Spindly species found in ocean’s crushing depths

Wed Nov 24, 6:07 am ET

PARIS (AFP) – Scientists unveiled on Wednesday a gossamer, ghostly creature discovered in the deepest reaches of the ocean between Indonesia and the Philippines.

The squidworm, up to 9.4 centimetres (3.7 inches) in length, is far more elegant than its name would suggest.

Swimming upright, it navigates by moving two body-length rows of thin, paddle-shaped protrusions that cascade like dominoes.

Ten tentacles as long or longer than its body stick out of its head, along with six pairs of curved nuchal organs that allow the squidworm to taste and smell underwater.

Using a remotely-operated submersible, a trio of marine biologists led by Karen Osborn of the Scripps Institution of Oceanography in California found the previously unknown animals in the Celebes Sea at a depth of 2.8 kilometres (1.7 miles).

“I was really excited,” Osborn said of her first glimpse. “It was so tantalising because the animal was so different from anything previously described, with the fantastic headgear.”

Squidworms live about 100 to 200 metres above the ocean floor, a layer rich in undiscovered fauna and flora, scientists say.

“I would estimate that when exploring the deep water column, more than half the animals we see are undescribed or new to science,” Osborn said in an email.

Up to now, this region has been largely inaccessible because tools for collecting samples either scraped along the ocean floor, or mangled specimens so badly that they were useless or unrecognisable once brought to the surface.

The squidworm, Teuthidodrilus samae, does not appear to be a predator, feeding instead on bits of so-called “marine snow,” a mix of sinking microscopic plants and animals, faecal material and cast-off mucus.

“Not the most appealing sounding food, but the large aggregates are rich in nutrients to feed on,” Osborn said.

The Celebes Sea, a deep pocket basin isolated from surrounding deep water, is part of the Coral Triangle, a conservation hot spot due to its diverse lifeforms and unique geological history.

The squidworm is so different from known animals that it required the creation of a new genus, the level above species in the taxonomical ladder for classifying animals and plants.

The study was published in Biology Letters, a journal of the British Royal Society.

Which Came First: Bees or Flowers?

By JOHN NOBLE WILFORD
Published: May 23, 1995 in The New York Times

BEFORE time turned them to stone at least 220 million years ago, the fossilized logs of the Petrified Forest in eastern Arizona stood as tall trees in a tropical environment. Many of them, scientists have now discovered, still bear traces of insect nests the trees once harbored. The logs are riddled with holes containing little chambers strung together in lines or clusters, nearly everything about them resembling the nests of modern bees.

The problem is that flowers date from only half as long ago. Could bees have lived before flowers? The very idea, once unthinkable, is upsetting traditional theory about the early history of bees and their supposed co-evolution with flowering plants, or angiosperms.

If confirmed by further research, the new findings at the Petrified Forest mean that bees were buzzing around some 140 million years earlier than previously thought. The oldest known fossil of a bee is an 80-million-year-old specimen trapped in amber from present-day New Jersey. Scientists now must be on the lookout for fossil bees to fill that huge time gap.

And then they must figure out what those bees were doing before the emergence of angiosperms, the earliest evidence for which is dated at 110 million to 120 million years ago. Either flowers actually appeared much earlier than anyone can conceive, or the first bees did without flowers for a long time, feeding on and pollinating cone-bearing, woody plants known as gymnosperms, a group that includes conifers, cycads and ferns.

In the latter and more likely case, scientists said, the discovery casts serious doubt on the standard theory that flowering plants and social insects like bees more or less evolved together, with the spread of flowers presumably influencing the development and proliferation of the bees.

“This new evidence suggests it was probably the other way around, and that insects like bees and wasps may have facilitated the evolution and diversification of angiosperms,” said Stephen T. Hasiotis, a paleobiologist at the United States Geological Survey in Denver and a doctoral student in geology at the University of Colorado at Boulder.

Mr. Hasiotis came upon the fossil bee nests while conducting studies aimed at reconstructing the ancient ecosystem and climate at the Petrified Forest, particularly as it applied to invertebrate life. He and other researchers found the remains of several hundred nests and cocoons, and tests put their ages at 207 million to 220 million years. Although no bee or wasp body parts were found with the fossil nests, they said, the only creatures that make similar structures today are bees and wasps.

The discovery was announced last week by Mr. Hasiotis at a regional meeting of the Geological Society of America, held at Montana State University in Bozeman. His collaborators were Dr. Russell Dubiel of the Geological Survey in Denver and Dr. Tim Demko of Colorado State University.

Despite the discovery’s stunning implications, other scientists tended to react favorably, in part because the evidence seemed compelling and it supported recent revisionist thinking about insect evolution. This stems from a growing recognition that the greatest expansion and diversification of insects occurred many millions of years before the appearance of flowering plants.

“We’re all very impressed,” said Dr. Charles D. Michener, an entomologist at Kansas University in Lawrence who is the author of “The Social Behavior of the Bees,” published by Harvard University Press in 1974. Mr. Hasiotis visited the Kansas campus earlier this year and showed the evidence to Dr. Michener and his colleagues.

Dr. Michener agreed that the fossil nests looked like the clusters of chambers, or cells, that make up the nests of modern bees. But like other scientists, he cautioned that more research would be needed to confirm the findings. It is always possible that some insect no longer extant made bee-like nests back then. The best evidence, of course, would be to find some fossil bees associated with the nests, he said.

“It’s exactly what we would have expected,” was the reaction of Dr. J. John Sepkoski Jr., a paleontologist at the University of Chicago. It was he and Dr. Conrad C. Labandeira, a specialist in fossil insects at the Smithsonian Institution’s National Museum of Natural History in Washington, who reported two years ago the results of a comprehensive study of insect evolution. Their conclusions challenged orthodoxy by pointing out that the appearance of flowering plants did not prompt the great diversification of insects because they had been flourishing at least 120 million years before that.

Mr. Hasiotis found the ancient nests over the last four years of field work among the fossil logs. They were usually in shallow hollows inside the trunks, reached through knot holes. Each nest consisted of 15 to 30 cells shaped like little flasks, each less than an inch long. Each shell had a narrow entrance that led to a wider chamber. The walls were probably constructed out of sap and resin from the tree.

In shape and size, Mr. Hasiotis said, each cell was “virtually identical” to similar enclosures in the nests of modern bees. Their practice is to deposit an egg in each cell, along with a store of pollen and resin as food for the larva that emerges from the egg.

The researchers also found the remains of other nests underground and clusters of cocoons in the logs. They closely resemble cocoons of present-day wasps. The evidence could push back the known origin of wasps by as much as 100 million years.

“The nest construction of these insects is fairly complex, indicating a highly developed behavior,” Mr. Hasiotis said.

The nest builders would not have been the same species as modern honeybees, he said, but probably primitive insects related to a smaller species today commonly known as the sweat bee. The appearance of the nest suggests the builders would have had an anatomy similar to that of today’s bees and wasps. That is, they would have needed a flexible and jointed head, thorax and abdomen with strong legs and the ability to fold the wings behind and flat against the back in order to maneuver around individual nest cells.

Because it is difficult to imagine bees without flowers, the new findings could have enormous implications for botany.

As it stands now, a tiny fossilized plant that lived 120 million years ago is considered the oldest known flower. Identified by Yale University botanists in 1990, it was apparently an herb, barely one inch tall and resembling the black pepper plant. Only later, it is assumed, did angiosperms evolve more dazzling flowers and nectar to lure insects, birds and bats to act as agents, transferring the pollen of one plant to the seed of another.

But recent research has led some botanists to suspect that the first angiosperms probably originated much earlier — perhaps as far back as 200 million years ago in the Triassic period, when dinosaurs were getting started. If it could be established that bees already existed then, theories of an earlier history for angiosperms would receive a big boost.

But the earlier bees would not necessarily have required angiosperms, said Dr. Thom Taylor, a paleobotanist at Ohio State University in Columbus. Although he has not studied the evidence for fossil bee nests, he could conceive of bees existing in a green world of ferns, conifers and cycads and other ancient gymnosperms, the dominant vegetation in the Triassic.

The pollen of these plants is normally scattered by wind, not by insects and birds. But Dr. Taylor said, “It would not surprise me to learn that bees and fern plants developed a relationship that involved pollination.”

In that case, as Mr. Hasiotis speculated, flowering plants did not so much open up new ecological niches for insects, including bees and wasps. Instead, they may have evolved to compete for the attention of insects that were already flourishing.

“Primitive angiosperms probably took advantage of this bee and wasp behavior by developing various colors of flowers as a pollination strategy to compete with gymnosperms,” the researcher said. “Over time, most of the insects actually shifted from gymnosperms to the flowering plants.”

Angiosperms may well be late bloomers as far as bees are concerned, but with the help of a lot of busy bees they have certainly flourished. Now there are 250,000 species of angiosperms, compared with fewer than 15,000 remaining varieties of gymnosperms.

Eggs with the oldest known embryos of a dinosaur found

By Katia Moskvitch
Science reporter, BBC News

Palaeontologists have identified the oldest known dinosaur embryos, belonging to a species that lived some 190 million years ago. The eggs of Massospondylus, containing well-perserved embryos, were unearthed in South Africa back in 1976. The creature appears to be an ancestor of the family that includes the long-necked dino once known as Brontosaurus. The study in the Journal of Vertebrate Paleontology also sheds light on the dinosaurs’ early development.

While the embryos are only about 20cm long, the adults are thought to have reached some five metres in height

The researchers used the embryos to reconstruct what the dinosaurs’ babies might have looked like when they roamed the Earth. Having studied the fossilised eggs, the team, led by Professor Robert Reisz of the University of Toronto Mississauga in Canada, discovered that the embryos were the oldest ones ever found of any land-dwelling vertebrate. “This project opens an exciting window into the early history and evolution of dinosaurs,” said Professor Reisz. “Prosauropods are the first dinosaurs to diversify extensively, and they quickly became the most widely spread group, so their biology is particularly interesting as they represent in many ways the dawn of the age of dinosaurs.”

‘Awkward’ bodies
Massospondylus belonged to a group of dinosaurs known as prosauropods, the ancestors of sauropods – huge, four-legged dinosaurs with long necks. Having studied the tiny (20cm-long) skeletons, the researchers noted that the embryos were almost about to hatch – but never had the chance. Interestingly, the report says, the embryos looked quite different compared to the adult animals. Once hatched, the babies would have had rather long front legs, meaning that they would have been walking on all fours rather than on two legs like the adults. The embryos’ heads were also disproportionally big, but it is believed the adult Massospondylus, which were about five metres in length, had relatively tiny heads and long necks. The little ones’ anatomy would have changed with age. The paper stated that the rather awkward body of the embryos suggested that just like humans, the hatchlings would have required parental care – and if in this case, it would be the earliest known example of parental care.

New Ocean Acidification Study Shows Added Danger to Already Struggling Coral Reefs

ScienceDaily (Nov. 13, 2010)

Over the next century, recruitment of new corals could drop by 73 percent, as rising carbon dioxide levels turn the oceans more acidic, suggests a new study led by scientists at the University of Miami Rosenstiel School of Marine and Atmospheric Science. The research findings reveal a new danger to the already threatened Caribbean and Florida reef Elkhorn corals.

“Ocean acidification is widely viewed as an emerging threat to coral reefs,” said Rosenstiel School graduate student Rebecca Albright. “Our study is one of the first to document the impacts of ocean acidification on coral recruitment.”

Albright and colleagues report that ocean acidification could compromise the successful fertilization, larval settlement and survivorship of Elkhorn corals. The research results suggest that ocean acidification could severely impact the ability of coral reefs to recover from disturbance, said the authors.

Elkhorn coral, known as Acropora palmata, is recognized as a critical reef-building species that once dominated tropical coral reef ecosystems. In 2006, Elkhorn was included on the U.S. Endangered Species List largely due to severe population declines over the past several decades.

The absorption of carbon dioxide by seawater, which results in a decline in pH level, is termed ocean acidification. The increased acidity in the seawater is felt throughout the marine food web as calcifying organisms, such as corals, oysters and sea urchins, find it more difficult to build their shells and skeletons making them more susceptible to predation and damage.

Recent studies, such as this one conducted by Albright and colleagues, are beginning to reveal how ocean acidification affects non-calcifying stages of marine organisms, such as reproduction.

“Reproductive failure of young coral species is an increasing concern since reefs are already highly stressed from bleaching, hurricanes, disease and poor water quality,” said Chris Langdon, associate professor at the Rosenstiel School and co-author of the study, published in the Proceedings of the National Academy of Sciences.

Cellular Communicators for Cancer Virus Identified

ScienceDaily (Nov. 8, 2010)

A new discovery by UNC scientists describes how cells infected by the Epstein-Barr virus (EBV) produce small vesicles or sacs called exosomes, changing their cellular “cargo” of proteins and RNA. This altered exosome enters cells and can change the growth of recipient cells from benign to cancer-producing.

In this way, virus-infected cells can have wide-ranging effects and potentially manipulate other cells throughout the body. The findings are reported in the Nov. 8 early online edition of the Proceedings of the National Academy of Sciences.

Nancy Raab-Traub, PhD, professor of microbiology and Immunology, said, “Exosomes may be the Trojan Horse through which EBV gains control of cells that are not even infected. Importantly, the production of exosomes may provide a new therapeutic target that can be blocked to reduce cancer growth.” Raab-Traub is a Sarah Graham Kenan Professor and member of UNC Lineberger Comprehensive Cancer Center.

Epstein-Barr Virus (EBV) is perhaps the world’s most successful virus as almost everyone is infected with it for life. EBV cannot be eliminated by the immune system and is constantly secreted into saliva where it is effectively transmitted. Infection with the virus rarely causes disease; however, EBV is found in several major cancers, including lymphoma and cancer of the nose and throat, where its proteins hijack the cell’s growth regulatory mechanisms to induce uncontrolled cell growth characteristic of cancer.

Through exosomes, a protein called latent membrane protein 1, that is considered the EBV oncogene, can be delivered to uninfected cells. Significantly, EBV also changes the entire contents of the exosomes to deliver cellular proteins that are also activated in cancers. This surprising finding reveals that one infected cell can have wide-ranging effects and induce the unchecked growth of neighboring cells.

The immune system is constantly on guard to identify foreign viral proteins. Through exosomal uptake, cancer cells would be stimulated to grow without the expression of proteins that “announce” infection to the immune system, thus allowing unchecked growth. The study also showed that the cells that produce blood vessels, the process called angiogenesis, readily take in the altered exosomes and are potentially induced to grow.

“The next step,” explains David Meckes, PhD, postdoctoral fellow in the Raab-Traub lab and first author of the paper, “is to determine how the virus controls which proteins are sorted into exosomes and how this process could be inhibited.”

Other UNC Lineberger authors, all members of the Raab-Traub laboratory, are: Kathy Shair, PhD;Aron Marquitz, PhD; Patrick Kung, PhD ; and Rachel Edwards, BS. The research was supported by a grant from the National Cancer Institute.

Editor’s Note: This article is not intended to provide medical advice, diagnosis or treatment.

Soy May Stop Prostate Cancer Spread: Experimental Soy-Based Drug Shows Benefits in Men With Localized Prostate Cancer

ScienceDaily (Nov. 8, 2010)

Northwestern Medicine researchers at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University have found that a new, nontoxic drug made from a chemical in soy could prevent the movement of cancer cells from the prostate to the rest of the body.

These findings are being presented at the Ninth Annual American Association for Cancer Research Frontiers in Cancer Prevention Research Conference.

Genistein, a natural chemical found in soy, is being used in the lab of Raymond Bergan, M.D., the director of experimental therapeutics at the Lurie Cancer Center, to inhibit prostate cancer cells from becoming metastatic and spreading to other parts of the body. So far the cancer therapy drug has worked in preclinical animal studies and now shows benefits in humans with prostate cancer.

A recent phase II randomized study of 38 men with localized prostate cancer found that genistein, when given once a day as a pill, one month prior to surgery, had beneficial effects on prostate cancer cells.

Researchers examined the cancer cells from the subjects’ prostates after surgery and found that genistein increased the expression of genes that suppress the invasion of cancer cells and decreased the expression of genes that enhance invasion.

“The first step is to see if the drug has the effect that you want on the cells and the prostate, and the answer is ‘yes, it does,'” said Bergan, a professor of hematology and oncology at Northwestern University Feinberg School of Medicine and a physician at Northwestern Memorial Hospital.

The next step is to conduct another phase II study to see if the drug can stop the cancer cells from moving out of the prostate and into the rest of the body, Bergan said. If confirmed, Bergan said this could be the first therapy for any cancer that is non-toxic and targets and inhibits cancer cell movement.

“All therapies designed to stop cancer cell movement that have been tested to date in humans have basically failed have because they have been ineffective or toxic,” Bergan said. “If this drug can effectively stop prostate cancer from moving in the body, theoretically, a similar therapy could have the same effect on the cells of other cancers.”

Funding from the National Institutes of Health supported this research.

Editor’s Note: This article is not intended to provide medical advice, diagnosis or treatment.

Engineered Plants Make Potential Precursor to Raw Material for Plastics


ScienceDaily (Nov. 8, 2010)

In theory, plants could be the ultimate “green” factories, engineered to pump out the kinds of raw materials we now obtain from petroleum-based chemicals. But in reality, getting plants to accumulate high levels of desired products has been an elusive goal. Now, in a first step toward achieving industrial-scale green production, scientists from the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory and collaborators at Dow AgroSciences report engineering a plant that produces industrially relevant levels of compounds that could potentially be used to make plastics.

The research is reported online in Plant Physiology, and will appear in print in the December issue.

“We’ve engineered a new metabolic pathway in plants for producing a kind of fatty acid that could be used as a source of precursors to chemical building blocks for making plastics such as polyethylene,” said Brookhaven biochemist John Shanklin, who led the research. “The raw materials for most precursors currently come from petroleum or coal-derived synthetic gas. Our new way of providing a feedstock sourced from fatty acids in plant seeds would be renewable and sustainable indefinitely. Additional technology to efficiently convert the plant fatty acids into chemical building blocks is needed, but our research shows that high levels of the appropriate feedstock can be made in plants.”

The method builds on Shanklin’s longstanding interest in fatty acids — the building blocks for plant oils — and the enzymes that control their production. Discovery of the genes that code for the enzymes responsible for so called “unusual” plant oil production encouraged many researchers to explore ways of expressing these genes and producing certain desired oils in various plants.

“There are plants that naturally produce the desired fatty acids, called ‘omega-7 fatty acids,’ in their seeds — for example, cat’s claw vine and milkweed — but their yields and growth characteristics are not suitable for commercial production,” Shanklin said. Initial attempts to express the relevant genes in more suitable plant species resulted in much lower levels of the desired oils than are produced in plants from which the genes were isolated. “This suggests that other metabolic modifications might be necessary to increase the accumulation of the desired plant seed oils,” Shanklin said.

“To overcome the problem of poor accumulation, we performed a series of systematic metabolic engineering experiments to optimize the accumulation of omega-7 fatty acids in transgenic plants,” Shanklin said. For these proof-of-principle experiments, the scientists worked with Arabidopsis, a common laboratory plant.

Enzymes that make the unusual fatty acids are variants of enzymes called “desaturases,” which remove specific hydrogen atoms from fatty acid chains to form carbon-carbon double bonds, thus desaturating the fatty acid. First the researchers identified naturally occurring variant desaturases with desired specificities, but they worked poorly when introduced into Arabidopsis. They next engineered a laboratory-derived variant of a natural plant enzyme that worked faster and with greater specificity than the natural enzymes, which increased the accumulation of the desired fatty acid from less than 2 percent to around 14 percent.

Though an improvement, that level was still insufficient for industrial-scale production. The scientists then assessed a number of additional modifications to the plant’s metabolic pathways. For example, they “down-regulated” genes that compete for the introduced enzyme’s fatty acid substrate. They also introduced desaturases capable of intercepting substrate that had escaped the first desaturase enzyme as it progressed through the oil-accumulation pathway. In many of these experiments they observed more of the desired product accumulating. Having tested various traits individually, the scientists then combined the most promising traits into a single new plant.

The result was an accumulation of the desired omega-7 fatty acid at levels of about 71 percent in the best-engineered line of Arabidopsis. This was much higher than the omega-7 fatty acid levels in milkweed, and equivalent to those seen in cat’s claw vine. Growth and development of the engineered Arabidopsis plants was unaffected by the genetic modifications and accumulation of omega-7 fatty acid.

“This proof-of-principle experiment is a successful demonstration of a general strategy for metabolically engineering the sustainable production of omega-7 fatty acids as an industrial feedstock source from plants,” Shanklin said.

This general approach — identifying and expressing natural or synthetic enzymes, quantifying incremental improvements resulting from additional genetic/metabolic modifications, and “stacking” of traits — may also be fruitful for improving production of a wide range of other unusual fatty acids in plant seeds.

This research was funded by the DOE Office Science, and by The Dow Chemical Company and Dow AgroSciences.

Bee mystery not over yet…

By Susan Milius
Web edition : Tuesday, October 26th, 2010

Ambushed on his way to the cafeteria one recent Wednesday after giving a talk, bee biologist Jeff Pettis proved remarkably gracious to this entomology paparazzo with a burning question.

On opening day at the 10th annual conference of the North American Pollinator Protection Campaign, Pettis allowed himself to be stopped for a chat in an echoing, block-long corridor in the U.S. Department of Agriculture’s central hive in Washington, D.C. Asked whether the recent media buzz over a fungus-virus pair of bee pathogens means science has finally figured out why bees are vanishing in a mysterious illness called colony collapse disorder, he replied directly.

“We have not,” Pettis said, sounding a bit wistful.

A recent scientific paper made news by suggesting that a newly discovered virus and a long-lamented fungus might be combining to hammer the bees. Pettis, of the USDA Bee Laboratory in Beltsville, Md., rates the headlines as “overblown.”

Other bee researchers too have been saying “wait and see” since the latest fungus-virus hypothesis appeared in a PLoS ONE paper online October 6. The cautious chorus even includes the scientist who led the study that caused the fuss, Jerry Bromenshenk of the University of Montana in Missoula. Excited as he sounds about his research, he’s not ready to claim that he has found the cause of colony collapse disorder.

What he and his colleagues say they have found is a link between the disorder and a pair of pathogens. All 45 of the collapsing or collapsed colonies the researchers sampled showed what look like signatures of infections by both a Nosema fungus, already well established in apiarists’ nightmares, and some form of what’s called an iridescent virus. Using a stand-in iridescent virus from moths, the researchers also found that combining the fungus and the virus did more damage to bees than either did alone.

The idea that a Nosema strain pairs up with another pathogen to cause colony collapse disorder is not new. As Science News’s Eva Emerson reported from the American Society for Microbiology meeting in June, Jay Evans of the USDA Bee Research Laboratory has also linked colony collapse disorder with a Nosema-plus-virus infection. He, however, was looking at several small RNA-based viruses.

What Bromenshenk’s team has not done, Bromenshenk himself explains, is meet the traditional standard for proving that a particular pathogen causes a disease, a set of criteria known as Koch’s postulates. Basically the team will have to isolate the honeybee pathogens, demonstrate that healthy honeybees inoculated with them get colony collapse disorder, and then recover the same pathogens from them.

The moth-virus inoculation that they have performed didn’t even reveal whether worker bees would fly away from their hives to die, the hallmark of colony collapse disorder. The lab setup kept the bees from flying much of anywhere, says coauthor and chemical ecologist Colin Henderson, also at Montana.

He and the bee team are eagerly hoping to work through Koch’s postulates, Henderson says. The tests could resolve some odd spots in the data. For example,the iridescent virus showed up not only in the collapsing colonies but in nine of the 13 apparently healthy ones. “Bee colonies are messy,” Henderson says.

The virus’ appearance in healthy colonies doesn’t automatically dash the fungus-virus hypothesis. An iridescent virus can lurk in an insect and not cause a fatal disease — at least in other species — says study coauthor Trevor Williams of the Institute of Ecology AC in Xalapa, Mexico. The new research is only the second report of one of these viruses in honeybees, Williams says, and he’s eager to see some actual infected material.

Lethal infections of these viruses in other insects create an iridescent sheen in the victim that can be quite pretty, in a sense, says Diana Cox-Foster of Pennsylvania State University in University Park. She, like Pettis, is waiting for more information. Neither she nor her colleagues have noticed iridescent viruses in hundreds of collapsing colonies examined in recent years.

The basic idea of combined menaces does make sense though, Cox-Foster says. She is investigating a different one-two combination: Pesticide exposure, she says, can substantially encourage the proliferation of viruses.

Article taken from: http://www.sciencenews.org/view/generic/id/64725/title/Bee_mystery_not_over_yet
For the wikipedia entry on colony collapse disorder go here: http://en.wikipedia.org/wiki/Colony_collapse_disorder

NASA Deep Impact spacecraft flies by small comet

By ALICIA CHANG
Thu Nov 4, 9:00 pm ET

PASADENA, Calif. – A NASA spacecraft sped past a small comet Thursday, beaming pictures back to Earth that gave scientists a rare close-up view of its center. Mission controllers burst into applause upon seeing images from the flyby that revealed a peanut-shaped comet belching jets of poisonous gases.

“It’s hyperactive, small and feisty,” said mission scientist Don Yeomans of the NASA Jet Propulsion Laboratory.

The close encounter occurred 13 million miles from Earth when the Deep Impact craft, hurtling through space, flew within 435 miles of comet Hartley 2. It’s only the fifth time that a comet’s core has been viewed up close.

Scientists are interested in comets because they’re icy leftovers from the formation of the solar system about 4.5 billion years ago. Studying them could provide clues to how Earth and the planets formed and evolved.

“The scientific work is just beginning now,” principal investigator Michael A’Hearn, of the University of Maryland, said at a post-mission news conference. “The engineers did a fantastic job of getting us data. Now we have to make sense of it.”

Thursday’s flyby is actually an encore mission for Deep Impact. It set off cosmic fireworks on July 4, 2005, when it fired a copper probe that crashed into comet Tempel 1. The high-speed collision spewed a cloud of debris into space, giving scientists their first peek of the interior.

After the $333 million comet-buster, NASA recycled Deep Impact for a new mission to visit another comet. It was supposed to target comet Boethin in 2008, but it was nowhere to be found. Scientists theorized the comet may have broken up into small pieces.

Deep Impact was then redirected to Hartley 2. Roughly 1 1/2 miles long, Hartley 2 is the smallest comet to be photographed up close. On its way there, the craft spent several months scanning a cluster of nearby stars with known planets circling them.

While its latest task lacks the Hollywood drama of the Tempel 1 crash, researchers still consider it an important mission. Unlike in 2005, viewers could not see Thursday’s comet encounter in real time since the craft’s antenna was not pointed at Earth as it flew past Hartley 2.

“There are a lot of open questions about comets and their life cycle,” said project manager Tim Larson of JPL, which manages the $42 million encore mission. “We have so little data that every time we have an opportunity to go near a comet, it’s a chance to expand our knowledge.”

Since September, Deep Impact has been stalking Hartley 2 like a paparazzo, taking images every 5 minutes and gathering data. It’s the first craft to visit two comets.

Deep Impact will observe Hartley 2 until Thanksgiving and then wait for further instructions from NASA. The space agency has not decided whether to reuse Deep Impact again. The craft does not have enough fuel on board to do another flyby.

The latest images add to scientists’ cometary photo album, said astronomer David Jewitt of the University of California, Los Angeles, who had no role in the project.

“We’re visual animals and nothing seems wholly real to us until we have a nice picture of it,” Jewitt said.

Hartley 2 passed within 11 million miles of Earth on Oct. 20 — the closest it has been to our planet since its discovery in 1986.

British-born astronomer Malcolm Hartley, who discovered the comet, said he never imagined a spacecraft would get so close to his namesake find.

“When I saw the comet, it was millions and millions of kilometers away,” he said. “I’m extremely excited and feel very privileged. After all, I only discovered it.”

The Lucky Genetic Variants That Protect Some People From HIV

by Richard Knox

Wednesday morning Harvard AIDS researcher Bruce Walker called one of his long-time patients with an announcement: “We’ve found the needle in the haystack!”

Actually, Walker and his colleagues have found a half-dozen needles. They pinpointed genetic variations that change amino acid building blocks in key proteins in the immune system. These differences help explain why some patients can be infected with HIV for decades, never get treatment and yet never progress to AIDS.

“We’ve found the five or six amino acids that explain the difference between people doing well or doing badly,” Walker says.

The discovery is being published online by the journal Science.

The patient Walker called Wednesday morning is a 54-year-old Episcopalian priest named Robert Massie who’s a fellow at Harvard’s Kennedy School of Government. Massie inspired Walker’s 17-year search for the secret of these HIV controllers.

Massie got infected with HIV way back in 1978 – several years before AIDS was recognized — from the constant injections of Factor VIII clotting factor he needed to treat his hemophilia.

Hemophiliacs were a bellwether group that helped scientists zero in on the AIDS virus. Many of them got infected early in the pandemic because Factor VIII was made from the blood of hundreds of donors. If even one was carrying HIV, the clotting concentrate was an efficient way to transmit the virus to unsuspecting hemophiliacs.

It turns out that the half-dozen amino acid variants that have protected Massie against AIDS are the same ones the Harvard-led team has found in others of European descent, those of African descent and Hispanics.

With the discovery, a number of other findings are falling neatly into place.

For instance, scientists have previously shown that people whose immune systems can control HIV are more likely to have certain “flavors” of an important immune trait called HLA (for Human Leukocyte Antigen). The HLA system allows the body to distinguish between its own healthy cells and those infected by foreign invaders, such as viruses.

But until now, scientists didn’t know what it was about the more favorable HLA subtypes that conferred protection against HIV.

The genetic instructions for the newly found amino acid variants resides in a region of chromosome 6 that codes for the HLA system. Five of the six variants are within a protein that controls how certain immune cells, called CD4s, display bits and pieces of viral protein on their outer shell – if they happen to be infected with a virus. HIV has a special affinity for infecting CD4 cells, and without constant antiviral treatment the virus slowly destroys the immune systems of most infected people.

But if a person has the newly discovered amino acid variants, his CD4 cells will be especially good at displaying pieces of HIV in a binding groove, or pocket of their outer coat. That enables killer cells, immune cells called CD8s, to target and kill the infected cells before they can spew forth more viruses.

For most people, the lack of these protective variants renders their HIV-infected cells invisible to their immune system.

“What we know for absolute certain is that these variants alter the way the viral protein sits in the binding groove,” Walker says. “Now we’re working on exactly how the protein is presented to induce a protective immune response.

“The exciting part of this finding,” he continues, “is that it helps us focus on something that clearly is important and hopefully will allow us to manipulate the immune response” of people without the protective trait.

Walker acknowledges that “we have a long ways to go before we can turn this finding into something that will prevent someone from becoming infected with HIV or augment their immunity. But this takes us a step closer to defining and effective immune response.”

Vaccines are one way to manipulate the immune response. But nobody has ever used a vaccine in such a targeted way.

Massie says he was “very, very happy” to hear of the discovery. “I know they’ve devoted a huge amount of time, money, effort and emotion to try and unlock this puzzle,” he says.

Meanwhile, Massie is keenly aware of his own good fortune – and not only at being born with the genetic talismans that have protected him from HIV.

He wasn’t protected, it turns out, against hepatitis C, also acquired from injections of Factor VIII concentrate. Hep-C destroyed his liver.

A year ago, he had a liver transplant. And, there’s a silver lining: The transplant has cured his hemophilia, because his new liver can make the Factor VIII he needs to prevent bleeding.

“I used to have four or five injections a day to maintain the right level of Factor VIII in my blood, ” Massie says. “All that’s behind me.”