Health Meaning

A gene that can cause breast and ovarian cancer when mutated also seems to play a key role in T cell development, the soldiers of the immune system, according to a study this month of Nature Immunology . The results do not explain how the gene BRCA1 , contributes to cancer, but they shed new light on how T cells mature.

The mutations in BRCA1 were involved in about 5% of breast and ovarian cancer. Researchers believe that the BRCA1 gene normally plays a crucial role in DNA repair. Some suspected the gene may also be important in T cells - which fight bacterial infections, viruses and parasites - because these cells produce large amounts of the BRCA1 protein and because DNA repair is a natural part the trip of a T cell at maturity. To produce a wide variety of different T cells that can fight against any invader, the DNA encoding the receptor cells is remodeled during ripening, which means DNA strand must be broken and glued together.

for how significant BRCA1 is the immune system, a team led by molecular biologist Razqallah Hakim of the University of Toronto has created mice that lacked the protein in their cells T. As a result, they had 0% fewer cells than a control group T. their T cell population was also very young, suggesting that the cells had not completed their maturation process, and less sensitive to various stimuli. The scientists found that p53, a protein that responds to DNA damage or by halting cell division or causing the cell to commit suicide, was apparently involved in their disappearance. The knockout mice have high levels of p53 in the T cells, whereas the protein was undetectable in the control group.

But a follow-up experiment surprised researchers. It showed that T cells do not die as a result of the DNA shuffling that went wrong. After eliminating BRCA1 and also the gene p53 - thus preventing the cells from killing - the researchers found that animals produced normal amounts of T cells In addition, DNA sites where their receiver has been broken and repaired were intact.

Although BRCA1 be critical for the development of T cells, it may not be crucial for DNA repair in the redistribution of the receptor genes, said Doug Green, a researcher at the apoptosis in the la Jolla Institute for allergy and immunology in San Diego, California. "Most of us assume that this was the main source of DNA damage in these cells," he said. The next step, says Green, is to understand the role of BRCA1 in cancer development.

Related Sites
Science news story about BRCA1

researchers have yet obtained the most detailed picture of how cancer tumors secure blood supplies that feed their growth. In August 18 number of Science , they show a set distinctly different gene is expressed in blood vessels of the human colon cancers compared to normal colon tissue. The work could pave the way for new drugs that stifle tumors by blocking the growth of blood vessels.

Scientists had already identified some "marker" gene that differ between normal blood vessels and presumably newly formed vessels that feed tumors growing. But a team led by Bert Vogelstein and Kenneth Kinzler Johns Hopkins University School of Medicine undertook to cast a much wider net. First, they had to overcome a serious obstacle - learning to isolate pure populations of endothelial cells that form blood vessels. These cells are only one of many types of cells present in the tumor and normal tissues, and are present in relatively small amounts. After trying for 2 years, Brad St. Croix the Hopkins group managed using a protein called P1H12, which occurs mainly on endothelial cells, as a handle to separate the cells.

Next, the team sought the active genes in endothelial cells of colon cancers and tissue from normal colon from the same patients. They found about 100,000 extracts of messenger RNA, representing more than 32,500 genes that had protein. Of these, 46 are substantially more active and 33 were less active in tumor endothelial cells than in normal colon tissue. In addition, the researchers found similar patterns of expression for most of the same genes in other vessels tumors, including lung, brain and metastatic liver cancers. "It is clear that the tumor vasculature is different from the normal vasculature," says Douglas Hanahan of the University of California, San Francisco.

Experts interested in the development of new treatments against cancer are intrigued. Philip Thorpe of the University of Texas Southwestern Medical Center at Dallas notes that the work could lead to compounds that block the protein products of genes overexpressed in the hope of cutting the growth of tumor vessels. Indeed, the researcher Judah Folkman Angiogenesis of Harvard Medical School in Boston, who launched the idea of ​​killing tumors by targeting the blood vessels, described the document as a "landmark".

St. Louis - Scientists have elucidated a critical step in emphysema, a progressive destruction of lung tissue that often occurs in smokers. A new study shows that debris of a protein called elastin attracts a class of immune cells that deal additional damage. The research was presented here October 14 at the International Conference on biology and pathology of the extracellular matrix.

Emphysema is the fourth leading cause of death in the United States. The damage is irreversible and no treatment except giving patients extra oxygen. In emphysema, a class of immune cells called macrophages flock to the lungs. There they churn enzymes that break down elastin, a fibrous protein which contributes to lung their shape and flexibility. The resulting fragments attract several types of immune cells, which led pulmonologist Steven Shapiro of the University of Washington in St. Louis to suspect that the fragments could also attract the same sort of macrophages that began the destruction of the elastin first.

Shapiro and colleagues have liquid lungs of the smoker in the upper half of a plastic container of which the two compartments are separated by a membrane. When they put human macrophages in the lower compartment filled with a cell culture medium, cells were grown to the membrane. This move was blocked when they added an antibody that latches on elastin fragments. And Shapiro and colleagues injected elastin fragments directly into the lungs of mice. Soon, macrophages were gathered in the lungs and began to produce an enzyme that destroys elastin.

Macrophages can hang in the lungs of smokers long after they get rid of their habit, so the damage can probably last for years, Shapiro said. That is why he is now looking for a compound that prevents cells from attacking elastin in mice.

The conclusion does not explain how emphysema is started, said pulmonologist Yale University Paul Noble, but it shows how it continues: Once the macrophages collect in the lungs, elastin fragments keep them coming. The next question, Noble said, is why all smokers have emphysema, while all have lungs macrophages. Perhaps genetic differences cause different immune responses, Noble said: "The response to these fragments ... may explain why some people smoke for 80 years and never get emphysema."

The National Emphysema Foundation

Emphysema information from the American Lung Association

National Emphysema Treatment Trial NIH

British scientists shoulds Their beef up research on alternative medicine, selon Issued a report last week by the House of Lords. Answering Their call, a foundation headed by Prince Charles offert to fund research into alternative medicine and is eagerly Awaiting the government's response.

Noting a dearth of high-quality research in alternative medicine, the House of Lords' Science and Technology Committee urged the National Health Service and the Medical Research Council on 28 November to Develop a few "centers of excellence." The committee pointed to the U.S. government's National Center for Complementary and Alternative Medicine in Bethesda, Maryland, as a feasible model. The report added que le work shoulds Ultimately be guided by a clearinghouse That Is Partly Funded by the government.

In a separate report, the Foundation for Integrated Medicine, an advocacy group headed by Prince Charles, offert to fill That role. Outlined It has 5-year, $ 7 million scheme to jump-start new research, media Existing studies at medical schools, and fund 5-year fellowships to process medical students in research methods for alternative medicine. Right now, the field is "not respectable PARTICULARLY have a research career," the foundation's rating Tricia Darnell. Increasing funding Would make it "more mainstream," she says.

The foundation hopes for backing from the U.K. Department of Health, goal allowed on que le agency has been "lukewarm" to the idea. Meanwhile, the foundation Welcomes feedback (see below) and is waiting for a government response to the House of Lords 'report.

Related Sites
The House of Lords' Report
To voice your opinion on the Foundation for Integrated Medicine's Plan
NIH's National Center for Complementary and Alternative Medicine

An antibiotic that helps to fight zits and bad breath may be able to prevent a much more serious disease. In the February issue of Nature Medicine , the researchers report that triclosan, often used in mouthwashes and acne creams can cure mice of malaria. The study also describes a new biochemical pathway in the malaria parasite that could be the target of several other drugs.

With 2.7 million deaths each year, malaria remains one of the most ruthless killers of the tropics. And because the parasite tends to develop resistance to all drugs, scientists are short of ideas to cure the disease. In search of alternatives, Namita and Avadhesha Surolia, Central Jawaharlal Nehru for Advanced Scientific Research in Jakkur, India, mice infected with the malaria parasite, and then inject them with triclosan. "We just thought we'd give it a try," says Namita Surolia. The two researchers were surprised to see that the animals were all healed within 4 days and remained healthy, while other infected mice malaria died after a week

the success was fascinating, because the attacks of triclosan one of the enzymes that help produce fatty acids -. things as cell membranes are made of - in plants and bacteria. But the parasite Plasmodium that causes malaria is a whole other unicellular organism, and until recently scientists thought it did not have the biochemical pathways to produce fatty acids . (instead, they assumed that Plasmodium borrowed its fatty acids from its animal host.)

the Surolias continued to show that, as in bacteria, triclosan is the key jams plasmodium s fatty acid machines; inhibits one of the key enzymes in biochemical conveyor belt. This brings the cycle of the fatty acid to a grinding halt, and the parasite can not divide unless new cell membranes.

Triclosan is normally used outdoors and can be dangerous to swallow at high doses. But if it proves to be safe, it could be tested as a treatment for malaria in humans, said James Beeson, a researcher of malaria at the University of Melbourne, Australia. In addition, all other enzymes involved in fatty acid production became suddenly potential targets, he said, giving science a much needed boost in the arms race with Plasmodium .

Related Sites
World Health Organization against the malaria sheets

If you want to stay young, do not light up. Smokers often look old before their time, because they have many more wrinkles than nonsmokers of the same age. Dermatologists now believe they may have discovered why. A study published in March 24 issue of The Lancet suggests that smoking stimulates production of an enzyme that makes the skin less elastic.

Scientists have known for some time that both smoking and exposure to ultraviolet (UV) predispose to premature aging of the skin. A team of dermatologists led by Anthony Young of the Institute of St. John of Dermatology at Kings College London first studied how UV light affected the levels of matrix metalloproteinase-1 (MMP-1), a enzyme that chops proteins. MMPs degrade collagen, a structural protein that is important for maintaining the elasticity of the connective tissue and constitutes up to 70% of the dry weight of the skin. When collagen is destroyed, the skin begins to sag and bend

Young and his fellow volunteers divided into two groups. a group of sites on their buttocks exposed to UV light, while the other did not. Skin biopsies revealed a curious fact: The levels of MMP-1 mRNA in the controls are not normally distributed, but are divided into two distinct groups. The team was perplexed. But then Young said he remembered seeing the results of a Japanese study showing that in vitro tobacco smoke solution induces transcription of the MMP-1 gene in cells of the human skin. When the team asked if they smoked, they discovered that smokers tend to have high levels of MMP-1 mRNA. He was completely "accidental discovery," says Young. Apparently, one of the thousands of chemicals in tobacco causes the MMP-1 levels to rise.

The results are important for several reasons, says Christopher Griffiths of Dermatology Centre at the University of Manchester. "This study shows that chemicals in cigarette smoke affect the whole body," he said, not only the parties who smoke is in direct contact with. "Inhaled products are transported through the bloodstream and make contact with all organs. "Griffiths also notes that emphysema, a lung disease common among smokers, is marked by a loss of connective tissue and may be related to the increase in MMP-1.

Related Sites

St. John Institute of Dermatology

DermWeb (skin care and dermatology information)

Vitamin C has long been touted as a healthy and balanced dietary supplement because it can protect against certain types of DNA damage. It also now seems to have an unpleasant chemical side effect. In the June 15 issue of Science , the researchers report that vitamin C may also stimulate the formation of molecules known to scramble the DNA.

Antioxidants such as vitamins C and E can disarm the highly destructive molecules called free radicals, so that many people believed that antioxidant supplements might help prevent cancer. This has not proven to be true in human trials, however. Now researchers led by Ian Blair of the University of Pennsylvania in Philadelphia may have an explanation.

In the process of destruction of free radicals, vitamin C is transformed into what is called a radical vitamin C. When certain metal ions are close to the radical vitamin C can transform compounds called lipid hydroperoxide in genotoxic, which switch bases around the DNA, disrupting its delicate code. However, these metal ions are rare in human blood

Something had to be the formation of genotoxic, although :. Even healthy people showed characteristic DNA damage induced by genotoxic. Blair and his colleagues decided to see if vitamin C alone would do. Working in the solutions thoroughly cleaned of all relevant metal ions, the researchers showed that the equivalent of an additional 0 milligrams of vitamin C could trigger the formation of genotoxic suspects.

It is not known how a great risk this reaction arises, however. Vitamin C concentrations researchers used are not much higher than those found in normal human blood. But not all people have high levels of commodity genotoxic lipid hydroperoxide. Blair and his colleagues plan to look more closely at the two patient populations that are :. Women with breast cancer and children who take certain drugs for leukemia

The prevalence of these genotoxic and DNA damage they cause was Puzzling cancer biologists for years because the relevant metal ions are rare in the blood and the conditions are not quite right. "No one had any idea where they came from," said Larry Marnett, a biochemist at Vanderbilt University in Nashville, Tennessee. The new explanation, that vitamin C could be the trigger, "a lot of chemical sense. "

Center for Cancer Pharmacology at the University of Pennsylvania
website laboratory Blair
Learn more about vitamin C Linus Pauling Institute

BARCELONA -. Motivated by more than one million deaths from malaria each year, scientists have fantasized about the ultimate method of eradication: replacing existing populations of mosquitoes incapable of spreading the disease. Two advances reported at the Third International Congress of Vector Ecology here on 20 September may help edge that dream closer to reality

Putting all new gene into mosquitoes was difficult .; a technique used in Drosophila does not work. Last year, scientists at the European Molecular Biology Laboratory in Heidelberg, Germany, reported that they genetically modified Anopheles stephensi , a species that transmits malaria in India. The team inserted a test gene that encodes green fluorescent protein (GFP). But the gene does not cause resistance to Plasmodium , the parasite that causes malaria.

Now, a team led by Marcelo Jacobs-Lorena, a molecular entomologist at Case Western Reserve University in Cleveland, Ohio, is spliced ​​in the same species of mosquito gene that. It encodes a peptide, called SM1, which appears to counteract Plasmodium by blocking receptors in the gut and salivary glands of mosquitoes. Without access to these receptors, Plasmodium can not replicate in the insect and infect humans when the mosquito bites. In carrying mosquitoes gene Plasmodium lost 85% to 95% of its ability to replicate, and the mice bitten by insects do get sick. In contrast, more than half the mice bitten by normal mosquitoes were infected.

Meanwhile, Mark Benedict Centers for Disease Control and Prevention (CDC) in Atlanta announced at the meeting that his team created the first transgenic Anopheles gambiae , malaria vector most prevalent in Africa. The team slipped GFP gene in A. gambiae as a first step. However, the realization is "very, very exciting," says Paul Eggleston of Keele University, UK. It is probably a matter of months before researchers produce a version of resistant malaria says Eggleston -. For example, by providing it with SM1

Skeptics warn that even such a feat would not mean the end of malaria; there are many obstacles, so that new mosquitoes replace existing ones to convince the public that it is safe to release them. But even if they are never released, says Eggleston, the altered mosquitoes will teach researchers about how malaria parasites interact with their host.

Related Sites

science story on the genetic modification of mosquitoes
CDC information on malaria
The homepage Paul Eggleston
The third International Congress of Vector Ecology

Scientists have developed transgenic mice that do not receive the healing of the deadly liver known as cirrhosis - even if exposed to environmental toxins or Swill equivalent gallon whiskey a day. Research shows a possible way to prevent cirrhosis, and also reveals that some proteins, thought to be specialists, may have more than one trick up their sleeves.

When the liver is injured by infection or toxins like alcohol, it repairs the damage by activating the liver cells, muscle smooth. chronic damage leads to excessive repair cells clog blood vessels. Eventually, the liver begins to starve. What starts the repair process is a molecular chain reaction set off by messenger proteins, which eventually activates a protein called C / EBPB.

Medical scientists Martina Buck and Mario Chojkier at the University of California, San Diego, wanted to know what C / EBPB done and how it is powered. Using radioactive tracers, they found that a phosphor molecule must attach to a certain place. Other biochemical studies revealed that C / EBPB usually keeps repair liver in check by caspase activation proteins called. But when the fastener phosphorus, caspases are inhibited instead. smooth liver cells accumulate, and the result is cirrhosis.

To see if this discovery could help prevent liver disease, high researchers transgenic mice with the version of C / EBPB that could not bind phosphorus. Even when exposed to a dangerous toxin, the mice do not develop cirrhosis; control animals, meanwhile, quickly fell ill. The researchers, who report their work in the October 26 issue of Molecular Cell, soon hope to create a modified version of the protein that works in humans.

The results were "remarkable," said biochemist Steven McKnight, University of Texas Southwestern Medical Center, Dallas, because they show that C / EBPB, previously known only to regulate transcription of DNA, regulates also the activity of other proteins. - two tasks thought to be independent and unrelated until recently the discovery of proteins with different functions, he said, calls into question the basic principle that proteins have evolved each attack a single specialized task.

Related Sites

Liver disease Columbia-Presbyterian Hospital home page
American Association for the study of diseases liver

CHICAGO -. cajoled by an advocacy group based in Boston, two giant pharmaceutical companies have released proprietary data on antibiotic resistance. The new figures presented December 17 at the meeting of the Interscience Conference on Antimicrobial Agents and Chemotherapy, show that microbes causing fatal pneumonia began to evade ciprofloxacin (Cipro) and other drugs in a class of antibiotics called fluoroquinolones.

for the last decade, physicians have relied on fluoroquinolones to clear various bacteria, including insects that cause pneumonia, skin infections, gonorrhea, and even anthrax. Microbes can develop resistance to fluoroquinolones in the laboratory. To determine if this is happening in hospitals, the Alliance for the Prudent Use of Antibiotics (APUA) in Boston began to press the big pharmaceutical companies to reveal the antibiotic resistance data. Recently, Bristol-Myers Squibb and GlaxoSmithKline agreed to share their information on testing on clinical isolates of Haemophilus influenzae , the second leading cause of death from bacterial pneumonia in children in the developing world.

Drug the company's researchers have been for years collecting thousands of H. influenzae isolating patients in hospitals and clinics across North America and Europe. In the laboratory, they push the samples in cultures containing various levels of one of the two fluoroquinolones, ciprofloxacin and ofloxacin. fully resistant insects can survive antibiotic concentrations 16 times higher than could kill a significant bug. But because the bacteria often develop resistance gradually undergoing a series of changes, the pharmaceutical company has counted those who survived drug levels only 2 times which is generally fatal. This strategy allows a glimpse of the strength in manufacturing, said microbiologist Stuart Levy of Tufts University School of Medicine in Boston, President of APUA.

The two companies have found that less than 0.1% of the samples of microbes collected before 1997 had acquired a drug resistance. But since 00, the incidence of partial resistance increased slightly to approximately 0.15%. Other pharmaceutical companies are thought to be as collect this type of data, even if it remains the owner.

pharmacologist Michael Dudley Mikrozid Pharmaceuticals Mountainview, California, called the study well done, although he warns that it is still unclear whether the resistance is on the rise because the impact is so low.

Related Sites

APUA backgrounder on the antibiotic resistance working
additional information about fluoroquinolones

The humble stool sample can be much more valuable than most people think. By carefully sifting through the genetic content of stool samples, researchers have developed a test that can detect colon and rectum in their early, most curable stages.

Although colorectal cancer is highly curable when caught early, it remains the second leading cause of cancer death in the United States. This is because many people do not seek preventive screening. The most effective tool detection is colonoscopy, which requires doctors to snake 2 meters long endoscope into the large intestine (slowly around curves, please) to look for abnormalities and tumors. In addition to being significantly uncomfortable, colonoscopies are also expensive. A simpler method of screening, analysis of blood samples for traces of stools (a symptom of colorectal cancer) is rarely conclusive.

The new technique involves testing samples of stool of a gene called CPA . Movements CPA can trigger the growth of tumors and mutated CPA is found in almost all malignant colorectal tumors. Now oncologists Bert Vogelstein and Kenneth Kinzler and their team at the Kimmel Cancer Center at Johns Hopkins University in Baltimore have shown that mutant CPA DNA can be detected in necrotic cells of the intestinal mucosa in faeces . The team used PCR - the standard method for DNA replication - to amplify the CPA DNA in stool samples from 74 patients. Samples containing mutated CPA dysfunctional protein gene products, allowing them to be easily identified.

The precise detected mutated ART CPA DNA in 61% of patients already diagnosed with cancer of precancerous colon at an early stage and identified mutations in 50% of patients known to have tumor benign, the team reports in the January 31 the New England Journal of Medicine . The test produced no false positives for a group without cancer.

"This work must absolutely be prosecuted," said Barbara Conley, an oncologist at the National Cancer Institute in Bethesda, Maryland. Although Conley stressed that more work needs to be done to improve test sensitivity she said it could one day provide a welcome alternative to colonoscopy.

Related Sites
Vogelstein / Kinzler Laboratory
information on colon cancer NCI

Stress can make people nervous, have ulcers, and even dying young. If that were not enough, new research suggests it may contribute to bad skin and play a role in hair loss. Scientists have found that the main body stress hormone triggers skin cells to multiply the oily lipid and to testosterone -. A key culprit in both baldness and excessive hair growth, depending on where it occurs

During a stressful event- -Say a final exam - the brain releases corticotropin (CRH), a master stress hormone that directs the body to pump adrenaline, tense muscles, or shiver. But researchers do not believe that CRH had an effect on the skin. Researchers have long thought the stress responses of the skin - such as tanning to prevent sunburn -. Was triggered by the immune system, which releases chemicals in the first signs of damage

Dermatologist Christos Zouboulis of the Free University of Berlin, Germany, and colleagues examined the effect of CRH on cells cultured from human sebaceous glands. These glands are located at the base of hair all over the body except the palms and soles. They house sebocyte called cells that are lipids, oily compounds that coat and protect the skin at low levels, but cause oily skin and acne in high concentrations.

The team found that Zouboulis sebocytes to CRH and have receptors for the hormone on their surfaces. Sebocyte meet CRH seepage up to 60% fat, the team reports in the May 14 issue of Proceedings of the National Academy of Sciences . HRC also caused the crank 50% cells of more than one enzyme which makes testosterone, which has been linked to both the male pattern baldness and hirsutism.

Call of labor "a big step forward" in understanding the skin stress response, biologist Andrzej Slominski skin of the University of Tennessee Health Science Center, Memphis, said that the production of the hormone stress of testosterone and oil in sebocytes could lead to new topical treatments for a variety of skin and hair disorders. Until then, the stress management courses are highly recommended.

Related Sites
Free University dermatology department page

Bacterial infections may trigger high levels of brain steroid which can make infants too sleepy to wake up when they encounter difficulties in breathing, suggests new research on lambs . Although a link between infections and sudden infant death syndrome (SIDS) has been suspected, this is the first time a clear mechanism was found that could explain such a link.

SIDS usually occurs during an infant sleeps at night. An emerging theory holds that the condition is caused by bacterial toxins encountered by virtually all infants in the first year of life. Researchers have proposed several theories to explain how these toxins could kill infants, but so far there has been little experimental evidence to back them up.

Now physiologist Saraid pool Monash University in Melbourne, Australia, found that even slight bacterial infection can cause brain levels of steroids to increase dramatically, leading lambs to become extremely drowsy and difficult to wake. In a trial involving 12 lambs a mild infection with Escherichia coli caused levels of allopregnanolone steroids in the blood to increase by 50%. The results were even more dramatic in the brain, where levels of allopregnanolone, which is known to have sedative and anesthetic properties, increased by two to three times. If the same thing happens in humans, even a mild infection could blunt the ability of infants to awaken, says billiards. "If they develop breathing problems during sleep that cause their blood oxygen in the fall, they are not the appropriate response exciting that allows them to wake up."

John Newnham, Director of Women and Infants Research Foundation in Perth, Australia, said the finding is an important step towards the understanding of SIDS. "This helps us with the idea that infection is involved." The research has been accepted for publication in the journal Pediatric Research later in the year.

Related Sites
Monash University Department of Physiology
General information on SIDS from the National Institute of Child Health and Human Development of the United States

Lupus, an incurable disease that strikes more than 16,000 Americans a year, causes the body's immune system to turn against itself, creating antibodies that will fight and kill their own cells. In a significant move, geneticists are now saying that a small change in a single gene contributes to the development of the disease in some people.

Lupus Symptoms can vary from joint pain, fever, arthritis, rash, and sensitivity to light for kidney and blood-clotting problems of life in danger. Although the disease seems to run in families, researchers have yet to identify the gene or genes that cause. However, mouse studies showing symptoms of lupuslike suggested that a gene called PDCD1 - which is known to help the body recognize foreign cells -. May play a role

Geneticist Marta Alarcon-Riquelme of Uppsala University in Sweden led an international team of researchers whether PDCD1 is also associated with lupus in humans . The team recruited 2510 people of European-American, Mexican, and African-American descent families with single or multiple cases of lupus, and families with no known history of the disease. The team decoded PDCD1 DNA of each person and found a single mutation - a change in a nucleotide letter of the genetic code -. Associated with lupus in 12% percent of European Americans and 7% of Mexicans

based on the location of the mutation in the DNA code, researchers believe that the mutation prevents a protein called RUNX1 of binding to the PDCD1 gene [ParcequeRUNX1estpensépouraiderlescellulescopientl'ADNcettedéconnexionpourraitperturberlacapacitédescellulesimmunitairesàdistinguerlesproprescellulesducorpscontrelesmicrobesenvahisseursenempêchantlescellulesd'exprimerlabonnequantitéde PDCD1 , the team argued in October 28 Nature Genetics . This mutation is not the only cause of lupus, though; it has also been found in 5% of European Americans and 2% of Mexicans who do not have lupus. And mutation was almost nonexistent in the African American population.

"This is a great advance for researchers to work with and we now have a testable hypothesis to continue," said rheumatologist Paul Utz of Stanford University in California. The next step, Utz said, is whether RUNX1 really play a role in the regulation of PDCD1 gene.

Related Sites
homepage Utz
Lupus Foundation of America

, the tiny disc-shaped platelets floating in the veins of the help blood clot, protect against excessive blood loss after injury. But new evidence shows that these cells have a darker side too. Researchers studying mice have shown that some are sticky platelets than normal can contribute to clogged arteries, which can lead to serious health problems.

atherosclerosis, or clogging of the arteries, is a major contributor to heart disease. The disease develops as white blood cells called monocytes cells attach to the walls of blood vessels, then the inventory to create fat deposits resembling hardened cottage cheese. Enough of this "plate" may reduce or block blood flow. Platelets are known to bind to monocytes, the doctors suspected a role in arterial disease. And in fact, inhibiting platelet drugs such as aspirin may help prevent blood clots in narrowed arteries. But he does not know if platelets contribute to arterial disease in the first place or just exacerbate the disease once it develops.

molecular physiologist Klaus Ley University of Virginia, Charlottesville, and his team studied activated platelets, hoping to find an answer. Activated platelets are revved beyond the resting state, but not yet committed to the formation of blood clots. For 12 weeks, the team injected platelet both resting and activated in mouse designed to be susceptible to atherosclerosis. They found that activated platelets express a molecular adhesive called P-selectin which attaches briefly arterial walls. This contact with the walls buffered with a chemokine residue, chemicals which attract monocytes. The mice injected with activated platelets developed plaque deposits that were 39% larger than those of mice injected with platelets rest online reporting team on December 16 in Nature Medicine . Mice can not produce P-selectin was not affected by injection of activated platelets.

Calling the study "stylish and exceptionally deep," cardiologist Anthony Rosenzweig of the Harvard Medical School and Massachusetts General Hospital in Charlestown said the next step will be to confirm that the platelet induce atherosclerosis in humans. Hematologist Zaverio Ruggeri from the Scripps Research Institute in La Jolla, California, said the findings could point to useful treatments that could prevent or slow the progression of atherosclerosis.

Related Sites
Klaus Ley website
Zaverio the site Ruggeri
Anthony Rosenzweig's website
basic information on atherosclerosis of American Heart Association

In war zones around the world, bandits steal food intended for starving civilians. One of the most feared pathogens medicine performs the same kind of piracy, new research suggests. To obtain the iron it needs to keep the bacteria Staphylococcus aureus steals the essential mineral from human blood cells. The chemicals that stop the crime could offer a new type large need antibiotics to kill dangerous infections resistant to drugs.

S. aureus causes diseases ranging from ear infections to meningitis. Antibiotics that kill it quickly lose their punch. Half of all hospital-acquired staph infections now resist all but one antibiotic, vancomycin. Some strains learn to avoid even one, so that new ways to kill the bug are urgently needed.

Nutrition is a possible weak point. S. aureus , like other bacterial pathogens and like us, needs iron to keep its engines running. There are a few years, a team led by Olaf Schneewind, now of the University of Chicago, hungry S. aureus for iron and took one of its proteins in the act. The protein had caught a chemical containing iron called heme in hemoglobin, the protein that makes red blood cells red

Now the postdoc Schneewind Eric Skaar has unraveled a conspiracy between this protein and six other that allows the microbe pilfer iron human red blood cells. Collectively, these proteins are known as surface determinants iron-regulated, or ISD proteins. After S. aureus hole punches protein in the red blood cell, Isd proteins form a bucket brigade flying heme in hemoglobin and pries out of his iron to feed the bacteria, Skaar, Schneewind and colleagues report in the 7 February science . They also identified two other proteins called sortases Isd proteins that bind to the cell wall so they can do their job. This means that drugs that block the way, perhaps by blocking sortases could prevent even the most wicked S. aureus strains to get the iron they need to grow, says Skaar.

"I liked [the study] much," said Klaus Hantke microbiologist at the University of Tübingen in Germany, adding that it offers the best description yet of how a bug extract iron from heme. But S. aureus and other microbes have backup plans for iron, he warns, to block flying heme iron may not kill them.

Related Sites
Backgrounder on antibiotic resistance
Centers for prevention pages S Disease Control. aureus , which are resistant to two common antibiotics, methicillin and vancomycin

pharmaceutical giants Merck and Aventis Pasteur decided to combine their experimental vaccines against HIV in a double blow. In tests on monkeys, the combination vaccine may work better than one of the two companies separately in human trials strategies. "We were driven by the data," says Emilio Emini, who heads the vaccine program against Merck HIV in West Point, Pennsylvania.

Merck and Aventis Pasteur, based in Lyon, France, the developed two vaccines against AIDS that the point of HIV genes into harmless virus. as explained Emini, Merck found in monkey studies between various combinations of vaccines against the other that the adenovirus-based HIV vaccine company continued with a booster dose of canarypox Aventis / vaccine against HIV has led to some of the strongest immune responses they observed. human trials of the Merck vaccine followed by Aventis preparation are awaiting US regulatory approval and could start in the coming months.

the proposed clinical trial is "an experience that needs to be done," said the vaccine against AIDS researcher Norman Letvin of Beth Israel Deaconess medical Center in Boston, Massachusetts. Letvin, who has directed several of these comparative studies in monkeys himself, said there are "very good data" that the smallpox virus such as canarypox can powerfully stimulate the so-called killer cells, warriors Immunity that selectively target and destroy cells infected with HIV and other invaders.

Merck also new data from a study of the human being. the company announced ago 2 years on monkey studies that led the company to launch human trials of vaccines against AIDS this year with a different strategy ( science , April 6, 01, p. 24). first they were vaccinated with an HIV gene sewn into a circular piece of bacterial DNA. they were then stimulated with the adenovirus / vaccines against HIV. But Emini said the first results of DNA studies in humans have disappointing. "Unfortunately, the DNA does not work as well in humans as it does in monkeys," he said.

Emini and colleagues plan to present their new monkey studies and human data from their trials, at a meeting of AIDS in Banff, Canada, which begins March 29.

a huge boost in funding for HIV prevention efforts could prevent up to 29 million new infections by 2010, according to a new analysis. Access to HIV Prevention: Closing the Gap , released today by a panel of AIDS experts known as the Global Working Group on HIV Prevention, provides that the group called the first book of the gap between the efforts to stop transmission of the virus and the continuing needs.

According to the report, in 02 the world spent $ 1.9 billion in low- and middle-income on prevention efforts such as condom distribution, education campaigns, counseling and voluntary testing programs, antiretroviral therapy for infected pregnant women and their newborns, and drug users and offers needles own treatment. This amount should be tripled by 05, estimates of the working group, if the world wants to avert 29 million new infections by 2010. "Without immediate intensification of HIV prevention interventions, we may see an explosion of HIV, "said Helene Gayle of the Bill & Melinda Gates Foundation, which co-convened the working group with the family Foundation Henry J. Kaiser.

The report, based on data from the Joint United Nations Programme on HIV / AIDS (UNAIDS), records how many effective prevention strategies still do not reach the majority of people most at risk of infection by HIV. Only 5% of pregnant women infected with HIV, for example, have access to drugs that can prevent transmission to their babies. More than 80% of injecting drug users have no access to so-called programs of "harm reduction" and only 42% of those at risk have condoms available.

Not only the rich governments must invest more in "combination prevention" efforts, the report concludes, but as if companies and foundations. "The realistic investment now will reap huge benefits in the future "says member of the working group Catherine Hankins of UNAIDS." This is not a dream. We really believe that this can happen if we are committed, and scale. "

Related Sites
Kaiser
Gates Foundation The Foundation

A steroid inhibitor which shrinks the prostate gland - and low-dose treated baldness - also helps to prevent the cancer prostate, the researchers found. The findings come from a massive test, 7 year nearly 19,000 men. But although the drug called finasteride, caused a 25% reduction in prostate cancer, it also increased the risk of aggressive prostate cancer in people diagnosed with the disease. Doctors now hope to find out who is most likely to benefit from the drug.

When finasteride was approved in 1992, it was designed to treat men with an enlarged prostate. (His hair-restoring properties were noted later.) The doctors also asked whether its ability to block the natural conversion of testosterone into a more potent male hormone called dihydrotestosterone, in the prostate may prevent cancer. Previous research had linked male hormones at the onset of prostate cancer. Some scientists worry that many men might start taking finasteride as a preventive measure before it has been proven to do the job. So they quickly - many at the time said too quickly - launched Prostate Cancer Prevention Trial, 18.882 recruiting older healthy men aged 55 and dividing them into two groups at random. A received finasteride, and the other received a placebo.

After 7 years, the researchers, led by Ian Thompson of the University of Texas Health Science Center at San Antonio, met with 060 men. In the finasteride group, 18%, or 804 men had developed prostate cancer. In the placebo group, the number was 24% or 1147 men. (The typical incidence is about 6%, the team believes it has found more because the biopsies were performed systematically at the end of the study.) The difference was so striking that Thompson and his colleagues arrested study a year ahead of

The drug has side effects, however, including problems with sexual arousal. Of greater concern were the highest rates of prostate cancer classified as aggressive. He developed in 6.4% of men in the finasteride group, compared to 5.1% in the placebo group

The difference in cancer rates of the most serious prostate, although small, "looks like a phenomenon, "said Peter Scardino, chief of urology at the cancer Center Memorial Sloan-Kettering in New York City notes that the increase could be misleading;. it is possible, for example, that the drug alters architecture of cancer cells in the prostate, making them only look worse. anyway, Scardino said, the study should be followed by others that evaluate the effect of the drug, for example, men high risk of prostate cancer.

Related Sites
Background on cancer prevention Trial prostate
National prostate cancer Coalition
information finasteride NIH

Radiation is one of the most effective means of killing germs, but it has been used clinically to treat only the cancer. This may be about to change. For the first time, researchers have turned radiotherapy against infection.

With antibiotic resistance on the rise in bacteria, medical researchers are looking beyond traditional drug therapies. One possible source of new weapons is radioimmunotherapy (RIT), a technique used to treat cancer patients. RIT works as a radiation treatment, but tumors blasting zone with radiation from outside, individual radioactive atoms are injected into the blood and circulate through the body. The trick is to fix the atoms emitting radiation to antibodies to proteins for locking onto the surface of the tumor cell. This ensures that the tumor cells overlap with RIT molecules while normal cells are spared the radiation DNA-blasting.

To see if RIT could be useful against an invading pathogen, Kate Dadachova, biologist at the Albert Einstein College of Medicine antibody in New York, and colleagues designed to bind to the surface of Cryptococcus neoformans , a tenacious fungus that plagues AIDS patients. In a paper published online this week in the Proceedings of the National Academy of Sciences , the team shows the courage to RIT as a fungus fighter. When infected mice were injected with the antibody alone, they died just as quickly as untreated mice. But when radioactive bismuth-213 or rhenium-188 atoms have been hung on the antibody, infections began to clarify and the survival of the mice increased up to 60% at the end of the tests. And the best news is that RIT does not seem to kill the bone marrow, a side effect that has limited the use of RIT in the treatment of cancer. Given this initial success in mice Dadachova believes that any kind of infection can potentially be treated with RIT.

"The data clearly indicate that RIT can be effectively used to treat fungal infections," said Gregory Adams, an oncologist at the Fox Chase Cancer Center in Philadelphia. Adams warns, however, that there could have difficulty scaling technique from mouse to man, and there could be damage to long-term tissue radiation.

Related Sites
research RIT Adams
About radiotherapy

The chronic underfunding field malaria research has just received a major new impetus. Traveling in Mozambique mogul software and philanthropist Bill Gates announced yesterday that the Bill & Melinda Gates Foundation will spend $ 168 million on new research in the fight against the scourge, which is estimated to sicken half a billion people every year and kills more than one million.

The money will be spent on three projects:

• The Malaria Vaccine Initiative (MVI), which aims to bring together governments, industry and academia to develop vaccines will receive $ 100 million. Despite decades of research, there is no vaccine against malaria. Founded in 1999 as part of the Program for Appropriate Technology in Health in Seattle, MVI has already received $ 50 million from the Gates Foundation.
  
• The drugs based in Geneva for Malaria Venture will receive $ 40 million for his efforts to develop new cheap drugs against the malaria parasite, Plasmodium falciparum , who developed resistance to many drugs currently available. The nonprofit, who pocketed $ 25 million from Gates in 00, has several drug candidates in the pipeline.
  
• Another $ 28 million will go to the study of an innovative prevention tool based on existing drugs. In intermittent preventive treatment in infants, children, the group most vulnerable to malaria, receive antimalarial drug three times during the first year of life, as well as routine vaccinations. A study in 701 children in southern Tanzania, published in 01, showed that the treatment could cut the number of malaria cases; Gates' contribution will pay for the bigger, cluster tests necessary to decide the implementation strategy widely.

The researchers say that the new initiatives could significantly advance the field, which is currently estimated to receive only $ 100 million a year - a fraction of what is spent on the study of diseases affecting richer countries. "Given the needs in malaria is a tremendous boost," said Michael Gottlieb, a program officer for parasitology at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland.

Related Sites
More information on grants
Malaria Vaccine Initiative
Medicines for Malaria Venture
Executive Summary of intermittent preventive treatment in infants

A new vaccine against the SARS coronavirus has shown promising results in early trials, researchers report in the December issue of 6 The Lancet . The vaccine revved up immune responses in six monkeys, but researchers have not yet tested its ability to fend off disease. No human vaccine exists yet.

To develop the vaccine, Andrea Gambotto and colleagues at the University of Pittsburgh have turned to adenovirus, the culprit behind the common cold. They were designed so that each three adenovirus expresses a component of the SARS virus of different proteins. The idea behind the vaccine is to stimulate a slight attack against the cold virus, and a fierce attack against the SARS protein. Make a vaccine with the only SARS protein was more expensive and took longer, said Gambotto. And it would not have triggered the production of both T cells and antibodies -. Two components of the immune system attack considered necessary to protect

To see if the vaccine could trigger an immune response, the team injected six macaques with adenoviruses and gave them a booster injection 28 days later. After 6 weeks, all monkeys had mobilized killer T cells against SARS and had high levels of protective antibodies. Two control monkeys injected with a common cold virus, do not mount an attack. Because the monkeys do not develop SARS, the monkeys are not infected with the virus.

It is a first step, but significant, says Gary Nabel, director of the research center on vaccines at the National Institute of Allergy and Infectious Diseases (NIAID), which earlier this year suggested ' use adenoviral vaccines against SARS. Get the immune response to two components is important, says Nabel. "If you have one but not the other, the protection that you see tends to be shorter," he said.

Although the team Gambotto is the first to publish results against SARS vaccine trials, the list of candidate vaccines is booming. Nabel said it is too early to say which is best. A Canadian team working on another adenovirus vaccine and Chinese researchers can begin human studies using an inactivated virus in a few months, Nabel said, adding that his group hopes to begin human trials later next year with an adenovirus vaccine which protects mice against SARS infection.

related sites
basic information on SARS NIAID
SARS Resources Centers for Disease Control and Prevention
the site Gambotto
Vaccine Research NIAID Center of

An enigmatic, highly lethal virus group has struck again. More than 40 people in Bangladesh seem to have fallen ill with encephalitis in the last month, and 14 died. Tests indicate the Nipah virus, which began with a devastating epidemic in Malaysia in 1999. Dozens of other cases are under investigation, according to the World Health Organization

The disease appeared in several clusters in central Bangladesh. most victims are children, said principal investigator Robert Breiman the Centre for Health and Population Research in Dhaka.

The Nipah virus and an Australian cousin, Hendra, both naturally infect Pteropus fruit bats. Using horses as an intermediate host, Hendra first jumped to humans in 1994, killing two. Nipah made its way to humans in Malaysia after causing a massive outbreak in pigs, killing 105 of its 276 victims (science, including April 16, 1999, p. 407). Grouped together in a new genre - the Henipavirus -. Attention within the paramyxovirus family, high mortality and the ability to jump the species barriers duo drew

Bangladesh had even small outbreaks in 01 and 03. Since the researchers from the Centers for Disease Control and Prevention (CDC) in Atlanta could detect antibodies against Nipah antigens in patients, but were unable to isolate the virus, they nicknamed "Nipah-like." This time, the virus was isolated, Breiman said, and CDC studies should soon make clear whether Nipah or a close relative

epidemiologically, "it is a very different disease than in Malaysia. - C is what makes it so fascinating, "said Breiman most victims were Malaysian pig farmers;. Bangladesh, there has been no outbreak of swine, and most patients were males . aged 8 to 15 years in Bangladesh bats Tests have shown that they, too, carry Nipah-like virus if an intermediate host, such as the outbreak of Malaysia is scrutinized is. also possible that the victims were directly exposed to feces of infectious bats, said Breiman.

There is no cure for Nipah, but a vaccine is under development. in the January issue of Journal of Virology , the french and Malaysian researchers reported that vaccinia virus, modified to express one or the other of two surface glycoproteins of Nipah protected golden hamsters with a mortal challenge Nipah. Because antibodies against Nipah and Hendra cross reaction, Institut Pasteur main virologist Vincent Deubel said he is "pretty confident" that the vaccine also protect against the virus Bangladesh.

Related Sites
WHO press release
Book on outbreaks of 01 and 03 in Bangladesh by the Center for Health and the research population
information about Nipah
vaccine document Summary

In some people, the immune system has a disturbing tendency to revolt: For some reason, he violently attacks the body itself. For years, scientists have wondered what triggers this rebellion. Now a team of immunologists may have hit on an important piece of the puzzle: an aggressive T cell overproduction of a class that attack the body's tissues. This blow of T cells can be avoided, they found, by exposing mice to bacteria early in life

The immune system is like a mini-ecosystem -. If there is a shortage of one type of cell, another will multiply furiously to fill the niche. To study how this can contribute to disease, immunologists Nora Sarvetnick, Cecile King, and their colleagues at the Scripps Research Institute in La Jolla, California, studied mice predisposed to type 1 diabetes and other autoimmune diseases -immunes. A few weeks before falling ill, these animals had about half the normal number of so-called memory T cells. Cells recall encounters with intruders and defense against future ones.Not surprisingly, the team found that Sarvetnick other T cells have been filling the void memory cells left behind. What was particularly striking is that these replacements were supposedly CD4 + and CD8 +, the same ones that go haywire and destroy the pancreas, which triggers type 1 diabetes rapidly proliferating cells, they found, also sported a specific cell signaling molecule. Although this marker, called IL21 has not yet been associated with autoimmune diseases, the gene product is to the right in the known DNA segment to these mouse susceptible to diabetes, suggesting that IL21 could make a drug target, said Sarvetnick.Furthermore, giving the animal a shot dead bacteria - similar to an immunization in humans - when they were newborns, Sarvetnick and colleagues prevented CD4 glut + and CD8 +. And the animals are not sick, they report in the April issue of Cell 16. The approach gives credit to the so-called "hygiene hypothesis," which argues that exposure to toxins early in life - in the case of mice, inoculated bacteria - helps prevent allergies and autoimmune diseases.Use finding provides evidence for a link between a low number of T cells and autoimmune diseases, although still not clear that it exists, said Michael Bevan, an immunologist at the University of Washington, Seattle. Sarvetnick now hopes to collect samples of human patients to see if his theory holds there.

Related Sites
Background of autoimmunity of the National Institutes of Health

SARS has sent the head of another senior official wheelchair China. Yesterday, the director Li Liming Center for Disease Control and Prevention (CDC) resigned and several officials of lower rank, after a report of an expert group showed the largest recent outbreak of severe acute respiratory syndrome China on a series of faults at National Institute of Virology CDC in southern Beijing.

epidemic earlier this year that sickened eight people in Beijing and in Anhui province and killed a ( science NOW, April 27), has started when two CDC laboratory workers, independently of each other, have developed SARS. The most likely source of their infection, the report concludes, is a lot of supposedly inactivated SARS virus was brought from a high containment facility in a research laboratory of the low security diarrhea where the two worked . Apparently, the inactivation process - the addition of a mixture of detergents to the virus - was not working properly, according to the study, only a summary of five paragraphs was released. In a breach of standard safety procedures, the researcher who conducted the inactivation - identified only by a surname, "Ren." - Had not tested whether the virus really was inactive, as the panel

Some scientists have welcomed the report and the resignation of Li. "This is a clear sign for Chinese scientists and the rest of the world that the Chinese government takes [biosafety] seriously, "said Guan Yi, a virologist in Hong Kong. University But others are disappointed that many details of the incident and laboratory operating procedures remain hidden." I was hoping a full account, more open to what happened, "said Tony Della-Porta, an Australian biosafety consultant who contributed to an earlier survey SARS escapes Singapore and Taiwan.

The government immediately named Wang Yu, currently deputy director of rural and social development within the Ministry of science and technology, as the new director of the CDC. A doctor and researcher trained at the medical University of China and Nihon University Tokyo, Wang has held a number of administrative positions and is a representative of a "new generation" of Chinese leaders more open and capable, says virologist David Ho of the Aaron Diamond AIDS Research Center in new York, who recently met. "I hope that the Chinese government gives enough support to put the CDC on track," said Guan

- .. LEI OF MARTIN and Enserink With reporting by Dennis Normile Tokyo related site
press releases on the investigation

a new study in mice shows that a chemical the body related to a compound in marijuana may complicate pregnancy if present in excessive amounts. The results could have implications for pregnant women, who can put their embryos at risk by getting high.

The psychoactive compound in marijuana, THC, is similar to some of the body's own signaling molecules, called endocannabinoids. These molecules mediate their effects by binding to two proteins, called CB1 and CB2. The exact role of these endocannabinoids in reproduction is uncertain, but high levels are associated with miscarriage in women.

To clarify this role, a team led by Sudhansu Dey, a biologist with the reproduction and development at Vanderbilt University Medical Center in Nashville, Tennessee, examined mice lacking CB1 and CB2 gene. Reporting in September 19 issue of Nature Medicine , the team discovered that embryos are often stuck in the oviducts of these mice and can not reach the uterus. The same problem occurred when the team injected booster injections of a synthetic endocannabinoid. Because the CB1 protein is found only in the muscles of the oviducts, the researchers conclude that endocannabinoids help coordinate the transport of embryos in the womb.

The study shows that the transport of the embryo depends chemical "fine tuning," said Vincenzo Di Marzo, a reproduction biologist at the National Institute of Molecular Biology in Naples, Italy. Dey warns that women who use marijuana may be at risk of ectopic pregnancy - the development of an embryo attached to the fallopian tube rather than the uterus - which can threaten the life of the mother and child, but Di. Marzo cautions that "the general picture in humans could be radically different," and he has not known whether THC reached dangerous levels in the fallopian tubes of women who use marijuana.

Related Sites
homepage of Sudhansu Dey
research group endocannabinoid Vincenzo Di Marzo

An Advisory Committee World Health Organization (WHO) recommended that scientists be allowed to genetically modify the smallpox virus. If the recommendation is accepted by WHO Director General Jong-wook Lee and the World Health Assembly, it would be the first time since smallpox was eradicated that scientists would be allowed this organization to genetically modify the virus.

Smallpox eradication is one of the greatest triumphs WHO: a disease that used to kill millions has been eliminated thanks to a vaccination campaign in the world. The samples of the smallpox virus still only known are stored frozen under tight security in the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, and the research center VECTOR in Koltsovo, Russia. Many involved in the eradication effort pushed for stocks remaining to be destroyed, but others argued that stocks should be kept to allow research on new treatments or safer vaccines in cases of terrorists or rogue countries have secret caches.

A WHO Advisory Committee must approve any research done with remaining stock, and CDC scientists recently requested permission to insert a marker gene encoding green fluorescent protein in the virus to make it easier to test the efficacy of new antiviral drugs. The modified virus would then be a green light under fluorescent light as long as the virus is intact. In the presence of effective drugs, the green glow will fade. The Advisory Committee approved these experiences last week, according to a WHO spokesman.

The experiment in question "has a clear scientific justification" with little or no chance of accidentally creating a more dangerous virus, said molecular biologist Richard Ebright of Rutgers University in Piscataway, New Jersey. The review process, it went through "is an example of how the process should work," he said.

Related Sites
Smallpox information from the CDC
Smallpox Information WHO

Is a diabetes treatment using targeted cancer drugs? This is a question asking two independent teams after giving leukemia patients Gleevec drug and watch their regression of pre-existing diabetes. A 70-year-old woman improved dramatically that she could be considered a type 2 diabetic, three physicians reported last week in the New England Journal of Medicine (NEJM) .

Gleevec was designed to disable a defect in a protein called tyrosine kinase that occurs in chronic myeloid leukemia (CML), a blood cancer. The connection with diabetes does not come as a complete surprise; Gleevec affect other kinases which indirectly contribute a control insulin signaling and the body's response to insulin secreted by the pancreas. And it strikes a known protein kinase growth factor, platelet derived which can stimulate conditions such as atherosclerosis, which are common complications of diabetes. Two mouse studies recently by Mark Cooper and colleagues from the Baker Heart Research Institute in Melbourne, Australia, showed that Gleevec helped animals with atherosclerosis induced by diabetes and kidney disease caused by diabetes .

The benefits may apply to humans, too. In November 04 Journal of Clinical Oncology , doctors from the University of Rome described seven patients with type 2 diabetes and CML. Six improved enough to reduce drugs against diabetes or insulin doses. The only patient whose diabetes did not help, the team said, was also the only one whose leukemia has not responded to Gleevec.

And now in NEJM , Enzo Bonora, an endocrinologist at the University of Verona, hematologist and two colleagues report improvements in three other cancer patients with diabetes, including older women. Italians can not tell if an effect on insulin signaling is behind the unusual observations. In addition, the cohort is tiny, Bonora stresses, so the results should be viewed with caution. "We do not know exactly what is happening," he said.

Neither do others. Brian Druker of Oregon Health & Science University in Portland, a hematologist-oncologist who helped develop Gleevec, said three or four diabetics with CML were treated at the center, and he does not remember changes in their diabetes while on the drug. Yet Druker said that the new findings are "hard to ignore."

Bonora considering asking Novartis, the Swiss company that makes Glivec to consider testing the type of medication 2 diabetes. Currently, Novartis " does not expect "the Gleevec study in type 2 diabetes, spokesperson for Novartis Kim Fox wrote in an email.

Related Sites
American diabetes Association
Information about Gleevec to the Food and Drug administration
Gleevec Context of the National cancer Institute
Clip NEJM letter

Humans put much stock in symmetry. People with symmetrical faces, for example, are often seen as more attractive and worthy companion. But the benefits do not end there. According to a new study, women with more symmetrical breasts are less likely to develop breast cancer than those with less breast perfect mirror

Many factors are known to influence the risk of breast cancer :. inherited genetic mutations ( science NOW, November 26, 26 03), the duration of breastfeeding ( science NOW, July 18, 03), and exposure to smoke from cigarette second hand ( science NOW, April 11, 00), for example. Another difference between healthy women and those with breast cancer is that the latter group more asymmetrical breasts. The question was: the breast asymmetry could predict the risk of breast cancer when measured in healthy women

The preliminary results suggest that it could ?. In a study published today in Breast Cancer Research , medical imaging Diane Scutt and Gillian Lancaster, University of Liverpool, UK, and John Manning of the University of Central Lancashire, UK , measured the volume of the breast mammograms of 504 healthy women. breast asymmetry was quite common. Among women who remained healthy breast averaged 53 milliliters, or 2.5%, larger than the other; for those who have developed cancer, the difference was significantly higher: 63 ml or 2.7%. Researchers have estimated that for each difference of 100 milliliters of breast volume, there was a 50% risk.

Such extreme volume difference is found in very few women, Scutt said, noting that other factors must be taken into account when assessing the risk of cancer. Still, she said, doctors may eventually be able to use breast asymmetry measures to monitor women already at high risk of breast cancer.

Anthropologist Robert Trivers of Rutgers University in New Brunswick, New Jersey, who is studying the effects of asymmetry, agrees and says that the sense of conclusions; breast asymmetry is caused by changes in estrogen levels, which are also associated with other breast cancer risk factors. He adds that the study is potentially "valuable" to quantify the risk of asymmetry.

Related Sites

• The study
• More information on the risk factors of breast cancer

experts have long feared that if a virus and human influenza strain H5N1 avian influenza currently circulating in much the world were to combine their genes, the result could be a disaster-- a deadly virus that spreads easily among people. But scientists at the Centers for Disease Control and Prevention (CDC) reported today that several of these hybrid viruses are, at least in ferrets, relatively benign.

Since 1997, the H5N1 virus has infected at least 231 people mostly in Asia, 133 of them died ( science NOW, February 9). So far the virus has not taken a form that passes easily between humans. This could occur if the H5N1 slowly developed the necessary changes, as probably happened with the Spanish flu of 1918 ( Science NOW, October 5, 05). Or H5N1 virus that infected a person could exchange some of its eight genes with those of a human flu virus - keeping its hemagglutinin (HA) surface protein, to which people have no immunity. Known as reassortment, this process led to two milder flu pandemics in 1957 and 1968.

Thus, CDC researchers and colleagues used a technique called reverse genetics laboratory to make combinations of H3N2 , a strain of human seasonal flu, and the virus strain H5N1 1997. to model the spread of the virus in people, they housed ferrets inoculated with reassortant in adjacent cages to healthy ferrets so that animals may transmit the virus through the air.

The hybrid proteins with H3N2 outside and H5N1 internal proteins well replicated in the cells, but not as easily transmitted among ferrets as H3N2 itself, the CDC team found. And potentially the most dangerous combinations - viruses containing genes for surface proteins of H5N1 and the virus proteins internal human flu - not only did not increase, and the H5N1 virus, but does not spread at all between ferrets. All reassortant would probably need, reports the CDC team today more genetic changes, such as those who made the 1957 and 1968 strains most able to bind to epithelial cells of the human respiratory tract in Acts of the national Academy of sciences . "The picture is more complex" than just the mixing of avian genes and flu, says co-author Jacqueline Katz of CDC.

This does not mean that the world can let down his guard against the H5N1 virus. "I'm cautious about using the word" reassuring, "said CDC Director Julie Gerberding reporters Friday, noting that the study only looked at simple combinations of a human flu virus and one strain H5N1. But it would have been bad news if a so-called reassortant had spread easily among ferrets, according to virologist Albert Osterhaus of the Erasmus Medical Center in Rotterdam, the Netherlands. We can be a "little" relieved, he said.

For wider coverage, please stay tuned for August 4 issue of Science.

Related site

• CDC facts on H5N1