Health Meaning

N EW O RLEANS - As for exercise? This may be the key to all the good your workout makes you. A neuroscientist announced today at the annual meeting of the Society for Neuroscience here that rats compelled to exercise a weakened immune system suffered, while those who exercised the same amount unconstrained showed healthy immune responses.

The exercise clearly has direct effects on health, such as building muscle mass and improve cardiovascular health, but research has also shown that it can have indirect benefits, such that strengthening the immune system and reduce stress-related illness. Furthermore, numerous animal studies on exercise have come to the opposite conclusion, suggesting that exercise suppresses the immune system. Monika Fleshner at the University of Colorado, Boulder, suspects that the blame may not lie with the drive itself, but the scheme.

Fleshner studied two groups of male rats. Those groups were forced to run on a treadmill once a day. The others had exercise wheels in their cages and were allowed to run whenever they wanted. At the beginning of the 8-week study, Fleshner challenged the immune systems of rats with a foreign protein, and by the end of the study, they were reminded of the same protein. Fleshner sampled rats antibodies made in response to the protein, and also verified the spleens of animals and lymph nodes for reactive immune cells.

Both groups exercised comparable amounts of time during the study, Fleshner said, and they lost similar amounts of weight. But the animals were forced to exercise "showed classic signs of chronic stress," including deleted antibody responses, as well as enlarged adrenal glands. The rats that were forced to exercise had immune responses 20% to 30% lower than those of control animals that did not exercise at all, while the immune responses of animals that exercised by choice have been improved. the forced exercise is probably causing stress animals because they feel out of control, said Fleshner.

the study could have important clinical implications, said researcher exercise Judy Cameron of the University of Pittsburgh, as he points out that "the perception of what exercise is like can have health effects. "Indeed, says Fleshner, military cadets, who are forced into the practice of training and punishment, have been shown to be immunocompromised, though it was not related to the exercise. The study may encourage members to reconsider the way it uses the exercise, said Fleshner. Similarly, heart doctors might want to consider that their patients benefit when designing exercise regimes.

Two other cases of a new and deadly influenza virus were diagnosed in Hong Kong. On Saturday, the public health authorities announced that a 54 year old male and a 13 year old girl, both had contracted a strain of flu that before this spring was thought to infect only birds. "It was not good news to hear. We are very worried," said Dominick Iacuzio, a specialist flu at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland.

Because flu strains that infect birds can not usually infect people ( science , 12 September, p. 10), the man has not built an immunity to these avian viruses. Therefore, almost everyone would be likely if the virus could spread. the latest infections are the third and fourth instance of an apparent human bird jumping in the last 8 months. the world Health Organization announced today ' hui that the man died of pulmonary complications. the girl is still hospitalized in intensive care, but his condition is improving.

A team of scientists from the Centers for Disease Control and Prevention (CDC) in Atlanta in Hong Kong, in collaboration with the authorities there to determine how the latest victims have caught the virus. No new victims is known to have been in contact with the two victims previously reported. "The main issue is to determine if the person to person transmission or [the victims] had been in contact with sick birds," said CDC epidemiologist Nancy Arden. "It is very difficult to know at this stage what [the new cases] means." However, she said, if the virus was easily transmissible, "we expect to see many more cases that we have seen so far. "

Many AIDS researchers suspected that the most common strain of HIV, HIV-1, has been lurking in the human population since the 1950s or even earlier. Now scientists have confirmed that is the case: HIV-1 fragments from a 1959 blood sample cases represent the earliest known HIV infection. The results, presented today at the 5th Conference on Retroviruses and Opportunistic Infections in Chicago, could provide a clue to how the virus could spread from primates to people, and could help vaccine designers learn to face the remarkable genetic diversity of modern strains of HIV.

a team led by David Ho, director of the Aaron Diamond Center for AIDS Research in New York, analyzed the plasma of a man who, in 1959, lived in what is now Kinshasa, Democratic Republic of Congo. The sample was collected as part of a larger study of the genetics of the immune system, and in 1986, he tested positive for HIV antibodies, indicating the possible presence of the virus.

Ho and his colleagues used a highly sensitive technology called polymerase chain reaction to detect and amplify small amounts of HIV genetic material in the sample. They got four small fragments - only 15% of the complete genome of HIV-1 - they then sequenced. When two experts in the history of the evolution of HIV virus compared to 1959 called ZR59, with modern strains of HIV, they found it to be very closely related to the common ancestor of the three strains found in Europe , North America and Africa. The team believes that this common ancestor must have been introduced into human animals sometimes in 1940 or 1950. The Ho Group describes its results in this week's issue of Nature .

The 1959 sample "provides a potential missing link" in the early origins of HIV, said Francine McCutchan, a molecular biologist at the Henry M. Jackson Foundation for the Advancement of Military Medicine in Rockville, Maryland . This information, McCutchan said, could help pharmaceutical companies develop a vaccine based on common features shared with the first HIV ancestors - highly conserved features and therefore probably crucial that may prove to be more universal targets to fight against the epidemic global vaccine based on a combination of a cocktail of modern HIV strains, the genetic codes differ from each other by 10% or more.

The recovery from surgery may be less of a trial if the nerves are numb right of patients prior to surgery. A clinical study reported in tomorrow's issue of Journal of the American Medical Association shows that blocking the potential pain impulses to the spinal cord before making a surgical incision instead of waiting for the results up that the procedure is completed in less pain and a faster recovery.

most physicians now provide pain relief to patients after surgery, by numbing the nerve receptors. However, research on laboratory animals have shown that traumatic experiences can rewire the nervous system to provide a persistent painful feeling long after the stimulus is removed. If the nerves do not feel the stimulus first, the pain response will not wired - and new pain signals can be blocked

To see if it works in people also directed team by Allan Gottschalk. and David Smith from the University of Pennsylvania Medical Center in Philadelphia followed 100 patients whose prostate glands were removed. They injected 66 subjects prior to surgery or with a narcotic anesthetic which prevents signals from reaching the spinal cord. During the hospital stay, the patients reported feeling pain which was 33% less intense than those who had not received treatment. In addition, 87% of these patients reported feeling any pain during the investigation 9.5 weeks after surgery, compared to only 47% of those treated conventionally.

The procedure can not become common in the operating room unless the benefits listed to outweigh the complications observed in the study, such as fluctuating blood pressure during surgery, says Smith . However, the implications of the study are much broader than the prevention of post-surgical pain, notes Daniel Carr, pain management professor at the New England Medical Center in Boston. For example, giving a child a local anesthetic before the blood sample could not only numb the needleprick, but also can reduce the emotional or physical sensitivity to long-term needleprick.

Dorothy Hodgkin, a British X-ray crystallography, which won the 1964 Nobel Prize in Chemistry for his pioneering work to determine the structures molecular complex organic molecules, was born on 10 May 1910. Hodgkin began studying sterols in 1932, when the rays were used as x to confirm that organic chemists already knew a chemical structure. Hodgkin improvements in X-ray crystallography high technology to an important analytical tool.

In 1934, Hodgkin had correctly analyzed the iodide cholesterol, the first complex organic molecule completely determined by X-ray crystallography His lab came later with structures for penicillin, which influenced the development of antibiotics and vitamin B-12, which determined its group with one of the first electronic computers. Hodgkin, who spent most of his career at the University of Oxford and the University of Bristol, died July 30, 1994.

[Source:RoyPorterEd The Biographical Dictionary of scientists (Oxford University Press, ed. 2, 1994).]

Babies who die from sudden infant death syndrome (SIDS) are more likely to have abnormal heartbeats few days after birth, according to a study tomorrow New England Journal of Medicine . If the finding is confirmed by other studies, it may help doctors identify high-risk babies and could lead to drug treatments that prevent some SIDS deaths.

When a child younger than 1 year dies suddenly of unexplained causes, doctors typically exclude SIDS as the cause of death. The researchers suspect that several abnormalities contribute to the deaths of SIDS, including difficulty breathing, gastrointestinal diseases and metabolic disorders. There are more than 20 years, several cardiologists, including Peter Schwartz of the Policlinico San Matteo in Pavia, Italy, suggested that babies with a long so-called QT interval in an electrical recording of their heartbeat may be more at risk SIDS. The measurements of the QT interval about the time it takes the heart muscle to recover after receiving an electrical signal to contract. If some heart tissue plates take longer to recover than others, they can beat out of sync, and lead to sudden death. The long QT syndrome, often caused by genetic defects, is a leading cause of sudden death in children and young adults.

Schwartz and his colleagues began a long-term study in 1976, recording electrocardiograms babies apparently healthy three or four days after birth. After 19 years, they had data on more than 34,000 children. Of the 33,034 they were able to follow through their first birthday, 34 had died, with 24 deaths attributed to SIDS. Of the 24, half had abnormally long QT intervals; none of the 10 who died of other causes had this problem. This suggests, the authors write, that detectable cardiac abnormalities in the first week of life may be responsible for a significant percentage of SIDS deaths.

Some experts are not convinced. While Schwartz team was collecting its data, other scientists have published several studies reporting no evidence of long QT intervals in groups of infants at high risk - the siblings of SIDS victims and babies who survived close calls. And another study of more than 7,000 babies randomly selected electrocardiograms revealed that 15 died of SIDS were not significantly different from those of healthy babies.

But if Schwartz's findings are replicated, they could be put to good use: Older children with long QT syndrome are usually treated with beta-blockers medicines called that help smooth the heart rhythms irregular. If the long QT interval is a risk factor, said Richard Friedman pediatric cardiologist at Baylor College of Medicine in Houston, some cases of SIDS "may be a preventable type of thing."

Today is the birthday of Alexander Fleming, a Scottish bacteriologist born in 1881 who accidentally discovered penicillin, one of the most important drugs 20th century. A strange and rare mold Penicillium notatum happened to be floating around in the laboratory of Fleming because another researcher studied him. Fortunately, Fleming looked messy habit of keeping its longest bacterial plates than usual, and when he returned from a week of vacation in 1928, he discovered mold growth. He determined that a compound produced by the mold, which he called penicillin could kill pathogenic bacteria, but not white blood cells or tissues. The conclusion lay dormant until 1940, when chemists Ernst Chain and Howard Florey isolated, purified, and tested the antibiotic in clinical trials. Fleming, Florey and Chain then received the Nobel in medicine in 1945 prices

[Source:EmilyMcMurrayEd Notable Twentieth Century scientists (Gale Research Inc., ITP, 1995).]

The Cold War may have ended several years ago, but it left some questions unresolved dangerous: 3000 nuclear waste sites in the United States only. Now researchers may have found a way to fight against this accumulation of waste using a genetically modified microbe resistant to radiation and chemicals down the sites. Experts say that the bug described in the October issue of Nature Biotechnology could possibly help the US government dig out of his 50-year-old toxic waste.

A team led by the pathologist Michael Daly of the Uniformed Services University of Health Sciences in Bethesda, Maryland, and Larry Wackett biochemist at the University of Minnesota, St. Paul, enlisted a fairly common bacteria grows in arid environments. Able to withstand higher levels of radiation than any other known microbe Deinococcus radiodurans is as easy to manipulate genetically. So the bug fortified team with four foreign genes that allow it to decompose organic substances.

The high modified microbes easily even in a radioactive chamber, quickly repairing DNA damaged by radiation. And they put their new genes to work, degrading toxic chemicals, such as chlorobenzene, which are commonly found on nuclear waste sites. "There is a potential new way of opening up" for waste disposal, Daly said. He hopes that the body may be further modified so that it uses toxic substances for energy rather than breaking them.

Deinococcus 's ability to withstand radiation makes "bug mind-blowing," says Dan Drell, a biologist with the Department of energy, which administers most sites nuclear waste. But he is not ready to sic the bug on the sites for now. "I want proof that the genome, once modified, is reasonably stable," he said, to prove that he will keep his new powers over time.

Smoking will kill 100 million men in China - one in three under 30 today - when they reach mean age or older, according to two articles published in tomorrow British Medical Journal . "This alarming study is a landmark in research on public health," said Jeffrey Koplan, director of the Centers for Disease Control and Prevention in Atlanta. "These data suggest the coming of a devastating epidemic in China in the 21st century."

The results are the fruit of a long-term collaboration between Chinese academies of Preventive Medicine and Medical Sciences in Beijing, Oxford University, and Cornell University. After examining the smoking habits of 1.25 million men in several Chinese cities and rural areas, the researchers found that smoking already causes about 750,000 deaths per year. The team interviewed the families of all who died in a sample of Chinese provinces to determine factors, including smoking, which may have contributed to death. This mortality rate is likely to increase 3 million by the time the young smokers reach middle age and older, the researchers estimate.

The health risks of smoking are not widely known among the Chinese population, which consumes a third of current global cigarette production. "A national survey in 1996 showed that two thirds believe smoking does little or no harm," said epidemiologist Richard Peto of Oxford University. Only 4% of adults know that smoking can cause heart disease he noted, and only 40% realize that cancer smoking lung risks.

tobacco-related deaths will likely keep mounting, the researchers say. at the turn of the century, cigarettes kill April 1 million annual people in the world. half in rich countries and half in developing countries if current smoking trends continue, the researchers predict that rates will rise to 10 million deaths per year in 2030, with 70% . poor countries many areas could soon get a better handle on this gloomy prospect: study team smoking behavior of young people and the cause of death of the elderly are being adopted by countries Asia, Africa, Eastern Europe, and Latin America to study their own emerging epidemics tobacco.

For the first time, researchers have created artificial bladders working dogs. Experts say the success described in the February issue of Nature Biotechnology , has significantly advanced the prospect of repairing or replacing damaged human bladder tissue grown from their own cells of a patient.

About 7000 patients need repair or replacement bladder each year in the United States. These include babies with birth defects, older people who have lost the normal function of the bladder, and those with bladder cancer, the fourth most commonly diagnosed cancer among white men. "Since you can not use plastics with bladders, we were forced to look for living tissue," says William Steers, a urologist at the University of Virginia School of Medicine in Charlottesville. "Sometimes we use amounts huge bowel to fashion a replacement bladder. "But these procedures frequently cause complications

After a search of 9 years, pediatric surgeon Anthony Atala and colleagues at Hospital Medical School and Harvard children Boston managed to grow a lot of muscle and urothelial cells. - specialized cells that layer inside the bladder. - from tiny samples chiseled dog bladders After generating about 60 million cells (enough covering about 3 square meters), the researchers used a pipette to paint the outside, a porous mold shaped with bladder muscle cells, and inside with urothelial cells. "We apply a layer at a time, then put in the incubator and cook," said Atala. The new body is ready in about a week, when successive layers of cells merged to cover both surfaces of the mold seamlessly.

artificial organs have started to work as soon as they were inserted in six beagles whose bladders had been removed. new blood vessels began to get inside of a month, biodegradable polymer mold is disintegrated by 3 months, and nerve endings have penetrated the muscle of 6 months. bladders grown in the laboratory were still operating normally when the experience of 11 months completed. Atala's team has now turned its attention to human transplants, even if the first test is still several years.

"It is a revolutionary work," says Steers. "It opens up unlimited possibilities for the replacement of the internal organs, especially those who are muscular." However, he warned that the organs may not work as well in older patients, and problems with the power connections and nerve blood may occur. So he said, "it's probably not quite ready for prime time yet."

P ARIS - The trial of three former French ministers long term HIV blood scandal in France came to an end today with a conviction and two acquittals. Although former Prime Minister Laurent Fabius and former Social Affairs Minister Georgina Dufoix were found not guilty, former Secretary of State for Health Edmond Hervé was convicted of manslaughter and other charges of Court Justice of the Republic, a special tribunal set up to try government ministers.

The case centered on the decisions taken by ministers in the early and mid-1980s, when the AIDS epidemic was breeding in France. Fabius, in particular, was accused of delaying a testing program nationwide with an AIDS test made by Abbott Laboratories based US while the French firm Pasteur Diagnostics preparing its own version. The court dismissed the charge, saying that Fabius had actually acted to accelerate the test program. His conviction was saved for Hervé, who was accused of continuing to allow prisoners and other high-risk individuals to donate blood for 2 years after warnings from health officials that their blood might be infected with HIV, the virus that causes AIDS. The decision, however, is mainly symbolic: Hervé will not receive punishment

Although the last chapter of the saga is now complete, the case can continue for many months to come .. 30+ others are accused in the case - most of the time poisoning - which noted French cell biologist François Gros, scientific adviser of Fabius in the 1980s, and AIDS epidemiology pioneer Jean-Baptiste Brunet. The judge for the accused, Marie-Odile Bertella-Geffroy, has completed its investigation and should recommend in the coming days at least some of these accused stand trial too. "This will last much longer," says a French biomedical researcher who asked not to be identified.

Six months after receiving the first transplant of the hand of the world, 48 years, Clint Hallam of New Zealand has a strong grip and feel in several fingers. His intervention was successful, Hallam doctors report in this week's issue of The Lancet .

The operation of Hallam helped fuel a growing demand for limb transplants, said Earl Owen, a transplant surgeon at Microsearch Foundation of Australia in Sydney. Some amputees adjust well to prosthetics, but others feel incomplete without flesh and bone member. Because doctors have reattached the severed hands successfully, Owen said that securing a share of donors could also be possible. September 23, 1998, Owen and an international team including Jean-Michel Dubernard surgeon at the Edouard Herriot Hospital in Lyon, France, transplanted to the right arm of Hallam, who lost his right hand a man of brain death 41 years hand in a 1984 circular saw accident when he was in prison.

To prevent rejection of the transplant, doctors gave Hallam drugs that suppress the immune system. These drugs increase the risk of skin cancer, diabetes, and a type of lymphoma, but Owen says only significant side effect of Hallam was until now a "touch of diabetes," which went away once his medication doses have been adjusted. His arm shows no rejection of the new hand sign, and the nerves that connect the two began to regenerate. Hallam now the feeling in his hand two fingers and the backs of his fingers, and muscle activity is constantly improving.

The team expects life with the hand of someone else could cause psychological problems, particularly because-- unlike a transplanted kidney or heart - a member is always visible . But Owen says that Hallam seems to have fully accepted the hand than his from the start. Such an attitude is essential, says transplant surgeon Jon Jones of the University of Louisville in Kentucky, a member of the US team that performed a second transplant hand in January. This is also considered a success, but Jones warns that it is too early to put too much faith in the operation. "It could be that we were lucky the first two times," he said. Both European and American teams are planning several operations. "If we can provide immunosuppressants that have minimal risk, this operation could become widespread," predicted Jones.

By tinkering with an enzyme in mouse brain cells, medical researchers may have opened the door to a treatment for Huntington's disease an as-yet- incurable progressive brain disorder. The results, which appear in tomorrow's issue of Nature show that an enzyme involved in cell suicide plays an unexpected role in the disease.

Huntington's disease is an inherited disease that causes dementia, spasms and ultimately death. Scientists know that it is caused by aberrant repetition of glutamine, an amino acid in a protein called huntingtin. Fragments of huntingtin containing glutamine sequence tuft as well as in the nuclei of brain cells and the cells die shortly thereafter. Many researchers believe that the cause of cell death is apoptosis, a programmed form of suicide. To complicate this image, called caspase enzymes are known to be involved in apoptosis in general, but also to cleave huntingtin in the test tube, where they produce fragments like those agglomerate in patients with Huntington's disease.

Harvard neurologist Robert Friedlander and his colleagues wanted to learn about the role of caspases in Huntington's disease. They studied a strain of mice with an altered gene huntingtin , which causes them to develop symptoms of Huntington-like. The team inhibited caspases in mice, either by introducing a defective copy of a gene of caspase in their genome, or by infusing a chemical inhibitor of caspase in their brains. Both strategies reported poorer physical coordination in mice and allowed to live about 20% longer than their huntingtin -altered mice that received no special treatment. And the mice that received the gene for huntingtin flawed accumulated caspase tufts fragmented slower. Because the mouse (as victims of human Huntington) had a normal copy of the huntingtin gene, they produced normal and defective huntingtin . The researchers found that fragments of the two versions accumulated in the brains of mice.

The results, says neurologist Serge Przedborski Columbia University, suggest that caspase does not just deliver the coup de grace by letting the cells of the brain cluttered with huntingtin fragments engage apoptosis; rather, the enzyme seems to be an accomplice who is on sickness. Friedlander assumes that caspase, in addition to producing aberrant huntingtin fragments, worsening matters by recruiting normal huntingtin tufts. "The results are phenomenal," says Ted Dawson neurologist at Johns Hopkins University, in particular because they show that blocking caspase may be a promising way to treat the disease.

research using cells from human embryos received an important seal of approval this week. In a decision that Stanford biologist Paul Berg called "gutsy", the National Bioethics Advisory Commission (NBCC) recommended July 14 that the federal government should fund not only research on human embryonic stem cells, but also the production cultures- - stem cell even if it involves the destruction of human embryos. In an official notice, the panel says it will send the notice to President Clinton "very soon".

Embryonic cells are considered to have great potential as a possible source of tissue transplantation. NBAC, a group of 17 members appointed by the President, deliberated on ethical guidelines for their use for 9 months. It concluded that only "spare" embryos from fertility clinics - which would otherwise be discarded - should be used to create stem cell cultures, and only if the two full consent of donors. In addition, the government should set up a permanent monitoring committee set of ethics rules and enforce

Decisions -. Not yet published in written form - could have an impact on legislative debates later this year. Congress passed an amendment to a 1999 appropriations bill that prohibited the support of the United States for any research that could destroy an embryo. This change will end at the beginning of the new fiscal year in October, but lawmakers in the House are expected to renew the request in the draft Finance Act of the Department of Health and Human Services for 00. A hearing on this bill has been tentatively scheduled for July 21.

Representative Jay Dickey (R-AR), a vocal opponent of research on embryonic stem cells, said he will try to persuade his Capitol Hill colleagues to reject the findings of NBAC. "We believe that science must serve man, not that humans should serve science," says Dickey. It intends to help take this battle to court if necessary to prevent federal funding of research using cells derived from human embryos.

But Berg, a spokesman for the American Society for Cell Biology, said NBAC hammered a conservative position he hopes to make sense for both scientists and the public. He calls the recommendations NBAC to monitor the "heavy" field and "bureaucratic", but says they are reasonable if they reassure the public that this research will be guided by ethical principles.

Today is the 83rd anniversary of Frederick Chapman Robbins, American pediatrician and virologist who played an important role in the development of vaccine against polio.

After investigating virus outbreaks for the US Army during the Second World War, Robbins joined a research team at Children's Hospital Boston. In 1948, he found a way to grow the virus in the laboratory, using cells grown in a nutrient solution -. This discovery was the isolation and study of the virus much easier

In 1952, the group Robbins had successfully propagated the polio virus in mixtures of cells of the skin and muscles human embryonic. This culture system not only helped Jonas Salk and Albert Sabin produce vaccines against polio, but also shed light on how the polio attacks the body. He suggested that the virus infects other first tissue before it invades the brain and spinal cord. Robbins and colleagues John Franklin Enders and Thomas Weller received 1954 Nobel Prize in Physiology or Medicine for their work

[Source: Britannica Online ].

The AIDS epidemic shows no signs of slowing down, according to the United Nations (UN) statistics released yesterday. Some 5.6 million people were infected with HIV this year, and 2.6 million died of the disease. For the first time, most African women in sub-Saharan Africa are infected than men. And while Africa still has the most cases, the former Soviet Union now has the rate of infection by the fastest rising HIV worldwide.

"The threat of HIV has not declined in all countries," Peter Piot, Executive Director of UNAIDS - the UN Special Programme on AIDS - at a press conference in London yesterday . Especially depressing was the news from Eastern Europe and Central Asia, where the number of people infected with HIV has increased by over a third in 1999 to about 360,000. The increase was faster in the greater Moscow region, where 2,700 infections have been reported in the first nine months of 1999 - three times more than in all previous years. Epidemiologists from UNAIDS and the World Health Organization, the group that published the report, attributed the dramatic increase in Eastern Europe - centered largely in the Russian Federation and Ukraine - . In a surge of drug intravenously

AIDS officials say they are particularly disturbed by the increase in infections among African women, who now account for about 55% of the approximately 23.3 million people with HIV in the sub-Saharan region. Although the reasons for this are not entirely clear, epidemiologists suspect several factors, including greater sensitivity of the female reproductive system for viral transmission. Young African women are particularly vulnerable to infection through forced sex with older men: Recent studies have shown that older African girls aged 15 to 19 are six times more likely to be infected than boys of the same age

the. UNAIDS figures contradict the notion that the epidemic is in decline, said Piot. "There is no room for complacency in any discussion of this epidemic."

W ASHINGTON , DC - Doctors have known for decades about a rare metabolic disorder that increases blood levels an amino acid called homocysteine, which causes mental retardation in children severely affected and early cardiovascular problems in others. Recently, however, scientists began looking for subtle effects, and they get a lot of them. Even the moderately elevated homocysteine ​​levels are associated with heart attacks, strokes, problems during pregnancy, and impaired cognition in middle and old age.

homocysteine ​​occurs naturally when another amino acid, methionine, is decomposed. Normally, it is quickly returned to methionine or converted to cysteine ​​- reactions requiring the presence of folic acid, vitamin B6 or vitamin B12. If these channels fail, however, blood homocysteine ​​levels begin to rise.

Dozens of observational studies have shown an association between moderately increased homocysteine ​​levels and the incidence of cardiovascular disease, noted epidemiologist Petra Verhoef the Wageningen Centre for Food Sciences in the Netherlands out there, who spoke February 18 at the meeting of the American Association for the advancement of science ( science is now editor). But until now, she said, no rigorous clinical study clinched the argument that the protein actually causes such diseases. Several major trials on this subject have begun recently, Verhoef said, and results are expected over the next two years. However, all seven speakers of the session on homocysteine ​​agreed that there is already enough evidence to recommend immediately reduce homocysteine ​​levels.

Many Americans, in fact, already do not know it. Grain products in the US are now "fortified" with folic acid to reduce the incidence of neural tube defects in the developing fetus. Besides, says Meir Stampfer of the Harvard School of Public Health, many people pop pills multiple vitamins, most correct all but the most severe homocysteine ​​abnormalities. The good news, said Stampfer, is that Americans reduce their chances of having a heart attack or stroke that way. The bad news is that, like almost everyone benefits, it will be increasingly difficult to launch a clinical trial that proves the point.

The respected, hyperkinetic supervisor of the research program on AIDS of $ 2 billion to the National Institutes of Health (NIH) announced his retirement yesterday. Neal Nathanson said his last day will be September 1st. "This is my birthday 73rd, and the family said you paid your dues and it's time to come home," said Nathanson, director of the AIDS Research Office (SRO).

Nathanson , viral renowned epidemiologist, was coaxed from his laboratory longtime University of Pennsylvania in Philadelphia (where he still keeps his home) in July 1998 by Harold Varmus, then director of the NIH. Nathanson had little experience of AIDS but he threw himself to the task with the enthusiasm of a graduate student. "part of the reason he was able to accomplish the things he did was because he was not an insider "said Philip Greenberg, an HIV immunologist at the University of Washington, Seattle, who sits on the board of OAR." he had no vested interest, and he did not have a career to expand. "

Greenberg and other credit Nathanson with the promotion of cooperation between NIH institutes, strengthening the vaccine research budget against AIDS, better coordination of research on primates, and save "section of study "HIV in specific hazard which reviews applications for external grants. Nathanson said to address the tensions between the various institutes presented him the biggest challenge of all. "The directors of the institutes are far too powerful and the NIH Director's far too low," says Nathanson. "The institutes do not play well together. And I did a lot of behind the scenes negotiations."

Nathanson plans to return to the University of Pennsylvania, and is interested in working in the vaccine against the AIDS area, Penn or elsewhere. "Who knows what will come," he said. NIH has not yet formed a search committee to find a replacement. "It will be hard to fill his shoes, I'll tell you," said Anthony Fauci, director the National Institute of allergy and infectious diseases.

A good dose of a single protein makes the crucial sensory cells grow again in the tissues of the ears of baby rats. The discovery, published in the June issue of Nature Neuroscience raises the prospect that gene therapy could treat some forms of hearing loss.

Inside the ears of mammals, said cells hair converting sound vibrations to electrical signals which then pass down the nerve fibers and brain. Unfortunately, the hair cells only grow as an embryo develops; once they are mutilated or worn in adult animals, cells are gone for good. That's why more than one third of adults over 64 suffer from hearing loss. For years, researchers had known that mice lacking a gene called Math1 - that turns some other genes on and off - are born without hair cells and are deaf. While neurobiologists Wei-Qiang Gao and Lisa J. Zheng Genentech Inc. in South San Francisco set out to see if an additional dose of Math1 would make the extra hair cells develop after pregnancy is over.

researchers took slices of the inner ear of newborn rats and put them in Petri dishes. After opening holes in cell membranes by zapping them with electricity, they slipped in a specially designed stretch of DNA containing Math1 gene. Equipped with the gene, the cells began to turn the crank on Math1 characteristic protein, and in the coming days, the cells containing the added gene germinated slowly into hair cells. Indeed, the electron microscope images showed that the transformed cells resembling bone fide hair cells.

The finding is an important step towards the restoration of hair cells in people, said neurobiologist Donna Fekete of Purdue University in West Lafayette, Indiana. But do not expect DNA eardrops charged to cure deafness anytime soon; there are still many uncertainties. For example, the researchers worked with tissue from young rats, not adult rats. "The question is," Fekete says, "it will work on older sensory organs, more mature?"

One in five Americans and Europeans has high blood pressure, a dangerous disorder with many genetic causes are only now being revealed. Now a team of researchers has discovered an important piece of the puzzle: a genetic mutation that leads to early onset hypertension. The mutation may help explain the causes of the most common forms of hypertension and may also explain why blood pressure of some women increases significantly during pregnancy.

The team, led by geneticist Richard Lifton of Yale Medical School, had earlier linked a series of genes with abnormal blood pressure. Finding new mutations in the genes that cause hypertension, they routine screening of patients with hypertension. Among them was a 15 year old boy with severe hypertension. The researchers discovered that he had a mutation in the mineralocorticoid receptor, a protein in the kidney cells that is involved in the handling of the salt body. When activated by the steroid hormone aldosterone receptor that normally triggers a cascade of molecular events that cause kidney cells to absorb salt and water for release back into the blood. This can help prevent dehydration on a hot summer day, but it also raises blood pressure.

Lifton and his colleagues then found that the mutation caused the hypertension before age 20 in all parents of the boy who had inherited. They found the reason for the engineering of cells in culture to shine when the mineralocorticoid receptor has been activated. The modified cells with the mutant receptor shone all the time - even in the absence of aldosterone. The mutant receptor seems to be permanently stuck in the "on" position, Lifton and colleagues report in the July issue 7 Science .

To their surprise, they also found that progesterone, which clog the normal receptor, strongly stimulated the mutant version. Because progesterone levels increase dramatically during pregnancy, Lifton wondered whether the hormone aggravate the blood pressure problems in pregnant women who have this mutation. EMail: Worsening hypertension had hit five pregnancies of two women carrying the mutated receptor. Lifton do not think that this particular mutation will prove to be common. But he says the results suggest that the salt recycling pathway, in which the acts of mutant receptors may be important in hypertension. They also suggest that hormones such as progesterone could in certain cases hyperstimulate track.

"It is a real tour de force," says nephrologist Friedrich Luft of the Max Delbrück Center for Molecular Medicine in Berlin, Germany. "He discovers new and unexpected mechanisms for hypertension" in humans, he said, which could one day lead to better treatments and new diagnostic tools for the disease.

Related Sites
Richard Lifton
Lifton laboratory
Information on hypertension National Institutes of Health

The bacterium that causes TB infects one third of the global population and kills up to 3 million people a year. The pathogen's success secret is that it can persist undetected in the lungs for decades. Now a team of researchers has discovered a vulnerability that suggests new ways to fight against this resilient bug.

When Mycobacterium tuberculosis initially infects a person, it flourished for a few weeks until the immune system marshals its defenses. The two then reach a dead end. The pathogen population will not increase, but the immune system can not get rid of already nestled bacteria in a class of immune cells called macrophages

During this so-called latent phase - which may last for decades - the bacterium is stuck with a restricted diet: It feeds carbon from lipids by a route called the glyoxylate shunt, which is present in bacteria and plants, but not humans. This makes the path of an attractive drug target, said John McKinney of Rockefeller University in New York, because there may be fewer side effects.

McKinney and colleagues investigated this way for a weak point. Now they have discovered that levels of an enzyme called isocitrate lyase (ICL), which is essential for this route are high in M. tuberculosis during its latent phase. To learn how the enzyme they created a knockout M. tuberculosis , which does not have ICL. These modified bacteria were cleared by the immune system in mice, the team reports in the August 17 issue of Nature .

"One of the things we do not understand is how M. Tuberculosis can sit in the tissues for years, even decades," says Jo Colston, an expert on microbial pathogenesis at the National Institute for medical research in London who was not involved in the study. "clearly, if you can knock a protein that allows [the bacterium] to survive, which represents a potential therapeutic target. "

McKinney and his colleagues are already looking for such compounds. In a second publication in the August issue Nature Structural Biology they and crystallographer James Sacchettini of Texas A & M University in College Station describe the protein structure of ICL. They also identified two compounds that stifle the active end of ICL and stop the enzyme, which can starve tuberculosis while he hides in macrophages.

Related Sites
John McKinney laboratory

homepage James Sacchettini

TB information Organization World health

Leaders of fundamental research organizations top of Germany met in Berlin on 14 October to dedicate a monument to victims of the research Nazi brain time, just days after a historic commission published a preliminary report on violations of biomedical sciences at the time of Hitler

new monument to "victims of Nazi euthanasia crimes" brand the site -. now the campus of the Max Delbrück Center for molecular Medicine- -Where scientists at the Kaiser Wilhelm Institute for brain Research experienced on the brains taken from Nazi victims, including the mentally disabled at the ceremony, the. biologist Hubert Markl, President of the Max Planck Society, said the new report of the Committee, it is clear that the "administrators, scientists and lab assistants in several biomedical Kaiser Wilhelm institutes were at the service of a regime criminal." Max Planck is the modern successor to Wilhelm institutes

Markl joined other leading German scientists -. Ernst-Ludwig Winnacker, President of the DFG funding agency, and Detlev Ganten, head of the Max Delbrück Center and the Association of German national research centers - to request a full account of the abuses of the Nazi era. Winnacker said a new DFG panel ( Science , June 2, p. 1576) provides historical information to share with the ongoing investigation of the Max Planck commission.

Related Sites

Presidential Commission for the history of the Kaiser Wilhelm Society in the National Socialist era

Max Planck Society

Deutsche Forschungsgemeinschaft (DFG)

Max Delbrück Centre for Molecular Medicine

AIDS researchers thought they were studying a cell ally in the fight against HIV. The molecule called RANTES, appears to delay the onset of disease. But now RANTES appears to be like two face as they come. Although the researchers tested the molecule slows AIDS, they also discovered that it makes them more likely to invite HIV first cells.

Three related molecules are known to inhibit the spread of HIV from cell to cell. All of these, including RANTES, are immune system molecules called chemokines. Test tube studies have shown that these molecules block the virus from infecting cells both in competition with HIV for entrance doors in T cells and somehow decreased the number of receptors available for HIV to hang.

RANTES comes in a few varieties genetically determined. To see if these types influence a person's response to HIV, a team led by Philip Murphy of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, analyzed data of immune cells from a study being called the Multicenter AIDS Cohort study (MACS) conducted in Chicago, Los Angeles, Washington, DC, and Pittsburgh. MACS has collected blood samples from the men to the risk of HIV infection for more than 15 years. The team compared 404 men who were infected at 123 men who remained HIV-free despite engaging in some of the same high-risk behaviors.

Murphy team divided the men into two groups, depending on the version of the RANTES gene they carried. The group with the G4 variant took about 2 years after infection with HIV develop AIDS than did the group with the G1 variant, the team reports in December 1 issue of the journal AIDS . In test tubes, the G4 gene variant produces more than RANTES version G1, supporting the idea that RANTES inhibits the progression of HIV and prevents the disease as well. But the news is not all good for men with G4 variant: They are about twice as likely to be infected with HIV as men G1

It is strange that a version of a gene appears to protect against HIV infection. but eventually allows the virus proliferates. Murphy does not know how to interpret the findings, and it is not alone. "It's weird," said chemokine researcher Robert Gallo of the University of Maryland, Baltimore; "I do not know of a study before which showed a molecule inhibiting HIV and helping at the same time it certainly is. a paradox."

Related Sites
The Multicenter AIDS Cohort Study
homepage Philip Murphy

A newly discovered protein may help explain why overweight often suffer from type II diabetes. The protein, dubbed resistin is produced by fat cells and appears to maintain the insulin response cells. The discoveries of new proteins often suggest a therapeutic gain, but in an unusual twist, the researchers made their discovery using an already popular class of drugs for patients with diabetes. Scientists say the findings should help explain how and why drugs work so well -. And can lead to more effective treatments for the disease

One of the health hazards of obesity is an increased risk of type II diabetes, also known as diabetes in adults. The disease begins when the body becomes mysteriously unable to respond to insulin, a key hormone that regulates blood sugar after meals. The cells of patients fail to absorb glucose, sending blood glucose levels to dangerous levels. Over the decades, this can lead to a host of complications, including nerve damage, kidney failure and blindness.

Some of the most effective treatments for type II diabetes belong to a known class of drugs thiazolidinediones (TZDs), which improve insulin response in patients. Scientists were intrigued, because the drugs seem to turn on a gene involved in the development of fat cells. Why a drug against diabetes would also increase the production of fat cells was a mystery - and a bit of a paradox, because the fat cells seem to be the cause of diabetes, said endocrinologist Mitchell Lazar of the University of Pennsylvania School of Medicine in Philadelphia. This connection led Lazar to speculate that drugs could shed light on what goes wrong in the first diabetes.

Lazar and colleagues guessed that the drugs could be turning off a gene that interferes with insulin response, so they looked for genes that become less active in the presence of TZD. In tomorrow's issue of Nature , they describe such a gene, which makes an unknown protein. They called resistin protein because it seems to cause insulin resistance.

The researchers found that fat cells in mice produce resistin and excrete into the bloodstream. overweight mice had significantly higher levels of resistin in their blood - and sugar levels in the blood higher - than did healthy mice. Blocking resistin appears to help animals respond more effectively to insulin. The researchers also found a human gene that is similar to resistin mouse. They provide for experiments to determine whether human cells respond in the same way as mouse cells.

The work "is quite an attractive story," says endocrinologist Jeffrey Flier of Beth Israel Deaconess Medical Center in Boston. Why mice and humans have a gene that causes insulin resistance is still a mystery, but Lazar speculates that evolution has favored organisms with "thrifty genes" that help store and use energy efficiently to help them survive lean times. When there is a lot of food, however, these genes can backfire.

Related Sites

the homepage of Mitchell Lazar

NIDDK information about diabetes

- traditional slaughter practices in many small European slaughterhouses seem to increase the risk of spread of the disease variant Creutzfeldt-Jakob disease (vCJD), the human form of mad cow. Five people in a village near Leicester, UK, probably contracted the disease in this way, British scientists announced today at a special meeting of the regional health authority. Because the techniques of killing were commonplace in many European countries where mad cow hit, experts fear that many more cases of vCJD occur.

Since 1996, at least 95 people in the UK died from the human version of mad cow disease, also known as bovine spongiform encephalopathy (BSE). Most scientists believe that vCJD can be caused by eating meat contaminated with BSE, but the link has not been firmly established. A chance for a breakthrough emerged in the last two years, when five young people died of vCJD within 5 kilometers from Queniborough, a small village northeast of Leicester.

Searching for the source of this group of diseases, Philip Monk, a communicable disease expert at Leicester Health Authority, and colleagues interviewed the relatives of the victims and 30 people matched the age in the region. The team also included 22 local butcher shops and grocery stores. The first butcher shop they visited gave them a hint: He split the head of a cow to remove the brains and sale. Meat can "easily be contaminated" in this way with potentially infectious materials of the brain, said Monk Other issues confirmed the suspicion. Four of the five victims - but only three of the 30 witnesses - purchased the four butchers meat that regularly used this practice of traditional butcher, banned in 1989 in Britain. the victims of vCJD were also 15 times more likely to have eaten meat from slaughterhouses who fired a bolt into the brain of a cow, which can leak brain tissue from the carcass.

This is the first evidence that vCJD is caused by contaminated meat during preparation, said Simon Cousens, a biostatistician at the London School of Hygiene & tropical Medicine. "They come with a very plausible explanation," he said. most European countries have recently banned these practices, but with an incubation period of 10 to 20 years, Monk said that "cases are likely emerge in other countries with BSE at least until 2016. "

to choose the best therapy for spreading the cancer, doctors need to know which created a fabric. Now researchers trained a computer program to distinguish DNA of four seemingly similar deadly tumors. The method could lead to a faster and more appropriate treatment diagnosis for a variety of cancers.

PinPoint pathologists often the origin of cancer by studying the size, shape and color of the cells under a microscope. This is a delicate task for any cancer cells that are alike, as a group of four rare childhood cancers collectively called tumors with small round blue cells. In these cases, doctors often use several spots that bind diagnostic proteins, which can delay diagnosis. Betting that the genetic fingerprint would be faster and more accurate molecular biologist Paul Meltzer and pediatric oncologist Javed Khan of the National Human Genome Research Institute (NHGRI) in Bethesda, Maryland, and colleagues examined gene activity in four cancers - neuroblastoma, rhabdomyosarcoma, non-Hodgkin lymphoma, and Ewing tumor family.

The team interviewed 6567 genes at once using DNA chips. On these chips called genes, the activity of each gene is represented by a colored dye intensity. To determine the expression profile of genes, the researchers then ran the color intensity data through a so-called artificial neural network, a program modeled on the behavior of neurons in the brain that can learn by trial and error. "You get a complete picture of what is happening with this cancer," says Meltzer.

After the program has learned the characteristics of each type of cancer, it has correctly identified all 20 test samples . He also correctly rejected five samples of other types of cancer as well as healthy cells, reports the team in the June issue of Nature Medicine .

"I think it's very encouraging, "said Lee Hartwell cell biologist research on cancer Fred Hutchinson in Seattle. Although the sample size is small, he warns, the work clearly shows that cancers the same cell and tissue type are similar enough to distinguish them from other cancers, despite genetic differences between people, he said. "If it continues to support these microarrays will be very, very important for the diagnosis, "he said.

Related Sites

project Overview NHGRI microarray
homepage Paul Meltzer
An introduction to neural networks

The use of alternative medicine-- which means all remedies herbal acupuncture to the imposition of hands - has been steadily increasing in the US and in no way limited to a particular segment of the population, according to a survey conducted by Harvard researchers

epidemiologist Ronald Kessler and colleagues used data from a telephone survey ago 3 years in which asked 2,049 people aged 18 years about their use of alternative therapies * 20 the previous year. Among the speakers, 68% had used replacement therapy and those, nearly half were long-term devotees. Women, whites, Westerners, educated colleges and people under 50 are the most likely to use alternative therapies. By comparing the data with earlier studies, the team found an upward trend which was uniform in all groups - who "suggests an increased demand continues to [alternative] therapies that will impact on all aspects . the delivery of health care over the next 25 years "

Some therapies remain stable - for example, the use of homeopathy has hovered around 3% for decades, Kessler said But. the use of herbal remedies has increased, thanks to a federal law passed in 1994, which exempted the Food and Drug Administration requirements them. Aromatherapy has also taken off, scientists report in the Aug. 21 Annals of Internal Medicine . the growing popularity of alternative medicine is "part of a larger trend of people taking charge of their own health," says Kessler.

Not everyone puts a positive spin on she. Wallace Sampson School of Medicine, Stanford University, a leading debunker of New Age medicine, said the Harvard group is trying to legitimize what in fact is still a "fringe" phenomenon and "grossly overestimated" the popularity of alternative medicine including in their definition of traditional practices such as self-help groups, relaxation, and dietary changes

* the survey asked about these alternative therapies :. acupuncture, aromatherapy, biofeedback, chiropractic therapy, commercial diet programs, "lifestyle plan" (as macrobiotics), energy healing, folk medicine, herbal medicine, homeopathy, hypnosis, imagery, massage, megavitamin therapy, naturopathy, osteopathy, relaxation, support groups, spiritual healing by others, and yoga.

Related site

The homepage Ronald Kessler
The National Centre complementary medicine and alternative

A new study casts doubt on a theory long about what goes wrong in the brain of patients with Huntington's disease . The findings suggest new approaches to drug design against the fatal neurological disorder.

The Huntington's patients have a mutated form of a protein called huntingtin, which contains between 36 and 0 repetitions of glutamine, an amino acid, where the unaffected individuals have just a couple of dozen repeats. Scientists have long assumed that the trouble arose from the interaction of huntingtin and called caspases, enzymes involved in the degradation of proteins routine. When caspase cut small peptides of mutant huntingtin region, they thought, peptides accumulated in abnormal blood cells observed in neurons of victims of Huntington. In laboratory experiments, the same peptides kill nerve cells.

But in the online issue on October 15 Nature Genetics , geneticists Roy Dyer and Cynthia McMurray at the Mayo Clinic in Rochester, Minn., Report that the theory does not stand up to the scrutiny. When they stained brain samples from victims of human Huntington, they found that the globs features include full-length mutant huntingtin, instead of peptide fragments of the mutant. Then, they showed that caspases not cut the peptides of the mutant protein at all. Instead, caspases normal huntingtin protein break down, as they are supposed to. Things go wrong when these fragments are attracted to the abnormal huntingtin balls, instead of being processed further. The researchers believe that this interaction ultimately kills the cell, but they are not sure how.

The study is "very important" and shows that the prevailing explanation for the origin of Huntington's disease needs to be "redesigned," said Scott Zeitlin, a neuroscientist at the University . of Virginia in Charlottesville Zeitlin said the study may also help scientists find new targets for drugs against Huntington -. Such as compounds that block agglutination of the abnormal huntingtin

Sites Related

Cynthia McMurray home
Disease Huntington Society of America

While asthma attacks are triggered by a series of environmental factors - mold for animals dusty teddy - the disease itself runs in families, which leads the researchers asthma in search of the genes responsible. Now researchers have found a set of genes that confer asthma susceptibility in mice.

Scientists already had their eyes on a region of human chromosome 5, called 5q23-35, where they suspect that a number of asthma-related genes reside: Many asthmatics have genetic mutations in this part of the chromosome. Several candidate genes controlling immune responses associated with asthma, but researchers do not know which genes make people more likely to come down with asthma in the first place.

To determine which candidate genes are responsible for asthma susceptibility, immunologist Rosemarie DeKruyff and colleagues at Stanford University in Palo Alto, California, sought to restrict 5q23-35 to a size manageable. They created two mouse strains that were genetically identical except in the region corresponding to 5q23-35 in humans: A strain had mutations that confer susceptibility to asthma and the other strain lacked these mutations. Then consider combinations of these mutations and identify which are most closely linked to asthma, they raised mice and had offspring inhale methacholine, which can trigger asthma. In this way, the researchers learned that the mice had inherited a genetic predisposition to the disease

After many reproductive cycles and tests, the stretch of chromosome that both mouse strains n did not share -. And conferred asthma susceptibility - was 0 times shorter than 5q23-35, the group reports in the December issue of Nature Immunology . There DeKruyff team identified two candidate genes Tim-1 and Tim-3 . Because mice of the subject asthma had multiple mutations in both genes, researchers could not determine whether the one, the other, or both cause asthma. mouse immune cells bearing the variety "sensitive" of Tim-1 , a new gene in search of asthma, have produced the same molecules as bent during an asthma attack. The other gene, Tim-3 , is already known to have a role in the immune system unrelated asset asthma attacks, but because many of the sick mice had mutations in Tim-3 , the researchers say they could not exclude the sensitivity until they can test it outside of Tim-1 .

The work "would be quite significant" if it holds up in humans, says immunologist Marsha Wills-Karp Medical Center Children's Hospital of Cincinnati, Ohio. The most appearance critical of Tim newly discovered genes is that they can cause not only asthma, but other diseases of the immune system as well.

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laboratory page author Dale Umetsu
Stanford Center for asthma and allergic disease
About asthma American Lung Association