Health Meaning

WASHINGTON, DC -. Amid a series of deadly attacks with anthrax, researchers today announced they have made significant progress in understanding the disease. Two studies presented at a press conference can stimulate the development of new drugs to prevent rapid death of inhalation anthrax.

Today, the tests confirmed that both Washington, DC, postal workers who died on Sunday, both suffered from inhalation anthrax; two others of the same mail sorting facility remain hospitalized with the disease, as does a third postal worker from New Jersey. Researchers believe they could save patients with inhalation anthrax if they had a way to block the deadly toxin produced by Bacillus anthracis . This toxin consists of three components, called edema factor (EF), lethal factor (LF) and the protective antigen (PA). This is primarily used to shuttle the two other macrophages, the cells that attack and kill.

Now, researchers from Harvard University and the University of Wisconsin, Madison, have identified the receptor on the surface of macrophages PA latches on. They do not yet know the natural function of this protein, called receptor toxin anthrax (ATR), but when they added a soluble version of ATR to macrophages grown in a test tube, it was able to bind toxin and block to enter the cells (see chart). This result gives hope that a drug might be able to 'clean' the toxin.

In another study, researchers from six institutions in the UK and the United States announced the three-dimensional structure of the LF. The structure may give researchers new clues for preventing LF macrophage killing and with it, patients, says lead researcher Robert Liddington of the Burnham Institute in La Jolla, California. Both studies will be published in the November 8 issue of Nature , but were made available online today.

The researchers acknowledge that their work, years away from producing new medicines, will be of little help in the current bioterrorist campaign. Yet studies can save lives in the future, said director Anthony Fauci of the National Institute of Allergy and Infectious Diseases, who spoke at the briefing. Fauci called the results "absolutely the most amazing, elegant science."

Related Sites

Both documents are available free here
recent science history of research on coal, including other ways to block the toxin ( science , 19 October 01, p. 40)
Page CDC with information on anthrax and updates about recent attacks
"anthrax as a biological weapon": a consensus statement published in Journal of the American Medical Association

Medieval as it may seem, scientists are testing a recipe of absinthe and iron on breast cancer cells, and so far the results are encouraging. In a new study, researchers report that artemisinin - a derivative of the wormwood plant - kills breast cancer cells enriched iron, but does not harm many healthy ones. destructive properties of artemisinin are triggered by above normal levels of iron in the cancer cells.

Many experiments have shown that artemisinin turns deadly in the presence of iron. Asia and Africa, artemisinin tablets are widely and in many cases successfully used to treat malaria, because the parasite has a high concentration of iron. Cancer cells can also be rich in iron because they often absorb the mineral to facilitate cell division. The cells provide an iron supplement with transferrin receptors, special reception points that channel the ore in the cell. Although normal cells also have transferrin receptors, cancer may have many more.

To test the effect of artemisinin on breast cancer cells, bioengineers Henry Lai and Narendra Singh of the University of Washington, Seattle, enriched separate normal breast cells and cancerous ones resistant to radiation with holotransferrin, a compound normally found in the body that transports iron to the cells. Then the team measured the cells with artemisinin. As reports in the November issue of Life Sciences 16 pairs, almost all cancer cells exposed to Artemisinin holotransferrin and died within 16 hours. The compounds killed just some normal cells. Lai believes that because of a breast cancer cell contains five to 15 more receptors than normal, it absorbs iron more easily and thus more sensitive to artemisinin attack.

"It looks very promising," said Gary Poser, an organic chemist at Johns Hopkins University in Baltimore, Maryland Yet he adds:.. "Other researchers need to replicate these findings" The next step, as the adhesive, is to treat a mixture of normal and cancer cells, instead of separating the two. Lai and others are also interested in the effect of artemisinin on other cancers.

Related Sites

abstract paper
Slideshow showing the absorption of iron in cells

Doctors prescribe morphine carefully. Patients quickly used to the powerful painkiller, and increasingly higher doses are needed to relieve pain. Now an article in the January 25 issue of cell shows that the development of tolerance in rats can be slowed by giving the animals a small amount of a second painkiller.

Many analgesics induce tolerance by decreasing the number of so-called opioid receptors, proteins on the surface of neurons and other cells that cling to the drug. With most drugs, these receptors - and the drug bound to them - are drawn into the cell through a process known as endocytosis. Some then recycled to the surface while others are destroyed. But morphine is different: The molecule remains on the surface, cradled in its receptor, and sends constant signals to the neuron

So how morphine induced tolerance.? Cell biologist Jennifer Whistler and colleagues at the University of California, San Francisco, decided to test the idea that cells with receptors stuck in the "on" position to ignore the signal unless the dose is increased. If there was a way to disable signaling, motivated researchers - eg using endocytosis periodically take the receivers out of commission. - Maybe they could prevent tolerance

The researchers dosed rats with a combination of morphine and a pinch of DAMGO, an opiate that triggers endocytosis. They then measured the morphine tolerance in rats by testing the sensitivity of their heat tails. All control rats on morphine noticed the heat by day 7 and would flick their tails out of the uncomfortable heat, indicating that the morphine was beginning to dissipate. But rats drugged with morphine and DAMGO remained unconscious. Tests on cells of the spinal cord showed that 10 times more opioid receptors in the group DAMGO were pulled inside neurons.

This is the first link between morphine tolerance and endocytosis receptors in living animals, says Brigitte Keiffer, studying the opiate receptors in the Louis Pasteur University in Illkirch, France. The work suggests that the addition of a component such DAMGO, researchers might be able to produce an analgesic that does not induce tolerance or dependence, she says.

Greene, Katie

Related Sites
homepage Jennifer L. Whistler
A page on the receptor mediated endocytosis

Surgeons could soon seal wounds difficult to reach using new son to change shape who know how to bind and never needs to be removed. The new biodegradable plastic fiber "smart" can be forged when heated to a few degrees above body temperature. The researchers say that the same material could be made to last much longer and one day be used for medical self-healing devices and shrink otherwise bulky implants -. Such as screws that hold the bones together

A growing class of materials have "shape memory" - they hold a form at a certain temperature and transform into another shape when heated. So far, none of these plastics have been used in medical devices, nor had any found to be biodegradable. The new material, described online April 25 in Science by the synthetic chemist Andreas Lendlein of mnemoScience GmbH in Aachen, Germany, and biomedical engineer Robert Langer of the Massachusetts Institute of Technology, is composed of two polymers, each already used separately in clinical applications such as drug delivery.

When combined, the two polymers react to temperature. The highest temperature form is "permanent" in the form of the plastic, which assumes after heating. After it cools down, the plastic can be stretched or crumpled into temporary forms up to four times larger or smaller than the permanent form. To make sutures, the researchers took a fiber of their shape-changing material and, after warming up for several minutes, cooled down and stretched. They used the loose sewing thread a wound on a rat. When heated to 40 ° C, tight suture with just the right amount of tension, avoiding damage to the surrounding tissue.

Medical devices that can fit into tiny holes in the body and develop forms designed with the request would be valuable, said Frederick Finelli laparoscopic surgeon at Medical Center of George Washington University in Washington, DC But he warned that the surgeons may feel uncomfortable not having direct control over the changing form implants. "If the size is predetermined and that you have it and you preheated then it turns out it is too small, what do you do then? These are the things the surgeons are concerned."

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changing the form of the son of Films
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Human embryonic stem (ES) cells receive no free pass of the immune system, unlike the early hopes of researchers. As the cells grow, they express increased levels of markers revealing the body uses to distinguish between native and foreign cells. This means that scientists hope to use the cells to treat Parkinson's disease, diabetes and other diseases have to worry about transplant rejection.

earlier evidence from human embryos raised the slim but tantalizing possibility that ES cells can be "immune privileged," unrecognizable by the body's defenses against foreign cells. One study reported that embryonic cells that give rise to ES cells express the so-called MHC proteins that help the immune system identify an invader; another produced inconclusive results.

Hoping a clear response, a team led by cell biologist Nissim Benvenisty of the Hebrew University of Jerusalem has sought MHC molecules in human ES cell lines. Researchers measured MHC molecules during three stages of development of ES cells using a fluorescent labeled antibody. As a control, they also tested a non-human ES cell line called HeLa. They found very low but constant expression of MHC class 1 molecules on ES cells undifferentiated, as they describe in a paper published online the week of July 8 by Proceedings of the National Academy science . However, as the differentiated cells, they stepped MHC protein production, but not as high as in HeLa cells.

The new findings lay to rest the hope that ES cells can stay under the radar of the immune system, said Hugh Auchincloss, a transplant surgeon at Harvard Medical School in Boston. But the news is not all bad, says Andrew Bradley, a transplant surgeon at the University of Cambridge, UK The relatively low levels of MHC expression could at least say that the tissues derived from ES cells would be less prone to rejection than whole organs transplants today.

Related site
website Nissim Benvenisty

in the beginning, it seemed impossible: a vaccine against the widely celebrated polio given millions of people in the 1950s were contaminated with a monkey virus - a virus that causes cancer in animals. But a report released Tuesday by the Institute of Medicine (IOM) soothes fears that the virus has caused a wave of cancer in the vaccinated population. It can be the cause of some rare cancers, but more research is needed to know.

some 40 years, SV40 was found in monkey kidney extracts used to produce the Salk vaccine. Since, concern grew that the vaccine may have triggered a cancer epidemic ( Science , 10 May, p. 1012). The virus turned cancerous cells cultured, and she kept causing tumors in animals. This heated debate in the last decade after researchers started finding SV40 DNA in four types of rare human cancers - it causes the same types in the animals - and press reports said that dozens of millions of people may have been exposed

the IOM committee examined all major epidemiological studies to see if people exposed to SV40-contaminated vaccine have a higher risk of developing cancer. Although the studies were flawed, the jury decided they were good enough to exclude a cancer epidemic. But it seems that millions of people may be infected with SV40, and the group concluded that the virus could very well come from the contaminated vaccine. Biological data also suggests but does not prove that the virus can sometimes cause human cancers. "We recognize that SV40 might at least have a carcinogenic effect, but epidemiological data do not suggest it actually did," said committee member of the IOM Steven Goodman, a biostatistician at Johns Hopkins School of Medicine in Baltimore . Despite this, he adds, "there is a body of evidence [on SV40 carcinogenicity] which must be taken very seriously."

Overall, the IOM report "really closes the book on focus "of past epidemiologic work, said pediatric oncologist Bob Garcea of ​​the University of Colorado Health Sciences Center in Denver. Although SV40 may yet turn to cause cancer in humans, the risk, if any, is" not remotely the stadium "well-known carcinogens such as tobacco smoke and asbestos, adds Goodman.

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IOM report
SV-40 and the vaccine against polio
Some causes of cancer

The researchers found that a variant gene in humans, common in Papua New Guinea, confers protection against malaria. At the same time, others have shown that the malaria parasite has multiple ways to evade this defense, casting doubt on efforts to find a single vaccine against the disease.

Plasmodium falciparum causes malaria by invading red blood cells, reproducing inside, then break open cells to release a new brood parasites. To enter the parasite corresponds to a protein on the outer membrane in a receptor protein on the surface of the blood cell, like a key in a lock. Researchers knew such a combination lock keys, and last year, several groups have identified a second possible "key" protein, called BAEBL or EBA140. Studies have suggested its corresponding "lock" could be a cellular receptor blood called glycophorin C.

In the January issue of Nature Medicine Alan Cowman parasitology at the Hall Institute of Medical Research Walter and Eliza in Melbourne, Australia, and colleagues demonstrate that EBA140 does indeed bind to glycophorin C. moreover, when they added antibodies to EBA140 to a mixture of noise and red blood cells, antibodies clung the protein, preventing extraneous to their insidious entry.

Cowman notes that the epidemiological work also seems to support a role for EBA140. In Papua New Guinea, an area plagued by malaria, nearly half of the population have a mutated version of glycophorin C, which makes them resistant to disease. The researchers showed that antibodies against EBA140 did not inhibit the entry into cells with glycophorin C mutated parasite, suggesting the parasite can not use EBA140 to lock on the modified receptor.

Meanwhile, the malaria researcher Louis Miller of the National Institute for Allergy and Infectious Diseases in Bethesda, Maryland, and colleagues studied the variation from EBA140 that binds the red blood cell. Parasites in samples from all over the world, they found four slightly different versions of the protein, only one of which binds to glycophorin C; the other three had not yet unknown targets, the team reports in December 2nd number of Journal of Experimental Medicine . Apparently, small changes in protein can lead to whole new ways to penetrate cells, researchers say - which would help the parasite evade mutations such as is common in Papua New Guinea

"the two additional documents. each other very well," says researcher malaria Peter Preiser National Institute for medical research in London. and together, he said, they rush all the hopes for development of a single vaccine that blocks the entry of pests. "There will not be a magic protein you vaccinate with which will solve all the problems of malaria." instead, he said, researchers will discover Plasmodium roads in the cell and to develop combined vaccines.

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search [deCowman
Miller's article in Journal of Experimental Medicine
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non-smoking adults become much less exposure to secondhand smoke than they were - but children are still plenty. That's one of the conclusions of a report published by the US Centers today for Disease Control and Prevention (CDC) which documents the levels of exposure to environmental chemicals. The study did not examine the effects of chemicals on health.

The first CDC report on environmental chemicals, published 2 years ago, suggested that efforts to curb secondhand smoke have paid off in the general population ( Science NOW, March 21, 01). In this study, the researchers measured the levels of 27 chemicals - including cotinine, a marker of tobacco smoke - in samples of blood and urine of 3,800 people participating in the CDC National Center for General health Statistics survey of health in the United States. . Today's progress report expands the list of 116 chemicals and breaks the volunteer population groups by age, race and gender

In the case of cotinine, the breakdown revealed an essential difference: the children have twice the cotinine levels than adults, the study found. Indeed, continine levels in adults have decreased by 75% since the early 190s, but only 58% in children. Secondhand smoke is associated with sudden infant death syndrome, ear infections, and respiratory infections, says Richard Jackson, deputy director of science for CDC. "If we had to choose something really go after, it would be that I would say is extraordinarily high priority, and something people can actually do something," says Jackson.

The report also reveals that some old bugbears are still hanging around. Although the pesticide DDT was banned in the US in 1973, a chemical called DDE, formed when DDT breaks down, showed adolescents who were born in the 1980s. the study also found that Mexican Americans had DDE levels three times higher than nonHispanic white or black Americans - perhaps due to exposure to agricultural jobs or Mexico, where DDT is banned but is probably still used, said Jackson. CDC does not know, however, how DDE levels observed to have an impact on health, Jackson said.

the report is "a wonderful addition" to what scientists familiar American exposure to environmental chemicals, says Linda Birnbaum, director of the division of environmental toxicology environmental protection Agency. "It can help us understand the improvements we've made, that our regulations have made," she said. It also gives a reference point for future studies, she said.

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Researchers seem to be on the heels of the cause of a mysterious illness, sometimes fatal gave the world jitters in recent days. Independent research teams in Germany and Hong Kong have examined samples of patients and found what appears to be a paramyxovirus - a member of a large family that has caused several serious outbreaks in recent years. Meanwhile, the Centers for Disease Control and Prevention (CDC) in Atlanta studied 11 possible cases of the disease, called severe acute respiratory syndrome (SARS) in the United States.

Yesterday, virologists institutes in Hamburg, Marburg and Frankfurt am Main in Germany said that the use of electron microscopy, they found particles that look visually known members of the Paramyxoviridae family in respiratory samples Singaporese a doctor who was hospitalized in Frankfurt last week after attending a conference in New York City. Today, researchers at the Prince of Wales Hospital, Hong Kong Chinese University have reported seeing the same virus particles. Both cautioned that the findings should be repeated in more patients, and even then, that this new virus may not be the culprit.

paramyxovirus gained notoriety after a vicious outbreak of Nipah virus in Malaysia and Singapore have killed more than 100 people and ravaged the Malaysian pig industry 4 years ago ( science NOW, April 13, 1999). A few years earlier, a member of the same family named Hendra had surfaced in Australia, killing two. fruit-eating bats proved to be the natural reservoir for the virus ( Science NOW, July 18, 00). But the family also includes the very common human viruses such as parainfluenza viruses, measles and mumps. Because reliable tests for all known members of the family have negative, "my presumption is that ... this may be a new virus," says CDC virologist Larry Anderson.

The disease also seems to have reached the US Today, CDC announced that there are 11 cases of SARS suspects under investigation. the number fluctuates, CDC director Julie Gerberding told reporters that patients are added or removed from the list. Flu- and pneumonia symptoms are as common; now that patients who have recently traveled to an area where local transmission of SARS took place - Guangdong province of China, Hong Kong, Hanoi, Singapore and Toronto - are considered potential cases

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After decades of painstaking efforts, a team of scientists purified a protein that stars in multiple cell dramas, development of the embryo to cancer. The protein, called Wnt, proves to have another power: He coaxes the blood stem cells divide quickly, prompting hopes that Wnt might make it easier to experiment on stem cells and one day of apply in therapy

the studies were released two collaborating laboratories of Stanford University in California involved in seemingly disparate activities. In a pioneering stem Irving Weissman cells Tannishtha Reya and colleagues were struggling to increase the number of stem cells in a petri dish without letting them become different tissue types. Produce a lot of undifferentiated stem cells is crucial to learn to direct cell development. Nearby, developmental biologist Roel Nusse and his lab members were struggling with their own albatross, the signaling protein Wnt, which had resisted all attempts to purify it.

The time "eureka" came when Nusse and postdoc Karl Willert was determined that Wnt hydrophobic - something its gene sequence has not suggested. Wnt acquires its avoidance of water from a lipid molecule that locks on it before it is the shuttle out of the cell, the researchers found. The team changed its Nusse purification plan that commonly used for proteins related to lipid and successfully isolated mouse Wnt protein.

With pure Wnt in hand, the researchers added the protein to mice stem cells from bone marrow, which generate a range of blood and immune cells. More than 1 week, the Wnt-treated stem cells produced at least six times more daughter cells than controls. Another set of experiments revealed that increased levels of a protein activated by Wnt called catenin had similar effects on stem cells. When these cells were infused into mice whose bone marrow was destroyed by radiation, they rebuilt the immune system of animals. Both papers Weissman Nusse and appear online today in Nature .

Others are enthusiastic about the results. "This is one of the first time you see the amplification of stem cell populations, which is what everybody was looking for," says Leonard Zon, a geneticist at the Hospital Boston children. Adds Guy Sauvageau, a stem cell biologist at the University of Montreal in Canada, "We are close to being able to tell people to clinics that yes, they now have proteins that allow the expansion" of stem cells

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the homepage Wnt Stanford
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A widely known for wading cancer protein appears to be part of a second line of defense :. It also keeps cancer cells that arise from spreading, according to a new job. The results highlight that goes wrong in allowing cancer metastasis; it can even refer to possible approaches to stop cancer from engaging in the end of mortal part

While many cancers remain in place, some shed cells into the bloodstream. these can be found elsewhere in the body, where they set up camp, producing fatal metastases. Researchers have long known that certain proteins help prevent the early stages of cancer. A failure of one of them, called Raf leads to both cancer and metastasis. The researchers wondered if a protein that stops Raf work, called RKIP (Raf kinase inhibitor protein), could only stop the spread of cancer, but not growth.

Earlier work by molecular biologist Evan Keller, University of Michigan, Ann Arbor, and colleagues have supported this idea. In studies of cancer cells of the cultured mouse prostate, they found that metastatic cells produced less RKIP that cells that do not. The next step was to determine whether RKIP had a role in the spread of prostate cancer in men. The team sought RKIP cancers in men removed within hours of their death. They found RKIP in the normal prostate tissue and reduced amounts of RKIP in breast cancer of the prostate, but they can not detect protein RKIP in cancers that have traveled to other parts of the body.

To verify that the loss of RKIP could cause cancer to metastasize, the researchers took a circuitous route. They RKIP overproduced in cultured cells which had already depicted metastatic ability; if the loss of RKIP helped promote metastasis, they reasoned, too should cause loss of metastatic ability. The intuition proved correct: When the Keller group injected these altered cancer cells into mice, the cancer remained in the prostate. unmodified cells spread to the lungs of mice, they report in the June 17 Journal of the National Cancer Institute .

tumor biologist Danny Welch of the University of Alabama, Birmingham, said the work exposes some of the biochemistry behind the spread of cancer. In addition, RKIP and other proteins that anchor cancer at a site may optionally be targets for gene therapy. "Doctors can cure cancer as long as it does not spread," he said, adding that the therapeutic use are years in the future.

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homepage Evan Keller
National Coalition against prostate cancer

End the practice of using antibiotics as growth promoters in livestock reduces the risk to human health without harming health or animal farmers, according a report by the World health Organization (WHO) released today. The WHO report based on the experience of Denmark, which eliminated the controversial practice.

For more than 40 years, breeders have used low doses of antibiotics to fatten livestock healthy, probably by relaxing the minor infections are not overtly sick animals. This regular treatment can lead to bacteria that are resistant to antibiotics, including strains that cause disease in humans. In 1998, Denmark became the first country to ban the practice, despite predictions of sick animals, more contaminated meat, and the economic pain to farmers industry. To see how the so-called "Danish experience" played, the researchers studied the prevalence of resistance to antibiotics in farm animals, in slaughterhouses, in meat sold in grocery stores and in healthy people ; and the impact of the ban on animal health and economic costs to farmers. The WHO committee, which is composed of 10 independent university and government researchers from eight countries met last fall in Foulum, Denmark, to see what has been learned.

Phase-out reduces the overall use of antibiotics in pigs and poultry by 54% from its peak of 1994 to 01, the committee concluded. The animals seemed to be fine: There was only a small increase in the use of antibiotics to treat infections. At the same time, there was no increase in the meat to infections such as Salmonella and Campylobacter . The annual net loss for hog producers was just 1% and was even lower for poultry farmers - a cost that could be offset by an increase in consumer confidence in the meat, followed by higher demand , according to the panel. "In circumstances similar to those of Denmark," the panel wrote, "the use of antimicrobials for the sole purpose of growth promotion can be discontinued."

Richard Carnevale of the Institute of Health of the United States of an animal, which represents manufacturers of antibiotics in animals, says that the benefits of public health in Denmark were negligible defects and Denmark, which provided the data, to minimize the "significant impacts on animal health and economic costs to producers," such as the construction of special barns to reduce exposure to bacteria. But Stuart Levy, president of the Alliance for the Prudent Use of Antibiotics, an advocacy group based in Boston, called the WHO report "important" and agrees with its conclusions. "The time has come to remove growth promoters," says Levy. "We do not need them."

Related Sites
WHO report
Information General on the use of antibiotics in animal husbandry of the Alliance for the prudent use of antibiotics (APUA)
APUA Summary of the report on the agricultural use of antibiotics

Two new studies cast more doubt on the theory that a mercury-based preservative in vaccines causes autism. Called thimerosal, the preservative has been eliminated in many industrialized countries, but is still used in the developing world. The new findings "provide additional data, extremely reassuring," says William Schaffner of Vanderbilt University School of Medicine in Nashville, Tennessee.

In 1999, attorneys parent groups such as Safe Minds suggested that thimerosal may explain the increasing incidence of autism, who often appears at about the same time as 2 years get a series of booster doses. many scientists were skeptical, but in 01 an Institute medicine panel concluded that there was not enough evidence to dismiss or accept the link.

Now the first large epidemiological studies weigh. People come from Denmark, which eliminated thimerosal from vaccines child in 1992 a team led by Kreesten Madsen epidemiology of the Danish science Centre in Aarhus said that if thimerosal were a major cause of autism, the incidence is expected to decline once it has removed. But he continued to soar after the phaseout 1992, according to a report in the September issue of the journal Pediatrics . A similar pattern emerges of health statistics in Sweden, where the total mercury in childhood vaccines began to decline in the late 1980s, as reported in the August issue of American Journal of Preventive Medicine .

But Mark Blaxill of Minds Safe argues that the Danish study is "misleading and distorted." He noted that in 1995, the Danish health registry began tracking a new category of patients, outpatient called autism. This and other factors, he says, are artifacts that confuse interpretation. Madsen replied that unpublished analysis without external consultation has shown the same upward trend.

epidemiologist Craig Newschaffer of Johns Hopkins University in Baltimore said that these ecological studies have inherent limitations, because they look at people rather than studying individual exposure. Although current studies are not likely to end the controversy in the United States, where many lawsuits have been filed, the new results are reassuring to the World Health Organization, which continues to recommend the use of small amounts of thimerosal to limit the costs of essential vaccines.

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the WHO policy on thimerosal
Minds Safe

The hopes of controlling the spread of HIV have been dealt another blow today when VaxGen of Brisbane, California, announced that its vaccine candidate failed in a large study among Thai heroin users. It is the second time that the vaccine, a genetically modified version of the gp0 surface protein of HIV, has shown ineffective.

The placebo-controlled study of 2546 Injecting drug users have found that HIV has infected 106 people who received the vaccine, a genetically engineered version of the HIV gp0 surface protein. The virus has infected 105 people who received dummy shots fire. Led by Bangkok Vaccine Evaluation Group of Thailand, the study involved scientists from VaxGen and the US Centers for Disease Control and Prevention.

The gp0 vaccine has a long and controversial history. The National Institute of Allergy and Infectious Diseases (NIAID) once defended the concept, partly because the researchers showed that antibodies in vaccinated individuals could "neutralize" HIV in test tube studies. But studies in 1993 showed that the antibodies triggered by the vaccine or immunogenic, constantly spirited strains of virus isolated directly from patients. Genentech, the original manufacturer of the vaccine, abandoned, which led epidemiologist Donald Francis leaves Genentech and co-found VaxGen.

In February, VaxGen reported the results of its first study of large-scale efficacy, which involved mainly gay men. The vaccine failed overall, but analysis suggested that gp0 might have worked in the few blacks and Asians in the study. The results were immediately challenged by some scientists ( Science NOW, February 27). VaxGen NIAID urged to follow up the results of the subgroup, but there is no intention to do so, said NIAID Director Anthony Fauci, who called today's results "not surprising at all."

The new findings do not mean gp0 is complete. A new study of 16,000 people just started in Thailand, which plans to use the protein as a wakeup call to any vaccine against AIDS that contains multiple HIV genes stitched into harmless canarypox. NIAID plans to provide significant funding for this study. Fauci said that the current negative results do not influence this decision: "As a boost, it could be qualitatively very different," said Fauci

Other AIDS researchers disagree .. "I think including gp0 is a waste of time, "said Dennis Burton, who studies antibodies against HIV in the Scripps research Institute in La Jolla, California. "It is bad immunogenic, and you can not get around that."

Related Sites
press release VaxGen

SEATTLE -. A simple cocktail of vitamins and supplements can significantly slow the loss of brain function associated with aging in dogs, according to a new study presented here on February 15 at the annual meeting of the AAAS. The results could have implications for delaying or preventing Alzheimer's disease in humans.

Aging dogs suffer from memory loss and the ability similar to that observed in humans who will develop Alzheimer learning. Canine brain also accumulate in plaques b amyloid fragments destructive proteins suspected of being associated with Alzheimer's disease in humans, which makes dogs a useful model for the study of disease. Previously, neuroscientist Carl Cotman of the University of California, Irvine, and colleagues tested the cognitive abilities of older beagles that were given a combination of vitamins C and E, some fruits and vegetables, and alpha-lipoic acid and acetylcarnitine, two compounds normally present in small quantities in the body which reduce production of free radicals thought to be involved in Alzheimer's disease. They found that the mixture has stimulated the learning and memory skills of dogs compared with dogs of the same age who did not take supplements.

To determine if the mixture has reduced the accumulation of b amyloid beta plaques, Cotman team compared the brains of beagles who took the supplements for years to those who had not. They found that dogs on the diet had developed 40% fewer plates. "We were blown away by the results," said Cotman. Studies in rodents have also found an improvement in cognitive function with one or more supplements. But because rodents do not naturally produce the plates, these studies used transgenic mice and rats. Because the neurological and cognitive decay dogs mimics more closely that of humans, Cotman said the beagle study offers new hope that humans may also benefit from the diet.

the work "is innovative and potentially very important," says John Breitner of the University of Washington, Seattle, who studies the impact of Alzheimer's disease in aging human populations. A treatment that delays the onset of the disease could be a huge benefit to public health and save millions of dollars per year, he and others say.

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Alzheimer's Association

Circumcision appears to offer some protection against HIV, but not other sexually transmitted diseases (STDs), according to a new study. The results support the idea that HIV interacts with the foreskin so unlike those of other STDs.

Previous studies have suggested that circumcised men have a lower risk of contracting HIV. But these studies also found that circumcised men had a lower risk of other STDs as well, suggesting that they can just participate in fewer sexual risk behaviors than uncircumcised men, possibly because of differences between cultures that encourage circumcision and those who do not. To determine if circumcision leads to a specific protection to HIV epidemiologist Robert Bollinger of Johns Hopkins University in Baltimore collaborated with scientists at the National Research Institute on AIDS in Pune, India.

The team followed nearly 2,300 men who visited STD clinics in India and were without HIV. About 10% of men were circumcised. The researchers determined the rates at which men became infected with HIV, gonorrhea or syphilis. Control of risky sexual behavior, the researchers found that men have contracted gonorrhea and just about syphilis the same rate, regardless of the circumcision, but circumcised men were six to seven times less likely to contract HIV, they reported in the Lancet March 27. Bollinger said the specificity of circumcision to reduced HIV infection "provides a clue" as to why it works "Other studies have shown that the foreskin has cells that are magnets for HIV." Removing the foreskin may hinder other STDs but not HIV, he said.

"It is a good study," said epidemiologist Stephen Moses from the University of Manitoba, Winnipeg. But it is still not convinced that circumcision protects against HIV infection. "Circumcision is a procedure surgical, it removes the natural tissue and can cause damage, "he said, so that the evidence must be strong before doctors recommend. He said the debate will be decided by three tests in which men are grouped at random to receive circumcision or not, then followed to determine if the procedure protects against HIV.

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Robert Bollinger
Research Institute of the National AIDS India

tumor suppressor genes are sentinels stand guard against cancer: knock them, and tumors may suddenly surface. Now researchers studying mice found a more potent suppressor genes tumor still -. The animals there are missing an amazing 50% chance of developing cancer

Tens of tumor suppressor genes have been identified, but most are poorly understood. Many, however, share one thing in common: The genes can not manage the damage to their DNA, and when mutated, they are the most likely cancer. Razqallah Hakem, a cancer biologist at the University of Toronto, Ontario, and colleagues studied normally a tumor suppressor called BRCA1 , variants that put women at high risk for breast cancer and ovarian. But recently, his attention was drawn to a mysterious gene that has been linked to cancer: Mus81 . Yeast lacking Mus81 were hypersensitive to radiation and other agents that damage DNA; in a yeast species, the gene appeared to be a crucial player in cell division.

team Hakem asked if Mus81 , with its sensitivity to DNA damage, could have a cancer link. To find out, the scientists raised mice lacking one or both copies of the gene. Only half of the animals with a good copy of Mus81 , and a quarter of those with no copies, remained healthy and survived a year. Tumors, especially lymphoma, raged through each of the diseased mice, reports the team in the June issue 18 Science . These mice were more likely to get tumors than mice lacking almost any other tumor suppressor, with the exception of the widely studied P53 gene, Hakim said.

The work also casts doubt on a widespread theory about the function of Mus81 . Yeast studies have suggested that Mus81 was critical for a specific step in cell division which is essential for chromosome recombination during reproduction. To the surprise of researchers, however, the missing animals one or two copies of Mus81 were fertile and produced normal sperm and egg cells. Apparently Mus81 works differently in mice.

" Mus81 really did play a crucial role" in suppressing tumors, says Stephen West, a biochemist at Cancer Research UK in London. It is particularly striking, he said, than mice with only one defective copy of Mus81 have cancer. Hakim said that came as a surprise to him, too. Although good copy of Mus81 can still make proteins, Hakim said was apparently not enough to ward off cancer.

Related Sites
Hakem and colleagues science article
homepage of Razqallah Hakem
Background on certain tumor suppressor genes

Researchers now understand why up to 40% of people poisoned by carbon monoxide mysteriously develop permanent brain damage weeks later. Changes to a protein found in the brain trigger a disastrous immune response. This knowledge could lead to new treatments for this common type of poisoning.

Carbon monoxide is a colorless, odorless gas, and more people die each year from inhaling than any other poison. carbon monoxide sticks to hemoglobin oxygen molecules carrying inside of blood cells much better than the oxygen molecules are, which means that the blood can not deliver oxygen to the brain and other organs. Doctors treat patients with pure oxygen and can remove carbon monoxide from the bloodstream within hours, but many people still develop permanent brain damage similar to Parkinson's disease. Until now, doctors could not explain why or how.

Through experiments with rats, Stephen Thom, a doctor of medical emergency at the University of Pennsylvania in Philadelphia, and his team tracked biochemical changes in the brain after carbon monoxide the exposure. They found that when carbon monoxide deprives the brain of oxygen, a common protein in the insulating sheaths around neurons - myelin basic protein (MBP) - becomes changed. The chemically modified MACM then triggers immune responses in the brain. But the immune system does not know when to stop. After clearing much of the MBP altered in a few weeks, immune cells continue to fight against normal PBM ", creating the potential risk of damage to permanent brain and continuous," says Thom.

To confirm that the MBP is at the heart of delayed brain damage, the team designed a group of rats unable to develop antibodies against MBP and exposed them to carbon monoxide. None of the rats developed delayed brain damage, and they normally played in a maze test designed to measure cognitive and motor skills, reports online this week in the team Proceedings of the National Academy of science . Thom now hopes to study the possibility of preventing permanent brain damage by the use of immunosuppressive drugs.

The study is a tour de force, says Lindell Weaver, a doctor of intensive care at the University of Utah in Salt Lake City. He added that the findings could have implications for treating other diseases and injuries that deprive the brain of oxygen.

Related Sites
Stephen Thom website
The Lindell Weaver website
information sheet about the CDC CO poisoning

artificial fragrances are in all kinds of detergents and personal care products, and they tend to go through the treatment of wastewater and persist in the environment. Although the chemicals are not toxic, a new study indicates that low concentrations could indirectly affect mussels and other aquatic animals. These synthetic musks interfere with the transport proteins that pump many types of toxins out of cells, which could allow them to build to dangerous levels. transport proteins are altered until 2 days after exposure to musks.

Other compounds are already known to block these so-called efflux transporters. (A positive application is the development of drugs to prevent such carriers help cancer cells resistant to chemotherapy.) Laboratory experiments have shown that environmental pollutants, such as polycyclic aromatic hydrocarbons, may have the same effect on carriers in sea urchins, fish, mussels, and other aquatic organisms, ultimately leading to toxicity.

Till Luckenbach and ecotoxicology marine biologist David Epel, both at Stanford University, examined the effects of six common synthetic musk compounds in personal care products. They removed the gills of mussels and bathe them in water with low concentrations of musks. Two hours later, they tested the effects on transport proteins in the gills by placing them in water containing a red dye. Absorbed and retained dye strips, showing that carrier cells were inhibited. The proteins remained impaired for 2 days, then recovered, reports in Environmental Health Perspectives pair online. "These seemingly harmless chemicals are harmful unexpectedly," says Luckenbach.

"They showed that [musks] may jeopardize an important defense system," said Tvrtko Smital, a molecular toxicologist at the Rudjer Boskovic Institute in Zagreb, Croatia. The concern is that musks could allow low-level pollutants to accumulate wildlife inside, he said. "We can expect with the prolonged effects of exposure to relatively low concentrations of chemicals," says Smital, adding that it will be important to monitor the habitat of these perfumes.

Related Sites
the EHP paper
the laboratory site of David Epel

The blockbuster drug sildenafil, sold as Viagra for men with erectile dysfunction, may have another benefit: preventing and reversing heart failure. In mice, the drug blunted an enzyme thought to help stimulate an oversized weakened heart. Mice with induced heart failure improved dramatically, but the approach has not been tested in humans.

Pfizer sildenafil originally developed to treat chest pain called angina. The drug blocks the phosphodiesterase 5A (PDE5A), a dispersed enzyme through smooth muscle cells in the body. Blocking PDE5A prevents the accumulation of another enzyme called cGMP, which in turn causes the arteries to dilate. narrowed arteries, as well as other potentially controlled by PDE5A forces can also play a role in heart failure.

Cardiologists David Kass and Eiki Takimoto of Johns Hopkins University, and colleagues decided to test the effects of sildenafil on the heart. The team recently found PDE5A in the heart muscle. Blocking with sildenafil, they thought, can inhibit the molecular cascade that leads to heart failure. Thus, the team subjected mice to surgery which constriction major cardiac artery and gave some of sildenafil animals. Within 9 weeks the animals who had acquired the drug had a heart much healthier, with improvements such as 67% less fibrosis, animals without drugs, the team reports online in the January 24 Nature Medicine .

to see whether sildenafil could reverse untreated heart failure, Kass group performed the same operation on another set of mouse, then waited 7-10 days. By then, the heart mass of the animals had reached 63%, a key sign of heart weakness. Half of the animals were sildenafil for 2 weeks and the other half received a placebo. Echocardiograms showed that in the treated animals, heart mass decreased gradually. The results may seem counterintuitive given that sildenafil carries warnings that it can cause heart problems, but says Kass, which is because the drug interacts with cardiac treatments such as nitroglycerin, which could trigger blood pressure drops .

"This drug is close the loop," says Robert Kloner, director of research at the Heart Institute at Good Samaritan Hospital and a faculty member of the University of Southern California, referring to Pfizer. Pfizer's early angina tests recently asked the Food and Drug Administration for approval to treat a disorder of life hazard, primary pulmonary hypertension.

Kloner called the new discovery "intriguing." It is also controversial: There is a debate about whether PDE5A is really present in the cardiac muscle, Kloner said, although several groups have recently detected there

Related Sites
information on heart disease. the American heart Association
information on cardiac hypertrophy

STOCKHOLM - public health efforts in the developing world are missing out on a market, eg group of researchers and health policymakers. They argue that efforts ramp up against the Big Three - HIV / AIDS, tuberculosis and malaria - will give far greater dividends if they are coupled to an attack against the so-called neglected diseases like hookworm, schistosomiasis and leishmaniasis. These parasites make their victims more susceptible to the Big Three, the scientists say, adding that the fight against both categories requires a similar public health infrastructure.

diseases such as lymphatic filariasis and onchocerciasis take their toll by stunted growth, anemia and blindness, contributing to widespread developmental delays and learning. These infections forgotten "is the leading global cause of growth deficits," but they would be relatively cheap to treat, says Peter Hotez, parasitology at George Washington University in Washington, DC In a paper published Jan. 30 in the Public Library of science Medicine Hotez and colleagues argue that the treatment of 500 million people with one or more of these neglected diseases would cost only 40 cents per person per year, against more than $ 20 per person per year for the fight against malaria. "It is the best buy in public health at the moment," says Alan Fenwick, schistosomiasis a researcher at Imperial College London and author on the paper.

At the same time, the authors these treatments may stimulate the struggle continues against the Big Three, they indicate a growing body of evidence that suggests that people infected with several parasites are more susceptible to other diseases -.. including major killers for example, Hotez underlines study in Senegal found that deworming medication reduced malaria cases by 0%. And the distribution systems for deworming medication can also distribute malaria nets, he said.

the team hopes to his ideas into practice soon at a meeting yesterday and today sponsored by the United Nations Millennium Project. - an advisory body that aims to reduce poverty, hunger and disease around the world - researchers, representatives of donor agencies, pharmaceutical companies and public health leaders from eight African countries met to develop a "quick impact initiative" that would create national programs of fight against malaria and neglected diseases together.

Getting medicines where they are most needed is the biggest challenge, said William Lin Johnson & Johnson. Lin is in charge of his company's effort to donate 50 million doses of mebendazole, used to treat hookworm and other helminths. "I asked them to increase production," he said. "I do not want to be left at the end of the year with stores in the warehouse -. And egg on my face "

Related Sites

• UN Millennium Project
• Global Alliance to Eliminate Lymphatic Filariasis
• control Initiative against schistosomiasis

Gleevec, the first of a vaunted line targeted cancer drugs with minimal side effects, can cause heart failure, according to new study . Researchers agree that the benefits of Gleevec worth the risk to patients desperately ill leukemia, but the study may encourage doctors to closely monitor for cardiac side effects.

For decades, drugs against cancer caused nausea and other debilitating side effects because they attack healthy tissue and cancerous tissue. Then, in 01, Novartis issued Gleevec (imatinib mesylate). The drug blocks a mutant protein that causes chronic myeloid leukemia (CML), becoming the first chemotherapy to specifically target cancer cells. CML was uniformly lethal, but today more than 70% of Gleevec patients in remission.

Cardiologist Thomas Force of Thomas Jefferson University in Philadelphia, Pennsylvania, began to doubt the safety of Glivec in 04 after the cardiologist Jean-Bernard Durand of MD Anderson Cancer Center in Houston, Texas, told him about 10 patients on the drug whose heart was normally pumped before treatment Gleevec but who had developed advanced heart failure after an average of seven months on the drug.

to see if heart failure was due to Gleevec, Durand and colleagues first examined biopsies of patient's heart muscles; they found abnormalities in the cell membranes which are characteristic of cardiac damages induced by the toxin. The work team then showed that Gleevec caused mouse hearts and mouse heart cells in culture to develop similar anomalies.

How Gleevec hearts be hurt? The drug targeting a mutant protein in cancer cells called Bcr-Abl, abnormal fusion of two normal cellular proteins, and Bcr-Abl. The team suspects that Gleevec may damage heart cells by disrupting Abl, a protein that normally regulates the growth and helps cells respond to stress. So strength and his colleagues took muscle heart cells cultured mouse and gave Abl either normal or variant Abl that is impervious to Gleevec. Even with additional normal on hand Abl, heart cells became sick again when we added Gleevec. But these cells with Gleevec-resistant Abl were fine, suggesting that targeting Gleevec Abl in normal heart cells causes heart failure in patients on medication. Force warns that other drugs against cancer that target enzymes linked Abl can also damage the heart. The researchers reported their findings online today in Nature Medicine .

hematologist George Daley of Boston Children's Hospital said that "they have marshaled a number of different pieces of evidence to suggest that there is [heart cell] direct toxicity." Novartis said in a statement says that more than 0,000 patients on Gleevec were checked, as life benefits are worth the risks, and that the cardiac side effects are "extremely rare." But the strength and cardiologists colleagues plan to check for themselves. They are planning a registry of 0 patients in their clinics that will monitor closely the hearts of cancer patients on Gleevec

Related Sites

• Background Gleevec FDA
• More information about CML

CHICAGO, ILLINOIS - mammography is still the gold standard for early detection breast cancer, but it is far from perfect: the technique lacks up to 20% of breast cancers. Soon, he can get some help. The researchers reported here today at the annual meeting of the American Chemical Society that they have developed a pair of compounds that help locate the tiny mineral deposits build up, a characteristic of breast cancer. If the compounds prove safe and effective in humans, they could prove a boon to the fight against a disease that affects 1-8 women in the United States at some point in their lives.

With mammography, radiologists use x-rays to identify the strong and the tiny calcium deposits in breast tumors. These deposits, called microcalcifications, are common to both benign and malignant tumors. While the most common mineral in benign tumors is called calcium oxalate, another called hydroxyapetite is more common malignancies. Mammography can not distinguish the two. But researchers have known for years that a drug against osteoporosis called bisphosphonates can, as it binds to hydroxyapetite.

several years, the chemist John Frangioni and colleagues at Harvard Medical School in Boston, Massachusetts, began to connect different imaging molecules called bisphosphonate contrast agents in the hope that they could use the drug to target tumors with contrast agents. They hit on a called PAM800 which is a combination of the bisphosphonate and a fluorophore which emits infrared light. Initial tests showed the compound worked to highlight hydroxyapetite microcalcifications in mice. But researchers could not produce sufficient compound to continue their studies.

So, for their ongoing work, Bhushan Kumar, a postdoctoral assistant in the laboratory of Frangioni, returned to the drawing board and came up with a new scheme for the synthesis of large amounts of PAM800. This allowed researchers to study the compound in pigs. And animal studies reported today show that subcutaneous injections of PAM800 easily allowed them to highlight microcalcifications in animals.

team Frangioni also reported that they created another series of hydroxyapetite-spotting compounds that not only gives off an infrared signal, but also hosts a chemical group gadolinium giving a strong signal in MRI machines. Although researchers have not yet tested this compound in animal studies, Bhushan said they hope it will eventually give doctors a way to identify tumors with ultra-sensitivity infrared imaging combined with the ability of the MRI to pinpoint their location in three dimensions.

"This looks like a good approach," said Bimal Banik, a medicinal chemist at the University of Texas Pan American, Edinburg. Banik warns that neither of contrast agents has been tested yet on animals injected with cell lines of breast cancer, which he called an important step to take. But the early work is promising, he says, because it offers hope that physicians will soon be able to cancer breast image with several techniques simultaneously, which greatly increases the chances of identifying the disease in its early stages.

related site

• Frangioni lab, with more research

Mice with a gene mutation linked to rare human cases of autism show a characteristic symptom of the disease: impaired social interaction. The discovery, published online today in Science adds to recent evidence that defects in synaptic connections between neurons may contribute to autism and related disorders.

Autism is a generalized disorder characterized by social and communication problems and obsessive or repetitive behavior. Scientists do not know what causes it, but genetics seem to be important. Changes in several genes have been implicated. For example, a 03 study identified a mutation - a single switch letter in the genetic code for a protein called neuroligin-3 - two Swedish brothers, one with autism and one with the related Asperger but softer. Neuroligin-3 lies at synapses, communication points between neurons, but little is known about its function, much less how it contributes to the symptoms of autism.

To study, researchers led by Katsuhiko Tabuchi and Thomas Südhof at the University of Texas Southwestern Medical Center in Dallas created a strain of mice with the same mutation found in Swedish brothers. The mutant mice had normal activity and coordination, but when researchers have mutant mice in a chamber with a mouse that had been held in a small cage, they were unusually shy, spend less time sniffing and interact with mouse cage that normal mice did. (The mouse has been withheld, because otherwise it would have initiated interactions with mutants, confusing the test.) However, there was no difference between the mutant and normal mice when it came to inquire into an empty cage, and even normal mouse mutants outperformed on a spatial learning and memory test, suggesting that the deficit was specific to social behavior.

then, the team examined Südhof slices of brain tissue of mutant mice. A neuron typically receives a variety of synaptic inputs from its neighbors: some that turn to send a message and others that inhibit this communication. inhibitory signaling was unusually high in the mutant mice, the researchers found. Much more work is needed to understand why the mutation impairs the inhibitory signaling and, in turn, how it could affect social behavior, said Südhof. Although, he said, the findings suggest that "the synapse is where things happen." Other recent work Südhof and others also points in this direction ( Science , July 13).

"This is really the science done well," said Daniel Geschwind, Neurogeneticist at the University of California, Los Angeles, adding that the mouse should be useful for further studies on autism. Huda Zoghbi, a geneticist at Baylor College of Medicine in Houston, Texas, agrees: "It's a great mouse to start looking," she said Geschwind Yet, Zoghbi and others caution that the findings. current may not apply to all cases of autism. Extremely small number of human cases of the disease are caused by mutated genes for neuroligin and related proteins, says Edwin Cook, an autism researcher at the University of Illinois Medical Center in Chicago. "We do not know how this mechanism will generalize," Cook said.

Related Sites

• Information on autism NINDS
• science section on the role of synaptic proteins and autismlike disorders

A new treatment may allow patients to avoid some of the grueling side effects of bone marrow transplants. The researchers reported in the November issue 23 Science they can use a specific type of antibody to remove the old stem cells from the marrow in mice, allowing costs to take their square. This discovery could allow patients to receive bone marrow without undergoing chemotherapy and other toxic procedures.

can improve bone diseases such as sickle cell anemia reconstitution of hematopoietic stem cells (HSCs) that generate white and red blood cells. But before receiving the marrow, patients should generally undergo conditioning, a cycle of chemotherapy (and sometimes radiation) that clears the immune cells that might attack the transplants and eliminates CSH, existing defective. However, the package also devastates the stem cells in the body, which triggers hair loss, diarrhea, mental decline and other side effects.

Finding a softer approach, postdoc Deepta Bhattacharya and immunologist Irving Weissman of the School of Medicine at Stanford University in Palo Alto, California, and colleagues have received doses with a mouse antibody that binds c-kit, a receptor on the surface of CSH promotes its division and survival. The antibody has sent the number of HSCs in the embedding of the bone marrow of animals more than 98% after 8 days, researchers report. This seemed to make room for new cells to rebuild the immune system of animals. Six months after a bone marrow transplant, 0% of a type of immune cell transfer were derived HSCs, the team found.

Weissman is considering a HSC removing antibody will be part of an attack on two fronts diseases such as sickle cell anemia, severe combined immunodeficiency, aplastic anemia, and thalassemia. First, patients will receive antibodies to suppress immune cells that might reject a bone marrow transplant; Such antibodies are already used, but they can cause flu-like symptoms and other side effects. Then, an HSC-deleting antibody would make room for new stem cells. Weissman cautions, however, that researchers need to find a human antibody that works as well as the version of the mouse. But if successful, the strategy could eliminate the need of chemotherapy and radiation and allow transplants for diseases such as type 1 diabetes, multiple sclerosis and lupus, wherein the traditional conditioning was considered too radical.

"There is an intriguing new approach," says stem cell biologist and clinician David Scadden of Harvard Medical School in Boston, Massachusetts. But stem cell biologist Kateri Moore of Mount Sinai School of Medicine in New York questions whether the antibody removes all HSCs. She noted that even without a transplant, the HSC numbers rebound in mice in about 3 weeks in a dose of antibody. CSH spared the antibody, it warns, could compete with the newcomers in space or even to produce T cells that attack transplants.

Related site

• More information about bone marrow transplants

For some alcoholics, alcohol gives an addictive thrill. For others, alcohol is a balm for stress and anxiety. A new study identifies a drug that can be particularly effective for the treatment of the latter group. The drug, which blocks the receptors for a neurotransmitter involved in stress responses, cravings significantly reduced in a group of rehabilitated alcoholics.

The drug most widely used for the treatment of alcoholism is naltrexone, which blocks the feeling of well-being of opioid receptors in the brain. But recent research has shown that naltrexone tends to work better for some 20% of alcoholics who start drinking early - before age 25 - and get hooked on alcohol because suddenly they get to drink, said Markus Heilig, a researcher at the US National Institute on alcohol abuse and alcoholism in Bethesda, Maryland. The drug is less effective in the other 80% of alcoholics, which generally develop addiction to alcohol later in life and drink primarily to relieve anxiety. Heilig and his colleagues hypothesized that drugs that reduce the stress response in the brain may be more useful for the treatment of the most common type of addiction.

In an article published online today in Science , the team describes experiments with a drug that blocks a receptor for substance P, a neurotransmitter involved in pain and stress signaling. The drug, known as LY686017 name, had proven safe in previous clinical trials for depression, but was not effective enough to continue developing, Heilig said. The researchers selected 50 volunteers, all recovering alcoholics who had a high score on a questionnaire measuring anxiety, and gave a daily half-dose of LY686017; the other half received a placebo pill.

Those who got the drug has received consistently lower on a standard questionnaire that measures the cravings of alcohol during the monthlong experience. To review the determination volunteer under stress, the researchers conducted mock interviews with three rear-facing assistants in white coats. Each volunteer had to give a 5 minute presentation to convince the "Committee" that he or she was the perfect person for a dream job, and then had to 5 minutes from difficult mental arithmetic. After this test, the volunteers were given a small container of their favorite beverage to handle and sniff but not drink. In the placebo group, blood tests showed high levels of cortisol, the stress hormone, and presentations of serious alcohol cravings questionnaires. Cortisol levels and cravings were much lower in volunteers taking the drug.

"I think it's a fascinating story," said neuroscientist Selena Bartlett of the Ernest Gallo Clinic and Research Center at the University of California, San Francisco. The frame work well with awareness growing as people become addicted to alcohol for different reasons, she said. "It seems that we are heading towards a sea change for new therapies for alcoholism."

Related Sites

• stress on information and alcohol
• information on other therapeutic targets for alcoholism
• information and General resources on alcoholism

signs a bold attempt to use gene therapy to treat a devastating rare disease that destroys the brains of children showed slower progression disease, according to a new paper. However, some experts are not convinced that the treatment, which involved streaming a virus in the brains of young patients actually worked.

The children all neuronal ceroid lipofuscinosis late infantile (LINCL), a form of the neurodegenerative disorder Batten disease. They were born without a working copy of CLN2 , a gene whose protein helps lysosomes - garbage elimination of the cell structures - decompose a waste called lipofuscin. Therefore, lipofuscin accumulates and eventually destroys the neurons, causing the brain to shrink. Children with LINCL appear normal at birth, but by the age of 2 to 4 show signs of development problems and often have seizures. Finally, blind and confined to a wheelchair, they usually die from 8 to 12 years.

few years, gene therapy researcher Ronald Crystal and colleagues at Weill Cornell Medical College in New York has slowed with LINCL success in mice using gene therapy in the brain. To test the safety of the approach in humans, the team treated 10 patients LINCL aged 3 to 10 years from 04. After anesthetizing children, researchers have drilled six holes 2 mm wide in their skulls. They then dripped into a solution of a harmless virus that was modified to carry a good copy of CLN2 gene. Four children had an immune response, but it was sweet. One patient developed seizures two weeks later and died 49 days after surgery. However, she has not had an inflammation of the brain, and Crystal said he did not know whether his death had anything to do with gene therapy.

Over the next 18 months, the Crystal team conducted neurological tests and magnetic resonance imaging (MRI). Although MRI scans have suggested that the brains of children treated were shrinking less than they would have otherwise, the results are not statistically significant. On measures of motor function, language, and the frequency of attacks, however, the children seemed to deteriorate more slowly compared to untreated patients, from about two points lower on a scale of new checkpoints. "This suggests [of efficacy] and encourages us to move forward," said Crystal, whose team reports its findings online today in Human Gene Therapy . The study of about $ 8 million was funded by the Nathan Battle Foundation, which was started by the parents of two siblings with LINCL, both of whom were enrolled in the study.

experts are shown the results with caution. "This is potentially exciting, but it is also potentially will not stand," says neurologist Jonathan Mink of the University of Rochester Medical Center in upstate New York. main flaw of the study, says Jonathan Cooper a neuroscientist at King's College London in the UK, these are untreated patients used for comparison. it is unclear how comparable these controls were in their stage of disease with patients, so it is difficult to be sure that patients did better than they would have otherwise.

Crystal hopes to improve on the results of his team using another type of viral vector that worked much better in mice in his later studies. He said the next trial could begin within a year.

Meanwhile, the researchers treated another disease of hereditary childhood brain called Canavan disease with gene therapy. The lead investigator on one of these tests, Paola Leone of the University of Medicine and Dentistry in Camden, New Jersey, said his team is preparing a manuscript on his study of 13 patients. At meetings, she reported "significant improvement" in some measures of cognitive and motor function.

Related site

• Information Batten disease

It seems that common sense :. Reduce insect populations, diseases and insects -Internet also decrease. But a new study of dengue fever, a viral disease transmitted by Aedes mosquitoes, suggests otherwise. Mosquito control can result in more cases of dengue hemorrhagic fever (DHF), a rare and sometimes fatal disease caused by the virus.

Researchers believe that tens of millions of people in tropical regions are infected with dengue virus each year. The pathogen can stimulate dengue fever, which is marked by painful muscle and joint pain, but is rarely fatal. Some patients, however, develop more severe DHF, which can cause bleeding and is fatal. There are still many questions about the epidemiology of both diseases -. Including the importance of mosquito abundance

An international team of data gleaned from a massive national survey of Aedes mosquitoes made between 02 and 04 in Thailand, where the Dengue . The researchers compared this information with data on the incidence DHF collected by the Thai Ministry of Health. Overall, 83 out of 100,000 Thai contracted dengue each year. As expected, the team found that the incidence DHF has increased the percentage of households by district containing larvae or pupae Aede (the index House). But the trend held up to a point. House when the index climbed beyond 30, DHF incidence gradually declined, the team reports this week PLoS Neglected Tropical Diseases .

Co-author Yoshiro Nagao Osaka University Graduate School of Medicine in Japan said the likely explanation - which was supported by computer models - is that DHF usually develops the second time a person is infected . When there are a lot of mosquitoes, the second infection is more likely to come shortly after the first, so there is a better chance that person still has a strong immune response. When mosquitoes are less abundant, the more time passes between infections, antibodies decline, and protection diminishes.

The data show that mosquito control can have unintended consequences, says Nagao. For example, lowering the index House for 30 through Thailand could lead to a 40% increase in DHF. In an unpublished study, Nagao and others plan to show that the only way out of the problem is a vaccine, many of which are now in clinical trials.

But dengue researcher Duane Gubler of the University of Hawaii, Honolulu, said the story is more complicated. On the one hand, the study models assume that all strains of dengue and mosquito populations are similar. In reality, there are "huge variations" between infectivity and potential spread of virus strains, he said, and some mosquito populations are much better than other vectors. In addition, the House index, which assesses mosquito breeding sites, may not be a good indicator of population exposure to a virus, says entomologist Paul Reiter of the Pasteur Institute in Paris. What is important is not the number sites, but the number of adult mosquitoes they produce, he said.

Bacteria get a bad name. Although most people exercise their Lysol as a sword against these organisms, in fact, many types of bacteria help us survive. Now, research has revealed that some microbes could also play a key role in the prevention of diabetes.

The human body runs on glucose and the hormone insulin prevents excessive outbreak. Every year about 15,000 people in the US are diagnosed with type 1 diabetes, which strikes when the immune system attacks cells in the pancreas that make insulin. Researchers have spent years trying to understand what triggers that attack the body's own cells.

Some studies have shown that mice exposed to different microbes develop type 1 diabetes at variable rates, suggesting that some bacteria can help modulate early stages of the disease. But specific information on how it works, and that bacteria were important, remained elusive.

Chervonsky immunologist Alexander of the University of Chicago in Illinois and colleagues evaluated how the microbial environment impacts of diabetes in mice. In some animals genetically predisposed to type 1 diabetes, the researchers hit a gene that protects against bacterial infections. The researchers then exposed five mouse prone to diabetes and five standard mouse germ vulnerable to a typical environment with lots of microbes. All normal mice and four of five mice prone germ developed diabetes, it seemed that the susceptibility to infection made no difference. But when the researchers studied the T cells, a marker of immune system activity in different tissues, they saw much less activity of T cells - something that is also a sign of incipient diabetes - in the ganglia pancreatic lymph from the general free mice, they reported in September 21 Nature .

Which microbes were behind the decreased T cell activity? The researchers keyed to a cocktail of bacteria known to live in the pancreatic lymph nodes normally. They placed mice susceptible to diabetes in an environment free of microorganisms and exposed to other bacteria. All mice in the germ-free environment developed diabetes; none of the mice exposed to the bacteria showed signs of the disease.

The Chervonsky group is examining whether the mice with type 1 diabetes living in otherwise normal lack these key microbes. "If we find the bacterial strain that is protective in mice, that should be enough to try convincing in humans," he said. But he noted that researchers need to understand exactly how these bacteria called off the attack of the immune system to produce treatments for patients with type 1 diabetes

developmental biologist Margaret McFall-Ngai of the University of Wisconsin, Madison, said the work reinforces the idea that microbes within our body can profoundly affect the way our bodies. And although David Relman immunologist at Stanford University in Palo Alto, California, warns against attributing too much importance to the role of microbes in human diabetes, it think the results are worth noting. "If nothing else, forcing us to another variable on the table that is not part of the mixture"