Health Meaning

BETHESDA, MARYLAND - The US government is ratcheting his attack against malaria, a disease which kills up to 1.5 million people per year. According to Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (NIAID), the Institute is taking steps to create a shared repository of research materials on malaria, malaria increase its budget to $ 1.8 million -delà the current $ 20 million (see table), and support the DNA sequencing of two new strains of malaria parasites

last year, an international consortium began sequencing the strain deadliest, Plasmodium falciparum , and now NIAID -. the largest donor in the world of malaria research --The adding P. vivax and P. berghei in the list. NIAID repository, meanwhile, will provide high-quality researchers, rare reagents, which Fauci hopes to attract newcomers to the field. The initiative is supported by the NIH director Harold Varmus, who pledged at a meeting in Dakar, Senegal, last winter to help build a new network, based in African malaria researchers ( Science , 17 January, p. 299). Varmus also spoke of the project at Columbia University last month, saying, "It's time for malaria and other tropical diseases called on exotic alcoves in which medical schools have traditionally housed and put them in the flow "of biology.

Varmus and other leaders of the NIH plan to meet European and African health officials in the Netherlands July 7 to examine 130 research proposals, they requested last winter and develop a shared funding plan . Said Stephen Hoffman, researcher malaria US Navy: "This is very exciting morale building aspects, I hope translates [long-term] funding."

A deadly disease that triggers heart failure in children - apparently never seen before - has resurfaced in Malaysia. A team of experts from the US Centers for Disease Control and Prevention (CDC) is now Malaysia trying to help the government learn what causes the disease, which has killed 31 children in just 3 months.

The epidemic has been limited so far to the Sarawak region of northwestern Borneo, an island off the coast of Malaysia's most populous. "We collected a fair bit of data with no clearly providing an answer as to what is happening," the CDC says Larry Anderson. Scientists think there could be a link to an epidemic of hand, foot and mouth (HFM) disease now raging in Malaysia. But HFM, which is caused by Coxsackie A16 and Enterovirus others, is rarely fatal and indeed has not resulted in deaths among children diagnosed with it in 2140 on peninsular Malaysia last month.

Malaysian health officials also suspect Coxsackie B virus that is linked to myocarditis, as a possible cause of heart failure disease. Another possibility is enterovirus 71, a bug that causes heart failure and has been isolated from many of the dead children. The culprit could even be seen pathogenic in people, said Anderson. At this point, he said, "it is detective work." The Department of Health Sarawak is posting updates epidemic on its website.

Scientists have identified the first gene with a strong resemblance to the p53 gene, a tumor suppressor significantly linked to near half of all human cancers. The researchers hope that the new gene, described in issue tomorrow Cell , give them a better understanding of the origins of many common cancers.

geneticist Daniel Caput and colleagues at the pharmaceutical company Sanofi Research in Toulouse, France, arrived on the new gene when looking for cell receptors of the immune system. When the French team tested a gene that came in the research, they were shocked to find that its sequence reminded p53 , a "security guard" cell that stops cell division when DNA damaged and allows the cell to make repairs. They then contacted their longtime collaborator Frank McKeon, who studies gene expression and cell division at Harvard Medical School in Boston.

Looking more closely, the team found striking parallels between p53 and the new protein, called p73. A p73 section closely resembles the so-called "core binding region" where p53 binds to DNA. Equally interesting, the p73 gene resides in a region chromosome 1, designed to host multiple suppressor genes unidentified tumors. (This area is lost in about half of childhood cancer called neuroblastoma nervous system, and in some melanomas and some cancers of the breast and colon.)

But the key evidence of tumor suppression is still lacking. When checked, several lines of neuroblastoma cells lacked mutations p73 would lead to rampant cell growth. as these mutations are found, or someone finds an inherited mutation of the gene in people with some form of hereditary cancer, it is "still to win" if p73 is a tumor suppressor says geneticist Bert Vogelstein cancer of the school of medicine at Johns Hopkins University.

One of the most worrying consequences of the outbreak of the Great Britain of the "mad cow" - that humans could be infected by the contaminated beef-- consumption? seems to be confirmed by the research to be published this week in Nature .

More than 20 Britons have died in recent months from what is called variant Creutzfeldt-Jakob disease (vCJD). The symptoms are similar to those of classical CJD, a fatal brain disease that progresses slowly. But vCJD tends to strike young people, and it is growing much faster. A link between vCJD and mad cow disease, bovine spongiform encephalopathy (BSE) was suspected, because both involve dementia, tremors, and this can be an infectious protein called a prion. But the evidence ( Science NOW, October 23, 1996) that the consumption of beef contaminated with BSE may cause vCJD was inconclusive.

In the new work, Moira Bruce of the Institute for Animal Health in Edinburgh, Scotland, and colleagues injected mice with infectious brain samples of cattle with BSE, patients died of vCJD, and patients with classic CJD. After considering how and where the mouse brains were damaged, and the symptoms and progression of the disease, the researchers concluded that vCJD and BSE in mice are the same, and the two are distinct from classical CJD.

A team from the Imperial College School of Medicine in London, led by John Collinge, adds further evidence to the puzzle in Nature separate. Collinge and colleagues demonstrate biochemically that the infectious agent responsible for BSE can turn normal human infectious prions in mice. The "inevitable conclusion" said Collinge, is that the new vCJD is the human equivalent of BSE and the consumption of infected beef is probably to blame.

A key question now is how many people may have been infected, but researchers still have no answers. "It may take several years before we can be sure that this is not a period of relative calm before the storm," says Jeffrey Almond at Reading University and John Pattison at University College London. "It all depends the average incubation period of vCJD, and, at present, we can not calculate. "

Livers are so delicate that even the most robust donor samples fail if they are not transplanted within 24 hours. But a fortuitous coincidence led to the discovery that interferon (IFN) , a powerful anticancer drug, may double the lifetime of donor livers. The discovery, published in the November issue of Gastroenterology , could greatly improve donor livers supply and relieve some of the pressure on the complicated transplant procedure.

fresh donor livers are immersed in a cold solution of electrolytes and sugars to preserve their hepatocytes. These cells pumped up to 5000 different proteins involved in any of the blood clotting to detoxification. But almost freezing temperature quickly bloats the sinusoidal cells of the liver, which cover the blood vessels. After transplantation, the hypertrophied cells detach hepatocytes and die, weakening blood vessels and starving the liver blood.

There are two years, researchers at Duke University Medical Center were investigating how to better preserve chilled livers. A member of the team at the time was also brushing up on research on breast cancer after a relative had been diagnosed with the disease. According to Duke liver transplant surgeon Pierre-Alain Clavien, team member noticed a "striking similarity" between the early stages of tumor development and injury to chilled livers. liver sinusoidal cells were swollen exactly like their counterparts, endothelial cells during angiogenesis, the growth of blood vessels in a tumor

The team tested as liver conservative three common cancer drugs - . fumagalin, minocycline and IFN - which inhibit angiogenesis. They injected the drug to rats before removing the livers of animals and organ extracts as well. IFN- was the only one to provide a "significant" improvement in the shelf life of sinusoidal cells, said Clavien. Because circulating IFN levels peaked in rats 2-6 hours after injection, he believes that a single dose given a few hours before an organ is removed from a rat - and the adding the drug to the preservation solution--Could do donor livers had perhaps 48 hours.

new research offers a "unique perspective" on the liver damage process, says Gregory Gores, transplant hepatologist at Mayo Clinic in Rochester, Minnesota. But the implication of the paper - the sinusoidal cells trying to develop blood vessels, rather than simply die - "is a hypothesis that has to be proven." This evidence, Gores says, is to identify the protein that triggers angiogenesis and looking for it in the liver.

White blood cells can play a crucial role in the development of Creutzfeldt-Jakob disease (CJD), the fatal human version of what is called "mad cow disease", Swiss scientists report in Nature tomorrow new -. on the basis of a related disease in mice and first presented at a closed meeting in November - calls prompted British blood banks to collect blood donations white blood cells.

neuropathologist Adriano Aguzzi of the University of Zurich in Switzerland and colleagues went to show that the infected blood can transmit CJD. Try to understand how spongiform infections reach the brain - where they kill cells, leaving the cloth full of holes - the researchers began to suspect that the immune cells could be unwitting collaborators. In their latest work, researchers tried to reduce the list of suspects by infecting different strains of mice immunosuppressed with scrapie, a related disease CJD. The team found that mice lacking T cells or interferon gamma can be infected as easily as controls, but mice lacking B cells that help produce antibodies, infection resisted. If B cells abet disease, due to the authors, they can also carry the infectious agent

Because nobody knows what causes CJD -. Many believe this is due to misfolded proteins that spread, while others think a slow-acting virus is to blame - it was difficult to nail down how the disease [infection] moves through the body. But few researchers are surprised by the latest news. Neuroscientist Paul Brown of the National Institute of Neurological Diseases and illnesses that he built on decades of previous research, including studies in the 1960s and 70 suggesting that blood can transmit these diseases, although less infectious than the tissues of the brain or nervous system.

clearly CJD can be transmitted through transfusion in laboratory animals, said Brown. But both Aguzzi and Brown point out that no human cases of CJD has been attributed to a blood transfusion. There is a "huge amount of Epidemiology that everything speaks against the possibility of blood transmission of the agent," says Aguzzi. However, he warns, the new variant ( Science now 23 October 1996), "could be a totally different story."

A rare incurable type of leukemia appears to be due to a mutant cell receptor that binds a signaling molecule closely if he is deaf to signals normally halt cell division. The researchers who discovered the mutant receptor hope the finding, reported in tomorrow's issue of Nature , can shed light on the most common forms of leukemia.

acute promyelocytic leukemia (APL) is an aggressive form of bone marrow cancer strikes about 3,000 people in the US each year. The problem starts when immune cells called leukocytes are divided and their two chromosomes fuse to create a mutant gene. Leukocytes then make a mutant receptor that can not fully respond to retinoic acid - a signal to a cell to stop dividing. Consequently, growth accelerates and becomes cancerous. In most cases, however, high doses of vitamin A - which produces retinoic acid - can slow the cancerous growth. But approximately 4% of patients do not respond to therapy.

To see why, a joint research team from the University of Pennsylvania Medical Center in Philadelphia and the European Institute of Oncology in Milan, Italy, analyzed the gene fusion in cell lines APL patients with incurable. They found that in these patients, the merger has a different mutant receptor. This receptor, it appeared, was a fatal affinity for a signaling protein called N-CoR that represses cell division. When the researchers added N-CoR in cells cultured with the rare mutant gene, the receptors bound so tightly that N-CoR failed to respond to retinoic acid and all the cells began to divide out of control . "Now we know the mechanism that causes APL, and we know why, in some cases, treatment can not," said team member Iris Zamir.

"There is a discovery intriguing, "says Thomas Waldmann, head of the metabolism of the National cancer Institute Management in Bethesda, Maryland. Although researchers have known for some time that retinoic acid treats leukemia, this research explains why. "It does not provide all the molecular details," says Waldmann, "but there is an opening" to discover future treatments.

Tumors can betray their presence by making cells that enter the bloodstream. Look for these rare cells takes a keen eye and good luck, but now researchers have developed a tool that ups the chances of detection. The technique, described in Proceedings of the National Academy of Sciences of tomorrow may eventually help doctors diagnose tumors earlier than current technology can -. Long before metastasis can take hold and frustrate effective therapies

necrotic cells by tumors represent only a fraction of minute blood or bone marrow, so that scientists need to meticulously comb through thousands cell cancer to find some of them. Jonathan Uhr, a microbiologist at the University of Texas Southwestern Medical Center in Dallas, and colleagues wanted to create an accurate census of fishing on cancer cells.

submicroscopic iron particles for bait, researchers coated with antibodies that bind to specific types of cancer cells. Then, they mixed the bait with blood samples from 33 patients with breast cancer or prostate cancer and 13 healthy people. Exposing the samples to a magnetic field to a total of 15 minutes made the railway cells migrate together, allowing scientists to extract a portion of the sample in which the concentration of cancer cells was stimulated about 10,000 times.

using a technique called flow cytometry, in which a shooting laser beam through a single file cell stream reveals clues to their size and make-up, the researchers were able to identify and precisely match the cells cancer of each sample in as little as 2.5 hours. The technique has found that suspicious cells, as expected, were much more numerous in all cancer patients than in healthy individuals. Other tests have ruled out cancer in healthy controls. The number of cancer cells have been possible using traditional techniques, the researchers say.

"It is precisely the kind of test we needed was" nab circulating cancer cells more effectively, said David Brown, a pathologist at the University of Virginia in Charlottesville. Uhr The group will then monitor people at high risk, such as women with a family history of breast cancer, and to test the ability of the method to identify tumor cells in early stages of cancer development.

A cold can make your headache - and perhaps your heart too. The chances of suffering a heart attack rocket for victims of colds and flu, the researchers report in Lancet tomorrow .

For decades, experts in public health have noticed that epidemics of colds and flu in the winter are often followed by a rash of heart attacks. But the link between infections and myocardial attracted relatively little attention until the 1980s when some studies have suggested that respiratory diseases can trigger heart attacks by encouraging blood clots or inflammation heart muscle.

Now, in the largest study of its kind, Christoph Meier and colleagues at the Boston University Medical Center in Lexington, Massachusetts, found that the chances of a heart attack can almost triple after respiratory tract infection. Meier team compared the medical records of 1,922 UK heart patients with 7649 randomly selected controls. They found that patients with a respiratory infection were 2.7 times more likely to have a heart attack within 10 days of becoming ill than were controls. The weak link over time. After 16 days, a respiratory disease did not increase the risk of heart attack

The results should "ring a warning bell" for physicians and heart patients, said David Spodick, cardiologist St. Vincent's hospital and the University of Massachusetts, Worcester, who published similar studies in the 1980s, but he and Meier agree that it is too early to establish specific treatments on the discoveries. Meier, for example, warns that the study could not determine whether bacterial or viral infections pose greater risks. As studies resolve this and other issues, he cautioned, the findings "should not be used to justify the wider use of antibiotics."

Some people who try smoking get hooked ever. Now scientists have found that these people are less susceptible to tobacco addiction because their bodies decompose under its addictive component, nicotine. The results, reported in tomorrow's issue of Nature , may lead to drugs that block the metabolism of nicotine and help addicted smokers quit.

In previous studies targeting the molecular roots of nicotine addiction, pharmacologist Rachel Tyndale of the University of Toronto and colleagues identified an enzyme called CYP2A6, which breaks down more than 48% of the nicotine To smoke. Because an estimated 18.5% of the population carries one or two defective copies of CYP2A6 gene and can not metabolize nicotine well, the team wonders if these people were protected dependence nicotine. This is because nicotine addicts seeking because their bodies are so effective in breaking the chemical.

To see which versions of the enzyme CYP2A6 smokers are, the researchers extracted CYP2A6 genes from white blood cells of 244 smokers and 184 people who had tried cigarettes, but which do to have developed a habit, became non-smoking. After millions of copies of the genes, they sort with enzymes that cut variants in different sizes. The researchers found that non-smokers who have not become addicted were 51% more likely to have defective CYP2A6 variants that smokers. Smoking with defective CYP2A6 enzymes 23% smoked fewer cigarettes each week, suggesting that inhibitors of these enzymes may one day help smokers reduce the number of cigarettes they smoke.

"This is the first study to demonstrate a genetic mechanism that could make you more vulnerable to nicotine addiction," says Alan Leshner, director of the National Institute on Drug Abuse. Enzymes may also help explain why some smokers can not just quit cold turkey, said oral pathologist Brad Rodu of the University of Alabama, Birmingham. the fact that drugs that block CYP2A6 can help these "inveterate smokers' cut and QUIT, Rodu added, "is very exciting and very interesting."

B Oston - already breathalyzers help police keep drunk drivers off the road. Now, they can become a quick and non-invasive way to diagnose diseases. A pair of scientists reported at the meeting of the American Chemical Society here today that they have developed a machine in minutes can detect trace compounds in the breath and the diagnosis of diseases such as diabetes, renal impairment, ulcers, and possibly cancer. Commercial versions of the instruments can be available in a few years.

To build their breath analyzer, chemist David Smith of Keele University in Staffordshire, UK, and Patrik Spanel, a physicist with the Academy of Sciences of the Czech Republic in Prague a piece of space technology spying on Earth. There are two decades, Smith and Keele colleagues developed an instrument known as a selected ion flow tube (SIFT) to analyze trace gases known to be present in interstellar gas clouds. The machine reacts with the test sample ions and feeds these products in a mass spectrometer. The unique chemical signals for each trace of compound are then compiled in a database.

For their work in progress, Smith and Spanel created a database for the breath of humans healthy and sick. They carefully selected ions which react with the volatile trace gases, but do not react with the abundant compounds in respiration, such as oxygen and nitrogen. The technique is so sensitive that scientists can distinguish tens of compounds at concentrations of only parts per billion. While the original SIFT machines are bulky table instruments, Smith said that in recent months, he and Spanel developed, a smaller portable version and tested with patients in the hospital.

When Smith and Spanel tested their device on patients with various disorders, the results are striking. Twenty patients with renal failure, for example, showed levels of ammonia and acetone over 10 times higher than in healthy controls, and researchers could monitor these levels fall back to normal patients received a dialysis treatment. Smith also said to be able to follow chemical markers of stress, diabetes and ulcers, and they say preliminary data suggest they may even be able to use the technique to detect bladder cancer prostate.

"These are very exciting results," said Michael Henchman, a chemist at Brandeis University in Waltham, Massachusetts. "The technique of David could be as important to medicine as MRI [magnetic resonance imaging]. "

There are sixty-one years old this month, W. Warrick Cardozo published a paper in Archives of Internal Medicine entitled "immunological studies in Sickle Cell Anemia", which reported the results of an early disease studies. Cardozo, a young American physician, discovered that sickle cell anemia - a condition in which the majority of the red blood cells are crescent - runs in families and that almost exclusively affects people of African descent. Also, Cardozo found that all the victims were killed by disease and all people whose blood contains sickle cell anemia suffered. These important observations came 13 years before researchers had identified the abnormal hemoglobin that causes sickle cell anemia

[Source:EmilyMcMurrayEd Notable scientists of the twentieth century (Gale Research Inc., ITP, 1995).]

bone marrow transplants can be a lifesaver, rebuilding the source of blood cells after radiation or chemotherapy destroyed. But for some patients with blood disease, no matching donor can be found. In tomorrow New England Journal of Medicine , the researchers report that umbilical cord blood transplants - which also contains immature blood cells - can be an effective alternative to bone marrow, even when the donor and the recipient are not related [

small studies have suggested that blood transplants cord could work, so Pablo Rubinstein, director of research at the New York blood Center, and his colleagues began a survey large. They collected information on 562 patients who received transplants of cord blood from unrelated donors since 1992. In more than 80% of the beneficiaries, the transplanted cells "transplanted" - have taken up residence in the bone marrow and began churning mature blood cells. Furthermore, less than a quarter of the patients suffered "disease of the graft against the host" severe or fatal disease (GVHD), a reaction in which the immune cells in the transplanted blood attack the recipient's body. (GVHD afflicts up to 35% of recipients of bone marrow.)

The results suggest that it is easier to find a successful match for cord blood transplants. To reduce the risk of GVHD, scientists try to match six types of cell surface proteins between donor and recipient. bone marrow transplants require at least five proteins for a game, but Rubinstein and his colleagues report that even in patients where only four matches, the cord blood cells can graft without triggering severe GVHD. Scientists have yet to settle whether some mismatches are better than others and how to determine an optimal dose cord blood for a given patient, said immunologist LeeAnn Jensen of the National Heart, Lung, and Blood Institute in Bethesda, Maryland.

The latest data are encouraging news for patients who can not find a matching bone marrow donor, said Eric Sievers at the Fred Hutchinson Cancer Center in Seattle. But he points out that up to 25% of cord over 12 years of blood of patients failed to engraft, which is often a death sentence. bone marrow transplants, secondly, to have a graft ratio of 97%. If the technique is to be useful for adult patients, he said, "clearly new ideas are needed."

P ARIS - One of the most publicized court cases modern French history during today's trial of former Prime Minister Laurent Fabius and two former ministers, who are accused of "manslaughter" and "involuntary assault on the physical integrity of persons" to have measures which have been delayed to protect the supply of blood and blood products to the nation from contamination by HIV. Pasteur Institute virologist Luc Montagnier and other top AIDS researchers should be called to the stand to testify

the case concerns the actions of Fabius and his two co-accused. - former social Affairs Minister Georgina Dufoix and former Secretary of State for Health Edmond Hervé - during the critical period between 1983, when HIV was was first isolated and 1985, while measures to try and protect the blood supply came into force in France. The three ministers are accused of having delayed the approval of an HIV test in France for several months in 1985. Dufoix and Hervé are also accused of delaying HIV destroys the heat treatment of blood products for hemophiliacs up that the existing supply of untreated products was exhausted. In previous tests, many doctors have been convicted of related charges, and more than 30 other defendants can be tried in the scandal, which was dragged for nearly 12 years ( Science , 16 June 1995, p. 1563).

in total, several dozen scientists, doctors, administrators and politicians should testify before the Court of the Republic, a special tribunal of jurists and parliamentarians that was created for testing former Justice Ministers . The testimony of AIDS researchers aims to shed light on key scientific issues in the case: What ministers know the AIDS epidemic, and when did they know? In particular, the court probing whether the French authorities have delayed the use of a blood test done by the American company Abbott Laboratories, based on the work of Robert Gallo and his colleagues at the National Cancer Institute, to give the French company Pasteur Diagnostics time to market its own version, based on the work of Montagnier group.

"We were called to put things in the context of the knowledge of the time," says immunologist Jean Claude Gluckman of the Pitié-Salpêtrière in Paris, a member of the team first isolated HIV. But some witnesses researchers have strongly differing views on critical issues in the trial, which may make conflicting evidence. "Even if this testimony is inconsistent, it has light information available to the political leaders of the time, "says Axel Kahn, a geneticist at the Institute Cochin the trial is expected to last several weeks. if convicted, the defendants face up to 3 years in prison and heavy fines.

The blood-brain barrier, which controls the chemical trafficking and brain, can be even more complex than previously thought. Certain compounds that seem to penetrate the entire brain, as indicated by the analysis of the brain, are caught by a second line of defense. Experts say the findings, reported in the February American Journal of Neuroradiology , underline the problem of providing drugs against a variety of brain diseases such as stroke, brain tumors and neurodegenerative diseases.

The blood-brain barrier is a filter at the base of your skull, rather it is a coating of cells that line hundreds of kilometers of blood vessels reach every crevice of the skull. These cells, called endothelial cells, are cemented with gluelike substances in structures called tight junctions. Normally only small molecules soluble in lipids can seep through this barrier. Glucose and other substances needed are the shuttle through specific conveyor systems. For anything else, such as drugs or virus particles designed to carry therapeutic genes, scientists must resort to a trick: Inject a concentrated sugar solution makes endothelial cells shrink, temporary opening pores between the cells

using this technique. The team neurosurgeon Edward Neuwelt at Oregon Health Sciences University and the Veterans Administration Medical Center in Portland has undertaken to develop a noninvasive means of monitoring the distribution of potential drugs. They injected rats with two types of iron oxide grains sugar-coated, the size of virus particles commonly used for gene therapy. The team visualized particles with MRI, suggesting that both compounds evenly distributed throughout the brain. But when Neuwelt watched some preparations of brain slices under the microscope at a higher resolution, was surprised: A compound had spent endothelial cells, but was stuck in a complex mesh of sugar and protein fibers, called the basement membrane surrounding the blood vessels. With most standard imaging techniques, Neuwelt said, trapping some compounds in the "web of the basement membrane" could give "false view that you got the uniform delivery, when in fact you do not have it. "

" the study shows that there is more to the blood-brain barrier tight junctions. It challenges mainstream thinking, "says neuroscientist Thomas Jacobs of the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. The findings, Jacobs said, emphasize the importance of setting aside more resources for the study of drug administration, the "Achilles heel" of the brain therapies. Neuwelt agreement: "The industry is spending hundreds of millions of dollars to develop new drugs [for the brain], yet virtually nothing about how to get there" The next step, he adds, is. "why some particles pass through and others do not."

smallpox, one of the most deadly viruses to infect humans, just got a reprieve of his own death sentence this week. According to a senior official at the White House, President Bill Clinton signed a memorandum ordering the US not to seek the destruction of smallpox currently held stocks in high security laboratories in Russia and the US officials. The action marks a reversal of the position of the government; for the last 3 years, US health authorities have supported a policy adopted by the leaders of the World Health Organization (WHO) in Geneva, calling for the annihilation of all smallpox samples in June 1999.

WHO eradication the plan-- now in question - began in 1967, when about 10 million people worldwide were infected with smallpox. In an all-out immunization program, WHO quickly overthrew the number of cases. In 1980, no new smallpox infection were reported, and routine vaccination began to decline. In 1983, the WHO members decided to turn on all the live smallpox samples to two standards: The US Centers for the Research Institute for Viral Preparations in Moscow Disease Control and Prevention in Atlanta. In 1996, WHO leaders proposed to destroy these stocks, too. The only member of WHO was openly oppose Russia, which argued that the samples should be kept for biological research.

However, the US government "has never been unified" on the plan, an official of the White House staff said science NOW. Proponents of destruction continued argue that the virus is too dangerous to keep, as a tool for biological studies, but others -. especially defense officials - have argued that the US should not destroy its stocks of smallpox when researchers in other countries almost certainly have secret supplies. "the big problem," the official White House said, "is that if you destroy official stocks, you will not know that it's all gone." Recently, holding stocks defenders highlighted a new concern - the need to respond to bioterrorist threats. The only way to discourage the use of smallpox as a weapon, they say, is to develop new drugs and vaccines antipox. And that research requires live virus.

Such arguments have convinced the president to order a change of policy, to the disappointment of eradication supporters. According to the White House, US health officials will join Russians in June to urge WHO to change its mind as well -. Maybe give a dead killer line a new lease on life

Today

is the birthday of Helen Dyer, a biochemist born in 1895 and known for his research on biological cancer precursors. Working at the National Cancer Institute, Dyer has found that vitamin B-6 may thwart a potent liver carcinogen in animals. The discovery has stimulated new research on the protective role of vitamin against cancer. In 1949, Dyer compiled the first global index of tumor chemotherapy

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

The man who coined the term "antibiotics" and pioneered their development is born this day in 1888. While studying plant and animal way rest breaks down in the soil microbiologist Selman Waksman at Rutgers University discovered a menagerie of bacteria filamentous soil. In 1943, while working on the molds, he found that the chemical is produced which removes bacterial attackers; streptomycin later became the first effective antituberculosis drug. Five years later, Waksman team developed neomycin, another important antibiotic. In 1952 he won the Nobel Prize in Physiology or Medicine for his discovery of streptomycin. Waksman died in 1973.

Sources: Nobel Foundation, Encarta

A new compound could one day help alleviate the severe side effects of cancer treatment for some people. In Science today , the researchers report that a small organic chemical protects mice against lethal doses of radiation.

Chemotherapy and radiotherapy not only kill tumor cells, they also damage healthy tissue and cause anemia, infections, vomiting, diarrhea and other problems. These side effects can be so severe that they prevent patients from receiving effective treatment. Although some compounds help protect healthy tissue cancer therapies, they have only limited effects, such as helping to restore the ability of the bone marrow to produce red blood cells.

Now, capitalizing on their knowledge of p53 , a powerful tumor suppressor gene, a team led by Andrei Gudkov of the University of Illinois, Chicago, may have found a best way to relieve side effects in some patients. Previous findings have shown, for example, healthy tissue from normal mice suffer more gamma radiation than do normal tissues of mice deficient in p53. This meant that the blocking p53 may prevent side effects -. But only if it could be done without triggering the formation of additional tumors

The team designed a system of cultured cells which could be used to screen rapidly for compounds that block this activation. And 10,000 synthetic chemicals, particularly one looked promising: pifithrin- a (PFT a ). It blocks cell death triggered by radiation and four chemotherapy drugs and it also inhibits the growth arrest induced by radiation. "Surprisingly," said Gudkov, "a single injection saved [normal] mouse completely" from a radiation dose that usually kills 60% of animals, while having no effect on p53-deficient animals. Further, the treated mice survived more than 8 months - about half the normal mouse lifespan - and none developed tumors

Before such a compound can be used in the clinic, Longer. -TERM animal studies are needed to ensure that the drugs do not cause the formation of tumors or have other dangerous side effects, warns medical oncologist Ronald Bukowski, Director of Experimental Therapeutics at the Cleveland Clinic. And people whose tumors contain p53 active gene - true for 50% of cancers - will not do be eligible for the drug, because it could help fight their tumors therapy. But if the new compounds pan out in humans, it would be good news for cancer patients.

Scientists may have found a new way to block a chain of molecular signals leading to the most common form of blindness. A compound that blocks the receptor for a signaling molecule successfully prevented half the growth of blood vessels rampant in the eyes of newborn mice. The condition can blind infants born prematurely, persons with diabetes, and the elderly, a team reports in this month Nature Medicine .

When the eyes are low in oxygen, the cells that line the retina send chemical distress signals. Such alarm, a molecule called vascular endothelial growth factor (VEGF), is trying to save the day by sprouting of new blood vessels. Ultimately, however, it spoils the rescue by causing the formation of leaking vessels - a condition known as hypoxia-induced proliferative retinopathy. Probing this chain of events, ophthalmologist Lois Smith and colleagues at Harvard Medical School and Hospital Boston Children examined the role of a signaling molecule called insulin growth factor-1 (IGF-1), which had been linked to the VEGF action in mice and humans.

Smith began imitating retinopathy in neonatal mice. She placed 7 days of age the pups and their nursing mothers in rooms infused with 70% oxygen and then removed animals after 5 days. As for premature babies, the lower oxygen concentration, oxygen-free in the eyes of infants. The researchers then gave newborns daily injections of either a peptide known to block the receptor for IGF-1 or control. Five days later, the growth of blood vessels in mouse eyes that received the inhibitor is half that of control animals.

The mechanism is not straightforward. Rather than blocking the production of VEGF, the compound prevents the receptor for IGF-1 release of the VEGF receptor, which normally remains on the order to make new blood vessels. The reason that some blood vessels have continued to grow in laboratory animals, Smith suggests, is that the signaling compounds other than IGF-1 may still be in operation.

"This study is interesting and shows that there is some interaction between IGF-1 and VEGF signaling pathways," said Peter Campochiaro ophthalmologist at Johns Hopkins Medical School in Baltimore, a researcher retinopathy long. But he believes that IGF-1 may not be the best receiver to target. Campochiaro and colleagues plan to start clinical trials on a VEGF receptor antagonist that is 100% effective at blocking VEGF. It is not yet known if this more radical approach will be safe in people. "What we're trying to do is look at the more complex interactions so that we can better modulate these pathways for clinical use," says Smith.

How the pharmaceutical industry can be encouraged to make medicines and vaccines for infectious diseases that sicken or kill billions of people in the world, but offer little in the way of economic benefits? Senior politicians strategies described last week at a meeting sponsored by the Institute for Global Health in San Francisco. Meanwhile, President Clinton has signaled its interest in launching an initiative to reduce the seemingly intractable gap in health between rich and poor countries, and last week a bill was introduced in the Senate US that would include a large number of suggestions for the meeting.

pharmaceutical companies already have the scientific knowledge and tools they need to develop drugs and vaccines for scourges like malaria, AIDS and tuberculosis. In addition, these drugs could save millions of lives and boost economic development in poor countries, said the group, which included representatives from the White House, the United States Congress, the World Health Organization, World Bank, World trade Organization, and pharmaceutical giants Glaxo Wellcome and Merck. Yet these diseases attract minimal attention from the pharmaceutical industry because executives do not see a market. Even when effective drugs are available - such as the cocktail of drugs against AIDS has reduced mortality in rich countries -. They may be too expensive for countries in Africa and Asia

The solution, the panel is in a set of incentives that would make it interesting for the pharmaceutical and biotechnology industries to take action. one approach is for governments and multilateral organizations to further research and development by subsidizing part of the enormous costs, either directly or through tax breaks. Another is to provide companies a future market - for example, by establishing "purchase money" and agreeing to purchase certain quantities of a product once it is available. The group also praised the partnerships in which scientists funded work with the industry, such as the Global Alliance recently created for Vaccines and Immunization (GAVI), as a means accelerate the discovery and development of drugs.

The Global Forum for Health approach has already found a receptive ear in Washington. In his State of the Union, President Clinton announced a contribution of US $ 50 million to GAVI, and a tax credit of up to $ 1 billion for companies that invest in new vaccines against malaria, AIDS and tuberculosis. A delegation from the World Health Forum was scheduled to meet Clinton this week to present their findings and discuss the proposals of Clinton, who are "absolutely on track," said Richard Feachem, head of the Institute for Global Health .

Meanwhile, Senator John Kerry (D-MA) introduced an ambitious bill, called Vaccines for the new Millennium Law, 24 February. Kerry has proposed "change the death spiral" by childhood immunization "a major objective of the foreign policy of the United States." His bill provides for donations of $ 150 million for GAVI and $ 30 million to the International Initiative for a vaccine against AIDS. It also offers several tax credits for the industry and a purchase fund to buy and distribute vaccines as soon as they are approved. To cover the cost, Kerry asks Congress to set aside $ 100 million per year for the next 10 years. The political fate of these plans is uncertain. Although Feachem is encouraged by these and other initiatives in the European Union and Japan. Feachem said, "The global awareness of this challenge is running at a level we have not seen before."

Shark cartilage is a popular folk remedy for cancer, although there is no scientific evidence that it works. But a new study may dull its appeal :. Scientists reported last week that not only sharks get cancer, but they may even have a cartilage cancer

Sharks have a low incidence of cancer, researchers say. This fact, as well as research in 1983 showing a shark cartilage protein that inhibits blood vessels supporting tumor was taken advantage of by alternative medicine entrepreneurs into a lucrative business selling shark cartilage powder and pills as combatants cancer. The craze went into high gear in the mid-190s, following the publication of a best-selling book, Sharks Do not Get Cancer (William Lane, the owner of a patent for the shark cartilage powder), and a large dose of advertising in a 1993 segment 60 Minutes CBS . The developers also praised the work of biochemist Carl Luer of Mote Marine Laboratory in Sarasota, Florida, who has tried unsuccessfully to induce cancer in sharks by exposing the two carcinogens. But Luer himself said "there is no evidence that the cartilage which protect them," and a clinical study of 1998 revealed the shark cartilage ineffective against human cancers.

Sharks outside the laboratory, however, seem to suffer from them tumors. Researchers on Gary Ostrander cancer at Johns Hopkins University in Baltimore, Maryland, and John Harshberger of George Washington University in Washington, DC, say they have found at least 40 cases of cancer in sharks and their close relatives after reviewing the scientific literature and fish tumor samples from the registry of the National Institute cancer tumors in lower animals. The three cases included cancers of cartilage. The results were announced today in San Francisco at the annual meeting of the American Association for Cancer Research

Ostrander hope the study will help to explode the "huge myth" that sharks are immune against the cancer. - A shared misunderstanding even by "people in my field," he said. He added that the right record may also help protect sharks, which the American Fisheries Society recently named as one of the most threatened groups of the world fish because of their low reproductive rate.

The number of deaths from breast cancer has fallen sharply since the 1980s, the researchers report in the matter on 20 May The Lancet . American women under 69 are 25% less likely to die from breast cancer in 00 than they were in 1987; the UK, the number is likely to fall by 30%. better screening methods and new or improved treatments are to thank, says co-author Richard Peto, an epidemiologist at the University of Oxford, UK

Death of many types of cancer have declined States STATES since around 190, researchers from the Centers for Disease Control and Prevention announced in 1998, a trend they attributed to better diagnosis and treatment. Cancer is still the second biggest killer, however, after heart disease and breast cancer is one of the "big four" - in collaboration with the lung, prostate and colorectal cancer -. Who claim the most victims

Analysis of breast cancer mortality in the US and UK, Peto and his team found a peak in the late 1980s, followed by a steady decline. Rates have fallen nearly 20% for women under 69 in the United States between 1987 and 1997, and appeared headed for an overall decline of 25% in 00; for women between 70 and 79, the decline was 9% between 1987 and 1997. The new chemotherapy regimens and the introduction of drugs such as tamoxifen that act on the estrogen-sensitive tumors were responsible for the majority of the fall, said Peto. Radiation therapy, improved methods of detection, and an overall increase awareness of breast cancer may also have contributed to saving lives.

The study reflects "tremendous progress, particularly in the treatment" of breast cancer, says epidemiologist Katrina Armstrong of the University of Pennsylvania in Philadelphia. Peto said the sharp fall suggests that mortality rates will continue to fall, but it is too early to say just how low they could fall.

Despite a diet full of fat chock- artery-clogging, people living in France are much less prone to heart disease than Americans or the British. Scientists now say they have identified the molecular basis of the French anomaly -. A compound found in red wine that may thwart heart disease and cancer

The French passion for fat laden foods such as butter, cheese, rich sauces and pâté made blanch US cardiologists. Yet the French death rate from cardiovascular disease was 50% lower than America, and 75% less than Britain's - a disparity that has become known as the French paradox. Deaths from breast cancer are also less frequent in France. Many scientists suspect that wine, another staple of French meals can be counteract the adverse effects of a fatty diet. There are nine years, a report 60 Minutes explore this possibility was bubbling winemakers; he uncorked a 40% increase in wine sales in the US.

But what myriad components of wine may protect? Some scientists alcohol to credit himself with much of the effect, but the cancer biologists Minnie Holmes-McNary and Baldwin Albert of the University of North Carolina, Chapel Hill, emphasized that beer drinkers do not seem benefit. That's why they focused on resveratrol, an antioxidant compound found in red wine that previous studies have indicated may suppress inflammation and cancer formation. They dosed human cells and in rat growth in culture with resveratrol and measured the effect on nuclear factor kappa B (NF k B), a known versatile protein to promote growth and cancer inflammation - which is thought to be important in atherosclerosis.

As the scientists report in the July issue of Cancer Research , resveratrol prevented the release of NF- k B from storage sites within of the cell. As a bonus, it stimulated the cancer cells to kill themselves. Since resveratrol is abundant in purple grape juice, raspberries and peanuts, teetotalers can enjoy the benefits of this compound so, Holmes-McNary said.

Eric Rimm, an epidemiologist at the Harvard School of Public Health, said points to possible new treatments for heart disease study. However, he says that there is "overwhelming evidence" that alcohol itself protects the hearts of wine lovers. For him, the French paradox is not a great mystery. Rimm said: "Hey, there is ethanol, stupid!"

Related Sites
The Baldwin Lab
Wine and Heart Disease - Review by Andrew Waterhouse of the University of California, Davis
American Heart Association statement on alcohol and heart disease

LONDON -. The British government today approved the cloning of human embryos to harvest stem cells, not likely to serve as seed material for growing fresh tissues to treat disease cells. The proposal was contained in a report presented in May a panel asked to review government policies on the use of embryos in research.

UK regulations now allow limited research on human embryos, including infertility treatments and studies contraceptives. Almost all embryos used in such projects come from in vitro fertilization clinics, and research is limited to embryos up to the age of 2 weeks. But recent advances in research on stem cells and other areas led the government of the United Kingdom last fall to form a group of experts, led by Liam Donaldson, chief medical officer of the British Ministry of Health.

The Panel recommended extending the use of embryos for research. At the top of his list is permission for researchers to extract stem cells from embryos remaining. Stem cells, which can be brought to form different types of cells, could help to replace many kinds of tissues (see table). Stem cells would be slaughtered from ages 5 to 6 days embryos. The report also recommends limited use of cloning - the creation of new embryos -. As a source of stem cells

Another line of research supported by the report would investigate the diseases caused by defective mitochondria, cellular power plants with their own set of DNA. When the sperm and egg unite, the resulting embryo retains the mitochondria from the egg only, which means that mitochondrial DNA is passed only through the mother. Some 50 rare diseases have been linked to damaged or defective mitochondrial DNA. A prevention method proposed involves transplanting the nucleus of an egg of a mother at risk in a donor egg with its nucleus removed and fertilize the ovum in vitro hybrid.

(In the United States, privately funded research on embryonic stem cells is not regulated, but the work funded by the federal government is waiting until the National Institutes of Health releases its final guidelines, expected in mid-September. according to the draft guidelines, work with stem cells derived from embryos newly created would be unacceptable for NIH funding. Some lawmakers and members of the public argued that research on embryonic stem cells is unnecessary because derived from adult tissue stem cells could be just as useful.)

Parliament should address the issue this fall. But the approval of large is uncertain. "I would not take the acceptance of these recommendations for granted by Parliament," says Harry Griffin, assistant director for science at the Roslin Institute in Edinburgh. "There will be a noisy opposition from pro-life groups, and a large part of the audience will see a moral dilemma. "

with reporting by Michael Balter.

Related Sites
Advisory Group medical Officer Chief experts on therapeutic cloning

PHILADELPHIA -. For years, researchers have difficulty knowing exactly why moderate drinkers are less prone to heart disease than those who abstain or drink away. Is the alcohol itself, or something in their drinks? Now a genetic study may tip the balance in favor of alcohol. But the discovery, announced here on October 6 at the annual meeting of the American Society of Human Genetics, also shows that the protective effects of a drink depends on your genes.

Since the early 1980s, studies have shown that moderate drinkers live longer and are less likely to suffer a heart attack than abstainers. Several compounds have been touted as responsible for this benefit. More recently, a study highlighted resveratrol, an antioxidant found in red wine ( Science NOW, 10 July). But Lisa Hines and colleagues at the Harvard School of Public Health in Boston believe that ethanol - the scientific word for alcohol in your drink - deserves credit

To back up his intuition, Hines watched. ADH3 , a gene responsible for the degradation of alcohol by oxidation. Its investigation was based on a previous observation: The rate at which the liver breaks down the ethanol depends copies of ADH3 genes people carry. So if there is ethanol that reduces the risk of heart disease, Hines speculated, then slow oxidizers should, on average, have healthier hearts, because ethanol would hang longer in their bodies.

And that's what she found, after analyzing DNA samples from 396 men with heart disease and 770 controls. Among the subjects with the metabolism of ethanol slow, moderate drinkers had a 86% lower risk of heart disease than abstainers. Moderate drinkers who metabolize ethanol quickly not so successful. Their risk of cardiovascular disease was only 38% less than those who abstained from alcohol. Drinkers with slow genes - which account for about 16% of the Caucasian population - also tend to have high blood levels of high density lipoproteins, which reduces the risk of heart disease

"It's a good start ., a good study, but not the whole answer, "said Sam Zakhari, a pharmacologist at the National Institute on alcohol abuse and alcoholism. other factors, such as weight and sex, influence also on the duration of the alcohol remains in the blood, Zakhari said, and they will play a role too if ethanol does indeed protect against heart disease. Hines, for his part, warned that his study shows benefits for mild to moderate alcohol consumption ". We are not advocating that everyone go out and drink "

Related Sites

Hines summary of the meeting of the American Society of Human Genetics

National Institute on alcohol abuse and alcoholism

scientists have moved closer to developing a vaccine against one of the deadliest diseases known. In the November 20 issue of Nature , they say a new DNA vaccine can protect macaques develop haemorrhagic fever Ebola, a highly contagious and sometimes fatal disease that is terrorizing the sub-Saharan Africa.

Ebola causes devastating symptoms such as shock and internal bleeding. The virus can kill up to 0% of its victims, often within 10 days after infection. At present, there is an epidemic in Uganda, which has so far sickened at least 337 people and killed 121. There are no drugs for Ebola, and most scientists believe that a vaccine is the best way to protect populations at risk. But so far, efforts to develop such a vaccine have failed.

Now a team of researchers from the National Institutes of Vaccine Research Center of Health in Bethesda, Maryland, and the Centers for Disease Control and Prevention in Atlanta has developed a DNA vaccine. This type of vaccine is comprised of a piece of viral DNA - in this case, an encoding section for the virus envelope - which is injected into the muscle. The hope is that the gene will be expressed as a harmless protein and teach the immune system how to defeat the actual virus

The team vaccinated four macaque monkeys. each first received three injections with the gene in the form of a piece of "naked DNA" and a few months later, a booster consisting of an adenovirus expressing the same gene. The vaccinated monkeys developed antibodies and immune cells against the virus; moreover, they survived injected with the Ebola virus and were healthy months later. Four unvaccinated monkeys were used as control group were dead or dying in a week after the injection.

Other scientists say the results look promising, but some point out that the vaccine may have worked because the team has challenged their monkeys with a relatively low dose of Ebola virus. "I am cautiously optimistic that [this vaccine] is an important step," says virologist Alan Schmaljohn the Medical Research Institute of the US Army Infectious Diseases in Frederick, Maryland. "I will be more comfortable once it is repeated with a higher challenge dose. "

Related Sites

Ebola Hemorrhagic Fever fact sheet from the CDC

The Ebola Outbreak in Uganda

The National Institute of Allergies and infectious diseases

DAVOS, SWITZERLAND -. In a huge boost to efforts to develop a vaccine against AIDS, Bill Gates announced at the World Economic Forum here on January 27 as the Bill and Melinda Gates Foundation will give $ 100 million to the International AIDS Vaccine initiative (IAVI). The grant 5 years turns the non-profit based in New York City on track to begin clinical trials of three of its most promising AIDS vaccine in 07.

With $ 21 billion of assets, the Bill and Melinda Gates Foundation gives away hundreds of millions of dollars annually for health and educational organizations. Preparing the ground for the big-time diving the foundation of vaccines against AIDS was a dinner party at the Gates mansion in 1998, assisted by the Chief IAVI Seth Berkley. Gates was seeking advice on how his foundation could significantly improve public health through contributions from big money. At the dinner, Mr. Gates asked Berkley, "Where is the money a limiting factor in stopping AIDS?"

Berkley had long argued that a vaccine is the best hope to stop AIDS . and after reading about vaccines against AIDS, Gates decided to support IAVI with a gift of $ 1.5 million in 1998 and another $ 25 million a year later. the new funds from the Gates Foundation will come in 20 million pieces each of the next five years is a challenge grant, which means that the foundation expects other organizations to help increase the IAVI $ 550 million needed to launch the three tests;. counting the silver Gates, IAVI $ 230 million. This puts the nonprofit in the big leagues HIV vaccines.

it is not clear how it will be to raise the rest. While Glaxo Wellcome helped IAVI, other pharmaceutical companies are taking a wait and see. Pfizer CEO Hank McKinnell said if IAVI comes through with an effective vaccine, Pfizer - which now does not work on a vaccine against AIDS -. Consider the production and sale of the vaccine

Related Sites
The Bill and Melinda Gates Foundation
The International Aids Vaccine Initiative

ORLANDO, FLORIDA - Doctors may keep open a blocked artery with a mesh tube, but as Dick Cheney discovered months last, these so-called coronary stents sometimes clog. Researchers are looking for new ways to limit the growth of cells that lodge in the devices. Now, a preliminary report suggests that ethanol can help keep clear stents.

Between 20% to 30% of patients who have stents inserted end with their reclogged arteries. A variety of new techniques are tested to fight against the dangerous buildup, such as the treatment of stents with radioactive material or covered with chemotherapy chemicals.

Knowing that ethanol can stop the growth of cells, a team led by cardiologist Ming Liu of the University of Alabama, Birmingham, tested a new procedure on 46 patients. Before inserting the stent, researchers have applied in a dilute ethanol solution to a portion of the artery which has been expanded using a small device balloon. Study patients had damage to their arteries that stretched for 10 millimeters or less. These patients normally represent a chance of clogged stents 15% to 20%. But a year after the operation, only 7% of patients treated with ethanol required to have their repaired stents, Liu reported here on March 18 at a meeting of the American College of Cardiology.

While encouraged by the early results, cardiologist Lawrence Laslett from the University of California, Davis, warned: "We must be careful with the use of alcohol may be toxic to the muscle heart. ". He is optimistic, however, that this and other new techniques could prevent accumulation of tissue inside stents.