Health Meaning

This is billed as "the first ethnic drug" - a heart drug for African Americans - is about to be tested clinical trials. NitroMed, a company in New Bedford, Massachusetts, announced earlier this month it won Food and Drug Administration (FDA) clinical trial authorization in black.

in the United States, blacks are more likely than whites to develop congestive heart failure and are nearly twice as likely to die of the disease. They do not benefit as much from the drug treatment of first line, known for ACE inhibitors. These drugs interfere with a metabolic process that causes constriction of blood vessels, increase blood pressure. However, the drug is more effective when patients respond with a sharp increase in the flow of nitric oxide (NO ). Black patients may have inherited a physiological difference that causes them to respond to ACE inhibitors with lower NO levels than whites, limiting the effect, said Jay Cohn, a heart researcher at the University Minnesota, Twin Cities.

--which BiDil combines two vasodilators with a source of NO - can help, said Cohn, who invented the drug and licensed the rights to NitroMed in 1999. Although BiDil had little effect on the overall mortality in a study conducted in the 1980s, Cohn analysis of a subset of black patients suggests that they have benefited. On this basis, the FDA accepted a 2-year trial that will compare BiDil and other drugs with placebo in 0 black patients at 100 sites.

Other researchers are intrigued but wary. "I'm skeptical of the approach," because it substitutes the color of the skin for genetic analysis, said Marc Pfeffer of Brigham Harvard and Women's Hospital in Boston. Conceding the point, an official NitroMed said "we are looking for better diagnosis" to target therapy.

Related Sites

NitroMed

Lyme disease, the tick -Internet bane from the outside, has scientists scratching their heads. The controversy over how to treat the disease continues this week with two studies in the June 12 issue of New England Journal of Medicine . A team contests the use of antibiotics to treat persistent symptoms of Lyme disease; another suggests that preventive antibiotics can reduce the risk of contracting the disease.

The symptoms of acute Lyme disease, caused by the bacterium Borrelia burgdorferi include a round rash of the skin, flu-like malaise, and seal the pain and stiffness. Antibiotics usually cure the infection and prevent long-term damage. But sometimes, patients who have recovered from the acute illness suffer from what is called post-Lyme disease syndrome characterized by chronic muscle pain, headache and fatigue.

No one knows what causes these long-term complications or how best to treat, so a team led by an infectious disease specialist Mark Klempner of the medical school of the University of Boston decided to test the antibiotics, some doctors use to treat the syndrome. The team worked with 107 patients with post-Lyme disease syndrome. Half received intravenous and oral antibiotics for 0 days; others placebos. Antibiotics do nothing special. About half of the people in each group improved

"long-term antibiotic treatment does not seem to be the answer" post-Lyme disease syndrome, says pediatrician and specialist in Eugene Shapiro Lyme disease medical school from Yale University.

A second study focuses on Lyme disease in its early stages. A team led by an infectious disease specialist Robert Nadelman the Westchester Medical Center in New York studied 482 people who had removed a potential carriers of tick skin diseases in the past 72 hours. Each patient was randomly assigned either a single dose of oral antibiotic or a placebo. In this case, the antibiotic appeared to help: 0.4% of those given antibiotics developed Lyme disease, against 3.2% of those receiving placebo

Although prophylactic antibiotics appear to work they can not tell the difference. in the big picture. The study shows that the risk of Lyme disease is low, Shapiro said, even in Westchester County, New York - one of the most hazardous areas of the country. And because many cases result of Lyme disease not recognized tick bites, he said, it is "unlikely" that preventive antibiotics will significantly reduce the overall incidence of Lyme disease.

Related Sites

Lyme Disease Resource Center
Information NIH Lyme disease

Scientists have identified a potential drug that may be able to hit a variety of cancer cells while leaving healthy cells unharmed. If it works in human trials already underway, the drug would be a significant advance over current chemotherapy agents and may one day help patients who do not respond to other medicines.

flavopiridol, like many other drugs, works by blocking proteins essential to cell division. It has been in clinical trials for kidney, prostate, colon and other cancers since 1998. Last year, a new talent came to light: flavopiridol also blocks a protein that helps transcribe DNA messenger RNA (mRNA), the first step in producing a protein from a gene and a process that all cells need to stay alive. researcher Louis Staudt cancer of the National Cancer Institute in Bethesda, Maryland, and colleagues was curious about the effects of flavopiridol on B-cell lymphoma.

When Staudt tested how flavopiridol inhibited genes, he was surprised to find that off transcription in a multitude. Yet rather than killing all the cell types targeted cancer flavopiridol. Puzzled, Staudt decided to measure how long the mRNA of each of 5000 genes lasts after treatment with flavopiridol. In September 13 issue of Genome Biology , the team Staudt reports that the mRNA of sustainability relates to gene function. The genes known to participate in cell death or cell division, two processes which, when awry, contribute to cancer, often had short mRNA. Once flavopiridol hit the cell, genes with short mRNA could not do more of it and mRNA rapidly degraded.

"He has a general effect on transcription, and patients are not Keeling more," said cancer researcher John Reed of the Burnham Institute in La Jolla, Calif. "It's pretty amazing. "

Related Sites The drug is being tested in small groups of patients (but none with a B-cell lymphoma), but Reed cautions that it is difficult to predict how successfully the drug against cancer.

research paper in Genome Biology
more on the way the flavopiridol of Journal of Biological Chemistry
Staudt laboratory Web site
Reed lab website

Since the emergence of a new human disease linked to eating beef from cattle with "mad cow" in 1996, the British public has been seized by a question: How bad will the epidemic? Hoping to dispel the confusion, two teams of scientists have refined their projections -. And they come to different answers

Although humans consumed about 750,000 cattle infected with bovine spongiform encephalopathy (BSE) between about 1980 and 1996, no one knows how many people have been infected, or how long it takes for an infected person to get sick. At the end of September 01, 107 people in the UK died from variant Creutzfeldt-Jakob disease (vCJD), an invariably fatal neurodegenerative disease. How many more are at risk is uncertain; the most authoritative estimate to date, the epidemiologist Roy Anderson Group at Imperial College in London, provides a few hundred to a maximum of 136,000.

A new mathematical analysis by researchers at the London School of Hygiene & Tropical Medicine provides encouraging news. The study, published online by Science on 25 October, concluded that the epidemic could be almost its peak. The team used an approach called "back-calculate" which focuses on a smaller number of assumptions, including speculation on the number of people infected with BSE when they were infected, and the incubation time. No matter how these parameters vary, the upper limit of the event is "less than 10,000," said London School epidemiologist statistical Simon Cousens, a co-author.

But those hopes are challenged by the Anderson Group. His newly completed analysis, but still unpublished uses different mathematical techniques and comes with maximum estimates that are "substantially higher," said Neil Ferguson member of the team. Both teams agree that their model may be too optimistic if a key assumption turns out to be false: that all victims of vCJD will share the same genetic profile. While this has been true for all cases of vCJD to date, a number of researchers believe that other genetic profiles may also be sensitive.

Given the lack of reliable tests for the infection of BSE in humans, it is surprising that different mathematical models produce different results, researchers say. Modelers are based on arbitrary assumptions, says epidemiologist Peter Bacchetti of the University of California, San Francisco. But because the London School predicted that the epidemic may soon peak, their projections may be in the short term more testable. Said veterinary epidemiologist Mark Woolhouse of the University of Edinburgh in Scotland: "We will soon know if they are right"

Related Link

Spongiform Encephalopathy Advisory Committee.

most pathogenic bacteria have been hunted for a long time, but for decades got a microbe with murder. Discovered in 1982, Helicobacter pylori triggers ulcers and cancer that kill 7 million people each year, scientists have learned much about the capabilities ulcer causing bug. Now a new study clarifies H. pylori deadliest talent, showing exactly how it forces the stomach cells to deform and migrate -. a first step in cancer transformation

People infected H. pylori are two to six times more likely than uninfected people to develop either the stomach or lymphoma cancer . When H. pylori infects the lining of the stomach, the stomach cells may lie until they resemble hummingbird beak. The microbe is known to inject a protein called CagA in stomach cells, where it is marked with phosphate groups. Because the addition or removal of phosphate from protein can interfere with cellular signals and help induce cancer, scientists have questioned whether it was H. pylori 's strategy.

Read, molecular oncologist Masanori Hatakeyama Hokkaido University in Sapporo, Japan, and colleagues first made an assumption that the human protein CagA interacts with cells of the stomach inside. They chose the hepatocyte growth factor (HGF), because the stomach cells treated with it exactly as CagA treated cells. HGF receptor alters a signaling protein called SHP-2, and the group wondered whether CagA done too.

Scientists have found that antibodies against CagA fish out SHP-2 from cell extracts of the stomach, and vice versa, indicating that the two proteins team up. Moreover, cells infected with a mutated version of CagA which does not bind SHP-2 helped CagA elongate cells. They proved the point by showing that SHP-2 clips additional signaling proteins phosphates, but only when it is related to CagA. Together, these results mean that CagA plugs into the normal cell signaling system, Hatakeyama said, leading the cell by mistake and put it at risk of becoming cancerous.

Cellular microbiologist Brett Finlay calls the work "a great step forward" in explaining how H. pylori tweaks normal cell signaling pathways, pushing the cells of the stomach a little more . malignancy other experts point out that most of the molecular links between H. pylori and cancer remain to be discovered - but H. pylori investigators are closing in on their careers

Related Sites

Facts H. pylori infection CDC
More background on H. pylori , sponsored by the pharmaceutical company AstraZenica
information H. pylori and ulcers of the National Institutes of Health
the benefits of H. pylori

Sometimes the biggest challenge for transplant patients just after receiving a new organ, when their bodies can reject as foreign. Now, scientists report in advance online edition of this week of Nature Immunology an immune cell that may be able to call out the immune system to launch such an attack. Although the work is still years from the clinic, it reinforces the idea that there may be ways to hide the strangeness of a new body.

Transplant patients today rely on powerful immunosuppressive drugs to keep rejection at bay. But these drugs can have serious side effects. Better treatment, scientists say, would encourage less of an immune response to a transplant recipient to start, rather than suppressing the response once it is already there.

immunologist Nicole Suciu-Foca and colleagues at Columbia University in New York stumbled on a possible approach while studying the biology of autoimmune diseases. The group was to mix two types of immune cells of two people: the dendritic cells, which the immune system warning invaders of a person, and T cells that fight the other. Normally, dendritic cells by adding to the mix should induce T cells to multiply to attack a threat. But in this case, the reverse is produced :. Dendritic cells Adding actually slowed the growth of T cells

T cell growth was inhibited only when both genes, ILT3 and ILT4 , were activated in the dendritic cells. Scientists believe that the so-called suppressor T cells turned on genes, because when they removed these cell culture, the growth of T cells resumes. This natural immune suppression may occur in cardiac transplant recipients who never rejected the organ, researchers say; T suppressor cells of these patients could induce dendritic cells from the donor to produce ILT3 and ILT4. This was not the case among those who rejected their new heart.

The work is "good news" for those trying to stem the immune rejection of grafts, said immunologist Mark Weinberg Emory University of Medicine School in Atlanta, Georgia. But, he adds, clinical intervention is still far.

Related Sites
The homepage of Nicole Suciu-Foca
transplant programs at Columbia University
American Society of Transplantation

CAMBRIDGE, MASSACHUSETTS -. It was not a mere bluster policy when US Sen. Edward Kennedy (D-MA), last week called Kendall Square in Cambridge the "epicenter of the world of biotechnology." The giant Swiss drug Novartis, based in Basel, has the intention to set up a research center of $ 250 million here to guide its overall efforts of R & D

the new center. - the Novartis Institute for biomedical research Inc .-- will coordinate $ . $ 2.4 billion a year R & D of the company's portfolio in the US, Japan and Europe the laboratory, which is expected to open next year, initially will house 400 scientists - possibly staffing up 1000 -. and will specialize in the development of drugs against diabetes, cardiovascular diseases and viral diseases Novartis market is increasingly focused on this side of the Atlantic Less than a third of sales. of the company are in Europe, while 43% is in the US

Novartis move is the latest blow to European research drugs and reflects the company's efforts to keep American competitors in its sites. "Europe has created its own problems by not ... provide a dynamic research environment," said Novartis chief Daniel Vasella direction. In Europe, there is more resistance to the links between industry and academia and European governments have managed to match the prodigious investment in biology and biotechnology made by both the US government and Venture Capitalists, Vasella said: "the United States has pursued a much more intelligent policy"

members of the Swiss scientific community agree that their research programs are underfunded and have few incentives to retain talent. Last November, the Council of science and technology Swiss launched a petition imploring Government to strengthen the 10% research budget within 5 years. "the Novartis movement is a very serious symptom during the descent of the Swiss research," said Catherine Nissen-Druey, vice president of the advisory body . "It sends a message to young Swiss scientists that research is more promising in the US than it is here."

With reporting by Helena Bachmann Geneva

Related Sites
Novartis Institute for Biomedical Research Inc.

BARCELONA, SPAIN -. Discourage new data presented at the XIV International AIDS Conference can significantly increase the bar for developers of vaccines against HIV

researchers took heart in the long observation that people with HIV seem able to repel infection with a second strain or subtype of the virus. This resistance to so-called superinfection makes a compelling argument that although the immune system can not clear an established HIV infection, it can go up sufficient immunity "cross reaction" to counter new strains. But immunologist Bruce Walker of Massachusetts General Hospital of Harvard reported today strong evidence that the patient is co-infected with a second strain of HIV.

"It is terrible news," said Brigitte Autran, immunologist of the Pitié-Salpêtrière Hospital in Paris, France.

The patient was part of a study of people who started treatment with anti-HIV drugs soon after infection. When the human virus fell below the most sensitive test for the detection level, he stopped taking drugs. he stayed drugs until the virus became detectable again. the third time its enriched viral levels, the researchers found that it had become infected with a new virus that was of the same subtype, called clade B.

most disturbing of all, they found that he had produced high levels of killer cells - so-called cytotoxic lymphocytes (CTL) that the clear cells infected with HIV. - his first against strain "We can not extrapolate from a single case, but we were really struck this cross-reactivity was not enough to protect against another clade B virus, "said Walker. His team was particularly surprised to find that although the genes of the two viruses B clade differed only by 12%, both viruses showed substantial difference in one essential characteristic: the parts of the virus that trigger the production killer cell. This indicates that the CTL responses that lack scale can not provide enough cross-reactivity necessary to protect people in the real world.

The finding made many researchers do a double take, especially those like Autran, who are trying to stimulate NK cells to attack HIV. But Emilio Emini virologist has warned his colleagues not to over-interpret this single case. "This observation indicates simply that you superinfection is possible," said Emini, who heads the vaccine program at Merck & Co. Rahway, Pennsylvania, which attempts to make a vaccine based killer cells. "What it does not tell you is the probability of that happening. "

Related Sites
Description Walker's research
Website of the XIV International AIDS conference

Chubby belly depriving their owners of more than a svelte figure, according to a new study. abdominal flab in middle age rats causes insulin resistance, a common precursor to diabetes that affects older people disproportionately. Surgically removing fat restores the function of insulin, suggesting that the disease develops because fat accumulates around the internal organs.

As people age, they acquire the beer belly and love handles. Their bodies also lose the ability to absorb glucose from the blood, a condition called insulin resistance. Circumstantial evidence linking the insulin resistance in visceral fat, fat found in the stomach, but not subcutaneous fat, which mold the love handles. Researchers have debated whether visceral fat is a byproduct or the cause of insulin resistance.

To study Nir Barzilai and colleagues at Albert Einstein College of Medicine in New York cut the fat of adult rats with insulin resistance. When subcutaneous fat was removed, the rats fared no better. But when visceral fat has been removed, the rats recovered and began extracting their blood glucose as well as youth is intact, the team reports in the October issue of Diabetes . The results suggest that visceral fat, but not subcutaneous fat crippled insulin function.

To determine how fat may alter the absorption of glucose, the researchers measured the production of blood molecules that fat cells secrete. They found that the elimination of visceral fat changes the signals sent by the subcutaneous fat cells. They produced about two-thirds less messenger RNA templates for the hormone leptin, which controls appetite and is overproduced in insulin-resistant people. There was also less TNF- a , a protein thought to counteract insulin by blocking its biochemical pathways. This observation implies that visceral fat causes insulin resistance by changing the output of molecules made by a wide range of fatty tissue.

"This is the first demonstration that I know that the elimination of visceral fat solves the problem of resistance," says endocrinologist Michael Schwartz of the University of Washington, Seattle. Endocrinologist Robert Schwartz of University of Colorado Health Sciences Center in Denver suggest how the scheme could be considered in the equation :. calorie restriction - which is known to reduce insulin resistance - could alter metabolism by influencing the types of fat calories build

Related Sites
A longer version of this article at SAGEKE
laboratory Nir Barzilai of Albert Einstein
American Diabetes Association

WASHINGTON, DC - After months of internal debate, President George W. Bush announced the details of its administration program to prepare today USA against a smallpox attack. About 450 000 health workers and others who may come into contact with the virus during an outbreak will be offered the vaccine between late January and the summer. Starting today, another half million in the army will get the plans on a mandatory basis.

Finally, up to 10 million police, firefighters, emergency medical technicians, and other so-called first responders will be offered the vaccine as well. And although the Administration does not recommend that the general public to get the shots, it will make available to those who "insist" they get vaccinated and are not known to be at risk of complications. Some researchers question the plan, citing rare but serious side effects of the vaccine, which include death

All vaccination against smallpox in the civil US was discontinued in 1972. 8 years later, disease was officially declared eradicated. But the US government is concerned that terrorists or rogue nations could access illegal virus stocks. During his address, the president said twice no information that such an attack is imminent. "However, it is prudent to prepare for the possibility of terrorists ... who kill indiscriminately would use disease as a weapon," he said.

Because some troops would be needed to take the vaccine, Bush said the commander, it would also be vaccinated. But as they are not first responders or other members of the Bush family or the staff of the White House will get the shots at -he added.

the smallpox vaccine provides good protection against the disease, but it causes serious side effects in a small number of people and kills one or two in every million people vaccinated. accordingly, vaccination policy was the subject of intense debate. in October, the Advisory Committee on immunization practices (ACIP) recommended that, as long as no attack has taken place, only those directly involved in the response should receive the vaccine - a group thought to number about half a million. But he did not inform broadening the policy to all first responders, and recommended not to offer the vaccine to the public. But ACIP chair John Modlin said the policy of the Bush administration is also reasonable. "The president and his advisers have obviously another global perspective on it," Modlin said

But others argue that vaccination as a bad idea - especially to make it accessible to the public. Getting vaccinated "happens to be an extremely complex decision that requires a sophisticated understanding of smallpox," said Michael Lane, a former director of the smallpox eradication unit of the Centers for Disease Control and Prevention in Atlanta. "For put this burden on the American people is a mistake. "

Related Sites
remarks and background information of the President
CDC extensive site about smallpox and side effects of the vaccine
the Advisory Committee on immunization practices recommendations of