Tuesday, October 13, 2009

UNUSUAL ARCTIC WARMTH, TROPICAL WETNESS LIKELY CAUSE FOR METHANE INCREASE

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Unusually high temperatures in the Arctic and heavy rains in the tropics likely drove a global increase in atmospheric methane in 2007 and 2008 after a decade of near-zero growth, according to a new study. Methane is the second most abundant greenhouse gas after carbon dioxide, albeit a distant second.

NOAA scientists and their colleagues analyzed measurements from 1983 to 2008 from air samples collected weekly at 46 surface locations around the world. Their findings appeared in the September 28 print edition of the American Geophysical Union’s Geophysical Research Letters and are available online now.

“At least three factors likely contributed to the methane increase,” said Ed Dlugokencky, a methane expert at NOAA’s Earth System Research Laboratory in Boulder, Colo. “It was very warm in the Arctic, there was some tropical forest burning, and there was increased rain in Indonesia and the Amazon.”

In the tropics, the scientists note, the increased rainfall resulted in longer periods of rainfall and larger wetland areas, allowing microbes to produce more methane. Starting in mid-2007, scientists noticed La Niña conditions beginning, waning and then intensifying in early 2008. This kind of climate condition typically brings wetter-than-normal conditions in some tropical regions and cooler sea surface temperatures in the central and eastern tropical Pacific Ocean. It can persist for as long as two years. In the United States, La Niña often signals drier-than-normal conditions in the Southwest and Central Plains regions, and wetter fall and winter seasons in the Pacific Northwest.

Observations from satellites and ground sites suggest that biomass burning – the burning of plant and other organic material that releases carbon dioxide and methane – contributed about 20 percent, of the total methane released into the atmosphere in 2007.

However, during the scientists’ 2007 measurement of methane for northern wetland regions, including the Arctic, temperatures for the year were the warmest on record. This temperature increase coincided with the large jump in the amount of methane measured in that area.

Dlugokencky and his colleagues from the United States and Brazil note that while climate change can trigger a process which converts trapped carbon in permafrost to methane, as well as release methane embedded in Arctic hydrates – a compound formed with water - their observations “are not consistent with sustained changes there yet.”

Methane is typically created in oxygen-deprived environments, such as flooded wetlands, peat bogs, rice paddies, landfills, termite colonies, and the digestive tracts of cows and other ruminant animals. The gas also escapes during fossil fuel extraction and distribution and is emitted during fires.

(Photo: NOAA)

National Oceanic and Atmospheric Administration

RESVERATROL: YOUR SECRET WEAPON AGAINST AGING?

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The claims in magazine ads, on TV, and all over the Internet are eye-catching: for instance, “Harvard researcher says resveratrol is the Holy Grail of aging research.” Research from other prestigious institutions such as Johns Hopkins, the Salk Institute, and the University of California is also often cited to prove that resveratrol holds the secret to longevity. It’s true that many eminent scientists are interested in resveratrol, and some findings have been tantalizing.

Resveratrol is one of many naturally occurring plant chemicals called polyphenols. It is found in grapes, peanuts, mulberries, and blueberries, as well as spruce, eucalyptus, and other plants (not all of them edible). Red wine is rich in it, and white wine has some, too. Many reports have called resveratrol the ingredient in wine that appears to protect wine drinkers from cardiovascular disease—the so-called “French paradox.” The “paradox” is that the French eat a lot of cheese and other fatty foods, but are healthier, presumably because of the red wine they drink. First isolated in 1940, the resveratrol molecule has been a subject of scientific study ever since. And, indeed, in laboratory studies it is the equivalent of a three-ring circus. Under a microscope, it appears to do nearly everything.

Here are some examples:

• In studies of yeasts, certain worms, and other small organisms, high doses of resveratrol have lengthened lifespan. Mice, too, live longer when given high doses of resveratrol. These findings brought forth loud exclamations of “eureka!” from some researchers, and gave rise to the anti-aging claims of supplement marketers.

• It is, or sometimes behaves like, a plant estrogen. As such, it may activate genes controlled by estrogen. This raises the possibility that it might promote certain cancers.

• On the other hand, it sometimes is, or behaves like, an anti-estrogen, and this raises the possibility that it might help suppress those same cancers.

• It is an antioxidant. Some researchers have proposed that it thus may help protect against cardiovascular disease, but this is far from proven. It’s true that wine, especially red wine, has heart benefits, but it’s not known to what extent resveratrol is involved in this.

• On the other hand, good studies have found that resveratrol, under some circumstances, can act like a pro-oxidant and can thus damage cells. It has been theorized that this property might be useful for treating cancer.

• It can have anti-inflammatory and anti-prostaglandin effects. (Prostaglandins are chemicals involved in many bodily processes, including pain.) That is, resveratrol has something in common with aspirin and other nonsteroidal anti-inflammatory drugs, which quell inflammation and pain.

• Lab studies suggest that resveratrol has neuro-protective properties. If these could somehow be harnessed, they might help prevent some of the degenerative diseases of aging.

Will our grandchildren take a resveratrol capsule every morning and live to be 100 without having to see a doctor? Should you get a supply of resveratrol pills and start taking them now?

We don’t know about the grandchildren, but the answer to the second question is no. There have been no good human studies of resveratrol. It appears, so far, to be safe, but its long-term effects are an open question. Any substance that seems to do almost everything and can play opposite chemical roles deserves careful study. Is it our friend or foe? Or both? Or neither? If it’s beneficial, what dose would you need? No one knows yet. Supplement marketers warn that delay could be dangerous, and they also say the big drug companies will one day be selling you resveratrol at 10 times the price. If that comes to pass, at least the drug companies will have had to show some evidence of safety and effectiveness via human studies. This is not the case with dietary supplements, which can make many vague health claims with no proof.

Science is not ignoring resveratrol. It is being tested at many research institutions here and abroad as a treatment for such disorders as diabetes, metabolic syndrome, and Alzheimer’s disease, as well as for preventing cancer. One hope, apart from its possible preventive or life-extending uses, is that resveratrol will prove useful for treating heart disease and cancer.

Many modern medicines come from plants—aspirin is perhaps the best known example. Still, not all remedies extracted from plants have proven successful. In addition, many nutrients and phytochemicals work best as team players—not as isolated elements to be swallowed in large doses.

UC Berkeley Wellness Letter

ASTROPHYSICISTS MOVE CLOSER TO UNDERSTANDING THE BEAUTY BEHIND STELLAR JETS

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Certain stars stream vast amounts of matter into space, creating some of the most beautiful objects in astronomers' telescopes. But while the astronomers can enjoy the beauty, they can't explain it.

Adam Frank, professor of physics and astronomy at the University of Rochester is hoping to change that.

Earlier this year, Frank and his colleague, Eric Blackman, professor of physics and astronomy, were part of what he called "one of the greatest astrophysical experiments that's ever been done." Recreating a stellar event in a laboratory is extremely difficult, says Frank, since most astrophysical phenomena require an entire star, "which is hard to fit in a lab."

But Frank, along with Professor Sergey Lebedev's team in the Department of Physics at Imperial College London, replicated the physics of a stellar jet in a laboratory, matching the known physics of jets amazingly well. That experiment was conducted using the Imperial College's MAGPIE pulsed power facility. Now, the U.S. Department of Energy has awarded Frank and his team $2.8 million to take the experiment to the next level.

Along with researchers from Rice University and the University of California at San Diego, Frank and Lebedev will re-conduct the initial experiment and carry out new ones on Sandia National Laboratories' Z-Machine—an X-ray generator 10 times more powerful than the MAGPIE facility. The new grant will allow Frank and the team to replicate jets even more accurately, as well as to get new astronomical observations to nail down exactly how stellar jets evolve in nature.

"It's a whole new way of doing astrophysics," says Frank, who specializes in using supercomputers to simulate astrophysical phenomena. "The DOE grant allows us to deepen and extend an unusual international collaboration of plasma physicists, astronomers, and computational scientists. The grant is for five years and that means we have the time and resources to come together to answer a very difficult problem from very different angles."

The original experiment at Imperial College showed how "knots" form in stellar jets. Though jets are believed to emanate from a star as a steady stream of matter, they quickly become knotted and twisted, creating the astonishing shapes they are known for, says Frank. Astrophysicists had long debated what caused the knotting of jets, but Frank, Lebedev, and the team managed to recreate a small-scale version of these jets at the Imperial College' facility.

At Imperial College, Lebedev sent a high-powered pulse of energy into an aluminum disk. In just a few billions of a second, the aluminum began to evaporate, creating a cloud of plasma very similar to the plasma cloud surrounding a young star, says Frank. Where the energy flowed into the center of the disk, the aluminum evaporated completely, creating a hole through which a magnetic field, generated in the process, could penetrate.

The field initially pushed aside the plasma, forming a "bubble with a jet inside," says Frank, who carried out the astrophysical analysis of the experiment. As the field penetrated further and the bubble/jet system grew, the magnetic fields began to warp and twist. Almost immediately, a new magnetic bubble formed beneath the first bubble, and the process repeated itself, creating a series of broken bubbles in the plasma.

The resulting cloud of plasma, pinched in by the magnetic fields, so closely resembled what astrophysicists observe in real stellar jets that Frank believes the same physics underlies both. Frank says other aspects of the experiment, such as the way in which the jets radiatively cool the plasma in the same way jets radiatively cool their parent stars, make the series of experiments an important tool for studying stellar jets.

"We can see these beautiful jets in space, but we have no way to see what the magnetic fields look like," says Frank. "I can't go out and stick probes in a star, but here we can get some idea."

(Photo: NASA)

University of Rochester

IOWA STATE UNIVERSITY RESEARCHER UNCOVERS POTENTIAL KEY TO CURING TUBERCULOSIS

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Tuberculosis is caused by Mycobacterium tuberculosis and is a contagious disease that is on the rise, killing 1.5 to 2 million people worldwide annually.

Reuben Peters, associate professor in the department of biochemistry, biophysics and molecular biology, is leading the team of scientists from Iowa State; the University of Illinois, Urbana-Champaign; and Cornell University, Ithaca, New York, that is attempting to find ways to minimize the disease. The group had their research published in the Aug. 28 issue of the Journal of Biological Chemistry, and their research is also scheduled to be the cover article in an upcoming issue of the Journal of the American Chemical Society.

When most infections are introduced into humans, the body defends itself with certain cells -- called macrophage cells -- that kill the invading micro-organisms. The macrophage cells engulf and destroy these microbes, such as the Mycobacterium tuberculosis.

Peters found that the mycobacterium tuberculosis produces a defensive molecule that prevents the macrophage cells from destroying them. Peters and his team named the defensive molecule edaxadiene.

Peters' next step was to try to find molecules that bind with the edaxadiene-producing enzymes from tuberculosis and neutralize them. This makes the tuberculosis cells unable to produce edaxadiene. Without edaxadiene, tuberculosis cells would have a reduced ability to resist being killed by the macrophage cells.

Peters thinks he may have already found one.

"We have inhibitors that bind tightly to one of the enzymes that make edaxadiene in a test tube," said Peters.

Finding an inhibitor that works outside of the test tube, and in humans, and is stable, and can be ingested safely by humans, and can help kill tuberculosis is a process that may take a decade.

But Peters sees a huge reward at the end of the process.

"This is the project where I tell my students, 'If we can make even just a 1 percent impact, we can save 15,000 - 20,000 lives a year.' That is really a significant contribution towards alleviating human suffering," said Peters.

Peters' group found the molecule by comparing the genetic makeup of tuberculosis - which kills humans - to the type that kills cattle but doesn't seem to have any effect on humans - Mycobacterium bovis.

"Their genetic sequences are more than 99.9 percent identical," said Peters. "However, whereas, tuberculosis causes disease in humans, the bovis variety is much less infectious in humans, although it does cause disease in cattle."

One of the small differences in the genetic information between the two mycobacteria may hold the key to why one infects humans while the other does not.

"The bovis mycobacterium is missing only one nucleotide in the gene for one of the edaxadiene-producing enzymes, but that turns out to be very important as it prevents that enzyme from functioning," he said.

"The critical piece for this idea is that Mycobacterium bovis doesn't make edaxadiene, and doesn't affect humans much, whereas Mycobacterium tuberculosis does make edaxadiene and is infectious in humans," Peters said.

"We think this is the big difference between the two mycobacterium, mainly because this is the only difference I know of that seems to affect their infection process," he added.

"This work presents tantalizing evidence that edaxadiene helps the tuberculosis bacterium evade the body's defenses," said Warren Jones, who oversees enzymology grants at the National Institutes of Health's National Institute of General Medical Sciences, which funded the research. "By exploring ways to block the production of this molecule, Dr. Peters is pioneering a new approach for combating this deadly pathogen."

One of the hurdles that will confront Peters in finding human cures is that the effect of edaxadiene may be specific to humans, so the normal testing process may be difficult.

The normal testing sequence involves testing in the laboratory, then on smaller animals, then larger animals, and then to humans.

Since edaxadiene may be important for the ability of tuberculosis to infect humans, rather than animals, preventing production of edaxadiene by tuberculosis may not have much effect in animals, which will be challenging for the process of bringing a cure to drugstore shelves, according to Peters.

Peters added that he is eager to take on the next challenge in the fight against tuberculosis.

(Photo: ISU)

Iowa State University

STUDY SHOWS THAT COLOR PLAYS MUSICAL CHAIRS IN THE BRAIN

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The brain's neural mechanisms keep straight which color belongs to what object, so one doesn't mistakenly see a blue flamingo in a pink lake. But what happens when a color loses the object to which it is linked? Research at the University of Chicago has demonstrated, for the first time, that instead of disappearing along with the lost object, the color latches onto a region of some other object in view – a finding that reveals a new basic property of sight.

The research shows that the brain processes the shape of an object and its color in two separate pathways and, though the object's shape and color normally are linked, the neural representation of the color can survive alone. When that happens, the brain establishes a new link that binds the color to another visible shape.

"Color is in the brain. It is constructed, just as the meanings of words are constructed. Without the neural processes of the brain, we wouldn't be able to understand colors of objects any more than we could understand words of a language we hear but don't know," said Steven Shevell, a University of Chicago psychologist who specializes on color and vision.

Shevell's findings are reported in a paper, "Color-Binding Errors During Rivalrous Suppression of Form," in the current issue of Psychological Science. Wook Hong, who received his Ph.D. at UChicago and is now a post-doctoral fellow at Vanderbilt University, joined Shevell in writing the paper and conducting the research.

Their work expands the understanding of how the brain is able to integrate the multiple features of an object, such as shape, color, location and velocity, into a unified whole.

"An aspect of human vision that we normally don't appreciate is that different features of an object, including color and shape, can be represented in different parts of the brain," said Shevell, the Eliakim Hastings Moore Distinguished Service Professor in Psychology and Ophthalmology & Visual Science.

If a person sees a basketball coming, it is perceived as having a particular color, shape and velocity. "The knitting together, or what can be called 'neural gluing,' of all those different features so we see a unified object is a complex function done by the brain. Our research focused on how the brain does that," Shevell explained.

To study how the brain represents the color of objects, the researchers used a technique called binocular rivalry. The technique presents a different image to each eye and thus pits signals from the right eye against signals from the left.

"The brain has difficulty integrating the two eyes' incompatible signals. When the signals from the two eyes are different enough, the brain resolves the conflicting information by suppressing the information from one of the eyes," Shevell said. "We exploited this feature of the brain with a method that caused the shape from one eye to be suppressed but not its color."

The researchers first showed subjects vertically oriented green stripes in the left eye and a horizontally oriented set of red stripes in the right eye. "The brain cannot fuse them in a way that makes sense. So the brain sees only horizontal or vertical," Shevell said. For their study, the researchers developed a new form of the technique that allowed the horizontal pattern to be suppressed without eliminating its red color, which continued on to the brain.

At this point, the brain has a musical chairs problem. Both the red and green colors reach consciousness but with only the one vertical pattern—one object but two colors. The surprising result was that the "disembodied red, which originated from the unseen horizontal pattern in one eye, glued itself to parts of the consciously seen vertical pattern from the other eye. That proves the idea of neural binding or neural gluing, where the color is connected to the object in an active neural process," Shevell said.

"To us it seems automatic," Shevell added. "Every basketball has a color. Every shirt has a color, but the brain must link each object's color to its shape."

(Photo: U. Chicago)

University of Chicago

LOSS OF TOP PREDATORS CAUSING SURGE IN SMALLER PREDATORS, ECOSYSTEM COLLAPSE

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The catastrophic decline around the world of "apex" predators such as wolves, cougars, lions or sharks has led to a huge increase in smaller "mesopredators" that are causing major economic and ecological disruptions, a new study concludes.

The findings, published today in the journal Bioscience, found that in North America all of the largest terrestrial predators have been in decline during the past 200 years while the ranges of 60 percent of mesopredators have expanded. The problem is global, growing and severe, scientists say, with few solutions in sight.

An example: in parts of Sub-Saharan Africa, lion and leopard populations have been decimated, allowing a surge in the "mesopredator" population next down the line, baboons. In some cases children are now being kept home from school to guard family gardens from brazen packs of crop-raiding baboons.

"This issue is very complex, and a lot of the consequences are not known," said William Ripple, a professor of forest ecosystems and society at Oregon State University. "But there's evidence that the explosion of mesopredator populations is very severe and has both ecological and economic repercussions."

In case after case around the world, the researchers said, primary predators such as wolves, lions or sharks have been dramatically reduced if not eliminated, usually on purpose and sometimes by forces such as habitat disruption, hunting or fishing. Many times this has been viewed positively by humans, fearful of personal attack, loss of livestock or other concerns. But the new picture that's emerging is a range of problems, including ecosystem and economic disruption that may dwarf any problems presented by the original primary predators.

"I've done a lot of work on wildlife in Africa, and people everywhere are asking some of the same questions, what do we do?" said Clinton Epps, an assistant professor at OSU who is studying the interactions between humans and wildlife. "Most important to understand is that these issues are complex, the issue is not as simple as getting rid of wolves or lions and thinking you've solved some problem. We have to be more careful about taking what appears to be the easy solution."

The elimination of wolves is often favored by ranchers, for instance, who fear attacks on their livestock. However, that has led to a huge surge in the number of coyotes, a "mesopredator" once kept in check by the wolves. The coyotes attack pronghorn antelope and domestic sheep, and attempts to control them have been hugely expensive, costing hundreds of millions of dollars.

"The economic impacts of mesopredators should be expected to exceed those of apex predators in any scenario in which mesopredators contribute to the same or to new conflict with humans," the researchers wrote in their report. "Mesopredators occur at higher densities than apex predators and exhibit greater resiliency to control efforts."

The problems are not confined to terrestrial ecosystems. Sharks, for instance, are in serious decline due to overfishing. In some places that has led to an explosion in the populations of rays, which in turn caused the collapse of a bay scallop fishery and both ecological an economic losses.

Among the findings of the study:

Primary or apex predators can actually benefit prey populations by suppressing smaller predators, and failure to consider this mechanism has triggered collapses of entire ecosystems.

Cascading negative effects of surging mesopredator populations have been documented for birds, sea turtles, lizards, rodents, marsupials, rabbits, fish, scallops, insects and ungulates.

The economic cost of controlling mesopredators may be very high, and sometimes could be accomplished more effectively at less cost by returning apex predators to the ecosystem.

Human intervention cannot easily replace the role of apex predators, in part because the constant fear of predation alters not only populations but behavior of mesopredators.

Large predators are usually carnivores, but mesopredators are often omnivores and can cause significant plant and crop damage.

The effects of exploding mesopredator populations can be found in oceans, rivers, forests and grasslands around the world.

Reversing and preventing mesopredator release is becoming increasingly difficult and expensive as the world's top predators continue to edge toward obliteration.

"These problems resist simple solutions," Ripple said. "I've read that when Gen. George Armstrong Custer came into the Black Hills in 1874, he noticed a scarcity of coyotes and the abundance of wolves. Now the wolves are gone in many places and coyotes are killing thousands of sheep all over the West."

"We are just barely beginning to appreciate the impact of losing our top predators," he said.

At OSU, Ripple and colleague Robert Beschta have done extensive research and multiple publications on the effect that loss of predators such as wolves and cougars have on ecosystem disruption, not only by allowing increased numbers of grazing animals such as deer and elk, but also losing the fear of predation that changes the behavior of these animals. They have documented ecosystem recovery in Yellowstone National Park after wolves were reintroduced there.

(Photo: Piper Smith)

Oregon State University

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