Health Meaning

Chemists have identified a family of compounds that may one day help prevent damage to the kidneys of lupus, a common autoimmune disease that afflicts up 2 million Americans.

one of the major complications of the disease, kidney damage, appears to come from antibodies that lock onto clean DNA from a patient. Normally, the kidneys filter blood damaged DNA, and in lupus patients misguided antibodies trigger inflammation when they bind to DNA that collects in the kidneys.

Gary Glick of the University of Michigan and Jonathan Ellman of the University of California, Berkeley, looked for a lure that mimic DNA and bind to antibodies troublesome. They have created more than 1,0 versions of a promising group of compounds called 1,4-benzodiazepines and identified those who locked in mouse antibodies with lupus. `` It's like playing the lottery every ticket you buy, '' said Glick. `` If you play big enough statistics, you are bound to win. '' Glick Ellman and report their findings in the current issue of the Journal of the American Chemical Society.

The President of the Medical Council of the Lupus Foundation of America, Evelyn Hess of the University of Cincinnati Medical Center, welcomes the conclusion with caution. It is `` an interesting test tube mechanism, '' she said, which must now be tested in animals.

This is precisely the next stage of Glick. His team is now testing the most promising compound in SLE mice prone to see if it effectively prevents kidney damage. Such treatment in humans, Glick said, could have fewer side effects than immune suppression drugs currently used to treat the disease.

Aspirin seems to protect against damage to the nerve cells of rats inflicted by glutamate, an amino acid, which has been involved in some chronic degenerative diseases. But some experts are skeptical about whether the test-tube findings, reported in today's issue of Science are relevant to humans.

Glutamate transmits messages in the brain. But at high concentrations it becomes a powerful excitotoxin that kills brain cells. Scientists have found evidence in recent years that the toxic effects of glutamate may play a role in nerve cell death seen in chronic neurodegenerative diseases such as Huntington's disease and amyotrophic lateral sclerosis, or Lou Gehrig's disease .

Knowing that neurodegeneration often accompanies inflammation, and aspirin reduces the inflammatory response, pharmacologist Mariagrazia Grilli and colleagues at the University of Brescia Medical School in Italy exposed to see if aspirin could prevent neurodegeneration. They have exposed rat brain cells to toxic levels of glutamate and either a cocktail of aspirin and its metabolite sodium salicylate, or a second anti-inflammatory drug indomethacin. Only aspirin cocktail at concentrations equivalent to those people who take aspirin protected against glutamate toxicity

The team traced Grilli protective effects of aspirin's ability to inhibiting the activation of two glutamate proteins -. nuclear factor kappa B and Rel. The proteins are transcription factors that switch on genes involved in immune function and inflammatory response. But he does not know how damp the transcription factors thwarts neurotoxicity.

In no way do the results suggest that aspirin conjure Huntington or other chronic neurodegenerative diseases, says a scientist pharmaceutical company who requested anonymity. The scientist who develops substitutes aspirin, said the popular painkiller has multiple effects in cell culture at concentrations used in the study. "Aspirin has been on the market for a hundred years," he said. "I think we've seen before." Nevertheless, said Johns Hopkins University researcher Jeffrey Rothstein glutamate, the results "sound really fascinating" and should be followed.

Scientists have found a biochemical pathway that may explain why sunburn and other injuries hurt when exposed to heat, according a report in the latest issue of Proceedings of the national Academy of sciences . The discovery could one day lead to treatments that blunt the heat sensitivity of an injured person.

Peter McNaughton and Paolo Cesare King's College in London nociceptors of isolated rat sensory neurons that collect painful stimuli. After quickly heated nerve cells at 49 degrees Celsius, they detected an increase in the electric current flowing through the cell membrane, suggesting that the current plays an essential role in the perception of pain. When they exposed these cells to injured another burst of heat, they should see an increased electrical response of the sensitized neuron. But the answer was unchanged. The team concluded that the culture was missing a key factor that sensitizes the injured tissues to heat.

This, the scientists quickly found, is bradykinin, a protein produced in the damaged tissue that is known to stimulate the pain receptors. When they added bradykinin to the mix, the current has almost doubled. Subsequent experiments teased that the increased current from the activation of bradykinin of protein kinase C. This enzyme, they found, triggers membrane current at lower temperatures in the damaged tissues, which lowers the threshold of pain sensation.

The results suggest that doctors might be able to remove the pain in patients sensitive to heat treating them with drugs that inhibit protein kinase C, said Jon Levine, a neuroscientist at the University of California, San Francisco. But he warned that clinical fruits are far away. An immediate advantage, Levine said, is that the study provides a model for studying how other types of painful stimuli can work. "This opens the door not closing," he said.

Tomorrow is the anniversary of German physiologist and surgeon Kaspar Friedrich Wolff, born in 1733. Considered the founder of embryology Wolff issued in 1759 called revolutionary work Theoria generationis , which challenged the prevailing theory that each organism develops from a homunculus - or a tiny version of an adult - inside a seed or semen. Wolff proposed that groups of cells, initially non-specialized, differentiated into various tissues, organs and systems. The idea that plants and animals are composed of cells was still controversial, and Wolff's findings were shunned for more than 50 years. But he finally did get a measure of recognition. The body of Wolff, an embryonic structure in animals that develops in the kidney, is named after him

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

The amino acid L arginine seems to reduce blood pressure and other heart disease risk factors. The finding, reported in the current issue of Journal of Clinical Investigation , may help explain why overweight people and some diabetics are at high risk of the disease.

The body converts L arginine to nitric oxide, a potent chemical that helps regulate blood pressure. Probe this link further, Dario Giugliano and his colleagues at the University of Naples in Italy infused L arginine in 10 healthy volunteers and kept track of several risk factors for cardiovascular disease: the pressure blood, blood viscosity, and agglutination of platelets - the cells that form blood clots. The researchers found that the three risk factors improved between 10% and 20% in response to the amino acid, and heart rate of the subjects and blood circulation in the legs increases. When the researchers repeated the experiment, but blocked the production of subjects of insulin, a hormone that controls blood sugar levels L beneficial effects were -arginine halved. When they infused insulin and amino acid, the effects have been restored.

The study is the first to show that insulin improves L The effects of arginine in people, Giugliano said, and may help explain why diabetics are overweight - who often have defective insulin receptors - are also at risk for cardiovascular disease. But all researchers are not convinced of the link. "They show an interesting phenomenon," says Michael Quon, who studies the relationship between insulin, nitric oxide, and L -arginine the National Heart, Lung, and Blood Institute in Bethesda, Maryland. "But the effect is small."

The National Institute of Allergy and Infectious Diseases (NIAID) today announced a new program that will quickly pay $ 6 million in grants pursue risky new ideas for a vaccine against AIDS. NIAID hope this cash injection will rev a field that has all but stalled.

The new funding mechanism, called the Innovation Grants Program for research approaches to HIV vaccine is the first realization of the vaccine against the AIDS Research Committee (AVRC), a group led by Nobel Prize David Baltimore, the Massachusetts Institute of Technology. At its first meeting on 17 February, the committee discussed what was broken in the vaccine research system that could help solve. "Part of what they saw as broken is that there is not enough of an opportunity to do research on vaccines that will through the system in a timely manner," says Carole Heilman NIAID, which is overseeing innovation.

the grants, each of whom will pay $ 150,000 in direct costs for 2 years, will fund research in three key areas. the first is a better understanding of protein surface of the AIDS virus, HIV Although this issue has been studied extensively, AVRC Norman Letvin member of Harvard Medical School says that critical gaps exist, such as the development of monoclonal antibodies that work against natural -. not only genetically. - versions of the protein AVRC would also like to see more work on the development of better animal models that Heilman said could include the application of new techniques used in the now famous lamb cloning experiments to develop a genetically population identical test animals. The third objective will be to maximize the immune response of the body against HIV by using different strategies for presenting pieces of the virus to the immune system.

Grant Proposals are due May 23, and NIAID will make September 30 price.

Scientists have developed an intelligent form of combat bug to bug the fight against Chagas disease, a potentially fatal infection transmitted by muscle aphidlike kissing bug. The new weapon is a bacterium normally found in the gut of the insect, which is designed to produce a lethal protein. The modified bacteria described in tomorrow Proceedings of the National Academy of Sciences , could help prevent Chagas disease, "a scourge that kills about 45,000 people a year in South and Central America. It could also provide a model approach compared to other diseases transmitted by insects.

A team of Yale University, Rockefeller University in New York, and the Centers for Disease Control and Prevention in Atlanta has developed a strain of the bacteria Rhodococcus rhodnii who lives in the gut of the insect kiss to produce an insect antibiotic called cecropin A. researchers exploited a food unappetizing habit of kissing bugs - they eat the feces on the other - by peppering fake feces with the modified bacteria. Bugs lapped it up. Once inside, the bacterial Trojan began pumping cécropine A bug in the bowels of the kiss, which are also home to Trypanosoma cruzi , the culprit behind Chagas disease. A cecropin kills trypanosomes, but leaves unharmed insects.

"It is fantastic," said Thomas Miller, an entomologist at the University of California, Riverside. "It changes the way we think about things." Besides kissing bugs, he says, this technique could be used to hijack a variety of other disease-carrying insects, mosquitoes that transmit malaria deer ticks that transmit . Lyme disease a member of the Yale team Frank Richards confirms: "It is a general principle that can be used in many systems."

One potential problem is that T. cruzi could quickly develop resistance to cecropin A: "If you try to treat anything with monotherapy, resistance develops quickly enough" , said a member of the Yale Ravi Duravasula team. He and his colleagues are probing ways to overcome potential resistance as obtaining the R. rhodnii to churn to a second antibiotic . Meanwhile, researchers are modified bacterium to the test in a controlled field trial in huts sealed in Guatemala.