Posts Tagged ‘Rebecca Boyle’
Five Reasons You Should Care About the New Ozone Hole Over the Arctic
Some answers from an atmospheric scientist
1: THIS IS A NEW PROBLEM
Most of the public probably knows about the infamous ozone hole over the South Pole, which became one of the great environmental recovery efforts of the 1980s. The Arctic loses some ozone every year, too, but not like this, said Gloria Manney, who works at NASA's Jet Propulsion Laboratory and the New Mexico Institute of Mining and Technology in Socorro.
“No previous year rivals 2011, when the evolution of Arctic ozone more closely followed that typical of the Antarctic,” Manney and colleagues write in the Oct. 2 online issue of Nature. For the first time, the Arctic loss was enough to be considered a hole.
Both holes are driven by chemical reactions involving chlorine. In cold air and sunlight, chlorine is converted into compounds that break down ozone (itself a harmful substance at the surface, but a protective one at stratospheric altitudes). Antarctica experiences an annual ozone hole as a result. The Arctic is cold, too, but usually not as cold as the Antarctic, and not for as long. But winter 2010-2011 was different. Scientists aren’t sure why.
“The processes that control temperatures in the stratosphere in the winter are so complex; it depends on various factors,” Manney said in an interview. “In December, we couldn’t have told you we were going to have this unusually long cold period.”
2: IT COULD HAPPEN AGAIN
Without ozone, more radiation would get through to interfere with our DNA, and that of other life forms on Earth.The planet’s climate is an extremely complex system, so it’s hard to say what will happen if global surface temperatures rise as expected. But it’s generally accepted that an increase in surface temperatures will translate to a chill in the upper atmosphere, Manney said. So as the Arctic loses more of its ice sheet in the summer, the air will get even colder up above, meaning more of the chlorine reactions will take place.
“If the stratosphere cools as a result of the changing climate, we might see severe ozone depletion more often in the future,” she said.
3: IT'S TOO LATE TO STOP
Humans have already emitted enough chemicals to seed the process. The , which took effect in 1989, prohibits production of chemicals involved in ozone destruction. But human activity belched out plenty of those chemicals before international governments ever started noticing, let alone signing treaties. There’s still enough in the atmosphere for this effect to persist for decades, Manney said.
4: PEOPLE NEED OZONE
The air over the Arctic is extremely mobile and turbulent, forming a vortex that covers the entire region. It’s a massive area, equivalent to maybe five Californias, and it churns and moves about the Arctic Circle. In April 2011, the vortex — and the hole — moved over northern Russia and Mongolia, Manney said. The climate-monitoring scientists didn’t notice it at the time, but ground-level ultraviolet radiation monitors started to spike.
The ozone layer’s main utility is in protecting Earth from the sun’s UV rays. Without ozone, more radiation would get through to interfere with our DNA, and that of other life forms on Earth. A mobile ozone hole in the northern latitudes thus poses a risk to lots of people.
5: WE NEED MORE DATA
International groups of scientists monitor the Arctic with a suite of Earth-observing satellites, balloons, ground stations and more. But some of their instruments, especially the satellites, are not designed to last for much longer. The instruments onboard NASA’s Aura spacecraft, whose trace gas and cloud measurements were key to this study, were designed to last about 5 years and they’re now about 7, Manney said.
And as we’ve seen before, it’s tough .
“There aren’t immediate plans for other satellites that give us the same kind of comprehensive measurements. So it is a concern as to whether and how much capability we’ll have to monitor not just ozone, but the other chemicals that contribute to destroying ozone,” Manney said.
... AND NOW FOR SOME GOOD NEWS
Combating greenhouse gas emissions and reversing global warming will help — if surface temps don’t rise dramatically, the stratosphere may not cool dramatically, and the chemical reactions that cause ozone depletion may not occur over the Arctic. What's more, humans have already made some progress with the Montreal Protocol, Manney said.
“Having done that, we expect that we are now on a path to where eventually, in several decades, we will stop having enough chlorine to form ozone holes,” she said. “And things we might be able to do to mitigate climate change would also decrease our odds of seeing more severe future ozone loss.”
As a scientist, Manney wouldn’t speculate about other possible solutions — like geoengineering or cloud-seeding projects that would warm up the stratosphere and prevent more ozone depletion, which we'll just go ahead and throw out there. But she does believe with better data and better models, she and others will eventually be able to predict where and when it happens, leading to better warning systems for people on the ground.
“There is the possibility of saying, ‘We’ve had severe ozone loss this winter, and the ozone vortex is expected to be here [in Russia or elsewhere], so you guys should put your sunscreen on,'” she said.
ALMA, the World’s Largest Radio Telescope, Grabs Its First Images
Appropriately enough, the first images captured the Antennae Galaxies, a pair of colliding galaxies replete with stars and stellar nurseries. ALMA’s 39- and 23-foot dish antennae can resolve areas of dense, cold gas that other telescopes could not detect.
sits in the high Chilean desert, about 16,000 feet above sea level and above much of the interfering atmosphere. These pictures were made with 12 telescopes situated relatively close together; science observations during the next few months will be even clearer.
Closer-situated antennae yield a wide field of view, so astronomers can search for items they want to study in more detail. Moving the antennae farther apart provides a narrower focus, like using a finer lens on a regular telescope. Instead of tunable knobs, ALMA has 192 separate antennae pads for the huge dishes to be moved around.
Astronomers submitted more than 900 research proposals for the telescope’s first 9 months of observations, which the European Southern Observatory whittled down to about 100. A few key subjects:
A nearby star system called AU Microscopii, just 33 light-years away, with an infant star harboring a ring of planetisimals;
The dusty disk surrounding HD142527, a young star 400 light-years away, which has enough material to make a dozen Jupiters;
and the great Sagittarius A, the supermassive black hole at the center of the Milky Way.
ALMA observes light at millimeter and sub-millimeter wavelengths, allowing observations of the farthest and oldest phenomena in the observable universe. It’s powerful enough to study the cold, dark remnants of exploded stars, including the first stars, which died a few hundred million years after the Big Bang — that’s an era known as the cosmic dawn.
While this is all going on, more of the 100-ton antennae will keep being added until the observatory is complete sometime in 2013.
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Nobel Prize for Medicine Awarded to Scientist Who Prolonged His Own Life With His Research
The prize, awarded jointly to three scientists, celebrates the discovery of the immune system's front-line responders--though one winner succumbed to cancer three days before
One half is awarded jointly to Bruce Beutler and Jules Hoffmann and one half goes to Ralph Steinman. But Steinman died on Friday after a battle with pancreatic cancer, according to in New York, where he was a cell biologist and director of its Center for Immunology and Immune Diseases. He was diagnosed four years ago, and was able to extend his life using a dendritic-cell based immunotherapy of his own design, the university said. He was 68.
The Nobel committee learned he died three hours after it officially bestowed him with the honor, the Nobel Assembly said Monday. Steinman's own university from his family, as officials were compiling information about his Nobel win. Nobel prizes are not awarded posthumously, but the Nobel Foundation's rules specify that if a person wins an award and dies before accepting it, the prize is still presented.
"The decision to award the Nobel Prize to Ralph Steinman was made in good faith, based on the assumption that the Nobel Laureate was alive," the assembly explained . "This was true – though not at the time of the decision – only a day or so previously." The foundation further explains that this situation is unprecedented in the history of the Nobel Prize.
The split award honors research into the immune system's dual nature. A group of first responder cells seek out and destroy invaders and block their ability to replicate, and a second group bats cleanup, producing antibodies that kill cells which have already been infected. Scientists now know a great deal about the genetic rules underlying these systems, but much of this knowledge stands on the shoulders of Beutler, Hoffmann and Steinman, the Nobel Assembly explains.
In 1996, Hoffmann, now 70, was working with some genetically modified fruit flies and infecting them with fungi or bacteria. He discovered that the activation of a gene called Toll is crucial for switching on the initial immune response that allowed his flies to fight off infection. Then in 1998, Beutler, now 54, was searching for a protein receptor involved in regulating septic shock, which results when the body is overwhelmed by infection. He found a mutation in a mouse gene that looked pretty similar to Hoffmann’s Toll gene. This gene codes for a receptor — nicknamed a Toll-like receptor — that binds to a bacterial product involved in septic shock.
Together, the work showed that insects and vertebrates shared similar molecules that activated the innate immune response — and now scientists knew what the molecules looked like. Since then, scientists have identified a dozen more Toll-like receptors in mice and humans.
Decades before that work, Steinman was pioneering research on the secondary immune response, the adaptive response. In 1973, he discovered the dendritic cell — so named because it has little tails, like dendrites in neurons — and set about explaining their function. They serve as the body’s surveillance cells, constantly moving around and sampling their environment. Steinman proved that dendritic cells activate T cells, a class of white blood cells that are important in .
The immune researchers’ work has been crucial in understanding treatment and prevention of disease, from AIDS to cancer. The research is also relevant for understanding auto-immune and inflammatory diseases, in which the immune system attacks the body’s own cells.
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Bats Have Unique Superfast Squeak Muscles to Make Superfast Echolocation Calls
Bats start out with shorter-rate chirps, increasing their frequency as they approach their quarry and culminating in a superfast pulse called the terminal buzz. Watch the video below to see what this sounds like. Coen Elemans and John Ratcliffe at the University of Southern Denmark set out to study how bats produce this buzz. They also wanted to determine whether the upper buzz limit is a function of how quickly the bats can hear the return signals that bounce off their prey, or whether it’s because of the bats’ own call-producing abilities.
They set up a chamber with 12 microphones and recorded the activities of five different free-flying Daubenton’s bats, little bats found in woodland areas from Britain to Japan. The bats hunted mealworms that were suspended in the chamber. The animals’ chirp rate was so rapid that the researchers knew they couldn’t be using normal skeletal muscle.
They attached the bats’ vocal muscles to a motor and a force monitor, and stimulated the muscles to flex. The researchers monitored how long it took a muscle to twitch, and determined the muscles were able to contract and relax at frequencies up to 180 Hz and, in one case, up to 200 Hz.
They also noticed that echoes from individual calls ended before the start of the next call, so the bats don’t confuse themselves. But a bat could theoretically produce calls at a greater frequency than 200 Hz — up to 400 Hz before echo interference would become a problem. The reason they don’t? The superfast muscles are only so fast.
Andrew Mead, a biology graduate student at the University of Pennsylvania’s School of Arts and Science, said the muscle performance could be equated to a car engine: “It can be tuned to be efficient, or tuned to be powerful depending on what you want it to do.”
Bats trade off some force to achieve the rapid oscillations, he said . “In a way it's like an engine that's been tuned for extremely high RPM.”
These laryngeal muscles contract at a rate 20 times that of the fastest human eye muscles, and about 100 times faster than typical skeletal muscles, the researchers say.
Previously, scientists thought these ridiculously quick muscle contractions were only found in the sound-producing organs of rattlesnakes and some types of fish. In 2008, Elemans , too, and now he’s found them in the first mammal. It suggests that these special muscles are more common than previously thought.
The research is published in today’s issue of the journal Science.
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Video: Plucky Fish Swims Far Away to Find Proper Tool For Eating Dinner
The orange-dotted tuskfish, a species of wrasse, is the second type of wrasse documented using tools in the past few months. A blackspot tuskfish was caught on camera earlier this year; now the first video has been .
The fish digs around in the sand to find a choice clam, picks it up, then swims for a while until it finds a good rock. It proceeds to throw the clam against said rock to open it. This is a fish, remember — not the type of creature you might expect to see using tools. , elephants, , sure — but a fish?
“It requires a lot of forward thinking, because there are a number of steps involved. For a fish, it's a pretty big deal,” said , professor of ecology and evolutionary biology at the University of California, Santa Cruz, who shot the video.
The fact that this behavior has been seen in other fish indicates it may not be a , but a deep-seated behavioral trait in wrasses — and maybe other fishes, too.
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BullDog: A Bigger, Scarier Version of BigDog Gets Closer to the Battlefield
Boston Dynamics is building a bigger, sturdier version of the military’s future trusty companion, and will likely unveil it within a few months. The company’s founder and president, Marc Raibert, shared the LS3 robot's progress Tuesday at a keynote speech at the 2011 IEEE International Conference on Intelligent Robots and Systems. Apparently LS3 (Legged Squad Support System) has been nicknamed BullDog, .
Alas, no fun video yet, as Boston Dynamics is apparently waiting for permission from DARPA to release it.
BullDog, like BigDog, is designed to carry hundreds of pounds of gear for armed forces, ambling over rough terrain and following humans without complaint. The larger version will carry 400 pounds, last 24 hours and carry enough fuel for a 20-mile trek. It will also be able to jump over obstacles, and more easily regain its footing after it falls over. BullDog will also have greater navigational autonomy than BigDog, IEEE says.
The most significant change may be that it’s significantly quieter than BigDog, which is quite obnoxiously, buzzingly loud:
Granted, a prancing, unstoppable four-legged metal beast probably doesn’t need stealth to look awesome and surprise the enemy.
BullDog is a 30-month, $32 million project funded by DARPA’s Tactical Technology Office and the U.S. Marine Corps Warfighting Lab. The project started in early 2010, so we anticipate a full unveiling sometime next year.
Until then, content yourselves with some of .
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Disarming HIV Could Protect the Immune System and Potentially Lead to a Vaccine, New Study Shows
HIV infection sends the immune system into overdrive and eventually exhausts it, which is what leads to AIDS. But removing cholesterol from HIV seems to cripple the virus' ability to over-activate part of the immune system, so it could potentially lead to a vaccine that lets the adaptive immune system attack and destroy the virus — just as it would if HIV was any other pathogen.
Dr. Adriano Boasso, an immunologist and research fellow at Imperial College London, said keeping the body’s first-responder immune cells quiet could have some benefits — the whole system may not burn out so quickly, and could potentially fight off HIV.
“Think of the immune system as a car. HIV forces the car to stay in first gear, and if you do that too long, the engine is not going to last very long,” he said in an interview. “But if we take the cholesterol away, HIV is not capable of attacking the immune system quite as well. Practically, what we’ve done is turn HIV into a normal jump-start of a car.”
Viruses replicate by invading cells and hijacking their machinery, which they use to churn out new copies of their genetic material. Among the repurposed material is cholesterol, which is important in maintaining cellular fluidity, something viruses require to interact with other cells. (This is not related to the way everyone thinks of cholesterol, which is cholesterol in the blood. That type of cholesterol, made of high-density and low-density lipoproteins, is related to heart disease, not HIV and AIDS.)
HIV quickly activates plasmacytoid dendritic cells, or pDCs, which are the first immune cells that respond to the virus. PDCs produce molecules called interferons, which both interfere with the virus’ replication and also switch on adaptive immune cells, like T cells. Boasso and other researchers believe this hyperactivation weakens the secondary immune system, undermining the body’s ability to respond.
But in a new study, Boasso and colleagues show that removing the cholesterol changes HIV, so that it cannot activate the pDCs like it normally would. By preventing these first responder cells from turning on in the first place, the secondary responders — the T cells — can organize a more effective counterassault.
“Modifying the virus affects the way the immune system sees it,” Boasso said. He said it’s like removing the weapons from HIV’s arsenal: “By removing cholesterol, we can turn those little soldiers into an armorless enemy, which can be recognized by the opponent’s army.”
Emily Deal is a postdoctoral fellow at the Gladstone Institute of Virology and Immunology, which is affiliated with the University of California-San Francisco. She studies pDC activation in viral infections, and said the cholesterol removal is allowing less of the HIV into the dendritic cells in the first place — which means there’s less of the virus for the cells to detect, which leads them to produce fewer interferons.
But keeping the pDCs from turning on could be both good and bad, she said.
“What is better for the host in the long run? Is it better to suppress replication early on, but potentially have some of your T cells die? Or what are the lon-term effects of having replication proceed in the absence of interferons, but have your T cells live?” she said. "It's a complicated system."
Ideally, further studies would look at this give-and-take relationship in monkeys, so researchers could determine if a de-cholesterolized version of HIV could be an effective form of vaccine, she said.
“I think it has a shot," she said. "However, pDCs control a lot of the immune system, and if they’re not getting turned on at all, that may have other effects. If you’re trying to use it as a vaccine, it may not induce enough of a response to be protective."
Boasso said the de-cholesterolized HIV could be studied for use in a potential vaccine, but it’s difficult to stimulate the immune system to fight off an invader when the system itself is the target.
“There’s going to be a lot of work to do,” he said.
The study, which also involved researchers at Johns Hopkins University, the University of Milan and Innsbruck University, is published in the journal .