal needed to complete low intensity activities for two minutes each awake hour over the course of one week.

"Based on these results we would recommend adding two minutes of walking each hour in combination with normal activities, which should include 2.5 hours of moderate exercise each week," says Beddhu. Moderate exercise strengthens the heart, muscles, and bones, and confers health benefits that low and light intensity activities can't.

The study examined 3,243 NHANES participants who wore accelerometers that objectively measured the intensities of their activities. Participants were followed for three years after the data were collected; there were 137 deaths during this period.

"Exercise is great, but the reality is that the practical amount of vigorous exercise that can be achieved is limited. Our study suggests that even small changes can have a big impact," says senior author Tom Greene, Ph.D., director of the Study Design and Biostatistics Center at the Center for Clinical and Translational Science.

Beddhu adds that large, randomized, interventional trials will be needed to definitively answer whether exchanging sitting for light activities leads to better health.


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Gravity data show that Antarctic ice sheet is melting increasingly faster -- ScienceDaily

Gravity data show that Antarctic ice sheet is melting increasingly faster -- ScienceDaily

The researchers "weighed" Antarctica's ice sheet using gravitational satellite data and found that from 2003 to 2014, the ice sheet lost 92 billion tons of ice per year, the researchers report in the journal Earth and Planetary Science Letters. If stacked on the island of Manhattan, that amount of ice would be more than a mile high -- more than five times the height of the Empire State Building.

The vast majority of that loss was from West Antarctica, which is the smaller of the continent's two main regions and abuts the Antarctic Peninsula that winds up toward South America. Since 2008, ice loss from West Antarctica's unstable glaciers doubled from an average annual loss of 121 billion tons of ice to twice that by 2014, the researchers found. The ice sheet on East Antarctica, the continent's much larger and overall more stable region, thickened during that same time, but only accumulated half the amount of ice lost from the west, the researchers reported.

"We have a solution that is very solid, very detailed and unambiguous," said co-author Frederik Simons, a Princeton associate professor of geosciences. "A decade of gravity analysis alone cannot force you to take a position on this ice loss being due to anthropogenic global warming. All we have done is take the balance of the ice on Antarctica and found that it is melting -- there is no doubt. But with the rapidly accelerating rates at which the ice is melting, and in the light of all the other, well-publicized lines of evidence, most scientists would be hard pressed to find mechanisms that do not include human-made climate change."

Compared to other types of data, the Princeton study shows that ice is melting from West Antarctica at a far greater rate than was previously known and that the western ice sheet is much more unstable compared to other regions of the continent, said first author Christopher Harig, a Princeton postdoctoral research associate in geosciences. Overall, ice-loss rates from all of Antarctica increased by 6 billion tons per year each year during the 11-year period the researchers examined. The melting rate from West Antarctica, however, grew by 18 billion tons per year every year, Harig and Simons found. Accelerations in ice loss are measured in tons per year, per year, or tons per year squared.

Of most concern, Harig said, is that this massive and accelerating loss occurred along West Antarctica's Amundsen Sea, particularly Pine Island and the Thwaites Glacier, where heavy losses had already been recorded. An iceberg more than 2,000 square miles in size broke off from the Thwaites Glacier in 2002.

In Antarctica, it's the ocean currents rather than air temperatures that melt the ice, and melted land ice contributes to higher sea levels in a way that melting icebergs don't, Harig said. As the ocean warms, floating ice shelves melt and can no longer hold back the land ice.

"The fact that West Antarctic ice-melt is still accelerating is a big deal because it's increasing its contribution to sea-level rise," Harig said. "It really has potential to be a runaway problem. It has come to the point that if we continue losing mass in those areas, the loss can generate a self-reinforcing feedback whereby we will be losing more and more ice, ultimately raising sea levels by tens of feet."

The Princeton study differs from existing approaches to measuring Antarctic ice loss in that it derives from the only satellite data that measure the mass of ice rather than its volume, which is more typical, Simons explained. He and Harig included monthly data from GRACE, or the Gravity Recovery and Climate Experiment, a dual-satellite joint mission between NASA and the German Aerospace Center. GRACE measures gravity changes to determine the time-variable behavior of various components in the Earth's mass system such as ocean currents, earthquake-induced changes and melting ice. Launched in 2002, the GRACE satellites are expected to be retired by 2016 with the first of two anticipated replacement missions scheduled for 2017.

While the volume of an ice sheet -- or how much space it takes up -- is also crucial information, it can change without affecting the amount of ice that is present, Simons explained. Snow and ice, for instance, compact under their own weight so that to the lasers that are bounced off the ice's surface to determine volume, there appears to be a reduction in the amount of ice, Simons said. Mass or weight, on the other hand, changes when ice is actually redistributed and lost.

Simons equated the difference between measuring ice volume and mass to a person weighing himself by only looking in the mirror instead of standing on a scale.

"You shouldn't only look at the ice volume -- you should also weigh it to find the mass changes," Simons said. "But there isn't going to be a whole lot of research of this type coming up because the GRACE satellites are on their last legs. This could be the last statement of this kind on these kinds of data for a long time. There may be a significant data gap during which the only monitoring available will not be by 'weighing' but by 'looking' via laser or radar altimetry, photogrammetry or field studies."

Harig and Simons developed a unique data-analysis method that allowed them to separate GRACE data by specific Antarctic regions. Because the ice sheet behaves differently in different areas, a continent-wide view would provide a general sense of how all of the ice mass, taken together, has changed, but exclude finer-scale geographical detail and temporal fluctuations. They recently published a paper about their computational methods in the magazine EOS, Transactions of the American Geophysical Union, and used a similar method for a 2012 paper published in the Proceedings of the National Academy of Sciences that revealed sharper-than-ever details about Greenland's accelerating loss of its massive ice sheet.

Robert Kopp, a Rutgers University associate professor of earth and planetary sciences and associate director of the Rutgers Energy Institute, said the analysis method Harig and Simons developed allowed them to capture a view of regional Antarctic ice loss "more accurately than previous approaches." Beyond the recent paper, Harig and Simons' method could be important for testing models of Antarctic ice-sheet stability developed by other researchers, he said.

"The notable feature of this research is the power of their method to resolve regions geographically in gravity data," Kopp said. "I expect that [their] technique will be an important part of monitoring future changes in the ice sheet and testing such models."


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How some beetles produce a scalding defensive spray -- ScienceDaily

How some beetles produce a scalding defensive spray -- ScienceDaily

Researchers had been baffled by the half-inch beetles' ability to produce this noxious spray while avoiding any physical damage. But now that conundrum has been solved, thanks to research by a team at MIT, the University of Arizona, and Brookhaven National Laboratory. The findings are published this week in the journal Science by MIT graduate student Eric Arndt, professor of materials science and engineering Christine Ortiz, Wah-Keat Lee of Brookhaven National Laboratory, and Wendy Moore of the University of Arizona.

"Their defensive mechanism is highly effective," Arndt says, making bombardier beetles "invulnerable to most vertebrates, and invertebrates" -- except for a few very specialized predators that have developed countermeasures against the noxious spray.

The liquid these beetles eject is called benzoquinone, and is actually a fairly common defensive agent among insects, Arndt says. But bombardier beetles are unique in their ability to superheat the liquid and expel it in an intense, pulsating jet.

The key is that they synthesize the chemical at the instant of use, mixing two chemical precursors in a protective chamber in their hindquarters. As the materials combine to form the irritant, they also give off intense heat that brings the liquid almost to the boiling point -- and, in the process, generates the pressure needed to expel it in a jet.

Seeing inside a living beetle

"For decades, the complex mechanism of how the bombardier beetle achieves spray pulsation as a chemical defense has not been understood, because only external observations were used previously," Ortiz says. In the current study, the researchers used high-speed synchrotron X-ray imaging to "see" inside the abdomens of living bombardier beetles during explosions. They used a facility at Argonne National Laboratory to carry out the experiments and produce detailed images that revealed, for the first time, how the process works, with a camera recording the action at a rate of 2,000 frames per second.

The X-ray images of the explosion reveal the dynamics of vapor inside the beetles' abdomens. They show that spray pulsation is controlled by the passageway between two internal chambers; two structures control this process: a flexible membrane and a valve.

The opening and closing of this passageway between a chamber holding the precursor liquid and an explosion chamber seems to take place passively; an increase in pressure during the explosion expands the membrane, closing the valve. Then, after the pressure is released when the liquid is ejected, the membrane relaxes back to its original state and the passage reopens, allowing the next pulse to form. This all takes place so rapidly -- not to mention inside the insect -- that the process had never been directly observed.

The explosive mechanism used by the bombardier beetle generates a spray that is not only much hotter than that emitted by other insects that use the same chemical irritant, but also propels the jet five times faster. Both the speed and the heat serve to make the spray even more effective against potential predators, Arndt says.

The pulsing nature of the spray may help protect the structure of the beetle's reaction chamber, Arndt says, allowing time for the chamber walls to cool a bit before the next pulse.

Understanding the beetles' ability to survive these intense internal explosions may help in designing blast-protection systems; this study shows how the sophisticated and specialized biological design of the system works to simultaneously achieve defensive and protective functions, Ortiz says. The reaction chamber, for example, possesses a rigid, reinforcing structure to minimize stretching and sustain temperature increases during an explosion, while other components allow for controlled, reversible stretching and movement to control the jet of fluid. The dynamics of the spray generation might also provide information useful in the design of propulsion systems, the researchers say.

R. Jeffrey Dean, a professor of biology at Cleveland State University who studies the defense mechanisms of the bombardier beetle, says the new work is a "wonderful confirmation of the qualitative passive 'pulse jet' model" first proposed by his team. "Although the findings are not unexpected, I'm amazed at the progressive advances in techniques," he adds.

This research was supported by the Department of Energy, the Department of Defense through the U.S. Army Research Office and the National Security Science and Engineering Faculty Fellowship, and the National Science Foundation.

Video: https://www.youtube.com/watch?v=TgqF-ND2XcY


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New origin theory for cells that gave rise to vertebrates -- ScienceDaily

New origin theory for cells that gave rise to vertebrates -- ScienceDaily

Now Northwestern University scientists propose a new model for how neural crest cells, and thus vertebrates, arose more than 500 million years ago.

The researchers report that, unlike other early embryonic cells that have their potential progressively restricted as an embryo develops, neural crest cells retain the molecular underpinnings that control pluripotency -- the ability to give rise to all the cell types that make up the body.

"This study provides deep new insights into the evolutionary origins of humans and other vertebrates," said evolutionary molecular biologist Carole LaBonne, who led the research. "It also provides critical new information about the molecular circuitry of stem cells, including cancer stem cells."

Regenerative medicine scientists now have an updated framework for future studies aiming to harness the power of stem cells to treat human diseases and congenital defects, LaBonne said.

The study also turns conventional thought on its head. Previously, scientists thought neural crest cells had to evolve to gain their incredible properties, but the Northwestern work shows the power was there all along. Researchers now can focus on the molecular mechanisms by which neural crest cells escaped having their potential restricted.

In a study using embryos from the frog Xenopus, a powerful model system used in studies of development, LaBonne and her team found that neural crest cells and the early pluripotent cells present in blastula embryos have surprising similarities, including shared expression of a key set of genes which work together to endow the cells with their unique properties.

The findings will be published as a Science Express article by the journal Science. The article also will be the cover story of the journal's June 19 issue.

"Neural crest cells never had their potential restricted at all," LaBonne said. "We believe a small population of early stem cells were set aside, so that when the time came, their immense developmental potential could be unleashed to create new features characteristic of vertebrates."

LaBonne is a professor of molecular biosciences in the Weinberg College of Arts and Sciences. She holds the Arthur Andersen Teaching and Research Chair and is co-leader of the Tumor Invasion and Metastasis program of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

Acquisition of neural crest cells more than 500 million years ago led vertebrates to evolve and leave behind less complex life forms (simple aquatic filter feeders, much like today's sea squirts and lancelets). With these cells, animals developed important new features such as a skull to house a complex brain, jaws for predation, a complex peripheral nervous system and many other cell types essential to the vertebrate body.

In their study, LaBonne and her research team studied the genetic toolkit that early embryonic cells use to promote pluripotency or "stemness" and compared it to the one used by neural crest cells. They found that the toolkit used by neural crest cells also is used by pluripotent blastula cells, and they showed that it is essential for pluripotency in both cell types. The proteins that derive from this toolkit work together to enable a dizzying array of tissues to arise from a population of single cells.

One of these proteins, called Snail1, has been the focus of previous studies by LaBonne's lab. They and others had shown that Snail1 plays key roles in controlling not only the immense developmental potential of neural crest cells but also their capacity for migratory and invasive behavior.

Cancer cells co-opt the function of Snail1 and other neural crest regulatory proteins to allow the formation of cancer stem cells and mediate the process of metastasis, whereby cancer cells disperse throughout the body to form new tumors, LaBonne said. Researchers therefore gain insights into Snail1's role in cancer by studying its function in the developing embryo.

In early blastula embryos, pluripotent cells were thought to exist only transiently; as an embryo develops, cells become restricted into categories of cells called germ layers and then into specialized cell types. The Northwestern study suggests that not all cells get restricted at those early stages. Instead, neural crest cells may have evolved as a consequence of a subset of blastula cells retaining activity of the regulatory network underlying pluripotency.

The study underscores just how much remains to be discovered about embryonic development. The human body has more than 10 trillion cells elaborately organized into tissues and organs that are intricate and highly complex, yet it all is self-assembled from a single cell, the fertilized egg.

"It's a fascinating process," LaBonne said. "One of the great frontiers in biology is understanding both how complexity is generated and how it evolves to create what Charles Darwin memorably called 'endless forms most beautiful.'"


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Engineering a better solar cell: Defects in popular perovskites pinpointed -- ScienceDaily

Engineering a better solar cell: Defects in popular perovskites pinpointed -- ScienceDaily

These superefficient crystal structures have taken the scientific community by storm in the past few years because they can be processed very inexpensively and can be used in applications ranging from solar cells to light-emitting diodes (LEDs) found in phones and computer monitors.

A new study published online April 30 in the journal Science by University of Washington and University of Oxford researchers demonstrates that perovskite materials, generally believed to be uniform in composition, actually contain flaws that can be engineered to improve solar devices even further.

"Perovskites are the fastest-growing class of photovoltaic material over the past four years," said lead author Dane deQuilettes, a UW doctoral student working with David Ginger, professor of chemistry and associate director of the UW's Clean Energy Institute.

"In that short amount of time, the ability of these materials to convert sunlight directly into electricity is approaching that of today's silicon-based solar cells, rivaling technology that took 50 years to develop," deQuilettes said. "But we also suspect there is room for improvement."

The research team used high-powered imaging techniques to find defects in the perovskite films that limit the movement of charges and, therefore, limit the efficiency of the devices. Perovskite solar cells have so far have achieved efficiencies of roughly 20 percent, compared to about 25 percent for silicon-based solar cells.

In a collaboration made possible by the Clean Energy Institute, the team used a technique called confocal optical microscopy, which is more often used in biology, and applied it to semiconductor technology. They used fluorescent images and correlated them with electron microscopy images to find "dark" or poorly performing regions of the perovskite material at intersections of the crystals. In addition, they discovered that they could "turn on" some of the dark areas by using a simple chemical treatment.

The images offered several surprises but also will lead to accelerated improvements in the materials' uniformity, stability and efficiency, according to corresponding author Ginger, the Alvin L. and Verla R. Kwiram Endowed Professor of Chemistry and Washington Research Foundation Distinguished Scholar.

"Surprisingly, this result shows that even what are being called good, or highly-efficient perovskite films today still are 'bad' compared to what they could be. This provides a clear target for future researchers seeking to improve and grow the materials," Ginger said.

The imaging technique developed by the UW team also offers an easy way to identify previously undiscovered flaws in perovskite materials and to pinpoint areas where their composition can be chemically altered to boost performance, Ginger said.

deQuilettes, who spearheaded the project as a Clean Energy Institute graduate fellow, estimates there are more than a thousand laboratories around the world currently researching the semiconducting properties of perovskite materials. Yet there is more work to be done to understand how to consistently make a material that is stable, has uniform brightness and can stand up to moisture without degrading. The UW research offers new ways for people to think strategically about how to improve the materials and how to extend their applications to high performance light-emitting devices such as LEDs and lasers.

"There are so many of us focusing on perovskites, so hopefully this technique will offer some new direction and steer us toward the places we can look to optimize their energy-capturing and emitting potential," deQuilettes said.

Co-authors of the study are Sarah M. Vorpahl, Hirokazu Nagaoka and Mark E. Ziffer of the UW and Samuel D. Stranks, Giles E. Eperon and Henry J. Snaith at Oxford.

Funding for the research was provided by the state of Washington through the UW Clean Energy Institute.


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Pesticides alter bees' brains, making them unable to live and reproduce adequately -- ScienceDaily

Pesticides alter bees' brains, making them unable to live and reproduce adequately -- ScienceDaily

To make their discovery, Connolly and colleagues fed bees a sugar solution with very low neonicotinoid pesticide levels typically found in flowers (2.5 parts per billion) and tracked the toxins to the bee brain. They found that pesticide levels in the bees' brains were sufficient to cause the learning cells to run out of energy. Additionally, the brain cells were even vulnerable to this effect at just one tenth of the level present. When the ability of the bee's brain to learn is limited, the bee is unable to master key skills such as recognizing the presence of nectar and pollen from the smell emitted from flowers. In addition, scientists fed bumblebee colonies this same very low level of pesticide in a remote site in the Scottish Highlands where they were unlikely to be exposed to any other pesticides. They found that just a few of the exposed colonies performed well, colonies were smaller, and nests were in poor condition with fungus taking over. This further suggests that bumblebees exposed to this type of pesticide become poor learners, become unable to properly gather food, and become unable to properly nurture the next generation of bees.

"It is ironic that neonicotinoids, pesticides developed to preserve the health of plants, ultimately inflict tremendous damage on plant life," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "These chemicals destroy the insect communities required by plants for their own reproduction."

"Our study shows that the neonicotinoid pesticides are a risk to our bees and we should stop using them on plants that bees visit," said Christopher N. Connolly, Ph.D., a researcher involved in the work from the Medical Research Institute at the Ninewells Medical School at the University of Dundee in Dundee, UK. "Neonicotinoids are just a few examples of hundreds of pesticides we use on our crops and in our gardens. Stop using all pesticides in your garden and see insect damage as a success. You are providing for your native wildlife. Nasty caterpillars grow into beautiful butterflies."


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New tool can switch behavior -- such as voracious eating -- 'on' and 'off' -- ScienceDaily

New tool can switch behavior -- such as voracious eating -- 'on' and 'off' -- ScienceDaily

When this complex signaling system goes awry, the results can lead to a plethora of diseases, including schizophrenia, depression, Alzheimer's Disease, Parkinson's Disease, eating disorders, and epilepsy. Cell surface receptors also play roles in cancers, diabetes, digestive conditions, and other diseases. This new technique could be modified to study them, as well.

This is the first technology to stem from the initial set of NIH BRAIN Initiative grants to create new cutting-edge research tools to improve our understanding of the brain.

"This new chemogenetic tool will show us how brain circuits can be more effectively targeted to treat human disease, " said Bryan L. Roth, MD, PhD, the Michael Hooker Distinguished Professor of Protein Therapeutics and Translational Proteomics at the UNC School of Medicine. "The problem facing medical science is that although most approved drugs target these brain receptors, it remains unclear how to selectively modulate specific kinds of receptors to effectively treat disease."

Roth addressed this problem by inventing a technology he dubbed "DREADDs" -- Designer Receptor Exclusively Activated by a Designer Drug.

The first-generation DREADD technology was developed in 2007.

Essentially, in lab experiments, Roth's team altered the chemical structure of G protein-coupled receptors so that the receptors expressed synthetic proteins when reintroduced into a mouse. This way, the mutated receptor could only be activated or inhibited by a specific synthesized drug-like compound. The receptor became like a lock; the synthetic drug became the only key that fit the lock. Depending on what Roth's team wanted to study, they could lock or unlock the specific brain circuits and behaviors associated with that one receptor.

This DREADD technology -- also known as chemogenetics -- is now used by hundreds of labs worldwide. It helped revolutionize our understanding of how brain circuits control normal and abnormal behavior, emotions, perception, pain sensation, memory, and many other processes. DREADDs have been used to improve the function of insulin-producing cells in mice as a way of treating diabetes. DREADD technology has also helped scientists treat epileptic seizures in mice.

But scientists could use this first DREADD to only manipulate a single receptor in one direction -- excite the receptor or inhibit it.

Last year, Roth and UNC colleagues Thomas Kash, PhD, and Jian Jin, PhD, received a $2.84-million NIH BRAIN Initiative grant to develop the next generation of DREADDs.

Today in the journal Neuron, UNC and NIH researchers revealed the first fruit of that grant -- a new chemogenetic technology they have named KORD (k-opioid receptor DREADD). This new tool, co-invented by Roth and Eyal Vardy, PhD, a former UNC postdoctoral fellow, can target two different kinds of receptors on the same neuron sequentially. This allowed them to study the function of two kinds of receptors as they relate to each other.

In the Neuron paper, Roth's team explain how they modified the receptors in the lab, packaged the receptors in an viral vector, and injected them into mice so that the synthetic receptors were expressed only in certain kinds of neurons in specific parts of the brain.

Then they administered the synthetic drug-like compound to demonstrate how neuronal signaling could be manipulated to turn the same neurons 'on' and 'off' and thereby turning 'on' and 'off' specific behaviors in mice.

In one type of experiment, the NIH lab of Michael Krashes, PhD, was able to turn 'on' and 'off' voracious feeding behavior in mice. In another type of experiment, UNC researchers were able to turn 'on' and 'off' behaviors similar to those induced by drugs such as cocaine and amphetamines.

Elliot Robinson, an MD/PhD student at UNC and co-first author of the Neuron paper, said, "These experiments have validated KORD as a new tool for researchers interested in controlling the function of specific populations of cells while also highlighting their therapeutic potential."

Reid Johnson, UNC graduate student and paper co-author, said, "Using genetically modified mice, we can now tease apart the interactions between seemingly disparate neuronal systems in a logical fashion."

Roth added, "We are now sharing KORD and other DREADD technology freely with other scientists, and it is likely that new uses for these technologies will appear in the near future."

Vardy, co-first author of the Neuron paper, is now a senior scientist at Merck Pharmaceuticals. Robinson conducted his experiments while in the lab of CJ Malanga, PhD, associate professor of neurology at the UNC School of Medicine and paper co-author. Johnson is part of the lab headed by Juan Song, assistant professor of pharmacology at UNC and paper co-author. Thomas Kash was also an author on this paper.


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Light -- not pain-killing drugs -- used to activate brain's opioid receptors -- ScienceDaily

Light -- not pain-killing drugs -- used to activate brain's opioid receptors -- ScienceDaily

In a test tube, the scientists melded the light-sensing protein rhodopsin to key parts of opioid receptors to activate receptor pathways using light. They also influenced the behavior of mice by injecting the receptors into the brain, using light instead of drugs to stimulate a reward response.

Their findings are published online April 30 in the journal Neuron.

The eventual hope is to develop ways to use light to relieve pain, a line of discovery that also could lead to better pain-killing drugs with fewer side effects.

"It's conceivable that with much more research we could develop ways to use light to relieve pain without a patient needing to take a pain-killing drug with side effects," said first author Edward R. Siuda, a graduate student in the laboratory of Michael R. Bruchas, PhD, an assistant professor of anesthesiology and of neurobiology.

But before that's possible, the researchers are attempting to learn the most effective ways to activate and deactivate the opioid receptor's pathways in brain cells. Bruchas, the study's principal investigator, explained that working with light rather than pain-killing drugs makes it much easier to understand how the receptors function within the complex array of cells and circuits in the brain and spinal cord.

"It's been difficult to determine exactly how opioid receptors work because they have multiple functions in the body," Bruchas explained. "These receptors interact with pain-killing drugs called opiates, but they also are involved in breathing, are found in the gastrointestinal tract and play a role in the reward response."

So the researchers sought a way to limit opioid receptors to performing a single task at a time, and it turned out to be almost as easy as flipping on a light switch, according to Bruchas, Siuda and their collaborators, including co-first author Bryan A. Copits, PhD, a postdoctoral research scholar in the laboratory of Robert W. Gereau, IV, PhD, the Dr. Seymour and Rose T. Brown Professor of Anesthesiology.

By combining the rhodopsin protein, which senses light in the eye's retina, with a specific type of opioid receptor called a Mu opioid receptor, the researchers were able to build a receptor that responds to light in exactly the same way that standard opioid receptors respond to pain-killing drugs.

When an opioid receptor is exposed to a pain-killing drug, it initiates activity in specific chemical pathways in the brain and spinal cord. And when the researchers shone light on the receptors that contained rhodopsin, the same cellular pathways were activated.

In a test tube and in cells, Siuda exposed the receptors to light and then watched as they released the same chemicals that standard opioid receptors release. Then, in mice, the researchers implanted a light-emitting diode (LED) device the size of a human hair into a brain region linked to the reward response. They injected the light-sensing receptors they had genetically manufactured into the same brain region. Neurons in that part of the brain release chemicals such as dopamine that create feelings of euphoria.

In decades of past opioid studies, researchers have observed mice and rats to press a lever to receive a dose of morphine, for example. The morphine would activate opioid receptors and the release of dopamine, and the animals would enjoy the response and press the lever again to continue feeling that reward sensation. This is one of the reasons opiates are so often abused in patients being treated for pain -- people like the way the drugs make them feel as much as the pain relief they provide -- and rates of abuse have skyrocketed over the past ten years.

Working to deliver a similar reward sensation using light, the researchers put the mice into an enclosed chamber. In one part of the chamber, the lighted laser fiber-optic device stimulated the release of dopamine in the brain. When the animals left that part of the chamber, the light in the brain turned off. Soon after, the mice returned to the part of the chamber that activated the fiber-optic device so that the brain could receive more light stimulation.

"By activating the receptors with light, we are presumably causing the brain to release more dopamine," Bruchas explained. "Rather than a drug such as morphine activating an opioid receptor, the light provides the reward."

The researchers were able to vary the animals' response depending on the amount and type of light emitted by the LED. Different colors of light, longer and shorter exposure to light, and whether the light pulsed or was constant all produced slightly different effects.

When a person takes an opioid drug such as Vicodin or OxyContin to relieve pain, such drugs interact with receptors in the brain to blunt pain sensations. But over time, patients develop tolerance and sometimes addiction. Opioids also can dramatically slow a person's breathing, too, and typically cause constipation.

In theory, receptors tuned to light may not present the same danger. Siuda said it someday may be possible to activate, or deactivate, nerve cells without affecting any of the other receptors that pain-killing drugs trigger, although achieving that goal will be difficult.

Bruchas' team is planning future studies that will use these receptors to test ways to control the brain cells that mediate pain and reward behavior with light rather than drugs.

The research was supported by a EUREKA award from the National Institute on Drug Abuse, the National Institute of Mental Health and the National Institute of General Medical Sciences of the National Institutes of Health (NIH); grant numbers R01 DA037152, F31 MH101956, K99 DA038725, TR32 GM108539 and NSTR01 NS081707. Additional funding from a W.M. Keck Fellowship in Molecular Medicine; and the Howard Hughes Medical Institute.

Siuda ER, Copits BA, Schmidt MJ, Baird MA, Al-Hasani R, Planer WJ, Funderburk SC, McCall JG, Gereau RW, Bruchas M. Spatiotemporal control of opioid signaling and behavior. Neuron, published online April 30, 2015.


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Wild bearded capuchin monkeys really know how to crack a nut -- ScienceDaily

Wild bearded capuchin monkeys really know how to crack a nut -- ScienceDaily

The monkeys are known to use stone "hammers" to crack nuts. The new study shows that the monkeys are quite careful about the amount of force delivered to those nuts. They adjust the force applied with each strike based on the condition of the nutshell, making it less likely that they'll end up smashing the tasty kernel inside.

"Wild bearded capuchin monkeys dynamically modulate their strikes based on the outcome of the preceding strike while using stone hammers to crack nuts," says Madhur Mangalam of the University of Georgia at Athens. "Until now, this level of dexterity was not suspected of any monkey."

Mangalam's graduate advisor, Dorothy Fragaszy, and her colleagues have studied nut-cracking in wild bearded capuchin monkeys since 2005, when they established the EthoCebus research project. They were especially curious how the monkeys managed to crack such hard nuts. They also wondered whether the monkeys might change their nut-cracking approach with nuts that are softer.

In the new study, the researchers videotaped 14 capuchin moneys cracking nuts. They carefully analyzed the tapes to determine the height and velocity of each and every strike. It typically takes several strikes with a stone to reach the nut inside.

And what they discovered came as quite a surprise.

"It was a 'eureka' moment when we realized that the monkeys modulated the strikes systematically according to the condition of the nut following the preceding strike," Mangalam says.

They had expected the monkeys to maintain the force of their strikes within a certain range, or possibly to increase it until the nuts cracked. It never crossed their minds that the monkeys might show such a sophisticated ability to match their action to the physical state of the nut. But that's exactly what they did.

"Our finding opens our eyes to the fact that non-human primates modulate their actions with a tool to accommodate the rapidly changing requirements of the task, which is a cognitive accomplishment," Mangalam says.

The researchers now plan to examine whether other species make adjustments in tool use on the fly. They'll also explore how this kind of dexterity influences each species' tool-use repertoire.


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