Tuesday, November 10, 2009

FIRST EVIDENCE FOR A SECOND BREEDING SEASON AMONG MIGRATORY SONGBIRDS

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Biologists for the first time have documented a second breeding season during the annual cycle of five songbird species that spend summers in temperate North America and winters in tropical Central and South America.

It was known that these species, which migrate at night when there are fewer predators and the stars can guide their journey, breed during their stay in temperate regions of the United States and Canada.

But it turns out that they squeeze in a second breeding season during a stopover in western Mexico on their southward migration, said Sievert Rohwer a University of Washington professor emeritus of biology and curator emeritus of birds at the Burke Museum of Natural History and Culture at the UW.

"It's pretty much unheard of to have a nocturnal migrant with a second breeding season. It's a pretty special observation," Rohwer said. "We saw these birds breeding and we were completely surprised."

Migratory double-breeding has been observed in two Old World bird species on their northward migration, but this is the first documented observation of "migratory double breeders" in the New World, and the first anywhere for the southward migration, Rohwer said.

The scientists traveled to the lowland thorn forests of coastal western Mexico to survey and collect songbirds that had raised their young in the United States and Canada and then immediately migrated to Mexico to molt, or shed and replace their feathers.

But during July and August in three consecutive summers, 2005-2007, the researchers found individuals from five species -- yellow-billed cuckoos, orchard orioles, hooded orioles, yellow-breasted chats and Cassin's vireos -- that were breeding rather than molting.

They found evidence that the birds had, in fact, bred earlier that year. Females of all five species examined in July had dry and featherless brood patches, indicating they had bred earlier that summer. (To more efficiently transfer heat to eggs, the abdominal brood patch becomes featherless and thickened with fluid when females are incubating, but as the young mature it dries out and remains featherless.). In the Mexican breeding ground, there was a complete absence of young birds, indicating the females had not bred in the area of the thorn forests.

Active nests were found for two species and males of all five species were singing and defending territories or guarding females, behaviors associated with breeding. In addition, isotopic analysis of the birds' tissues showed that many had recently arrived in west Mexico from temperate areas farther north.

Rohwer is lead author of a paper describing the findings, published the week of Oct. 26 in the online edition of the Proceedings of the National Academies of Science. Coauthors are Keith Hobson of Environment Canada, a national agency charged with preserving environmental quality, and Vanya Rohwer, a graduate student at Queen's University in Kingston, Ontario. He is Sievert Rohwer's son and took part in the work while a UW undergraduate. The research was funded by the Burke Museum Endowment for Ornithology, the Hugh and Jane Ferguson Foundation, the Nuttall Ornithological Club and Environment Canada.

The observation is much more than an oddity in bird behavior, Sievert Rohwer said. He noted that orchard orioles might raise a first brood in the Midwestern and south-central U.S. and a second on Mexico's western coast, yet both sets of offspring find the same wintering area in Central America. The question is how both groups find the right place, since they must travel in different directions.

Then there is the yellow-billed cuckoo, once commonly seen throughout the western United States and as far north as the Seattle area but now seldom seen along the West Coast. Disappearing habitat in the U.S. is usually cited as the reason.

But Rohwer believes the real problem could be the transformation of thorn forests of southern Sonora and Sinaloa, states in northwestern Mexico, into irrigated industrial farms. That loss of habitat, he said, could mean not enough young are produced in the second breeding season to sustain the populations previously seen on the U.S. West Coast.

"It turns out that many of those migrants, both molt migrants and the newly discovered migratory double breeders, are dependent on the low-altitude thorn forests that become very productive during the monsoon," Rohwer said.

The thorn forests lie in an arid and forbidding scrubland that springs to life with the monsoon lasting from June through August. The monsoon brings virtually all of the area's annual rainfall. The small trees leaf out and insects become abundant, making an ideal stopover for migrating songbirds.

However, with plenty of biting insects, temperatures often at 100 degrees Fahrenheit and humidity hovering near 100 percent, it is a difficult place for researchers to work, so there has been little previous documentation of life in the thorn forest. The new findings could spur more work there.

"For western North America, the conservation implications are pretty serious," Rohwer said. "Biologists know theoretically that they should pay attention to these migration stopover sites, but they've been largely ignored for their conservation implications."

(Photo: UW/Burke Museum)

SCIENTISTS TURN STEM CELLS INTO PRECURSORS FOR SPERM, EGGS

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Human embryonic stem cells derived from excess IVF embryos may help scientists unlock the mysteries of infertility for other couples struggling to conceive, according to new research from the Stanford University School of Medicine. Researchers at the school have devised a way to efficiently coax the cells to become human germ cells — the precursors of egg and sperm cells — in the laboratory. Unlike previous research, which yielded primarily immature germ cells, the cells in this most-recent study functioned well enough to generate sperm cells.

“Ten to 15 percent of couples are infertile,” said senior author Renee Reijo Pera, PhD. “About half of these cases are due to an inability to make eggs or sperm. And yet deleting or increasing the expression of genes in the womb to understand why is both impossible and unethical. Figuring out the genetic ‘recipe’ needed to develop human germ cells in the laboratory will give us the tools we need to trace what’s going wrong for these people.” Reijo Pera is a professor of obstetrics and gynecology at the medical school and the director of Stanford's Center for Human Embryonic Stem Cell Research and Education. The study was published online by Nature on Oct. 28.

Previous efforts to study infertility have been hampered by the fact that — unlike many other biological processes — the human reproductive cycle cannot be adequately studied in animal models. And because germ cells begin to form very early in embryonic development (by eight to 10 weeks), there’s been a dearth of human material to work with. “Humans have a unique reproductive system,” Reijo Pera said. “Until now we’ve relied on studies in mice to understand human germ cell differentiation, but the reproductive genes are not the same. This is the first evidence that you can create functional human germ cells in a laboratory.”

The scientists built on previous research in the mid-1990s by Reijo Pera that identified a number of genes involved in male infertility. Members of what’s called the DAZ family, the genes are unusual in that they encode RNA-binding proteins rather than the DNA transcription factors more commonly known to regulate cellular events.

In the current study, the researchers treated human embryonic stem cells with proteins known to stimulate germ cell formation and isolated those that began to express germ-cell-specific genes — about 5 percent of the total. In addition to expressing key genes, these cells also began to remove modifications, or methyl groups, to their DNA that confer cell-specific traits that would interfere with their ability to function as germ cells. Such epigenetic reprogramming is a hallmark of germ cell formation.

They then used a technique called RNA silencing to examine how blocking the expression of each of three DAZ family members in the embryonic stem cells affected germ cell development. Conversely, they also investigated what happened when these genes were overexpressed.

They found that one family member, DAZL, functions very early in germ cell development, while two others, DAZ1 and BOULE, stimulate the then-mature germ cells to divide to form gametes. Overexpressing the three proteins together allowed the researchers to generate haploid cells — those with only one copy of each chromosome — expressing proteins found in mature sperm. (When a sperm and an egg join, the resulting fertilized egg again has two copies of each chromosome.) When treated in this manner, about 2 percent of the differentiated human embryonic stem cells were haploid after 14 days of differentiation.

The effect of the DAZ family members on the embryonic stem cells varied according to whether the cells were derived from a male or a female embryo. Overexpression of BOULE increased the relative proportion of putative germ cells from 2 to 12 percent in female, but not male, cell lines. This suggests that BOULE may play a larger role than the other proteins in the development of female germ cells.

The researchers plan to use a similar strategy to optimize the production of eggs from embryonic stem cells, as well as investigating whether reprogrammed adult cells called induced pluripotent cells, or iPS cells, can also be used to create germ cells. By charting the milestones of gamete development, they hope to identify potential problems that would lead to infertility or fetal disability.

“Although most of our birth defects are caused by problems in the development of eggs or sperm,” said Reijo Pera, “it’s not clear why there are so many errors. This research gives us a system we can use to compare errors in the germ line vs. somatic cells. For instance, we can now begin to directly investigate the effects of environmental toxins on germ cell differentiation and gamete development. We’ve already seen that, even in a dish, germ cells appear to be more sensitive to these compounds.”

(Photo: Stanford U.)

Stanford University

NEW CLUES TO WHY STEM CELLS STOP DIVIDING

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Scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory have pieced together a mechanism that causes a type of human adult stem cell to permanently stop dividing after being exposed to ionizing radiation.

Their research can be used to help refine cancer treatments that utilize ionizing radiation, and may help inform future work to protect the health of astronauts on missions to deep space. It also sheds light on cellular senescence, a process in which cells permanently stop dividing that is linked to cancer and aging.

Specifically, Lab scientists zeroed in on the protein that triggers senescence in human mesenchymal stem cells. Found in the bone marrow of juveniles and adults, these stem cells are critical for maintaining and repairing tissues such as bone, cartilage, and muscle.

Like all stem cells, human mesenchymal stem cells have the ability to proliferate and differentiate into specialized cell types. They sometimes stop dividing when they’re damaged, however, which can contribute to the transformation of normal cells into cancer cells and is believed to play a role in the aging process.

Now scientists have a better understanding of how this breakdown occurs.

“We found that X-ray induced cellular senescence of human mesenchymal stem cells is a highly complex process that is mediated by a critical protein kinase called CK2,” says Daojing Wang of Berkeley Lab’s Life Sciences Division, the principal investigator of a study that is published in the October 15, 2009 issue of the journal Cancer Research.

There has been tremendous interest in utilizing human mesenchymal stem cells in regenerative medicine and disease therapy because they are relatively easy to work with and are much less controversial than human embryonic stem cells, Wang says. But few studies have looked at the consequences of exposing these cells to ionizing radiation, which is used in CT scans, cancer radiotherapy, and nuclear medicine, he adds.

To address this problem, Wang and colleagues exposed human mesenchymal stem cells in culture to X-ray radiation, then imaged the telltale changes in a cell’s shape and proteins that indicate senescence. They also used a technique called gene knockdown, in which the expression of a gene is reduced, to home in on the specific protein that triggers senescence.

Their search led them to a type of protein, called a kinase, which modifies other proteins by adding a phosphoryl group to them.

They found that a protein kinase called CK2 plays a key role in controlling the structural reorganization of a cell’s scaffolding after the cell is exposed to ionizing radiation. The scaffolding gives a cell its shape and helps it divide, among other functions. Structural changes in this cellular scaffolding are a defining characteristic of cellular senescence — and now the protein that sets these changes in motion has been identified.

Their work may help explain why radiation therapy can sometimes lead to unintended secondary bone cancers in a small minority of cancer patients years after the patients undergo treatment. It also offers the best glimpse yet into the highly coordinated mechanism that drives X-ray induced cellular senescence of human mesenchymal stem cells.

In a related study published earlier this year in the International Journal of Radiation Oncology*Biology*Physics, Wang and colleagues found that space radiation encountered by astronauts during space travel exerts more damaging effects on human mesenchymal stem cells than X-rays. They used radiation from iron-56 isotopes to mimic space radiation, and found that it perturbs key protein networks inside the cells.

“Much more work is needed to further understand the health risks associated with ionizing radiation in order to provide countermeasures. We will continue to investigate the fate of mesenchymal stem cells in response to ionizing radiation in the context of aging and cancer,” says Wang.

(Photo: LBNL)

Lawrence Berkeley National Laboratory

A LITTLE NANO, A LOT OF OIL

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A wall of graphene a single nanometer wide could be the difference between an oil well that merely pays for itself and one that returns great profit.

Rice University and Houston-based M-I SWACO, the world's largest producer of drilling fluids for the petrochemical industry, have signed an agreement for research funds to develop a graphene additive that will improve the productivity of wells.

The company will spend $450,000 over two years for research by the lab of James Tour, Rice's Chao Professor of Chemistry and professor of mechanical engineering and materials science and of computer science.

Tour's lab will work with M-I SWACO’s researchers to optimize the effectiveness of graphene additives to drilling fluids, also known as muds.

Water- or oil-based muds are typically forced downhole through a drill to keep the drillhead clean and to remove cuttings as the fluid streams back up toward the surface. But the fluids themselves can clog pores in the shaft through which oil should flow.

The nanoscaled graphene additive, just a little per barrel, would be forced by the fluid's own pressure to form a thin filter cake on the shaft wall; this will prevent muds from clogging the pores.

When the fluids are removed along with the drill head, the formation pressure -- that is, the pressure of the oil or gas inside the ground – would force the filter cake out through the pores and into the shaft. "When you release the hydrostatic pressure and pull the drill bit out, there's much more pressure inside the rock than in the hole," Tour said. "The filter blows out and the oil flows."

James Bruton, M-I SWACO's vice president for research and engineering, said the time is right for his company to investigate the use of nanoparticles. "It's something we've wanted to get into, but it was obvious we would have to partner with those who are in the know about nanotechnology. So when a friend of our CEO’s who knows Professor Tour asked if we were interested in visiting with him, we were happy to say yes."

Bruton said the cost of drilling fluids can reach $200 to $300 per barrel, and a well in the Gulf of Mexico might require more than 20,000 barrels to drill. "It's not a cheap undertaking for our customers, so the performance of the fluids is paramount," he said.

Tour emphasized the nanomaterials being studied are "clean tech" components in an environmentally sensitive field. "We've shown them to be nontoxic in many forms," he said. "It's all graphite-based, and that often comes from the ground anyway."

While the company's current focus is on drilling muds, Bruton said future research would focus on using graphene in completion fluids and other drilling products. "The ideas for using nanotechnologies are endless," he said.

"People often ask me what are we developing, and most of the time they want to know what's coming out tomorrow, next week, next month or next quarter," Bruton said. "In reality, I have to worry about things we're going to implement two to five years from now. That's where the step changes are. That's where we hope and believe nanotechnology, with Rice and Jim's group, will help us get to where we need to go."

Rice University

BLAST FROM THE PAST GIVES CLUES ABOUT EARLY UNIVERSE

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Astronomers using the National Science Foundation's Very Large Array (VLA) radio telescope have gained tantalizing insights into the nature of the most distant object ever observed in the Universe -- a gigantic stellar explosion known as a Gamma Ray Burst (GRB).

The explosion was detected on April 23 by NASA's Swift satellite, and scientists soon realized that it was more than 13 billion light-years from Earth. It represents an event that occurred 630 million years after the Big Bang, when the Universe was only four percent of its current age of 13.7 billion years.

"This explosion provides an unprecedented look at an era when the Universe was very young and also was undergoing drastic changes. The primal cosmic darkness was being pierced by the light of the first stars and the first galaxies were beginning to form. The star that exploded in this event was a member of one of these earliest generations of stars," said Dale Frail of the National Radio Astronomy Observatory.

Astronomers turned telescopes from around the world to study the blast, dubbed GRB 090423. The VLA first looked for the object the day after the discovery, detected the first radio waves from the blast a week later, then recorded changes in the object until it faded from view more than two months later.

"It's important to study these explosions with many kinds of telescopes. Our research team combined data from the VLA with data from X-ray and infrared telescopes to piece together some of the physical conditions of the blast," said Derek Fox of Pennsylvania State University. "The result is a unique look into the very early Universe that we couldn't have gotten any other way," he added.

The scientists concluded that the explosion was more energetic than most GRBs, was a nearly-spherical blast, and that it expanded into a tenuous and relatively uniform gaseous medium surrounding the star.

Astronomers suspect that the very first stars in the Universe were very different -- brighter, hotter, and more massive -- from those that formed later. They hope to find evidence for these giants by observing objects as distant as GRB 090423 or more distant.

"The best way to distinguish these distant, early-generation stars is by studying their explosive deaths, as supernovae or Gamma Ray Bursts," said Poonam Chandra, of the Royal Military College of Canada, and leader of the research team. While the data on GRB 090423 don't indicate that it resulted from the death of such a monster star, new astronomical tools are coming that may reveal them.

"The Atacama Large Millimeter/submillimeter Array (ALMA), will allow us to pick out these very-distant GRBs more easily so we can target them for intense followup observations. The Expanded Very Large Array, with much greater sensitivity than the current VLA, will let us follow these blasts much longer and learn much more about their energies and environments. We'll be able to look back even further in time," Frail said. Both ALMA and the EVLA are scheduled for completion in 2012.

(Photo: NRAO/AUI/NSF)

National Radio Astronomy Observatory

VOLCANOES PLAYED PIVOTAL ROLE IN ANCIENT ICE AGE, MASS EXTINCTION

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Researchers here have discovered the pivotal role that volcanoes played in a deadly ice age 450 million years ago. Perhaps ironically, these volcanoes first caused global warming -- by releasing massive amounts of carbon dioxide into the atmosphere. When they stopped erupting, Earth’s climate was thrown off balance, and the ice age began.

The discovery underscores the importance of carbon in Earth’s climate today, said Matthew Saltzman, associate professor of earth sciences at Ohio State University.

The results will appear in the journal Geology, in a paper now available online.

Previously, Saltzman and his team linked this same ice age to the rise of the Appalachian Mountains. As the exposed rock weathered, chemical reactions pulled carbon from Earth’s atmosphere, causing a global cooling which ultimately killed two-thirds of all species on the planet.

Now the researchers have discovered the other half of the story: giant volcanoes that formed during the closing of the proto-Atlantic Ocean -- known as the Iapetus Ocean -- set the stage for the rise of the Appalachians and the ice age that followed.

“Our model shows that these Atlantic volcanoes were spewing carbon into the atmosphere at the same time the Appalachians were removing it,” Saltzman explained. “For nearly 10 million years, the climate was at a stalemate. Then the eruptions abruptly stopped, and atmospheric carbon levels fell well below what they were in the time before volcanism. That kicked off the ice age,” he said.

This is the first evidence that a decrease in carbon from volcanic degassing -- combined with continued weathering of the Appalachians -- caused the long-enigmatic glaciation and extinction in the Ordovician period.

Here is the picture the researchers have assembled: 460 million years ago, during the Ordovician, volcanoes along the margin of what is now the Atlantic Ocean spewed massive amounts carbon dioxide into the atmosphere, turning the world into a hothouse. Lava from those volcanoes eventually collided with North America to form the Appalachian Mountains.

Acid rain -- rich in carbon dioxide -- pelted the newly exposed Appalachian rock and wore it away. Chemical reactions trapped the carbon in the resulting sediment, which formed reefs in the vast seas that covered North America.

For about 10 million years, the volcanoes continued to add carbon to the atmosphere as the Appalachians removed it, so the hothouse conditions remained stable. Life flourished in the warm oceans, including abundant species of trilobites and brachiopods.

Then, 450 million years ago, the eruptions stopped. But the Appalachians continued weathering, and atmospheric carbon levels plummeted. The Earth swung from a hothouse to an icehouse.

By 445 million years ago, glaciers had covered the south pole on top of the supercontinent of Gondwana (which would eventually break apart to form the continents of the southern hemisphere). Two-thirds of all species had perished.

When they started this research, Saltzman and his team knew that Earth’s climate must have changed drastically at the end of the Ordovician. But they didn’t know for certain that volcanoes were the driving force, explained Seth Young, who did this research for his doctoral degree at Ohio State. He is now a postdoctoral researcher at Indiana University.

“This was not necessarily what we expected when we started investigating, but as we combined our data sources, the story began to fall into place,” Young said.

Using a computer model, they drew together measurements of isotopes of chemical elements -- including strontium from rocks in Nevada and neodymium from rocks in Virginia and Pennsylvania -- with measurements of volcanic ash beds in the same locations. Then they factored in temperature models developed by other researchers.

The ash deposits demonstrated when the volcanoes stopped erupting; the strontium levels indicated that large amounts of volcanic rock were being eroded and the sediment was flooding Earth’s oceans during this time; and the neodymium levels pinpointed the Appalachians as the source of the sediment.

The new findings mesh well with what scientists know about these ancient proto-Atlantic volcanoes, which are thought to have produced the largest eruptions in Earth’s history. They issued enough lava to form the Appalachians, enough ash to cover the far ends of the earth, and enough carbon to heat the globe. Atmospheric carbon levels grew 20 times higher than they are today.

This study shows that when those volcanoes stopped erupting, carbon levels dropped, and the climate swung dramatically back to cold. The timing coincides with today’s best estimates of temperature fluctuations in the Ordovician.

“The ash beds start building up at the same time the Appalachian weathering begins, but then the record of volcanism ends, and the temperature drops,” Saltzman said. “Knowing these details can help us understand how carbon in the atmosphere is changing Earth’s climate today.”

Next, the researchers will examine the role of the ancient volcanic ash more closely. While the ash was in the atmosphere -- before it settled around the globe -- it might have blotted out the sun, and cooled the earth somewhat. Saltzman and his team want to make some estimate of this short-term cooling effect to refine their computer model.

Meanwhile, Young is just starting to re-analyze the same rock samples, this time looking for a different isotope -- sulfur. This, he hopes, will offer clues to how much oxygen was in the oceans, and how that oxygen may have affected life in the Ordovician.

(Photo: Matthew Saltzman, Ohio State University)

Ohio State University

CALTECH SCIENTISTS FIRST TO TRAP LIGHT AND SOUND VIBRATIONS TOGETHER IN NANOCRYSTAL

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Researchers at the California Institute of Technology (Caltech) have created a nanoscale crystal device that, for the first time, allows scientists to confine both light and sound vibrations in the same tiny space.

"This is a whole new concept," notes Oskar Painter, associate professor of applied physics at Caltech. Painter is the principal investigator on the paper describing the work, which was published in the online edition of the journal Nature. "People have known how to manipulate light, and they've known how to manipulate sound. But they hadn't realized that we can manipulate both at the same time, and that the waves will interact very strongly within this single structure."

Indeed, Painter points out, the interactions between sound and light in this device—dubbed an optomechanical crystal—can result in mechanical vibrations with frequencies as high as tens of gigahertz, or 10 billion cycles per second. Being able to achieve such frequencies, he explains, gives these devices the ability to send large amounts of information, and opens up a wide array of potential applications—everything from lightwave communication systems to biosensors capable of detecting (or weighing) a single macromolecule. It could also, Painter says, be used as a research tool by scientists studying nanomechanics. "These structures would give a mass sensitivity that would rival conventional nanoelectromechanical systems because light in these structures is more sensitive to motion than a conventional electrical system is."

"And all of this," he adds, "can be done on a silicon microchip."

Optomechanical crystals focus on the most basic units—or quanta—of light and sound. (These are called photons and phonons, respectively.) As Painter notes, there has been a rich history of research into both photonic and phononic crystals, which use tiny energy traps called bandgaps to capture quanta of light or sound within their structures.

What hadn't been done before was to put those two types of crystals together and see what they are capable of doing. That is what the Caltech team has done.

"We now have the ability to manipulate sound and light in the same nanoplatform, and are able to interconvert energy between the two systems," says Painter. "And we can engineer these in nearly limitless ways."

The volume in which the light and sound are simultaneously confined is more than 100,000 times smaller than that of a human cell, notes Caltech graduate student Matt Eichenfield, the paper's first author. "This does two things," he says. "First, the interactions of the light and sound get stronger as the volume to which they are confined decreases. Second, the amount of mass that has to move to create the sound wave gets smaller as the volume decreases. We made the volume in which the light and sound live so small that the mass that vibrates to make the sound is about ten times less than a trillionth of a gram."

Eichenfield points out that, in addition to measuring high-frequency sound waves, the team demonstrated that it's actually possible to produce these waves using only light. "We can now convert light waves into microwave-frequency sound waves on the surface of a silicon microchip," he says.

These sound waves, he adds, are analogous to the light waves of a laser. "The way we have designed the system makes it possible to use these sound waves by routing them around on the chip, and making them interact with other on-chip systems. And, of course, we can then detect all these interactions again by using the light. Essentially, optomechanical crystals provide a whole new on-chip architecture in which light can generate, interact with, and detect high-frequency sound waves."

These optomechanical crystals were created as an offshoot of previous work done by Painter and colleagues on a nanoscale "zipper cavity," in which the mechanical properties of light and its interactions with motion were strengthened and enhanced.

Like the zipper cavity, optomechanical crystals trap light; the difference is that the crystals trap—and intensify—sound waves, as well. Similarly, while the zipper cavities worked by funneling the light into the gap between two nanobeams—allowing the researchers to detect the beams' motion relative to one another—optomechanical crystals work on an even tinier scale, trapping both light and sound within a single nanobeam.

"Here we can actually see very small vibrations of sound trapped well inside a single 'string,' using the light trapped inside that string," says Eichenfield. "Importantly, although the method of sensing the motion is very different, we didn't lose the exquisite sensitivity to motion that the zipper had. We were able to keep the sensitivity to motion high while making another huge leap down in mass."

"As a technology, optomechanical crystals provide a platform on which to create planar circuits of sound and light," says Kerry Vahala, the Ted and Ginger Jenkins Professor of Information Science and Technology and professor of applied physics, and coauthor on the Nature paper. "These circuits can include an array of functions for generation, detection, and control. Moreover," he says, "optomechanical crystal structures are fabricated using materials and tools that are similar to those found in the semiconductor and photonics industries. Collectively, this means that phonons have joined photons and electrons as possible ways to manipulate and process information on a chip."

And these information-processing possibilities are well within reach, notes Painter. "It's not one plus one equals two, but one plus one equals ten in terms of what you can do with these things. All of these applications are much closer than they were before."

"This novel approach to bringing both light and sound together and letting them play off of each other exemplifies the forward-thinking work being done by the Engineering and Applied Science (EAS) division," says Ares Rosakis, chair of EAS and Theodore von Kármán Professor of Aeronautics and Mechanical Engineering at Caltech.

(Photo: M. Eichenfield, et. al., Nature, Advanced Online Publication (18 October 2009)

California Institute of Technology

ANTI-CANCER AGENT COULD BE USED TO PREVENT PREMATURE BIRTH

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Around 50,000 babies are born too early in the UK each year, yet little is known about what causes premature birth or how to prevent it. Premature birth is the biggest single cause of death in infants, and around 1,500 babies die in the UK as a result of this. A variety of drugs are used to reduce the incidence of premature labour, but few are effective and some have serious side effects.

It has been previously shown that protein kinase A (PKA), is involved in controlling the relaxation of the uterus during pregnancy, and that levels of PKA are higher in pregnant woman compared to non-pregnant woman and then decrease at the start of labour.

Researchers using uterine muscle samples from patients at the Royal Victoria Infirmary, Newcastle showed that the drug, Trichostatin A, increased the levels of a protein subunit of PKA and also inhibited smooth muscle contractions in these tissues.

The research, carried out by a team at Newcastle University, was funded by leading children’s charity, Action Medical Research.

Professor Nick Europe-Finner, the project leader and Professor of Myometrial Science at Newcastle University, said: “This is an exciting new discovery as we now know that protein kinase A has an important role in controlling relaxation of the uterus during pregnancy. The discovery that Trichostatin A can inhibit contractions, presumably due to its effect on PKA, means that this drug could potentially be used to prevent premature labour, however further laboratory studies are needed to assess the effectiveness of this and similar anti-cancer agents.”

Dr Magdalena Karolczak-Bayatti, Research Fellow, Newcastle University commented: “More laboratory research should help us to determine exactly how Trichostatin A regulates PKA levels and affects uterine muscle contraction. ”

Premature birth can have negative, long-lasting effects on both the mother and the baby. For many women, preterm labour is shocking, frightening and unexpected.

“This project has uncovered some of the molecular pathways that regulate uterine contractions and so could be linked to premature birth. The results showing that Trichostatin A can inhibit contractions in the uterus means it could have a role in preventing premature birth. Finding a new treatment for early labour would be a major step forward,” says Dr Yolande Harley, Deputy Director of Research at Action Medical Research.

There are several factors which can increase a woman’s risk of going into premature labour including age, infection and inflammation. However, often, the first indication of a problem is when a woman arrives at hospital in preterm labour. Many premature babies, particularly those who are born very early, are at risk of developing serious problems, such as cerebral palsy, blindness, deafness and developmental delay.

(Photo: Newcastle U.)

Newcastle University

'FEEL-GOOD' HORMONE SEROTONIN REGULATES BLOOD SUGAR CONCENTRATION

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Diabetes is the most prevalent metabolic disease in developed countries and one that engenders - in addition to its high fatality - enormous health care costs. The physiological meaning of the ‘feel-good’ hormone serotonin in insulin-producing cells of the pancreas was not understood for more than 40 years but has finally been resolved by scientists of the Max Planck Institute of Molecular Genetics in Berlin.

The researchers Diego J. Walther, Nils Paulmann and colleagues report in the current issue of PloS Biology, that a lack of serotonin in the pancreas causes diabetes. The interdisciplinary research team identified the underlying molecular and physiological mechanisms. The close interdisciplinary collaboration with Marjan Rupnik, head of the Institute of Physiology in Maribor, Slovenia, and a former group leader at the Max Planck Institute for Biophysical Chemistry, as well as the collaboration with Heidrun Fink, executive director of the Institute of Pharmacology and Toxicology of the School of Veterinary Medicine, Free University Berlin, was particularly instrumental to allowed untangling these findings.

Prior studies of the team from Berlin have identified a novel mechanism of serotonin’s action in blood platelets that relies on the permanent covalent coupling of the hormone to signalling proteins, the so-called ‘serotonylation’. The scientists now identified this mechanism also in β-cells of the pancreas. As in thrombocytes, serotonylation regulates the secretion of storage granules from these cells. "Under normal conditions serotonin controls the release of insulin, the most important hormone in the regulation of blood glucose concentration of humans and animals", explains Diego Walther. When the serotonin levels are low like in serotonin-deficient mice, proper insulin secretion is hampered and blood glucose concentration rises to noxious levels after a meal, a hallmark of diabetes. The identification of the insulin-releasing action of serotonin opens new avenues for intervention in diabetes, a main research objective for further studies by the international team.

The pancreas is the third disease-associated context of serotonylation identified since the first description of this mechanism in bleeding disorders by the research team. In addition to the study’s contribution to the understanding of serotonin’s role in the widespread disease diabetes, the special case of serotonylation highlights the general physiological relevance of protein monoaminylation exemplarily. Other kinds of monoaminergic hormones like histamine, dopamine, and norepinephrine can act in similar ways. Like the phosphorylation of proteins, monoaminylation also has a profound impact on several cellular processes and their identification is a challenge accepted by the group from Berlin. Furthermore, the present study might change the text book knowledge about the mode of action of hormones. "In contrast to that which was long assumed, water-soluble hormones like serotonin, histamine, and catecholamines act not only at the cell’s interface via surface receptors, but also within cells via monoaminylation", Walther explains.

The results, published by the researchers from Berlin, solve the puzzle of what serotonin is doing in the β-cells of the pancreas and widen the concept of protein monoaminylation in disease-relevant physiological processes. The scientists plan to investigate in further studies why diabetic serotonin-deficient mice have a normal life expectancy and show none of the typical diabetes-associated secondary damage. Such research could help to improve the quality of life and to prolong life expectancy of diabetic patients.

(Photo: Nils Paulmann, MPIMG)

Max Planck Institute of Molecular Genetics in Berlin

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