Health Meaning

infectious disease researchers are hoping to return to the Democratic Republic of the Congo soon to try to trace an exotic infection is alarming experts public health: the largest outbreak ever observed in humans of a virus called monkeypox well known. A first cousin of smallpox, once feared, monkeypox causes almost identical symptoms.

According to a Research News in tomorrow's issue of Science * between February 1996 and February 1997 at least 92 cases of the disease and three deaths were reported in remote area of ​​what was then Zaire. Only 37 documented cases were reported from 1981 to 1986. These results led to in-depth discussions on what could be the cause of the epidemic -. In particular, if the virus moves from man to man more easily than before

medical epidemiologist Ali Khan Centers for Disease Control and Prevention (CDC) in Atlanta led an international team, organized by the Organization World health (wHO) and the Zairian Ministry of health, who visited 12 villages in the center of the epidemic of five days in February, cutting short his trip due to civil unrest. As Khan and his colleagues detailed in Morbidity and Mortality Weekly Report from the CDC ( MMWR ) April 11, they believe 73% of 89 people they studied were infected with d 'other people. It would be a big jump from "secondary contact" rate of 30% reported by epidemiologist and expert monkeypox Czechoslovak Zdenek Jezek, who was from 1981 to 1986 studies in Zaire. The recent survey also found a patient who seems to have been the source of eight other infections, which is twice the highest chain of transmission observed previously. "This is not only an outbreak of a rare exotic disease in the middle of nowhere," Khan said. ". Personally, I am concerned about what would happen if the disease manifests itself in a big city"

an explanation of the epidemic, launched by Jezek and others, is that vaccination against smallpox - which also confer immunity to monkeypox - were so successful that they were arrested there almost 2 decades, creating an ever-increasing pool of people who are sensitive to animal viruses. Immunity is further compromised because the Democratic Republic of Congo has high rates of HIV infection, which paralyzes the immune system. Civil war may have contributed another factor: Faced with a growing threat of famine because of the unrest, villagers may have increased their hunting animals that carry monkeypox, which include monkeys, squirrels and rats

In. virologist Peter Jahrling of the Medical Research Institute of the US Army Infectious Diseases at Fort Detrick, Maryland, "low probability" that the epidemic spreads further. "But it is not zero," he added. To get closer, WHO hopes to organize another mission in a month if the political situation is relatively calm. Khan is eager to return. "It is important to go back there and ask what is the extent of the disease and how transmission occurs," said Khan. "We are all waiting for better data."

* For details, Science Online subscribers can link to the full text of the news story about the search.

A strain of bacteria causing the plague that is resistant to antibiotics normally used to treat the disease occurred in Madagascar. Although researchers have isolated it say they know of no other instances of resistant bacteria, they note that genes that confer drug resistance can easily spread to other plague strains, which pose a threat new pandemics of disease.

Transmitted primarily by flea bites, the last bubonic plague broke out as a pandemic, there are more than 100 years in Hong Kong before spreading around the world. Today, although the disease is always fatal if not treated in time, antibiotics have reduced mortality in patients with fever of about 10%.

But tomorrow New England Journal of Medicine , a team of researchers from the Institut Pasteur in Paris and Antananarivo, Madagascar, reports having isolated a drug-resistant strain of Yersinia pestis , the bacterium responsible for plague, a patient in Madagascar. The patient has not responded to conventional therapy of the disease, a cocktail of antibiotics chloramphenicol, streptomycin and tetracycline. Y. pestis isolated patient also failed to respond to another antibiotic mixture containing sulfonamides and tetracycline, which is often given to people who may have been exposed to plague. The patient survived, however, thanks to another antibiotic, trimethoprim, which the virus strain was not resistant.

Just how the bacterium manages to outsmart the drugs are not yet clear. But researchers report the isolation of the new strain of a small circular DNA strand, known as a plasmid. Similar plasmids carry the genes for resistance to an antibiotic with other resistant bacteria such as Enterobacteriaceae and E. coli inhabiting the intestines of humans and other animals. The team showed that in the test tube plasmid could be transferred to the resistant Y. pestis both a laboratory strain of the bacterium E. coli . "The transfer [of plasmids] occurs at a high frequency," said team member Elisabeth Carniel of the Institut Pasteur in Paris, suggesting that antibiotic resistance could easily spread.

David Dennis of the Centers for Disease Control and prevention in Fort Collins, Colorado, cautions that this discovery could have international implications, "it is an isolated case, but it seems a warning that we must be alert to the possibility that it could spread to other strains, "he said. "If it does, it would be a significant public health problem."

One of the keys to a long life is to eat less - at least for laboratory rats and fruit flies. Now a study of primates, published in this month of American Journal of Physiology suggests that reducing caloric intake to 30% below the level regarded as normal may benefit the heart. Rhesus monkeys on the low-calorie diet have higher levels of cholesterol and triglycerides lowest levels of 'good', the two that guard against heart disease and stroke in humans. The advantage is greater for young people of middle-aged monkeys and shrinks in old age.

For the last decade, molecular biologist George Roth of the National Institute on Aging has been studying the effects of calorie restriction on rhesus monkeys. All 60 monkeys given the same diet, but half are only allowed 70% of the calories normally consumed as a monkey. In previous research, Roth and colleagues have slightly lower blood pressure, improved glucose tolerance and insulin sensitivity (which means that the animals are less likely to develop diabetes), and lower body temperatures in the low-cal group. "What we think is that animals that are restricted are shifting their metabolic strategy of growth and reproduction in a life care strategy," said Roth.

In this document, Roth announcement of results relative to compounds surveillance levels that influence cardiovascular health. the monkeys who ate less had higher levels of normal HDL2B, a type of high-density lipoproteins and protective cholesterol. the largest increase (83%) was for the youngest group of monkeys - 10 years - and the least (16%) for older monkeys, until the age of 28. the levels of people of old age means. about 13 to 15 years in triglycerides were 41% lower than the monkeys on the full meal plan calories. juvenile levels were 11% below normal, and levels were 8% higher than normal for the older monkeys.

"There is solid information," said Richard Weindruch, a gerontologist at the University of Wisconsin, Madison. The next step, says endocrinologist William Cefalu of Bowman Gray School of Medicine in Winston-Salem, North Carolina, is to relate the results to disease. Indeed, the monkeys will soon be tested to determine if they develop heart disease and to what degree, Roth said.

Potent cocktails of anti-HIV drugs can fight the AIDS virus to undetectable levels in the blood. But a pair of tomorrow's paper Science (pp. 1291 and 1295), report that the virus can survive the bombing in a small number of T cells, immune cells that are the main HIV target. Viruses in this hidden reservoir, moreover, can be awakened from their shock shell and allowed to reproduce, at least in the test tube. Or current treatment regimens can take many years to completely rid the body of HIV, experts say, or they are not powerful enough to do it

Although HIV had already been taken lurking in cells Immunity after medical treatment, some scientists had speculated that the virus might exist in a damaged form of impotence. To check this perspective, two research teams - one led by immunologist Robert Siliciano at Johns Hopkins University School of Medicine in Baltimore, and the other by virologist Douglas Richman of the University of California, San Diego, School of Medicine in La Jolla --looked for HIV in the so-called memory T cells, which help lead the attack when the immune system encounters microbial invaders it has seen before.

researchers took blood cells, including memory T cells, HIV-positive patients who were on a strict diet of multi-drug therapy and cultured with cells from people not infected. When the researchers triggered the memory T cells become activated, the virus began to replicate and infect HIV-negative cells - even if viral levels in HIV-infected cells were tiny. Although the results seem to confirm that HIV survives an attack of chemotherapy, the researchers did find some good news. There was no evidence that the virus had mutated survivor, suggesting that it had not become drug resistant

AIDS researchers are not surprised by the viral return. "We knew that the patients during this time period become positive virus if treatment is withdrawn," said retrovirologist John Coffin of Tufts University in Medford, Massachusetts. "The virus still has to be somewhere." Indeed, the results "should not have any impact on what we recommend to patients," said Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in Bethesda, Md. "We are reaping huge benefits for patients bearing the virus as low as possible for as long as possible. "

Like a captain on a shoot a rocket to call for help sinking ship, distressed arteries attract immune cells. But instead of saving the arteries, immune cells appear to accelerate their decline. The findings, reported in today's issue of Journal of Clinical Investigation , suggest that put a damper on some of this distress call may be a new way to treat heart disease.

Everyone knows that "bad" cholesterol tends to accumulate in the arteries and often leads to atherosclerosis. But for many other risk factors - such as cigarette smoke and certain bacterial infections - the cause of the disease mechanism is unclear. One thing these risk factors have in common, however, is that they trigger an inflammatory response and repair, said Robert Terkeltaub Hospital of the Veteran Administration in San Diego. We knew that the precursor macrophages - wandering cells made by the immune system to consume bacteria and dead cells - accelerates the deposition of fat in the arteries bruised

Terkeltaub enlisted colleagues at Scripps Research Institute La Jolla. In California, and the University of California, San Diego, to try to understand how these precursors called monocytes could be attracted to the injury. Working on mice, Linda Curtiss Scripps transplanted bone marrow that churn white blood cells, with or without the mouse version of CXCR-2, a receptor for chemokines - the distress call from the injured cells to the lesion . The team fed two groups of mice a diet of artery hardening ". And a milkshake over it" the equivalent of one hamburger per day, Terkeltaub said, After 4 months, the mice with the receptor exhibited arterial lesions 2.5 times the size of lesions in mice lacking the receptor; the CXCR-2 mice also had significantly higher macrophage account.

The discovery shows that the modification of the immune response can change the course of atherosclerosis, said Alan Greater Columbia University. The implication, he said, is that compounds that block chemokine receptors could someday be used to protect people injured arteries.

In the war against cancer vaccines designed to teach the immune cells to look for proteins on cancer cells and fuse to kill has been less sparkling results provided that. Now, researchers report in the March issue of Nature Biotechnology that inoculating mice with a protein fragment that mimics the shape of abnormal cancerous cells sugars attached to proteins seems to do the trick. The new therapy is currently being studied in clinical trials

The new work -. Directed by Vasso Apostolopoulos, Austin Research Institute, Heidelberg, Australia - target the sugar molecules on the surface of a protein called mucin (MUC1), which is secreted by the epithelial cells of the mucous membranes of the kidney, lung, breast and other tissues. MUC1 on cancer cells is strewn with sugar molecules that are shorter and less numerous than those of normal cells. Previous experiments had shown that these sugars Nabot themselves make good vaccines because they are poor to stimulate immune cells to attack.

Apostolopoulos and his colleagues got around this problem by using a short protein fragment that mimics the structure of aberrant sugar molecules and is able to trigger a stronger immune response. They tested the mimetic in mice that received human breast cancer cells transplanted expressing the modified MUC1 protein. The mice that received the vaccine injections fake sugar will not continue to develop cancer, while the control animals did.

In an accompanying review Olivera Finn, University of Pittsburgh School of Medicine and Sandra Gendler of the Mayo Clinic in Scottsdale, Arizona, called the new strategy an important approach that "could prove useful in a clinical context. "in fact, efforts are already underway to begin clinical trials, said member Ian McKenzie group." Initially, the test will be performed on cancer patients, "he said. "If this is successful, it will be done on patients in [high risk] groups."

The dangerous pathogen Staphylococcus aureus causes infections ranging from skin abscesses toxic shock syndrome. About a third of currently isolated strains from patients who acquire S. aureus then hospital infections are resistant to all antibiotics except one, vancomycin - and now the resistance to this antibiotic began cropping. But new research suggests an approach to the fight against S. aureus that can bypass the ability of the organism to develop resistance.

In Science tomorrow , the researchers say they can decresase the incidence and severity of S. aureus infections in mice by blocking the ativity of a protein called RAP, which controls the production of toxins and other proteins that make the pathogenic bacterium. The work suggests that disabling RAP - perhaps by vaccinating people with the protein so that the immune system takes out of commission, or by developing drugs that prevent it from doing its job - could keep microbe to spread in the body before the patient's immune system exhausts outside. These drugs do not directly kill the organism, and in the absence of such selective pressures, resistant strains may be less likely to develop.

Naomi Balaban, a researcher of infectious diseases at the University of California, Davis Medical Center in Sacramento discovered RAP and its role in the last few years. His previous work has suggested that S. aureus multiplies it secretes HBP. When the protein reaches a critical concentration, it sends a signal which activates genes for toxin production. This suggested, Balaban said, the protein could be a good target for prevention strategies. She and her colleagues inoculated mice with purified RAP from S. aureus cultures. Vaccinated animals developed antibodies to RAP, and when the researchers injected S. aureus under the skin of animals, only 28% developed skin lesions, against 70% of controls.

Because it takes weeks to mount an immune response, such a vaccine could benefit those whose risk could be expected, such as diabetics and kidney dialysis and surgery patients. But "it opens up a new strategy for treating or preventing one of the most serious nosocomial infections that we strongly support," said Julie Gerberding, an infectious disease specialist at the University of California, San Francisco. "The methods that prevent disease without selection for drug resistance could really help us. - And we're going to need help quickly"

Researchers have made a new compound aspirin that promises to provide the same pain relief as aspirin, but without stomach ache or the risk of kidney damage. The compound described in tomorrow Science , can also help reduce the risk of certain cancers and Alzheimer's disease.

This new "superaspirin" is one of a dozen new compounds under development that soothe joint pain by blocking the activity of an enzyme called COX-2, which promotes the inflammation, pain and fever. The problem with aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) is that they also interfere with the activity of the COX-1 enzyme, which protects the walls of the stomach and kidneys. Thus, pharmaceutical companies have been eager to find drugs that target only COX-2, especially since epidemiologic and laboratory studies now indicate the long-term use of these drugs may protect against cancer colon and Alzheimer's disease.

At least two companies, Monsanto Corp. in St. Louis, Missouri, and Merck and Co., based in Whitehouse Station, New Jersey, tested COX-2 inhibitors in people and hope to be marketing their new superaspirin next year. "Finally, all these [NSAID] marketing molecules become dinosaurs," predicts Philip Portoghese, a medicinal chemist at the University of Minnesota in Minneapolis.

So far, however, all new inhibitors COX-2 pain relief for only as long as they were attached to the COX-2. But now biochemist Lawrence Marnett at Vanderbilt University school of Medicine in Nashville, Tennessee, and colleagues describe one that works much like aspirin and chemically modifies COX-2, permanently blocking the production of hormones until the body makes more enzyme COX-2.

to build the next generation of these selective inhibitors, Amit and Kalgutkar Vanderbilt Marnett made a molecule which retains original side group acetylated aspirin, aspirin which transfers to the COX-2 enzyme to destroy it. This new molecule also has a carbon ring attached to a sulfur atom, and short chain of carbon atoms which hang sulfur. They found that it could reduce the activity of COX-2 by as much as temporary COX-2 inhibitors exist. Marnett, whose university has patented this class of COX-2 inhibitors permanent, hopes to partner with a pharmaceutical company to come up with a more efficient version of the new superaspirin.

A chemical in marijuana may protect against brain damage from a stroke, according to a report in The Acts of the future national Academy of Sciences . The compound known as cannabidiol in the test tube SOP damage by oxygen free radicals more effectively than vitamins C and E, the more potent known food antioxidants.

As every knows pothead, marijuana and its component psychoactive tetrahydrocannabinol (THC) inhibit the activity of certain brain areas. Aidan Hampson, in collaboration with colleagues from the National Institute of Mental Health and also undertook to check whether the inhibitory effects of THC may also prevent the toxic overstimulation of brain cells that occurs when brain cells become starved for oxygen and sugar, and are then unable to pump the neurotransmitter glutamate.

researchers simulated a stroke while bathing a Petri dish full of neurons in the neurotransmitter glutamate, which is toxic in high doses. When they added purified THC, half as many neurons died. First, the researchers speculated that THC binds to the cannabinoid receptor, but when they added another chemical that blocks the receptor, THC always protected the cells. "It should not have protected the neurons, but it also works well," says Hampson. Other tests have shown that THC was raking free radicals such as hydrogen peroxide, which are spewed from the excited neurons. They have also shown that cannabidiol, a component of marijuana similar to THC but its psychoactive effects, provided that the same antioxidant benefits.

Hampson is already at work simulating shots rats and try to prevent damage with cannabidiol. But pharmacologist Steve Childers, Wake Forest University Medical School in Winston-Salem, NC, is skeptical that cannabidiol would be effective in preventing strokes in people at safe doses. "They are not testing a very low concentration of the compound," he said.

L ONDRES - Since the first indication in 1995 that "mad cow" had crossed the species barrier in people, causing a deadly new form of brain disease, a key question remains unanswered: How many cases are likely to occur given the long period of illness latency? - perhaps 10 years or more. - It's hard to say whether Britain is facing a silent epidemic or just a handful of cases in excess of 27 diagnosed far

Late last week, the British government announced that it is about to launch a groundbreaking study to try to find. It will review hundreds of tonsils and appendices stored, removed during surgery in recent years, for traces of protein misshapen called "prion" that have been associated with brain disease known as new variant Creutzfeldt-Jakob disease (vCJD).

study was prompted by the case of Tony Barrett, a 45 year old coastguard southwest England, who died of vCJD in June. According to an article in August 29 issue of The Lancet , Barrett had his appendix removed in a local hospital eight months before he first showed symptoms of the disease. When doctors examined the tissue stored evidence misshapen prions, he tested positive. This was the first demonstration that vCJD can be detected before symptoms appear, said James Ironside of the National CJD Surveillance Unit, a co-author of Lancet paper.

The government now expects test more than 1,000 of the 800,000 samples of tonsils and 45,000 samples of the removed appendix and stored each year. Comparison of tissue removed before and up to the outbreak of mad cow in the late 1980s can provide a rough estimate of the extent to which the population harbors prion protein vCJD. The study is too small, however, provide something more than an indication of whether or not there is a widespread problem. "Interpretation of [data] require great caution," said Kenneth Calman, Chief Medical Officer of Great Britain, who announced the study last week.

Government officials and their advisors not yet worked on the ethical rules that will govern the testing program, however. One option is to remove all identifiers so that the fabric can be traced back to the patient. If this is not done, the researchers will face the question of whether to tell patients if prions are detected in their organs.