Health Meaning

SAN DIEGO - When you hear of insulin, you probably think of diabetes, but perhaps it could soon bring to mind the disease Alzheimer. The connection is an enzyme that breaks insulin and a protein that causes Alzheimer's disease. Now, a preliminary study suggests that dysfunction of this enzyme may be responsible for Alzheimer's disease in some families.

Alzheimer patients suffer from excessive amounts of a protein called b amyloid, which for some reason built into their brain. In some cases, it appears that genetic mutations increase the production of b amyloid. Alternatively enzymes - so far unknown - which break b amyloid simply do not work fast enough. In 1994, researchers found the first candidate: Insulin-degrading enzyme (IDE) breaks down b amyloid in a test tube. FDI but does not seem likely to be clinically important, because it is normally found in the cytoplasm, and b amyloid built between the inner closed cells or vesicles in the cell.

New evidence for the importance of FDI came from Dennis Selkoe, Wesley Farris and colleagues from Harvard Medical School in Boston. Although screening of brain cells to proteins that destroy b amyloid, they discovered that FDI seemed to have more naturally secreted b amyloid. At the annual meeting of the Society for Neuroscience here Farris November 11 reported that blocking FDI activity stopped approximately 70% of b amyloid ventilation in isolated cell membranes from brain tissue. And causing cells to overproduce FDI intensified the rate of b amyloid ventilation.

The team also worked with the geneticist Rudolf Tanzi and his colleagues from Massachusetts General Hospital to see whether mutations in the gene for FDI could contribute to Alzheimer's disease in people with a family history of disease. The Tanzi group provided data on the seven families of Alzheimer's disease appears to be related to the region of chromosome 10 that contains idea. Selkoe's team analyzed the cells of these families and found that members of the same family had significantly fewer b amyloid degradation than normal, suggesting that FDI can contribute to broken disease. The team is looking for more families with Alzheimer's disease that can have such mutations.

The data are "very encouraging," says Alzheimer's researcher Frank Laferla of the University of California, Irvine, but he remains convinced that IDE cleans most of b amyloid . "It will not be a single enzyme that degrades b amyloid," he said.

Related Sites

Summary of the Society for Neuroscience meeting
learn more about Alzheimer's disease from the National Institute on Aging

Scientists have modified a common respiratory viruses to destroy cancer cells while leaving healthy unharmed, said a report in tomorrow's issue of Science . The next step - a clinical trial in human cancer patients - is already underway

The cancer killer pathogen is genetically modified lung and a family member of adenovirus .. Biochemist Frank McCormick and ONYX Pharmaceuticals colleagues in Richmond, California, found that the modified virus is unable to replicate in normal cells, but it develops into cancer cells lacking the gene p53 that suppresses tumor growth. The p53 gene, leaving cells vulnerable to the virus when it is out, is one whose loss or inactivation is linked to the development of 50% of human cancers. Consequently, the virus could be widely applicable in the treatment of cancer, particularly because the loss of p53 also allows to make cancers resistant to conventional chemotherapeutic drugs. The modified virus has killed human tumors implanted in mice while sparing normal cells.

`` What I like is how smart he is, '' said Richard Klausner, director of the National Cancer Institute. `` It has been a longstanding fantasy to find a [anti-cancer] virus. '' However, he warned that `` not all [new cancer treatment] who is intelligent and focused [to tumor cells] will end up being useful. ''

ONYX team tests the safety of the virus in people with cancer of the head or neck that do not respond to conventional therapies. The tests should be completed in 1997. To date, the virus, which is injected directly into the tumors of patients appears to be safe. But it is too early to say whether the virus has the same ability to kill tumors in humans it has in mice.

WASHINGTON, DC - A deadlock that has gripped the longest and most expensive war in modern times - war against cancer - can finally eased. The cancer death rate in the US fell by 2.6% between 1991 and 1995, the National Cancer Institute (NCI) announced today, marking the first sustained decline 6 decades of modern cancer cases.

"This looks like a turning point in the war 25 years on cancer," Donna Shalala, Secretary of Health and Human Services, said in a statement today. "It is not just a blip once, but a trend of real and promising fall." After a 6.4% increase in mortality from cancer between 1971 and 190, the decline suggests that lifestyle changes and improved treatments start paying.

For example, lung cancer mortality among men dropped 6.7%, representing more than half of the overall decline of 4.3% of cancer deaths in men. NCI attributes this decline in part to the 15% decrease between 1955 and 1970, the percentage of men who smoke. For women, however, lung cancer deaths increased, apparently because smoking among women increased in the 1960s increasing numbers of lung cancer offset strong gains against breast cancer because of diagnostic earlier and better treatment, keeping the overall decline in women's cancer mortality to only 1.1%.

African Americans seemed to make the biggest gains. They experienced an overall decline of 5.6% of cancer mortality, compared with an increase of 18.3% between 1971 and 190.

definitive cancer rates for 1995 will not be released before next year, but experts predict the downward trend will remain relatively unchanged. Says the NCI Director Richard Klausner, "The 190s will be remembered as the decade when we turned measurably tide against cancer."

LONDON - claims in the British media this week that the government is ready to give fire green transplantation of organs from genetically modified pigs in human patients were dismissed as "pure speculation" by a Ministry of Health official. The official said a decision will be announced in 1997.

The London Times and the BBC reported yesterday that the government had accepted the recommendation of an inquiry it was safe to advancing transplants. They reported that the inquiry, chaired by Ian Kennedy, professor of medical law and ethics at the College, London King raised the issue that pig organs could spread to humans potentially dangerous animal viruses. Nevertheless, the Committee has concluded that neither the security nor the ethical issues blocking the way for pig to human transplants. Transgenic pigs are a regulatory protein that helps prevent the immune system from attacking a transplanted organ.

A Ministry of Health official has neither confirmed nor denied that the government planned to approve pigs to humans. "The report will be published in the new year, and we will have to wait until then," he said. A spokesman Imutran, the company based in Cambridge UK, which developed transgenic pigs, says the company n has no information on the content of the report. "speculation is new for us," she said.

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a laboratory of tests indicated that a chemical found in grapes and other fruits and vegetables is a potential antitumor agent. But experts warn that the compound, described in a report in tomorrow's issue of Science , is at least 2 years of testing in humans, and early results do not justify more trips the wine rack.

medicinal chemist John Pezzuto and colleagues at the University of Illinois, Chicago, did not expect it to improve the image of red wine when they began their study. His team was one of many who just a few years began testing some 1,000 plant extracts from around the world for the presence of potential antitumor agents. Their main assay revealed that extracts which inhibit an enzyme called cyclo-oxygenase-1, a cog in the body's inflammatory response. Pezzuto says, "anti-inflammatory agents tend to be good antitumor compounds."

> The team narrowed the 1000 extracts down to three that seemed particularly promising. The most powerful came from Peru roots of Cassia quinquangulata tree, extracts of which are used in traditional medicine to treat fever. Further experiments on a hosted component of the extract called resveratrol, a compound produced in some plants when they are subjected to a stress or pathogen attack. The compound did well in the anti-tumor tests. In addition to inhibition of cyclooxygenase, it impeded the DNA mutations in Salmonella bacteria, increasing the activity of an enzyme in the liver of mice that detoxifies carcinogens, precancerous lesions inhibited in mouse mammary cells, and growth upset of skin tumors in mice exposed to a powerful skin. carcinogenic

Resveratrol is particularly useful as anti-cancer drug candidate because it is easy to obtain: The chemical is abundant in grape skin and has been found in at least 70 other species of plants, including peanuts and mulberries. But experts warn that the compound has a long way to go before the beginning of the pharmacy. "This is a good lead, but it is very early," says Peter Greenwald, director of the division Prevention and fight against cancer from the National Cancer Institute. Greenwald adds that resveratrol is facing at least 2 years' other animal testing and safety testing before it is considered a human cancer prevention trial: "We are certainly far from saying" drink lots of red wine "

A vaccine against cholera cheap performed well in a pilot in Vietnam. The discovery, published in the tomorrow The Lancet , is a breakthrough in the search long and frustrating in developing countries an effective vaccine against cholera, a potentially fatal disease spread by contaminated drinking water.

at the end of 1992, a team led by researchers at the National Institute of Hygiene and Epidemiology in Hanoi, Vietnam, and the National Institute of Child Health and Human Development United States has given the oral vaccine - which is to kill all Vibrio cholerae , the cholera bacteria - to more than 67,000 residents of Hue, Vietnam. A number approximately equal did not receive the vaccine. In 1993, 37 people were vaccinated admitted to a hospital with cholera, against 92 cases in the control group. Thus, the vaccine decreased hospital admissions for cholera by 60%.

Developed and produced at the institute in Hanoi, the vaccine is relatively cheap to produce and easy to distribute as it remains active without refrigeration. He also seems to be equally effective in children and adults. What surprised the researchers, because a similar set, tested vaccine killed in Bangladesh in the 1980s seems to be less strong in children.

"This study is important," said Myron M. Levine, director of the Center for Vaccine Development at the University of Maryland School of Medicine, "because it demonstrates that a developing country can design, produce and evaluate a moderately effective vaccine in a large field trial with little outside help. "

researchers plan to launch a larger trial in Vietnam later this year between the vaccine against placebo. If proven effective, the vaccine could be pressed into service quickly in Vietnam, where more than 3,000 people receive cholera every year. Levine adds that a similar vaccine against other strains of cholera could be produced in developing countries such as Zaire, where an outbreak has killed 12,000 people in the Rwandan refugee camps in July 1994.

Creating a new organism from a single cell was more science fiction than science. Not anymore. Scientists have cloned a sheep using a cell nucleus taken from the udder of an adult sheep, according to a report is expected later this week Nature . The breakthrough has generated a fierce reaction from ethicists and others who fear the prospect of human cloning.

embryologist Ian Wilmut and his colleagues at the Roslin Institute Scotland first increased udder cells in laboratory dishes, then put the nuclei of these cells into egg cells whose DNA had been removed . They found that in the bud, the genome transferred back to embryonic pattern of gene expression, prompting the egg to start dividing. The viable embryo was then placed into the uterus of the ewe that had produced the egg.

Wilmut team first used this technique a year ago, producing lambs with nuclei transplanted from very early embryos. In their latest work, the group reports how cells taken from sheep at any time in their life will do the job. In addition to the lamb of the breast tissue of a sheep 6 years, four children were produced with cores 9 day old embryos and three from the cells of the skin 26 days fetus.

Others have new bodies, mainly amphibians and mice using embryonic nuclei, but failed when they used adult cells. "We now have strong evidence that it is feasible," said researcher Colin Stewart embryo Centre for Research and Development Frederick Cancer National Cancer Institute in Frederick, Maryland.

We thought that in mature somatic cells, certain genes necessary for the development have been transformed permanently, even lost. Thus the success of the group was a "surprise," says Wilmut. "The mechanisms that regulate the expression of genes are more labile than we could have imagined." Finally, Wilmut said he hopes to use nuclear transplantation to create sheep or cattle with genes added to their specific genomes

Theoretically, people could also be cloned. Imagine how much someone would pay for a basketball team fielding five versions of Michael Jordan. Wilmut said Science Now that his group was opposed to human cloning ethically. "We do not know if it will work [in people]," he added. Activists, however, take measures to counteract this possibility. For example, the critic Jeremy Rifkin Biotechnology of the Foundation on Economic Trends announced yesterday his group, as well as some religious leaders and non-governmental organizations, "is determined to mount a global effort opposed human cloning and will seek legislation to ban this technology in every nation. "Several countries - including Germany and the United Kingdom. - Have the laws on the books banning human cloning, but the United States is not among them

People with too little dopamine in their brains develop the debilitating symptoms of Parkinson's disease. Now scientists have identified a molecule that helps the brain get just the right amount of this neurotransmitter. The discovery, published in today's issue of Science * raises the possibility enticing that increasing or restoring the activity of this molecule, called Nurr1, omitting nerve cells could relieve or prevent Parkinson's disease.

researchers already knew that a gene called Nurr1 is most active in brain cells that produce dopamine. To find out what the gene's protein fact, a team led by Thomas Perlmann of the Ludwig Institute for Cancer Research and Lars Olson of the Karolinska Institute, both in Stockholm, Sweden, has created a strain of mice lacking the Nurr1 gene. These mice failed to nurse and died one day after birth. The only physical difference that the group could detect between KO and normal animals of the same age was in the midbrain region, which contains neurons that degenerate in Parkinson's disease. The cells were poorly organized, suggesting that they had never specialized in dopamine-producing neurons.

The team confirmed this suspicion by testing the presence of proteins known to be produced by these particular neurons. Nurr1, tyrosine hydroxylase (an enzyme essential for the production of dopamine) and of other proteins were all absent. Other experiments have suggested that Nurr1 not only causes dopamine cells to form in the first place, but it also helps produce the right amounts of dopamine. "Finding [protein] that affects such a specific [section] brain is very exciting," said neurobiologist Ron McKay of the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. The results raise the tantalizing possibility that the increase or the restoration of Nurr1 activity in failing nerve cells can delay or prevent Parkinson's symptoms.

It may also help researchers track down the cause of the disease. Because Parkinson's disease does not seem to run in families, experts have long sought an external cause, such as a toxic environment. It may now be possible to narrow the search by looking at how the potential toxic substances affect Nurr1. And that could lead to treatment, says molecular biologist Orla Conneely Baylor College of Medicine in Houston, whose team discovered the origin Nurr1: "If we find [toxicants] that inhibit the activity of Nurr1, we can then be able to identify drugs that can counteract that. "

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The number and shape of moles on your skin can indicate your risk of malignant melanoma, the most dangerous type of skin cancer. The results, reported in tomorrow's issue of The Journal of the American Medical Association , suggest that doctors should regularly examine moles of patients during physical examinations.

Although researchers have long known that large, irregular shaped moles are most likely to go wrong, Margaret Tucker of the National Cancer Institute and colleagues at Harvard Medical School wanted to identify the relation between the size, number and type of mole and melanoma risk. They asked dermatologists in two research centers on the major skin cancer - the Melanoma Clinic at the University of California, San Francisco, and the pigmented lesion clinic of the Hospital of the University of Pennsylvania - take detailed notes on the characteristics of moles for patients and melanoma moles turned into

having collected data on 738 patients with melanoma and 1,030 melanoma patients, Tucker's team found that subjects with more than 100 small moles -. 2-5 millimeters in diameter - were twice as high a risk of melanoma as did people with fewer moles. In addition, having one mole with an irregular contour or a color marbled also doubled the risk. Patients with 10 or more moles irregular had 12 times the risk of cancer patients without these moles.

The results are not surprising, as other epidemiological studies have implicated the moles as a risk factor for melanoma, said Sewa Legha, a clinical oncologist at MD Anderson Cancer Center in Houston. However, he said, better quantify the risk is important because too few doctors understand the importance of regular skin examinations. "Doctors are not well versed in recognizing abnormal moles," he said. "It should be a part of a routine physical examination." Tucker added that the data his team "allow doctors to determine, based on physical examination, if a person is at moderate risk or very high risk."

Scientists have linked two major air pollutants with mortality rates increased in 12 European cities. The findings, published in the issue of tomorrow British Medical Journal , are sure to fuel a contentious debate in Europe and the United States on proposed standards that greatly reduce exposure to air pollutants.

An international team led by Klea Katsouyanni of the University of Athens analyzed the daily fluctuations in the levels of two pollutants - sulfur dioxide and particulates - and mortality rates in cities. They found that the average increase of 50 micrograms per cubic meter either sulfur dioxide or black smoke (small particles) on a given day was associated with an average increase of 3% of deaths in western European cities studied - Athens, Barcelona, ​​Cologne, London, Lyon, Milan and Paris. Such levels of pollutants, however, have been linked to a lower increase in mortality rates in the cities of Eastern Europe and Central Bratislava, Krakow, Lodz, Poznan and Wroclaw sulfur dioxide is linked to increased 0.8% of deaths, and the black smoke she gave up 0.6%.

we do not know why people in Eastern and Central Europe, with higher levels of pollution means, seem to be less exposed to daily increases in air pollution. "It was not an effect we expected," said Katsouyanni. One possibility, she and other experts speculate, is that older people are more vulnerable to the adverse effects of air pollution and because Europeans East have an expected shorter life, their cities are less at risk.

the regional difference is treated in other studies on air pollution and health of the European Union . A European project approach

The scientists found that immune systems ravaged by AIDS patients can bounce back from the state of the art drug treatment kept the HIV at bay for a year. But the findings, reported in tomorrow's issue of Science * it clear that the complete reconstruction of a devastated immune system of HIV is a challenge, especially given the limitations of treatment available today.

The new HIV treatments are ward off illness and death in thousands of people. To get a better idea of ​​how prices of the immune system after therapy immunologist Brigitte Autran of H ™ pital Pitié Salpétrire in Paris and colleagues analyzed white blood cells or T cells, which have a receptor known as CD4 name on their surfaces. HIV selectively infects the cells of the immune system, leading to their destruction. In time, people with HIV are left with so few CD4 their immune system can not repel even the wimpiest bacteria, viruses or fungi.

A major benefit widely observed in people receiving powerful new treatments is bouncing CD4 dramatically. Yet overall, but most healthy people infected CD4 do not return to normal levels. Moreover, it is unclear whether patients really regenerate CD4 or simply "redistribute" those who were sequestered in the lymph nodes and other tissues. This, in turn, determines how the effectiveness of the "new" are CD4 fight against infections.

The group analyzed the CD4 Autran who returned in eight adults taking a powerful combination of three anti-HIV drugs. After 1 year, the drugs had pushed the virus and CD4 cells had jumped twice. But because all the CD4 are not created equal, the researchers used other markers on the surfaces of these cells in order to classify them as belonging to the "memory" or subset "naive". A memory cell only responds to invaders it has seen before, while the naive cells can initiate an immune response - and create memory cells - against newcomers. In the first 4 months of treatment, the group found, CD4 return were mostly of the memory cells. But after this initial phase, the naive population rose sharply, indicating that the new cells were generated. - And by providing a "directory" more diverse CD4 capable of responding to new invaders

The study is "the best that the analysis of T cells back after a triple drug therapy that I saw "says immunologist Donald Mosier of the Scripps research Institute in la Jolla, California. However, he warns, the chances are "slim to none" that HIV drugs will eventually allow the immune system to replenish completely with fully functional CD4, both because of the limitations of medicine and the ability of the immune system to settle. "I would be really surprised if you can keep doing this year after year," he said. Autran has hope, however. "I'm very optimistic that if we could reduce the level of virus replication enough, we could discuss this, "she said.

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A computer that can diagnose common psychiatric disorders could be a useful aid for busy physicians and make screening more common mental disorders. And for some disorders, patients seem more willing to confide in telephony based system than in their personal physicians, according to a study in tomorrow's issue of Journal of the American Medical Association .

With medical examinations for 10 minutes or less, many primary care physicians do not have time to ask questions that can help diagnose mental illness - and patients do not usually wear volunteers these informations. "There is a high rate of undetected mental disorders in the population," says Kenneth Kobak, a psychologist who led the study at the Dean Foundation for Health, Research and Education, Middleton, Wisconsin. "These people go to their regular doctors in the family, but doctors are not catching it."

So Kobak and his colleagues created a computer to ask questions based on a common questionnaire called the primary care evaluation of mental disorders, which is used to diagnose alcohol abuse, major depression, bulimia and other disorders. They set up an interactive voice response system, similar to that used by many directory assistance for telephone companies, where the computer asks a question, and the listener responds. in the review of 0 patients in four primary care clinics, a clinical eating disorder, and alcohol treatment facility, computer and medical disorders professional each found in approximately 60% of their patients. Even more striking, patients with alcohol abuse were twice as likely to admit their illness to the computer as their primary care physician.

Experts say that the computer system could be a useful aid for busy doctors. "It works very well for what it is, which is a screening device," says Jean Endicott, a psychologist at the College of Physicians and Surgeons of Columbia University, New York. "I think the availability of these types of programs and procedures should certainly improve screening and detection, and hopefully treat these diseases. "

A vaccine against rotavirus significantly reduced the number of deaths from childhood diarrhea in Venezuela, according to a study published in the tomorrow of New England Journal of Medicine . But critics say that the effectiveness of the vaccine has not been confirmed in the poorest countries, where inadequate nutrition could work against her, and they argue that most developing countries will not be able to pay anyway.

Nearly 00,000 infants and children die each year, mostly in developing countries, severe diarrhea caused by rotavirus infections. Although the virus infects almost everyone in the world, it only kills children. A child with severe rotavirus diarrhea can suffer from 10 to 15 episodes of diarrhea and vomiting every day. And although treatment with rehydration salts and the right food can save lives, researchers have worked for years on a vaccine that could reduce the severity of the disease, especially in poor countries health care and developing nutrition.

In the early 190s, Albert Kapikian and colleagues at the National Institute of Allergy and Infectious Diseases developed a vaccine, and tests in Finland and the United States have shown that it could reduce the incidence of severe diarrhea. But in tests in developing countries such as Brazil and Peru, it has reduced the cases of 30% to 45%. Kapikian and his colleagues decided to create their own vaccine trial in a poor urban area near Caracas, Venezuela, with a dose 10 times stronger vaccine

Unlike previous trials -. Which counted all cases in which a child was sick and would not be detected a reduction in the severity of the disease - the researchers counted the number of cases where a child has been hospitalized with severe diarrhea. In the study of 20 infants, the vaccine reduced the incidence of severe disease by 88% compared to the control group. The only side effect of the vaccine was a slight fever.

But other researchers say diarrhea vaccine efficacy in Venezuela does not mean it will work everywhere. Richard Cash, of the Harvard School of Public Health and Harvard Institute for International Development, explains the impressive results in Venezuela could be due to better nutrition that strengthens the immune system, and a lower rate of overall diarrhea than Brazil or Peru. "What you really need to do is try to Bangladesh or in countries in sub-Saharan Africa where sanitation is worse," he said. Treasury also emphasizes that, at $ 30 per dose, the vaccine is too expensive for many developing countries, where five average annual health care spending only $ $ 20 per person.

For vaccines to teach the body to recognize a pathogen, they must insert a diagnostic fragment in macrophages and other cells of the immune system. Viruses can do the job, but they can be dangerous - especially in patients whose immune system is already weakened by a viral infection. Now researchers report that a single bacterial protein may act as carrier, priming the immune system to respond to specific foreign proteins. The new technology, reported in the current issue of Proceedings of the National Academy of Sciences could be adaptable in a delivery system for vaccines against AIDS.

The key to the new technology is a protein called hsp70, which belongs to a group of proteins called "heat shock proteins" or "stress proteins" have been found in bacteria and higher organisms. These protein strongly stimulate the immune system of mammals. in recent years, several research groups have created vaccines that protect mice against cancer by injecting them isolated stress proteins from own tumor cells of the mouse. Now, Rick Young immunologist and his colleagues at the Whitehead Institute and Massachusetts Institute of Technology have coaxed a mouse immune system to recognize other proteins by attaching them to a heat shock isolated tuberculosis bacilli proteins and injecting the combination into the animal.

the group has created a prototype vaccine to mice by binding a protein to chicken ovalbumin called hsp70 tuberculosis proteins. They then implanted in mice genetically a cancer cell line festooned with the ovalbumin protein. Generally, these cancer cells overwhelm the immune system of the host. But because hsp70 somehow made known target the immune systems of host mice, ovalbumin on cancer cell surfaces was like a bull's eye in the sights of a sniper. The mouse immune system responded enthusiastically, killing invasive cancer cells. After 40 days, 80% protected mice were still alive, whereas all the control mice died of tumors.

Heat shock proteins are "much safer" than viral vaccines, said Michael Starnbach, immunologist at Harvard Medical School in Boston. And although researchers do not know how the heat shock proteins to sneak into killer T cells, they might be able to deliver almost any antigen. "It's exciting," says Starnbach.

Blood vessels, such as highways and roads that reach most addresses, run through almost all tissues of the body. The problem for doctors is that drugs of this transportation system moving almost everywhere find their way to many more nooks and crannies than they are supposed to. Now, German researchers have found a low-tech solution to get the goods to specific places of the body: tiny polymer spheres with drugs that can be accommodated in specific sets of narrow vessels called capillaries before releasing their loads. The technique, reported in the next month of Nature Biotechnology , could provide a new vehicle for delivering drugs to people with heart disease and other ailments.

heart attacks occur when clogged arteries prevent the heart to circulate enough blood to sustain itself. Treatment is possible to create new pathways for blood to reach the heart muscle using a protein called fibroblast growth factor (FGF) to stimulate the growth of new blood vessels. FGF, use has however not found widespread as a treatment again because of two major problems :. Enzymes quickly disable FGF outstanding, and high doses can dilate blood vessels and lower blood pressure dangerously

To deliver FGF where it is needed more precisely, a team led by physiologist Wulf Ito Institute Max Planck physiology and clinical research in Bad Nauheim, Germany, FGF attached to small letters - resin spheres, 7 micrometers in diameter, which are too big to squeeze through capillaries. A sphere of drug loaded "looks like a golf ball with FGF in small bumps," says Ito.

The researchers tested the technique on healthy pigs, injection of spheres in an artery feeds a part of the heart muscle. in seconds, 60% of the spheres inserted into capillaries fed by the artery. the remaining 40% were probably slightly smaller and squeaked through, said Ito. Do not worry, the rest of body "gets a very, very small dose," he said. Indeed, the remaining spheres were so diffusely distributed outside of the heart tissue that researchers could not find one.

If other research shows that injecting spheres trigger a new hair growth, they could have "huge clinical implications," said Elazer Edelman, director of the Harvard-MIT biomedical engineering Center in Cambridge, Massachusetts. Already, similar spheres get their first test in people: Edelman has conducted tests in which FGF-bearing areas are located in people's chests as they are open for coronary bypass surgery. "It will be interesting to see how these injectable spheres work in clinical trials," he said.

New blood test can quickly reveal whether a child has a bacterial infection. If the test, described in the March Journal of Pediatrics , can be developed for widespread use, it could help doctors save the lives of some infants, as well as millions of dollars in treatments for babies appear to have infections.

Because infants are so vulnerable to infections, doctors must make hasty decisions as to whether a baby who looks ill really needs an antibiotic. Often wandering on the safe side, the doctors end up treating 17 healthy babies for everyone who is later confirmed to have an infection. For a decade, immunologists have sought a molecule in the immune system of the newborn which could serve as a warning flag for an infection. But the molecules tested so far, none have been proven.

Leonore Herzenberg, Erica Weirich, and their colleagues at Stanford University Medical Center has undertaken to develop a simple blood test for the latest and most promising sentinel molecule called CD11b. The molecule appears on the surface of neutrophils, a type of immune cell, within 5 minutes of being exposed to a bacterial toxin called saccharide lipopoly. Researchers designed a fluorescent marker that clings to CD11b and can be accessed regularly by Laserlight. They screened blood of 106 children suspected of having an infection, or high risk for one. They also come with a proven, but slower test for an infection that flags C-reactive protein (CRP). Every 15 babies tested positive for CRP, which is produced in large quantities during infection, were also positive for CD11b. In addition, there were no false positive results CD11b.

If confirmed, the results "could ultimately change how doctors decide how to treat newborns," said Herzenberg. But Robert Baltimore, a pediatrician at Yale University Children Hospital, is not so sure. Although the test "has a very high predictive value", he said, he could suffer the fate of many previous laboratory tests for babies - doctors ignore. "Very often, they will order the test and treat babies anyway," even if the test comes out negative, he said.

Blood is known spiral as it flows through the arteries, but researchers at a conference Royal Academy of Engineering announced yesterday in London that the helical flows Whirl like a corkscrew. In addition, the twists and branches of blood vessels promote the swirling flow, which runs through the plaque and helps prevent atherosclerosis.

Until recently, researchers lacked the power of the computer to accurately model the blood flow in the complex, three-dimensional geometries, said Spencer Sherwin, a fluid dynamicist at Imperial College London science, technology and medicine. But a new computer program written by Sherwin and colleagues seems to have finally managed to accurately model the arterial blood flow: Their calculations correspond to the MRI data on the speed of blood within the arteries, says Danesh of Tafti national Center for Supercomputing Applications in Champaign, Illinois.

the new program could open the way for more sustainable arterial grafts, natural or artificial replacements for the arteries, which do not work mate Colin said Caro, a physiologist also at Imperial College. About half of arterial grafts fail in 10 years, after being blocked by a thickening of the inner wall. This can happen because surgeons tend to join grafts perpendicular to the vessel wall in a single flat plane, rather than the curve as a freeway onramp that ships are natural.

Sherwin now considering the use of simulations and real arteries MRI to determine the optimum angle of arterial grafts to maintain swirling blood flow that could prevent blockages.

"the results of the blood are obviously important to improve arterial graft construct," said Michael Bettmann, a cardiovascular specialist at Medical Center Dartmouth-Hitchcock Dartmouth in New Hampshire, "but they can also be useful to the development of new techniques, primarily those not operating for the treatment of peripheral arterial disease. "

AIDS patients survive longer these days, but most still succumb to opportunistic infections that escape an immune system weakened by HIV. Now, however, scientists have evidence that immuno-cell field which stops naturally with age may be able to return to active duty in some people. The discovery, reported in the current Journal of Clinical Investigation , suggests that the body could resume production of certain immune cells after the drug hitter HIV in submission

immune cells called T lymphocytes - . Frontline troops into battle against foreign microbes - are produced in the bone marrow and then battle prepared in the thymus, a small gland at the base of the neck. This training is considered to occur before birth until puberty, when the thymus atrophy and is generally thought to stop functioning. In adulthood, according to most medical textbooks, thymus treated the T cells enough to deal with most microbial invaders one person is likely to encounter in a lifetime. But attacks against HIV destroys T-cells, leaving patients infected defenseless against many pathogens. Nevertheless, some studies have shown that patients on powerful new antiviral therapies seem able to regenerate some of these cells once viral loads were reduced for a sufficient period of time -. Leading researchers to question the source of these new T cells

To see if the thymus may be the source of these new T cells, immunologist Joseph McCune and his colleagues at the Gladstone Institute of Virology and immunology in San Francisco thymus size measured in 99 HIV-positive patients. The team used a technique called computed tomography, which creates an image in three dimensions X-ray of internal organs. About half of the subjects had a much more thymus tissue that HIV-negative controls. In addition, the size of the thymus gland of a subject closely related to blood levels of T cells - indirect proof that the thymus may be working and the release of these immune cells, say the authors

Experts warn that rejuvenation. thymus tissue alone does not prove that the gland is working properly. Yet the results are "a good argument" for a revival of the thymus function, says immunologist Brigitte Autran of the Pitié-Salpêtrière Hospital in Paris, whose team discovered some of the first evidence that immune reconstitution could be possible. "It is clear that the immune system is more difficult to try to raise the number of T cells," adds Mario Roederer, an immunologist at the University of Stanford.

An epilepsy drug used in Europe removes key signs of addiction to cocaine in baboons and rats, according to a study in Synapse this week . If confirmed in human studies, the finding may lead to a new way to help cocaine addicts kick the habit.

The drug, called gamma vinyl-GABA (GVG), seems to erase a chemical characteristic of cocaine and other addictive drugs: a surge of dopamine, a neurotransmitter in the brain's reward centers. GVG does not act on dopamine directly, but increases levels of a neurotransmitter called gamma-aminobutyric acid (GABA) that acts as a brake on dopamine release; that GABA may boost curb excessive neuronal activity leading to seizures. In the early 190s neuropharmacologist Stephen Dewey of Brookhaven National Laboratory in Upton, New York, and colleagues began to test whether GVG also removes dopamine-induced increase in cocaine.

In the current study, the team gave Dewey cocaine 20 baboons, some of whom had previously received injections of GVG and followed dopamine levels in the brain baboons using a technique imaging called positron emission tomography. While cocaine produces a large increase in dopamine in baboons not given GVG, the researchers did not see this increase in animals treated with GVG, suggesting that the drug "blocks the neurochemical action of cocaine," says . -member of Charles Ashby team, neuropharmacologist at St. Johns University in Jamaica, New York

the researchers then investigated whether GVG could also block a behavior related to drug addiction in rats: their tendency to return to a place they had already received an addictive drug. This behavior reflects the ability of rats to link environmental signals with drug taking, an association that often triggers drug cravings in people. researchers discovered that GVG stopped the behavior, indicating that it could weaken drug cravings.

"We hope that GVG will dramatically reduce the tendency of an addict back to cocaine," said Ashby . Of course, if this hope is realized will depend on the results of clinical trials are expected to begin later this year. "This is obviously something that should be followed," said Frank Vocci neuropharmacologist of the National Institute on Drug Abuse.

A drug combination therapy for hepatitis C cured almost half of the patients tested. Experts say the results described in tomorrow New England Journal of Medicine , make a good case to give both ribavirin and interferon alfa-2b as a standard treatment. But they note that more effective drugs will be needed to eliminate the virus in all patients

One of the most common infections in the world., Hepatitis C is carried by about 170 million people . While most people have no symptoms, about 20% develop chronic inflammation that scars and destroys the liver. The virus kills about 10,000 people each year. Until recently, the only accepted treatment was 6 months interferon repeated injections to stimulate an immune response against the virus. This approach, experts say, is able to cure less than 20% of patients who undergo this. Recent clinical trials have shown that the antiviral ribavirin may enhance the effectiveness of interferon, but few patients were tested.

Two teams have now studied the combo drug in randomized controlled trials. John McHutchinson the Scripps Clinic in La Jolla, California, gave daily doses of the association or interferon alone in 912 previously untreated patients. After 6 months the combination had cleared the virus from the blood of 31% of the subjects in this group. "For a chronic condition, we have something that is very impressive," said McHutchinson. Another trial, conducted by Gary Davis of the University of Florida, Gainesville, tried the combo drug on 345 patients who had been treated successfully with interferon alone, but later relapse. This cured 49% of patients. (the success rate is higher than in the Scripps trial because the relapsed patients Florida trial have been known to respond to interferon.) the studies were funded in part by Schering-Plough, which makes both drugs.

the results represent "a breakthrough in the treatment of hepatitis C," says Jake Liang, a researcher at the National Institute of diabetes and digestive and kidney diseases. But he says it will take the discovery of new drugs to see the most dramatic improvements in treatment.

A NAHEIM , C ALIFORNIA - Many toxicologists can remember of be stubborn at some point by people opposed to chemical testing on animals, particularly mammals. Now, a researcher has taken another step to facilitate the disapproval that he and his colleagues often feel. At the annual meeting of the American Association for the Advancement of Science, which publishes Science NOW, aquatic toxicologist Richard Winn, University of Georgia, Athens, describes a promising new line of fish that can help replace the rats for screening toxic chemicals.

to improve their ability to detect chemical changes could result in the mid 1980s, toxicologists have begun using laboratory mice with bacterial genes that can be folded out and screened for damage. This is much easier than, for example, the screening of the whole mouse genome or waiting for the tumors to develop. Hoping to find an alternative to rodents, Winn and his colleagues turned to Medaka fish, which are already used for toxicology tests. They brought in the animals two bacterial genes, called Lad and eyelash , used in the lines of transgenic rodents to detect mutations caused by chemicals.

In the first tests, they spilled the mutagenic widely used N -ethyl- N -nitrosourea (ENU) in their fish tanks, and after waiting 1 to 16 hours, ground fish and bacterial DNA recovered for analysis. The researchers found they could detect even slight genetic changes, mapping of two to threefold increase in mutations at low exposure to ENU. Winn also describes a transgenic medaka with a third gene called LacZ said it works well to detect radiation damage. Radiation tends to knock out or rearrange chunks of DNA, and this gene is large enough - and its support, a circular piece of DNA called a plasmid, is strong enough - there is enough DNA for left analysis after radiation shot.

If the research pans, it could not only save the lives of many mammals, but also do toxicology tests cheaper and easier. Keep a cost of fish "a few cents a year," compared to 20 cents per day per mouse, Winn said. "I'm really happy" to hear about the progress of Winn says toxicologist Shane Barbara of Louisiana State University in Baton Rouge, who studies cancer in mice. She and others are eager to start tests on transgenic medaka .

A gene linked to breast cancer can stimulate cancer growth of advanced prostate that kills some 44,000 American men each year. The finding, from a study of transplanted tumors in mice and reported this month in Nature Medicine , raises the prospect of one day prostate cancer treatment with a drug that reduces breast tumors in women.

caught early, prostate cancer can be treated chemically castrate the patient. At this stage, the tumors thirst androgens - male hormones such as testosterone - and will shrink if they are blocked by drugs. But eventually (usually after a few years) tumors are learning to live without hormones and start to grow and spread again. Once this happens, no treatment can control them. The cancer itself weans of androgens, oncologist Charles Sawyers and colleagues at the University of California, Los Angeles, believe, developing the taste of the protein produced by the gene HER-2 / neu . The gene also allows some breast cancers grow without estrogen.

Sawyers and the company found that advanced tumor stage prostate grafted into mice contained numerous times more protein HER-2 / neu tumors to androgen-dependent stage earlier. They also found that androgen dependent tumors grow without hormones if they were infected with a genetically modified gene loaded with the virus. The researcher concluded that the protein / neu HER-2 stimulated androgen receptors in cells in late phase, triggering the continuous cell division without the need of androgens.

If HER-2 / neu fuels cancer growth in advanced human prostate, the disease might respond to Herceptin, a drug against breast cancer which binds the protein / HER-2 neu. But Tapio Visakorpi, an oncologist at the University of Tampere, Finland, whose commentary on the results also appear in Nature Medicine warns: "There is still a very, very long way to browse to say whether Herceptin be useful in the treatment of prostate cancer. "Visakorpi said that researchers should then determine whether HER-2 / neu is also prevalent in tumors of advanced prostate in men as it is in the transplanted cancers in mice. Sawyers, who intends to test Herceptin mice, agrees. "My hope," Sawyers said, "is that this document will force people to answer this question."

Today is the birthday of Ines Mandl, an American biochemist who has conducted pioneering research on enzymes and elastic tissue that led to progress in the understanding of pulmonary emphysema.

Mandl, who was born in 1917, studied collagenase - a group of about 20 enzymes that can break down the collagen in a soluble form - and was the first to isolate and purify an enzyme. As director of obstetrics laboratories / Gynecology at the Delafield Hospital (affiliated with the University of Columbia), Mandl studied respiratory distress and emphysema in neonates and identified the role of elastin, an elastic tissue in the lungs. It showed that emphysema patients have elastin degradation, which destroyed lung tissue. Smoking, she found, elastin also damaged

In 1972, Mandl founded the magazine Connective Tissue Research

Source: Benjamin F. Shearer and .. Barbara S. Shearer, remarkable women in the physical sciences :. A biographical dictionary (Greenwood Press, 1997)

For people missing an arm or a leg, a sophisticated artificial limb can do more than simply restore some of their capabilities. A report in the June issue of Nature Neuroscience suggests that a so-called "myoelectric prosthesis" - which captures the electrical signals of the muscles in the stump to drive an artificial hand - can prevent phantom pain, feeling that a member hurts, even if it has disappeared.

Almost all patients who undergo amputation can still feel their missing limb during the first weeks after the amputation, and often . missing arm or leg hurts in two of the patients, the pain persists for years or decades the source of phantom pain is enigmatic, but appears to involve rewiring of the cortex, the superior control center of the brain. neurons of the neighboring regions in the cortex seem to establish links with the area which formerly controlled the cut branch, but is now fallow. sensory stimulation of a body part on the other hand, is known to extend the zone the cortex involved in its control.

In a myoelectric prosthesis, electrodes sense, muscle contractions and send electrical signals to a motor driving the movements of the hand. Neurologist Martin Lotze and his colleagues at the University of Tübingen, Germany, wondered whether tactile stimulation as a prosthesis provides or requires muscle activity could prevent expansion in the cortical center used by a neighboring region, control the movement of the lips, and reduce phantom pain.

team interviewed 14 patients on the severity of their pain and their use of the prosthesis. To assess cortical rewiring, they asked the patients to purse your lips, while brain activity in their lip-control region was measured using imaging functional magnetic resonance. Although almost all patients recalled having phantom pain immediately after the amputation, the team found that five patients who wore their functional prosthesis for longer periods and used the most were more or less painless, and showed almost no expansion of the area control lip into the cortex.

Psychologist Ronald Melzack of McGill University in Montreal, Canada, welcomes the work. "These are good things," he said. "There is no doubt that the use of prostheses should be initiated as soon as possible," he said, because it could spare patients from having to take strong painkillers with potentially serious adverse effects. Melzack adds, however, that the myoelectric devices are very sophisticated yet "a very expensive luxury treatment" for amputees.

Ticks, already notorious as carriers of disease, get another black mark tomorrow New England Journal of Medicine . A document, it indicates that ticks can infect people with a new, potentially life-threatening disease. The culprit is a bacterium known as Ehrlichia ewingii , which until now was thought to infect only dogs.

The microbe is a relative of E. chaffeensis , humans can also contract ticks. Attacking his victim white blood cells E. chaffeensis causes a disease called ehrlichiosis, characterized by fever, malaise, muscle pain, and, if untreated, organ failure. Ehrlichiosis was first reported in 1986; Since then, hundreds of cases have arisen in the US, with the highest incidence in Missouri.

Because his flu symptoms are much like those of many other diseases, ehrlichiosis is difficult to diagnose. Doctors can get an early indication of the number of white blood cells from patients' blood, said Gregory Storch, professor of pediatrics at Washington University in St. Louis, but to confirm their diagnoses, clinicians use the polymerase chain reaction to search for the patient's blood for a typical ribosomal gene from several Ehrlichia bacteria.

Between 1994 and 1998, the team Storch ran this test, and another more specific that detects only E. chaffeensis of 413 people suspected of ehrlichiosis. Sixty patients were tested positive for the general test, but of those, only 56 were confirmed to have E. chaffeensis . Suspect that the other four have dealt a new Ehrlichia species, the researchers sequenced the bacterial gene in the blood and compared to a database containing sequences from known infectious bacteria. To their surprise, the "new" species had already been identified - by veterinarians. Called E. ewingii , it usually infects dogs that have been bitten by ticks. "This is the first time anyone has seen this in humans," says Storch.

The symptoms of E. ewingii infection seems indistinguishable from E. chaffeensis , but many other things about the disease is unknown. "it might be unusual or common," says Storch, "and it could be carried by deer ticks and Lone Star ticks." Three of the four patients had weakened immune systems - may have contributed to E. ewingii foothold - but the fourth was healthy before

"They opened a new chapter in history of pathogens by ticks, "said Jesse Goodman doctor from the University of Minnesota .. the next step is to try to develop E. ewingii in the laboratory and perhaps learn how to prevent ehrlichiosis, he said. "We'll keep working on medical aspects," says Storch, "perhaps in collaboration with veterinarians."

A virus that has made the human genome permanent residence for a long time can be a major cause of breast cancer, if a study presented last week at a conference in Sydney Virology, Australia is correct. Researchers say they have found a piece of the virus - which resembles a known virus that causes breast cancer in mice - in a high percentage of samples of cancerous breast tissue. If confirmed, and if a link can be established between the presence of the virus and development of cancer, the discovery could help doctors predict who is at high risk for the disease.

In recent years, scientists have identified two genes that, when mutated, can cause breast cancer, but they can not account for the great majority of cases. By the 1940s, however, virologists across a virus that causes breast, or breast tumors in mice. The mammary tumor virus of mouse called virus (MMTV) is a so-called retrovirus, a type of virus that can stick its genome into the chromosomes of infected hosts. If the land of the viral genome near one of several oncogenes of the cell, it can cause the gene to become abnormally active, leading to uncontrolled cell division and ultimately to cancer.

The discovery of MMTV sparked a hunt for a similar virus in human breast cancers. But while many researchers picked up at least indirect evidence that such viruses might be present there, a clearcut identification was hampered by the fact that the human genome carries thousands of so-called "human endogenous retroviruses elements" leftovers essentially harmless retrovirus of the ancestral man who found a permanent place in our chromosomes long ago. "This made the search for a 'HMTV' like finding a needle in a haystack," said virologist Robert Garry Tulane University in New Orleans.

Garry and his colleagues decided to take another look. They used the chain reaction highly sensitive polymerase (PCR) to search in human breast cancer samples for an MMTV gene, known as about . They chose this one because its sequence differs most from that of the comparable gene in endogenous retroviruses to ensure that any sequence they picked up was actually a linked MMTV gene. And researchers have discovered such a sequence in over 85% of the 30 samples of breast cancer. To their surprise, however, they also found in about 30% of breast tissue samples and other organs healthy people. This suggests that for Garry HMTV is an intact retrovirus that is inserted into the relatively recent human genome and is probably passed from parent to child through the germ line.

Currently, however, the finding raises more questions than answers. In 1995, for example, a team led by molecular virologist Beatriz Pogo of the School of Medicine Mount Sinai in New York also found notes of a virus like MMTV in human breast cancer tissue. But the team Pogo almost never found signs of the virus in healthy tissue or other organs - that led them to believe that HMTV was not part of the genome, but an infectious agent. And in any case, simply detecting signs of a virus in cancer tissue does not necessarily mean that it plays a causal role. One way to learn, said Alan Storey, an expert on cancer virus at the Imperial Cancer Research Fund in London, perhaps to check whether the virus-infected cells in culture become cancerous. In the meantime, Storey said, the new findings "clearly stimulate much research" in the breast-cancer virus.

Researchers have found a new approach for the treatment of chronic pain: destroy a small group of spinal cord nerve cells pivots with a chemical " smart bomb. " Treatment is less sensitive to pain rats, according to a study published in the current issue of Science . If the strategy works in humans, it could become an alternative to morphine.

Chronic pain is associated with a range of illnesses and injuries, but its cause is often quite mysterious. Sufferers may experience severe pain and unabated long after the original source - tissue damage, for example - seems to have healed. Often the pain is aggravated by innocuous stimuli, such as pressure of a blanket or even a gentle breeze against your skin.

Previous research had indicated Some, however, that neurons of the spinal cord that communicate using a neurotransmitter called substance P plays a role in chronic pain. So neurobiologist Mantyh Patrick and colleagues at the University of Minnesota and Veterans Affairs Medical Center in Minneapolis found a way to kill only those neurons in rats. They attached to the substance P saporin, a toxin that brings the ribosomes of the protein assembly of the cell stopped. Then they infused hybrid molecule in the spinal cord of rats. Nerve cells that normally bind substance P also took in the complex -. and died after the toxin released their ribosomes

to see if it would go against chronic pain, the team induced the condition in rats. Even a slight pressure on the legs would cause animals to jerk them back - a response that mostly disappeared in the rats given the complex P-saporin substance. However, the rats reacted still really painful stimuli, a response that could be moistened with morphine. This is important Mantyh said, because doctors are not likely to advise their patients to undergo this kind of treatment if it were to make morphine analgesic their best, ineffective.

"These are very important experiences," said Tony Yaksh of the University of California, San Diego, who looks forward to any new approach for the treatment of patients with cancer, arthritis or other diseases associated with chronic pain. before the technique strikes clinics, however, Mantyh team should look for side effects and test the therapy in larger animals before proceeding to human trials. Finally, Mantyh said, perhaps the treatment would use a chemical that stuns rather than destroys neurons.

Some 20 million people in the US alone suffer from liver disease, and more than 40 000 of them die every year. liver transplants could save many of these lives, but there are only enough donor livers to treat about 4,000 US patients each year. Now researchers have developed a way to grow liver cells in the laboratory by temporarily making them cancerous, then use them to reconstruct a damaged rat liver. The technique could one day help prolong the lives of patients waiting for a donor organ, or even eliminate the need for a transplant

When the liver suffers chronic damage -. Often hepatitis or too alcohol-- cells eventually stop division and member fails. So far it has been difficult to grow liver replacement cells in the laboratory. But in 1996, Philippe Leboulch of the Massachusetts Institute of Technology and Harvard Medical School have developed a technique of introducing a cancer oncogene called T antigen in cells, so "immortalizing" that they continually increase in culture. To keep the cells of cancer remain forever, he designed the oncogene so that it can be cut to the DNA of cells later by an adenovirus carrying a pair of "genetic scissors."

When Ira Fox, a surgeon liver transplantation at the University of Nebraska Medical Center in Omaha, has heard of this system, he immediately called Leboulch and proposed a collaboration to a trial in liver cells. the new team set to see if they could grow enough cells to save the life of rats that had been about 0% of their livers surgically removed. This treatment is always fatal, but when the researchers injected their hepatocytes in the spleens of the animals up 60% of the animals survived, they report in February 18 Science .

the success is "very encouraging," says hepatologist Roy Chowdhury of the Albert Einstein College of Medicine in New York . But he noted that the liver failure in humans is different; a virus or a toxin may persist, said Chowdhury, and perhaps damage the transplanted cells, too.

Rides, thinning hair, bones and weak muscles - physical degeneration of aging is well known. But it is still a mystery why the body breaks down as it gets older. Now, using a hot new technology, researchers finally found the genes that make cells show their age.

DNA microarrays, also called DNA chips, fueled the excitement in the research community because they can test the activity of many genes immediately. In essence, microarrays are embedded size nail chips with known DNA extracts. To find out what is happening inside a cell, the researchers expose the chip fluorescently labeled genetic material that is sent inside the cell. Active genes leave telltale traces as they correspond with mapped locations on the chip.

A team led by Richard Lerner and Peter Schultz of the Scripps Research Institute in La Jolla, California, used microarrays to analyze gene activity in fibroblasts, the cells that help form skin and connective tissue. They tested the cells of healthy people of different ages and also children with Hutchinson-Guilford progeria, a rare inherited disease that resembles an accelerated form of aging

The researchers found that expression of only 61 genes -. Out of a total of some 6300 tested - changed with age. Many of the same changes have also taken place in fibroblasts of patients with progeria, a finding indicating that these individuals are in fact age abnormally fast, they report to March 31 Science . Among the genes depending on the age, many are known to help cells divide, providing support to the idea that aging stops cell division.

It will take more work to confirm that these genes are differentially active in aging people, not just cell lines differently aged, says Leonard Guarente aging specialist at the Massachusetts Institute of Technology. But Guarente said, "This is an extremely interesting piece of work." It is still a way to the beauty salon, however. Lerner said: "The Fountain of Youth here ... I do not think"

A new transplant technique has enabled eight diabetic patients to completely stop their insulin injections. The study, described this morning at the meeting Transplant 00 in Chicago, is "truly a milestone in the treatment of diabetes," said Hugh Auchincloss transplant surgeon at Harvard Medical School.

Type I or childhood onset, diabetes affects hundreds of thousands of people in the United States is believed to start when the immune system kills insulin-producing cells in the pancreas. insulin plays a key role in regulating the blood glucose by promoting the conversion of sugar into glycogen. to compensate for the lost cells, diabetics must inject insulin several shots a day. Even with these injections, however, wide variations in the levels of sugar in the blood trigger side effects ranging from kidney failure and nerve damage to blindness.

for years, researchers have sought ways to transplant cells producing healthy insulin in diabetic patients. Most were only partially; patients less than one in 10 can do without insulin injections one year after the transplant, and they all have to endure the side effects of immunosuppressive drugs.

A new protocol developed by transplant surgeons James Shapiro, Jonathan Lakey, and colleagues from the University of Alberta in Edmonton, Canada, has had much better initial results. The eight team patients - one of them treated there more than a year -. Have normal blood sugar without insulin injections

The team attributes the success to several factors. First, they transplanted islet cells as soon as possible after the removal of an organ donor. Second, do not use any non-human proteins for preparing the cells prior to transplant. Finally, they used a new anti-rejection drug that blocks a protein CD25 specific immune system, instead of steroid drugs used commonly. These drugs are known to be hard on the pancreatic cells, says immunologist transplant Norma Kenyon of the University of Miami in Florida, but the cells seem to tolerate the new drug more easily.

Kenyon warns that patients who are age 29-53, must remain on immunosuppressive drugs for the rest of their lives. Auchincloss and stresses that each graft requires two donor pancreases, so that the treatment would only be available for "a small fraction" of diabetics. To help more patients, researchers will learn how to grow human islet cells in culture or to find a way to use animal islets. The protocol is "a really great step," Auchincloss said. "But is was only a step. It is actually not the cure. "

In people with schizophrenia, a brain circuit that regulates emotion is overwhelmed by a chemical messenger called dopamine. The new discovery confirms a long-standing hypothesis about schizophrenia and provides the most direct evidence to date on why schizophrenics lose touch with reality.

The devastating symptoms of schizophrenia include delusions, hallucinations and paranoia. Like all effective antipsychotic drugs block a receptor for the neurotransmitter dopamine, the researchers guessed there are more than 30 years that dopamine circuits were overactive in people with the disease. This could be caused by an excess of dopamine, a too large number of dopamine receptors, or both. Indeed, the autopsies showed schizophrenics an overabundance of one type of dopamine receptors in the striatum, a part of the brain that helps to regulate emotion. But because most people with schizophrenia were treated with antipsychotic drugs, some researchers have argued that it was a result of drug treatment rather than the disease.

To measure whether the circuitry of dopamine-sensitive were overactive in schizophrenia, Anissa Abi-Dargham of Columbia University College of Physicians and Surgeons in New York and colleagues compared 18 schizophrenia with 18 normal subjects . First they treated patients and controls for 2 days with a drug that knocks off dopamine receptors. Then they gave the patients a mimetic radiolabeled dopamine which could accumulate on dopamine receptors emptied. Using a brain imaging method called emission tomography single photon, they compared the amount of dopamine molecules like landed on the receptors in the two groups.

In people with schizophrenia, the amount of dopamine-like molecules bound to the receptors increased twice that in controls, they report in the edition July 5 of Proceedings of the national Academy of sciences . It most likely means that schizophrenics have both more dopamine available and most of the dopamine receptors. In addition, the increase occurred in the October 2 chronic patients - who had used antipsychotic drugs in the past -. And in the eight newly diagnosed patients who had never been treated with medication

The search for "can potentially help us understand how antipsychotic drugs work," says psychiatrist and neuroscientist Francine Benes from Harvard Medical School in Boston. But psychiatrist Shitij Kapur of the University of Toronto is warning that researchers still need a way to measure dopamine directly into the brains of live schizophrenic. But "assuming this is in place," dit- it, "the whole story [dopamine] will start to come together."

For more information on schizophrenia of the National Institute of Mental Health: www.nimh.nih. gov / publicat / schizoph.htm

An international team of scientists is homing on the site of a third gene that might be involved in the development of hereditary breast cancer. If the gene is found, the work will pave the way to improved genetic counseling and cancer screening and treatment for family members with breast cancer history.

The shortcomings of so-called "susceptibility genes" contribute to the development of 5% to 10% of all breast cancers, which greatly increases the risk of contracting the disease from a woman. In to date, researchers have identified two genes predisposing to breast cancer, called BRCA1 and BRCA2 , but faults in these genes probably represent no more than one third of all hereditary breast cancer.

to track other susceptibility genes, research teams from Finland, Sweden, Iceland and the United States have joined forces. They identified 37 families that are affected with high rates of breast cancer, but who are not known BRCA1 or BRCA2 mutations. using a technique called comparative genomic hybridization of tumor DNA and normal tissue of 61 women, researchers found five probable areas for breast cancer genes. To refine their search, dim teams throughout these regions using two new mathematical models. Finally, they drew on the well-established methods of genotyping and linkage analysis to identify similar DNA segments shared by patients with breast cancer in a family.

Together, these techniques have given a region on chromosome 13 as the probable site of a third susceptibility gene, the teams reported in the August 15 Proceedings of the National Academy of Sciences . While it may take months to years to identify the faulty gene, this work is "an important intermediate step in seeking the reduction," said team member Olli Kallioniemi, a geneticist cancer in National Institute of research on the human genome in Bethesda, Maryland.

other scientists welcomed the announcement carefully, however. population geneticist mark Skolnick, scientific director for Myriad Genetics Inc. of Salt Lake City, which led the team that identified BRCA1 , finds the work "potentially very important," but warns that the statistical data are not conclusive.

Mary-Claire King, a geneticist at the University of Washington, Seattle, pioneered research of genes predisposing to breast cancer, leases integrative approach of the teams. But she noted that both Skolnick and BRCA2 also lies on chromosome 13. It is possible, they note that undiscovered faults around this gene may have confused the analysis. definitive proof that the team had indeed found a new gene linked to breast cancer, they say, will not come until researchers reproduce their work in other family groups or find gene itself.

Related Sites
The NCI's information page on Breast Cancer (CancerNet)

The old saying "put a thief to catch a thief" is best known as the inspiration for Alfred Hitchcock's 1955 film To Catch a Thief . But with a twist, it's also a good description of a new technique to fight against common infections: set a microbe to catch a microbe. By orchestrating common bacteria to produce microbicides, researchers hope to find a first line of defense against infections of all kinds.

all bacteria are bad. Some live safely and on humans, including one called strain Streptococcus gordonii than that normally found in the mouth. To supplement this easy living microbe and arm themselves against pathogens, a team of researchers led by microbiologist Luciano Polonelli the University of Parma in Italy changed S. gordonii so it secretes antibodies . Imitations of antibodies the action of a "killer toxin" naturally produced by certain strains of yeast, and destroys microbes such as Candida albicans , a fungus that causes vaginal yeast infections; Pneumocystis carinii , which causes a kind of pneumonia often deadly for AIDS patients; strains and multi-resistant tuberculosis drugs.

To test whether the engineered microbe could fight against the disease, the researchers infected vaginally with rats Candida . They then introduced vaginal colonies established engineering S. gordonii in eight rats, and microbes cleared the infection in 75% of animals. None of the untreated animals recovered from infection. This makes the microbe as effective as flucanozole, an antifungal drug commonly used to treat yeast infections. And since microbes produce antibodies continuously, they also prevent Candida infections. Antifungal drugs, however, are used to fight against established infections.

In principle, the same technique could be used to develop bacteria that could repel all kinds of infections, said immunologist Larry Zeitlin Epicyte Pharmaceutical Inc. of San Diego. But obtaining regulatory approval to release genetically modified bacteria will be difficult, he said. "It is a really smart idea," Zeitlin said the new technique, "but whether it will pan out is difficult to predict."

Related Sites

Technical Information Candida albicans , the University of Minnesota

researchers are trying to assess the hazards of arsenic have encountered an obstacle: They need an arsenic isotope for their studies, and the only place in the world which makes it is exhausted. It could take until mid-01 before enough is produced to replenish the two dozen laboratories around the world who need the isotope.

The shortage comes at a particularly bad time. In May, the Environmental Protection Agency of the United States (EPA) proposed a cost reduction of levels of arsenic, a natural contaminant in drinking water. EPA also funds a burst of research into the causes of cancer how arsenic because immobilizing the elusive mechanism could reveal whether the limit should be so strict. To understand the mechanism, researchers use arsenic-73 to find genes that metabolize arsenic and explore how these metabolites enter cells and damage DNA.

But the Department of Los Alamos National Laboratory Energy in New Mexico did not produce any arsenic-73 since the beginning of 1999. They were the isotope smashing protons an accelerator in a rubidium bromide target, but the source of the protons - a tritium production program - closed. A new facility isotope production was expected to open next year, but the massive fires that swept the region this spring pushed the completion date to mid-02. Los Alamos ran out of its inventory arsenic-73 around July.

"None of us knew about it until it is too late" to make other plans, said Marc Mass, an EPA toxicologist. There are other plotters, he said, but they are expensive and too insensitive to some experiments. Los Alamos officials say they can do arsenic-73 to another accelerator, perhaps in Canada - but it can still be six months before any arsenic-73 is available, said Gene Peterson, Programme Director and Isotope Production distribution of laboratory

that's little comfort to arsenic researchers, who are at the end of their minds. Vas Aposhian toxicologist at the University of Arizona in Tucson, who bought the last arsenic-73 millicuries this summer, said he and his colleagues "will scream bloody murder" when provisioning their laboratory works a few weeks. Miroslav Styblo, a biochemist at the University of North Carolina, Chapel Hill, tried to convince his colleagues of an accelerator in his native Prague to do a lot of arsenic-73. But "so far," he said, "we do not have realistic promises."

Related Sites

Los Alamos Isotope Production and Distribution Program

EPA proposed rule arsenic from drinking water

chemotherapy may save lives, but it comes with unpleasant side effects. Drugs target rapidly dividing cells, allowing them to home to tumors, but they also kill normal cells as those of the hair follicles. Although the resulting hair loss is not life threatening, it can be extremely distress for patients. Now a team reports that they can prevent hair loss caused by chemotherapy in first rats rub the skin of animals with a newly developed drug.

The new drug targets an enzyme called cyclin-dependent kinase 2 (CDK2), which results in key stage in the cycle of cell division. Many researchers in industry and academia are looking for CDK inhibitors, mainly in the hope of developing agents to block the growth of cancer cells. But William Kaelin of the Dana-Farber Cancer Institute in Boston, who is among those who do this work, emphasizes that CDK inhibitors offer two possibilities. They can be used, he said, to find "be smarter ways to kill cancer cells or smarter ways to protect normal cells."

Focusing on the latter objective, a team led by Stephen Davis Glaxo Wellcome Research and Development in the Research Triangle Park, North Carolina, has developed a powerful CDK2 inhibitor for topical application. The researchers tested the drug in both animal models. In one, the researchers transplanted human scalp hair in mice. When they applied the CDK2 inhibitor to growing hair transplants, the researchers report in the January 5 version of Science , temporarily inhibited cell division of the hair follicle. In a second model, rubbed the drug in hair newborn rats and gave them a chemotherapeutic agent. The drug prevented hair loss in half of the animals and reduced in another 20%. It was not as effective against a combination of two chemotherapy drugs, protection of only 33% of hair loss in animals. Davis also said his team did not detect any interference with the ability of chemotherapy drugs to kill cancer cells in animal tumor models.

Oncologist David Fisher of the Dana-Farber described the work to date as a "huge advance." He hypothesizes that it may also be possible to design inhibitors to protect other tissues normal which were damaged by chemotherapy drugs the lining of the intestine. - where damage causes nausea and vomiting. - It is a possibility, if a non-resorbable version can be produced

When the Albany Medical Center in New York announced last November that it would assign a new annual award in biomedical research, something made the price stand out: a cool half million dollars. Now the center has given its top prize on Arnold Levine, president of Rockefeller University in New York and co-discoverer of a protein that goes wrong in cancer.

The award was established with a gift of $ 50 million to the Albany Medical Center in Morris Silverman, a businessman from New York who was educated near Albany. The award recognizes researchers who have made important contributions to medicine and biomedical research. It is the largest annual award in science or medicine in the US, according to a spokesman Albany door probably only a second award for the Nobel Prize, which last year was worth $ 915,000.

Levine won the award, announced on March 14, for his contribution to cancer biology. In 1979, p53, a protein that is defective in more than 50% of co-discovered human cancers. The protein normally cleans up after the cells with damaged DNA by clamping down on cell division or inducing cell suicide; otherwise, cancer cells proliferate. Levine has not only helped to recognize the role of p53 in cancer, he also played a leading role in the cloning of the first DNA p53 and identification of a key protein that binds p53 and modulate its function. It is now testing compounds that could kick a defective p53 protein back in action or crank up the amount of p53 available to limit the damage.

"Arnie has made a fundamental contribution to each step in the development of the p53 field," said Frank McCormick, director of the University of California, San Francisco Comprehensive Cancer Research Center and author of several reviews p53. He praises Levine for an open and collaborative style of research that has influenced many p53 researchers. "In such a competitive field this is a major achievement in itself," said McCormick.

Related Sites

The Albany Price Medical Center

Rockefeller University

More on p53

The children suffer lasting brain damage from poisoning lead moderate even when treated quickly with a drug that removes lead in their blood, according to a large clinical trial reported in issue 10 May the New England Journal of medicine . The results mean that the only way to avoid permanent brain damage from lead poisoning is to prevent it in the first place, experts say.

Severe lead poisoning causes brain damage, seizures and death, especially in children. Low to moderate levels of lead, which occur in 1 to 20 children under 6 in the US, cause more subtle damage. Even years after exposure, young children have reduced attention span and decreased ability to think and reason abstractly. A drug called succimer orally mops that lead in the blood can save the lives of children seriously poisoned. But no one knew if it could prevent brain damage in moderately poisoned children.

To find out, epidemiologist Walter Rogan of the National Institute of Sciences of Environmental Health in Research Triangle Park, North Carolina, colleagues enlisted medical centers four cities that regularly treat children poisoned lead. The double-blind trial, eventually included 780 2 years, 75% were African American, who had been poisoned, mostly dust from deteriorating lead paint in their urban homes. The research team removed the lead paint and cleaned houses. Then they gave the children either succimer or placebo pills for several months. The children were tested three years later, when they were 5 -. The youngest age at which cognitive deficits can be measured reliably

Although drug therapy reduced blood lead values ​​significantly compared to placebo treated children showed no differences in IQ, memory, conceptual thinking, or hyperactive behavior of untreated children. The researchers will test again the differences after the children enter primary school, but so far "there is not even a hint" of a difference, said Rogan.

The document is "very important because it shows that you can treat children up to the kazoo with a chelating agent and you get nowhere," says pediatrician John Rosen, who heads the main program to children's Hospital of Montefiore in the Bronx, new York. Together with other studies, the new results underline the need to remove or replace the lead-based paint, which was banned in 1976 in the United States, but still coats the walls of 25 million homes. "This is an entirely preventable disease and healing is decontamination," Rosen said.

Related Sites

Page the treatment of children exposed to lead host (TLC) clinical trial of lead poisoning prevention program
Childhood Centers for
general information about lead poisoning and housing policy of the national advocacy group Center for Disease Control and Prevention Lead-Safe Housing