First an alga, then a squid, enigmatic fossil is actually a fish

A photo of the Platylithophycus cretaceus specimen. The scale bar is 5 centimeters.

A fossil slab discovered in Kansas 70 years ago and twice misidentified -- first as a green alga and then as a cephalopod -- has been reinterpreted as the preserved remains of a large cartilaginous fish, the group that includes sharks and rays. In a study published in the Journal of Paleontology, American Museum of Natural History researchers describe the fishy characteristics of the animal, which lived between 70-85 million years ago.

"There are many examples of temporarily misplaced taxa in paleontological history, including ferns that were once thought to be sponges and lungfish teeth thought to be fungi," said the lead author, Allison Bronson, a comparative biology Ph.D.-degree student in the Museum's Richard Gilder Graduate School. "In this case, the misidentification didn't happen because of a lack of technology at the time -- scientists familiar with cartilage structure could easily see this was a chondrichthyan fish. The researchers used reasonable arguments for their interpretations, but didn't look outside of their own fields."

The enigmatic specimen, Platylithophycus cretaceum, is roughly 1.5-feet long by 10-inches wide and from the Niobrara Formation in Kansas. The Niobrara Formation is one of the most diverse fish-fossil sites in North America, preserving late Cretaceous animals that lived in and around the Western Interior Seaway, a broad expanse of water that split North America into two land masses.

In 1948, two paleobotanists from the Colorado School of Mines and Princeton University compared the texture of the fossil slab with that of green algae. They described two parts of a plant: surfaces covered with hexagonal plates, which they called "fronds," and supposedly calcium carbonate-covered thread-like filaments. In 1968, two researchers from Fort Hays Kansas State College studying cephalopods from the Niobrara Formation compared the specimen with a cuttlefish, based primarily on its textural similarities to a cuttlebone -- the unique internal shell of cuttlefish. The reclassification made Platylithophycus the oldest sepiid squid then on record.

In both of these earlier studies, the hard tissue was assumed to be composed of calcium carbonate, but no tests were performed. For the new study, Bronson and co-author John Maisey, a curator in the Museum's Division of Paleontology, applied a small amount of dilute organic acid to the specimen -- a method that has been widely used in paleontology since the time of the initial description of Platylithophycus. If there is a reaction, the fossilized material is likely made from calcium carbonate. But if there is no reaction, which was the case when Bronson and Maisey performed the test, it is likely made from calcium phosphate, as are the fossilized skeletons of cartilaginous fish like sharks and rays.

The most obvious clue that Platylithophycus was a cartilaginous fish are the hexagonal plates on the surface of the specimen. After taking a closer look with a scanning electron microscope, Bronson and Maisey reinterpreted that feature as tessellated calcified cartilage, found on both extinct and living sharks and rays. The new study suggests that the "filaments" earlier described are actually part of the gill arches, made up of tessellated cartilage. Gill arches are cartilaginous curved bars along the pharynx, or throat, that support the gills of fish. The "fronds" are reinterpreted as gill rakers, finger-like projections that extend from the gill arches and help with feeding.

"We think this was a rather large cartilaginous fish, possibly related to living filter-feeding rays such as Manta and Mobula," Maisey said. "This potentially expands the range of diversity in the Niobrara fauna."

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Education, not income, the best predictor of a long life

This is a curve showing the relationship between income and life expectancy in 1970, 1990 and 2010.

Rising income and the subsequent improved standards of living have long been thought to be the most important factors contributing to a long and healthy life. However, new research from Wolfgang Lutz and Endale Kebede, from IIASA and the Vienna University of Economics and Business (WU) has shown that instead, the level of education a person has is a much better predictor of life expectancy.

In 1975, Samuel Preston developed the Preston Curve, which plotted the GDP per person on the horizontal axis against life expectancy on the vertical axis. The curve shows a clear but flattening upward trend in life expectancy with increasing GDP. The curves also shift upwards over time which has been explained by better healthcare.

In 1985, John Caldwell and Pat Caldwell suggested instead that lowered mortality resulted from better female education. In their new paper, Lutz and Kebede used global data from 174 countries from 1970-2015 to test the two hypotheses. Whether income or education is more important for improving health and life expectancy is an important question for policymakers deciding where to direct funding.

Lutz and Kebede also plotted life expectancy against the mean years of schooling of the adult population. The curve created is much more linear, suggesting that education is a much better predictor. There is no upward shift of the curve requiring explanation by other factors. Data was subject to multivariate analyses to validate the findings. The same link was found when the curves were adjusted for child mortality.

The researchers point out that better education leads to improved cognition and in turn to better choices for health-related behaviours. Recent decades have seen a shift in the disease burden from infectious to chronic diseases, the latter of which are largely lifestyle-related. As time goes on, the link between education and better health choices, and therefore life expectancy, will become even more apparent.

"This paper is more radical than previous analyses in terms of challenging the ubiquitous view that income and medical interventions are the main drivers of health. It even shows that the empirical association between income and health is largely spurious," says Lutz.

Previous lines of research at the Wittgenstein Centre, a collaboration between IIASA, WU and the Vienna Institute of Demography, have emphasised the importance of improving education for poverty eradication and economic growth, as well as the ability to adapt to climate change. These findings further back up the call for improved access to education.

The apparent link between health and income found by Preston can be explained by the fact that better education results in both better health and higher incomes.

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Dinosaurs ended -- and originated -- with a bang!

Dinosaur fossil

It is commonly understood that the dinosaurs disappeared with a bang -- wiped out by a great meteorite impact on the Earth 66 million years ago.

But their origins have been less understood. In a new study, scientists from MUSE -- Museum of Science, Trento, Italy, Universities of Ferrara and Padova, Italy and the University of Bristol show that the key expansion of dinosaurs was also triggered by a crisis -- a mass extinction that happened 232 million years ago.

In the new paper, published today in Nature Communications, evidence is provided to match the two events -- the mass extinction, called the Carnian Pluvial Episode, and the initial diversification of dinosaurs.

Dinosaurs had originated much earlier, at the beginning of the Triassic Period, some 245 million years ago, but they remained very rare until the shock events in the Carnian 13 million years later.

The new study shows just when dinosaurs took over by using detailed evidence from rock sequences in the Dolomites, in north Italy -- here the dinosaurs are detected from their footprints.

First there were no dinosaur tracks, and then there were many. This marks the moment of their explosion, and the rock successions in the Dolomites are well dated. Comparison with rock successions in Argentina and Brazil, here the first extensive skeletons of dinosaurs occur, show the explosion happened at the same time there as well.

Lead author Dr Massimo Bernardi, Curator at MUSE and Research associate at Bristol's School of Earth Sciences, said: "We were excited to see that the footprints and skeletons told the same story. We had been studying the footprints in the Dolomites for some time, and it's amazing how clear cut the change from 'no dinosaurs' to 'all dinosaurs' was."

The point of explosion of dinosaurs matches the end of the Carnian Pluvial Episode, a time when climates shuttled from dry to humid and back to dry again.

It was long suspected that this event had caused upheavals among life on land and in the sea, but the details were not clear. Then, in 2015, dating of rock sections and measurement of oxygen and carbon values showed just what had happened.

There were massive eruptions in western Canada, represented today by the great Wrangellia basalts -- these drove bursts of global warming, acid rain, and killing on land and in the oceans.

Co-author Piero Gianolla, from the University of Ferrara, added: "We had detected evidence for the climate change in the Dolomites. There were four pulses of warming and climate perturbation, all within a million years or so. This must have led to repeated extinctions."

Professor Mike Benton, also a co-author, from the University of Bristol, said: "The discovery of the existence of a link between the first diversification of dinosaurs and a global mass extinction is important.

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Study identifies more than a hundred new genes that determine hair color

Scientists have discovered 124 genes that play a major role in determining human hair color variation.

A team of scientists, led by academics from King's College London and Erasmus MC University Medical Center Rotterdam, have discovered 124 genes that play a major role in determining human hair colour variation.

The discovery sheds new light on our understanding of the genetic complexity underpinning variations in human pigmentation, and could advance our knowledge of conditions linked to pigmentation, such as skin, testicular, prostate and ovarian cancers. The new findings are also relevant for forensic sciences.

Although previous studies have found that a large percentage of hair colour variation is explained by heritable factors, previous genetic studies only identified a dozen or so hair colour genes. The new study, published today in Nature Genetics, largely explains the genetic knowledge gap.

In order to identify the previously unknown hair colour genes, researchers analysed DNA data from almost 300,000 people of European descent, together with their self-reported hair colour information. The data was supplied by UK Biobank, 23andMe Inc., the International Visible Trait Genetics Consortium and their study partners.

By comparing the hair colour of the group with their genetic information, stored at several million locations across the human genome, the team identified 124 genes involved in the development of hair colour, of which more than 100 were not previously known to influence pigmentation.

The scientists also demonstrated that predicting hair colour with this new genetic information is more accurate than with previously known genes.

Joint lead author Professor Tim Spector from King's College London said: "This work will impact several fields of biology and medicine. As the largest ever genetic study on pigmentation, it will improve our understanding of diseases like melanoma, an aggressive form of skin cancer.

The genes that affect hair colour also affect other cancer types, while other pigment genes affect the chances of having Crohn's and other forms of bowel disease.

"Our work helps us to understand what causes human diversity in appearance by showing how genes involved in pigmentation subtly adapted to external environments and even social interactions during our evolution. We found that women have significantly fairer hair than men, which reflects how important cultural practices and sexual preferences are in shaping our genes and biology."

Joint lead author Professor Manfred Kayser from Erasmus MC said: "Besides substantially increasing our understanding of human pigmentation genetics in general, finding these new hair colour genes is also important for further increasing the accuracy of hair colour prediction from DNA traces in future forensic applications, which can help to find unknown perpetrators of crime."

Read more at Science Daily

'Mono' virus linked to 7 serious diseases

Blood sample for Epstein-Barr virus (EBV) test.

A far-reaching study conducted by scientists at Cincinnati Children's reports that the Epstein-Barr virus (EBV) -- best known for causing mononucleosis -- also increases the risks for some people of developing seven other major diseases.

Those diseases are: systemic lupus erythematosus (SLE), multiple sclerosis (MS), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, and type 1 diabetes. Combined, these seven diseases affect nearly 8 million people in the U.S.

Study results published April 12 in the journal Nature Genetics. The project was led by three scientists: John Harley, MD, PhD, Director of the Center for Autoimmune Genomics and Etiology (CAGE) at Cincinnati Children's and a faculty member of the Cincinnati VA Medical Center; Leah Kottyan, PhD, an immunobiology expert with CAGE; and Matthew Weirauch, PhD, a computational biologist with the center. Critical contributions were provided by Xiaoting Chen, PhD, and Mario Pujato, PhD, both also in CAGE.

The study shows that a protein produced by the Epstein-Barr virus, called EBNA2, binds to multiple locations along the human genome that are associated with these seven diseases.

Overall, the study sheds new light on how environmental factors, such as viral or bacterial infections, poor diet, pollution or other hazardous exposures, can interact with the human genetic blueprint and have disease-influencing consequences.

"Now, using genomic methods that were not available 10 years ago, it appears that components made by the virus interact with human DNA in the places where the genetic risk of disease is increased," Harley says. "And not just for lupus, but all these other diseases, too."

The full impact of this study could take years to explore. Here are some of the initial implications:

New concern about the 'kissing disease'

EBV is a strikingly common virus. In the US and other developed nations, more than 90 percent of the population becomes infected by age 20. In less-developed nations, 90 percent of people become infected by age 2. Once infected, the virus remains in people for their entire lives.

Mononucleosis, which causes weeks of extreme fatigue, is the most common illness caused by EBV. Mono was nicknamed the "kissing disease" years ago because the virus spreads primarily via contact with saliva.

Over the years, scientists have linked EBV to a few other rare conditions, including certain cancers of the lymphatic system. Harley, who has devoted much of his career to studying lupus, found possible connections between lupus and EBV years ago. That work includes proposing mechanisms that the immune system uses in response to the virus that lead to lupus, and showing that children with lupus almost always are infected with EBV.

Today's study adds weight to those lupus findings and adds six more well-known diseases to the list.

"This discovery is probably fundamental enough that it will spur many other scientists around the world to reconsider this virus in these disorders," Harley says. "As a consequence, and assuming that others can replicate our findings, that could lead to therapies, ways of prevention, and ways of anticipating disease that don't now exist." So far, no vaccine exists that will prevent EBV infection.

"I think we've come up with a really strong rationale for encouraging people to come up with more of an effort," Kottyan says. "Some EBV vaccines are under development. I think this study might well encourage them to push forward faster and with rededicated effort."

How EBV hijacks our immune system

When viral and bacterial infections strike, our bodies respond by commanding B cells within our immune systems to crank out antibodies to battle the invaders. However, when EBV infections occur, something unusual happens.

The EBV virus invades the B cells themselves, re-programs them, and takes over control of their functions. The Cincinnati Children's research team has discovered a new clue about how the virus does this, a process that involves tiny proteins called transcription factors.

Our bodies have about 1,600 known transcription factors at work within our genome. Each cell uses a subset of these to become what they are and to respond to their environment. These proteins constantly move along the strands of our DNA, turning specific genes on and off to make sure cells function as expected.

However, when the transcription factors change what they do, the normal functions of the cell can also change, and that can lead to disease. The Cincinnati Children's team suspects that the EBNA2 transcription factor from EBV is helping change how infected B cells operate, and how the body responds to those infected cells.

The new paper shows that seven seemingly unrelated disease states actually share a common set of abnormal transcription factors, each affected by the EBNA2 protein from the Epstein-Barr virus. When these EBNA2-related clusters of transcription factors attach themselves to one portion of the genetic code, the risk of lupus appears to rise. When those same transcription factors land on another part of the code, the risk of multiple sclerosis appears to rise. And so on.

"Normally, we think of the transcription factors that regulate human gene expression as being human," Kottyan says. "But in this case, when this virus infects cells, the virus makes its own transcription factors, and those sit on the human genome at lupus risk variants (and at the variants for other diseases) and that's what we suspect is increasing risk for the disease."

New leads emerge for improving treatment

It remains unclear how many cases of the seven diseases listed in the study can be traced to prior EBV infection. More genomic analyses involving many more patients with these diseases will be required to make reliable estimates.

"The impact of the virus is likely to vary across the diseases," Harley says. "In lupus and MS, for example, the virus could account for a large percentage of those cases. We do not have a sense of the proportion in which the virus could be important in the other EBNA2-associated diseases."

However, the breakthrough identification of specific transcription factors connected to EBV infections opens new lines of study that could accelerate efforts to find cures.

"This same cast of characters is a villain in multiple immune-related diseases," Weirauch says. "They're playing that role through different ways, and doing it at different places in your genome, but it's the same sinister characters. So if we could develop therapies to stop them from doing this, then it would help multiple diseases."

A number of compounds -- some experimental, some approved as medications for other conditions -- already are known to be capable of blocking some of the high-risk transcription factors listed in the paper, Weirauch says. Teams at Cincinnati Children's have begun deeper studies of some of these compounds.

Findings go far, far beyond EBV

While the EBV-related findings involved more than 60 human proteins linked to seven diseases, the Cincinnati Children's research team already has taken a huge next step. They applied the same analytic techniques to tease out connections between all 1,600 known transcription factors and the known gene variants associated with more than 200 diseases.

The results of that massive cross-analysis also appear in today's study. Intriguing associations were documented involving 94 conditions.

"Our study has uncovered potential leads for many other diseases, including breast cancer," Harley says. "We cannot possibly follow up on all of these, but we are hoping that other scientists will."

After devoting decades of research to hunting down the causes of lupus, Harley says this study represents the most important discovery of his career. "I've been a co-author in almost 500 papers. This one is more important than all of the rest put together. It is a capstone to a career in medical research," he says.

Software behind discoveries to be made public

Detecting and tracking the activities of these transcription factors took years of work involving dozens of laboratory and computational experts.

The project required gathering massive sets of genetic data, then analyzing every genetic change affecting the activity of the virus. Doing this required creating two new algorithms, called RELI and MARIO, which were developed at Cincinnati Children's by Weirauch and colleagues.

Both software tools and a related website will be made publicly available.

"We are going to great lengths to not only make the computer code available, but all of the data and all of the results," Weirauch says. "We think it's an interesting approach that could have implications for many diseases, so we're contacting experts on the various diseases and sharing the results and seeing if they want to collaborate to follow up on them."

GLOSSARY OF TERMS

What is the Epstein-Barr virus?

The Epstein-Barr virus (EBV) is an extremely common virus usually spread by saliva. EBV causes mononucleosis, and has been associated with a growing number of other diseases. A study led by Cincinnati Children's, published today in Nature Genetics, adds seven diseases to that list.

What is mononucleosis?

Also known as "mono," and nicknamed the "kissing disease," the symptoms of this condition include extreme fatigue, fever, sore throat, head and body aches, swollen lymph nodes in the neck and armpits, swollen liver or spleen or both, and rash, according to the Centers for Disease Control and Prevention. Most people get better in two to four weeks. However, some people may feel fatigued for several more weeks.

What is a B cell?

B cells are a type of white blood cell found in the immune system. These cells produce antibodies in reaction to infections by bacteria, viruses and other invaders. Epstein-Barr virus infects a small proportion of these cells.

What is a transcription factor?

Transcription factors are proteins that "turn on and turn off" genes. These proteins help direct cell growth, division, and death. They also control cell migration and organization. There are about 1,600 known human transcription factors that do their work along the human genome. These proteins change the expression of genes to make RNA, which in many cases results in forming other proteins that change how cells form and function.

What is a DNA variant?

The DNA genome of every person contains over 3 billion DNA bases. Most of the bases are exactly the same for every person. However, about 1 percent of the bases can be different and these create diversity between people. The variants can change the way proteins are made or change the regulatory processes that lead to protein production.

Read more at Science Daily

Circumbinary castaways: Short-period binary systems can eject orbiting worlds

This artist’s concept illustrates Kepler-16b, the first planet known to orbit two stars – what’s called a circumbinary planet. The planet, which can be seen in the foreground, was discovered by NASA’s Kepler mission. New research from the University of Washington indicates that certain shot-period binary star systems eject circumbinary planets as a consequence of the host stars’ evolution.

Planets orbiting "short-period" binary stars, or stars locked in close orbital embrace, can be ejected off into space as a consequence of their host stars' evolution, according to new research from the University of Washington.

The findings help explain why astronomers have detected few circumbinary planets -- which orbit stars that in turn orbit each other -- despite observing thousands of short-term binary stars, or ones with orbital periods of 10 days or less.

It also means that such binary star systems are a poor place to aim coming ground- and space-based telescopes to look for habitable planets and life beyond Earth.

There are several different types of binary stars, such as visual and spectroscopic binaries, named for the ways astronomers are able to observe them. In a paper accepted for publication in Astrophysical Journal, lead author David Fleming, a UW astronomy doctoral student, studies eclipsing binaries, or those where the orbital plane is so near the line of sight, both stars are seen to cross in front of each other. Fleming will present the paper at the Division on Dynamical Astronomy conference April 15-19.

When eclipsing binaries orbit each other closely, within about 10 days or less, Fleming and co-authors wondered, do tides -- the gravitational forces each exerts on the other -- have "dynamical consequences" to the star system?

"That's actually what we found" using computer simulations, Fleming said. "Tidal forces transport angular momentum from the stellar rotations to the orbits. They slow down the stellar rotations, expanding the orbital period."

This transfer of angular momentum causes the orbits not only to enlarge but also to circularize, morphing from being eccentric, or football-shaped, to perfect circles. And over very long time scales, the spins of the two stars also become synchronized, as the moon is with the Earth, with each forever showing the same face to the other.

The expanding stellar orbit "engulfs planets that were originally safe, and then they are no longer safe -- and they get thrown out of the system," said Rory Barnes, UW assistant professor of astronomy and a co-author on the paper. And the ejection of one planet in this way can perturb the orbits of other orbiting worlds in a sort of cascading effect, ultimately sending them out of the system as well.

Making things even more difficult for circumbinary planets is what astronomers call a "region of instability" created by the competing gravitational pulls of the two stars. "There's a region that you just can't cross -- if you go in there, you get ejected from the system," Fleming said. "We've confirmed this in simulations, and many others have studied the region as well."

This is called the "dynamical stability limit." It moves outward as the stellar orbit increases, enveloping planets and making their orbits unstable, and ultimately tossing them from the system.

Another intriguing characteristic of such binary systems, detected by others over the years, Fleming said, is that planets tend to orbit just outside this stability limit, to "pile up" there. How planets get to the region is not fully known; they may form there, or they may migrate inward from further out in the system.

Applying their model to known short-period binary star systems, Fleming and co-authors found that this stellar-tidal evolution of binary stars removes at least one planet in 87 percent of multiplanet circumbinary systems, and often more. And even this is likely a conservative estimate; Barnes said the number may be as high as 99 percent.

The researchers have dubbed the process the Stellar Tidal Evolution Ejection of Planets, or STEEP. Future detections -- "or non-detections" -- of circumbinary around short-period binary stars, the authors write, will "will provide the best indirect observational test of the STEEP process.

Read more at Science Daily

NASA’s Newest Satellite Will Scan the Universe for Undiscovered Exoplanets

NASA's Transiting Exoplanet Survey Satellite

NASA's Transiting Exoplanet Survey Satellite will zero in on 200,000 stars, which could potentially yield hundreds of new exoplanet discoveries. TESS will target areas of the sky where new planets will likely be easier to spot than those studied by the venerable Kepler Space Telescope, giving observatories on the ground a better chance of confirming the discovery of new exoplanets.

TESS is scheduled to launch from Vandenberg Air Force Base April 16 and will make its way to an Earth orbit with lowest and highest altitudes of 67,000 miles and 232,000 miles. It will study different parts of the sky in observing campaigns of almost one month each, ferrying data back to Earth about what it sees.

Like Kepler, TESS will examine stars and look for the telltale dimming, or “transit,” that takes place when a planet goes across the star's face. The observatory's information will be beamed back to the ground where other telescopes can look for small tugs or wobbles in the star's position, which would confirm a planet has been discovered.

"TESS was designed so the targets would be optimally based for ground-based follow up," principal investigator George Ricker, a senior scientist at the Massachusetts Institute of Technology, told Seeker. "We want to make sure we can communicate to ground-based observers the information that we get in terms of candidate transit events, or planets."

With 200,000 high-priority targets, TESS investigators expect the first possible planets will come back to Earth within just a few weeks or months. The mission is currently funded for two years. In that time, it will locate hundreds of possible exoplanets, including a few dozen that are close to the size of Earth. Kepler has already located well over 2,000 planets, but the TESS stars will be brighter, closer, and easier to examine.

Kepler investigators, however, will get the second chance to look at planets discovered by the telescope during the second year of TESS’s operations. At first, TESS will spend a year moving its view around the southern hemisphere. Kepler's original field of view was the constellation Cygnus, in the north. Sometime during its second year of operations, TESS will spend a month staring at the same spot that Kepler examined for four years, between 2009 and 2013.

Engineers constructed TESS to last well beyond its original mission lifetime, as long as funding persists. The telescope will act as a finder telescope, searching for objects that are interesting, which other telescopes might zoom in on. A prominent follow-up telescope will be the James Webb Space Telescope, which is now expected to launch in 2020. Ideally, TESS and James Webb observations will overlap.

"The longer the mission will operate, the more precisely we can determine the properties of the [planetary] transits," Ricker said. Once they pinpoint the time it takes for a planet to go around a star, Webb can peer at the planet to learn more about its atmosphere. Other instruments, such as HARPS (High Accuracy Radial velocity Planet Searcher) at the La Silla Observatory, could measure a planet’s wobbles in order to estimate its mass.

Read more at Seeker

Mountain erosion may add CO2 to the atmosphere

A new study found that the process of mountain erosion can be a source of new carbon dioxide gas that can release it back into the atmosphere far faster than it's being absorbed into newly exposed rock. The researchers conducted fieldwork in one of the most erosion-prone mountain chains in the world -- the central range of Taiwan (above).

Scientists have long known that steep mountain ranges can draw carbon dioxide (CO2) out of the atmosphere -- as erosion exposes new rock, it also starts a chemical reaction between minerals on hill slopes and CO2 in the air, "weathering" the rock and using CO2 to produce carbonate minerals like calcite.

A new study led by researchers from the Woods Hole Oceanographic Institution (WHOI), however, has turned this idea on its head. In paper released on April 12th in the journal Science, the scientists announced that the erosion process can also be a source of new CO2 gas, and can release it back into the atmosphere far faster than it's being absorbed into newly-exposed rock.

"This goes against a long-standing hypothesis that more mountains mean more erosion and weathering, which means an added reduction of CO2. It turns out it's much more complicated than that," says Jordon Hemingway, a postdoctoral fellow at Harvard University and lead author on the paper.

The source of this extra CO2 isn't entirely geological. Instead, it's the byproduct of tiny microbes in mountain soils that "eat" ancient sources of organic carbon that are trapped in the rock. As the microbes metabolize these minerals, they spew out carbon dioxide.

The researchers came to this realization after studying one of the most erosion-prone mountain chains in the world -- the central range of Taiwan. This steep-sided range is pummeled by more than three major typhoons each year, each of which mechanically erode the soil and rock through heavy rains and winds.

Hemingway and his colleagues examined samples of soil, bedrock, and river sediments from the central range, looking for telltale signs of organic carbon in the rock. What they found there surprised them.

"At the very bottom of the soil profile, you have basically unweathered rock. As soon as you hit the base of the soil, layer, though, you see rock that's loose but not yet fully broken down, and at this point the organic carbon present in the bedrock seems to disappear entirely," notes Hemingway. At that point in the soil, the team also noticed an increase in lipids that are known to come from bacteria, he adds.

"We don't yet know exactly which bacteria are doing this -- that would require genomics, metagenomics, and other microbiological tools that we didn't use in this study. But that's the next step for this research," says WHOI marine geochemist Valier Galy, senior author and Hemingway's advisor in the MIT/WHOI Joint Program.

The group is quick to note that the total level of CO2 released by these microbes isn't severe enough to have any immediate impact on climate change -- instead, these processes take place on geologic timescales. The WHOI team's research may lead to a better understanding of how mountain-based (or "lithospheric") carbon cycles actually work, which could help generate clues to how CO2 has been regulated since the Earth itself formed.

Read more at Science Daily

Bad antibodies made good: The immune system's secret weapon uncovered

These new findings will fundamentally change thinking about how the immune system protects us.

The 'bad apples' of the immune system are also its secret weapon, according to major Australian research published today in the world-leading journal Science.

In a world first, scientists from Sydney's Garvan Institute of Medical Research have revealed how a population of 'bad' antibodies in the immune system -- which are usually 'silenced' because they can harm the body -- can provide crucial protection against invading microbes. The research was carried out in mice.

The 'bad' antibodies are known to react against the body's own tissues and can cause autoimmune disease. For this reason, it was once thought that they were discarded by the immune system or that they were made inactive in the long term. However, the new findings show for the first time that 'bad' antibodies go through a rapid 'redemption' process and are activated when the body is faced with a disease threat that other antibodies cannot tackle.

As a result, the 'redeemed' antibodies no longer threaten the body, but instead become powerful weapons to fight disease -- and particularly diseases that evade the immune system by disguising themselves to look like normal body tissue.

Professor Chris Goodnow, who co-led the new research with A/Prof Daniel Christ (both Immunology Division, Garvan), says the new findings will fundamentally change thinking about how the immune system protects us.

"We once thought that harmful antibodies were discarded by the body -- like a few bad apples in the barrel -- and no one had any idea that you could start with a 'bad' antibody and make it good.

"From these new findings, we now know that every antibody is precious when it comes to fighting invading microbes -- and this new understanding means that 'bad' antibodies are a valuable resource for the development of vaccines for HIV, and for other diseases that go undercover in the body."

This study was made possible by the generosity of The Bill and Patricia Ritchie Foundation, and through funding from the National Health and Medical Research Council (Australia).

Carrying out the immune system's toughest task

The new research appears to solve an enduring mystery that has puzzled scientists for decades: How does the immune system attack invading microbes that look almost identical to the body's own molecules, without mounting an attack on the body at the same time?

Campylobacter, HIV and others are particularly problematic targets for the immune system because they have evolved to appear almost identical to the body's own molecules; they are 'wolves in sheep's clothing'. This makes it difficult for the immune system to attack them, because it systematically avoids using antibodies that can attack 'self'.

To understand how the immune system recognises these 'wolves in sheep's clothing', scientists from the Garvan Institute zeroed in on a mysterious army of immune cells in the bloodstream.

'Bad' antibodies are hiding inside silenced B cells

The silenced cell army contains millions of immune cells known as B cells -- which produce antibodies to fight diseases. Unlike other B cells, though, the cells of this army pose a danger to the body. This is because they can make 'bad' antibodies, which can attack 'self' and cause autoimmune disease. For this reason, they are kept in a long-term silenced state (known as anergy).

Professor Chris Goodnow discovered the silenced cells 30 years ago -- and has been working to understand their function ever since.

"The big question about these cells has been why they are there at all, and in such large numbers," says Prof Goodnow. "Why does the body keep these cells, whose antibodies pose a genuine risk to health, instead of destroying them completely, as we once thought?"

The new findings appear to answer that question, showing that selected cells in the army can be reawakened to fight invaders -- but only once their 'bad' antibodies are made good.

"We've shown that these silenced cells do have a crucial purpose, says Deborah Burnett, a PhD student at Garvan whose work forms the basis of the study. "Far from 'clogging up' the immune system for no good reason, they're providing weapons -- bad apples made good -- to fight off invaders whose 'wolf in sheep's clothing tactics make it almost impossible for the other cells of the immune system to fight them."

Three tiny DNA changes turn bad into brilliant

Working with a sophisticated preclinical mouse model, which was developed at Garvan by Prof Rob Brink (Immunology Division) and his team, the researchers showed that the silenced cells can produce antibodies when they encounter an invader that appears highly similar to 'self'.

Crucially, before the cells attack, the antibodies they make are first redeemed through tiny alterations to their DNA sequence. This ensures the antibody that each cell makes no longer attacks 'self', but rapidly becomes a 5000 times more potent weapon against the invading foreigner.

Remarkably, in the model system tested, only three DNA changes were needed to transform antibodies from dangerous cells to effective weapons against disease: a first change to stop the antibody from binding to 'self', and a further two changes to increase their ability to specifically bind the invader.

At the atomic level, a dimple makes the difference

In experiments conducted at the Australian Synchrotron, the research team showed how the three DNA changes rearrange the tips of the antibody in defined ways, so that it becomes much better at recognising the foreign molecule and worse at recognising 'self'. In particular, the redeemed antibody fits neatly around a nanoscale 'dimple' that is present on the foreign molecule but is absent on self.

"This research has taken us on an exciting journey," says A/Prof Christ. "Not only have we uncovered a new kind of immunity, we've been able to confirm precisely how a bad antibody can be made good.

"Crucially, these redeemed antibodies are by no means a fall-back option. In fact, our findings show the opposite -- that antibodies made by tweaking 'bad' antibodies can be even better than those developed through established pathways."

Read more at Science Daily

New insight into how Giant's Causeway and Devils Postpile were formed

This is the Giant's Causeway.

A new study by geoscientists at the University of Liverpool has identified the temperature at which cooling magma cracks to form geometric columns such as those found at the Giant's Causeway in Northern Ireland and Devils Postpile in the USA.

Geometric columns occur in many types of volcanic rocks and form as the rock cools and contracts, resulting in a regular array of polygonal prisms or columns.

Columnar joints are amongst the most amazing geological features on Earth and in many areas, including the Giant's Causeway, they have inspired mythologies and legends.

One of the most enduring and intriguing questions facing geologists is the temperature at which cooling magma forms these columnar joints.

Liverpool geoscientists undertook a research study to find out how hot the rocks were when they cracked open to form these spectacular stepping stones.

In a paper published in Nature Communications, researchers and students at the University's School of Environmental Sciences designed a new type of experiment to show how as magma cools, it contracts and accumulates stress, until it cracks. The study was performed on basaltic columns from Eyjafjallajökull volcano, Iceland.

They designed a novel apparatus to permit cooling lava, gripped in a press, to contract and crack to form a column. These new experiments demonstrated that the rocks fracture when they cool about 90 to 140?C below the temperature at which magma crystallises into a rock, which is about 980?C for basalts.

This means that columnar joints exposed in basaltic rocks, as observed at the Giant's Causeway and Devils Postpile (USA) amongst others, were formed around 840-890 ?C.

Yan Lavallée, Liverpool Professor of Volcanology who headed the research, said: "The temperature at which magma cools to form these columnar joints is a question that has fascinated the world of geology for a very long time. We have been wanting to know whether the temperature of the lava that causes the fractures was hot, warm or cold.

"I have spent over a decade pondering how to address this question and construct the right experiment to find the answer to this question. Now, with this study, we have found that the answer is hot, but after it solidified."

Dr Anthony Lamur, for whom this work formed part of his doctoral study, added: "These experiments were technically very challenging, but they clearly demonstrate the power and significance of thermal contraction on the evolution of cooling rocks and the development of fractures."

Dr Jackie Kendrick, a post-doctoral researcher in the Liverpool group said: "Knowing the point at which cooling magma fractures is critical, as -beyond leading to the incision of this stunning geometrical feature- it initiates fluid circulation in the fracture network. Fluid flow controls heat transfer in volcanic systems, which can be harnessed for geothermal energy production. So the findings have tremendous applications for both volcanology and geothermal research."

Understanding how cooling magma and rocks contract and fracture is central to understand the stability of volcanic constructs as well as how heat is transferred in the Earth.

Professor Lavallée added: "The findings shed light on the enigmatic observations of coolant loss made by Icelandic engineers as they drilled into hot volcanic rocks in excess of 800?C; the loss of coolant in this environment was not anticipated, but our study suggests that substantial contraction of such hot rocks would have opened wide fractures that drained away the cooling slurry from the borehole.

Read more at Science Daily