Saturday, 26 February 2011

Johnald's Fantastical Daily Link Splurge

Johnald's Fantastical Daily Link Splurge

Exotic Superfluid Found in Ultra-Dense Stellar Corpse

Posted: 25 Feb 2011 01:38 PM PST

The ultra-dense meains of the galaxy's youngest supernova are full of bizarre quantum matter.

Two new studies show for the first time that the core of the neutron star Cassiopeia A, is a superfluid, a friction-free state of matter that normally only exists in ultra-cold laboratory settings.

"The interior of neutron stars is one of the best kept secrets of the universe," said astrophysicist Dany Page of the National Autonomous University in Mexico, lead author of a paper in the Feb. 25 Physical Review Letters describing the state of the star. "It looks like we broke one of them."

Cassiopeia A (Cas A) was a massive star 11,000 light-years away whose explosion was observed from Earth about 330 years ago. The supernova left behind a tiny, compact body called a neutron star, in which matter is so densely packed that electrons and protons are forced to fuse into neutrons. Neutron star material is some of the most extreme matter in the universe. Just a teaspoonful of neutron star stuff weighs about 6 billion tons.

The neutron star in Cas A was first spotted in 1999, shortly after the Chandra X-Ray Observatory began scanning the sky for objects that emit X-rays.

Last year, astronomers Craig Heinke of the University of Alberta and Wynn Ho of the University of Southampton noticed something odd: The neutron star was cooling down at an alarmingly fast rate. In just 10 years, the star had cooled from 2.12 million degrees to 2.04 million degrees, a drop of 4 percent.


Theoretical models predicted that neutron stars should cool slowly as the neutrons inside decayed into electrons, protons and nearly-massless particles called neutrinos that flee the star quickly, taking heat with them.

But ordinary neutron decay is too slow. Two competing groups of physicists, one led by Page and one including Heinke and Ho, saw that something else must be going on in Cas A.

Almost simultaneously, both teams came to the same solution: The matter inside the neutron star is converting to a superfluid as astronomers watch. Heinke and Ho's paper will appear in the Monthly Notices of the Royal Astronomical Society.

Here's how it works: Normally, the laws of quantum mechanics dictate that a collection of neutrons can get only so cold, but no colder. But at extremely cold temperatures in the lab, or the extremely high pressures inside a neutron star, pairs of neutrons can link up. Together, the neutron pairs relax into the lowest energy state quantum physics allows, and convert to a superfluid.

"A superfluid is essentially a macroscopic quantum liquid, in which if you take any given particle in the fluid, it's moving in essentially the same way as the particles around it," said Bennett Link of the University of Montana, who was not involved in the new studies. "The whole system behaves as a quantum system even though it's large in size."

Superfluids flow without friction. On Earth, they can climb walls and escape from airtight containers. When the particles in a superfluid are charged, the fluid is a superconductor, which carries electricity with no resistance.

As the neutrons and protons in the neutron star link up to form superfluids, they release massive amounts of neutrinos. The mass exodus of neutrinos fleeing Cas A explains the rapid cooling, the physicists conclude.

The idea that neutron stars should contain superfluids had been around since the 1950s. Page and colleagues had even predicted theoretically that the core of Cas A in particular should be a superfluid.

"We knew that it was there, our models had it all included before, but we did not have the data to actually hang our coats on," said Madappa Prakash of Ohio University, a coauthor on Page's paper.

Page didn't expect that superfluidity would actually show itself in Cas A. When he learned that Heinke and Ho had seen the star's temperature drop precipitously, "I jumped and my head hit the ceiling," he said.

Both teams knew the other group was working on the same idea, and raced in friendly competition to publish their theory first. Page's team ended up winning the race by one day. Heinke and Ho were waiting for one more observation from Chandra, taken in November 2010, before submitting their paper for publication.

The papers differ only in the details. The two teams made different assumptions about how hot the neutrons were to begin with, so their calculations for the temperature at which the superfluid state is possible are different.

Both teams predict that Cas A will continue to cool down over the next 10 years.

"That allows people to test it against alternative hypotheses, such as, it's some kind of episodic thing," Link said. "If it's still cooling at the same rate, that would give evidence for their hypothesis, that we are actually seeing a superfluid form."

X-ray Image: NASA/CXC/UNAM/Ioffe/D.Page,P.Shternin et al; Optical Image: NASA/STScI; Illustration: NASA/CXC/M.Weiss

"Rapid Cooling of the Neutron Star in Cassiopeia A Triggered by Neutron Superfluidity in Dense Matter." Dany Page, Madappa Prakash, James M. Lattimer, and Andrew W. Steiner. Physical Review Letters, Vol. 106 No. 8, Feb. 25, 2011. DOI: 10.1103/PhysRevLett.106.081101.
"Cooling neutron star in the Cassiopeia A supernova remnant: Evidence for superfluidity in the core." Peter S. Shternin, Dmitry G. Yakovlev, Craig O. Heinke, Wynn C. G. Ho, Daniel J. Patnaude. Monthly Notices of the Royal Astronomical Society, accepted.

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Brain-Wasting Prions Amass Before Dealing Deathblow

Posted: 25 Feb 2011 01:30 PM PST

Infectious proteins that cause brain-wasting conditions like mad cow disease appear to build up in the brain long before initiating the cascade of deterioration that leads to dementia and death, a new study of mice finds.

The findings suggest that other factors besides the misshapen infectious proteins characteristic of prion diseases may control the lethality of the disease. If scientists can determine what those factors are, future treatments may be able to prevent the infectious protein diseases — which include mad cow disease, scrapie in sheep and Creutzfeldt-Jakob disease in people — from progressing to a fatal stage.

"We don't know what's going on here, but we do know there's something interesting," says John Collinge, director of the United Kingdom Medical Research Council Prion Unit in London, who headed the new study.

Findings reported by Collinge and his colleagues in the Feb. 24 Nature contradict the idea that infectious versions of a normal brain protein called PrP accumulate slowly, gradually twisting all of the healthy copies of the protein into a disease-causing form. Researchers have thought that the disease-causing prions slowly build up to toxic levels that spell the death of brain cells.

But the new study shows that the process is anything but gradual, and that infection and toxicity are independent stages of the disease. Prions quickly build up in the brains of mice over the course of a month or two, Collinge and his colleagues found, peaking at about 100 million infectious particles per brain.

That level remains constant for months with no evidence of disease.

"Whatever you do, it sort of stops at that level and remains there for the duration of the infection," says Collinge.


Researchers had expected that if they increased the amount of the normal PrP protein in the mice's brains, the number of infectious particles would increase as well. But instead, prion levels plateaued. No one knows what stops mice from making ever more infectious particles, but the researchers speculate that there may be some substance that puts a ceiling on the number of prions in the brain.

Although the number of infectious particles in the brain didn't change, the length of the incubation period between the initial infection and the onset of disease was faster in mice that made more PrP in their brains. The result suggests that how fast an animal will get sick depends upon how much PrP is in the brain.

The lag time between prion buildup and disease suggests that infection is a separate process from toxicity. Collinge and his colleagues speculate that some other as-yet-unknown molecule or cellular process might be needed to make the switch between infectious and toxic prions.

"It's provocative," says Reed Wickner, a geneticist at the U.S. National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland, of the study. The idea that some other substance might be needed to convert the prion into a lethal form is "a reasonable suggestion, but there may be other explanations, too," he says.

He speculates that number of prions in the brain may be limited, but the size of each particle is not. It could be that filaments of prion protein inside cells just keep getting bigger and bigger until they finally become lethal to the cell.

Collinge agrees that the size of the prion filament may matter, but says that the new research clearly shows that prions don't directly kill brain cells. Another possibility is that the production of prions depletes some important factor from brain cells, he says. When that substance is used up, cells die.

He and his team are now trying to determine if the toxic form of the prion protein is biochemically distinct from the infectious form.

Image: A cow affected in 2003 by bovine spongiform encephalopathy (BSE), a prion-based disease that degrades the nervous system. (Dr. Art Davis/CDC)

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How One Nuclear Skirmish Could Wreck the Planet

Posted: 25 Feb 2011 12:00 PM PST

Image: A nuclear bomb test. Nevada Division of Environmental Protection

WASHINGTON — Even a small nuclear exchange could ignite mega-firestorms and wreck the planet's atmosphere.

New climatological simulations show 100 Hiroshima-sized nuclear bombs — relatively small warheads, compared to the arsenals military superpowers stow today — detonated by neighboring countries would destroy more than a quarter of the Earth's ozone layer in about two years.

Regions closer to the poles would see even more precipitous drops in the protective gas, which absorbs harmful ultraviolet radiation from the sun. New York and Sydney, for example, would see declines rivaling the perpetual hole in the ozone layer above Antarctica. And it may take more than six years for the ozone layer to reach half of its former levels.

Researchers described the results during a panel Feb. 18 at the annual meeting of the American Association for the Advancement of Science, calling it "a real bummer" that such a localized nuclear war could bring the modern world to its knees.

"This is tremendously dangerous," said environmental scientist Alan Robock of Rutgers University, one of the climate scientists presenting at the meeting. "The climate change would be unprecedented in human history, and you can imagine the world … would just shut down."

To defuse the complexity involved in a nuclear climate catastrophe, sat down with Michael Mills, an atmospheric chemist at the National Center for Atmospheric Research, who led some of the latest simulation efforts.

'It's pretty clear this would lead to a global nuclear famine.' In your simulation, a war between India and Pakistan breaks out. Each country launches 50 nukes at their opponent's cities. What happens after the first bomb goes off?

Michael Mills: The initial explosions ignite fires in the cities, and those fires would build up for hours. What you eventually get is a firestorm, something on the level we saw in World War II in cities like Dresden, in Tokyo, Hiroshima and so on.

Today we have larger cities than we did then — mega cities. And using 100 weapons on these different mega cities, like those in India and Pakistan, would cause these firestorms to build on themselves. They would create their own weather and start sucking air through bottom. People and objects would be sucked into buildings from the winds, basically burning everything in the city. It'll burn concrete, the temperatures get so hot. It converts mega cities into black carbon smoke.


Atmospheric scientist Michael Mills of NCAR. Dave Mosher/ I see — the firestorms push up the air, and ash, into the atmosphere?

Mills: Yeah. You sometimes see these firestorms in large forest fires in Canada, in Siberia. In those cases, you see a lot of this black carbon getting into the stratosphere, but not on the level we're talking about in a nuclear exchange.

The primary cause of ozone loss is the heating of the stratosphere by that smoke. Temperatures initially increase by more than 100 degrees Celsius, and remain more than 30 degrees higher than normal for more than 3 years. The higher temperatures increase the rates of two reaction cycles that deplete ozone. And the ozone layer is in the stratosphere, correct?

Mills: OK, so we live in the troposphere, which is about 8 kilometers [5 miles] thick at the poles, and 16 km [10 miles] at the equator.

At the top of the troposphere, you start to encounter the stratosphere. It's defined by the presence of the ozone layer, with the densest ozone at the lowest part, then it tails off at the stratopause, where the stratosphere ends about 50 km [30 miles] up.

We have a lot of weather in the troposphere. That's because energy is being absorbed at the Earth's surface, so it's warmest at the surface. As you go up in the atmosphere it gets colder. Well, that all turns around as you get to the ozone layer. It starts getting hotter because ozone is absorbing ultraviolet radiation, until you run out of ozone and it starts getting colder again. Then you're at the mesosphere.

How Nukes Gobble Up Ozone

When we talk about ozone, we're talking about the odd oxygen family, which includes both ozone (O3) and atomic oxygen (O). Those two gases can interchange rapidly within hours.

Ozone is produced naturally by the breakdown of molecules of oxygen, O2, which makes up 20 percent of the atmosphere. O2 breaks down from ultraviolet solar radiation and splits it into two molecules of O. Then the O, very quickly, runs into another O2 and forms O3. And the way O3 forms O again is by absorbing more UV light, so it's actually more protective than O2.

Ozone is always being created and destroyed by many reactions. Some of those are catalytic cycles that destroy ozone, and in those you have something like NO2 plus O to produce NO plus O2. In that case, you've gotten rid of a member of the odd oxygen family and converted it to O2. Well, then you've got an NO which can react with ozone and produce the NO2 back again and another O2. So the NO and NO2 can go back and forth and in the process one molecule can deplete thousands of molecules of ozone.

It's a similar process to chlorofluorocarbons, Those are the larger molecules that we've manufactured that don't exist naturally. They break down into chlorine in the stratosphere, which has a powerful ozone-depleting ability. —Michael Mills Where do the nukes come in? I mean, in eroding the ozone layer?

Mills: It's not the explosions that do it, but the firestorms. Those push up gases that lead to oxides of nitrogen, which act like chlorofluorocarbons. But let's back up a little.

There are two important elements that destroy ozone, or O3, which is made of three atoms of oxygen. One element involves oxides of nitrogen, including nitrogen dioxide, or NO2, which can be made from nitrous oxide, or N2O — laughing gas.

The other element is a self-destructive process that happens when ozone reacts with atomic oxygen, called O. When they react together, they form O2, which is the most common form of oxygen on the planet. This self-reaction is natural, but takes off the fastest in the first year after the nuclear war.

In years two, three and four, the NO2 builds up. It peaks in year two because the N2O, the stuff that's abundant in the troposphere, rose so rapidly with the smoke that it's pushed up into the stratosphere. There, it breaks down into the oxides like NO2, which deplete ozone. So firestorms suck up the N2O, push it up into the stratosphere, and degrade the ozone layer. But where does this stuff come from?

Mills: N2O is among a wide class of what we call tracers that are emitted at the ground. It's produced by bacterias in soil, and it's been increasing due to human activities like nitrogen fertilizers used in farming. N2O is actually now the most significant human impact on the ozone, now that we've mostly taken care of CFCs. You did similar computer simulations in the past few years and saw this ozone-depleting effect. What do the new simulations tell us?

Mills: Before, we couldn't look at the ozone depletion's effects on surface temperatures; we lacked a full ocean model that would respond realistically. The latest runs are ones I've done in a community earth system model. It has an atmospheric model, a full-ocean model, full-land and sea-ice models, and even a glacier model.

We see significantly greater cooling than other studies because of ozone depleting. Instead of a globally averaged 1.3-degree–Celsius drop, which Robock's atmospheric model produced, it's more like 2 degrees. But we both see a 7 percent decrease in global average precipitation in both models. And in our model we see a much greater global average loss of ozone for many years, with even larger losses everywhere outside of the tropics.

I also gave this to my colleague Julia Lee-Taylor at NCAR. She calculated the UV indexes across the planet, and a lot of major cities and farming areas would be exposed to a UV index similar to the Himalayas, or the hole over the Antarctic. We're starting to look at the response of sea ice and land ice in the model, and it seems to be heavily increasing in just a few years after the hypothetical war.

Massive global ozone loss predicted following regional nuclear conflict. Michael Mills/NCAR/NSF What would all of this do to the planet, to civilization?

Mills: UV has big impacts on whole ecosystems. Plant height reduction, decreased shoot mass, reduction in foliage area. It can affect genetic stability of plants, increase susceptibility to attacks by insects and pathogens, and so on. It changes the whole competitive balance of plants and nutrients, and it can affect processes from which plants get their nitrogen.

Then there's marine life, which depends heavily on phytoplankton. Phytoplankton are essential; they live in top layer of the ocean and they're the plants of the ocean. They can go a little lower in the ocean if there's UV, but then they can't get as much sunlight and produce as much energy. As soon as you cut off plants in the ocean, the animals would die pretty quickly. You also get damage to larval development and reproduction in fish, shrimp, crabs and other animals. Amphibians are also very susceptible to UV.

A 16 percent ozone depletion could result in a 5 percent loss in phytoplankton, which could result in a 7 percent loss in fisheries and aquaculture. And in our model we see a much greater global average loss of ozone for many years; the global average hides a lot. This doesn't sound very good at all.

Mills: No, as we said it's a real bummer. It's pretty clear this would lead to a global nuclear famine.

You have the inability to grow crops due to severe, colder temperatures and also the severe increases in UV light. You have the loss of plants and proteins in the oceans, and that leads to widespread food shortages and famine (PDF).

The first three layers of the atmosphere. NOAA There have been thousands of nuclear tests. Why hasn't this already happened?

Mills: We're not talking about direct impacts of the explosions themselves, but the firestorms that result when you detonate these in cities. Most tests were in deserts or atolls or space or underground. When you talk nuclear reductions, you're wading into political territory. As a scientist, how do you handle that?

Mills: The response to this from the policy community has been rather underwhelming. We know, from what both Gorbachev and Reagan have said in anecdotes, that these kinds of studies had a big impact on thinking at the time. People started realizing nuclear war was not something you can win. You'd just destroy the whole planet.

That led to some of the dramatic reductions we saw in the original START treaty, but we still have the ability to basically destroy the planet with one-tenth of 1 percent of the world's current arsenals.

By the way, there's nobody really funding these kinds of studies. All of us here are doing these on our own time. You can't get grants to do this kind of research. It's puzzling to me. What would you like to see happen?

Mills: We'd all like to see much more dramatic reductions in the number of nuclear weapons we're seeing proposed in the new START treaty, and the SORT treaty under the Bush administration. These just seem like refinements, in which the number of weapons is reduced, but each airplane counts as one weapon that can carry multiple bombs. So we might not be seeing any reductions. Should nations have any nukes?

Mills: How many times do you need to explode a nuclear weapon in your enemy's capital to deter them? I think just once. But given the consequences, I don't think it's reasonable to have any.

Ultraviolet radiation indexes before and after a simulated regional nuclear war, with compensation for black carbon (BC) soaking up some of the radiation. A level of 11 or higher is considered an extreme risk of harm from unprotected sun exposure. Michael Mills/NCAR/NSF

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Mosquito-Attacking Fungus Engineered to Block Malaria

Posted: 25 Feb 2011 10:45 AM PST

By John Timmer, Ars Technica

Although public health efforts have eradicated some diseases and helped limit the impact of many others, malaria continues to present a massive public health issue. A large fraction of the world's population lives in areas where the parasite poses a risk, and it kills a million people annually, most of them in the developing world.

The malarial parasite, Plasmodium, has proven tough to tackle for a variety of reasons. Once in a human, it manages to change the proteins that cover its surface often enough that our immune systems have trouble mounting a successful response. Unlike a bacteria or virus, the parasite is a eukaryote, just like humans, which means that it's harder to find unique biochemical properties that would let us target it with drugs. Plasmodium has also been able to evolve resistance to the few drugs that we've been using to treat it. That evolution of resistance extends to its vectors, a few species of mosquitoes, which have also evolved resistance to many of the pesticides we have used to keep them in check.

All of that might seem to be enough to make tackling malaria seem like an intractable problem. But some researchers are reporting some success with a new approach to limiting its spread: engineering a mosquito parasite to attack it before it can reach humans.

The species of mosquitoes that transmit malaria are themselves vulnerable to parasites, including some forms of fungus. This has led to interest in using these fungi as a form of biological insecticide. But the fungus doesn't always kill quickly enough, and if it did, it might end up facing the same sorts of problems that chemical insecticides do: the mosquitoes would simply evolve resistance to the fungus as well.

The solution the researchers arrived at is to use a form of fungus that doesn't kill the mosquitoes until late in their lives, after they've had a chance to reproduce. This keeps them from evolving resistance, but wouldn't keep them from spreading Plasmodium. To do that, they turned to a bit of genetic engineering, creating fungi that produce various proteins that attack the parasite.


The authors tried a variety of approaches. These parasites exit the mosquito through its salivary gland, so the authors created a modified protein that coated the glands, blocking Plasmodium's attempts to latch on to them. They also used a fragment of an antibody that binds directly to Plasmodium's, as well as a toxin present in scorpion venom that kills it. They merged two of the approaches, fusing the venom protein to the one that coats the salivary gland.

To a degree, all of them worked. The fungus alone had a weak effect on the invasion of the salivary glands by Plasmodium, dropping it by 15 percent. But the engineered fungi dropped it by anywhere from 75 to 90 percent. Two of the combined approaches dropped it by 97 and 98 percent. Thus, in the presence of these modified parasites, Plasmodium had a hard time getting to where it could infect humans.

Depending on the precise timing of fungal infection, the authors estimate that it could reduce transmission by 75-90 percent if it reaches the mosquitoes within 11 days of their picking up the Plasmodium. And that's a conservative estimate, given that this estimate was based simply on the presence or absence of the malarial parasite in the salivary glands. The levels in the fungus-infected animals were greatly reduced, which should limit transmission even further.

Although this shouldn't select for resistant mosquitoes, it still has the potential to drive the evolution of Plasmodium that can resist the scorpion toxin. There are two reasons the authors think this might not be a huge problem. For one, the fungus can obviously express a number of toxins at the same time, which makes it much more difficult for Plasmodium to evolve a way around it. The other thing is that there are many proteins that could potentially be used to target it; this is especially appealing, given that an antibody fragment was one of the proteins used in this experiment, suggesting that it should be possible to create a large panel of interfering molecules.

The other nice thing about this approach is that this fungus (or its relatives) can attack other mosquito species, including the ones that spread Dengue fever. This is a very promising fungus.

The general approach holds promise as well, since we reported on another use of an engineered, disease-fighting pathogen already this month. There have been millions of years of evolution that help pathogens target specific species and tissues, something that we're rarely able to do with drugs. If it's possible to take advantage of that specificity, it can be a powerful tool.

Image: A mosquito drawing blood. (James Gathany/CDC)

Citation: "Development of Transgenic Fungi That Kill Human Malaria Parasites in Mosquitoes." Weiguo Fang, Joel Vega-Rodríguez, Anil K. Ghosh, Marcelo Jacobs-Lorena, Angray Kang, and Raymond J. St. Leger. Science, Vol. 331, No. 6020, Feb. 25, 2011. DOI: 10.1126/science.1199115

Source: Ars Technica.

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Navigational ‘Magic’ of Sea Turtles Explained

Posted: 24 Feb 2011 03:28 PM PST

For centuries, determining longitude was an extremely difficult task for sailors, so difficult that it's been thought improbable — if not impossible — for animals to do it.

But migratory sea turtles have now proved capable of sensing longitude, using almost imperceptible gradients in Earth's magnetic field.

"We have known for about six years now that the magnetic map of turtles, at a minimum, allows turtles to … detect latitude magnetically," said biologist Ken Lohmann of the University of North Carolina, who describes the turtle's power Feb. 24 in Current Biology. "Up until now, that was where the story ended."

Lohmann specializes in animal navigation, and work from his laboratory and others have exhaustively demonstrated how sea turtles — along with many birds, fish and crustaceans — use gradients in Earth's magnetic field to steer.


Magnetic Reception Found in Pigeon Ears

It's not just sea turtles showing off geomagnetic tricks. Birds, known to use geomagnetic location through magnetically sensitive particles in their eyes and beak, also appear to sense magnetism with their ears.

In another Current Biology study published Feb. 24, Washington University neurobiologists Le-Qing Wu and David Dickman follow up on earlier observations of magnetically sensitive compounds in birds' vestibular lagena, an inner-ear structure.

Wu and Dickman held 23 homing pigeons in total darkness for 72 hours within a rotating magnetic field. Aftewards they killed the birds and searched their brains for activation in regions linked to orientation, spatial memory and navigation.

The researchers then repeated the study with five birds whose lagenae were surgically disabled. The brain navigation patterns were altered, suggesting a navigational role for the lagena.

According to Wu and Dickman, cell receptors in the lagena, which are known to respond to head tilt in relation to gravity, likely interact with those magnetically sensitive particles. The results may encode a "geomagnetic vector" that links motion, direction and gravity.

Fish, amphibians and reptiles also possess the same ear structure, raising the possibility of the mechanism being widespread in the animal kingdom.

Those differences, however, are far greater by latitude than by longitude. Travel north or south from Earth's magnetic poles, and their pull weakens noticeably. Travel straight east or west, and the pull doesn't change. Instead the pull's angle changes, and only to an infinitesimally slight degree.

That turtles and other migratory animals could detect such a small change was considered unrealistic, but experiments on animals released in out-of-the-way locations repeatedly described them finding home with unerring accuracy and efficiency, explicable only as a product of both longitudinal and latitudinal awareness.

Several nonmagnetic explanations were proposed, foremost among them a "dual clock" mechanism analogous to human methods of calculating longitude, which sailors perform by comparing precise differences between the time locally and at an arbitrary longitudinal line, such as the Greenwich Meridian. No such mechanism has been found, however, and longitudinal differences in local airborne or waterborne chemicals don't seem to explain animals' uncanny long-distance steering.

"A skeptic could reasonably believe that the latitudinal cue is magnetic, but that determining east-west position depends on magic," wrote James L. Gould, a Princeton University evolutionary biologist, in a 2008 Current Biology commentary on animal navigation.

In the new study, researchers led by Lohmann and graduate student Nathan Putnam, also a UNC biologist, placed hatchling loggerhead sea turtles from Florida inside pools of water surrounded by computer-controlled magnetic coil systems.

By varying the currents, Lohmann and Putnam could precisely reproduce the geomagnetic characteristics of two points at identical latitude, but on opposite sides of the Atlantic. Into each pool they placed the hatchlings, which in the wild would instinctively follow a migratory path from their home beach and into the currents that circle the Sargasso Sea and loop around the Atlantic.

In the first pool, programmed to the geomagnetic field in the western Atlantic near Puerto Rico, the turtles swam northeast, on the same trajectory as loggerheads in the wild at that locale. In the other pool, set to the geomagnetics of the eastern Atlantic near the Cape Verde islands, the turtles swam northwest.

No other cues could explain their directions. Against reasonable expectation, the turtles clearly sensed differences in geomagnetic angle.

Gould, who was not involved in the study, wrote an accompanying commentary. Whereas his earlier article was titled "Animal Navigation: The Longitude Problem," this was called "Animal Navigation: Longitude at Last." The findings are "the final piece of the puzzle," he wrote.

Lohmann now plans to study whether currents affect the turtles' longitudinal compass, and whether the turtles detect differences over short distances. He also suspects that other animals may have a similar longitudinal compass.

"The mechanism we've found in turtles might also exist in birds," he said.

Image: Upendra Kanda/Flickr.

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Citations: "Longitude Perception and Bicoordinate Magnetic Maps in Sea Turtles." By Nathan F. Putman, Courtney S. Endres, Catherine M.F. Lohmann, and Kenneth J. Lohmann. Current Biology, Vol. 21 Issue 4, Feb. 24, 2011.

"Animal Navigation: Longitude at last." By James L. Gould. Current Biology, Vol. 21 Issue 4, Feb. 24, 2011.

"Magnetoreception in an Avian Brain in Part Mediated by Inner Ear Lagena." By Le-Qing Wu and J. David Dickman. Current Biology, Vol. 21 Issue 4, Feb. 24, 2011.