Racial disparities exist among diabetes patients treated by the same physicianBlack patients with diabetes are less likely than white patients to achieve long-term control of their blood

glucose, blood cholesterol and blood pressure levels, even when they are treated by the same physician, according to a report in the June 9 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

Racial disparities in the quality of diabetes care have been previously documented, according to background information in the article. Black patients with diabetes are less likely to receive recommended components of care, including hemoglobin A1C testing (HbA1C, a measure of blood glucose control over time) and lipid testing, and to achieve treatment goals, such as controlled blood pressure, cholesterol and blood glucose levels. In addition, black patients are more likely than white patients to develop diabetes-related eye and kidney disease and to have amputations of their lower extremities. "Identifying the underlying reasons and potential solutions for these differences in quality of care and outcomes is a high priority," the authors write.

Thomas D. Sequist, M.D., M.P.H., of Harvard Vanguard Medical Associates, Boston, and colleagues analyzed electronic medical records from 4,556 white patients and 2,258 black patients with diabetes treated by 90 primary care physicians in eastern Massachusetts. Each physician treated at least five black patients and five white patients; all patients were age 18 or older and had visited the physician within the last two years.

Black patients and white patients received tests of low-density lipoprotein (LDL or "bad") cholesterol and HbA1C at similar rates. However, white patients were more likely than black patients to reach commonly accepted benchmarks for controlled levels of HbA1C (47 percent vs. 39 percent), LDL cholesterol (57 percent vs. 45 percent) and blood pressure (30 percent vs. 24 percent).

"Patient sociodemographic factors explained 13 percent to 38 percent of the racial differences in these measures, whereas within-physician effects accounted for 66 percent to 75 percent of the differences," the authors write. "Thus, racial differences in outcomes were not related to black patients differentially receiving care from physicians who provide a lower quality of care, but rather that black patients experienced less ideal or even adequate outcomes than white patients within the same physician panel."

The variation in diabetes care was not related to overall performance or the volume of black patients treated by individual physicians, the authors note. "Our data suggest that the problem of racial disparities is not characterized by only a few physicians providing markedly unequal care, but that such differences in care are spread across the entire system, requiring the implementation of system-wide solutions," they write. "Efforts to eliminate these disparities, including race-stratified performance reports and programs to enhance care for minority patients, should be addressed to all physicians."(Arch Intern Med. 2008;168[11]:1145-1151. Available pre-embargo to the media at www.jamamedia.org.)Editor's Note: This study was funded by the Robert Wood Johnson Foundation Finding Answers: Disparities Research for Change National Program. Dr. Sequist serves as a consultant on the Aetna External Advisory Committee for Racial and Ethnic Equality. Co-author Dr. Ayanian serves as a consultant to RTI International and DxCG Inc. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.Editorial: Results Offer Opportunity for Physician Leadership

"The findings presented by Sequist et al build nicely on prior work and are important and provocative," writes Carolyn Clancy, M.D., of the Agency for Healthcare Research and Quality, Rockville, Md., in an accompanying editorial.

"They now have an opportunity to examine physicians' reactions and how care changes when physicians are provided feedback on their performance," Dr. Clancy writes. "Eliminating disparities in health care will require that all patients have access to care, as well as physician leadership to assure that the care provided is evidence-based, patient-centered, effective, consistent and equitable."(Arch Intern Med. 2008;168[11]:1135-1136. Available pre-embargo to the media at www.jamamedia.org.)

Arsenic and new riceAmid recent reports of dangerous levels of arsenic being found in some baby rice products, scientists have

found a protein in plants that could help to reduce the toxic content of crops grown in environments with high levels of this poisonous metal. Publishing in the open access journal BMC Biology, a team of Scandinavian researchers has revealed a set of plant proteins that channel arsenic in and out of cells.

Arsenic is acutely toxic and a highly potent carcinogen, but is widespread in the earth's crust and easily taken up and accumulated in crops. Contaminated water is the main source of arsenic poisoning, followed by ingestion of arsenic-rich food, especially rice that has been irrigated with arsenic-contaminated water. According to the WHO, arsenic has been found approaching or above guideline limits in drinking water in Argentina, Australia, Bangladesh, Chile, China, Hungary, India, Mexico, Peru, Thailand, and the US.

Until now, scientists have been unable to identify which proteins are responsible for letting arsenite, the form of arsenic that damages cellular proteins, into plant cells. Now Gerd Bienert and his colleagues from the University of Copenhagen, Denmark and the University of Gothenburg, Sweden, are the first to show that a

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family of transporters, called nodulin26-like intrinsic protein (NIPs), can move arsenite across a plant cell membrane. NIPs are related to aquaglyceroporins found in microbes and mammalian cells and which have already been shown to function as arsenite channels in these other organisms. Bienert's team put the plant genes coding for different NIP transporters into yeast cells in order to test the cells for arsenic sensitivity. The researchers found that the growth of yeast containing certain plant NIPs was suppressed when arsenite, one of the predominant forms of arsenic found in soil, was added to the mix. They showed that the arsenite was channelled by NIPs and accumulated inside the yeast cells. Further investigations showed that only a subgroup of NIPs had arsenite transport capabilities, and have now been identified as metalloid channels in plants.

More surprisingly, the researchers also found that when they added arsenate some yeast, cells actually grew better and arsenite was released out of the cells. "It appears that some NIPs don't just transport arsenite in one direction", says Bienert. "They are bidirectional and, given the right conditions, can clear cells of toxic arsenite as well as accumulate it. This striking exit of the accumulated arsenite in cells could have an important role to play in the detoxification of plants, especially coupled with possibility of engineering a transporter that discriminates against arsenite uptake in the first place."Notes to Editors:1. A subgroup of plant aquaporins facilitate the bi-directional diffusion of As(OH)3 and Sb(OH)3 across membranes Gerd P Bienert, Michael Thorsen, Manuela D Schuessler, Henrik R Nilsson, Annemarie Wagner, Markus J Tamas and Thomas P Jahn BMC Biology (in press)

ADHD an advantage for nomadic tribesmen?A propensity for attention deficit hyperactivity disorder (ADHD) might be beneficial to a group of Kenyan

nomads, according to new research published in the open access journal BMC Evolutionary Biology. Scientists have shown that an ADHD-associated version of the gene DRD4 is associated with better health in nomadic tribesmen, and yet may cause malnourishment in their settled cousins.

A study led by Dan Eisenberg, an anthropology graduate student from Northwestern University in the US, analyzed the correlates of body mass index (BMI) and height with two genetic polymorphisms in dopamine receptor genes, in particular the 48 base pair (bp) repeat polymorphism in the dopamine receptor D4 (DRD4) gene.

The DRD4 gene codes for a receptor for dopamine, one of the chemical messengers used in the brain. According to Eisenberg "this gene is likely to be involved in impulsivity, reward anticipation and addiction". One version of the DRD4 gene, the '7R allele', is believed to be associated with food craving as well as ADHD. By studying adult men of the Ariaal of Kenya, some of whom still live as nomads while others have recently settled, the research team investigated whether this association would have the same implications in different environments.

While those with the DRD4/7R allele were better nourished in the nomadic population, they were less well-nourished in the settled population. Although the effects of different versions of dopamine genes have already been studied in industrialized countries, very little research has been carried out in non-industrial, subsistence environments like the areas where the Ariaal live, despite the fact that such environments may be more similar to the environments where much of human genetic evolution took place.

Eisenberg explains, "The DRD4/7R allele has been linked to greater food and drug cravings, novelty-seeking, and ADHD symptoms. It is possible that in the nomadic setting, a boy with this allele might be able to more effectively defend livestock against raiders or locate food and water sources, but that the same tendencies might not be as beneficial in settled pursuits such as focusing in school, farming or selling goods".

These findings suggest that behavior differences previously associated with the DRD4 gene, such as ADHD, are more or less effective depending on the environment. Research into how this might occur in Ariaal children is planned in the near future.Notes to Editors1. Dopamine receptor genetic polymorphisms and body composition in undernourished pastoralists: An exploration of nutrition indices among nomadic and recently settled Ariaal men of northern Kenya Dan T.A. Eisenberg, Benjamin Campbell, Peter B. Gray and Michael D. Sorenson BMC Evolutionary Biology (in press)

World's oldest woman had normal brainAlzheimer's disease isn't inevitable, suggests unique case in Neurobiology of Aging

Amsterdam, 9 June 2008 -- A 115-year-old woman who remained mentally alert throughout her life had an essentially normal brain, with little or no evidence of Alzheimer's disease, according to a study in the August issue of Neurobiology of Aging (http://neurobiologyofaging.org/).

The findings question the assumption that Alzheimer's disease or other forms of dementia will inevitably develop, if people live long enough. "Our observations suggest that, in contrast to general belief, the limits of human cognitive function may extend far beyond the range that is currently enjoyed by most individuals, and 2023/05/19 2

that improvements in preventing brain disorders of aging may yield substantial long-term benefits," according to a study led by Prof. dr. Gert Holstege of University Medical Centre Groningen, The Netherlands.

Dr. Holstege and colleagues had a unique chance to test the mental functioning of one of the world's oldest humans, and then to compare their findings with the condition of the subject's brain after death. The patient was a Dutch woman who, at age 82, made arrangements to donate her body to science after death. At age 111, she contacted the researchers to ask whether her body would still be useful for research or teaching purposes. They assured her that, contrary to what she thought, they were especially interested because of her age: "She was very enthusiastic about her being important for science," Dr. Gert Holstege and colleagues write.

The researchers found the patient to be "an alert and assertive lady, full of interest in the world around her, including national and international politics and sports." She had lived independently until moving to a residential care home at age 105, mainly because of poor eyesight. Ironically, she had been very small at birth and was not expected to survive.

A series of neurological and psychological examinations were performed when the patient was 112 and 113 years old. The results were essentially normal, with no signs of dementia or problems with memory or attention. In general, her mental performance was above average for adults aged 60 to 75.

As planned, her body was donated to science when she died at age 115. At the time, she was the world's oldest woman. Examination after death found almost no evidence of atherosclerosis (narrowing of the arteries) anywhere in her body. The brain also showed very few abnormalities - the number of brain cells was similar to that expected in healthy people between 60 and 80 years old.

A key finding was the absence of brain abnormalities typical of Alzheimer's disease. There were almost no deposits of a substance called beta-amyloid, which are characteristic of Alzheimer's patients. The other abnormalities present, including "neurofibrillary tangles," were very mild - too early to cause significant mental impairment.

The unique case lends new insights into the potential for preserving brain function in very elderly patients. Previous studies have found at least mild abnormalities in the brains of nearly all "cognitively normal" elderly people. As the number of people living to age 100 and beyond continues to increase, the findings suggest that deterioration of the brain is not inevitable.In addition to the article, commentaries by Dr. Joseph L. Price of Washington University, St. Louis, Panteleimon Giannakopoulos of University Hospitals of Geneva, Switzerland and colleagues, and Drs. Kelly Del Tredici and Heiko Braak of the Institute for Clinical Neuroanatomy in Frankfurt/Main, Germany are available.Notes to Editors:The full text of the article is available upon request by contacting the Elsevier press office, newsroom@elsevier.com.About Neurobiology of AgingNeurobiology of Aging (http://neurobiologyofaging.org/) publishes the results of studies in behavior, biochemistry, cell biology, endocrinology, molecular biology, morphology, neurology, neuropathology, pharmacology, physiology and protein chemistry in which the primary emphasis involves mechanisms of nervous system changes with age or diseases associated with age.

Solid tumor cells not killed by radiation and chemotherapy become strongerDURHAM, N.C. -- Because of the way solid tumors adapt the body's machinery to bring themselves more oxygen, chemotherapy and radiation may actually make these tumors stronger.

"In a sense, these therapies can make the tumor healthier," said Mark W. Dewhirst, D.V.M., Ph.D., professor of radiation oncology at Duke University Medical Center. "Unless the treatment is very effective in killing many if not most tumor cells, you are shooting yourself in the foot."

Dewhirst and colleagues Yiting Cao, M.D., Ph.D., of Duke Pathology, and Benjamin Moeller, M.D., Ph.D. have introduced this counter-intuitive idea at recent conferences and in a review article featured in the June issue of Nature Reviews Cancer.

Radiation and chemotherapy do kill most solid tumor cells, but in the cells that survive, the therapies drive an increase in a regulatory factor called HIF1 (hypoxia-inducible factor 1), which cells use to get the oxygen they need by increasing blood vessel growth into the tumor. Solid tumors generally have low supplies of oxygen, Dewhirst explained and HIF1 helps them get the oxygen they need.

The review article concludes that blocking HIF1 would provide a clear mechanism for killing solid-tumor cells, particularly cells that are proving resistant to radiation or chemotherapy treatments.

As a part of this work, Dewhirst's team has been studying the phenomenon of rising and falling oxygen levels in tumors, called cycling hypoxia. Oxygen levels have been found to naturally cycle up and down in individual blood vessels as well as large tumor regions. This instability in the tumor's oxygen levels can increase HIF-1 production and cause radiation therapy to fail, Dewhirst said.

"It is my opinion that the whole tumor grows more aggressively because of this pulsation of oxygen at low levels," Dewhirst said. "Most people thought cycling hypoxia was caused by temporary stoppage of blood flow 2023/05/19 3

in single blood vessel in tumors. In fact, however, oxygen levels cycle up and down virtually everywhere in the tumor, which is caused by fluctuations in blood flow rate. It has been a challenge to convince people of this."

Dewhirst and colleagues have made movies of oxygen transport in a tumor of a living animal that show the oxygen levels cycle up and down significantly, pulsing in waves seen as color changes in the movies. (View these movies at the Nature Reviews Cancer site: http://www.nature.com/nrc/journal/v8/n6/suppinfo/nrc2397.html )

The Duke team argues that blocking HIF1 is the consistent answer to tumor growth problems. Blocking HIF1 activity interferes with the tumor's ability to undergo glycolysis (energy production) in low-oxygen conditions, which blocks tumor growth, the authors wrote. Exactly how to accomplish chemotherapy or radiation treatment in the safest, most effective ways, in combination with HIF1 blockade, is still open for exploration, Dewhirst said.

For example, targeting HIF1 in the early stages of tumor growth, especially in very early cancer spread, may help, Dewhirst said. "For a woman who has had a primary breast tumor removed, and who is at high risk for cancer spread, this might be a situation in which you'd target HIF1," he explained. "Blocking HIF1 makes sense during the early stages of angiogenesis, which is the accelerated phase of blood vessel formation. In this way, you could keep the early metastasis sites inactive and prevent them from growing."

The Duke team has completed a phase I trial with a HIF1 inhibitor. "We are actively pursuing this clinically and will be moving this study into Phase 2," Dewhirst said. "We are interested in other applications of HIF-1 inhibition in combination with radiation and chemotherapy for different diseases."

Stem cell discovery sheds light on placenta developmentGAINESVILLE, Fla. ― Researchers studying embryonic stem cells have explored the first fork in the developmental road, getting a new look at what happens when fertilized eggs differentiate to build either an embryo or a placenta.

By manipulating a specific gene in a mouse blastocyst ― the structure that develops from a fertilized egg but is not yet an actual embryo ― scientists with the University of Florida's McKnight Brain Institute and the Harvard Stem Cell Institute caused cells destined to build an embryo to instead change direction and build the cell mass that leads to the placenta.

Writing in today's (Monday, June 9) online edition of Nature Genetics, the scientists reveal a cellular signaling mechanism in place at the earliest developmental stage.

Understanding the conditions that cause these cells to go off to different fates may have a bearing on health problems such as ectopic pregnancy, which occurs when the embryo develops outside of the womb in about 1 of 60 pregnancies, or molar pregnancy, which is abnormal tissue growth within the uterus that affects about 1 in every 1,000 pregnancies.

"We originally were exploring factors that might cause embryonic stem cells to become malignant ― there is a concern that these cells may cause tumors," said Chi-Wei Lu, Ph.D., an associate neuroscientist at the UF College of Medicine and lead author of the study. "Our experiments led us to discover the signal that initiates the process of embryonic tissue differentiation."

By activating a gene called Ras in cells bathed in a very specific culture medium, scientists were able to cause embryonic stem cells ― which originate from the inner cell mass of the blastocyst ― to become more like the trophoblastic stem cells that give rise to the placenta from the outer portion of the blastocyst.

Researchers marked these newly minted cells, which they called ES-TS cells, and injected them into mouse embryos. Instead of joining the stem cells that build the embryo, ES-TS cells joined the stem cells that build the placenta. Furthermore, when scientists transferred the engineered mouse embryos to foster mothers, the ES-TS cells went to work exclusively laying the foundation for the placenta.

"This paper highlights the value of embryonic stem cells for understanding early development," said senior author George Q. Daley, M.D., Ph.D., an associate professor of biological chemistry and molecular pharmacology at Harvard Medical School and an associate professor of pediatrics at Children's Hospital Boston. "Embryonic stem cells are more plastic than we had thought. By simply activating the Ras gene, we changed the fate of embryonic stem cells to an entirely unexpected tissue ― the placenta. This surprising result has given us an unanticipated insight into early embryo development."

The technique of genetically modifying the cells and growing them in a special medium could be valuable for additional research.

"This is exciting because events that only occur in the early stages of embryonic development are very difficult to study," Lu said. "Just a few models exist, and even in mice, only a limited amount of embryos can be harvested. Now we can culture these cells and have unlimited material to study."

Researchers are only beginning to understand the natural chemical environments that allow for production of different tissues.2023/05/19 4

"What is nice is that what she has observed in cultures appears to be quite similar to what goes on in early development in animals," said R. Michael Roberts, D.Phil., a professor of molecular biology at the C.S. Bond Life Sciences Center at the University of Missouri-Columbia who did not participate in the research. "Normally, mouse embryonic stem cells aren't easily converted along the pathway to form placental cells, while human embryonic stem cells undergo this transition quite easily. This has always been a puzzle. What she has shown is you can make mouse embryonic stem cells convert unidirectionally to trophoblasts by activating a single gene. This is very helpful for understanding how the placenta develops."

Pesticides blamed for plummeting salmon stocks* 12:52 09 June 2008

* NewScientist.com news service* Ewen Callaway

A weak mix of pesticides in river water dampens a salmon's sense of smell, say researchers. In experiments, Steelhead rainbow trout exposed to low levels of 10 common agricultural pesticides could not perceive changes in levels of a predator's scent.

"You can imagine if a fish is unable to detect just how close it is to a [wading] bear, it's a problem," says Keith Tierney, a toxicologist who led the study while at Simon Fraser University in Burnaby, British Columbia.

A depressed sense of smell might also keep fish from finding mates and food. Trout are closely related to salmon, and, though the theory is unproven, pesticides may be a cause of plummeting salmon stocks in Canada and the US, Tierney says.

Fisheries researchers have long suspected that pesticides can deaden fishes' olfactory sense. But most of the evidence was based on fish exposed to artificially high levels of a single chemical and for a short period.

In the wild, however, salmon swim through waters polluted with low levels of pesticides and other chemicals that can change from day to day, depending on the amount and nature of the runoff entering the river system.Chemical cocktail

After the US Clean Water Act and similar legislation in Canada forced drastic cuts in easily tracked water pollutants, such "nonpoint sources" of pollution -- those affecting a water body from diffuse sources -- have become more common.

To get a better handle on how dilute pesticides stymie a fish's sense of smell, Tierney, now at University of Windsor, Ontario, and his colleague Christopher Kennedy measured the water quality in British Columbia's Nicomekl River -- a 34-kilometre flow that empties into the Pacific Ocean just south of Vancouver.

Tierney's team found no fewer than 40 chemicals in the river, most at trace concentrations.Simplifying matters, the researchers created a weak mix of the 10 most abundant pesticides, which included

atrazine and diazinon, then exposed trout to the brew for four days. Next, they tested how the chemicals affected odour-sensing cells exposed to a scent molecule produced by predators.Permanent damage

Pesticide-treated trout could still sense the odour -- an amino acid called L-serine -- but they couldn't detect changes in the scent's concentration, the researchers found. Sensing changes in the levels of a scent is important because animals, including humans, tend to "tune out" smells that don't change, Tierney says.

"If you go into a pizza joint, you get used to the smell," he says. "You go back outside and it smells completely different."

The damage also seems permanent -- a protein that detoxifies harmful chemicals appears overwhelmed by the pesticides. "This [contaminated] water is causing problems in very, very sensitive tissue," he says.

In unpublished experiments, Tierney's team has found that trout exposed to low levels of pesticides have trouble finding food and mates. All told, the deadened sense of smell may mean that fewer salmon survive to spawn each year.Cleaner water

Pesticides are probably just a part of the problem facing salmon, says Nathaniel Scholz, an ecotoxicologist at the National Oceanographic and Atmospheric Administration in Seattle, Washington. Overfishing and climate change have also been blamed for declines.

Untangling the role of water pollutants will help conservationists and policy makers "get the most bang for their buck," Scholz says.

And even if field research proves that low levels of pesticides contribute to declining stocks, stemming the trickle of chemicals into rivers won’t be easy. The toxic compounds come from a myriad of sources, including farms, cities and suburbs, and their levels often fluctuate from day to day, depending on storm runoff.

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Yet safer pesticides and better runoff controls offer some hope, Tierney says. "The water will have to be a little cleaner if we want to have salmon in the water."Journal reference: Environmental Science & Technology (DOI: 10.1012/es800240cu)

New research refutes myth of pure Scandinavian raceA team of forensic scientists at the University of Copenhagen has studied human

remains found in two ancient Danish burial grounds dating back to the iron age, and discovered a man who appears to be of Arabian origin. The findings suggest that human beings were as genetically diverse 2000 years ago as they are today and

indicate greater mobility among iron age populations than was previously thought. The findings also suggest that people in the Danish iron age did not live and die in

small, isolated villages but, on the contrary, were in constant contact with the wider world.

On the southern part of the island of Zealand in Denmark, lie two burial grounds known as Bøgebjerggård and Skovgaarde, which date back to the Danish iron age (c. 0-400 BC). Linea Melchior and forensic scientists from the University of Copenhagen analysed the mitocondrial DNA of 18 individuals buried on the sites and found that there was as much genetic variation in their remains as one would expect to find in individuals of the present day. The research team also found DNA from a man, whose genetic characteristics indicate a man of Arabian origin.The ancestors of the Danes were in contact with the wider world

Archeologists and anthropologists know today that the concept of a single Scandinavian genetic type, a Scandinavian race that wandered to Denmark, settled there, and otherwise lived in complete isolation from the rest of the world, is a fallacy.

"If you look at the geographic position of Denmark, "then it becomes clear that the Danes must have been in contact with other peoples," says scientist, Linea Melchior. "We know from other archeological excavations that there was a good deal of trade and exchange of goods between Denmark and other parts of Scandinavia and Europe. These lines of communication must have extended further south as one of the Danish burial grounds, which dates back to the iron age also contained the remains of a man, who appears to have been of Arabian origin.People from distant lands were absorbed in Danish iron age communities

At the beginning of the Danish iron age, the roman legions were based as far north as the river Elbe (on the border of northern Germany) and it is thought that the man of Arabian descent found in the burial grounds in Southern Zealand would have either been a slave or a soldier in the roman army. It is probable that he possessed skills or special knowledge, which the people in Bøgebjerggård or Skovgaard settlements could make use of, or he could have been the descendant of a female of arabian origin, who for reasons unknown, had crossed the river Elbe and settled down with the inhabitants of Zealand.

"This discovery is comparable to the findings of a colleague of mine, who found a person of Siberian origin on the Kongemarke site," continues scientist, Linea Melchior. He was buried on consecrated ground, just as the circumstances of the Arab man's burial was identical to that of the locals. The discovery of the Arab man indicates that people from distant parts of the world could be and were absorbed in Danish communities.The iron age peoples moved away from their place of birth

"All of our ancestors, no matter when they arrived have contributed to our history and the development of our lifestyle," explains Linea Melchior. "Indeed, Danish identity is more a definition of where one is physically located and lives today than a question of our past history - since we're all originally African in origin. That we ended up in Europe was accidental, which is in itself remarkable".

"Another interesting feature of the approximately 50 graves assessed so far on the two sites and also from other burial sites and time periods in Danish history is that none of the individuals seem to be maternally related to one another", explains Linea Melchior. "We couldn't see any large families buried in the same location. This suggests that in the Danish iron age, people didn't live and die in the villages of their birth, as we had previously imagined".The findings have been published in the American Journal of Physical Anthropology 135:206-215 (2008) and PLoSOne 3(5): e2214.

Ancient cave found under churchBuilt in 230 A.D., church is one of Christianity's oldest in the world

By Dale Gavlak The Associated PressAMMAN, Jordan - Archaeologists in Jordan said Monday they have discovered a cave underneath one of the world's oldest churches that may have once been an even more ancient site of Christian worship.

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Archaeologist Abdel-Qader Hussein, head of the Rihab Center for Archaeological Studies, says the cave was unearthed in the northern Jordanian city of Rihab after three months of excavation and shows evidence of early Christian rituals.

The cave lies under St. Georgeous church, built in 230 A.D., making it one of the oldest churches in the world, along with one unearthed in the Jordanian southern port of Aqaba in 1998 and another in Israel discovered in 2005.

Hussein said there was evidence that the underground cave was used as a church by 70 disciples of Jesus in the first century after Christ's death, which would make it the oldest Christian site of worship in the world.

He described a circular worship area with stone seats separated from a living area that had a long tunnel leading to a source of water. He said the early Christians hid there from persecution.

A mosaic inscription on the floor of the later church of St. Georgeous above refers to "the 70 beloved by God and the divine" who founded the worship there.

Thomas Parker, a historian at the University of North Carolina-Raleigh, who led the discovery of the church in Aqaba, said that while he hadn't seen the Rihab site, any such claim should be taken with a degree of caution.

"An extraordinary claim like this requires extraordinary evidence," he said. "We need to see the artifacts and dating evidence to suggest such an occupation in the 1st century A.D."

Parker asked how archeologists could be certain whether the "cave was actually a center of Christian worship."

The archeologist also noted that mosaics are difficult to date unless there is a precise date in the text of the mosaic inscriptions themselves and typical mosaic inscriptions with Christian themes are from the 5th to 6th century.

"It's quite possible that there was a cave with earlier occupation which was later converted to Christian use. But to make the jump that this was actually used by Christians fleeing Jerusalem in the 1st century A.D. seems like a stretch to me," Parker said.

Archimandrite Nektarious, Bishop Deputy of the Greek Orthodox Archdiocese in Amman hailed the discovery, calling it an "important milestone for Christians all around the world and right here at home."

"It confirms that Christians in this region are not strangers," he said. "They are real citizens who have always had roots in this region from those days until the present."(c) 2008 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed. URL: http://www.msnbc.msn.com/id/25061134/

Engineer develops detergent to promote peripheral nerve healing; 100 patients treated successfully in first year of use

By Daniel J. Vargas June 10, 2008AUSTIN, Texas– A detergent solution developed at The University of Texas at Austin that treats donor nerve grafts to circumvent an immune rejection response has been used to create acellular nerve grafts now used successfully in hospitals around the country. Research also shows early promise of the detergent solution having possible applications in spinal cord repair.

The solution – combined with an enzyme treatment conceived at the University of Florida in Gainesville – is licensed by AxoGen, an Alachua, Florida-based company, and is used to create an acellular nerve graft from human cadaver tissue, called AVANCE Nerve Graft. Nationwide, nearly 100 patients suffering nerve injuries have received AVANCE grafts, all involving peripheral nerves which transmit sensory information between the brain and muscles.

Christine Schmidt, a biomedical engineering professor, developed the detergent solution in her lab with Terry Hudson and Curt Deister, chemical engineering graduate students at the time, who are now with Genentech in California and with AxoGen, respectively.

“Surgeons are reporting some early successes,” she says.These grafts are being used to treat people with traumatic injuries potentially resulting from lacerations,

gunshots and everyday accidents, but it also has been used to treat cavernous nerves after the removal of the prostate. The AVANCE product has treated wounded soldiers and can treat the nerves in hands, arms, legs and the face.

Traditional treatment of these types of nerve trauma required harvesting an intact nerve from the patient’s body and transplanting it to repair the damaged area. However, that requires two surgeries, is more costly and leads to loss of nerve function and possible infection at the donor nerve site, Schmidt says.

Synthetic, tubular grafts are another surgery repair option. However, Schmidt says they are limited to repairing very small injuries. She adds AVANCE nerve grafts are able to bridge long nerve gaps, provide a

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three-dimensional pathway supporting nerve regeneration and are easily bendable because they are human nerve harvested from tissue donors, making it easier for surgeons to handle. “This method has broader applicability,” Schmidt says. “Formerly a patient’s only option was to use their own nerve or the completely synthetic grafts.”

By using the detergent solution, the donor nerve is stripped of the cellular lipid components, which causes the immune rejection response when implanted. Schmidt’s laboratory spent four years developing the solution to be strong enough to remove rejection-inducing factors, but mild enough to preserve the delicate physical architecture of the nerve essential for regeneration. The resulting tolerated transplanted nerve provides a type of scaffolding that serves as a bridge between the two ends of the severed nerve to promote regrowth. And because the immunogenic lipid components have been extracted, patients don’t require immunosuppressant drugs.

AxoGen learned about the detergent processing work in Schmidt’s lab, licensed it and combined it with the University of Florida enzyme treatment that removes other regrowth inhibiting factors, creating the AVANCE product.“So they’ve taken something from our lab that works really well and made it work even better,” Schmidt says.

Schmidt now is conducting spinal-cord lab testing in animals using detergent-treated peripheral nerve grafts. She is working with post-doctoral fellow Zin Khaing, a central nervous system expert.AxoGen’s AVANCE Nerve Graft was first used on a patient in July 2007, when a 38-year-old man underwent surgery to repair a facial nerve at the Mayo Clinic in Rochester, Minn. In a recent case, it was used to repair several damaged nerves in three fingers of a Dallas resident at University Hospital – Zale Lipshy. For photos of Schmidt, go to: http://www.engr.utexas.edu/news/action_shots/pages/schmidt_07.cfmFor information on AxoGen, visit: www.axogeninc.com.For more information, contact: Daniel J. Vargas, Cockrell School of Engineering, 512-471-7541, Daniel.vargas2@engr.utexas.edu; Christine Schmidt, Cockrell School of Engineering, 512-471-1690, Schmidt@che.utexas.edu; Anna Tietz, AxoGen, 386-462-6844, atietz@axogeninc.com

The cause of all hereditary sensory and autonomic neuropathy type II cases has been established

Mutations in a neuronal specific isoform of WNK1 cause this very serious diseaseA major discovery that details the existence of a neuronal specific form of the WNK1 gene, henceforth

referred to as the WNK1/HSN2 isoform, was recently completed by the research group of Dr. Guy A. Rouleau and published in the scientific journal The Journal of Clinical Investigation. The group led by Dr. Rouleau is part of the University of Montreal Hospital Centre (CHUM), the CHUM Research Centre (CRCHUM) and the Sainte-Justine University Hospital Centre. Dr. Rouleau is also a professor at the University of Montreal. Their recent results will hereafter help to explain all the cases of hereditary neuropathy type II.

Hereditary sensory and autonomic neuropathy type II (HSANII) is a severe and early onset disorder that starts early during childhood. It is characterized by loss of perception to pain, touch and heat attributable to a loss of peripheral sensory nerves in the lower and upper limbs. Unfortunately no therapy is currently available for individuals suffering from hereditary neuropathy type II. In 2004, Dr. Rouleau's team identified the DNA sequence of HSN2 as encoding a novel gene but their more recent investigations have now shown that this sequence is more precisely linked to the expression of a WNK1 isoform that is exclusively detected in the nervous system. Till their discovery, the presence of mutations in WNK1 were only observed in individual suffering from a rare form of hypertension known as Gordon syndrome and no WNK1 isoform were exclusively expressed in the nervous system. The observation of mutations specific to the WNK1/HSN2 isoform in individuals with hereditary sensory and autonomic type II will henceforth allow the generation of animal models of the disease and help to better understand the implication of this gene and its mutations in the sensorial loss mentioned above.

Despite the severity of the symptoms observed in hereditary sensory and autonomic neuropathy type II, this important discovery points to the role of proteins like WNK1/HSN2 that are involved in the perception of pain and henceforth open new avenues for the development of pain treatments. A better understanding of the disease also provide a valuable genetic test to asses the risk or the cause of the disease in individuals at risk or presenting symptoms of it.This study of WNK1/HSN2 was realized in the laboratory of Dr. Rouleau by two postdoctoral fellows, Dr. Nathalie Girard and Dr Masoud Shekarabi. Dr. Laurence Faivre from the Hôpital d'enfants, CHU Dijon, also participated to this study.This work was funded by the Canadian Institutes of Health Research.The article is available online at: www.jci.org/articles/view/34088/pdf.

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Arecibo joins global network to create 6,000-mile telescopeBy Lauren Gold

On May 22, Arecibo Observatory in Puerto Rico joined other telescopes in North America, South America, Europe and Africa in simultaneously observing the same targets, simulating a telescope more than 6,800 miles (almost 11,000 kilometers) in diameter.

The telescopes are all members of the Express Production Real-time e-VLBI Service (EXPReS) project, and May 22 marked a live demonstration of their first four-continent, real-time, electronic Very Long Baseline Interferometry (e-VLBI) observations.

VLBI uses multiple radio telescopes to simultaneously observe the same region of sky -- essentially creating a giant instrument as big as the separation of the dishes. VLBI can generate images of cosmic radio sources with up to 100 times better resolution than images from the best optical telescopes.

The results were immediately transmitted to Belgium, where they were shown as part of the 2008 Trans-European Research and Education Networking Association Conference.

The Arecibo team called the demonstration a major milestone in the telescope's e-VLBI participation, with a data-streaming rate to the central signal processor at the Joint Institute for VLBI in Europe (JIVE) in the Netherlands four times higher than Arecibo had previously achieved.

"These results are very significant for the advance of radio astronomy," said JIVE director Huib Jan van Langevelde. "It shows not only that telescopes of the future can be developed in worldwide collaboration, but that they can also be operated as truly global instruments."

EXPReS, funded by the European Commission, aims to connect up to 16 of the world's most sensitive radio telescopes to the JIVE processor to correlate VLBI data in real time. This replaces the traditional VLBI method of shipping data on disk and provides astronomers with observational data in a matter of hours rather than weeks, allowing them to respond rapidly to transient events with follow-up observations.

Cornell's National Astronomy and Ionosphere Center manages Arecibo Observatory for the National Science Foundation.Scenes of nature trump technology in reducing low-level stress

Technology can send a man to the moon, help unlock the secrets of DNA and let people around the world easily communicate through the Internet. But can it substitute for nature?

Apparently not, according to a new study that measured individuals' heart recovery rate from minor stress when exposed to a natural scene through a window, the same scene shown on a high-definition plasma screen, or a blank wall. The heart rate of people who looked at the scene through the window dropped more quickly than the others. In fact, the high-definition plasma screen had no more effect than the blank wall.

In addition, the research done through the Human Interaction with Nature and Technological Systems Lab at the University of Washington showed that when people spent more time looking at the natural scene their heart rates tended to decrease more. That was not the case with the plasma screen.

The study, funded by the National Science Foundation, is published in the current issue of the Journal of Environmental Psychology.

"Technology is good and it can help our lives, but let's not be fooled into thinking we can live without nature," said Peter Kahn, a UW associate professor of psychology who led the research team.

"We are losing direct experiences with nature. Instead, more and more we're experiencing nature represented technologically through television and other media. Children grow up watching Discovery Channel and Animal Planet. That's probably better than nothing. But as a species we need interaction with actual nature for our physical and psychological well-being."

Part of this loss comes from what the researchers call environmental generational amnesia. This is the idea that across generations the amount of environmental degradation increases, but each generation views conditions it grew up with as largely non-degraded and normal. Children growing up today in the cities with the worst air pollution often, for example, don't believe that their communities are particularly polluted.

"This problem of environmental generational amnesia is particularly important for children coming of age with current technologies," said Rachel Severson, a co-author of the study and a UW psychology doctoral student. "Children may not realize they are not getting the benefits of actual nature when interacting with what we're calling technological nature."

To see how people reacted to nature and a technological representation of it, the researchers recruited 90 college students to participate in an experiment that had them work on four mental tasks while sitting at a desk in an office. With 30 of the students, the desk faced a window overlooking a campus scene that included a large fountain and trees. For a second group of 30 students, the window was replaced with the plasma screen that showed the same nature scene in real time. For the remaining 30 students, curtains covered the plasma screen and the desk faced a blank wall.2023/05/19 9

Participants were tested individually. Each was welcomed by a researcher, hooked up to a heart rate monitor and told to wait for five minutes while the researcher stepped out of sight. A camera mounted on the wall near the window or plasma screen was synchronized with the heart monitor and tracked participants' eye movements. At the end of the waiting period, the researcher returned, explained the first task and stepped out of sight. This was repeated for the remaining three tasks and then the subject was told to wait again for five minutes.

Heart recovery rate was based on how quickly each participant's heart rate dropped in the 60 seconds after being told to wait or to have one of the tasks explained. Each person's performance was tallied on the basis of six measurements, once after every task and the two waiting periods. Low-level stress was created by having to deal with another person in a social situation and the anticipation or performance anxiety each might have experienced to do well on the four tasks.

The researchers found that participants with the plasma screen actually looked at it just as often as did those who had the window. However, the window held the students' attention significantly longer than the plasma screen did. When participants spent more time looking at the window, their heart rates decreased faster than on tasks when they spent less time looking at the window. This was not true with the plasma screen.

"I was surprised by this," said Kahn. "I thought the plasma screen would come somewhere between the glass window and the blank wall. This study is important because it shows the importance of nature in human lives and at least one limitation of technological nature.

"In the years ahead, technological nature will get more sophisticated and compelling. But if it continues to replace our interaction with actual nature, it will come at a cost. To thrive as a species, we still need to interact with nature by encountering an animal in the wild, walking along the ocean's edge or sleeping under the enormity of the night sky."Co-authors of the study are Batya Friedman, Jennifer Hagman, Erika Feldman and Anna Stolyar of the UW, Brian Gill of Seattle Pacific University, Nathan Freier of Rensselaer Polytechnic Institute and Sybil Carrẻre of California State University, San Bernardino. Freier and Carrẻre were both at the UW when they worked on the study.

Cutting-edge weapons result of prehistoric experimentationMU researchers find stone projectile variations point to early technological

experimentationCOLUMBIA, Mo. – In today's fast-paced, technologically advanced world, people often take the innovation of new technology for granted without giving much thought to the trial-and-error experimentation that makes technology useful in everyday life. When the "cutting-edge" technology of the bow and arrow was introduced to the world, it changed the way humans hunted and fought. University of Missouri archaeologists have discovered that early man, on the way to perfecting the performance of this new weapon, engaged in experimental research, producing a great variety of projectile points in the quest for the best, most effective system.

"Technological innovation and change has become a topic that interests people," said R. Lee Lyman, professor and chair of the University of Missouri Department of Anthropology. "When the bow and arrow appeared in North America, roughly 1,500 years ago, it eventually replaced the atlatl (spear thrower) and dart. The introduction of the bow and arrow, a different weapon delivery system, demanded some innovative thinking and technology. In other words, one could not just shoot a dart from a bow. Components like the shaft and arrow point needed to be reinvented.".

Arrow points (top) were reworked and refined through experimentation, often using dart points (bottom) as a starting place. The difference between the two types of points (size and neck/stem width) can be observed in this photo.

University of MissouriBecause the necessary flight dynamics and mechanics of the arrow wouldn't have been fully understood, the

indigenous people at the time would have experimented—trying all sorts of points with different types of shafts, attempting to discover the best combinations. This reinvention process can be seen archaeologically through an increase in the number and variation of projectile points—indicating the transition period between the atlatl and the bow and arrow.

"Everyone is looking for the better mouse trap," Lyman said. "Once a change is made in one variable, it may prompt changes in another variable because the two are mechanically linked. For example, if something gets

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longer, generally, it will get heavier. This is called a cascade effect. This, in combination with experimentation, resulted in the tremendous variation in projectile points."

Lyman said there is evidence of an initial burst of variation in projectile points at the time bow-and-arrow technology was introduced and that prehistoric artisans experimentally sought arrow points that worked effectively. Following that initial burst, less-effective projectile models were discarded, causing archaeologists to see a reduction in variation.In the course of this research, Lyman and his collaborators, T.L VanPool and M.J O'Brien, analyzed the data from more than 1,000 projectile points from three separate geographical locations. Lyman's study, "Variation in North American dart points and arrow points when one, or both are present," will be published in an issue of the Journal of Archaeological Science in fall 2008.Note: Photos of the dart and arrow points representative of the ones used in the study are available at http://munews.missouri.edu/ or by contacting Bryan E. Jones, Sr. Information Specialist, JonesBry@missouri.edu or 573-882-9144.

'Party chat' brain filter discovered* 01:00 10 June 2008

* NewScientist.com news service* Colin Barras

The brain region responsible for one of humankind's neatest mental tricks may have been identified.We think nothing of singling out one person's voice at a party buzzing with people chatting. But researchers

have struggled to understand just how the human brain manages to filter out a single thread of conversation from a tangle of similar background noises.

The phenomenon was labelled the "cocktail party effect" in the 1950s by Colin Cherry, a British cognitive scientist.

Now, if we don't know exactly how, at least we may know where. Researchers conducting brain scans of people listening to multiple sounds, say that the secondary auditory cortex – located in the temporal lobe at the side of the head – does much of the work.Hidden tone

Alexander Gutschalk at the Ruprecht-Karl University of Heidelberg in Germany and his team decided to study brain activity during this "informational masking".

They hooked volunteers up to a Magnetoencephalography (MEG) imager and played them a sound file containing a large number of randomly repeating tones across a range of frequencies (listen to the track, mp3 format).

Hidden inside the track was one regularly repeating tone (listen to the hidden tone, mp3 format), masked by random beeping (listen to the masking sound, mp3 format). Subjects were asked to ignore the random tones and press a button when they heard the regular tone.

Gutschalk's team found that when subjects became aware of the regular tone, there was a surge of activity in the secondary audio cortex. "In fact, we see the activity even before the subject presses the key, which is interesting," says Gutschalk.Missing pitch

However, because the repeating sound was buried deeply in the sound file, some subjects failed to find it in the mix. When this happened there was no extra activity in these subjects' secondary auditory cortex.

The results suggest that sound travels a long way – through the outer and inner ear, the thalamus and the primary auditory cortex – before the brain begins understand what it is hearing.

Guy Brown at the University of Sheffield, UK, points out that Gutshalk's experiments did not include all the factors involved in the cocktail party effect. For example variations in pitch and timbre would also be involved in a real life situation.

Gutschalk agrees: "This isn't exactly the cocktail party phenomenon, but the mechanism we have identified probably plays an important role in the cocktail party effect," he says.Journal reference: PLoS Biology (DOI: 10.1371/journal.pbio.0060138)

Robot Asimo can understand three voices at once* 15:55 10 June 2008

* NewScientist.com news service* Colin Barras

Advanced humanoid robot Asimo just got a new superpower – it can understand three humans shouting at once.

For now the modified Asimo's new ability are being used to judge rock-paper-scissors contests, where three people call out their choices at once. But the number of voices and the complexity of the sentences the software can deal with should grow in future.2023/05/19 11

Hiroshi Okuno at Kyoto University, and Kazuhiro Nakadai at the Honda Research Institute in Saitama, both in Japan, have designed the new software, which they call HARK.Quality control

HARK uses an array of eight microphones to work out where each voice is coming from and isolate it from other sound sources. The software then works out how reliably it has extracted an individual voice, before passing it onto speech-recognition software to decode.

That quality control step is important. The other voices are likely to confuse speech recognition software. So any parts of the sound file that contain a lot of background noise across a range of frequencies are automatically ignored when the patched-up recording of each voice is passed on to a speech-recognition system.

The HARK system actually goes beyond normal human listening capabilities, Okuno told New Scientist. "It can listen to several things at once, and not just focus on a particular single sound source."

While focusing on a single voice among many is known as the "cocktail party effect", Okuno calls the ability to focus on multiple voices at once the "Prince Shotoku Effect".

"According to Japanese legend, Prince Shotoku listened to 10 people's petitions at the same time," he says.Eight 'ears'

Although the HARK software can't comprehend 10 voices at once yet, Okuno and Nakadai say it can follow three players calling simultaneously at 70 to 80% accuracy when installed into Honda's Asimo robot.

The array of eight microphones is placed around the Asimo's face and body, which helps it to accurately detect and isolate simultaneous voices. "The number of sound sources and their directions are not given to the system in advance," says Nakadai.

Guy Brown at the University of Sheffield, UK, is impressed with the work, although he points out that it is largely built from existing elements used to process sound, such as getting an array of microphones to localise a sound, and using automated software to block out difficult-to-interpret parts of a voice recording.Small vocabulary

"The main achievement has been to embed this technology in a robot and to get it all working in a real-time, interactive manner," Brown says.

Rock-paper-scissors uses a small vocabulary, making the task easier. "Clearly there's a long way to go before we can match the performance of human listeners in 'cocktail party' situations," he says. In fact, when Okuno and Nakadai tried using their software to follow several complicated sentences at once, as three people shouted out restaurant orders, it could only identify 30 to 40% of what was said.

Alexander Gutschalk at the Ruprecht-Karl University of Heidelberg in Germany has just conducted one of the first studies of brain activity when dealing with the cocktail party effect, and says future collaboration between neuroscientists and roboticists could make robots better party conversationalists.

Okuno and Nakadai presented their work at the 2008 IEEE International Conference on Robotics and Automation in Pasadena, California, last month.

Personal HealthDisorder Magnifies Blood Clot Risk

By JANE E. BRODYWhen David Bloom, 39, went to Iraq in 2003 to cover the war for NBC

News, his wife, Melanie, naturally feared for his safety. Would a bullet or a bomb claim him? A land mine? An ambush?

Instead it was a blood clot lodged in his lungs that ended his life. Ms. Bloom subsequently learned that her husband carried a genetic abnormality, factor V Leiden, that greatly increased his risk for developing blood clots.

Mr. Bloom had three other risk factors for clots: a long plane ride to Iraq, erratic eating habits that could have caused dehydration, and cramped sleeping space in Army vehicles. But had he not had this genetic quirk — or had he known about it and the higher risks it carried — he might have escaped his fate.A Hidden Problem

Factor V Leiden (pronounced factor five) is the most common hereditary clotting disorder in the United States, present in 2 percent to 7 percent of Caucasians, less often in Hispanics and rarely in Asians and African-Americans.

Andy MartinThe disorder accounts for 20 percent and to 40 percent of cases of deep vein thrombosis, or D.V.T., the clot

that Mr. Bloom developed in his leg before it broke loose and traveled to his lungs, resulting in a pulmonary embolism that caused his death.2023/05/19 12

Factor V Leiden is more often than not a hidden disorder, until someone in a family — often someone like Mr. Bloom, who was athletic and healthy — develops a deep vein thrombosis or another unexpected clot. Because screening for this problem is not routine, factor V Leiden is usually not detected until several members of a family develop clots or one person develops a succession of clots.

Even then, a possible carrier of the gene defect may not be tested.Dr. Rinah Shopnick, medical director of the Hemophilia and Thrombosis Center of Nevada, described the

case of Ann, 20, who reported to the center about her doctors’ reactions to her family history. Ann told doctors that her otherwise healthy cousin had suffered a major heart attack in his 40s and was found to have factor V Leiden. Her grandmother died while pregnant, and her aunt, uncle and grandfather died of heart problems.

Ann reported that she had had blood pressure problems since age 8, and developed a serious blood pressure disorder during pregnancy and that her brother had just tested positive for the defect.

Yet she was advised by two doctors not to be tested, she said. The reasoning was that the disorder was rare, that she would have to pay for the test (it is not expensive) and that if she was found to carry the gene it could affect her ability to buy affordable life and health insurance. (Federal legislation has just been passed to protect against such discrimination.)Inherited Risk

In someone with factor V Leiden, clots can arise in veins anywhere. The abnormality can increase the risk of heart attack, stroke, miscarriage, gallbladder dysfunction and toxemia of pregnancy. Clots are also more likely to develop after surgery and childbirth and in women taking oral contraceptives or estrogen therapy.

The disorder results from a mutation in the factor V gene that participates in forming clots in response to an injury, for example. Without two fully functional factor V genes, the body’s ability to put a brake on clot formation is inhibited.

Normally, a molecule called activated protein C, or APC, prevents clots from becoming too large by inactivating coagulation factor V. But factor V Leiden impairs this protein’s ability to suppress the coagulation factor because it is longer lasting and stickier.

A parent who carries the mutated gene has a 50 percent chance of passing it on to each child. Someone who inherits one mutated gene faces a five- to seven-fold increased risk of developing a serious and potentially life-threatening clot. Someone with two of the damaged genes has a 25- to 50-fold increased risk. Approximately one person in 5,000 among whites in the United States and Europe has two of the mutated genes.

Because the risk of suffering a clot is about one in 1,000 people a year in the general population, the increased risk associated with factor V Leiden is not to be taken lightly: 5 to 7 in 1,000 people each year for those with one mutant gene and 25 to 50 per 1,000 in those with two mutant genes. The risk is greatest in individuals who have more than one clotting defect, as well as in people who smoke or are overweight.

A Danish study of 9,253 adults found that in people who did not smoke, were not overweight and were younger than 40, the 10-year risk of clots and emboli was 1 percent in those with one mutated gene and 3 percent in those with two damaged genes. But the risk increased to 10 percent in people with one mutated gene and 51 percent in those with two abnormal genes if they smoked, were overweight and were older than 60.Screening

Two blood tests can detect factor V Leiden. One, the APC resistance assay, is 95 percent accurate and could be used for screening. It measures the anticoagulant response to activated protein C. A definitive but more costly diagnosis, also performed on blood, can be made by genetic analysis of the factor V gene.

One or both tests is recommended for people with D.V.T., pulmonary embolism, premature stroke, repeated miscarriage, a family history of clots or a known factor V mutation in a blood relative. Thus, Mr. Bloom’s three daughters should be tested, because each has a 50 percent chance of carrying the defective gene.

For people with a personal or family history of clots, testing can help avert clotting complications when they undergo major surgery, are treated for cancer, anticipate pregnancy or plan to take oral contraceptives, estrogen therapy or a drug like tamoxifen.

In women with factor V Leiden, for example, treatment with an anticoagulant during pregnancy can reduce the risk of pregnancy loss. Women needing contraception might be wise to avoid birth control pills and instead choose a method that would not increase their risk of clots. And a person who is hospitalized or needs surgery can be treated with blood thinners and mechanical compression boots.

Though factor V Leiden alone does not seem to raise the risk of arterial clots, something as simple as daily therapy with low-dose aspirin may help prevent a heart attack or stroke in people with factor V Leiden if they have additional risk factors.

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Preventive action is also important during long periods of immobilization, including long car and plane rides. Drinking plenty of water to prevent dehydration, avoiding alcohol, taking frequent walks and wearing elastic stockings can lower the risk of clots on such excursions.

Vital SignsOutcomes: Tooth Loss Tied to Pregnancy

By NICHOLAS BAKALARA new study suggests that the more babies a woman has, the more likely she is to lose teeth.In a nationwide sample of 2,635 women ages 18 to 64 who had had at least one pregnancy, the number of

teeth lost increased with the number of pregnancies. The association persisted even after controlling for age, smoking, socioeconomic status and the number of dental visits a woman reported. The study appears online in The American Journal of Public Health.

Why this happens is not clear, but Stefanie L. Russell, the lead author of the study and an assistant professor of epidemiology at New York University, said that one possible reason was that pregnant women simply do not go to the dentist often enough.

“I’m not sure why that’s the case,” she said. “Previously it was thought that women should only be treated during the second trimester,” in part because of fears of the effects of dental X-rays on the fetus.

“But you have to look at the individual case and see what kind of treatment a woman needs,” Dr. Russell said. “Preventive care during pregnancy is really important.”

The authors cite studies showing rates of gingivitis and other dental problems in pregnant women ranging from 30 percent to 100 percent. Although disease usually subsides after giving birth, existing periodontal problems may worsen during pregnancy.

CasesShowing the Patient the Door, Permanently

By RAHUL K. PARIKH, M.D.It wasn’t the boy I had a problem with. It was his mother.We had met a few months earlier, when I gave her 14-year-old son a diagnosis of mild asthma. I didn’t mind

her tough questions, but her tone of voice put me on edge. She seemed suspicious, almost angry. Still, in the end I decided she was just a smart, assertive parent, and I let it go.

This time, she was more confrontational. She complained she had been “forced” to bring in her son for a physical because his school needed a doctor’s clearance before he could play sports. What kind of racket did we doctors have with schools? Why did she have to bring in her son when she knew he was healthy? I was taking her money for doing this?

I bit my tongue and tried to tell her why I thought they belonged here. Yes, he was probably very healthy. But an annual checkup could help him learn to take charge of his own health as he grew up, and it would give me a chance to encourage healthy choices and to get a good sense his emotional health during these challenging years. Finally, I pointed out, he was due for a tetanus booster.

She was unimpressed. “I don’t believe in preventive care,” she said. “I’ll treat him for tetanus if he needs it.”The rest of the visit went more smoothly, mainly because Mom left the room so I could examine her son.

But before they left, she again accused me of taking her money, saying I hadn’t done anything different from their previous visits. Before I could reply, her son politely confirmed that this visit had been more comprehensive.

I have had my share of difficult patients and parents. But putting up with this lady had taken more time than it was worth, and it interfered with my taking care of her son. I wasn’t sure I wanted to do it again.

I considered my options. I could be stoic, do my job and keep the boy in my practice. I could call his mother and ask her to keep her opinions to herself so I could focus on her son, though my instincts told me that this wouldn’t stop her. Finally, I could decline to see her son, and therefore her, ever again. In other words, fire my patient.

The physician-patient compact basically states that a doctor will care for a patient in exchange for compensation and that the patient will heed the doctor’s advice. Patients who disagree with their physicians, or just dislike them, are free to go elsewhere.

By the same token, this mutual contract gives a doctor the right to dismiss a patient. The most obvious reasons are failing to pay or missing multiple appointments. Refusing to adhere to treatments can lead to dismissal. So can being abusive to the medical staff.

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Of course, we need to exercise this option sensibly. Doctors cannot fire a patient in dire straits like severe pain, bleeding or a life-threatening situation. And of course, we cannot refuse to see patients because of their race, age, sexual orientation and so on.

But could I fire a patient because I didn’t like his mother? Colleagues who had studied the ethics and legal issues told me that the answer wasn’t clear-cut. Obviously, I couldn’t just abandon them. Yet like a lot of legal jargon, the word “abandonment” is open to interpretation. I decided it meant that as long as I wasn’t leaving anyone out to dry with a serious, immediate medical problem, that I gave a patient reasonable notice and provided options about where to continue getting care, I was within my rights.

I thought about our conversation on the tetanus booster, when the mother said she didn’t believe in preventive care. I’m a pediatrician — prevention is in my DNA. If I accepted her view, I’d be compromising my conscience and my professional ethics. I couldn’t do that.

I wrote a letter addressed to my patient’s mother and sent by certified mail. I kept it brief: “Sometimes, a patient or family and doctor aren’t compatible. ... Therefore, I will be dismissing you from my practice.” I went on to advise them how they could get a new pediatrician and told them that until they found a new doctor, I would continue to care for her child’s mild asthma.

Two weeks later, I received notice that they had gotten it. The child had signed for it, which made me feel bad because I didn’t have anything against him. Checking his chart, I saw that his mother had chosen a new pediatrician, a colleague of mine. They hadn’t seen him yet.

I considered telling my colleague about my experience. Perhaps warning him so he could remember to take extra care would help get them off to a better start. On the other hand, perhaps I would unfairly bias him against this child and his mother.

I decided to keep quiet. After all, it could have just been me.Rahul K. Parikh is a physician in Walnut Creek, Calif. He writes about medicine for Salon.

BasicsTallying the Toll on an Elder of the Sea

By NATALIE ANGIERMILFORD, Conn. — Horseshoe crabs may look ancient and alien and battery-operated, they may look like Wilma Flintstone’s idea of a Roomba vacuum cleaner, yet to the sixth-grade students from Columbus School in nearby Bridgeport, the most outrageous thing about the bronze-helmeted creatures crawling clumsily along the beach was not their appearance but their size — or rather sizes.

One boy pointed to a linked pair of horseshoe crabs, a relatively compact specimen maybe seven inches across clinging to the tail end of a much larger companion. A kid crab hitching a ride on its mother? No, explained Jennifer H. Mattei, head of the biology department at Sacred Heart University in Fairfield, who led the expedition. They were both full-grown, a male and a female, and the female was the bruiser out front.

Serge BlochAmong horseshoe crabs, Dr. Mattei explained, adult females are a good 25 to 30 percent bigger than their

mates, a fact that the girls greeted with hoots of triumph, boys of indignation. Why are the females bigger? a boy demanded. It’s supposed to be the other way around!

As it turned out, the answer to that question was closely tied to the reason the students from Cheryl Crevier’s class had ventured out on a flawless June morning to the shores of Long Island Sound. With clipboards purposefully in hand and tape measures jauntily around neck, the 22 children were there to help catch, measure and tag as many specimens as they could find of the American horseshoe crab, or Limulus polyphemus, one of the oldest and most tenacious species on Earth. Fossils found this year in Manitoba reveal that the animal’s architecture has hardly changed in 445 million years.

The student project is part of a major effort now under way from Maine to Florida, as researchers and volunteers race to take advantage of the spring spawning season, when the crabs lumber from their wintering seabeds on the continental shelf and head inward to the shoreline to breed, and thus can be readily counted (www.projectlimulus.org). Experts are desperate to know whether their suspicions are correct — that as a result of being harvested en masse for use as fishing bait, horseshoe crab populations are beginning to crash.

The loss of the horseshoe crab would be tragic, researchers said, not only because the creatures are fascinating and cute and predate the dinosaurs by 200 million years, but also because so many contemporary life forms depend on them. Their annual spawns draw hundreds of species of migratory birds, predatory fish, reptiles, amphibians and various other alimentary canals eager to brunch on the freshly deposited Limulus eggs.

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“Horseshoe crab eggs are like filet mignon around here,” Dr. Mattei said. “They’re a very popular item on the menu.”

A bounteous one, too. “A single female horseshoe crab can put down 80,000 eggs a year, four million in her lifetime,” said John T. Tanacredi, a professor of earth and marine sciences at Dowling College in Oakdale, N.Y.

We, too, are multiply tethered to the ancient mariners. From their blood we extract a protein that is exquisitely sensitive to bacterial toxins and is used to test surgical instruments and intravenous drugs to ensure they are safe. The relatively simple visual circuitry of the horseshoe crab has proved an ideal model system for decoding the basis of sight. “Only with the horseshoe crab eye is it possible to predict what each nerve fiber in the retina will send to the brain as it sees,” said Robert B. Barlow, a professor of ophthalmology at the State University of New York Upstate Medical University.

The Columbus School students, after being assured that the crab was harmless and surmounting their squeamishness at holding something that, when turned over, looks very much like a large version of the scorpions and spiders to which the horseshoe crab is more closely related than it is to standard crabs like the Dungeness, took to their task with gusto.

They scooped the crabs out of the water carefully and held them, as instructed, like bowls of soup. They punctured small holes in the hard, chitinous shell with special tools designed by Dr. Mattei and her colleagues Mark Beekey and Barbara Pierce. And before a crab could ooze more than a spot of its distinctive blue blood — the color the result of the crab’s blood using copper as an oxygen ferrier rather than iron, as we do — they inserted the white numbered tag.

While they worked, the students learned about the horseshoe crab, how it uses its ice-pick-like tail, or telson, to steer in the water and to right itself should it be overturned in the sand, how the crab is a generalist willing to feed on plankton, bits of fish and worms, and how it lacks jaws for chewing and so grinds up its food with the help of bristles on its legs and an internal gizzard that contains bits of sand and gravel.

Dr. Mattei explained that in the ever-shifting tidal environment, the solid crabs are coveted real estate. “Over 20 species of organisms can be found living on their shells,” she said, including barnacles, slipper shells, blue mussels, sponges, flatworms and leeches, a baggage sum that, if not helpful to the crabs, doesn’t usually hurt them either.

She described the crab’s life cycle, how the animals shed their shells some 17 times before reaching adult size at around nine years of age. The males emerge from that final shell-shucking with a distinguishing pair of “boxing gloves” on their front claws, which they use for the all-important task of clinging to the back of a female for months at a time. While conjoined, the couple doesn’t have sex. But whenever the female lays a clutch of eggs, the male is well positioned to fertilize them by releasing a spermic plume.

“Females are bigger just for the physics of carrying all those eggs,” Dr. Mattei said. Sperm, by contrast, is gossamer, and male-male combat rare. “It’s whoever gets there first,” Dr. Mattei said, a reproductive strategy that may, in fact, reward the petite.

Alas, sometimes the first comer is a large warm-blooded crab with opposable thumbs. In the last few years, the Asian market for North American eel and conch meat has soared, and it seems that gravid female horseshoe crabs make the best bait. Even the stalwart Limulus can’t last if all its eggs end up in one basket — shaped like a fisherman’s boat.

Loyal to Its RootsBy CAROL KAESUK YOON

From its diminutive lavender flowers to its straggly windblown stalks, there is nothing about the beach weed known as the Great Lakes sea rocket to suggest that it might be any sort of a botanical wonder.

Yet scientists have found evidence that the sea rocket is able to do something that no other plant has ever been shown to do.

The sea rocket, researchers report, can distinguish between plants that are related to it and those that are not. And not only does this plant recognize its kin, but it also gives them preferential treatment.TAKING ADVANTAGE A Cuscuta pentagona moving toward a tomato plant. Brian McClatchy/De Moraes and Mescher

LabsIf the sea rocket detects unrelated plants growing in the ground with it, the plant aggressively sprouts

nutrient-grabbing roots. But if it detects family, it politely restrains itself.

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The finding is a surprise, even a bit of a shock, in part because most animals have not even been shown to have the ability to recognize relatives, despite the huge advantages in doing so.

If an individual can identify kin, it can help them, an evolutionarily sensible act because relatives share some genes. The same discriminating organism could likewise ramp up nasty behavior against unrelated individuals with which it is most sensible to be in claws- or perhaps thorns-bared competition.

“I’m just amazed at what we’ve found,” said Susan A. Dudley, an evolutionary plant ecologist at McMaster University in Hamilton, Ontario, who carried out the study with a graduate student, Amanda L. File.

“Plants,” Dr. Dudley said, “have a secret social life.”Since the research on sea rockets was published in August in Biology Letters, a journal of the United

Kingdom’s national academy of science, Dr. Dudley and colleagues have found evidence that three other plant species can also recognize relatives.

The studies are part of an emerging picture of life among plants, one in which these organisms, long viewed as so much immobile, passive greenery, can be seen to sense all sorts of things about the plants around them and use that information to interact with them.

Plants’ social life may have remained mysterious for so long because, as researchers have seen in studies of species like sagebrush, strawberries and thornapples, the ways plants sense can be quite different from the ways in which animals do.

Some plants, for example, have been shown to sense potentially competing neighboring plants by subtle changes in light. That is because plants absorb and reflect particular wavelengths of sunlight, creating signature shifts that other plants can detect.

Scientists also find plants exhibiting ways to gather information on other plants from chemicals released into the soil and air. A parasitic weed, dodder, has been found to be particularly keen at sensing such chemicals.

Dodder is unable to grow its own roots or make its own sugars using photosynthesis, the process used by nearly all other plants. As a result, scientists knew that after sprouting from seed, the plant would fairly quickly need to begin growing on and into another plant to extract the nutrients needed to survive.

But even the scientists studying the plant were surprised at the speed and precision with which a dodder seedling could sense and hunt its victim. In time-lapse movies, scientists saw dodder sprouts moving in a circular fashion, in what they discovered was a sampling of the airborne chemicals released by nearby plants, a bit like a dog sniffing the air around a dinner buffet.

Then, using just the hint of the smells and without having touched another plant, the dodder grew toward its preferred victim. That is, the dodder reliably sensed and attacked the species of plant, from among the choices nearby, on which it would grow best.

“When you see the movies, you very much have this impression of it being like behavior, animal behavior,” said Dr. Consuelo M. De Moraes, a chemical ecologist at Pennsylvania State University who was on the team studying the plant. “It’s like a little worm moving toward this other plant.”

Although a view of plants as sensing organisms is beginning to emerge, scientists have been finding hints of such capabilities and interactions for 20 years. But discoveries have continued to surprise scientists, because of what some describe as an entrenched disbelief that plants, without benefit of eyes, ears, nose, mouth or brain, can and do all they are seen to do.

“A lot of the examples of plant behavior are examples in which the phenomena are pretty easy to observe,” said Dr. Richard Karban, a plant ecologist at the University of California, Davis.

The problem, for many scientists, is that as obvious as the behaviors sometimes are, they can seem just too complex and animal-like for a plant. “Maybe if we understood more mechanistically how it’s happening,” Dr. Karban added, “we’d feel more comfortable about accepting the results that we’re finding.”

It does not help credibility that scientists in the field often find themselves having to distinguish the results of careful experimental studies from decidedly nonscientific, even kook-fringe, discussions about phenomena like plant sentience and emotion.

Plants are not “sensitive new age guys who cringe when something around them gets hurt and who love classical music and hate rock,” Dr. Dudley said as she referred to depictions in popular works of plants living tender, emotion-soaked existences, in particular the 1970s “The Secret Life of Plants.”

Even mainstream researchers do not always completely agree on which ideas are clearly within the realm of science and which have gone a bit too far.

Recent debates have revolved around a longstanding question: which of the abilities and attributes that scientists have long considered the realm of just animals, like sensing, learning and memory, can sensibly be transferred to plants?

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At the extreme of the equality movement, but still within mainstream science, are the members of the Society of Plant Neurobiology, a new group whose Web site describes it as broadly concerned with plant sensing.

The very name of the society is enough to upset many biologists. Neurobiology is the study of nervous systems — nerves, synapses and brains — that are known just in animals. That fact, for most scientists, makes the notion of plant neurobiology a combination of impossible, misleading and infuriating.

Thirty-six authors from universities that included Yale and Oxford were exasperated enough to publish an article last year, “Plant Neurobiology: No Brain, No Gain?” in the journal Trends in Plant Science. The scientists chide the new society for discussing possibilities like plant neurons and synapses, urging that the researchers abandon such “superficial analogies and questionable extrapolations.”

Defenders point out that 100 years ago, some scientists were equally adamant that plant physiology did not exist. Today, that idea is so obviously antiquated that it could elicit a good chuckle from the many scientists in that field.

As for the “superficial analogies,” the new wave botanists are well aware that plants do not have exact copies of animal nervous systems.

“No one proposes that we literally look for a walnut-shaped little brain in the root or shoot tip,” five authors wrote in defense of the new group. Instead, the researchers say, they are asking that scientists be open to the possibility that plants may have their own system, perhaps analogous to an animal’s nervous system, to transfer information around the body.

“Plants do send electrical signals from one part of the plant to another,” said Dr. Eric D. Brenner, a botanist at the New York Botanical Garden and a member of the Society of Plant Neurobiology.

Although those signals have been known for 100 years, scientists have no idea what plants do with them.“No one’s asked how all that information is integrated in a plant, partly because we’ve convinced ourselves

that it isn’t,” Dr. Brenner said. “People have been intimidated from asking that question.”

The mention of the possibility of plant neurobiology elicits such visceral responses that Dr. Brenner said he had at times worried that it could harm his career.

“I see a lot of people waiting on the sidelines,” he said, “to see how this all pans out.”Brainpower May Lie in Complexity of Synapses

By NICHOLAS WADEEvolution’s recipe for making a brain more complex has long seemed simple enough. Just increase the

number of nerve cells, or neurons, and the interconnections between them. A human brain, for instance, is three times the volume of a chimpanzee’s.

A whole new dimension of evolutionary complexity has now emerged from a cross-species study led by Dr. Seth Grant at the Sanger Institute in England.

Dr. Grant looked at the interconnections between neurons, known as synapses, which until now have been regarded as a standard feature of neurons.

But in fact the synapses get considerably more complex going up the evolutionary scale, Dr. Grant and colleagues reported online Sunday in Nature Neuroscience. In worms and flies, the synapses mediate simple forms of learning, but in higher animals they are built from a much richer array of protein components and conduct complex learning and pattern recognition, Dr. Grant said.

The finding may open a new window into how the brain operates. “One of the biggest questions in neuroscience is to answer what are the design principles by which the human brain is constructed, and this is one of those principles,” Dr. Grant said.

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If the synapses are thought of as the chips in a computer, then brainpower is shaped by the sophistication of each chip, as well as by their numbers. “From the evolutionary perspective, the big brains of vertebrates not only have more synapses and neurons, but each of these synapses is more powerful — vertebrates have big Internets with big computers and invertebrates have small Internets with small computers,” Dr. Grant said.

He included yeast cells in his cross-species survey and found that they contain many proteins equivalent to those in human synapses, even though yeast is a single-celled microbe with no nervous system. The yeast proteins, used for sensing changes in the environment, suggest that the origin of the nervous system, or at least of synapses, began in this way.

The computing capabilities of the human brain may lie not so much in its neuronal network as in the complex calculations that its synapses perform, Dr. Grant said. Vertebrate synapses have about 1,000 different proteins, assembled into 13 molecular machines, one of which is built from 183 different proteins.

These synapses are not standard throughout the brain, Dr. Grant’s group has found; each region uses different combinations of the 1,000 proteins to fashion its own custom-made synapses.

Each synapse can presumably make sophisticated calculations based on messages reaching it from other neurons. The human brain has about 100 billion neurons, interconnected at 100 trillion synapses.

The roots of several mental disorders lie in defects in the synaptic proteins, more than 50 of which have been linked to diseases like schizophrenia, Dr. Grant said.

Dr. Edward Ziff, a synapse expert at New York University, said Dr. Grant’s work was the first in which synapses had been analyzed from a cross-species perspective. “I would say this work is unique,” he said. “Grant’s been a leader in making this type of analysis and he deserves a lot of credit for it, although a certain amount of guesswork is involved.”

'Electron turbine' could print designer molecules* 12:31 11 June 2008

* NewScientist.com news service* Kate McAlpine

A carbon nanotube that spins in a current of electrons, like a wind turbine in a breeze, could become the world's smallest printer or shrink computer memory, UK researchers say.A simple microscopic motor can be made by slotting three nanotubes together and hooking them to an electric current

– the so-far theoretical design could be used as a tiny printer to make designer molecules (Image: C Lambert)The design is simple. A carbon nanotube 10 nanometres long and 1 nm wide is suspended between two

others, its ends nested inside them to form a rotating joint. When a direct current is passed along the tubes, the central one spins around.

That design has as yet only been tested using advanced computer simulations by Colin Lambert and colleagues at Lancaster University, Lancashire, UK.

But Adrian Bachtold of the Catalan Institute for Nanotechnology, who was not involved in the work, intends to build the electron turbines and says it should be straightforward.

Researchers have made or designed a range of small-scale motors in recent years, using everything from DNA to light sensitive molecules to cell-transport proteins.

The Lancaster design is one of the simplest yet. Imagined applications for nanomotors range from shrinking optical communications components to new forms of computer memory.Tiny turbine

Conventional water or wind turbines spin by deflecting oncoming air or water in one direction. This causes a reaction force to push them in the opposite direction.

Similarly, when electrons move through the nanotube turbine, they tend to bounce off its spiral arrangement of carbon rings in a particular direction. This redirects the electrons into a spiral flow, and causes the tube to rotate in the opposite direction.

The Lancaster team is confident this electron "wind" can overcome any friction forces that would prevent the middle tube spinning. They also hope to minimise friction at the joints by making the nanotubes as smooth as possible.Tiny inkjet

The Lancaster researchers say their motor could be used to pump atoms and molecules through the spinning middle tube. Multiple pumps could precisely control a chemical reaction, driving atoms in a pattern to engineer new molecules. "It's like a nanoscale inkjet printer," says Lambert.

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Atoms pumped through the motor could also be used to represent digital data, with an array of motors shuttling atoms between the 1 and 0 ends of the middle tube to store or process information. This method could store data in a space about 10 times smaller than today's state-of-the-art commercial systems, says Lambert.

"The work of Lambert's group is exciting," says Bachtold, "the proposed motors should be rather straightforward to fabricate". But he points out that only experiments will reveal whether this new nanomotor design lives up to its promise.A paper on the electron windmills will be published in Physical Review Letters this month. A pre-review version is available on the arXiv pre-print website.News Release - IAU0804: Plutoid chosen as name for Solar System objects like

PlutoJun 11, 2008, Paris The International Astronomical Union has decided on the term plutoid as a name for dwarf planets like Pluto at a meeting of its Executive Committee in Oslo.

Almost two years after the International Astronomical Union (IAU) General Assembly introduced the category of dwarf planets, the IAU, as promised, has decided on a name for transneptunian dwarf planets similar to Pluto. The name plutoid was proposed by the members of the IAU Committee on Small Body Nomenclature (CSBN), accepted by the Board of Division III, by the IAU Working Group for Planetary System Nomenclature (WGPSN) and approved by the IAU Executive Committee at its recent meeting in Oslo, Norway.

Plutoids are celestial bodies in orbit around the Sun at a semimajor axis greater than that of Neptune that have sufficient mass for their self-gravity to overcome rigid body forces so that they assume a hydrostatic equilibrium (near-spherical) shape, and that have not cleared the neighbourhood around their orbit. Satellites of plutoids are not plutoids themselves, even if they are massive enough that their shape is dictated by self-gravity. The two known and named plutoids are Pluto and Eris. It is expected that more plutoids will be named as science progresses and new discoveries are made.

The dwarf planet Ceres is not a plutoid as it is located in the asteroid belt between Mars and Jupiter. Current scientific knowledge lends credence to the belief that Ceres is the only object of its kind. Therefore, a separate category of Ceres-like dwarf planets will not be proposed at this time.

The IAU has been responsible for naming planetary bodies and their satellites since the early 1900s. The IAU CSBN, who originally proposed the term plutoid, is responsible for naming small bodies (except satellites of the major planets) in the Solar System. The CSBN will be working with the IAU WGPSN to determine the names of new plutoids to ensure that no dwarf planet shares the name of another small Solar System body. The WGPSN oversees the assignment of names to surface features on bodies in the Solar System. These two committees have previously worked together to accept the names of dwarf planet Eris and its satellite Dysnomia.

In Oslo, members of the IAU also discussed the timing involved with the naming of new plutoids. Again, following the advice of the Division III Board and the two Working Groups, it was decided that, for naming purposes, any Solar System body having (a) a semimajor axis greater than that of Neptune, and (b) an absolute magnitude brighter than H = +1 (see Notes) magnitude will, for the purpose of naming, be considered to be a plutoid, and be named by the WGPSN and the CSBN. Name(s) proposed by the discovery team(s) will be given deference. If further investigations show that the object is not massive enough and does not qualify as a plutoid, it will keep its name but change category.

In French plutoid is plutoïde, in Spanish plutoide and in Japanese 冥王星型天体.From Canada to the Caribbean: Tree Leaves Control Their Own Temperature,

Penn Study RevealsPHILADELPHIA –- The temperature inside a healthy, photosynthesizing tree leaf is affected less by outside environmental temperature than originally believed, according to new research from biologists at the University of Pennsylvania.Surveying 39 tree species ranging in location from subtropical to boreal climates, researchers found a nearly constant temperature in tree leaves. These findings provide new understanding of how tree branches and leaves

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maintain a homeostatic temperature considered ideal for photosynthesis and suggests that plant physiology and ecology are important factors to consider as biologists tap trees to investigate climate change.

Tree photosynthesis, according to the study, most likely occurs when leaf temperatures are about 21°C, with latitude or average growing-season temperature playing little, if any, role. This homeostasis of leaf temperature means that in colder climates leaf temperatures are elevated and in warmer climates tree leaves cool to reach optimal conditions for photosynthesis. Therefore, methods that assume leaf temperature is fixed to ambient air require new consideration.

“It is not surprising to think that a polar bear in northern Canada and a black bear in Florida have the same internal body temperature,” Brent Helliker, professor of biology in the School of Arts and Sciences at Penn, said. “They are endothermic mammals like us ,and they generate their own heat. However, to think that a black spruce in Canada and a Caribbean pine in Puerto Rico have the same average leaf temperature is quite astonishing, particularly since trees are most definitely not endothermic. Our research suggests that they use a combination of purely physical phenomena — like the cooling from water evaporation or the warming caused by packing a lot of leaves together — to maintain what looks like leaf-temperature homeostasis.”

Leaf temperature, cooled by the physiological and morphological techniques of evaporation, leaf angle or reflection and heated by a decrease in evaporation and an increase in the number of leaves per branch, can now be considered adaptations towards achieving homeostasis. Researchers do not suggest that tree canopies maintain a constant temperature through a day or a season, but rather that this ideal temperature is a long-term target value.

The study also presents a new hypothesis for why certain trees grow in certain climates and provides a new theory for how and why trees in the north will suffer from global warming, by overheating due to the mechanisms they have evolved to keep their leaves warm.

In addition, weather-forecasting models rely on accurate estimates of surface-water evaporation, much of which comes from tree leaves. Knowing the temperature of these leaves is crucial to an accurate prediction of future climate scenarios.

The research, published online in this week’s Nature, contradicts the longstanding assumption that temperature and relative humidity in an actively photosynthesizing leaf are coupled to ambient air conditions. For decades, scientists studying climate change have measured the oxygen isotope ratio in tree-ring cellulose to determine the ambient temperature and relative humidity of past climates. The assumption in all of these studies was that tree leaf temperatures were equal to ambient temperatures.

Researchers at Penn, using measures of oxygen isotopes and current climate, determined a way to estimate leaf temperature in living trees and as a consequence showed this assumption to be incorrect. This is an unfortunate finding for the potential to reconstruct climate through tree-ring isotope analysis but a boon to ecologists because it creates potential for the reconstruction of tree responses to both average climate and climate change over the last couple of centuries.The team used their method to reconstruct tree canopy leaf temperatures in 39 species across 50 degrees of latitude and found that in warmer climates leaves were cooler than ambient temperatures and in cooler climates the opposite was true. Perhaps the more remarkable finding was that across such a large area and across so many types of tree that the leaves seemed to be operating at the same temperature, probably a result of natural selection acting to maintain optimal temperature for photosynthesis in the face of widely varying ambient climates.

The continental-scale dataset used in this research was part of a separate study done by Suzanna Richter, a contributor to this study and post-doctoral researcher in the Department of Earth and Environmental Science at Penn. “Multi-million-year-old wood that colleagues and I collected in Arctic Canada and Siberia was so well preserved that it both looked like modern wood and burned like modern wood. Its fantastic preservation brought about questions as to whether the chemistry of the wood could be used to determine the climate that the trees grew in millions of years ago.”

Although there are few studies that compare tree-canopy temperatures throughout an entire growing season, a recent study using infrared thermal imaging of a mixed forest in Switzerland agreed with the current study: canopy temperature was 4-5 degrees (Celsius) higher than the cool, ambient air temperature of Switzerland.Funding for this study was provided by the Department of Biology at the University of Pennsylvania and the Andrew W. Mellon Foundation.

EULAR PRESS RELEASEAt Least 50% Of Recent Onset Rheumatoid Arthritis Patients Become Free Of

Signs And Symptoms Within 36 Weeks

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The results of a systematic step-up DMARD treatment schedule in combination with tight control

Paris, France, Wednesday June 11th 2008: At least 50% of recent onset rheumatoid arthritis patients achieve remission (a state free of signs and symptoms) within 36 weeks when following a systematic approach of step-up DMARD treatment in combination with tight control, according to results of a study presented today at EULAR 2008, the Annual Congress of the European League Against Rheumatism in Paris, France. Results of this study indicate that achieving remission is not only possible during clinical trials but can be a realistic goal of standard clinical care.Of 169 early RA patients, remission (defined as DAS28<2.6) was achieved in 15.5% at week 8 (23/148), 22.2% at week 12 (24/108), 30.7% at week 20 (23/75), 38.8% at week 24 (33/85), 52.1% at week 36 (38/73) and 51% at week 48-52 (26/51).The researchers achieved these results through implementation of a tightly regulated DMARD treatment scheme, as follows:Methotrexate 15mg/week was initiated following diagnosis* If remission was not achieved at week 8, the dose was increased to 25mg/week* If not achieved at week 12, sulfasalazine was added (2grams/day)* If not achieved at week 20, the dose was increased to 3grams/day* If not achieved at week 24 adalimumab was added to methotrexate* Every 3 months thereafter, therapy could be adjusted based on DAS28, also using other TNF-blockers. Patients were allowed to take NSAIDs, and prednisolone .10mg/day and intra-articular corticosteroid injections could be administered 1

Dr. H. Kuper and Prof M. van de Laar of Medisch Spectrum Twente & University Twente, the Netherlands, who led the study, said; “In many large clinical trials, remission can be considered a realistic goal. We set out to determine whether all patients presenting in daily clinical practice can reasonably expect to achieve a state free of signs and symptoms, if a strict treatment schedule was followed. Our results show that remission is indeed achievable in as many as half of clinical practice patients following this schedule, which could indicate that remission is a realistic treatment goal of daily clinical practice.”As part of the Dutch Rheumatoid Arthritis Monitoring Registry (DREAM), investigators performed a prospective descriptive study of a cohort of recent onset rheumatoid arthritis DMARD-naive, patients in daily clinical practice, between January 2006 and January 2008. 190 consecutive patients with recently diagnosed RA under the care of the rheumatology clinics of three hospitals in the Netherlands were included. Results were taken from the first 169 patients with DAS28>3.2 at inclusion.At baseline, patient characteristics between the hospitals were comparable . average patient age was 57.3 years (13.7), 63.9% were female, 52.7% of which were rheumatoid factor positive, with an average disease duration of 16 weeks (1-52), ESR 33.2 (20.5), CRP 23.5 (26.4), DAS28 5.1 (1.1), HAQ 1.3 (0.6).For further information on this study, or to request an interview with the study lead, please do not hesitate to contact the EULAR congress press office on:Email: eularpressoffice@uk.cohnwolfe.comRory Berrie: Onsite tel: +44 (0) 7789 270 392Camilla Dormer: Onsite tel: +44 (0) 7876 190 439Abstract number: OP-0003

Fossils found in Tibet by FSU geologist revise history of elevation, climateAbout 15,000 feet up on Tibet's desolate Himalayan-Tibetan Plateau, an international research team led by

Florida State University geologist Yang Wang was surprised to find thick layers of ancient lake sediment filled with plant, fish and animal fossils typical of far lower elevations and warmer, wetter climates.

Back at the FSU-based National High Magnetic Field Laboratory, analysis of carbon and oxygen isotopes in the fossils revealed the animals' diet (abundant plants) and the reason for their demise during the late Pliocene era in the region (a drastic climate change). Paleo-magnetic study determined the sample's age (a very young 2 or 3 million years old).

That fossil evidence from the rock desert and cold, treeless steppes that now comprise Earth's highest land mass suggests a literally groundbreaking possibility:

Major tectonic changes on the Tibetan Plateau may have caused it to attain its towering present-day elevations — rendering it inhospitable to the plants and animals that once thrived there -- as recently as 2-3 million years ago, not millions of years earlier than that, as geologists have generally believed. The new evidence calls into question the validity of methods commonly used by scientists to reconstruct the past elevations of the region.

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"Establishing an accurate history of tectonic and associated elevation changes in the region is important because uplift of the Tibetan Plateau has been suggested as a major driving mechanism of global climate change over the past 50-60 million years," said Yang, an associate professor in FSU's Department of Geological Sciences and a researcher at the National High Magnetic Field Laboratory. "What's more, the region also is thought to be important in driving the modern Asian monsoons, which control the environmental conditions over much of Asia, the most densely populated region on Earth."

The fossil findings and implications are described in the June 15, 2008 issue of the peer-reviewed journal Earth and Planetary Science Letters.The journal can be accessed online at www.elsevier.com/locate/epsl.

Yang co-authored the paper ("Stable isotopes in fossil mammals, fish and shells from Kunlun Pass Basin, Tibetan Plateau: Paleoclimatic and paleoelevation implications") with paleontologists from the Department of Vertebrate Paleontology at the Natural History Museum of Los Angeles County, and the Institute of Vertebrate Paleontology and Paleoanthropology, Chinese Academy of Sciences (Beijing). The collaborative research project, which since 2004 has featured summer field study on the remote Tibetan Plateau, is funded by a grant from the Sedimentary Geology and Paleobiology Program of the U.S. National Science Foundation.

"The uplift chronology of the Tibetan Plateau and its climatic and biotic consequences have been a matter of much debate and speculation because most of Tibet's spectacular mountains, gorges and glaciers remain barely touched by man and geologically unexplored," Yang said.

"So far, my research colleagues and I have only worked in two basins in Tibet, representing a very small fraction of the Plateau, but it is very exciting that our work to-date has yielded surprising results that are inconsistent with the popular view of Tibetan uplift," she said.

This summer, Yang and her colleagues from Los Angeles and Beijing will conduct further fieldwork in areas near the Tibetan Plateau. "The next phase of our work will focus on examining the spatial and temporal patterns of long-term vegetative and environmental changes in and around the region," she said. "Such records are crucial for clarifying the linkages among climatic, biotic and tectonic changes."

There is much still to learn and understand about those changes."Many of the places we've visited in Tibet are now deserts, and yet we found those thick deposits of lake

sediments with abundant fossil fish and shells," Yang said. "This begs the question: What came first and caused the disappearance of those lakes? Global climate change? Or, tectonic change?"

Woolly-Mammoth Gene Study Changes Extinction Theory9 June 2008—A large genetic study of the extinct woolly mammoth has revealed that the species was not one large homogenous group, as scientists previously had assumed, and that it did not have much genetic diversity. "The population was split into two groups, then one of the groups died out 45,000 years ago, long before the first humans began to appear in the region," said Stephan C. Schuster, associate professor of biochemistry and molecular biology at Penn State University and a leader of the research team. "This discovery is particularly interesting because it rules out human hunting as a contributing factor, leaving climate change and disease as the most probable causes of extinction." The discovery will be published later this week in the early online edition of the Proceedings of the National Academy of Sciences (PNAS).

The research marks the first time scientists have dissected the structure of an entire population of extinct mammal by using the complete mitochondrial genome -- all the DNA that makes up all the genes found in the mitochondria structures within cells. Data from this study will enable testing of the new hypothesis presented by the team, that there were two groups of woolly mammoth -- a concept that previously had not been recognized from studies of the fossil record.

The scientists analyzed the genes in hair obtained from individual woolly mammoths -- an extinct species of elephant adapted to living in the cold environment of the northern hemisphere. The bodies of these mammoths were found throughout a wide swathe of northern Siberia. Their dates of death span roughly 47,000 years, ranging from about 13,000 years ago to about 60,000 years ago.

Schuster and Webb Miller, professor of biology and computer science and engineering at Penn State, led the international research team, which includes Thomas Gilbert at the University of Copenhagen in Denmark and other scientists in Australia, Belgium, France, Italy, Russia, Spain, Sweden, the United Kingdom, and the United States. The team includes experts in the fields of genome evolution, ancient DNA, and mammoth paleontology, as well as curators from various natural-history museums.

Another important finding for understanding the extinction processes is that the individuals in each of the two woolly-mammoth groups were related very closely to one another. "This low genetic divergence is surprising because the woolly mammoth had an extraordinarily wide range: from Western Europe, to the Bering Strait in Siberia, to Northern America," Miller said. "The low genetic divergence of mammoth, which we 2023/05/19 23

discovered, may have degraded the biological fitness of these animals in a time of changing environments and other challenges."

Our study suggests a genetic divergence of the two woolly-mammoth groups more than 1-million years ago, which is one quarter the genetic distance that separates Indian and African elephants and woolly mammoths," Miller said. The research indicates that the diversity of the two woolly-mammoth populations was as low centuries ago as it is now in the very small populations of Asian elephants living in southern India. "The low genetic divergence of the elephants in southern Indian has been suggested as contributing to the problems of maintaining this group as a thriving population," Schuster said. Intriguingly, the mitochondrial genomes revealed by the researchers are several times more complete than those known for the modern Indian and African Elephants combined.

Whereas studies before this research had analyzed only short segments of the DNA of extinct species, this new study generated and compared 18 complete genomes of the extinct woolly mammoth using mitochondrial DNA, an important material for studying ancient genes. This achievement is based on an earlier discovery of the team led by Miller, Schuster, and co-author Thomas Gilbert, which was published last year and that revealed ancient DNA survives much better in hair than in any other tissue investigated so far. This discovery makes hair, when it is available, a more powerful and efficient source of DNA for studying the genome sequences of extinct animals. Moreover, mammoth hair is found in copious quantities in cold environments and it is not regarded as fossil material of enormous value like bone or muscle, which also carries anatomical information.

"We also discovered that the DNA in hair shafts is remarkably enriched for mitochondrial DNA, the special type of DNA frequently used to measure the genetic diversity of a population," Miller said. The team's earlier study also showed that hair is superior for use in molecular-genetic analysis because it is much easier than bone to decontaminate. Not only is hair easily cleaned of external contamination such as bacteria and fungi, its structure also protects it from degradation, preventing internal penetration by microorganisms in the environment.

An important aspect of the new study is that the hair samples it used had been stored in various museums for many years before being analyzed by the researchers, yet the scientists were able to obtain lots of useful DNA from them. "One of our samples originates from the famous Adams mammoth, which was found in 1799 and has been stored at room temperatures for the last 200 years," Schuster said. This research technique opens the door for future projects to target interesting specimens that were collected a long time ago and are no longer available from modern species, the scientists said. Even the molecular analysis of entire collections seems now possible, an effort that the team calls "Museomics."

"We plan to continue using our techniques to untangle the secrets of populations that lived long ago and to learn what it might have taken for them to survive," Schuster said. "Many of us also have a personal interest in learning as much as we can about how any species of large mammal can go extinct."The research was supported, in large part, by Penn State University, Roche Applied Sciences, and a private sponsor. Additional support was provided by the National Human Genome Research Institute, Marie Curie Actions, the Australian Research Council, the Russian Foundation for Basic Research, and the Pennsylvania Department of Health.CONTACTS -- Stephan Schuster: (+1)814-863-9278 or (+1)814-441-3513, scs@bx.psu.edu, Penn State Center for Comparative Genomics and Bioinformatics-- Webb Miller: (+1)814 865-4551, webb@bx.psu.edu, Penn State Center for Comparative Genomics and Bioinformatics-- Barbara Kennedy (PIO): 814-863-4682, science@psu.eduBACKGROUND INFORMATION:Woolly mammoths, descended from ancestors in Africa, were widespread in northern Europe, Asia, and North America during the last Ice Age. However, by 11,000 years ago, they all had died out, except for tiny isolated populations that held out for another few thousand years

Indonesia. Long-Tailed Macaques Spotted Catching Fish.By Lauren Miura

Long-tailed macaques eat mostly fruit — but when resources are scarce, they’ve been known to get creative with their cuisine. When living near humans, they raid gardens and learn to beg for food. Sometimes they even steal food from inside houses.

Now, for the first time, scientists have observed long-tailed macaques fishing with their bare hands.Nature Conservancy scientist Erik Meijaard and other researchers are the first to scientifically document this

rare conduct. In a recent article published in the International Journal of Primatology, Meijaard and his

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coauthors say that, while conducting field studies in Indonesia, they have repeatedly observed long-tailed macaques catching fish from fast-flowing rivers.

“This is interesting behavior and some of the first observations of primates catching fish,” says Meijaard, the Conservancy's senior ecologist in Indonesia.

A macaque fishing in Indonesia.© Mel WhiteA Very Hungry Monkey?

In the first sighting back in 1998, researchers describe seeing five female macaques sitting alongside the Ketambe River in the Indonesian province of North Sumatra.

The macaques’ eyes scanned the water. After about three minutes, one of the macaques reached into the river. With her bare hands, she pulled out a fish and quickly ate it. Other macaques watched her — and one even tried unsuccessfully to catch a fish herself.

“Clearly it may raise the question of whether there is some sort of learning going on," says Meijaard. "If perhaps a couple of generations back, one primate caught a fish and it was subsequently copied.”

Researchers documented a similar sighting in 2006 in a separate macaque population in the Lesan Conservation Area, a Nature Conservancy program site in East Kalimantan, Indonesia. There, on two separate occasions, a macaque was observed swiftly grasping a fish out of the shallows before retreating into the forest with the fish still in its mouth.

While the fishing macaque sighting in Lesan coincided with a time of low fruit availability, Meijaard is hesitant to blame the fishing behavior on resource scarcity or draw conclusions about its meaning.

“It might be nothing more than a hungry monkey who is smart enough to extract nutrients from its environment,” he says.Protecting Indonesia's Forests

Meijaard is also the Kalimantan coordinator for the USAID-funded Orangutan Conservation Services Program.

But he says that forests — not macaques or orangutans — are the Conservancy’s real focus.The Conservancy is fighting an ongoing battle to protect the forests around the Lesan Conservation Area.

These forests, which harbor a substantial orangutan population, are slated to be destroyed for agriculture and plantations.

The Conservancy is working around the clock to convince local communities and governments to instead consider their long-term economic needs and put the forests into permanent, sustainable management.

“Macaques and orangutans are neat symbols, but they’re not going to convince people here,” Meijaard says. “What we need is data that shows the microeconomic implications of forest conversion."

"Depending on the decisions made now, the forest could be around forever, or it could be gone forever by next year.”Lauren Miura is a senior writer at The Nature Conservancy.

Primary tumors can drive the growth of distant cancersPrimary tumors can encourage the growth of stray cancer cells lurking elsewhere in the body that otherwise

may not have amounted to much, according to a new study in the June 13 issue of the journal Cell, a publication of Cell Press. As people age, most may have such indolent cancer cells given the sheer number of cells in the body, although their rarity makes them impossible to detect, the researchers said.

The primary tumors under study, which were derived from human breast cancers, seem to "instigate" the growth of other cancers by mobilizing bone marrow cells, which then feed the secondary tumors' growth, they report.

One key to the process is the secretion of a substance known as osteopontin by the instigating tumor, a finding that may have therapeutic implications. Indeed, the researchers noted that osteopontin is present at elevated levels in women with metastatic breast cancer, supporting the notion that the new findings may hold clinical significance.

“If metastases depend on stimulation by primary tumors, interception of the signal through neutralizing antibodies" might block cancer spread, said Robert Weinberg of the Massachusetts Institute of Technology. "That's still speculative, but it's an interesting idea to ponder," he added, noting that treatments today don't specifically target metastases, which are responsible for the vast majority of cancer deaths.

The researchers noted that while the effects of the tumor microenvironment has been much studied, much less was known about how the systemic environment in the body contributes to tumor growth. Several earlier reports had shown that assorted bone marrow-derived cells can be incorporated to various extents into the supportive framework, or stroma, of tumors. However, it wasn't clear whether tumors actively recruit stromal

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cells by directly perturbing other cell reservoirs, such as the bone marrow, or whether tumors are just passive recipients of stromal cell precursors that normally circulate throughout the body.

In the new study, the researchers injected "instigating" human tumor cells into mice along with indolent "responding" cancer cells also derived from humans. Those indolent cells formed vigorously growing tumors only in the presence of the instigating tumor cells, they reported. They found further evidence that the instigating tumor somehow perturbs the makeup of the bone marrow, although Weinberg said they don't really know how that happens. They also show that osteopontin is necessary to the process, but that it does not act alone.

Finally, they showed that the same instigation process can encourage the growth of disseminated metastatic cancer cells. Instigating breast tumors in the mice also drove the growth of implanted fragments of human colon tumors, a finding that they said shows the generality of the physiologic signaling.

Nonetheless, the researchers said they don't yet know how universal this systemic instigation of tumor growth might be. Still, the findings challenge the "prevailing view that primary tumors suppress the growth of derived metastases," Weinberg said. "We argue they can foster cancer's spread by activating bone marrow that is then recruited by distant metastases."

The findings also have important implications for the preclinical study of human cancers, Weinberg emphasized.

“The ability of instigating tumors to foster the growth of a human colon tumor surgical specimen underscores the powers of systemic instigation," the researchers wrote. "Indeed, to our knowledge, methods to expedite the growth of human tumor surgical specimens in vivo have not been previously described. These results suggest that the presently described procedure can be used to study aspects of human tumor biology that would otherwise be difficult if not impossible to study.

“In the longer term, identification of additional tumor-derived factors that perturb the host systemic environment in one way or another may allow one to predict the effects that a given primary tumor type has on the outgrowth of indolent cancer cells that have disseminated to distant sites."Researchers include Sandra S. McAllister, Whitehead Institute for Biomedical Research, Cambridge, MA; Ann M. Gifford, Whitehead Institute for Biomedical Research, Cambridge, MA; Ashley L. Greiner, Whitehead Institute for Biomedical Research, Cambridge, MA; Boston University, Boston, MA; Stephen P. Kelleher, Whitehead Institute for Biomedical Research, Cambridge, MA, Williams College, Williamstown, MA; Matthew P. Saelzler, Whitehead Institute for Biomedical Research, Cambridge, MA; Massachusetts Institute of Technology, Cambridge, MA; Tan A. Ince, Whitehead Institute for Biomedical Research, Cambridge, MA; Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Ferenc Reinhardt, Whitehead Institute for Biomedical Research, Cambridge, MA; Lyndsay N. Harris, Yale University Medical Center, New Haven, CT; Bonnie L. Hylander, Roswell Park Cancer Institute, Buffalo, NY; Elizabeth A. Repasky, Roswell Park Cancer Institute, Buffalo, NY; and Robert A. Weinberg, Whitehead Institute for Biomedical Research, Cambridge, MA, Massachusetts Institute of Technology, Cambridge, MA, MIT Ludwig Center for Molecular Oncology, Cambridge, MA.

Ancient antibody molecule offers clues to how humans evolved allergiesScientists funded by the Biotechnology and Biological Sciences Research Council (BBSRC) have

discovered how evolution may have lumbered humans with allergy problems. The team from the Randall Division of Cell & Molecular Biophysics, King's College London are working on a molecule vital to a chicken's immune system which represents the evolutionary ancestor of the human antibodies that cause allergic reactions. Crucially, they have discovered that the chicken molecule behaves quite differently from its human counterpart, which throws light on the origin and cause of allergic reactions in humans and gives hope for new strategies for treatment. The work is published today (13 June) in The Journal of Biological Chemistry.

Researcher, Dr Alex Taylor said: "This molecule is like a living fossil – finding out that it has an ancient past is like turning up a coelacanth in your garden pond. By studying this molecule, we can track the evolution of allergic reactions back to at least 160 million years ago and by looking at the differences between the ancient and the modern antibodies we can begin to understand how to design better drugs to stop allergic reactions in their tracks."

The chicken molecule, an antibody called IgY, looks remarkably similar to the human antibody IgE. IgE is known to be involved in allergic reactions and humans also have a counterpart antibody called IgG that helps to destroy invading viruses and bacteria. Scientists know that both IgE and IgG were present in mammals around 160 million years ago because the corresponding genes are found in the recently published platypus genome. However, in chickens there is no equivalent to IgG and so IgY performs both functions.

Lead researcher, Dr. Rosy Calvert said: "Although these antibodies all started from a common ancestor, for some reason humans have ended up with two rather specialised antibodies, whereas chickens only have one that has a much more general function.

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"We know that part of the problem with IgE in humans is that it binds extremely tightly to white blood cells causing an over-reaction of the immune system and so we wanted to find out whether IgY does the same thing."

By examining how tightly IgY binds to white blood cells the researchers have found that it behaves in a much more similar way to the human IgG, which is not involved in allergic reactions and binds much less tightly.

Professor Brian Sutton, head of the laboratory where the work was done said: "It might be that there was a nasty bug or parasite around at the time that meant that humans needed a really dramatic immune response and so there was pressure to evolve a tight binding antibody like IgE. The problem is that now we've ended up with an antibody that can tend to be a little over enthusiastic and causes us problems with apparently innocuous substances like pollen and peanuts, which can cause life-threatening allergic conditions."

The next stage of the work is to examine in very fine detail the interaction between the antibodies and the surface of the white blood cell. This is with a view to designing drugs that could alter this interaction and therefore 'loosen' the binding of IgE, making it more like its chicken counterpart.Contact Please contact BBSRC Media Office in the first instanceNancy Mendoza, Tel: 01793 413355, Mobile: 07785 710 536, email: nancy.mendoza@bbsrc.ac.ukAuthorsDr Rosy Calvert, Tel: 0207 848 8088, e-mail: rosy.calvert@kcl.ac.ukDr. Alex Taylor, Tel: 0207 848 6496, e-mail: alexander.taylor@kcl.ac.ukProfessor Brian Sutton, Tel: 0207 848 6423, e-mail: brian.sutton@kcl.ac.ukNotes to Editors This research is published in The Journal of Biological Chemistry: Taylor et al., 'Avian IgY binds to a monocyte receptor with IgG-like kinetics despite an IgE-like structure', The Journal of Biological Chemistry, 283: 16384-16390This research is funded by a £300K grant from the UK's Biotechnology and Biological Sciences Research Council (BBSRC).

Tsunami in the Brain11.06.2008

After a stroke, waves of electrical discharge in the human brain cause more nerve cells to die / Researchers from Heidelberg an Cologne publish a study in the “Annals of Neurology”

After a stroke, even unaffected areas of the brain are at risk – depolarization waves arise at the edges of the dead tissue and spread through the adjacent areas of the brain. If these waves are repeated, more cells die. This has previously been observed only in animal studies.

A clinical study at the university hospitals of Heidelberg and Cologne along with the Max Planck Institute of Neurological Research in Cologne has shown for the first time that this phenomenon occurs after a stroke in humans and is a warning sign that more nerve cells will die. The study, published in June 2008 in the renowned journal “Annals of Neurology,” may allow to translate more than 60 years of experimental research for the diagnosis and therapy of stroke patients.

More than 150,000 people a year in Germany suffer a cerebral stoke, the third most frequent cause of death in industrialized countries. When deposits clog vessels to the brain, some areas of the brain do not receive sufficient oxygen and the tissue dies. Depending on the size of the area affected, the patients may die or suffer permanent damage such as paralysis.

Spreading depolarizations first proven in stroke patientsThe depolarization waves in the brain – known as cortical spreading depression (CSD) – have been studied

only experimentally since the 1940s. Many features are thus known from animals – the waves of depolarization that can spread out at a speed of two to five millimeters per minute are followed by silence – brain activity comes to a halt for a short time. In this time, the nerve cells recover. “The impact of these waves is several times greater for nerve cells than an epileptic seizure,” says Professor Dr. Rudolf Graf from the Max Planck Institute of Neurological Research and co-founder of the international study group COSBID (Cooperative Study on Brain Injury Depolarisations).

“After the stroke, circulation in the tissue surrounding the affected area of the brain is initially poor, but it can still be saved,” explained Dr. Christian Dohmen of the Neurology Department at Cologne University Hospital. The spreading depolarizations additionally impair the metabolism of the weakened nerve cells. “The more frequently such waves occur, the longer the nerve cells require to recover, until finally they die off entirely,” says the main author of the study. To what extent the brain is damaged after a stroke depends thus on the number of these spreading depolarizations. This correlation is becoming apparent in humans as well.Know-how from 60 years of research can now be used for treating stroke patients

The spreading depolarizations, which also occur after head injuries or hemorrhages, can be measured only on the surface of the brain. For this study, the physicians therefore selected 16 patients whose brain had to be partially exposed due to a life threatening swelling of brain tissue. Electrodes were applied to the surface of the

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brain around the affected tissue (electrocorticography), the incisions were closed, and brain waves were measured for five days. All patients were in an artificial coma during this period due to their serious condition.

"Our study puts an end to the discussion as to whether these waves also occur in a human brain following a stroke,” says Dr. Oliver Sakowitz, physician at the Department of Neurosurgery of the University of Heidelberg Hospital and co-author of the study. Now comes the question of how to prevent or at least contain them. “As they cause additional damage to the weakened tissue surrounding the stroke area, it is conceivable that we could prevent further damage by suppressing the waves,” said the neurosurgeon.

In previous experimental studies on animals, a few therapy approaches were already developed which physicians can now apply. “The spreading depolarizations are a warning sign that other areas of the brain are at immediate risk and may be also useful as diagnostic measures,” says Dr. Sakowitz. In a follow-up study on a larger number of stroke patients, the COSBID team under the direction of Dr. Christian Dohmen wants to clarify whether cortical spreading depression has an influence on the extent of sequelae such as paralysis.

First space ad targets hungry aliens* 19:46 12 June 2008

* NewScientist.com news service* Colin Barras

It could be the longest commercial break in history. Over a six-hour period this morning, high-powered radars in the Arctic Circle broadcast an advertisement into space for the first time.

The advertisement, for Doritos tortilla chips, was being directed towards a solar system in the Ursa Major constellation, just 42 light years from Earth. The solar system contains a habitable zone, and could host an Earth-like planet and extraterrestrial life.

The EISCAT European space station on the Norwegian island of Svalbard sent the message using its array of radars. Those radars are normally used to study the Earth's upper atmosphere.

"They are among the brightest signals coming off our planet – almost like a lighthouse beaming out of the solar system," says Tony van Eyken, EISCAT director. That makes the radars ideal for transmissions far into space, he says.

The advert itself is unlikely to be decoded by extraterrestrial life, according to van Eyken. "We're sending it as an MPEG file coded into 1s and 0s. It's going to look pretty random," he says. But repeating the message in a series of regular pulses over several hours should help extraterrestrials identify the message as intelligent, he thinks.

EISCAT will receive an undisclosed donation from Doritos for the use of their facilities. "It's not big money, but it could be the thin end of the wedge to using our resources in a new way," says van Eyken.

In 2007, the UK Science and Technology Facilities Council (STFC) announced it was ending funding for a number of astronomy projects, and will no longer fund UK researchers hoping to work at EISCAT.

"Some years in the future, the money that comes from this kind of commercial service could be used to fund pure research," says van Eyken.

Residents of the UK can view the Doritos advert, entitled "Tribe", on ITV1 at 7:44 pm on Sunday, 15 June.Researchers find drugs being tested for Alzheimer's disease work in

unexpected and beneficial waysWednesday, June 11, 2008

JACKSONVILLE, Fla. – Researchers at Mayo Clinic, with their national and international collaborators, have discovered how a class of agents now in testing to treat Alzheimer's disease work, and say they may open up an avenue of drug discovery for this disease and others.

In the June 12 issue of Nature, they report that agents known as gamma-secretase modulators (GSM) work to reduce production of long pieces of the amyloid beta protein (Abeta) that readily stick together and form clumps, and increase production of shorter Abeta that can inhibit the longer forms from sticking together.

This is critical because only when Abeta aggregates and accumulates is it harmful and can trigger Alzheimer's disease, the researchers say.

"So, as these compounds lower the amount of the bad, longer sticky Abeta peptides in the brain, they increase the quantity of shorter Abeta peptides that may protect against development of Alzheimer's disease," says senior author Todd Golde, M.D., Ph.D., Chair of the Department of Neuroscience at Mayo Clinic in Jacksonville.

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"In a very general sense the action of these GSM on Abeta might be analogous to some cholesterol lowering drugs that can lower LDL, the bad cholesterol that sticks to your arteries, and can raise HDL, the good cholesterol that sweeps out LDL," he says.

Not only that, GSM agents actually stick to the Abeta already in the brain, keeping it from aggregating. A hallmark of Alzheimer's is formation of "plaques" and other assemblies of Abeta protein in the brain, which are believed to damage neurons in complex ways that are not yet fully understood, researchers say. "Surprisingly, this means that these compounds may do three things that may be beneficial with respect to Alzheimer's disease: they inhibit production of long Abeta, block aggregation of Abeta, and increase production of shorter Abeta peptides that may in turn inhibit Abeta aggregation," says the study's lead investigator, Thomas Kukar, Ph.D.

As exciting as these discoveries are, the investigators – which number 29 in all and are from four nations - also found that GSMs work in a way that has not been seen before in other drugs. "Most drugs target enzymes, which act on proteins, or cell surface receptors, which proteins bind to," he says. "These agents work on the structure, or substrate, of the protein itself, which had not been believed to be druggable."

"This broadens the notion of what drugs can do, and therefore, has wide reaching implication for future drug discovery for many different disorders," Dr. Golde says.

The findings also suggest that GSMs now being tested or in development to treat Alzheimer's may prove to be valuable, the researchers say. One such drug, tarenflurbil (FlurizanTM), is in Phase III clinical trials, and results from the first, a 1,600-patient US study, are expected this summer. Results of a phase II study, published online in April in Lancet Neurology, suggest it provides benefit in patients with mild Alzheimer's, Dr. Golde says.Understanding the agent Mayo discovered

Mayo Clinic helped discover that tarenflurbil was a GSM. Previously, Dr. Golde, along with Eddie Koo, M.D., of the University of California at San Diego, found that the agent tarenflurbil, then called r-flurbiprofen, inhibited production of Abeta 42, and increased the quantity of the shorter Abeta38 but they did not know why. Myriad Genetics, a biotechnology company, had been testing the drug to treat prostate cancer, an indication that is not currently being pursued. But after cell and animal studies in the laboratories of Dr. Golde and Dr. Koo suggested that tarenflurbil could influence Abeta production and reduce cognitive deficits in a mouse model of AD, the company began testing it to treat Alzheimer's in humans.

At the same time, Mayo researchers, led by lead investigator Thomas Kukar, Ph.D., worked to understand how tarenflurbil and other so-called GSMs work. The Abeta protein is normally generated from a larger protein (the amyloid precursor protein) by the sequential cutting action of two different enzymes that act as molecular scissors. Such enzymes that cut other proteins are referred to as proteases. First the protease, beta-secretase, cuts the protein above the cell membrane. A second protease, gamma-secretase, then clips the portion that sticks inside the cell. Where gamma-secretase cuts the amyloid precursor protein determines how long the Abeta peptide will be. The most commonly produced fragment is Abeta 40, but some are longer (Abeta 42) and some, such as Abeta 38, are shorter. None clump together as quickly as Abeta 42 does, however, and emerging evidence indicates that these shorter pieces may actually keep the longer Abeta 42 from clumping together.

The discovery of gamma-secretase initially led to development of agents designed to block its action. One strategy was to directly target and block gamma-secretase, but because the protease acts on many different proteins, this approach proved to be too toxic, Dr. Golde says. Companies then focused on developing "selective" scissor targeting gamma-secretase inhibitors that predominantly inhibit Abeta production without affecting other targets of the protease. At least one such compound, tarenflurbil, is in clinical trials with several more expected to be entering human trials over the next year or two.

Researchers at Mayo thought that tarenflurbil must also be directly targeting gamma-secretase, but it took almost three years of experimentation using multiple methods to discover that the agent actually acts on the substrate of the scissors –the amyloid precursor protein itself. It is thought that the compounds somehow push the protein around in the membrane so that when the gamma-secretase scissors finally cut it, toxic abeta 42 fragments are not produced.Relevance for future drug discovery

"We now think most GSMs, including tarenflurbil, work this way," Dr. Kukar says. "This is one of the few examples of a small molecule drug that targets a protein substrate rather than the enzyme that works on it, and from a therapeutic point of view, that can offer many beneficial effects."

"If results from tarenflurbil and other GSM agents are less beneficial than hoped, these findings may help drug designers create newer, more potent drugs," Dr. Golde says. "Anytime we gain an increased understanding of the precise molecular action of a drug, that enhances our ability to make better drugs."2023/05/19 29

The study was funded by grants from the National Institute on Aging, the American Federation for Aging Research Rotary CART Fund, the American Health Assistance Foundation, and Mayo Clinic. Mayo Clinic and the University of California own a joint patent on Abeta42 lowering compounds and their use for treating AD, which the institutions licensed to Myriad Genetics.Dr. Golde has sponsored research funded by Myriad Genetics.Study co-authors include researchers from the Swiss Federal Institute of Technology in Lausanne, Switzerland; Harvard Medical School; the Technische Universitaet in Darmstadt, Germany, University College in Dublin, Ireland; and the University of California at San Diego.To access Mayo Clinic's News Blog, which contains video of Dr. Golde discussing information contained in this news release, and links to other Alzheimer's research from Mayo Clinic, please click: http://newsblog.mayoclinic.org/2008/06/09/drugs-being-tested-for-alzheimers-disease-work-in-unexpected-beneficial-ways/You will need this pass code to view this post in advance of the embargo time: 1f7bacTo obtain the latest news releases from Mayo Clinic, go to www.mayoclinic.org/news. MayoClinic.com is available as a resource for your health stories.

What's wrong with selling kidneys?Doctors in this week's BMJ debate the issue of selling kidneys.

A regulated system of compensation for living donors may be the solution to the growing shortage of kidneys for transplantation, writes Arthur Matas, Professor of Surgery at the University of Minnesota.

In many areas of the United States the average wait for a transplant from a deceased donor is five years, but in some parts it is as long 10 years. Because of this the annual death rate for suitable transplant candidates has risen from 6.3% in 2001 to 8.1% in 2005.

Current unregulated systems in developing countries only benefit the rich, and provide no long term donor follow-up, or protection for either buyer or seller, he says.

In contrast, Matas argues, a regulated compensation system in the Western world would increase the number of available organs. Such a system would provide strict control and limit harm by allowing every candidate an opportunity for transplant, full donor evaluation, informed consent, long term health follow-up, with payment managed by the government or insurance companies, and the banning of any other commercialisation.

We already compensate people for sperm, ova, surrogate motherhood, and loss of body parts in court cases without any loss of dignity or humanity. Similarly, Matas concludes that we should allow a trial of compensation for living donation to learn if we can increase the number of kidneys while protecting the dignity and humanity of the donors.

But Jeremy Chapman, from the Centre for Transplant and Renal Research in Sydney, argues that this could reduce the supply of all organs.

He believes that the idea of the regulated market is a myth, which could have devastating consequences on the less easily regulated environments of Asia and Africa.

According to Chapman, selling organs does not help lift people out of poverty. In India and Pakistan people sell their kidneys to pay off debts, but they continue to live below the poverty line, and recent data show that 86% report deteriorating health after organ removal.

In addition, he asks, which family member would donate if the government is willing to pay for a kidney? Many would prefer a stranger rather than a family member to take the risk. What's more, if a kidney is worth money before death, then rather than donating, families may demand money for all sorts of organs after death.

The reality of regulated organ purchase will be a reduction in organ donation, and the destruction of kidney, heart, lung, liver, and pancreas transplantation, he concludes.Contact:Professor Jeremy Chapman, Centre for Transplant and Renal Research, University of Sydney, Westmead, Australia. Tel: +61 419 751 656 Email: jeremy_chapman@wsahs.nsw.gov.au

1 patient's account of becoming a live kidney donorAnnabel Ferriman, an editor at the BMJ, gives a frank first person account of her journey through the

"protracted" and sometimes "frustrating" process of becoming a live kidney donor to her friend, Ray, who had been suffering from polycystic kidney disease for eight years.

Although overall a positive experience, she describes how 16 months of tests, some of which had to be repeated after her notes went missing, and some unnecessary delays, at times left her "seething with rage".

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In one instance, she describes how after turning up for the results of tests on a liver lesion, she waited for 90 minutes only to be told that they were still unsure about the nature of the lesion and that she would have to return a week later.

Thankfully the lesion was benign and during the final stages progress was swift, she recalls. The operation was performed laparoscopically and her recovery was fast and she has had no adverse effects. Ray took a little longer to recuperate, but is doing well and is also back at work.

Because of the shortage of cadaver organs and the higher success rates with living organ transplants, the Royal Free Hospital, where she had the operation, is keen to expand its programme. But, she says, her experience has left her "wondering if it has the capacity to do so."

"I am recounting the tale partly to encourage other people to consider kidney donation, but also in the hope that hospitals might make the path for donors a little easier", she concludes.

"Annabel's helpful account describes a process that we recognise [in this instance] was extended", says Dr Bimbi Fernando, one of Annabel's transplant surgeons from the Royal Free Hospital, in an accompanying article. This was due in part to the difficulties of managing her unexpected liver abnormality, but it was compounded by some administrative delays.

Over the past 12 months, he explains, the trust has made substantial changes and investment in the transplant process, and the average time it takes from the beginning of donor testing to the transplant operation has fallen from 200 days to 116 days.

Drug commonly used for alcoholism curbs urges of pathological gamblersMINNEAPOLIS / ST. PAUL (June 13, 2008) – A drug commonly used to treat alcohol addiction has a similar effect on pathological gamblers – it curbs the urge to gamble and participate in gambling-related behavior, according to a new research at the University of Minnesota.

Seventy-seven people participated in the double-blind, placebo controlled study. Fifty-eight men and women took 50, 100, or 150 milligrams of naltrexone every day for 18 weeks. Forty percent of the 49 participants who took the drug and completed the study, quit gambling for at least one month. Their urge to gamble also significantly dropped in intensity and frequency. The other 19 participants took a placebo. But, only 10.5 percent of those who took the placebo were able to abstain from gambling. Study participants were aged 18 to 75 and reported gambling for 6 to 32 hours each week.

Dosage did not have an impact on the results, naltrexone was generally well tolerated, and men and women reported similar results.

"This is good news for people who have a gambling problem," said Jon Grant, M.D., J.D., M.P.H., a University of Minnesota associate professor of psychiatry and principal investigator of the study. "This is the first time people have a proven medication that can help them get their behavior under control."

The research is published in the June issue of the Journal of Clinical Psychiatry.Compulsive gamblers are unable to control their behavior, and the habit often becomes a detriment in their

lives, Grant said. He estimates between 1 to 3 percent of the population has a gambling problem.While the drug is not a cure for gambling, Grant said it offers hope to many who are suffering from

addiction. He also said the drug would most likely work best in combination with individual therapy."Medication can be helpful, but people with gambling addiction often have multiple other issues that should

be addressed through therapy," he said.Naltrexone is sold under the brand names Revia and Depade. An extended-release formulation is sold under

the name Vivitrol.The research was funded by the National Institute of Mental Health. Grant has served as a consultant to Pfizer and has received grant/research support from GlaxoSmith Kline and Forest.

Genetic building blocks may have formed in space* 21:59 13 June 2008

* NewScientist.com news service* Rachel Courtland

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Some fundamental building blocks of our genetic code might have come from outer space, according to a controversial new meteorite study.

The study suggests that some organic compounds associated with genetic material might have formed in a meteorite called Murchison before it landed in Australia in 1969. The chemicals are two kinds of nucleobases, ring-like carbon molecules that are essential for the creation of nucleic acids like DNA and RNA.

The find might bolster claims that meteorites delivered some of the chemicals needed to create life. "It boosts the idea that the origin of life on Earth may have had an important contribution from an extraterrestrial object," says lead author Zita Martins, a chemist at Imperial College London in the UK.

But it may be too early to conclude these nucleobases formed beyond the Earth, says Sandra Pizzarello, a chemist at Arizona State University in Tempe, US. The study "raises a very interesting question that was raised a very long time ago, but I don't think it solves it", she told New Scientist.

No one knows how life got its start. Primitive Earth conditions might not have been favourable for the chemistry needed to create life's building blocks.

The Murchison meteorite contains the building blocks of DNA and RNA, which may have an extraterrestrial origin (Copyright: Chip Clark/Smithsonian Institution/www.si.edu)

Meteorite impactsInstead, researchers have argued that frequent bombardments by meteorites 3.8 billion years ago – when life

is suspected to have first emerged – could have delivered the material to Earth, where it might have helped further the development of life.

Studies of meteorites, as well as astronomical observations of interstellar dust and gas, have turned up a number of organic compounds, including sugars and phosphates.

But nucleobases are also needed to make a nucleic acid like DNA or RNA. Such chemicals have been found in a number of meteorites, but no one was sure whether they were extraterrestrial in origin or the result of earthly contamination.Noisy signal

To study the origins of these nucleobases, Martins and colleagues studied the mass of organic chemicals isolated from the meteorite.

The team looked at two different isotopes of carbon in the chemicals, which included the nucleobases uracil and xanthine. The lighter version, carbon-12, is present on Earth in large amounts. Carbon-13 is more common in sweeping clouds of cold, interstellar gas. Large amounts of the stuff usually indicate the material did not form on Earth.

The ratio of carbon-13 to carbon-12 was unusually high in the two nucleobases, leading the team to conclude the materials likely formed in the meteorite itself rather than on Earth.

But Pizzarello says too many other chemicals were present in the samples to clearly distinguish the carbon ratio. "Analytically, it's not convincing," Pizzarello told New Scientist.Journal reference: Earth and Planetary Science Letters (vol 270, p 130)

Ancient mineral shows early Earth climate tough on continents

MADISON - A new analysis of ancient minerals called zircons suggests that a harsh climate may have scoured and possibly even destroyed the surface of the Earth's earliest continents.

Zircons, the oldest known materials on Earth, offer a window in time back as far as 4.4 billion years ago, when the planet was a mere 150 million years old. Because these crystals are exceptionally resistant to chemical changes, they have become the gold standard for determining the age of ancient rocks, says University of Wisconsin-Madison geologist John Valley.

Valley previously used these tiny mineral grains - smaller than a speck of sand - to show that rocky continents and liquid water formed on the Earth much earlier than previously thought, about 4.2 billion years ago.

In a new paper published online this week in the journal Earth and Planetary Science Letters, a team of scientists led by UW-Madison geologists Takayuki Ushikubo, Valley and Noriko Kita show that rocky continents and liquid water existed at least 4.3 billion years ago and were subjected to heavy weathering by an acrid climate.2023/05/19 32

Ushikubo, the first author on the new study, says that atmospheric weathering could provide an answer to a long-standing question in geology: why no rock samples have ever been found dating back to the first 500 million years after the Earth formed.

"Currently, no rocks remain from before about 4 billion years ago," he says. "Some people consider this as evidence for very high temperature conditions on the ancient Earth."

Previous explanations for the missing rocks have included destruction by barrages of meteorites and the possibility that the early Earth was a red-hot sea of magma in which rocks could not form.

The current analysis suggests a different scenario. Ushikubo and colleagues used a sophisticated new instrument called an ion microprobe to analyze isotope ratios of the element lithium in zircons from the Jack Hills in western Australia. By comparing these chemical fingerprints to lithium compositions in zircons from continental crust and primitive rocks similar to the Earth's mantle, they found evidence that the young planet already had the beginnings of continents, relatively cool temperatures and liquid water by the time the Australian zircons formed.

"At 4.3 billion years ago, the Earth already had habitable conditions," Ushikubo says.The zircons' lithium signatures also hold signs of rock exposure on the Earth's surface and breakdown by

weather and water, identified by low levels of a heavy lithium isotope. "Weathering can occur at the surface on continental crust or at the bottom of the ocean, but the [observed] lithium compositions can only be formed from continental crust," says Ushikubo.

The findings suggest that extensive weathering may have destroyed the Earth's earliest rocks, he says."Extensive weathering earlier than 4 billion years ago actually makes a lot of sense," says Valley. "People

have suspected this, but there's never been any direct evidence."Carbon dioxide in the atmosphere can combine with water to form carbonic acid, which falls as acid rain.

The early Earth's atmosphere is believed to have contained extremely high levels of carbon dioxide - maybe 10,000 times as much as today.

"At [those levels], you would have had vicious acid rain and intense greenhouse [effects]. That is a condition that will dissolve rocks," Valley says. "If granites were on the surface of the Earth, they would have been destroyed almost immediately - geologically speaking - and the only remnants that we could recognize as ancient would be these zircons."Additional information and images are available on the authors' web sites Zircons Are Forever (http://www.geology.wisc.edu/zircon/zircon_home.html) and the Wisc-SIMS ion microprobe facility (http://www.geology.wisc.edu/facilities/wiscsims/wisc_sims.html).Other co-authors on the paper include Aaron Cavosie of the University of Puerto Rico, Simon Wilde of the Curtin University of Technology in Australia and Roberta Rudnick of the University of Maryland.

Can you 'daydream' your way out of a coma?Source: New ScientistDate: 13 June 2008

Daydreaming your way out of a coma? Unlikely as it sounds, keeping track of a wandering mind may one day help doctors to discover whether a brain-damaged individual is still 'in there'.

When a healthy person is daydreaming, their brain is not occupied with specific tasks and the 'default network', a series of specific, connected regions in the brain's cortex, kicks in. The network's purpose is still hotly debated but recent evidence suggests it keeps the brain primed and ready to take on new tasks. Problems activating the default network have been linked to cognitive diseases like Alzheimer's and schizophrenia.

Now Steven Laureys and colleagues at the University of Liège in Belgium have used brain scans to measure the activity of the default network in 13 brain-damaged people whose levels of consciousness were different.

Their study, presented at this week's meeting of the European Neurology Society in Nice, France, found that activity varied in proportion to the amount of brain damage. Minimally conscious patients had a ten per cent reduction compared with healthy individuals, while activity was reduced by 35 per cent in coma patients and those in a persistent vegetative state (PVS). There was no activity at all in the default network of a brain-dead patient.

Laureys concludes that such a scan could act as a 'consciousness meter'. "This could turn into an utterly useful way to diagnose residual consciousness in brain-damaged patients," he says. Such a test could dramatically affect the fate of brain-damaged patients, by helping to determine whether to treat them with drugs or therapies, and in some cases, whether to keep them alive at all, says Laureys.

Usually, consciousness is measured by running a battery of behavioural tests. But these may miss some people who are minimally conscious. Two years ago, researchers at the University of Cambridge, together with Laureys's group, investigated an alternative. They found that the correct brain areas lit up in someone they

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thought was in a PVS when she was asked to imagine playing tennis. This indicated that she must in fact be conscious (New Scientist, 7 July 2007, p 40).

However, the test is difficult to carry out and negative results are hard to interpret as the patient may simply not be able to think about a particular task. Measuring activity in the resting brain is quicker - and doesn't depend on the patient responding. "We just scan someone for ten minutes and get an easily quantifiable read-out," says Laureys.

John Whyte at the Moss Rehabilitation Research Institute in Philadelphia, Pennsylvania, who is testing drugs that may help restore consciousness, says that although larger studies are needed to determine how reliably the default network indicates consciousness, assessing awareness in the resting brain is crucial to treating unresponsive, brain-damaged patients: "To find the right treatments, we need to be able to classify patients better, and resting assessments like this one should help with that."

Joseph Giacino at the JFK Medical Center in Edison, New Jersey, agrees: "If this can help us to sort patients by how well connected their brains are, we might be able to use it one day to better predict who will wake up and who won't."

Is a sniff of coffee as good as a sip?DRINKING a cup of coffee can wake you up, but perhaps just a whiff of Java is enough to reverse the

effects of sleep deprivation on the brain.A team led by Yoshinori Masuo at the National Institute of Advanced Industrial Science and Technology in

Tsukuba, Japan, deprived rats of sleep for a day. When they examined their brains they found reduced levels of mRNA - messenger molecules that indicate when a gene is being expressed - for 11 genes important to brain function. When the rats were exposed to the aroma of coffee, the mRNA for nine of the genes was restored to near normal levels, and pushed to above normal levels for two - GIR, involved in neuro-endocrine control, and NFGR, thought to control oxidative stress (Journal of Agricultural and Food Chemistry, DOI: 10.1021/jf8001137).

We don't know if the same genes are suppressed in sleep-deprived humans, nor whether we would feel tired if they were, but many of these genes do have human equivalents. So the team says gene suppression may help explain why people feel bad when they haven't had enough sleep - and that gene reactivation could explain why people love the smell of coffee.

Next the team hopes to identify the molecules in coffee aroma that affect gene expression. They suggest pumping them into factories to help revive tired workers who can't sip coffee while operating machinery.

How Montezuma gets his revengeJohns Hopkins researchers discover clue to how dysentery parasite might evade

immune systemEvery year, about 500 million people worldwide are infected with the parasite that causes dysentery, a global

medical burden that among infectious diseases is second only to malaria. In a new study appearing in the June 15 issue of Genes and Development, Johns Hopkins researchers may have found a way to ease this burden by discovering a new enzyme that may help the dysentery-causing amoeba evade the immune system.

"This is the first enzyme to be identified that looks like it could mediate immune system evasion," says Sin Urban, Ph.D., an assistant professor of molecular biology and genetics at Hopkins.

The EhROM1 enzyme, it turns out, is part of an ancient group of enzymes—they are found in every branch of life from bacteria to man—known as rhomboid enzymes. In most animals, rhomboid enzymes seem to play a role in cell-to-cell communication, but a couple of years ago Urban found that malaria parasites use rhomboid enzymes for a more sinister purpose: to enter host cells uninvited.

That led his team to scour the DNA of other parasites to see if any of them also had genes that encode rhomboid enzymes. They found that the dysentery-causing amoeba Entamoeba histolytica contains one rhomboid enzyme and named it EhROM1.

"Plasmodia, the parasites that cause malaria, grab onto a host cell and push their way in," explains Urban. "Once inside they use rhomboid enzymes to cut themselves loose." But amoebas don't enter cells to cause dysentery, so Urban's team set out to figure out how these parasites use EhROM1.

They first identified protein targets cut by EhROM1 by looking for amoeba proteins that had structural signatures similar to those cut by malaria rhomboids. They found these signatures in a family of proteins—lectins—that are found on cell surfaces. The researchers put both proteins into cells and verified that EhROM1 does cut one particular lectin, and the more EhROM1 they added, the more lectin pieces resulted.

Every cell has on its surface proteins recognizable by sentries of the immune system that constantly survey the body for intruders, and amoebas are no different. To evade the immune system, amoebas shift all their surface proteins to the rear end of the cell then, like a dump truck, shed these proteins into the fluid around them.2023/05/19 34

Lectin, it turns out, is one of the proteins that during immune evasion moves to the rear and is shed by the amoeba. So collaborating researchers at Stanford University then looked to see if EhROM1 follows lectin and sure enough found that EhROM1 clusters at the cap—the cluster of surface proteins waiting to be shed.

"We're excited to see if EhROM1 plays a specific role in the cap shedding during immune evasion," says Urban.

What's more, the EhROM1 enzyme is remarkably similar to those found in malaria parasites, suggesting that any potential drugs targeting EhROM1 might be able to treat two of the world's most prevalent diseases.The research was funded by the National Institutes of Health and the Burroughs-Wellcome Fund.Authors on the paper are Leigh Baxt and Upinder Singh of Stanford University, and Rosanna Baker and Urban of Hopkins.On the Web: http://biolchem.bs.jhmi.edu/bcmb/faculty/Faculty_detail.asp?PersonID=1232 http://www.genesdev.org/

Here, there be dragonsStrange beasts evolve on islands: flightless bats and birds, amphibious or monstrous lizards, huge tortoises, giant rodents, dwarf elephants and even humans, such as the

famous ‘hobbit’, H. floresiensis.Graeme O'Neill 13/06/2008 15:20:20

When fossils of a diminutive, recently extinct race of humans were discovered in a cave on Flores, one of the most easterly islands of the Indonesian archipelago, researchers can be forgiven for assuming they were down-sized by the peculiar selection pressures that act upon insular species.

On Flores, natural selection has morphed several familiar species to unfamiliar sizes. There be dragons: three metre, 200kg monitor lizards, also known as the Komodo dragon, plus the fossilised remains of an extinct giant rodent, Spelaeomys, and extinct Stegodon pigmy elephants.

The tiny skulls of the Flores fossils ignited a heated, sometimes ad hominin, debate about whether they represented a new species of Homo, or were merely microcephalic mutants of a Floresian form of H. erectus, or even a microcephalic H. sapiens.

But a new cladistic analysis by an Australian National University PhD student suggests the diminutive, gracile humans who lived on Flores as recently as 12,000 years ago, now popularly known as 'hobbits', might not have been dwarfed by insular life.

Debbie Argue, of the Australian National University's School of Archaeology and Anthropology, has produced strong evidence that Homo floresiensis was tiny because its African ancestors were tiny.If Argue is right, H. floresiensis descends from the first hominins to leave Africa, and this might have happened some 2.25 million years ago, around the time when the first, primitive Homo species was emerging in Africa.

If so, the hobbits' forebears could have colonised the Indonesian archipelago up to half a million years before the first large hominin species, Homo erectus - Java Man - crossed the deepwater gaps separating Java and Lombok, and Sumbawa and Flores, by means that did not involve swimming.Comparisons

Argue, who is supervised by renowned ANU human evolutionist Professor Colin Groves, described the results of her morphometric and morphological analysis at the ANU's recent Archaeological Science Conference in Canberra.

She compared anatomical structures of the type specimen of H. floresiensis, LB1, with several modern humans, and many ancient hominins such as H. erectus, H. ergaster, H. habilis, and the Dmanisi specimens.

Cranially, it is most similar to H. ergaster or H. habilis - Argue says this indicates only that H. habilis and H. floresiensis shared an ancestor. But H. floresiensis had long arms in proportion to its legs, and is close to the primitive arm-to-leg ratio of the gracile australopithecine, Australopithecus garhi.

When A. garhi was discovered in 1996, it was hailed as a missing link between Australopithecus and Homo, but is now regarded as the most advanced of the australopithecines.

A. garhi, which lived about 2.2 million years ago, had a cranial capacity of 450cc, less than a third that of modern humans and 33cc larger than that of LB1, the type species of H. floresiensis, which has been set at 417cc according to a study last year by Dean Falk and colleagues. Given the pronounced variation in modern human brain size, A. garhi and H. floresiensis are in the same headspace.

But australopithecines never made it out of Africa. Or did they?"Floresiensis seems to have evolved around the time of A. garhi, given its primitive arm-leg ratio, whereas

H. habilis was moving towards the modern human ratio around the same time," Argue says."If we're right, it means some hominin must have moved out of Africa about two million years ago, which is

half a million years earlier than the Dmanisi hominin, which is supposedly the earliest out of Africa.

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"Not long after H. floresiensis was discovered, someone drew attention to the skull's resemblance to one of the sub-adult skulls from Dmanisi, but morphologically, the Dmanisi crania are very similar and they are quite different from H. floresiensis.

"The 'hobbit' had a relatively small head in relation to its body, and it stood about one metre tall. Australopithecines started at just under one metre, and range up to 1.2 metres, so height is not really an issue.

"We don't have to invoke the island law - the hobbit has some very ancient australopithecine characteristics, which suggest its ancestors were tiny.

"The question is: how did it get to Flores, and when? It's likely to have left Africa between two million and 2.25 million years ago, but that doesn't mean it got to Indonesia immediately - it could have evolved along the way.

"But its presence on Flores means it must have been present on islands back up the Indonesian archipelago. If we knew where to look.

"There is a new Australian-Indonesian program to excavate other targeted areas and it could have reached Flores via Sulawesi, as some others have suggested."Skull and mandibles

Argue confined her cladistic analysis to the skull and mandibles of H. floresiensis and the comparative sample. She compared 40 character states related to the face, basal area of the skull, the dimensions of the back of the skull, and 30 characters of the mandibles of the various species. She is confident of her conclusions.

"If someone had found these skulls in Africa, nobody would have argued they are microcephalic," she says. A lone microcephalic individual from Flores, or even two, would cast doubt upon the claim that H. floresiensis is a new species of Homo.

But the cave on Flores has yielded partial remains of at least two other adults and one child of similar or even smaller proportions.

Argue says stratigraphic and other evidence indicates that they occupied the cave for more than 80,000 years, from about 94,000 years ago until around 12,000 years ago - around the time a major volcanic eruption devastated the island, possibly extinguishing the tiny and extraordinary Floresians.

Stem cell researchers give old muscle new pepBerkeley - Old muscle got a shot of youthful vigor in a stem cell experiment by bioengineers at the University of California, Berkeley, setting the path for research on new treatments for age-related degenerative conditions such as muscle atrophy or Alzheimer's and Parkinson's diseases.

In a new study to be published June 15 in an advanced online issue of the journal Nature, researchers identified two key regulatory pathways that control how well adult stem cells repair and replace damaged tissue. They then tweaked how those stem cells reacted to those biochemical signals to revive the ability of muscle tissue in old mice to repair itself nearly as well as the muscle in the mice's much younger counterparts.

Irina Conboy, an assistant professor of bioengineering and an investigator at the Berkeley Stem Cell Center and at the California Institute for Quantitative Biosciences (QB3), led the research team conducting this study.

Because the findings relate to adult stem cells that reside in existing tissue, this approach to rejuvenating degenerating muscle eliminates the ethical and medical complications associated with transplanting tissues grown from embryonic stem cells.

"We are one step closer to having a point of intervention where we can rejuvenate the body's own stem cells so we don't have to suffer from some of the debilitating diseases associated with aging," said the study's lead author, Morgan Carlson, a recent Ph.D. graduate of Conboy's lab.

The researchers focused on the interplay of two competing molecular pathways that control the stem cells, which sit next to the mature, differentiated cells that make up our working body parts. When the mature cells are damaged or wear out, the stem cells are called into action to begin the process of rebuilding.

"We don't realize it, but as we grow our bodies are constantly being remodeled," said Conboy. "We are constantly falling apart, but we don't notice it much when we're young because we're always being restored. As we age, our stem cells are prevented, through chemical signals, from doing their jobs."

The good news, the researchers said, is that the stem cells in old tissue are still ready and able to perform their regenerative function if they receive the appropriate chemical signals. Studies have shown that when old tissue is placed in an environment of young blood, the stem cells behave as if they are young again.

"Conversely, we have found in a study published last year that even young stem cells rapidly age when placed among blood and tissue from old mice," said Carlson, who will stay on at UC Berkeley to expand his work on stem cell engineering either as a QB3 fellow or a postdoctoral researcher. He will be supervised by Conboy; Tom Alber, professor of biochemistry; and David Schaffer, associate director of the Berkeley Stem Cell Center and professor of chemical engineering.2023/05/19 36

Adult stem cells have a receptor called Notch that, when activated, tells them that it is time to grow and divide, the researchers said. But stem cells also have a receptor for the protein TGF-beta that sets off a chain reaction activating the molecule pSmad3 and ultimately producing cyclin-dependent kinase (CDK) inhibitors, which regulate the cell's ability to divide.

"Interestingly, activated Notch competes with activated pSmad3 for binding to the regulatory regions of the same CDK inhibitors in the stem cell," said Conboy. "We found that Notch is capable of physically kicking off pSmad3 from the promoters for the CDK inhibitors within the stem cell's nucleus, which tells us that a precise manipulation of the balance of these pathways would allow the ability to control stem cell responses."

Notch and TGF-beta are well known in molecular biology, but Conboy's lab is the first to connect them to the process of aging, and the first to show that they act in opposition to each other within the nucleus of the adult stem cell.

Aging and the inevitable march towards death are, in part, due to the progressive decline of Notch and the increased levels of TGF-beta , producing a one-two punch to the stem cell's capacity to effectively rebuild the body, the researchers said.

"What we discovered is the interplay between two pathways - one an aging pathway, and the other a youthful pathway," said Conboy.

But what would happen if researchers blocked the adult stem cells in old tissues from reacting to those TGF-beta signals? The researchers put that question to the test in a living organism by comparing the muscle regeneration capacity of old, 2-year-old mice, comparable in age to a 75- to 80-year-old human, with that of 2-month-old mice, similar in age to a 20- to 25-year-old human.

For a group of the old mice, the researchers disabled the "aging pathway" that tells stem cells to stop dividing by using an established method of RNA interference that reduced levels of pSmad3. The researchers then examined the muscle of the different groups of mice one to five days after injury to compare how well the tissue repaired itself.

As expected, the researchers found that muscle tissue in the young mice easily replaced damaged cells with new, healthy cells. In contrast, the areas of damaged muscle in the control group of old mice were characterized by fibroblasts and scar tissue.

However, muscles in the old mice whose stem cell "aging pathway" had been dampened showed levels of cellular regeneration that were comparable to their much younger peers, and that were 3 to 4 times greater than those of the group of "untreated" old mice.

The researchers cautioned that shutting down the TGF-beta/pSmad3 pathway altogether by turning off the gene that controls it could lead to many health problems. The ability to suppress cell division is critical in controlling the development of tumors, for instance.

"When we are young, there is an optimal balance between Notch and TGF-beta," said Conboy. "We need to find out what the levels of these chemicals are in the young so we can calibrate the system when we're older. If we can do that, we could rejuvenate tissue repair for a very long time."

The researchers also warn against interpreting this research as the cure-all for aging."We're not at a point where we're ready to inject ourselves with TGF-beta antibodies and call it a day," said

Carlson. "There are multiple mechanisms involved in how our body functions. We know that TGF-beta is involved in one aspect of aging, but we don't know where it fits in the global scheme of aging."

In addition to their work on adult stem cells, Carlson and Conboy have also discovered that human embryonic stem cells can actually neutralize the effects of aging. Conboy received funding last year from the California Institute for Regenerative Medicine (CIRM) to pursue this line of research.Michael Hsu, a former UC Berkeley postdoctoral researcher in bioengineering, also co-authored this paper.This study was primarily supported by the National Institutes of Health and The Ellison Medical Foundation, with additional funds from a pre-doctoral training grant from CIRM.

Hunger hormone increases during stress, may have antidepressant effectDALLAS – June 15, 2008 – New research at UT Southwestern Medical Center may explain why some people who are stressed or depressed overeat.

While levels of the so-called "hunger hormone" ghrelin are known to increase when a person doesn't eat, findings by UT Southwestern scientists suggest that the hormone might also help defend against symptoms of stress-induced depression and anxiety.

"Our findings in mice suggest that chronic stress causes ghrelin levels to go up and that behaviors associated with depression and anxiety decrease when ghrelin levels rise. An unfortunate side effect, however, is increased food intake and body weight," said Dr. Jeffrey Zigman, assistant professor of internal medicine and psychiatry 2023/05/19 37

at UT Southwestern and senior author of a study appearing online today and in a future print edition of Nature Neuroscience.

Dr. Michael Lutter, instructor of psychiatry at UT Southwestern and lead author of the study, said, "Our findings support the idea that these hunger hormones don't do just one thing; rather, they coordinate an entire behavioral response to stress and probably affect mood, stress and energy levels."

It is known that fasting causes ghrelin to be produced in the gastrointestinal tract, and that the hormone then plays a role in sending hunger signals to the brain. Research groups including Dr. Zigman's have suggested that blocking the body's response to ghrelin signals might be one way to help control weight by decreasing food intake and increasing energy expenditure.

"However, this new research suggests that if you block ghrelin signaling, you might actually increase anxiety and depression, which would be bad," Dr. Zigman said.

To determine how ghrelin affects mood, Dr. Zigman and his colleagues restricted the food intake of laboratory mice for 10 days. This caused their ghrelin levels to quadruple. As compared to the control mice, which were allowed free access to food, the calorie-restricted mice displayed decreased levels of anxiety and depression when subjected to mazes and other standard behavior tests for depression and anxiety.

In addition, mice genetically engineered to be unable to respond to ghrelin were also fed a restricted-calorie diet. Unlike their calorie-restricted wild-type counterparts, these mice did not experience the antidepressant-like or anti-anxiety-like effects.

To test whether ghrelin could regulate depressive symptoms brought on by chronic stress, the researchers subjected mice to daily bouts of social stress, using a standard laboratory technique that induces stress by exposing normal mice to very aggressive "bully" mice. Such animals have been shown to be good models for studying depression in humans.

The researchers stressed both wild-type mice and altered mice that were unable to respond to ghrelin. They found that after experiencing stress, both types of mice had significantly elevated levels of ghrelin that persisted at least four weeks after their last defeat encounter. The altered mice, however, displayed significantly greater social avoidance than their wild-type counterparts, indicating an exacerbation of depression-like symptoms. They also ate less than the wild-type mice.

Dr. Zigman said the findings make sense when considered from an evolutionary standpoint.Until modern times, the one common human experience was securing enough food to prevent starvation.

Our hunter-gatherer ancestors needed to be as calm and collected as possible when it was time to venture out in search of food, or risk becoming dinner themselves, Dr. Zigman said, adding that the anti-anxiety effects of hunger-induced ghrelin may have provided a survival advantage.

Dr. Lutter said the findings might be relevant in understanding conditions such as anorexia nervosa."We're very interested to see whether ghrelin treatment could help people with anorexia nervosa, with the

idea being that in a certain population, calorie restriction and weight loss could have an antidepressant effect and could be reinforcing for this illness," Dr. Lutter said.

In future studies, the researchers hope to determine which area in the brain ghrelin may be acting on to cause these antidepressant-like effects.Other UT Southwestern researchers involved in the study were Dr. Ichiro Sakata, postdoctoral researcher in internal medicine; Sherri Osborne-Lawrence, senior research scientist; research assistants Sherry Rovinsky and Jason Anderson; Saendy Jung, student intern in psychiatry; Dr. Shari Birnbaum, assistant professor of psychiatry; Dr. Masashi Yanagisawa, professor of molecular genetics and a Howard Hughes Medical Institute investigator; Dr. Joel Elmquist, professor of internal medicine and pharmacology; and Dr. Eric Nestler, chairman of psychiatry.The work was supported by the National Institutes of Health, the Foundation for Prader-Willi Research, the National Alliance for Research on Schizophrenia and Depression and the Disease-Oriented Clinical Scholars Program at UT Southwestern.

Ebb and flow of the sea drives world's big extinction eventsMADISON - If you are curious about Earth's periodic mass extinction events such as the sudden demise of the dinosaurs 65 million years ago, you might consider crashing asteroids and sky-darkening super volcanoes as culprits.

But a new study, published online today (June 15, 2008) in the journal Nature, suggests that it is the ocean, and in particular the epic ebbs and flows of sea level and sediment over the course of geologic time, that is the primary cause of the world's periodic mass extinctions during the past 500 million yearssc1.

"The expansions and contractions of those environments have pretty profound effects on life on Earth," says Shanan Peters, a University of Wisconsin-Madison assistant professor of geology and geophysics and the author of the new Nature report.

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In short, according to Peters, changes in ocean environments related to sea level exert a driving influence on rates of extinction, which animals and plants survive or vanish, and generally determine the composition of life in the oceans.

Since the advent of life on Earth 3.5 billion years ago, scientists think there may have been as many as 23 mass extinction events, many involving simple forms of life such as single-celled microorganisms. During the past 540 million years, there have been five well-documented mass extinctions, primarily of marine plants and animals, with as many as 75-95 percent of species lost.

For the most part, scientists have been unable to pin down the causes of such dramatic events. In the case of the demise of the dinosaurs, scientists have a smoking gun, an impact crater that suggests dinosaurs were wiped out as the result of a large asteroid crashing into the planet. But the causes of other mass extinction events have been murky, at best.

"Paleontologists have been chipping away at the causes of mass extinctions for almost 60 years," explains Peterssc2, whose work was supported by the National Science Foundation. "Impacts, for the most part, aren't associated with most extinctions. There have also been studies of volcanism, and some eruptions correspond to extinction, but many do not."

Arnold I. Miller, a paleobiologist and professor of geology at the University of Cincinnati, says the new study is striking because it establishes a clear relationship between the tempo of mass extinction events and changes in sea level and sediment: "Over the years, researchers have become fairly dismissive of the idea that marine mass extinctions like the great extinction of the Late Permian might be linked to sea-level declines, even though these declines are known to have occurred many times throughout the history of life. The clear relationship this study documents will motivate many to rethink their previous views."

Peters measured two principal types of marine shelf environments preserved in the rock record, one where sediments are derived from erosion of land and the other composed primarily of calcium carbonate, which is produced in-place by shelled organisms and by chemical processes. "The physical differences between (these two types) of marine environments have important biological consequences," Peters explains, noting differences in sediment stability, temperature, and the availability of nutrients and sunlight.

In the course of hundreds of millions of years, the world's oceans have expanded and contracted in response to the shifting of the Earth's tectonic plates and to changes in climate. There were periods of the planet's history when vast areas of the continents were flooded by shallow seas, such as the shark- and mosasaur-infested seaway that neatly split North America during the age of the dinosaurs.

As those epicontinental seas drained, animals such as mosasaurs and giant sharks went extinct, and conditions on the marine shelves where life exhibited its greatest diversity in the form of things like clams and snails changed as well.

The new Wisconsin study, Peters says, does not preclude other influences on extinction such as physical events like volcanic eruptions or killer asteroids, or biological influences such as disease and competition among species. But what it does do, he argues, is provide a common link to mass extinction events over a significant stretch of Earth history.

"The major mass extinctions tend to be treated in isolation (by scientists)," Peters says. "This work links them and smaller events in terms of a forcing mechanism, and it also tells us something about who survives and who doesn't across these boundaries. These results argue for a substantial fraction of change in extinction rates being controlled by just one environmental parameter."- Terry Devitt, (608) 262-8282, trdevitt@wisc.edu[sc1]The study starts in the Ordovician [sc2]100 years would refer to larger-scale changes in faunal composition

Plastics unite to make unexpected 'metal'* 18:00 15 June 2008

* NewScientist.com news service* Colin Barras

Jamming the right two pieces of plastic together creates a thin but strongly conducting channel along the junction that acts like a metal, say Dutch researchers. The discovery could lead to a whole new way of making electronics from non-metallic materials, and even new superconductors.

Alberto Morpurgo's team at Delft University of Technology in the Netherlands attached a micrometer-thick crystal of the organic polymer TTF to a similarly thin organic crystal of the polymer TCNQ.

The thin, flexible crystals conform to each other's shape and stick together due to van der Waals forces, says Morpurgo.Metal surprise

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Both TTF and TCNQ are electrical insulators. But Morpurgo's team found that a 2-nanometre-thick strip along the interface between the two crystals conducts electricity as well as a metal.

It was known that a blend of the two materials could conduct electricity, but it does so relatively poorly.

When laid side-by-side the two materials are physically unchanged, but the way electrons behave is subtly altered along the interface where the different materials are in close proximity, says Morpurgo. In tests, they tried cooling down the combined materials, expecting the odd behaviour to disappear because the two plastics become more insulating at lower temperatures.

Instead the interface became a better conductor, just as metals offer less resistance to electricity when they are cooled.

Usually the electrons inside each of the materials are unable to travel freely. But Morpurgo thinks that at the interface electrons from the TTF molecules are able to jump over to vacant spaces known as "holes" in the TCNQ molecules.Interesting properties

The result is that, in the 2-nm gap between the molecules of the two different materials, they can travel freely, allowing current to flow. "Such an electron-hole system is really something new and it may have interesting electronic properties," Morpurgo says.

Jochen Mannhart at the University of Augsburg in Germany agrees. "You do get exciting things happening at interfaces – physics at interfaces is responsible for the behaviour of semiconductors, for instance."

But the TTF-TCNQ interface conducts electricity much better than standard semiconductors. "The electron concentration there is an order of magnitude higher," Mannhart says. "That has the power to create new effects, from magnetism to superconductivity." Journal reference: Nature Materials (DOI: 10.1038/nmat2205)

The Face of Fear ExplainedBy Clara Moskowitz, LiveScience Staff Writer

An image showing four different facial expressions (clockwise from top-left: fear, disgust, sadness, happiness). Overlaid on top of each expression is a set of vectors (arrows) indicating how the facial features move from the neutral pose. Larger movement is conveyed by red-yellow arrows. For example, the eyebrows raise in fear relative to neutral. Credit: Susskind et al.

Everyone knows the face of fear.Upon beholding the chainsaw-wielding ax-murderer in a slasher movie, the damsel in distress usually widens her eyes

and flares her nostrils in horror.It turns out this expression isn't merely for cinematic effect, but actually serves a biological function, scientists have

found, by altering the way our senses perceive the world.An image showing four different facial expressions (clockwise from top-left: fear, disgust, sadness, happiness).

Overlaid on top of each expression is a set of vectors (arrows) indicating how the facial features move from the neutral pose. Larger movement is conveyed by red-yellow arrows. For example, the eyebrows raise in fear relative to neutral.

Credit: Susskind et al."Our hypothesis was that different changes on the face would lead to different amounts of sensory intake," said Joshua

Susskind, a psychology graduate student at the University of Toronto who worked on a study testing the function of facial expressions. "The idea is that fear is for vigilance. You'd expect that changes on the face, such as opening the eyes, would be characteristic of fear, because you're trying to assess more information in your environment." Squinty eyes and pinched nose

To test this hypothesis, Susskind and his advisor, Adam Anderson, and colleagues took images of people's faces as they posed with expressions associated with fear and disgust. Using statistical models, the team analyzed the faces and found that the two expressions produced opposite facial effects.

The scientists then tested what function these facial changes served. They took various measures of sensory perception, such as volume of air intake, width of the visual field and peripheral vision, and speed of visual tracking. Across the board, the researchers found that when making fearful expressions, subjects breathed in more air, saw a wider field of view, and could visually track targets more quickly.

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"We found certain patterns in the ways faces change between fear and disgust," Susskind told LiveScience. "Those changes were very consistent with the idea that fear is expanding the sensory surfaces. Disgust seems to produce the opposite effect, contracting the sensory intake."

When pinching their noses and squinting their eyes in disgust, people simply saw and smelled less."We're claiming that these emotions oppose in appearance as well as function," Susskind said. "One is the need to take

in more information, and the other is the need to reject information."Darwin's idea

Darwin was the first to suggest that emotional facial expressions might have evolved for a reason."He suggested that they're not just symbolic or arbitrary — they have a purpose," Susskind said. "They increase the

likelihood that the animal or the species would survive."Darwin and others hypothesized that expressions such as happiness (smiling) and sadness (frowning) may serve a

social function, by communicating the internal emotion a person is feeling.Later scientists, such as Silvan Tompkins and Paul Ekman, discovered that the expression of emotions is strikingly

similar across cultures — horror and disgust look pretty much the same on the face of a New Yorker as they do on a Nigerian, and people from different cultures can recognize emotions such as happiness, anger and surprise on others' faces, even if they don't share a language.

The fact that emotional expressions seem to be universal led scientists to believe they weren't used only for communication and social purposes, but also served an additional adaptive biological function.Future studies

The new study may be the first to measure changes in sensory intake that accompany these facial expressions."As far as we know, we're the first to look at the actual consequences on intake of information," Susskind said. "It's

only been speculated before."The scientists don't believe their results are confined to the two emotions they tested. Other emotional face changes

may also serve biological functions."We'd like to see how this extends to other expressions," Susskind said. "Can you get a measurement of changes in

intake with anger? Perhaps you find you're narrowing your intake. We're not trying to say this is specific to fear and disgust."

Susskind and his colleagues would also like to test whether animals express emotions with similar facial changes, and whether these serve the same purposes in other species.

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