Health Meaning

The treatment of patients with gene therapies requires a safe vehicle to transport useful genes and adeno-associated virus (AAV) is widely considered one of the safest. But a new study shows that at least some human cancer cells treated with the virus develop abnormal chromosomes, raising concerns about the safety of long-term gene therapy AAV-based.

Some researchers thought was safer AAV for gene therapy than other so-called viral vectors, because AAV infection is common and causes no known adverse effects. AAV-based therapies gathering also adopted several safety tests. Yet it was unclear exactly how the virus supply and activates genes in human cells. Scientists wondered how DNA AAV jumped into the cell's chromosomes and if it's damaged by doing so.

To find out, geneticist David Russell of the University of Washington, Seattle, and colleagues studied the impact of AAV on genes in a culture cell line cancer. The researchers used a strain AAV adapted to output chromosomes when the cells are treated with a certain drug, bearing parts near the chromosome with it. Then analyzing the DNA sequences of these pieces of chromosomes, the team was able to reconstruct how AAV had altered the cell's chromosomes when inserting itself.

As reported in the February issue of Nature Genetics cell chromosomes had small parts missing or added where the virus itself had inserted. In a cell line of two different chromosomes had abnormally merged. Despite this connection, it is not known if the type of cells studied - a cancer cell line commonly used by researchers - somehow AAV allowed to cause additional damage. More tests on other types of cells is necessary, Russell said, to determine whether patients treated with AAV are at greater risk of chromosomal disturbance, which can lead to cancer.

The study raises a warning flag. "We'll have to monitor these patients" named in safety testing, says therapist Malcolm Brenner gene from Baylor College of Medicine in Houston, adding the results suggest that AAV vectors are probably not safer than other viral vectors currently used. However, Brenner adds, it is far too early to consider dropping AAV, as other evidence suggests it is safe.

Related Sites
Context gene therapy of the US Department of Energy
questions and answers on gene therapy of the National cancer Institute
animated gene therapy primer

For decades, researchers have struggled to find ways to help patients with Duchenne muscular dystrophy, a devastating genetic disease that kills most victims in their 20s . Now they have had some success in mice. The scientists found that by stimulating the production of an enzyme on the membranes of the muscle fibers, they can prevent Duchenne animals that would normally have the disease

caused by a missing or defective gene on the X chromosome Duchenne affects 1 5,000 children, almost all boys (women with a faulty copy of the gene are carriers). The gene codes for dystrophin, a protein that helps the muscle fibers attach to surrounding connective tissue. Lack of dystrophin causes progressive muscle weakness. While some research groups are working on gene therapy treatments, others have focused on approaches that would slow down the relentless disease.

neuroscientist Paul Martin and his team at the University of California, San Diego, believes that a solution might be to coax the body to produce more utrophin, a protein similar to dystrophin. There is a catch: dystrophin and utrophin are not usually found in the same parts of muscle tissue. The trick is the production of utrophin where dystrophin would normally. To do this, the team developed a strain of mice with multiple copies of a gene that produces high doses of a certain enzyme. This enzyme, called CT GalNAc transferase generates sugars thought to stimulate the production of utrophin and anchor the protein in place. The group then multiplied mice with men who had the disease and women who were carriers.

Strikingly, none of the children had any muscle degeneration. The analysis of muscle tissues showed the enzyme and utrophin dotted over the entire surface of each muscle fiber. Scientists still can not explain how to make more of the enzyme allows the propagation utrophin around. But the work demonstrates that even in mice that would normally Duchenne, improving the amount of utrophin can help build strong muscle tissue healthy, the team reports in the April 15 issue of Proceedings of the national Academy of sciences .

"This is really exciting," said neuroscientist Stephen Kaufman of the University of Illinois, Urbana-Champaign, who think an enzyme-based treatment may be easier to develop that therapy gene. The body is less likely to reject an enzyme, it is already in production, he said, compared with a foreign gene.

Related Sites
The Web page of Paul Martin
Muscular Dystrophy Association

BARCELONA - HIV infects 40 million people today around the world, will have a balance sheet even more this decade that previously thought, researchers said the surprisingly sober opening plenary session of the biggest AIDS conference ever held.

the first scientific presentation of the International AIDS Conference XIV, a week-long meeting that attracted 17,000 participants, here July 7 offered a big-picture perspective - and it was dark. Another 45 million people will be infected with HIV by 2010 unless the world steps up efforts to prevent transmission of the virus, said epidemiologist Bernhard Schwartländer the World Health Organization, citing an analysis he and colleagues published in July 6 issue of the Lancet . "One of the most disturbing trends of all," said Schwartländer the packed house, is the impact the virus is having on adolescents and young adults. Nearly half of newly infected people in the world are between 15 and 24

Schwartländer stressed that young children were walloped by collateral damage from the virus - and will probably hit harder in the future . Backing up his point is an analysis published at this meeting by the US Census Bureau, the Joint United Nations Programme on HIV / AIDS (UNAIDS) and other groups estimating that 13.4 million children under 15 have lost one or both parents to AIDS, and by 2010 that number will nearly double

These frightening trends are not just limited to developing countries :. Eastern Europe had little HIV 10 years ago, but now has more people infected than the whole of Western Europe, Schwartländer said. And he noted that some cities in the richest countries, including the US, have recently seen jumps in new infections. "The richest countries of the world are not immune to the growing epidemics either," he said.

"It is now clear that the AIDS epidemic is still in its infancy "said Peter Piot, head of UNAIDS. "This is the worst epidemic in human history."

Related Sites
The UNAIDS website
Conference's website XIV International AIDS

In another blow to the long-term hormone therapy prospects, the Medical Research Council UK (MRC) today set a term to a large British study planned to enroll at least 20,000 women. The decision is a direct consequence of the judgment of a similar trial in the US there are 3 months, which found that the benefits of the same combination of hormones outweigh the increased risk.

Researchers have long debated the pros and cons of "replace" hormones decline in postmenopausal women with pills. To the surprise of many, the National Institutes of Health recently decided to stop an important part of the Initiative for Women's Health (WHI), which tested a combination of popular hormone called Prempro. An interim analysis showed that hormones increased the risk of heart disease and breast cancer more they reduced the chances of osteoporosis, bone fractures, and colorectal cancer ( Science NOW, the July 9).

Initially, the leaders of the international study of long duration estrogen women after menopause (WISDOM), which began in the UK in 1999, said trial could continue. The results of the WHI have left enough room for scientific doubt, they argued, to continue the enrollment of women ( Science NOW, July 23). But two weeks later, the MRC Council overturned this decision and asked an independent committee to examine more closely. Now, that group concluded that WISDOM should stop too. The study of $ 32 million was already years behind because the enrolled women have proved much more difficult than researchers had thought, said the Chairman of the Committee, Ray Fitzpatrick of the University of Oxford. In addition, the results not expected before 2016, were unlikely to differ much from those of WHI, he said.

WISDOM researchers are "very disappointed" Janet Derbyshire, director of the MRC Unit for clinical trials, wrote in a press release. Richard Gray, who chaired the WISDOM of monitoring data and the Ethics Committee, called the "premature" decision. It is very unlikely that anyone will fund a similar randomized trial of hormone therapy in the future, he said, which means that questions about its effectiveness persist.

But WISDOM would continue ethically questionable, given the results of previous tests, says Elizabeth Barrett-Connor of the University of California, San Diego - and the increased risk would have made recruiting participants even more difficult. "It is simply not a glimmer of hope."

Related Sites
MRC press release about the decision, additional information about WISDOM
Learn more about the health of women stopped Initiative trial
of in the paper Journal of the American Medical Association with the results of the WHI study

Leave antiparasitic drugs just once a year could be enough to stop the spread of tropical parasite that causes elephantiasis of the deformity disease. The spectacular results, reported in December 5 number of The New England Journal of Medicine , suggest that a global campaign underway to eradicate the pest could be very successful.

Throughout the tropics, wired to cause big problems. They damage the lymphatic systems of tens of millions, causing painful limbs and genitals and swollen grotesquely in some people. Infection occurs years before the onset of symptoms, when mosquitoes transmit thousands of filaria larvae in the blood. Some of the larvae penetrate nodes and lymph vessels, where they can turn into thread-like worms that churn out up to 12,000 larvae per day. Mosquitoes that feed on an infected person continues the cycle.

Not good treatments exist for advanced elephantiasis but health workers learned in the 1980s only one annual dose of diethylcarbamazine antiparasitic: blocked blood larvae levels. In 1997, the World Health Organization launched a global campaign to eradicate the disease. As health workers were preparing researcher in tropical diseases James Kazura Case Western School Reserve University of Medicine in Cleveland, Moses Bockarie of Papua New Institute Guinea Medical Research in Goroka, and their colleagues began to give annual dose of diethylcarbamazine and other antiparasitic drug, ivermectin, residents of 14 remote villages in the highlands of Papua New Guinea.

The mass treatment strategy worked like a charm. After 4 years, the percentage of people infected with the larvae dropped from 47% to 1% in moderately affected villages, and 77% to 5% in villages heavily affected. local mosquitoes has also become less contagious mosquitoes biting had 97% fewer larvae. The percentage of infected 5 years children fell eightfold 5%. And most surprisingly, the annual drug treatment, which is designed to prevent new infections, elephantiasis even reversed in many patients.

"The study was terrific," says researcher Eric Ottesen of tropical disease Rollins School of Public Health at Emory University in Atlanta. It represents the first "proof of principle," he said, that give annual salaries of drugs to all community members could sufficiently reduce infection levels to make the peter disease for good.

Related Sites
Papua New Institute -Guinée, medical research
Background on lymphatic filariasis global Alliance for ending lymphatic filariasis
Background of lymphatic filariasis from the World health Organization

Less than a year ago, Swedish scientists have caused widespread concern among health officials and the general public when they detected high concentrations of acrylamide - a potent carcinogen in laboratory animals - in bread, potato chips and french fries. But a new study finds no link between dietary acrylamide and cancer in humans.

Acrylamide forms when the starch-based foods are baked or fried at high temperatures. Because the substance causes cancer in rats and mice, acrylamide is known to be neurotoxic in humans and is considered potentially carcinogenic to humans too. So far, however, no direct evidence supported this hypothesis.

Lorelei Mucci of the Harvard School of Public Health in Boston and colleagues at the Karolinska Institute in Stockholm studied the diets of 987 cancer patients and 538 healthy people. Based on detailed questionnaires, the team estimated the contribution of each of acrylamide. In what appears to be good news for junk food lovers, they found no link between acrylamide consumption and cancers of the colon and rectum, kidney or bladder cancer - the most common cancers associated with food carcinogenic. While Mucci warns that it is too early to declare acrylamide sure. "We do not want to generalize from these initial data," she said, citing the need to investigate links to other forms of cancer. The team reports its findings in the January 13 of British Journal of Cancer .

"There are many things in animal studies that pan when we look at the man," said Harvard University epidemiologist Eric Rimm's, which was not associated with 'study. "For me, it does not come as a surprise." However, he cautions that the study is not definitive, in part because of the lack of comprehensive data on acrylamide levels in various foods. And epidemiologist Lars Hagmar of Lund University, Sweden, added that the study may have been too small to detect risks likely involved with acrylamide minute. "I find conclusive study," said Hagmar

Related Sites
Karolinska Institute in Stockholm. The Research Network on Cancer
Harvard School of Public Health: Department of Epidemiology
University of Lund: Department of Occupational and Environmental Medicine
International Agency for Research on Cancer in Lyon, France

Scientists say they have shown for the first time in a live animal cells from bone marrow can become insulin-producing cells in the pancreas. They hope that this could be the first step towards developing a treatment for diabetes that do not require regular injections of insulin.

A team led by Andreea Ianus University of New York transplanted bone marrow cells from male mice into female mice whose bone marrow had been destroyed by radiation. The donor cells were engineered to produce a fluorescent protein (GFP) they began to produce insulin. About 6 weeks after transplantation, the researchers discovered male cells (identified by their Y chromosomes) in the pancreas of females. Cells produced to insulin and other substances associated with the pancreatic beta cells. They report their findings in the March Journal of Clinical Investigation.

The work is "fascinating" and "important ... if it turns out to be right," said Douglas A. Melton diabetes researcher at Harvard University. Other researchers, like Markus Grompe Oregon Health Sciences University in Portland, maintain a healthy skepticism. "many laboratories have studied pancreatic cells derived from bone marrow and not seen similar results," said Grompe, who wonders if the insulin signals a sign that the donor cells fused with simply producing beta cells resident insulin instead of turning into beta cells themselves.

Ianus and his colleagues, however, believe they have excluded this possibility. Co-author Mehboob Hussain said that they tested for fusion by inserting the male marrow cells in females whose beta cells contained an inactivated form of GFP. Male cells contain no GFP but had an enzyme that activates the inactive form of the GFP. Cells not shine, indicating that the cells of the male marrow had not fused with the beta cells of women.

High hopes are riding on the next experience, which is whether the marrow cells will actually restore insulin in a mouse model of diabetes. Although the rate of production of new cells is low in experiments with non-diabetic mice, Hussain predicts that the new beta cells production rate will be much higher in the damaged pancreas.

Related Sites
Information on diabetes from the National Institute of Diabetes and
Digestive and Kidney Diseases
pancreatic physiology Overview

a recently discovered peptide can prevent iron accumulation associated with a common genetic disorder, a new study. The disorder called hereditary hemochromatosis, affects one in 0 to 300 people, making it the largest of all known genetic diseases. The study points the way to new treatments for the disease.

Although iron deficiency is the worst nutritional problem in the world, it is possible to have too much of a good thing. Patients with hereditary hemochromatosis - most of which have two defective copies of a gene called HFE - absorb excess iron from their diet, overloading their bodies with metal, which can lead to lesions of large scale organ. Although the precise role of HFE in the iron flow control remained mysterious, scientists have suspected that the answer may come from a kind of "iron hormone," predicts a molecule to relay signals from the liver - which detects iron levels in the blood. - intestinal in particular, a hormone that can inhibit iron absorption could help explain what goes wrong in hereditary hemochromatosis, because the loss of such hormone probably lead to excessive iron absorption.

Now, a team led by Sophie Vaulont, a molecular biologist at the Cochin Institute in Paris, provided strong evidence that the long sought iron hormone hepcidin is. This small peptide is expressed at abnormally low levels in patients with hereditary hemochromatosis. previous work by the group and other Vaulont had shown that high iron levels trigger the liver to hepcidin and high hepcidin lowers the amount of iron in the body. In their current paper, published online this week by Nature Genetics Vaulont, Gaël Nicolas postdoctoral researcher, and colleagues tested the importance of the low production of hepcidin in hereditary hemochromatosis. They treated mice, which like humans with the disease had defective copies of HFE gene by adding a gene for hepcidin. Mice without the added gene showed the accumulation of iron toxicity characteristic of the disease, but the livers of mice with the transgene showed "no iron accumulation whatsoever," said Vaulont. And that, she says, means a lack of hepcidin really causes hereditary hemochromatosis.

"It is a very interesting document and important," said Hal Drakesmith, a molecular biologist at the Weatherall Institute of Molecular Medicine in Oxford, UK It is appropriate that hepcidin could "in theory" provide treatment . of hereditary hemochromatosis That would be a dramatic step beyond the current treatment of choice - old but effective -. from bleeding, periodic removal of the patient's blood to remove excess iron

Related Sites
the CDC page on iron overload and hemochromatosis
the American Society hemochromatosis
hemochromatosis National digestive diseases information Clearinghouse

A controversial theory that the AIDS epidemic was accidentally started by Western health workers in Africa has been severely compromised by a new study of the origins of HIV. The results show that viruses like HIV can jump between closely related primates that eat each other, indicating that African markets in which monkey meat is sold could be a source of new diseases.

Stalking the evolutionary history of HIV has been a thorny issue. In 1999, researchers showed that the nearest ancestor of HIV-1, the most common of the AIDS virus, is a virus called SIVcpz, which seems to produce no symptoms in African chimpanzees. A controversial theory holds that vaccines against polio administered in Africa in the 1950s were accidentally tainted with SIV virus which then mutated humans to become HIV-1. Many scientists have criticized the improbable idea, but there was little evidence for alternative channels of transmission.

reports in the June issue 13 Science , a team led by Paul Sharp, an evolutionary biologist at the University of Nottingham, UK, argues that chimpanzees were HIV-1 virus precursor eating monkeys. A comparison of the amino acid sequences of four SIVcpz protein with other SIV strains reveals that SIVcpz was created by the merger of two strains that infect monkeys.

Like humans, chimpanzees are omnivores that hunt other animals when they can. The team says that chimpanzees could have been infected by eating freshly killed monkeys, leaving the two viruses mix their DNA. It is not known if SIVcpz mutated into something closer to the HIV-1 before or after being transmitted to humans. But what is clearer than ever, says Sharp, is that the virus can jump the line here.

"I am totally convinced," says Eddie Holmes, an evolutionary biologist at the University of Oxford, UK "It shows that the butchering of animals is really a viable mechanism of viral transmission." L the study also avoids the theory that HIV was introduced by vaccination against polio, Holmes says, as chimpanzee meat sold in Africa is generally infected with SIVs.

Sites Related
home [Sharp
UN Web page on chimpanzees and the impact of their hunting

Researchers have developed a unique vaccine against the West Nile virus that puts the disease in mice. The vaccine, which uses a small cousin of the West Nile virus to stimulate the immune system, joins two other experimental vaccines that could one day prevent infection in humans.

The epidemic of West Nile has spread to 32 states, Mexico, and much of Canada. Although most people exposed to West Nile virus to escape unharmed, in 02 alone, the virus sickened 284 and killed 4156 Americans, causing brain infections. There are no drugs to banish the virus people, and to date no vaccine to prevent it. Several vaccine candidates have been developed, including a virus, yellow hybrid West Nile fever, which took place off the disease in monkeys, and a Nile virus hybrid Western-dengue has prevented in mice ( Science NOW March 5, 02). Virologists and Roy Hall Khromykh Alexander of the University of Queensland in Brisbane, Australia, instead working with a well-studied and harmless cousin of the West Nile virus called Kunjin virus.

Because the genome Kunjin virus is almost a carbon copy of the genome West Nile, and it causes only the mildest symptoms, it seemed like an ideal candidate for a vaccine. To make sure it was harmless, the researchers made a copy RNA to DNA virus genome and tweaked a gene to make it even safer virus. Low doses of the injected DNA in the mouse thigh muscles caused them to produce antibodies that neutralize both Kunjin and a virulent strain of West Nile virus in test tube experiments. Then the vaccine has passed the acid test: When the researchers injected what would have been lethal doses of West Nile virus directly into the brain of mice immunized, almost all have been protected

Thomas Monath of OraVax Cambridge, Massachusetts. , Company that developed a vaccine against yellow fever in the hybrid competition, called the work "elegant" but wondered whether the weakened virus would provoke an immune response strong enough to protect monkeys and human expansion. Diane Griffin virologist at Johns Hopkins School of Public Health, however, welcomed the new contender; because other vaccine candidates can not take place, "it is good to have other candidates in the wings."

Related Sites
CDC West Nile homepage
virus inserts West Nile from the US Department of Agriculture

the best way to block the transmission of HIV during sexual intercourse is condoms, but men sometimes oppose use. Now, researchers have developed an idea to help women protect themselves, especially in developing countries. Their modified bacteria could be used to colonize the vagina and fight against the spread of HIV. But even if the approach promises to help women directly reduce their risk of infection, several obstacles stand in the way.

All women with HIV-combat Lactobacillus bacteria on the main site of HIV infection, says Peter Lee, a molecular biologist at Stanford University. These bacteria coat inside the vagina and excrete agents of lactic acid and hydrogen peroxide antimicrobial. To see if the capacity of Lactobacillus could be exploited, a team led by Lee and John Lewicki, a molecular biologist at Osel, a biomedical company in Santa Clara, California, inserted the virus gene -Kill human CD4 protein - molecular target HIV - in bacteria. CD4 is a membrane protein on human immune cells that HIV is anchored before infecting the cells. Lactobacillus engineered to secrete CD4 could block the virus from attaching to human cells, they reasoned.

The technique shows promise, at least in vitro, they report online this week in the Proceedings of the National Academy of Sciences . When mixed with human cell cultures, bacteria decreased infectivity of HIV-1 Appearance laboratory strain of 95%. Although the technique does not work as well with wild strains, experiments provide "proof of principle," says Lewicki. He and Lee are now trying to make the most effective technique for engineering Lactobacillus to express CD4 on its surface. These bacteria, they say, could collect HIV and kill them with his lactic acid and hydrogen peroxide. Eventually, the team hopes to concentrate engineering Lactobacillus in a vaginal suppository. Osel is already a product using unmodified Lactobacillus (to fight against vaginal infections), but approval of a basic modified bacteria to treatment could be tricky.

"I think this is a good approach in principle," said Ed Berger, a molecular biologist at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, because it is potentially cheap to produce, discreet to use, and above all "controlled by women." However, there are obstacles to overcome, said Berger, as to ensure that the alteration Lactobacillus is surpassed by natural Lactobacillus or cause inflammatory reactions.

Related Sites
bacterial pills Osel
The search for new ways to fight against HIV

SEATTLE - Cancer cells are a mishmash of DNA damage: broken chromosomes, rearranged bases, chromosomes or too short too long. But despite the wealth of observed associations between DNA damage and tumors, scientists are just beginning to understand the genetic accidents that result in tumor progression. Now, a team found that mice with defects in DNA repair are especially prone to tumors.

A crowd of insults can damage DNA, ultraviolet light or certain chemicals to defects in the own ability of DNA to replicate. Cells have two repair options closely related: the shift repair and proofreading, each based on a separate group of enzymes called polymerases. It was ten years ago, scientists linked mutations in mismatch repair genes to a rare cancer called hereditary colon cancer without polyposis. But no other human cancers have been linked to DNA repair replication defects.

Bradley Preston, a pathologist at the University of Washington, Seattle, wondered whether defects in proofreading, another repair mechanism, could also faster tumors. He and his colleagues created mice with defects in one of the two DNA polymerases critical for replay. He compared those animals with another strain of mice with defects in mismatch repair. All three died of cancer, but not the same: A defective-replay strain succumbed to skin cancer, while other gastrointestinal tumors developed, such as mismatch-faulty strain

Next the Preston group mated mice. generate animals with defects in both repair mechanisms. The mice that were homozygous - in other words, animals that had inherited the defective gene from both parents - for both defective mismatch repair defective and were not born at all. Most striking were homozygous animals for mismatch repair and heterozygous for proofreading; all died of cancer, most lymphomas, 3 months of age. DNA in their cells mutated 0 times more often than normal, Preston reported here since February 13 at the annual meeting of the AAAS. "It is the highest mutation rate we've ever seen," he said.

"It is the first real evidence" that the DNA polymerases disruption can cause cancer, said Lawrence Loeb, biochemist at the University of Washington. the backup job the idea that the difficulty in repairing defects in DNA replication can cause cancer in mice, said Preston, and he and others are on the lookout for human cancers that follow this model.

Related Sites
homepage Bradley Preston
DNA repair Context

exposure to insect repellents may be the decrease in the size of newborns? A new study suggests that happening in New York until two pesticides were banned 4 years ago. But the link is confirmed yet.

Scientists worry low birth weight because it correlates with a host of misdeeds such as low IQ. Maternal smoking is a factor that can lead to smaller babies, and pesticides are a suspect. In 1998, researchers from Columbia Robin Whyatt University Frederica Perera, and co-workers tested the umbilical cord blood of 314 babies Dominican and African American mothers for levels of chlorpyrifos and diazinon, organophosphates that have until was recently found in sprays insecticide home.

In a paper published online this week by Environmental Health Perspectives ( EHP ), the team reports that infants with levels of pesticides were higher shorter and weighed, on average, almost a quarter of a kilogram less than those with no signs of pesticides. Most striking among babies born after the ban took effect, blood levels decreased and the link with birth size have disappeared. "This is evidence of a relationship of cause and effect" - as has already been shown in animal studies, said Perera

Others are more cautious .. Epidemiologist Matthew Longnecker Institute National science environmental health points out that no association between chlorpyrifos exposure and birth weight was found in two new studies in the press EHP , one in California and one in new York City. But the University of California, Berkeley epidemiologist Brenda Eskenazi, who led one of them, says he has found a link between organophosphate biomarkers in the urine of mothers and reduce the gestation time . She thinks that differences in exposure measurements may help explain the discrepant results. Still, she said, "the jury is still out" on the risks that pesticides pose to the developing fetus.

Related Sites
Center Columbia Children's Environmental Health
environmental Protection Agency chlorpyrifos page
page Natural Resources Defense Council on insecticides

NEW ORLEANS -. researchers have identified a compound in tears that appears to protect the cornea from infection by a microbe known. The results, presented here on May 26 at the annual meeting of the American Society for Microbiology, could help prevent eye infections in contact lens wearers or lead to new treatments.

A notorious microbe called Pseudomonas aeruginosa is the leading cause of eye infections in people wearing contacts; in severe cases, infection can lead to permanent vision loss. Previously, Suzanne Fleiszig, a microbiologist at the University of California, Berkeley School of Optometry, had discovered that the human tear fluid can prevent the microbe from cells of cornea damage or invasion. For this study, it has raised more volunteers tears ( "onions work well enough," she said) to find out which component of the chemical soup that makes tears is responsible.

Among the potential candidates Fleiszig and his colleagues tested was a group of molecules known as collectins name, some of which play a role in protecting the lungs against infection. Indeed, they found that one of these, called surfactant protein D (SP-D) is abundant in human tears. They also found that the protein layers mouse corneas. In Petri tests, both the human version and SP-D mice could reduce P. aeruginosa "the ability to infect cells of the cornea; but when SP-D was removed from the human tear fluid, tears are no longer offered any protection. Fleiszig now considering whether people who wear contact lenses have less SP-D on their corneas or lenses diminish somehow the activity of the protein.

"It's great," Harvard microbiologist Gerald Pier said after studying Poster Fleiszig the meeting. The risk of corneal infections is low for individual lens wearers, says Pier - but because many people wear contacts, it is still a big problem. "Discover why people are resistant when they are not wearing contact lenses is very important," he said. And SP-D, or something like it, could be used to prevent or treat infections of the cornea, he said.

Related Sites
The homepage of Fleiszig
home [dePier
more on Pseudomonas aeruginosa
How to prevent eye infections

PHILADELPHIA - Despite the name, not all "good" cholesterol can be good for everyone. In patients whose coronary arteries are clogged with plaques, up to half of the high-density lipoprotein (HDL), the particle that carries the good cholesterol, is chemically modified so that it can fight against the accumulation of cholesterol deposits, researchers reported here on August 25 at a meeting of the American Chemical Society. The new work should lead to improved diagnosis of heart disease, as well as new drugs that prevent atherosclerosis by blocking the damage to HDL.

The research is an offshoot of efforts to find better ways to track heart disease risk. Last year, Stanley Hazen, a physician and chemist at the Cleveland Clinic in Ohio and colleagues identified two chemical fingerprints that were much better than existing markers to highlight the risk of heart disease a person . The first of these markers was myeloperoxidase (MPO), a key enzyme that immune cells use to fight microbial invaders. Of the patients who need emergency care for chest pain, those with high levels of MPO had a higher short-term risk of heart attacks, bypass surgery, or death. The second was a set of proteins modified by the addition of a chemical group known as nitrotyrosine, a reaction which can be carried by MPO and other compounds. Patients with high levels of nitrotyrosine these modified proteins were more likely to have atherosclerosis. Hazen's group wanted to know if a particular protein is more likely than others to be hit with nitrotyrosine.

They found that the preferred target of DFO is apolipoprotein A-1 (ApoA-1), the primary HDL protein. And when they looked at blood samples from 0 patients, half with and half without cardiovascular disease, they found that patients with lots of apoA-1 were changed 16 times more likely to belong to the group with heart disease . However, currently used clinical markers - cholesterol and C-reactive protein - are far worse to predict disease. The results also appear in the current Journal of Clinical Investigation . Hazen suggests that when DFO reacts with apoA-1, it changes the protein to one or more key sites interfere with the ability of the protein to transport cholesterol out of cells and eventually leading to atherosclerosis.

"This is very exciting," said Ian Blair, a disease biomarker expert at the University of Pennsylvania in Philadelphia. "He seems to have a biomarker that is much better than existing biomarkers for diseases cardiovascular. "Moreover, he adds, for the first time the new work provides a clear molecular mechanism that explains why high HDL levels may not always have a protective effect against heart disease. Hazen said his group and others are already working on the follow-MPO diagnostic, and pharmaceutical companies are looking for compounds to inhibit MPO and prevent HDL deactivation.

Related Sites
Stanley Hazen's website
atherosclerosis bases of the American Heart Association
cholesterol bases of the American Heart Association

Malaria infects 30 million pregnant women annually, causing anemia and other problems that kill about 0,000 newborns. researchers have now identified a protein that the parasite needs to infect the placenta -. a first step toward a vaccine that could prevent malaria in pregnant women

Most adults who live where malaria is endemic have developed immunity. Exceptions are pregnant with their first or second child; a particular strain of parasite infects red blood cells and causes them to accumulate in the placenta of women, leading to severe malaria, premature births, low birth weight infants and stillbirths.

In 1995, researchers found the first clues as to why these women were vulnerable. In pregnant women, infected red blood cells stick to chondroitin sulfate A (CSA), a sugar molecule made by the placenta. To find out how they stick, Thor Theander parasitology from the University of Copenhagen in Denmark and colleagues studied the genes of the parasite that are transformed in the presence of CSA. They reported in 03 that a gene called VAR2CSA , which encodes a protein that the parasite membrane inserts on the red-blood-cell, the regime when he meets CSA.

To see if the parasite uses its protein to make VAR2CSA infected red blood cells stick to the placenta, the researchers made antibodies against VAR2CSA rabbit, then labeled with a dye. Dye-labeled antibodies VAR2CSA glued to stains on the surface of infected red blood cells that bind to CSA - circumstantial evidence that VAR2CSA was in the right place to do the job. antibodies isolated from the blood of infected pregnant women stuck Dye scored exactly the same places, showing that humans, too, could produce antibodies targeting this protein

Women with fewer antibodies -. and therefore a lower immune response - against VAR2CSA were four times more likely than women with high levels of antibodies to give birth to children seriously underweight, suggesting that they did not fight off the parasite and, the report of the team in the November 1st issue of the Journal of Experimental Medicine . Because VAR2CSA gene is widely conserved among parasite strains, researchers believe a vaccine containing part of the VAR2CSA protein could make an effective vaccine against malaria associated with pregnancy.

"It is final, high quality work that checks the target of a vaccine" against malaria associated with pregnancy, says molecular parasitologist Kirk Deitsch of Weill Medical College of Cornell University in New York. The specific strain vaccine strategy could also work to prevent P. falciparum brain infections, he said, which means that "you can eliminate two of the three leading causes of death by malaria."

Related Sites
Facts on Malaria in Pregnancy Centers for
More information on malaria associated with pregnancy of the World Health Organization Disease Control and Prevention

many widely used pesticides may have unpredictable effects on wildlife as they degrade in the environment, a new study suggests. Chemicals that make up these pesticides are chiral, meaning that they occur as two identical but mirror structures. The researchers who conducted the new study found a "dramatic difference" in toxicity and persistence between chiral, and argues that regulators should therefore consider chirality when the pesticide risk assessment.

Although mirrored versions, or enantiomers of a molecule has the same chemical properties, they can interact with enzymes in different ways. There are about a dozen years, researchers noted that microbes tend to preferentially break down specific enantiomers of persistent pesticides such as DDT and other pollutants. Therefore, the enantiomeric ratio of these pesticides has become asymmetrical in some food chains. The researchers also showed that the enantiomers may vary in their toxicity, although most of this work has been done in the chemicals banned.

Chemist Jay Gan and colleagues at the University of California, Riverside, have decided to examine the pesticides that are widely used today. They examined five common insecticides, including organophosphates such as profenofos, and synthetic pyrethroids, such as permethrin. For all these compounds, one of the enantiomers is at least 10 times more toxic than the other Daphia, a small crustacean often used to assess toxicity.

The researchers also found that the enantiomers differ in two organophosphorus they persist in sediment. For example, one enantiomer of permethrin has become almost twice as common as the other during a year, they report online today in the Proceedings of the National Academy of Sciences. This means that the environmental impact of these pesticides may depend on the behavior of a particular enantiomer, the team concludes. "The difference in terms of risk assessment and regulation could be pretty drastic," Gan said.

Derek Muir National Research Institute on Waters in Burlington, Canada, agrees that the variation of the enantiomers can play a big role in determining ecotoxicity. selective degradation "is important for the risk assessment of pesticides to non-target organisms," he said. The key is that regulators can not get the true picture if they do not take into account changes in the ratio of enantiomers and their individual toxicity, says chemist Charles Wong environment at the University of Alberta in Edmonton, Canada.

Related Sites
the basics isomers, enantiomers, and the like
a recent meeting session on chiral pollutants
information on pesticide regulation

How do you treat an infection that robs the body of iron? The simplest answer - with more iron - may not be the best, according to a new study. hookworm infected animals fed moderate amounts of iron became sicker and more anemic than those who eat very little iron. The results may have implications for how doctors treat these infections in humans.

740 million people are estimated to be infected with hookworm, mainly in tropical regions of the developing world. The worms usually enter the body through the skin (often burrowing through the bare feet of children playing in the dirt) and wriggle their way to the intestines. There they hang and begin to suck blood and nutrients. Untreated infections can lead to growth retardation, learning difficulties, malnutrition and severe anemia. Many victims have already anemia to begin with, however, because of low levels of iron in their diet or other infections such as malaria.

To see if being anemic increases the severity of hookworm infections, researchers at Yale School of Medicine hamsters infected with hookworms. During the infection, the animals were placed on diets containing standard iron or low levels. To the surprise of researchers, after 20 days the standard diet hamsters were nearly 10 times more worms in their intestines that hamsters low iron content. Hamsters on a diet with intermediate levels of iron were even worse, reports the team in the January issue of Infection and Immunity .

iron supplements People with hookworm infections are often given to deal with their anemia, but this could be a mistake, says study author and specialist Michael Cappello disease . He said the relationship between the levels of iron and hookworm infection intensity resembles a bell curve: At levels of very low and very high iron, the parasite is not great, but he raged at levels intermediaries. Cappello suspects that high iron levels can poison hookworm, and a low level of iron prevents worms to develop into their adult form of sucking blood. Stimulate people infected with moderate iron levels with supplements could put them in the ideal range for hungry hookworms, he said.

Parasitologist and pediatrician Peter Hotez of George Washington University in Washington, DC, warns against taking too much of the results in hamsters severely restricted iron, noting that low iron content in the blood is associated with devastating problems for children and pregnant women. But he notes the study is in line with results in humans that suggest iron balance is essential to ward off the worst effects of hookworm infection.

Related Sites

• WHO info on hookworm infection
• Plans for a vaccine against hookworm
• More information about iron deficiency anemia

With products of nanotechnology worth over $ 32 billion already on the market, the United States needs to develop a systematic approach $ 50 million-a force -Year to investigate the risks of nanomaterials to human health and environmental safety potential. This is according to a report released today by Andrew Maynard, scientific director of the Woodrow Wilson Center for International researchers Project on Emerging Nanotechnologies in Washington, DC But at least one federal official who helps coordinate nanotechnology research says that a large part of what the report calls is already being done.

nanomaterials have long been cherished in the world of research because of their small size gives them unique chemical behavior of light emission, electric, and. But because these particles can get inside cells, toxicologists must take a careful look at their security ( Science NOW, June 15). The National Nanotechnology Initiative United States (NNI) currently spends about $ 11 million per year in research that is "very relevant" to the environmental health and safety (EH & S), a fraction of its budget more $ 1 billion, according to the report. Critics argue that the security effort is not well coordinated. "People are everywhere, doing a little of this and a little of that," said David Warheit, a toxicologist at DuPont in Newark, Delaware. . This ad hoc approach creates "significant knowledge gaps" about the fate of nanoparticles, said Maynard "At best, these gaps create uncertainties - and the worst dangers - for workers, businesses, consumers, investors and insurers. "He adds

Maynard argues that the federal government needs a comprehensive global strategy and define research priorities. first, they would be designed to measure human exposure and environmental nanomaterials and their toxicity. Ultimately, the goal is to accurately predict the impact of hundreds of nanomaterials being developed around the globe. the process should be conducted by federal agencies with a clear mandate to oversee EH & S risks such as the environmental protection Agency. research should also be coordinated at the international level, and the costs should be shared with the industry where possible.

Paolo Gargini, director of technology strategy of Intel Corporation, a leading manufacturer of semiconductor chips in Santa Clara, California, calls the new report "an important contribution to building much needed consensus around the need for targeted research on the implications and applications of nanotechnology. "Clayton Teague, director of the US National nanotechnology Coordination Office to help coordinate research efforts between the 25 organizations financing participating in the NNI, agrees. But he argues that the current funding EH & S is $ 44 million rather than the Maynard estimate of $ 11 million, and that agencies already cooperate to establish research priorities and even finance joint research projects. Teague said the agenda EH & S coordinated federal should be described in a report to be published in the next two months.

Related site

• The

If you want to protect people against malaria, the disease keep on mosquitoes. It is an interesting approach, but its implementation is more difficult than it sounds: In nature mosquitoes malaria-free tend to be less well than their susceptible counterparts. Enter a genetically modified mosquito to fight against the disease. A new study, transgenic insects beat mosquitoes nonengineered when both feed on the blood of infected parasites. If confirmed, the study means that the plans to replace the entire populations of mosquitoes with those resistant to disease may have better chances of success.

After mosquitoes bite a host with malaria, the parasite that causes the disease proliferates in the insect, is preparing to infect the next human victim. It is not fun to be infected, and one would think that mosquitoes have developed resistance to the malaria parasite over time. But several studies have suggested that mosquitoes designed to build defenses against malaria are less fit than the insects that have chosen to live with pests.

Now it is necessary to take heart. It several years ago, a group of medical entomologists at Johns Hopkins University has created a strain of Anopheles stephensi (a mosquito that bites rodents) with a gene called SM1 makes the mosquitoes resistant to infection Plasmodium berghei , a parasite of rodents malaria. In the new study, published online this week in Proceedings of the National Academy of Sciences , the group conducted a series of experiments in which 250 of these insects were placed in a cage with 250 counterparts wild type and allowed to feed on mice infected with malaria. Resistant insects lived longer and produced more eggs than those who lived not resistant to the parasite, and after nine generations, some 70% of the population was resistant. Researchers think the realization SM1 is a cheaper strategy than what the defenses against mosquitoes resistant to malaria develop in nature.

Yet the apparent benefits of resistance may not be large enough to help the spread of genes in a population in the wild, where all hosts are infected, says co-author Jason Rasgon. However, he said the study is the first demonstration that natural selection can help, rather than harm, genetically insects. And mosquitoes with SM1 gene could help keep malaria when he was licensed from an area using other means, such as bed nets, drugs, or future vaccine, he adds.

entomologist Bart Knols of Wageningen University in the Netherlands warned that the conditions of the cage are very different from those of the field where many other factors affect the survival of an insect; what is more, the results may not hold in the human malaria, he said. Yet it is "very encouraging" to see if mosquitoes engineering laboratory made in the edge of evolution, said Kenneth Vernick of the University of Minnesota

Related Site

• science story about mosquitoes resistant malaria

scientists are excited about what they see as a possible breakthrough in the treatment schizophrenia: the first human trials showing the effectiveness of a new class of antipsychotic drugs. The study represents the "leading edge of a new generation of drugs" for schizophrenia, says Yale University researcher John Krystal drug.

During the last half century, many drugs were developed to treat schizophrenia, which affects about 1% of the population but each of them have activity on the same target.. the dopamine D2 receptor the "dopamine hypothesis" is based on the fact that the excess of dopamine causes psychosis.

in recent years, however, scientists have been probing another theory, the "glutamate hypothesis." Glutamate is the major excitatory neurotransmitter in the brain and activates other neurochemicals. The theory is that the low activity in some type of glutamate receptor (NMDA) paradoxically leads to excess glutamate also damage the brain connections. This results in psychosis, thought disorder, and numbing of emotions associated with schizophrenia. In animal studies, compounds that act on glutamate receptors appear to block the effects of amphetamines better than do most conventional drugs mimicking psychosis.

In an article published online Sunday Nature Medicine , researchers from Eli Lilly and Co. in Indianapolis, Indiana, have shown that these compounds work in humans too.

The team, led by Sandeep Patil and Darryle Schoepp, compared a compound called LY140023 both placebo and conventional antipsychotic olanzapine. The randomized trial included 118 patients with schizophrenia who spent four weeks closely monitored in hospital. More than a third of patients in both treatment groups responded with 25% or more reduction in symptoms using a standard scale - compared to only 3% in the placebo group. The difference between treatment groups was not statistically significant; However, those taking LY140023 did not show parkinsonian movement problems or weight gain, two side effects of conventional antipsychotic drugs.

"I could not exaggerate this exciting breakthrough," says Jeffrey Conn of Vanderbilt University in Nashville, Tennessee, who worked on medication for schizophrenia for Merck & Co. "It is the first clear demonstration that you can get an antipsychotic efficacy without inhibiting the D2 dopamine receptors. "Conn said the new drug may be targeting brain pathways" downstream "of those applied by conventional antipsychotic drugs. Thus, it is said it, the medicament "may be closer to the primary pathology" of schizophrenia.

Related Sites

• More information on schizophrenia
• More information about glutamate receptors and the hypothesis of glutamate

Federal regulators have given the green light to a test of arthritis gene therapy who was arrested last summer after that one patient died. New tests indicate that the therapy had no role in the death. The decision is a relief for gene therapy researchers who had worried about a potential new side of their field.

The trial by Targeted Genetics Corp. was arrested after the Death July 24 to 36 year old Jolee Mohr of Taylorville, Illinois, which received an injection of gene therapy to treat her rheumatoid arthritis in a knee 3 weeks earlier ( science , 3 August). During September 1 meeting of the Recombinant DNA Advisory Committee Federal (CAR), the experts noted that Mohr apparently died mainly from a fungal infection called histoplasmosis that his immune system was unable to fight ( Science NOW , September 17). Mohr immune system may have been compromised by a drug she was taking against arthritis, Humira, which blocks an inflammatory molecule called α tumor necrosis factor (TNF-a). The protein produced by the gene therapy is also a blocker of TNF-α, and if it spreads beyond the knee Mohr, combination with Humira can be left vulnerable to the fungus.

This was not the case, according Targeted Genetics. The company stresses the new test results from a survey conducted by the company and external researchers, which were presented at the American College of Rheumatology annual meeting earlier this month. The level of TNF-α blocker detected in the blood of Mohr with a binding assay was "well within the normal range expected" from the dose of Humira that she was taking, says President and CEO H. Stewart Parker. The new tests have also dismissed the idea that the gene therapy vector, adeno-associated virus reproduces in the body of Mohr. While the vector DNA turned in other tissues, the amounts were extremely low. Today, the company announced that the US Food and Drug Administration lifted the hold on the trial.

Others agree that the case is closed. "It does not look like gene therapy has been instrumental to the best of our knowledge," said the doctor Kyle Hogarth of the University of Chicago in Illinois, who treated Mohr and took part in. However investigation the Hogarth question whether it makes sense to include patients who are already taking TNF-blockers in the study, because it is difficult to distinguish between the effects of gene therapy product and drugs. Parker is disagreed, noting that rheumatologists say "there is a significant unmet need" for treatment for patients with joints that do not respond to systemic medications.

the company now plans to resume the trial of 127 patients but does give a second dose to as many as 35 patients waiting if they have a fever, as Mohr did. "We are being conservative," said Parker. She said the only change in the consent document will be lit to confirming death earlier. RAC will publish its final conclusions on the case at a meeting next week. RAC President Howard Federoff of Georgetown University in Washington, DC, declined to comment in advance of the meeting.

Related Sites

• Targeted Genetics press release
• Information 17 RAC meeting in September on the death arthritis

Although rapid famous, cheetahs can not seem to overcome a deadly disease called amyloid (AA) amyloidosis. The disease kills up to 70% of cats in captivity and has frustrated breeding efforts. In a new study, the researchers provide the first convincing evidence that could explain how the disease is transmitted.

AA amyloidosis resembles mad cow. Like mad cow, a misfolded version of a protein - in this case amyloid A - converts the normal proteins into abnormal, a process that snowballed into large deposits of damaging proteins in tissues such as the spleen and liver. (The protein mad cow did most of its damage in the brain and central nervous system.) The animals often die of renal failure and the incidence of AA amyloidosis has climbed from 20% to 70% cheetahs in captivity since the 1980s

AA amyloidosis is caused by a bacteria or virus, but there is reason to suspect that it can spread from animal to animal as a infectious disease. The mad cow and scrapie - a related disease in sheep - appear to be contagious. When captive cheetahs are kept in small enclosures close, AA amyloidosis strikes younger animals and with more severity, a finding that confirms the hypothesis of contagion. However, biologists have been hard to understand how the disease moves from cat to cat.

To examine potential routes of transmission, Keiichi Higuchi, a biologist at Shinshu University in Matsumoto, Japan, and colleagues isolated the AA protein from livers of infected animals. Of the protein, the researchers were able to develop a fluorescent marker, in other experiments, picked up the AA protein in the feces of diseased cheetahs. The discovery supports earlier studies that had marked feces as a possible route of infection for similar diseases in deer and mice. Furthermore, the AA protein in the feces was more transmissible and more effective in inducing the disease in mice that the protein isolated from the liver, probably because of its small size and greater instability, researchers report online today in Proceedings of the national Academy of sciences .

It is still unclear how captive cheetahs come into contact with the feces of another. Higuchi's team suspects that this may occur when cats lick their fur during grooming or when they eat food that has touched the contaminated soil. Based on their findings, the researchers suggest that zoos or breeding colonies in captivity can limit the spread of AA amyloidosis eliminating feces promptly or keeping animal food separate areas that have come into contact with feces. "These results provide possible measures to save the cheetah from extinction," says Higuchi. There are only about 12,500 cheetahs living on the planet today, he notes, so any cheetah death is a blow for survival of the species.

Sarah Durant, a conservation biologist at the Zoological Society of London and the Wildlife conservation Society in the United States, said limiting the spread of AA amyloidosis in captive animals is a good strategy. Although the disease is unlikely to affect the cheetahs release, she said that the conquest in captivity could raise awareness about the plight of wild cheetahs.

Related Sites

• More about cheetah diseases
• More information about cheetah conservation

Contagious cancer was sweeping the populations of Tasmanian devils, killing most adults. Now, young devils spawn earlier than ever before. But is this a case of rapid change or just a temporary response to a changing environment?

Tasmanian devil facial tumor disease resurfaced in Tasmania there about 10 years and now affects the majority of devils on the island ( science , 18 February 05, p. 1035). Lesions around the animal's mouth can reach a size of ping-pong balls and spread on the face; unable to eat, demons are starving in the months of the onset of cancer. The disease is highly contagious, and adults are particularly vulnerable, perhaps because the tumor cells are often spread during sexual contact. The problem was so devastating that the Tasmanian devils were declared a threatened species in May.

zoologist Menna Jones of the University of Tasmania has also noticed a surge in pregnancies 1 year devils. Normally, the animals, which live about 6 years do not occur before age 2. But when Jones and his colleagues gauged the age and reproductive status of demons - via tooth erosion and organ development sex - they have found evidence for the breeding of several months to a year earlier than normal at the four sites of the five studied. The proportion of first breeding females has reached an astonishing 83% in one place, the team reports this week in the Proceedings of the National Academy of Sciences .

The transition to early farming could be an evolutionary response, Jones said. By killing adults that breed after two years, the cancer could be genetic selection for younger breeding females, she notes. If so, the results would make the devil the first mammal known to rapidly evolve their reproductive modes in response to a disease.

Evolutionary biologist Nelson Hairston Cornell University is skeptical. Young devils may have started breeding early simply because they have better access to food and mates, now that fewer adults are on the scene. To really make the case for genetic evolution, he said, the team should demonstrate that the devils from zoos, for example, would not adopt early reproduction in response to more food and mates.

Hairston also note that scientists have shown the rapid evolution of mammals such as rabbits and sheep, but not in response to the disease ( science , 16 March 07, p . 1571). Thus, the history of Tasmania would not cause a change in our understanding of evolution. "But it would add a sexy example [of the phenomenon]," he said.

With reporting by Lauren Cahoon.

ROCKVILLE, MARYLAND - The first major epidemiological study of bisphenol A, a common ingredient in baby bottles and beverage containers, suggests that relatively high doses of the chemical double the risk of diabetes and cardiovascular disease. The result is presented as a Scientific Review Committee meets here to start the assessment of the Food and Drug Administration of the United States (FDA) draft risk assessment for the health of the compound.

Many laboratory studies have examined the health impact of bisphenol-A, but the results were contradictory. A concern is that the chemical binds weakly to the estrogen receptor. Some researchers have found evidence of rodent reproductive problems, developmental disorders, cancer and neurological problems, while others do not ( Science NOW, April 16).

A team led by David Melzer, an epidemiologist and physician at the Peninsula Medical School in Exeter, United Kingdom examined data from the US Centers for Nutrition Examination Survey, a representative sample of the general population Disease Control and National Health and prevention. Over 0% had detectable levels of bisphenol A in their urine.

Melzer and his colleagues then examined the levels of bisphenol A and health status for adults in 1455, sampled in 03 and 04. Divided by the amount of BPA measured in urine, those in top fourth had double the risk of type 2 diabetes and cardiovascular disease compared to those in the rest of the bottom. The levels of enzymes routinely used to diagnose liver problems were also higher, they report in tomorrow's issue of Journal of the American Medical Association ( JAMA ).

The logical link diabetes, Melzer said, pointing to recent animal and cell studies finding that BPA interferes with insulin production in mice. However, the increased risk of cardiovascular disease was a surprise, he admits. Approximately gauging exposure from urine levels Melzer suspect in the investigation adults with higher levels of BPA were still consumes much less than the current daily level considered safe by the FDA for adults ( 50 micrograms per kilogram of body weight).

The study was released early to coincide with today's hearing. An ad hoc advisory group of six scientists examined the draft of the FDA assessment of bisphenol A, released last month. In the evaluation, the FDA reviewed the current literature. Focus heavily on two major studies funded by industry, the agency decided that the current safety level remains adequate. He rejected many other animal studies, mostly by academics, as too small, inconsistent or unreliable. (This contrasts with a final report released September 3 by the National Toxicology Program, managed by the National Institute of Health Sciences of the environment, which found "minimal" to "some" concern when evaluating these studies.)

the JAMA paper is not included in the project evaluation, and some members of the panel were skeptical of the findings. "I fear that this article will let people with the message that BPA causes heart disease and diabetes, "says Garret FitzGerald cardiovascular biologist at the University of Pennsylvania School of Medicine in Philadelphia, which concerned the small sample size; only 79 people reported cardiovascular disease.

Environmental groups urged the panel recommended that the FDA considers JAMA paper, as well as the full range of animal studies, and to revise its calculation of a safety deposit high level. This is not a simple task. "How in the world do you put all these things together in a quantitative risk assessment?" Member of Philip Bushnell group Neurotoxicology division of the Environmental Protection Agency wondered aloud. The panel will report to the Scientific Council of the FDA by October 31.

A powerful cholesterol drug cut the incidence of heart attack and stroke in half when given to people with elevated levels of inflammation, as a? new clinical trial. The results have attracted much attention because people in the study had normal levels of cholesterol and therefore are not recommended cholesterol-lowering drugs. But the long awaited trial called JUPITER, also comes with notes; more importantly, it is unclear why the drug, Crestor, actually helped these people, and if and how it should change for disease prevention strategies.

led by Paul Ridker, a cardiologist at Brigham and Women's Hospital in Boston, the JUPITER study enrolled nearly 18,000 people who had normal levels of cholesterol and moderate or high levels of protein C reactive protein (CRP), a marker of inflammation in the blood. For about 2 years, half received Crestor, a powerful anti-cholesterol drug in a class known as statins, and half received a placebo. The trial was stopped in March, three years early because Crestor worked so well. Those who took it had 50% fewer heart attacks and strokes, and overall mortality was 20% lower than the placebo group. In absolute terms, however, the differences were quite small: 1.8% of those taking placebo, or 157 people, had a "cardiac event" during the study, compared with 0.9%, or 83 people, taking the drug. The drug also increased the risk of diabetes somewhat.

Crestor reduced LDL or "bad" cholesterol by an average of 50% and CRP 37%, the JUPITER running researchers reported Nov. 9 online in the New England Journal of Medicine and the meeting of the American Heart Association in New Orleans.

test "challenges ... how we do prevention," said Ridker. The fact that patients with CRP received Crestor - much like those taking medication for high cholesterol - means that doctors can use CRP levels to identify people at risk who are now sailing under the radar, said -he. This could help reduce the number of heart attacks and strokes in people with healthy cholesterol level.

Others believe that the situation is more nuanced and that CRP may be less important than JUPITER suggests. For example, it is unclear whether the benefits of JUPITER were entirely due to the decrease in LDL cholesterol, which has long shown to prevent heart disease, and lowering LDL and CRP. "We know there is a straight line of LDL cholesterol in cardiovascular risk," regardless of the starting number, said Mark Pepys of University College London, who has studied CRP for decades. LDL decreased to about 50% by JUPITER - a decline that is consistent with the 54% reduction of heart attack was observed, said Pepys. Although study participants were described as healthy volunteers, most also were overweight, 15% were current smokers, and 40% had metabolic syndrome. These risk factors, not CRP may explain why having more aggressive cholesterol lowering goals can help

Regardless, JUPITER confronts a problem that cardiologists have struggled for a while with nothing to see with CRP :. How to treat patients who have normal cholesterol levels, but some common risk factors such as high blood pressure or obesity. If these people are on statins, too, in order to even lower cholesterol? "I think [JUPITER] broadens thinking about risk factors," says Benjamin Scirica cardiologist at Brigham and Women's Hospital, who was not involved in the trial. Scirica, for his part, said that JUPITER "brings the target goal down to everyone" regarding cholesterol, and expects to treat more aggressive cholesterol now that it serves.

Fearing that the US Congress will force the hand because of public interest, the National Institutes of Health is moving to change its rules on conflicts financial interest for scientists who receive grants. A new set of regulations could be ready in 6 months to 1 year, according to Acting Director Raynard Kington NIH during a meeting Friday in Bethesda, Maryland. Last week, the NIH submitted a draft list of issues in the White House in which he wants public participation, which will help shape the new rules: -

How to determine whether "significant." a financial interest if the current definition, which exempts any financial dispute is less than $ 10,000, will be replaced by a stricter limit or no lower limit at all

- What NIH should strengthen its policy to make institutions respect by requiring independent confirmation of the institutions of reports

- What NIH should seek conflicts involving financial agreements between universities and businesses

- What NIH should require investigators to disclose any and all financial interests

the latter possibility prompted Christine Seidman, professor of medicine and genetics at Harvard medical School in Boston, to observe that the new requirements could mean that the amount of required paperwork to disclose the links financial could "quickly exceed the scientific content" of a grant application.

She spoke at a meeting of the Advisory Committee of the NIH director, which was distributed and will soon appear archived online. The questions will be published soon for public comment, officials said.

Current regulations require recipients of NIH to submit financial conflicts "important" to their institution, which must then report the conflict to the NIH and ensure it was managed or eliminated. This year the NIH has reviewed 20 cases of alleged non-compliance. Six are still under investigation, but so far, the NIH found a single case in which rules were broken: that of a psychiatrist at Emory University in Atlanta who failed to report payments that it has received from pharmaceutical companies and device.

The Ebola-Reston virus recently discovered for the first time in pigs in the Philippines, has now been confirmed infected at least a human being. Scientists are relieved because the person was not ill and is unlikely to have transmitted the virus to others. The virus is related to Ebola strains that caused the deadly hemorrhagic fever in humans in Africa. Ebola-Reston but did not cause serious disease in two dozen people previously infected by contact with monkeys dying from the viral disease. Officials are concerned about the discovery of the virus in pigs because farm animals live near humans and are thought to be "mixing vessels" in which animal viruses mutate in hazardous to humans.

The virus was known to be circulating in the Philippines since 1989, regularly appearing in deadly epidemics in monkeys. The virus was confirmed in pigs for the first time last fall, causing a survey jointly conducted by the World Health Organization, the United Nations Food and Agriculture Organization, and the Organization World Paris-based animal health. The person in the Philippines has been found that the disease was announced jointly by the ministries of health Philippines and agriculture January 23, stays healthy, and officials believe that it is extremely unlikely that the virus was transmitted to other humans. International and local experts are still trying to determine how the person was infected, if the virus causes disease in pigs, and if it is in wider circulation in pigs. Their findings will likely lead to recommendations to prevent pigs from being exposed to the virus.