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

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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

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A longer version of this article at SAGEKE
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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. "

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remarks and background information of the President
CDC extensive site about smallpox and side effects of the vaccine
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cancer cells have the ability to divide indefinitely, thanks to an enzyme called telomerase giving young. Now scientists have shown how cancer cells keep this handy potion and took a first stab to block. If the technique pans, it could eventually lead to a new class of cancer drugs, the team said.

telomerase is turned off in normal cells but is particularly active in 85% of cancers. Telomerase protects DNA to complete the protective bumpers on the ends of chromosomes. This process is essential in early life because DNA could obtain otherwise degraded as cells divide rapidly. However, said Robert Newbold, a geneticist cancer at Brunel University in Uxbridge, UK, the body stops producing telomerase before birth, and a strict limit is placed on the number of times cells can divide . The ability to turn off telomerase probably evolved as an anticancer defense in the long term creatures such as humans, he said.

To study how cancer cells manage to keep the gene turned on telomerase Newbold Brunel and his colleagues and the Swiss Research Institute in Lausanne against cancer treated cells cancerous and normal fibroblasts with enzymes that digest DNA. With the applied enzyme, they found that the gene for telomerase was easier to cut and can be cut into several pieces in cancer cells - suggesting that the DNA of telomerase has been disentangled and prepared for use, the team reports in the February 1 years Cancer Research .

In a second series of experiments, this time with breast cancer cells, the team at Newbold found that genes of telomerase rolled back when the researchers added a normal copy of chromosome 3, which they had previously found to contain potentially able to turn off telomerase genes.

"Blocking this outcome would be a very able chemoprevention if it could be done specifically [for the telomerase gene]," agrees Woodring Wright, a cell biologist at the University of Texas Southwestern Medical Center in Dallas. "But it may be difficult," he warns.

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Lab Newbold

NEW ORLEANS - Nanoscale electronics experts are often streaked to manufacture circuits Microchip companies already make millions of times better. But at the meeting of the American Chemical Society here yesterday, researchers described a nanoscale device that does something fleas can not touch: tracking proteins indicative of two different forms of cancer. On the road, the tables of these sensors could enable doctors to instantly screen patients for various diseases.

Researchers have been experimenting with electronic diagnostics for years, but with mixed success. The detectors typically use field-effect transistors (FET) devices in which a voltage applied to an electrode, called the gate, alters the current flow between two electrodes. For diagnosis, researchers have generally replace the gate of a material coated with proteins or other compounds to capture molecules of interest. As the captured molecules are charged, their presence alters the conductance between the two electrodes of the transistor. But although these devices operate frequently, they are generally not very sensitive, because they require a large number of target molecules to bind.

Hoping to improve the sensitivity, chemist Charles Lieber of Harvard University and his students have tried the same configuration with nanoscale transistors. Lieber's group has made these transistors for years, typically using son as small as 1 to 2 nanometers in silicon. For this study, they have shaped silicon nanowires doors coated with antibodies to the specific antigen of the prostate (PSA), prostate cancer marker. They then positioned the transistors in a patterned plastic pad with tiny channels which allowed fluid flow over them.

When the team injected a dilute solution containing PSA, the negatively charged protein bound to the antibody and modified conductivity FET, the graduate student Lieber Wayne Wang said at the meeting. In fact, he said, he and his colleagues managed to detect PSA at levels of 0,025 picograms per milliliter, making the detector more sensitive PSA yet created - over 100 times more sensitive than commercial PSA tests . Wang also noted that a similar sensor picked up the presence of CEA, a marker for colorectal cancer. And a simple array of nanosensors detected two cancer markers simultaneously.

"They did really good progress," said Liu Jie, a chemist at Duke University in Durham, North Carolina. "The question is, can they be made reliable and inexpensive manner in large quantities?" nanowire sensors, he said, still have a long way to go before reaching the market. But if successful, they could provide physicians instant playback of whether a patient has a wide variety of diseases.

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The site laboratory Leiber
American Chemical Society meeting in 03

RNA molecules Millions can protect mice against the damage caused by hepatitis B, a new study shows. The technique disables the virus genes. The discovery takes scientists a little more to the use of this new approach, called RNA interference (RNAi), in people.

Researchers discovered in the late 190s that the RNA molecules might shortened off specific genes. In recent years some biologists began to study how these so-called small interfering RNAs (siRNA) can be used to suppress the disease. In February, a team reported using siRNA to stop a gene in the liver in mice and protect against inflammatory attack like hepatitis ( Science NOW, February 10. Gene therapist Mark Kay and his postdoctoral student Anton McCaffrey, both from Stanford University in California and colleagues wanted to know whether RNAi could target the virus directly behind the hepatitis -. the only way to finally cure people of disease

the researchers first mimicked an infection with hepatitis B by inserting the genome of hepatitis B in liver cells in mice. they then turned to the two types of siRNA each targeting different parts of the genome of the hepatitis. Kay's team placed the siRNAs in DNA loops called plasmids. infusing the mice with a considerable number of these high pressure plasmids allowed the animals to 92% less RNA of hepatitis B than control animals, the researchers report in the May 12 issue of Nature Biotechnology. mice did not suffer serious side effects detectable, although Kay points out that this delivery method can not be used in humans. He and others are experimenting with more benign ways to reach a large number of cells with siRNA.

Judy Lieberman of Harvard University, lead author on the paper hepatitis in February that used a different approach, is encouraged that the study of Kay was successful, but warns that numerous obstacles remain. Philip Sharp of the Massachusetts Institute of Technology in Cambridge agrees. "The question is, can you get [siRNAs] it effectively, appropriately, have an impact on the process that causes the disease?" he says. "I remain optimistic, but I do not consider as a dead certainty."

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B Foundation Hepatitis

Supported by a billionaire entrepreneur and two prestigious universities, a team of scientists is preparing to take a big leap beyond the human genome. Today, the Massachusetts Institute of Technology (MIT) and Harvard University unveiled plans for a new institute designed to transform genetic research in clinical medicine. The institute is supplied with an initial commitment of $ 100 million Eli Broad, a Los Angeles businessman, and will be led by Eric Lander, head of the center of the genome-MIT Whitehead Institute in Cambridge.

The Broad Institute has emerged after two years of difficult negotiations on financing, location and organization ( science 21 December 01, p. 2451). Broad may be best known in Los Angeles as an art lover. But he also invested millions of dollars in a laboratory of biological sciences at the California Institute of Technology in Pasadena.

In addition to Broad $ 100 million commitment, MIT and Harvard have pledged to mobilize up to $ 0 million more in the next decade. The Broad Institute will aim to bring together specialists in more than half a dozen disciplines for understanding the cell and use genetic information to create tools in the fight against cancer, diabetes and inflammatory and infectious diseases. The ambitious effort will be based in Cambridge, Massachusetts, where a dozen professors and 30 associated members of the faculty will be supported by a starting budget of $ 30 million per year. Unlike Whitehead, the Broad Institute will not be an independent entity; MIT will administer on behalf of the partners.

Broad Institute leaders have not yet managed to bring the private sector into the picture. Novartis, the pharmaceutical company based in Basel, has moved its R & D center in Cambridge last year and expressed interest in joining this partnership. Negotiators failed to agree before the MoU was signed last week, however. Mark Fishman, director of biomedical research at Novartis, said that "we want to be part of these things, and this is just one of the possible ways." Lander and Stuart Schreiber, a Harvard chemist who will be part of the faculty foundation, said the new institute will focus on the need to make data available for free, and they predict that companies understand the need to collaborate openly.

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ad Broad Institute
Eric Lander homepage

women trying to conceive should not take two aspirin and call your doctor in the morning, according to a new study. It shows that aspirin and ibuprofen, but not acetaminophen, taken at the time of the design almost double the risk of miscarriage. The findings may change the way doctors recommend over-the-counter painkillers to pregnant women.

About 15% of pregnancies end in miscarriage, and doctors know little about the factors that put women at increased risk. A study last year suggested a link between a class of painkillers called nonsteroidal anti-inflammatory drugs (NSAIDs) and miscarriages. NSAIDs, which include common painkillers such as ibuprofen and aspirin, reduce pain by purging prostaglandins, which fertilized eggs must be planted in the womb.

To test whether NSAIDs rattle pregnancies, a team of researchers led by epidemiologist reproductive-Kun Li of the Research Institute of the Kaiser Foundation in Oakland, California, surveyed 1055 women who conceived in the 40 previous days. They requested the use of pain-around time, women trying to get pregnant and have followed pregnancies in women who have succeeded. The researchers took into account activities such as drinking coffee or hot-tubbing and excluded women at risk of miscarriage in the absence of treatment, such as women who reported cramps.

The risk of miscarriage is 80% higher than normal for women who took aspirin or ibuprofen (the active ingredient in Advil) regularly for more than a week, the team reports in the issue of British Medical Journal August 16 Acetaminophen (the active ingredient in Tylenol) has no effect on pregnancies at all. The risk jumped dramatically if women took the drugs in a week of design: Five times the number of women taking one of two NSAIDs had miscarriages, compared with women who took nothing or have taken acetaminophen. In the end, Li said, the Federal Drug Administration will decide whether to reclassify aspirin and ibuprofen. Li noted that newer NSAIDs, COX-2 inhibitors such as Celebrex, were tested for reproduction and are not recommended for pregnant women.

Epidemiologist Gunnar Nielsen of Odder Hospital in Denmark said the study shows "almost beyond doubt" that NSAIDs, it will be harder for some women to get pregnant. "If pregnant women need analgesics during pregnancy," he suggests, "they should ask their doctor if [acetaminophen] will be enough."

Related Sites
The page of De-Kun Li at Kaiser
NSAIDs on the net

the fight against a problem that hematologists and blood banks it has long abandoned it, a team of scientists has determined how to store platelets in the refrigerator instead of the temperature ambient. If maintained in other experiments, the technique could stabilize supply of platelets and reduce the risk of bacterial infections transfusions.

Platelets are disk-shaped cells that help blood clot. Every year millions of units transfused in people around the world to stem the bleeding. But because platelets must be stored at warm temperatures, they last only five days after donation. (In contrast, the red cells can be refrigerated for more than a month, and plasma may be frozen for a year). They can also host bacteria that are a major cause of the original infection through transfusion. In January, scientists at Harvard Thomas Stossel, Karin Hoffmeister, and their colleagues found that when platelets are cooled, some protein receptors on their surfaces stick together, revealing a sugar molecule. This triggers a response in the liver. When platelets are infused, liver cells yank them out of circulation

Now, the team of Hoffmeister found a potential cure, as reported in this week's issue of science . Other experiments in test tubes showed any part of the liver cells sugar molecule were noticed. Scientists reasoned that if they threw a coat over sugar - in the form of another type of sugar molecule with a different chemistry, which covers the first - the liver does not recognize the pads, and they circulate freely.

Hoffmeister and his colleagues extracted the mouse blood platelets mixed with a solution containing the second and sugar concoction refrigerated for 2 hours. They then injected platelets modified into mice, and the cells appeared not the worse for wear. The group also studied human platelets with a similar sweet disguise. After cooling platelets up to 12 days and examine them in a petri dish and then, the team Stossel found that function seemed intact.

The technique "seems to offer real promise" not only to reduce pathogens, but also to extend the storage time, said Roger Dodd, executive director of biomedical safety for the American Red Cross in Rockville ., Maryland After more expansive tests, modified cold rooms can allow blood banks - and beneficiaries - to start counting their savings

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of Thomas Stossel laboratory
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__gVirt_NP_NN_NNPS <__ Backgrounder on the blood, PBS

The long dreaded superbug surface on a Friday summer in 02. The new strain of the resistance Staphylococcus aureus , cultured from a patient with diabetes at Detroit, had developed to vancomycin, one of the few antibiotics left to reliably kills staph. Now a study shows how the microbe became a threat.

S. aureus lives on the skin and in the nose of healthy people, causing nothing worse than pimples and boils. But in hospitalized patients, it causes tens of thousands of infections each year, including serious infections and surgical wound sometimes fatal, infections of the bloodstream, and pneumonia. The microbe has learned to evade antibiotic after another, and in the late 1980s, vancomycin was the drug of last resort.

When the Detroit vancomycin-resistant S. aureus (VRSA) strain appeared the detective work began. Doctors two strains almost identical patient. The only difference seems to be vancomycin resistance or sensitivity. Doctors also grown Enterococcus faecalis of ulcers resistant to vancomycin foot of the patient. circular loops of DNA called plasmids of VRSA and E. faecalis strains, but not sensitive S. aureus strain had a gene called vanA as wards of vancomycin. This suggests that the drug resistance gene had jumped species, says Weigel.

To see how he made the jump, microbiologists Linda and Fred Weigel Tenover of CDC and colleagues examined the plasmids for a mobile genetic element called a transposon, a DNA extract that can jump from a plasmid and worm its way into another. Indeed, the two strains resistant to vancomycin welcomed with a plasmid containing a transposon vanA .

The results suggest that E. faecalis in the woman's ulcer crept up S. aureus and passed along its resistance plasmid, the researchers report in the November issue 28 Science . Enzymes in S. aureus seem to have destroyed abroad E. faecalis plasmid, but before that happened, the transposon jumped like a rat escape from a sinking ship, and infiltrated the S. aureus plasmid resident to create a new hybrid. This created a new S villain. aureus strain that can spread easily in hospitals, withstand almost all drugs to kill him, and share his weapons with S. aureus cousins ​​who remain vulnerable to vancomycin. "What we have is really isolated the triple threat," says Tenover.

Two antibiotics, linezolid (Zyvox) and quinupristin / dalfopristin (Synercid), always stop VRSA, said microbiologist Donald Low University . Toronto But it is important that pharmaceutical companies intensify efforts to develop alternatives, he said. " At this point, we have something in our back pocket, but that could change quickly "

Related site
record CDC VRSA

Federal regulators should be allowed to use controversial studies in which people are intentionally dosed with pesticides, a group of experts decided. The report from the National Research Council (NRC) concluded that these tests may be acceptable if they meet the scientific and ethical standards. Environmental groups criticized the report as full of loopholes and urged the Environmental Protection Agency (EPA) to put a moratorium on pesticide testing, they maintain are unethical.

The question has been raised because of a 1996 law that requires EPA to tighten the limits on exposure to pesticides to protect children. To compensate for this, companies have started sending EPA human studies to move a fudge factor used in the standards based on rat data. This factor is called the security is applied to the results from animals in cases where people are more sensitive than rats. But the EPA has placed a hold on human testing after the Environmental Working Group (EWG), an advocacy group based in Washington, released a report slamming several of these studies in the UK. Later, the agency asked the NRC to take a look at all human dosing studies, including volunteers exposing to air pollutants and water. Meanwhile, last year a court ordered the EPA to consider pesticide tests on a case by base basis.

The panel, chaired by James Childress ethicist at the University of Virginia, found that these tests are not intrinsically unethical: Improve the science behind a regulatory decision "is a benefit to society which may justify the conduct of a human dosing study, "the report said. EPA should accept the data, he adds, if they are scientifically valid, the information can not be obtained in other ways, and studies comply with federal ethics standard known as the common rule.

In addition, a kind of test - which is to try to eliminate animal to human safety factor - should be accepted if the participants not experience adverse effects. This usually means the metabolism studies wherein volunteers are given lower doses which do not cause symptoms, but cause chemical changes detectable in the blood and urine.

The report recommends new obstacles, however. He said the EPA, which has no ethics committee of its own, should establish a review panel for the Humanities to offer companies advice before they undertake a study and to help EPA decide which studies to accept.

Regarding the 19 trials have already been submitted to the EPA, most of them metabolism studies, the report said they could be used if they are found to meet the standards the report. According to Patrick Donnelly, executive vice president of CropLife America, "They all will." But toxicologist Jennifer Sass of the Natural Resources Defense Council disagrees. It examined several, and "none of them have any [scientific] validity," she said

Related Sites
Intentional of human dosing studies to the EPA regulatory purposes: scientific and ethical issues
Environmental Working Group press release and the 1998 report

the idea that a low calorie diet can reduce the risk of breast cancer has allowed to sell several popular books on cancer prevention diet. But a short and sudden combat famine may do just the opposite, according to a new study that found higher rates of breast cancer among Dutch women who lived a brief famine at the end of World War II.

As Allied forces tried to wage war to a quick conclusion advancing on the Rhine bridge at Arnhem, Netherlands, in the fall of 1944, the German authorities have imposed an embargo on food . For 6 months, the hungry Dutch. Adult calorie intake dropped from 1,500 to 700 kilocalories per day. Supply suddenly became abundant again when the Netherlands was released on May 5, 1945.

To determine whether the famine had an effect on the incidence of breast cancer epidemiologist Sjoerd Elias and colleagues from Julius center for health sciences and primary care in Utrecht analyzed data from a study of breast cancer that began in 1974. Between 1983 and 1986, as part of the screening protocol for the study, a 15.396 group of participants who experienced famine responded to a detailed questionnaire. From their responses, the Elias group calculated a "famine score" which estimated the degree of malnutrition each participant. They then randomly selected 2352 women and their health records referenced against various cancer registries.

Women who reported having been hit hard by the famine had a significantly increased risk of breast cancer, 1.5 times higher than those who had the most room, the group reports in 7 April issue of Journal of the National cancer Institute . The risk was even more pronounced, twice as high for older persons 2 to 9 to the time of famine. Researchers suspect that the temporary malnutrition followed by plentiful food at a young age may have had a lasting effect on the balance of hormones - insulin like growth factor I and sex steroids -. Which have been linked to breast cancer

"the rather surprising results ... [also] remind scientists to keep an open mind about the meaning of all the effects of famine on the risk of cancer" said the cancer epidemiologist Tim Key of Oxford University, UK He adds that the study is an "important contribution" because it is the first to bear the risk of breast cancer in the self-reported estimates women of the intensity of the famine, which are more accurate than only demographic, but warned that the results need to be confirmed.

related site
Context "hunger winter" of 1944-1945

a growl of a new nasal spray vaccine may soon keep severe acute respiratory syndrome (SARS) at bay. The new vaccine, a hybrid of SARS and a human respiratory virus, prevented infection in monkeys and may soon lead to a new nasal spray in people.

Since SARS emerged in China in 02, the virus has infected 8,000 people, causing pneumonia in many of them and killing 774. The outbreak was controlled in 03 and health authorities have contained recent epidemics, including an outbreak in China in April, isolating patients. But the disease still lurks, and new strains could emerge and start another epidemic, says virologist Peter Collins of the National Institute of Allergy and Infectious Diseases.

No vaccine against SARS has not been proven in clinical trials, but researchers have developed several prototypes, including a virus of SARS and died a DNA vaccine, both of which have to be injected. Since the laboratory Collins makes genetically nasal spray vaccine against childhood respiratory diseases and SARS is a respiratory virus, "it seemed natural," Collins said, to make a hybrid strain of vaccinia virus to ward off SARS.

The researchers spliced ​​the gene encoding the spike protein of SARS, which is on the surface of the virus and allows it to invade human cells, in an attenuated variant of human parainfluenza virus 3. This strain was designed as a nasal spray vaccine to protect children against pneumonia. After the growth and isolation of the hybrid virus were administered to a group of African green monkeys. A month later, the researchers infected each monkey with SARS. Then they stamped nose and throat each day and tested hardware. A group of vaccinated false green monkeys remained infected by SARS up to 8 days, while the vaccinated animals showed no signs of infection, according to the results to be published Saturday The Lancet . Because parainfluenza vaccine strain has already tested safe in a clinical trial, the hybrid vaccine is ready for clinical trials in children and, with modifications, for adults, Collins said.

"It is a very smart job," said Ruth Foxwell mucosal immunologist at the University of Canberra in Australia. The new vaccine could protect infants and children, although the immune system in adults can neutralize the vaccine, she said. But to develop a vaccine just a year after the virus was discovered "is fantastic compared to what is normal."

related Site
WHO RAD page
CDC SARS FAQ

A new study gives ammunition to researchers who claim that Crohn's disease, an often devastating inflammation of the intestine is caused by a microbe usually infects cattle. But the study, published in this week's issue of The Lancet , it is unlikely to end the long debate on the role of the microbe.

Crohn's disease is a chronic inflammation of the small intestine, which can cause severe pain, diarrhea, ulcers and tissue damage which sometimes requires surgery. For over 15 years, some researchers have blamed Mycobacterium avium subspecies JD , a bacterium that causes severe intestinal infection called Johne or Johne's disease in cattle, goats and sheep worldwide. Infected animals lose bacteria in their milk, and some studies have shown that the pasteurization does not kill all the microbes. Contaminated drinking water may be another route of infection. The same Mycobacterium species was found in the tissue of the intestine of patients of some Crohn; proponents of the hypothesis believe that only people with a certain genetic or immunological predisposition getting the disease.

Four years, Saleh Naser of the University of Central Florida in Orlando and colleagues cultured breast milk of two women with Crohn bug - a finding that they say provides further evidence that the Crohn's disease is really the human equivalent of Johne's disease. In the new document, Naser and his colleagues show that half of the 28 Crohn's patients had bacteria in the blood, while not one of the 15 people who had bowel diseases unrelated or were healthy did.

It is not known why the bacteria have shown in the blood of patients with certain Crohn's disease, but not in others. However, "this is a very important piece of the puzzle," says researcher Robert Greenstein Crohn's Veterans Affairs Medical Center in New York, a proponent of the hypothesis of infection. Finding microbes in the blood, which is normally sterile, "is an indication that the immune system loses the battle" in patients with Crohn's, he said. in an accompanying editorial in the Lancet , Warwick Selby, University of Sydney , Australia, cautions that the study does not clinch the case. Even if he writes, "the sight of all that, [ Mycobacterium ] can not continue to be ignored in Crohn's disease. "

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More Crohn disease
website awareness and paratuberculosis Research Association, with links to the literature scientific

When the early 1880s vulcanized rubber and the 1930 advent of latex mark the latest advances, we quickly understand the sorry state of male contraceptives. Researchers in this field have tried hard pressed to provide men with other options, but has not had much success. Now a team in the United States and India reported promising preliminary results for its new contraceptive vaccine for men.

reproductive biologist Michael O'Rand of the University of North Carolina, Chapel Hill, manufactured the vaccine after reporting his discovery of a new protein only male in 01. The protein, called Eppin, has been found so far on the surface of sperm cells and elsewhere in the testis and epididymis. Its function is not clear. But O'Rand said that if a man harbored antibodies to this protein, his sperm may malfunction.

O'Rand teamed up with colleagues from the Indian Institute of Science Bangalore, which hosts a large research center for primates. The researchers injected nine monkeys with human protein Eppin and gave six monkeys a dummy vaccine. Two of the vaccinated monkeys Eppin were discontinued from the study, however, because they do not produce enough antibodies to the protein, a mysterious problem other immunocontraceptives met.

The monkeys booster vaccine every 3 weeks. To test if it worked, men vaccinated spent several days each with three different females during the fertile peak of the menstrual cycle of women. The result: None of the seven vaccinated monkeys managed to impregnate a female. Four of the six control monkeys did. Although aimed the contraceptive effect of the vaccine to be reversible, only five of the seven vaccinated monkeys, some of which received the vaccine for nearly 2 years, recovered their fertility during the study, the group reports in the issue November 12 of science . "It's hard to say" what it means, O'Rand said. "Maybe they recovered two weeks after we leave" test.

"There seems to be a promise," said Ronald Swerdloff, a reproductive endocrinologist at the University of California, Los Angeles. Still, "it's just the beginning of the game," with too few monkeys tested, concluding that pan out approach, he adds. O'Rand and his colleagues are now trying to understand how their vaccine disrupts fertility. One possibility is that it leaves the slower sperm.

Related Sites
O'Rand and colleagues Science paper
home [MichaelO'Rand

WASHINGTON, DC - The doctors may have demonstrated why a common drug given to patients with heart failure fails to help nearly half of them: a genetic difference resulting in a change of a single amino acid appears to determine patient response to the drug. The results, announced today at the annual meeting of the American Association for the Advancement of Science, could help doctors better prescribe medication for patients with heart failure, and perhaps for those with pressure high blood well.

In the late 190s, Stephen Liggett pulmonologist from the University of Cincinnati, and his colleagues have identified a genetic variation in humans has not been seen in a variety of species, including mammals, suggesting that it has recently evolved in humans. The change occurs in a single amino acid - Humans or arginine or glycine. Everyone has two copies, inheriting one from each parent; This means that a person may have two copies of glycine, arginine, two, or one of each. Studies have suggested that mice with two copies of arginine were more susceptible to heart failure and more sensitive to beta blockers -. A class of drugs used to treat

Liggett decided to test how this affected human variation. His team found 1,040 volunteers, all people with severe heart failure. Almost half had either two copies of arginine or an arginine and a glycine; the rest had two copies of glycine. Patients were randomized to receive either a placebo or the drug bucindolol, a beta-blocker.

When observed for about 2 years (and in some cases up to 5), 82% survived to drugs, compared to 65% compared to placebo. Those with one copy of each amino acid or two copies of glycine, however, have not helped at all by drugs, fare nearly as badly as placebo. Liggett hopes to establish a larger study to see if the results are robust. All patients received the drug because he believes that the results show that it is unethical to give patients arginine double copy placebo

"He found a polymorphism." - Genetic variation - "that seems to predict response" to bucindolol says Kathy Giacomini from the University of California, San Francisco. The result, she says, is "very exciting" and "very specific." We do not know, Liggett said, if the results are applicable to other beta-blockers, which are also used to treat high blood pressure.

related site
homepage Liggett

DENVER, COLORADO -. Patients whose HIV infections have developed resistance to most available drugs may soon have a new and powerful new antiretroviral drug to add to their treatment.

The drug, manufactured by Merck and known as MK-0518, inhibits the enzyme critical integrase that the virus uses to drag its genetic material into human chromosomes, and then copy itself. Antiretroviral drugs currently on different target parts of the HIV life cycle market.

At the 13th Conference on Retroviruses and Opportunistic Infections here February 8 Beatriz Grinsztejn of the Oswaldo Cruz Foundation in Rio de Janeiro, Brazil, revealed results of a multisite, placebo-controlled study in 167 people infected with multidrug-resistant HIV. The results showed how MK-0518 could reduce the level of virus below 400 copies per milliliter - a drop of 99% - 80% of treated participants. "This is a difficult population, and for 80% [of patients] below 400 copies is about as good as it gets," said Michael Saag, director of the AIDS Research Center at the University of Alabama, Birmingham.

a smaller shorter study, reported at a meeting last fall, found that the drug was as safe and effective in people with HIV who n has never taken antiretroviral medication. Constance Benson, an organizer of the retrovirus meeting and an AIDS researcher at the University of California, San Diego, said that if the drug works in larger trials and toxicities not serious area, "it will change the treatment paradigm."

the current study only looked at the impact of the drug after 16 weeks and did not assess whether it has improved the health of participants who had been on anti-HIV drugs for an average of 9 years. Merck launches two studies in several countries to evaluate the safety and efficacy of MK-0518 in large groups of same-drug resistant

"We move the drug through the [pipeline] as quickly as possible. "said Robin Isaacs Merck, head of clinical research for infectious diseases. If all goes well, the company plans to seek approval from the US Food and Drug Administration next year. Merck also began organize larger trials with patients who were not drug-resistant HIV.

related site

• The retrovirus conference

Editors of the journal Analytical Chemistry yellow flags raised today on a paper on the toxicology of silicone breast implants . The original study, published on 1 May of the magazine, reported finding high levels of a potentially dangerous form of platinum in blood and tissues of women who had silicone implants in their bodies for years. Since then, however, experts have disputed several of the methods used to reach conclusions. Two of these criticisms appear in the August 1 issue of the journal, with an editorial by two editors of the newspaper that said at least one of the method of the newspaper "falls short of the standard of this newspaper." Consequently, publishers advise their readers to "exercise caution" when evaluating the paper.

The dispute stems from work published by Ernest Lykissa of ExperTox Inc., a company of toxicology tests in Deer Park, Texas, and Susan Maharaj Centre for Research on Environmental Medicine in New Market, Maryland. They reported that women they studied showed not only high levels of platinum in their bodily fluids and tissues, but also chemically reactive forms of the metal, including one known as platinum (VI), which is highly reactive and unstable. A less reactive form of platinum was used as a catalyst for making gels incorporated in many silicone breast implants. Lykissa Maharaj and the report suggested that platinum turned more reactive in the body of women with implants and thus became a potential source of toxic reactions experienced by those with silicone implants.

Among the complaints about the work, but that was Lykissa Maharaj and relied on a device called an ion chromatograph, which is usually used to differentiate reactive platinum. In addition, experts noted that the control subjects had platinum levels were not statistically different experimental subjects, which are not expected.

Lykissa and Maharaj could not be reached for comment, but the pair did not retract their paper.

Royce Murray, a chemist at the University of North Carolina, Chapel Hill, and chemical analysis 's editor, said the paper Lykissa and Maharaj was sent to a normal contingent of three examiners, but these authors failed to catch many problems. Therefore, he said, "a mistake was made, I think in the publication of this document." Under normal circumstances, Murray said, the newspaper is willing to let scientists dispute play in the correspondence between critical and the authors. However, in this case, he said, "we thought we should not expect the scientific community to set the record straight because of the public interest."

related site

• chemical analysis publishing

A new technique can convert type A and type B red blood cells into type O, the "universal donor" blood type that can be transfused for all patients. The advance may help prevent blood shortages

The four types of primary human blood -. A, B, AB and O - resulting from differences in molecules known as antigens dotting the surface of red blood cells and elicit responses of the immune system of the organism. Individuals with type A antigens make antibodies to the type B antigen, which causes the body to attack and reject transfused type B blood as foreign. The same scenario unfolds dark for people who get type B type A blood. Blood type O individuals lacks both antigens and can be transfused safely in people with all four blood types. Type O individuals can receive only O blood type, however, which means that during blood shortages, they may want for blood that was shed to patients with other blood types.

To alleviate type O blood shortages, Henrik Clausen, a glycobiologist at the University of Copenhagen in Denmark, and scientists ZymeQuest team, a biotechnology company based in Beverly, Massachusetts, hunted for enzymes that convert other blood types to type O. a and B antigens consist of similar branched carbohydrate molecules that differ in the sugars that cap their tips. The researchers looked for enzymes that snip the sugars off the two antigens without damaging red blood cells. The company had previously isolated a coffee bean enzyme that stripped the B antigen that worked, but too inefficiently. To identify and mass-produce more efficient enzymes, they tested extracts of 2500 kinds of bacteria and fungi. They focused on two enzymes: one from a bacterium that causes infant meningitis, converted type A blood into type O, while another, a human gut bacterium, converted type B type O. (the two enzymes together convert the type AB to type O.)

Each enzyme denuded much of its target antigen from red blood cells that the antigen can not be detected by a test blood group, the Food and Drug administration approved and by subsequent chemical analysis, the researchers reported online yesterday in Nature Biotechnology . ZymeQuest tests the enzyme type A-conversion efficiency in clinical blood and hope to conduct a clinical trial of the B-type enzyme conversion starting later this year, said Clausen.

"I'm impressed" by the study, said scientific transfusion Geoff Daniels of the Bristol Institute of Science transfusion in Bristol, UK Type O blood runs short of time blood is in short supply, Daniels said. If the technology proves safe and effective in humans and financially viable for blood banks, he concludes, in a few years the new enzyme technology "would be able to reduce the pressure on [type] O".

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• Facts about blood donation of the American Red Cross
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Tamoxifen, a drug commonly used to prevent breast cancer recurrence, is also effective against the manic phase of bipolar disorder, new research suggests

bipolar disorder -. formerly known as manic depression - affects about 1% of the population. As its nickname indicates exceeded, patients experience periods of deep depression and mania, extremely hyperactive condition that can lead to wild spending, risk taking, and extreme sexual activity. When mixed with depression, mania also leads to suicide.

Lithium has been the mainstay of bipolar treatment for over 50 years, but about 40% of patients do not respond to it, said Husseini Manji psychiatrist National Institute of Mental Health (NIMH) in Bethesda, Maryland . In recent years, both anticonvulsant and antipsychotic drugs have proven effective for mania, but can take weeks for the shot. Now it seems that an alternative may be to fast action horizon.

Tamoxifen protects against breast cancer by blocking the receptors for the hormone estrogen, which some tumors depend on. But the drug has another function: It inhibits an enzyme called protein kinase C (PKC) that regulates the excitability of brain cells. Studies have shown increased PKC activity in the brains of people with bipolar disease, and a recent study of the whole genome found that the gene with the strongest association with the disease is that governing PKC. It is found that tamoxifen is the only PKC-inhibiting compound approved for direct human use which can pass from the bloodstream into the brain.

So over several years, a NIMH group led by psychiatrist Carlos Zarate conducted a controlled study with 16 patients hospitalized for mania. Over a period of 3 weeks, each person was given either tamoxifen or placebo. In a paper appearing online today in the journal Bipolar Disorders , the team reports that the tamoxifen treated patients began to improve by the 5th day, and five of the eight showed a reduction of 50% or more symptom reduction on a rating scale-mania -. compared to only one of eight in the placebo group

"This is potentially a major development if replicated," says psychiatrist Paul Keck of the University of Cincinnati in Ohio. "It potentially opens a whole new avenue for targeted treatments."

Manji, a co-author of the study, said doctors have provided a lot of anecdotal evidence that patients with bipolar breast cancer on tamoxifen did not have that much trouble with mania. He said that there were no gender differences in response to drugs in the NIMH trial shows the effect is not related to estrogen receptors. Now, he notes, the work is to test potential drugs that do not mess with estrogen and are "pure PKC inhibitors."

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• More about bipolar disorder
• study on the use of lithium to treat mania

Skin cells reprogrammed to act like embryonic stem cells -. A first breakthrough reported in human cells there 2 weeks - already showing promising as a therapeutic agent. In today's online edition of Science , researchers describe the use of induced pluripotent stem (iPS) to relieve the symptoms of sickle cell anemia in mice. The technique is not safe to try in people, but scientists say it is proof of principle that iPS cells could one day treat human disease.

induced pluripotent stem cells excite scientists because they represent a way to get custom-made stem cells without the ethical barriers to the use of embryos or oocytes ( science Today ay, November 20). Researchers hope they might be able to use the technique to replace defective cells in the body with healthy cells containing the patient's own DNA.

Tim Townes of the University of Alabama, Birmingham, and colleagues wondered whether iPS cells could be useful in a mouse model of sickle cell anemia. (The blood cells are much easier to replace than are the cells that make up the fabric). In afflicted humans, red blood cells become curved and can not flow easily through blood vessels. The mice show many of the symptoms that patients are human, and they were particularly good candidate to test the capabilities of iPS cells, said Rudolf Jaenisch cell researcher strains of the Whitehead Institute and Massachusetts Institute of Technology, once in Cambridge, who worked with Townes on the project.

The first step was the creation of specific iPS mice. Researchers took cells from the skin of the tail of mice to sickle cell and the inserted copies of four genes that render the cells have the characteristics of embryonic stem cells. They also added a corrected hemoglobin gene in cells and caused to become producing blood stem cells. Finally, the researchers injected these partially differentiated cells in sickle cell mice that had been treated with radiation to kill their own blood stem cells. Within weeks, the new cells produce mature blood cells, and the symptoms of sickle cell disease have improved dramatically, reports the team.

Townes and Jaenisch said he initially collaborated on a project that has used nuclear transfer to the corrected stem cells, a process called therapeutic cloning. But experiments have failed, he said, because nuclear transfer was too inefficient to produce the necessary cells. The technique of iPS cells "is amazingly effective," he said.

The document is an important step, said Jose Cibelli of Michigan State University in East Lansing. Laboratory results for iPS cells have been impressive so far, he said, "but if they do not have a therapeutic value, they will be far from getting to the point of replacing the idea of ​​therapeutic cloning."

the next important step for the field, Cibelli said, is to find reliable ways to differentiate the cells into various types of cells useful and be sure that no undifferentiated cells remain to cause potential tumors. Other experiments with iPS cells have suggested that they might tend to cause cancer, but none of the treated mice showed no signs of tumors after 12 weeks. This is a promising sign, Townes said, but would need much longer studies before the technique could be considered safe enough to try in humans.

Related site

• More information about sickle cell anemia

scientists have for the first time pushed the cells human embryonic stem to become functional pancreatic cells. The work, published online today in Nature Biotechnology , an important step towards the use of embryonic stem cells to treat diabetes.

One of the most sought after prize in embryonic stem (ES) cell research is a method of transforming cells in pancreatic beta cells. These cells produce insulin in response to sugar in the blood, and they are damaged or missing in type 1 diabetes If scientists could find a reliable way to make beta cells from human ES cells, they could be able to replenish the supply of patients. But so far nobody has managed to produce functional beta cells in the laboratory.

Now, developmental biologist Emmanuel Baetge and colleagues of the biotechnology company Novocell in San Diego, California, report that they have managed to coax human ES cells behave like beta cells in mice . For several years, the group has attempted to use the molecular signals that prompt pancreatic development in a fetus to direct human ES cells to become beta cells in a dish. In previous work, the researchers describe a technique that seemed to produce insulin-producing cells, but the cells do not respond to glucose, a key characteristic of working beta cells.

Thus, researchers have supported a step. Instead of trying to get mature beta cells in a dish, they treated ES cells with signals that coaxed them to form pancreatic endoderm, a type of cells similar to those in a human fetus aged 6 to 9 weeks. They implanted these immature cells into mice, hoping that the final signal that the formation of rapid beta cells could be provided by the organs of animals. Thirty days after implant, the researchers were able to detect the human version of C-peptide, a byproduct of the production of insulin in the blood of animals. (The researchers studied C-peptide instead of insulin, because it is easier to differentiate between versions of man and mouse.) After 2 months, the C-peptide levels human increased when mice received a dose of glucose, indicating that the implanted cells responding to blood sugar. Finally, the researchers selectively killed own beta cells of animals with a toxin, which usually leads to becoming diabetic mice. But rodents who received implanted human cells do not develop diabetes, showing that the implanted cells may take the place of the beta cells of the animals.

The work is "very important for the area," says diabetes expert Teresa Ku of the Beckman Research Institute in Duarte, California, whose group also worked on ways to turn the ES cells beta cells. Baetge said Novocell already meets the US Food and Drug Administration to discuss additional safety testing will be required before you can consider starting human trials. But Ku notes that it is difficult to determine whether the pancreatic endoderm cells are the self-renewal. If not, she said, they might give in a few years, and patients will undergo multiple transplants. A fully differentiated cell beta in the culture dish is always the safest bet, she said.

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• More information on efforts to understand the beta cell
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