Health Meaning

A new vaccine can prevent dangerous infections among infants and their mothers. A vaccine against group B streptococcus (GBS) - which causes severe infections in nearly two 1,000 newborns and kills about 10% of infected people - triggered the production of antibodies against the bacteria in tests clinical

vaccines work. by exposing the body to a lure representing an infectious agent, so that when the real pathogen comes along the body will see a resemblance and mount an attack. The recognizable part of GBS is a complex sugar coating, which immunizes only about 60% of people. To make a vaccine that can protect most of the rest, infectious disease expert Dennis Kasper and colleagues at Brigham and Women's Hospital in Boston used a relatively new technique to connect the complex sugar tetanus toxoid, a protein known to elicit a strong immune response.

conjugate vaccine seems to do the trick, triggering levels of protective antibodies in 54 of the 60 women tested, with no serious side effects. The killed GBS antibodies in the test tube, and, at least in mice, were able to cross the placenta and fetus immunize. After Kasper researchers injected pregnant mice with antibodies from immunized women, mouse gave birth to puppies immune to GBS. "The characteristics of the antibody were what we expected, '' said Kasper, who with Carol Baker of Baylor College of Medicine in Houston in detail the clinical trial in the latest issue of Journal of Clinical Investigation .

conjugate vaccine is the first demonstrated both safe and effective, said Pamela McInnes, project manager for the Initiative streptococci group B at the National Institute of allergy and infectious diseases . More human trials are needed, especially to see if the vaccine is safe for pregnant women McInnes said the vaccine also offers the promise to reduce the number of reproductive age women carrying GBS - now estimated at 10 .. % to 30% of the search can now, she said, "with a more clinical approach and with real hope for prevention. ''

In a surprising finding, daily supplements of the trace element selenium have been found to reduce the risk of several types of cancer in patients with skin cancer history. The results, reported in tomorrow's issue of Journal of the American Medical Association , surprised researchers, which discourage people from loading the supplement until the results are replicated in other people .

A team led by epidemiologist Larry Clark of the Arizona Cancer Center in Tucson had observed lower rates of skin cancer in people with high levels of selenium. So the group has undertaken to test whether selenium could reduce the risk of recurrence of basal cell or squamous cell carcinoma in people previously treated for skin cancer. Beginning in 1983, they began to enroll patients from seven dermatology clinics in the eastern United States, giving half the group a placebo daily and the other half to 0 micrograms of selenium beer yeast tablet. A total of 1312 patients, three quarters were men, received selenium or placebo for an average of 4.5 years.

The group found that selenium was no better than placebo in preventing a return of skin cancer, refuting initial thesis. But he demonstrated some anticancer properties. For example, the selenium group recorded only 77 cases of secondary cancer compared with 119 in the control group. For prostate cancer, the ratio was 13 cases vs. 35; for colorectal cancer, eight against 19; and for lung cancer, 17 against 31. The selenium group also experienced 17% fewer deaths, including half the number of tests from a variety of cancers. The trial was to continue for 2 years, but Clark pulled early decision "so that doctors can know of this potential for cancer prevention."

Experts say the results should be considered with caution. the study is "very, very encouraging," said Clement Ip, a cancer researcher at Roswell Park cancer Institute in Buffalo, but he and others say more studies are needed to determine how selenium affects tumors . and how it affects a broader spectrum of patients There are also questions about its safety when taken on a long term basis: Selenium can lead to hair loss and nail doses above 1 milligram . "We recommend that we do an additional test to confirm these results and see how it spread to other people," said Clark, especially women and people with certain types of cancer.

Scientists have created a new species of mouse suffering from atherosclerosis when fed a Western diet rich in fats. The discovery, reported in Science tomorrow * offers a model for probing the causes of a human disorder - familial combined hyperlipidemia (FCHL) - which occurs in about 2% of people in Western countries and can lead to premature coronary heart disease.

In a simple and elegant experience, Alan R. Great and his colleagues high mouse Columbia University with a human gene linked to FCHL with mice lacking receptors for several proteins that bind to low density lipoprotein ( LDL), a fat molecule to which elevated blood levels is associated with atherosclerosis. The human gene, apolipoprotein C-III is linked to high blood levels of low density lipoprotein (VLDL), also a culprit in heart disease. Thus, the offspring of mice had the worst of both worlds :. VLDL and expenses of a crippled ability to remove LDL circulating blood

Tall team fed mice a diet consisting of approximately 20% saturated fat which was also high in cholesterol. "The big surprise," said Grand, "is that both genetic defects do not simply add to each other. They were clearly synergistic." The mice four times the normal normal levels of VLDL and LDL compared to mice developed arterial clogging and earlier and more severely than did mice and genetically modified food on a regular hybrid. The finding adds weight to a theory that APOC3 and defective LDL receptors play a key role in all the high lipid levels observed in FCHL says Grand.

"There is an imaginative study," says Richard Havel, a lipid researcher at the University of California, San Francisco. But APOC3 is probably not the only villain in FCHL, which is considered from defects in several genes. yet, Havel said, the work "is a step in the right direction." the next step will be to try to breed mice with defects in several genes that mimic the human condition more closely.

* Science online subscribers can link to the full text of the report.

A protein that triggers the growth of blood vessels appears to play a key role in the development of Kaposi's sarcoma. The discovery, published in the tomorrow of the Proceedings of the National Academy of Sciences, may lead to better treatments for the disfiguring and potentially fatal cancer that strikes nearly a third of AIDS patients.

pathologist Parkash Gill and his colleagues at the University of Southern California School of Medicine had suspected that vascular endothelial growth factor (VEGF), a protein that regulates the permeability of blood vessels and stimulate growth, could be involved in Kaposi's sarcoma, because tumors - that appear as purple spots on the skin - twisted masses of disorganized blood vessels and capillaries that leak. The team found that the Kaposi sarcoma cells indeed produce scads of VEGF. They also noted that tumor cells with elevated levels of two receptor proteins that bind to VEGF, whereas the skin cells from the adjacent unaffected areas had no receptors.

Gill group next tried to block VEGF with the hope of preventing tumor growth. They injected with antisense DNA - a mirror image so of the DNA segment in the gene encoding the VEGF protein - into mice with tumors. The antisense DNA can bind to the cell an RNA template for the protein, thus strangling its production. The treatment seems to work :. Tumors in mice that received the antisense DNA has not increased as rapidly as those mice that received random DNA fragments

"If it holds up that VEGF is an very central player "in Kaposi sarcoma, said Harvard University cell biologist Judah Folkman, it may open multiple avenues of treatment. Although the initial antisense DNA tests were promising, Gill said compounds that block VEGF receptors can also be a weapon against cancer, which can kill patients when tumors invade the lungs or other organs.

BETHESDA, MARYLAND NCI-tU-Turn on mammograms - Cancer The National Cancer Institute (NCI) has once again breast approved test for women in their forties. The action brings NCI's recommendations in line with those of the American Cancer Society and other groups, but puts the body against external scientific group recently concluded that these tests save Lives.

At a press conference today, the National Advisory Council of Cancer (NCAB) announced its support for mammograms every 1 to 2 years for women aged 40 to 49 with a normal risk breast cancer. These X-ray tests could save lives per year 1500-00, says NCI Director Richard Klausner, although the board noted that a third of all diagnoses may be false alarms. Klausner welcomed the recommendation of the Board and said the policy would become effective immediately.

Although most experts agree that regular mammograms can reduce breast cancer deaths among women over 50, they have fiercely debated the value of universal screening for women in their forties . Clinicians who treat breast cancer patients are among the staunchest supporters of screening, while many epidemiologists find little statistical evidence for a benefit. In 1993, citing a lack of clear scientific evidence, NCI reversed its policy and decided not to recommend screening in this age group. In January, a panel of 14 members of epidemiologists side and reiterated this position after having evaluated seven randomized trials.

But the NCAB came to a different conclusion, deciding that mammograms every 1 to 2 years to reduce breast cancer mortality by about 17%. The advantage is "difficult to detect with a high degree of certainty," admitted President NCAB Barbara Rimer, a behavioral scientist at Duke University, but adds that universal screening is "scientifically defensible." The only dissenting voice on the board of 17 members was epidemiologist Kay Dickersin of the University of Maryland School of Medicine.

The new policy does not apply to women in their forties with a high risk of breast cancer, those family history of the disease, certain genetic mutations, or who gave birth after age 30. These women said the council should consult a physician for the appropriate interval for testing. The board made its decision a month earlier than planned because of public controversy stirred by the position of the consensus group, Rimer said, but it did not influence the result. "We made our separate work all this "ACS officials applauded the new NCI policy and said it was in line with its recommendation for annual screening in this age group.

low-tar cigarettes can reduce your chances of getting a type of lung cancer, but they increase your risk of another type of lung cancer, according to a study reported in next month's issue of cancer . The work, carried out in Switzerland, supports the prevailing belief that low tar cigarettes are not much safer than their predecessors high octane.

Fabio Levi of Vaud tumor registry in Lausanne, Switzerland, and colleagues analyzed 7423 cases of lung cancer reported between 1974 and 1994 in two Swiss states, Vaud and Neuchâtel. The group found that the incidence of squamous cell tumors in larger lung tubes in men fell 27% from 1974 to 1979 in 1989-1994. Meanwhile, the rate of adenocarcinoma, which affects cells secreting mucus from the lungs, increased by 142% over the period. Overall, the rate of lung cancer in the region increased slightly, from 55.6 to 57.5 cases per 100,000 people.

Swiss researchers blame the cancer rates of lung shift on phase-in since the mid-1950s to mid '80s cigarettes containing lower tar, which is rich in carcinogens. Therefore, they say, smokers have less tar deposits in major pulmonary tubes, which represents the rate of less tumor there. But the smoke low tar cigarettes is easier to breathe and tends to get sucked deep into the lungs. Levi's group suggests that this deep breathing offers more carcinogens in smaller pulmonary branches, where adenocarcinoma develops

The authors acknowledge that other factors -. dietary changes to air pollution - can be at least partly responsible for the shift in the type of lung cancer. Nevertheless, the study confirms similar trends in US cancer rates, said Neal Benowitz, a researcher of nicotine at the University of California, San Francisco. Switching to low-tar cigarettes, he said, can reduce the risk of certain diseases, but it will not protect you against the real killers: "You will not change your risk of cancer or heart disease. "

SAN FRANCISCO - A therapeutic vaccine against severe rotavirus diarrhea, which kills nearly 00,000 children worldwide each year, succeeded in clinical trials. The vaccine works best "to mitigate the outcome of the disease" - not necessarily to prevent it, said Hsieh Chia-Lung, Senior Director of Vaccine Development at Wyeth-Lederle Vaccines and Pediatrics. Featured here at the annual meeting of the American Chemical Society, the vaccine of the company, called RotaShield, should be on the market by the middle of next year.

Hsieh announced that clinical trials involving 10,500 children in nine countries showed that RotaShield limit the severity of the disease in 80% to 95% of cases. The vaccine is composed of human viral proteins inserted in a similar virus affecting rhesus monkeys.

The experts were initially disappointed that prevention is not the strong point of the vaccine, said pediatrician S. Michael Marcy of the Kaiser Foundation Hospital Panorama City, California, a member of the American Academy of committee of Pediatrics infectious diseases. However, he said the new vaccine will be a great improvement over existing treatments, which amount to just give fluids to sick infants. For this reason, Marcy said, "This vaccine is a winner."

Although rotavirus sickens 3.5 million people - mostly infants - in the United States each year, it is the deadliest in developing countries, where access to health care is limited and poor sanitation. It is also common in the southern United States and within the African-American families, says Hsieh. She says Wyeth-Lederle considering recommending the universal oral vaccination for infants at 2, 4 and 6 months of age.

BETHESDA, MARYLAND - Nobel Laureate David Baltimore Price challenged a fundamental principle of research AIDS: a type of immune cell is regularly able to seek and destroy cells infected with HIV. Speaking yesterday at the Ninth Annual Conference on progress in the development of vaccines against AIDS, Baltimore, virologist at the Massachusetts Institute of Technology (MIT) and the head of a National Institutes of vaccine advisory committee health against AIDS, suggested that HIV effectively disarm the immune cells, white blood cells called cytotoxic T lymphocytes (CTL). The findings may shed light on why some experimental vaccines work in monkeys.

A crucial problem in the vaccine work against AIDS is to determine which immune responses to a vaccine must stimulate. Many researchers focused on antibodies, which GLOM the virus in the blood and help mount a successful infection. Much attention was also paid to CTL, who is like smart bombs, target and destroy cells that HIV has already infected. But the laboratory Baltimore has cast doubt on CTL can do the job themselves

Baltimore and Kathleen Collins MIT CTL guru Bruce Walker of Massachusetts General Hospital, started with two deceptively simple questions :. CTL can actually kill cells infected with HIV? Or to the target cells, such as those infected with cytomegalovirus and other pathogens, produce a factor that protects against CTL? To answer these questions, researchers have developed a test to gauge whether HIV interferes with the production of CTLs. For the immune system to produce CTL against specific pathogens, an infected cell must hold pieces of the pathogen on its surface, spreading what the enemy looks like. The Baltimore team found, however, that an HIV protein called NEF prevents infected cells display fragments of HIV to the CTL-part of the immune system, essentially blindfolding it.

"It seems very interesting," said Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases, the meeting of the sponsor. "We need to take a step further and see up where you can push it. " Baltimore emphasizes that it is impossible to extrapolate from test-tube results to people. But he said the study may help explain why apes and humans infected with HIV that lack NEF gene appear to be unharmed by the virus: Maybe the infected cells stimulate the production of anti-HIV CTL antibody which butterfly infection early on.

- Scientists have genetically Alzheimer's a new strain of mice that can be a model of the early stages of Alzheimer's disease. Even before the brains of human patients develop a characteristic of the disease - the clusters of proteins called plaques - their memories are deteriorating and they lose neurons. The new mice, described in tomorrow's issue Nature , also show neurons and memory loss without plaques, suggesting they could provide a testing ground for drugs intended to slow the progression of the disease in humans. But all the experts are not convinced that the team created an accurate model for early Alzheimer's disease.

In recent years, plaques, which accumulate over time from sticky protein, called insoluble amyloid, became the first suspect to cause the debilitating symptoms of Alzheimer's disease . But some researchers have come to suspect that another protein, produced as an intermediate step when cells chop a long molecule called amyloid precursor protein (APP) to form amyloid could injure neurons before scar plates the brain. test tube studies, for example, suggested that the APP fragment is toxic to neurons.

Now Jo Nalbantoglu, a molecular biologist at McGill University in Montreal and colleagues created mice that have brains that are riddled with these precursor fragments. To do this, they added that the part of the APP gene for amyloid precursor mouse embryos. When they grew into adults, the experimental group had much more trouble remembering how to solve a maze that made the mice in a control group.

Researchers then dissected the brains to see why. When they electrically stimulated living slices of the hippocampus, a memory center for the signal persisted in neural pathways known for 0 minutes in the control mice, but died after about 15 minutes in mice with large amounts of amyloid precursor fragment. In addition, 18-month-old experimental mice had a lower density of 20% of the neurons in the CA1 region of the hippocampus - an effect observed in human Alzheimer's patients. Previous mouse models, however, have failed to show that death characteristic of nerve cells.

neuroscientist Mark Mattson of the University of Kentucky, Lexington, called the work "important progress." But Sangram Sisodia Johns Hopkins University School of Medicine, who is working on mouse models of Alzheimer ' Alzheimer others think neuronal loss could be an artifact of how the Canadian team had neurons to be a true Alzheimer model mice are going to produce amyloid plaques and develop -. and they show no biochemical evidence either. then Nalbantoglu plans to seek these plaques in aged mice while investigating how the precursor proteins could be the cause of memory loss.

PARIS - A common virus may help the AIDS virus to infect certain types of cells and wreak havoc on the immune system. The results, reported in tomorrow's issue of Science * require closer symbiotic relationship between HIV and its possible ally - Cytomegalovirus (CMV) -. Imagined before

CMV, a member of the herpesvirus family that infects 80% of adults and almost all HIV-infected homosexual men, has long been a prime suspect as a cofactor AIDS. A team led by Marc Alizon at the Cochin Institute in Paris, in collaboration with Michel Seman at the University of Paris, began probing whether HIV can use a protein called CMV US28 to enter into certain types of cells. The protein is expressed in cells experimentally infected with CMV. US28 had previously been shown to act as a reception point, or receptor, for the same immune system molecules called chemokines that bind to CCR5, a receptor used by HIV strains which dominates during the early stages of signaling infection.

In determining whether US28 could act as HIV accomplice, the French group has inserted the US28 gene in a human cell line that HIV normally do not infect. The group then sets Alizon those cells that express the protein US28 on their surfaces, various strains of HIV. In these and related experiments, the team found that Alizon US28 bearing cells were easily infected with HIV strains that normally use the CCR5 receptor on human chemokine, and a little less easily by strains that use another human receptor, CXCR4.

"the results are provocative and potentially important for HIV pathogenesis," says Philip Murphy, a chemokine receptor expert at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. Adds David Posnett immunologist at Cornell University Medical College in New York who has studied CMV: "I wonder what it all means in real life."

Indeed, it is not yet clear if the French group results, which are limited to cell lines laboratory are relevant to people with HIV. "There is a total lack of information about when, where, and how many US28 is expressed in people infected with CMV," Murphy said. So experts continue to debate whether CMV is simply an opportunistic organism enjoying the immune suppression caused by HIV, or a partner in the destruction of the immune system.

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