Friday, 14 January 2011

Johnald's Fantastical Daily Link Splurge

Johnald's Fantastical Daily Link Splurge

Tiny Silicon Chip Uses Quantum Physics to Slow Light Down

Posted: 14 Jan 2011 10:37 AM PST

Scientists have built an optical device smaller than a dime that slows light down to 155 miles per second, the slowest ever managed on a chip.

The tiny silicon chip works at room temperatures and can be mass-produced, with 32 chips on a 4-inch silicon wafer. Previous efforts slowed light to just 0.01 miles per second, but this required a roomful of equipment and temperatures near absolute zero.

Those experiments were "fantastic and very inspiring, but with limited practical applications," said electrical engineer Holger Schmidt of the University of California, Santa Cruz, who led the study published in November's Nature Photonics.

Chips based on Schmidt's work could be used to create all-optical systems that would potentially be "cheaper, faster and use less power," said physicist John Howell from the University of Rochester, who was not involved in the study. Slowing light on a chip could eventually be used for optical memory, quantum cryptography, and to create simple quantum computers, he said.


Schmidt's team's method involves shining a red laser through a tabletop maze of mirrors into the optical chip. The laser, just a few times stronger than a laser pointer, travels through a channel on the chip, and hits a 4-mm-long capillary full of rubidium atoms. As the light smacks into the atoms, they absorb it and don't let it through.

The scientists then shine another red laser into the rubidium atoms, triggering a quirky quantum mechanical effect that causes the rubidium's electrons to occupy a different physical state. This turns the previously dense rubidium vapor transparent.

"That was really exciting," Schmidt said. "Without that second beam, it would be opaque."

As the light passed through the rubidium atoms, they acted like a speed bump, slowing it down by a factor of 1,200. The 6-meter-long incoming light pulse was squashed like a Slinky, fitting into just 5 mm on the chip. Reducing the second laser's intensity could slow light even more, potentially even bringing it to a stop, Schmidt said.

"The work is extremely impressive, and a big step forward," said Stephen Harris, an electrical engineer and physicist at Stanford University. Being able to slow down light on a chip at room temperature "could have a lot of impact," he said.

Images: 1) A diagram of the chip, showing the channel through which light travels to hit a capillary full of Rubidium atoms. The capillary connects the two chambers where the Rubidium atoms are stored. (Credit: Brigham Young University). 2) Each of the 32 units fabricated on this four-inch silicon wafer can be used to control the speed of light pulses. (Photo by C. Lagattuta). 3) The tiny light-slowing chip, smaller than a coin, contains two chambers where Rubidium atoms are stored. (Credit: Brigham Young University).

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Airborne Prions Make for 100 Percent Lethal Whiff

Posted: 13 Jan 2011 03:24 PM PST

When sprayed into the air, prions that cause mad cow and other neurodegenerative diseases may be in one of their most lethal forms.

A new study has revealed one short exposure to sprayed prions can be 100 percent lethal in mice. While the discovery doesn't present any foreseeable public health threat, it comes as a surprise to scientists who study prion-based diseases and calls existing safety rules for laboratories and slaughterhouses into question.

"Common knowledge is that prions aren't airborne, and can't cause infection that way," said neuropathologist Adriano Aguzzi of University Hospital Zurich, co-author of a study appearing today in PLoS Pathogens. "We were totally surprised and also a bit frightened at how efficient [airborne infections] were."

Most infectious diseases are spread by bacteria or viruses, which use genes to copy themselves. But prions are a third form of disease discovered in 1982, and they're made only of misfolded proteins. The molecules resemble regular proteins found in the brain cells and other nervous tissues, but their abnormal shape converts healthy proteins into long fibrils that ultimately kill cells.

Like a chain reaction, fibrils create more prions until the host dies from destroyed brain and nervous tissue. All prion infections are 100 percent fatal, and symptoms appear suddenly months or years after infection.

"Prions are like an enemy within, the alien in some B-movie that transforms people to an evil version," said prion biologist Edward Hoover of Colorado State University, who was not involved in the study. "The immune system doesn't see them coming."


Five known human prion diseases exist, including Creutzfeldt-Jakob disease, as well as six non-human diseases, including scrapie, chronic wasting disease and mad cow disease (which sometimes jumps to humans through contaminated meat).

Although prions infect only one to two people per million in the United States each year, as much as 15 percent of deer in some Colorado populations carry chronic wasting disease. Such diseases spread via infected body fluids and tissue, yet only inconclusive evidence on airborne transmission existed until now.

To see if airborne prions could cause infection in mammals, Aguzzi and his team exposed several small groups of mice to different concentrations and exposure times of aerosolized prions that cause scrapie.

All mice except one group, which was exposed to a very light concentration of prions, got infected and died about 150 to 200 days after exposure. When it came to a lethal dose, the researchers also found that prion concentration didn't matter as much as exposure time. A group of four mice exposed for one minute to a light dose of prion-infected fluid, for example, died from scrapie in about 200 days.

Other forms of prion exposure typically require high concentrations of them to do anything, so Aguzzi said the lethality wasn't what he expected. Roughly 100,000 times more prions, for example, are required to cause an infection through the mouth compared to brain-to-brain contamination.

"That's part of the reason why we don't see more cases of prion diseases," Aguzzi said.

Because the incidence of prion disease is so low among humans — and continues to remain low — it's unlikely airborne forms are a significant threat to most people.

"I think this study is interesting and comprehensive, but my big question is this: Where do prions exist in aerosolized form?" said prion biologist Anthony Kincaid of Creighton University, who also was not involved in the research. "People who remove brains or spinal chords often use bone saws, so those might make infected tissue airborne. Otherwise I'm not sure."

Slaughterhouse environments may also be a concern, Kincaid added, but the jury is out until further research is done. Until then, he agreed with Aguzzi and Hoover that laboratory protocols are worth revising.

"My real hope in studying prions is apply what I learn to much more common but similar diseases, such as Alzheimer's," Aguzzi said. "Knowing why aggregated proteins damage neurons will allow us to understand how they affect brain function."

Image: Flickr/Darin House – MOmilkman

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Two New Views of Stunning Starburst Galaxy

Posted: 13 Jan 2011 03:15 PM PST

SEATTLE — This gorgeous new X-ray image of the nearby galaxy M82 shows a frantic burst of star formation that may have been triggered by a close encounter with a nearby galaxy.

M82 is "the prototypical starburst galaxy in the nearby universe," said astronomer Roy Kilgard of Wesleyan University, who presented the new image in a press conference Thursday at the meeting of the American Astronomical Society. The galaxy lies just 12 million light-years from the Milky Way, and is the brightest galaxy in the sky in infrared wavelengths.

The image above was captured by the Chandra X-Ray Observatory over the course of nearly two years.

"It's extraordinary. I've never seen detail like this in an X-ray image before," Kilgard said.

More than 100 point-like X-ray sources show up in Chandra's view of the galaxy, eight of which may be black holes stealing gas and other matter from companion stars much more massive than the sun.

NASA's WISE (Wide-Field Infrared Survey Explorer) also observed M82 (the golden galaxy at the top of the image below) before the telescope ran out of coolant in October 2010. WISE's infrared view covers an area 11 times the area of the full moon, and also captures M82's galactic neighborhood.

The blue grand-spiral galaxy M81 dominates the bottom center of the image, and the small elliptical galaxy NGC 3077 lies to the bottom left. The faint green streaks that crisscross the image are lanes of dust in the Milky Way.

The huge burst of star-forming activity in M82 was probably triggered by a recent near-miss collision with M81, said astronomer Ned Wright of the University of California, Los Angeles. The encounter stopped M82's rotation, and dumped a huge amount of gas into the galaxy's center, where it collapsed into bright, young stars.

Near-miss collisions often result in distorted, wonky-looking galaxies. But for M81, the flyby with M82 may have enhanced its spiral structure.

"Eventually these things will merge into some giant mega-galaxy," Wright said.

The data from the two space telescopes is "quite complimentary," Kilgard said. Combining the X-ray and infrared views of M82 can help astronomers determine how star formation is related to the birth of black holes with stellar companions.

Image: 1) NASA/CXC/Wesleyan/R.Kilgard et al. 2) NASA/JPL-Caltech/UCLA

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Secret Service Study Probes Psyche of U.S. Assassins

Posted: 13 Jan 2011 11:44 AM PST

With public speculation mounting about what motivated a 22-year-old man to attempt to kill a congresswoman, a little-known study by the Secret Service suggests the truth may be frighteningly mundane.

The study of U.S. assassinations over the last 60 years debunks some key myths about the miscreants behind the attacks. The Exceptional Case Study Project, completed in 1999, covers all 83 people who killed or attempted to kill a public figure in the United States from 1949 to 1996.

"We approached a number of people, many in prison," says forensic psychologist Robert Fein, who co-directed the study with Bryan Vossekuil of the Secret Service. "We said you're an expert on this rare kind of behavior. We're trying to aid prevention of this kind of attack. We'd welcome your perspectives."

Fein interviewed 20 of the attackers who were still living and sifted old evidence from cases. His goal was to understand the sequence of thoughts, plans and motivations that transformed a downtrodden, but unremarkable person into an aspiring killer over a period of months or years.

Contrary to popular assumptions about public killings, the attackers didn't conform to any particular demographic profile. But when Fein reconstructed their patterns of thinking, he was able to distill them into a handful of recurring motives for killing a public person — motives that seemed consistent regardless of whether a given individual was delusional or not (and three quarters of those who pulled the trigger were not).


Some hoped to achieve notoriety by killing a well-known person. Others wanted to end their pain by being killed by Secret Service. Still others hoped to avenge a perceived, idiosyncratic grievance unrelated to mainstream politics. Some hoped, unrealistically, to save the country or call attention to a cause. And some hoped to achieve a special relationship with the person they were killing.

Beyond these findings, the study overturns the image of the political or celebrity killer as a menacing stalker. It's true that politicians and celebrities receive hundreds of threats each year — but those threats come from people other than the itchy-fingered trigger-pullers.

Unlike terrorists, who sow panic with public threats, just 4 percent of assailants in the study warned their targets by sending threats. That silence underlined their desire to fly under the radar, says J. Reid Meloy, a forensic psychologist at the University of California in San Diego who studies public figure killings.

The aspiring assailants often chose between several possible victims. And once they chose, they spent weeks, even sometimes years, planning and mulling their attacks.

Undated file photo of Sirhan Sirhan. On June 5, 1968 Sirhan shot Senator Robert F. Kennedy to death minutes after Kennedy claimed victory in the California presidential primary. /AP

Sirhan Sirhan, the man who assassinated Senator Robert Kennedy in 1968, practiced for months at a shooting range. He was seen practicing just eight hours before the killing. And in the investigation that followed, reviews of film footage revealed that Kennedy had been approached by his killer several times in what may have been dry runs in the weeks before his death.

All of this bears on the case of Jared Loughner, the 22-year-old accused of shooting U.S. representative Gabrielle Giffords on Jan. 8. "As it has unfolded," says Meloy, "it's very consistent with what we know about public-figure attackers."

Loughner apparently met Giffords at a rally in 2007, where her answer to a question he asked is said to have disappointed him. "If he felt angry and perhaps humiliated," says Meloy, "that could have been the beginning of the grievance" that eventually made her a target.

Or, if Loughner was driven by another motive — say, notoriety, suicide, or calling attention to a cause — then bumping into Giffords might simply have brought to his attention a local, accessible target, in much the same way that female TV news anchors — locally grown and available for nightly viewing — are also targeted by stalkers.

One thing is certain: In the months leading up to his attack, Loughner slid into decline. Outbursts in class led to meetings with school administrators, which led to his withdrawal from community college. On Nov. 30 he bought a gun.

These meltdowns are common in the year preceding an attack. Nearly half of the assailants in the Secret Service study lost their marriage, job, health or a loved one. That disintegration set them onto another path: The unthinkable gradually became thinkable. The assailant-in-the-making developed tunnel vision around a single obsession — and other opportunities in life seemed to recede from their view.

"Think of people circling the drain," says Fein. "Before they went down the drain they came to see that violence was acceptable as a way to solve their problem."

One of the cases in the study was a man named H.J. who during the Reagan and Bush-senior years of the 1980s was troubled by voices that he believed emanated from illegal government satellites. He spent several years buying weapons and making threats to the voices, in hopes that threats alone would quiet them.

Several times the voices became so intolerable that H.J. began driving to Washington with the intent of killing someone. But each time as he drove they faded, prompting him to abandon a bloody errand that no longer seemed necessary.

This hesitance to spill blood isn't unique. "Many people," says Fein, "are quite ambivalent about bad things they're thinking about doing."

John W. Hinckley Jr. is shown in this undated photo. A divided appeals court panel cleared the way Friday, Jan. 15, 1999 for Hinckley to make supervised day trips away from the mental hospital where he has been confined since he tried to assassinate former President Reagan. /AP

H.J. eventually arrived in Washington, intent on killing a member of the president's cabinet, spurring a Watergate-style investigation, and ending the satellite program he had imagined. He was arrested before he got off a shot.

But the Secret Service prefers to spot people like H.J. earlier on, and if possible, guide them to a different path without resorting to handcuffs.

A suspicious letter to a prominent official is likely to generate a knock on the door from two well-dressed agents, says Fein.

Those agents, after sitting down in the living room, are likely to afford the letter writer the kind of polite listening that normally costs $150 an hour in a therapist's office, as they assess whether he or she represents a threat.

"Far more people are investigated, examined and spoken with than actually end up being hospitalized," says Robert T.M. Phillips, a Maryland-based forensic psychiatrist who worked with the Secret Service for 15 years to assess people who threatened the president.

Sometimes the Person of Concern is referred for mental health services. Other times the Secret Service agents themselves continue to engage the person with frequent visits and calls.

Fein tells of one letter he read, written by a Person of Concern to the Secret Service agent charged with preventing him from harming a government figure. The letter was addressed: "To Agent Smith, my only friend in the whole world."

Efforts to turn problem people away from doing unfortunate things don't always succeed. A woman, called Ms. Doe, cited in a separate study by Phillips, showed up at the White House with flowers for Bill Clinton. Another time she traveled to D.C. hoping to jog with him. She gave no indication of posing a threat, and so was released after each incident.

But after years of frequenting presidential events and sending gifts and love letters, Ms. Doe crossed a line both figurative and real: She breached the security zone around Clinton's limousine while carrying a cellphone, an item easily mistaken for a handgun.

In light of the danger she posed to herself — and fears that her affection for Clinton, if rejected, might give way to rage — Ms. Doe was committed to a mental ward.

Jared Lee Loughner, unlike the others, was never detected by the system meant to intercept him. His true thoughts leading up to the massacre, if they are ever revealed, will take time to emerge. But history provides some hints.

"The reality of American assassination is much more mundane, more banal, than assassinations depicted [in movies]," concludes Fein in his report on the Secret Service study. These people aren't especially interesting, he adds: They are "neither monsters nor martyrs."

Top image: Satan tempting Booth to the murder of the president. /Library of Congress.

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Mystery Disease Found in Pacific Salmon

Posted: 13 Jan 2011 11:05 AM PST

Traces of viral activity have been found in a mysteriously dwindling population of Pacific salmon, hinting at an explanation for deaths that have so far baffled scientists.

In fish returning to Canada's Fraser River, site of the die-off and home to one of North America's last great sockeye salmon runs, researchers discovered patterns of gene expression usually seen when a body fights a virus.

The findings are not conclusive, and pose many as-yet-unanswered questions. "This is the discovery stage," said Scott Hinch, a University of British Columbia salmon ecologist. "But it raises all kinds of concerns."

The importance of salmon in the Fraser and elsewhere isn't only in the intrinsic marvelousness of creatures that are born far from the sea, spend adulthood thousands of miles away in the open ocean, and return in a final blaze of upstream glory to spawn and die in the waters of their birth.

The Fraser River's wild salmon fishery is worth about $1 billion annually. And that's just the obvious value. Salmon migration is also a physical circuit to the sea, each body a mass of nutrients carried from ocean to continental interior, scattered by scavengers across the land.

Some researchers think the Pacific northwest's forests are so lush not just because of the region's climate, but because its soils were fertilized for thousands of years by salmon bodies — an extraordinary line of natural credit, now threatened by dams and overfishing.

Unlike other major river systems on North America's Pacific coast, however, the Fraser is largely undammed. Even as other Pacific salmon populations vanished or entered boom-and-bust cycles typical of ecosystems on the brink of collapse, its own populations persisted. Until the early 1990s, about 8 million sockeye salmon returned each year to spawn. Then their numbers started drop.


In some years, half of the Fraser's returning sockeye die before spawning. In other years, mortality is closer to 95 percent. "The causal mechanisms of this premature mortality have eluded multidisciplinary research by scientists and fisheries managers," wrote Hinch and his colleagues, led by biologist Kristina Miller of Fisheries and Oceans Canada, in a Jan. 14 Science paper.

In less academic terms, the fish are dying, and nobody can figure out why.

Five years ago, the researchers noticed that some Fraser sockeye appeared to show unusual signs of physiological stress while at sea. In the new study, they take that work to the genomic level. Salmon were caught, biopsied and tagged with radio transmitters in the ocean, about 120 miles from the Fraser; at the Fraser's mouth; and again on their spawning grounds. For each stage, the researchers could look for patterns in gene expression, then see if they tracked with differences in fate.

A pattern stood out. Many of the fish displayed high activity in a set of genes typically activated in response to viral infection. When this genomic signature was found in ocean fish, they were 13.5 times more likely to die before reaching the Fraser. When the signature was found in fish tagged in the river, they were 50 percent more likely to die before reaching their spawning grounds. In fish tagged on their spawning grounds, those with the signature were 3.7 times more likely to die without mating.

"It's excellent science," said fish microbiologist James Winton of the U.S. Geological Survey, who was not involved with the research. "This appears to be quite important." Winton applauded the researchers' approach, which had never before been used in salmon, a species for which researchers only notice the most obvious diseases.

"The fact that, within the physiology of these fish, you can see signs of who is likely to make it and who won't, is amazing," said Michael Webster, a program officer at the Gordon and Betty Moore Foundation's Wild Salmon Ecosystems Initiative.

However, though a virus is the most likely culprit, it hasn't yet been isolated. The findings open up a range of new questions, said each of the researchers: If the pattern is indeed caused by a virus widespread in the Fraser, where did it come from? Was it introduced, just as infectious hematopoietic necrosis — a lethal virus endemic in Pacific salmon — has been transferred around the world? If it was always there, did it suddenly evolve into a more virulent form? Or is something else exacerbating its effects?

The researchers suspect climate has a role in the answers to some of these questions. In the last 40 years, the Fraser's waters have warmed by about 4 degrees Fahrenheit, with most of that coming in the last 15 years. "In some cases, that temperature alone is pushing fish stocks to the edge," said Hinch.

Heat and stress can weaken fish, making them more vulnerable to disease. Changing temperatures also change the ranges of microbes and parasites, allowing them to move into new regions. Over the last decade, the Yukon River has been invaded by Ichthyophonus, a parasite that threatens the river's Chinook salmon population. It's believed to have spread because of changing temperatures.

"We use the term emerging diseases. In humans, it's the SARS coronavirus, or avian flu. They also occur in fish. Part of [their increasing incidence] is due to the fact that more people are looking, with better tools. Part of it is due to us moving pathogens around the globe. And part of it due to increasing stress on these animals," said Winton. "At some point, we're going to add the last straw."

Images: Kristina Miller.

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Citation: "Genomic Signatures Predict Migration and Spawning Failure in Wild Canadian Salmon." By Kristina M. Miller, Shaorong Li, Karia H. Kaukinen, Norma Ginther, Edd Hammill, Janelle M. R. Curtis, David A. Patterson, Thomas Sierocinski, Louise Donnison, Paul Pavlidis, Scott G. Hinch, Kimberly A. Hruska, Steven J. Cooke, Karl K. English, Anthony P. Farrell. Science, Vol. 331 No. 6014, January 14, 2010.