Health Meaning

The legislation proposed by the Bush administration to stimulate the production of medicines and vaccines antibioterrorism is running into opposition in Congress. Although project "BioShield" was approved by a Senate committee last week, members of the House expressed strong reservations about its potentially astronomical costs and the negative impact on competition between pharmaceutical and biotechnology companies to design new treatments.

President George W. Bush first announced BioShield in his State of the Union in February. BioShield aims to accelerate research efforts and development base of the National Institute of Allergy and Infectious Diseases (NIAID), which was allocated a record $ 1.7 billion to research bioterrorism during exercise 03. It also includes a provision to distribute drugs and vaccines to fight against potential bioterrorist attacks without the usual clinical tests mandated by the Food and drug Administration.

But it was third provision BioShield that caused widespread concern among members of the two subcommittees, one of the House Committee on Energy and Commerce and one of the commission of Homeland security, which organized jointly today for their first discussion of the law. Representatives have doubts about the administration's plan to enter into multi-year contracts with companies that produce products antibioterror and provide guaranteed financial support of products once they reach fruit. This is necessary "to create a market" for products that would not have another one, said Tommy Thompson, secretary of the Department of Health and Human Services. Without BioShield, "it will not be a lot of companies are lining up to do."

But members of the House have pointed out potential flaws in this strategy. For example, if the government contracted with a production company, for example, a vaccine against the plague, then a second company developed a superior vaccine, the first contract was nevertheless held, and the government would be stuck paying for a potentially inferior product. "You can indeed stifle innovation" by discouraging competition, said Jim Turner (D-TX), and waste money. Bush tentatively proposed to spend $ 6 billion over 10 years on BioShield, but Thompson said during today's hearing that the amount is actually "indefinitely" without limit in a year. In addition, because the Project BioShield Act installs the current bill, a future administration would be bound to support it, even if displaced national security priorities, noted Christopher Cox (R-CA).

The Energy and Commerce and Homeland Security committees will now determine how, if necessary, modify the existing draft BioShield Act before voting on it.

Related Sites
information from the White House on BioShield
Senate Bill BioShield

Shooting millions of tiny RNA molecules in the blood of mice can protect the liver against the ravages of hepatitis. This is apparently the first time that this technique, called RNA interference (RNAi) was used to fight against the disease in an animal. But biologists warn that the therapy has a long way to go before it can be safely applied to humans.

RNAi uses thumbnails RNA molecules to silence specific genes ( Science NOW, December 19, 02). Normally, large RNA molecules convert genetic information into protein; but in the late 190s, researchers found that the truncated RNA could be induced to turn off genes. Hepatitis has become a center RNAi studies, because the liver easily absorbs molecules.

Harvard University immunologist Judy Lieberman and Premlata Shankar and colleagues wanted to see whether RNAi could prevent liver damage. They gave mice three injections massive high pressure - equivalent to about half the volume of blood "animals - a solution that forced the molecules in the liver. The molecules are designed to stop a gene called Fas , which when overactive, induces liver cells to self-destruction; Fas is also involved in human liver diseases.

The next day, the animals received an antibody that sends Fas in hyperdrive, causing liver failure. Control mice died within a few days, but 82% of the treated mice survived. About 80% to 0% of liver cells incorporated RNA molecules. In addition, RNA molecules hung around for 3 weeks, about three times longer than previous studies, the authors report online today in Nature Medicine

During this time, other mice face a distinct challenge :. Over six weeks, they received weekly injections of cells called Con, which Goad the immune system to attack the liver, producing the kind of scars seen in viral hepatitis. Some animals also received an RNA infusion during this time, and this group developed any damage to the liver. Despite the traumatic delivery method, the mouse does not seem to suffer any side effects.

"It is amazing how it worked," marvels Charles Rice of the Rockefeller University in New York City Still, he added, the delivery method is clearly problematic. In humans, the "hydrodynamic shock ... is not the way to go." Researchers have yet to determine if a more gentle approach might prove fruitful.

Related Sites
The homepage of Judy Lieberman
General Hepatitis Foundation International
Hepatitis C Information from NIH

Shooting millions of tiny RNA molecules in the blood of mice can protect the liver against the ravages of hepatitis. This is apparently the first time that this technique, called RNA interference (RNAi) was used to fight against the disease in an animal. But biologists warn that the therapy has a long way to go before it can be safely applied to humans.

RNAi uses thumbnails RNA molecules to silence specific genes ( Science NOW, December 19, 02). Normally, large RNA molecules convert genetic information into protein; but in the late 190s, researchers found that the truncated RNA could be induced to turn off genes. Hepatitis has become a center RNAi studies, because the liver easily absorbs molecules.

Harvard University immunologist Judy Lieberman and Premlata Shankar and colleagues wanted to see whether RNAi could prevent liver damage. They gave mice three injections massive high pressure - equivalent to about half the volume of blood "animals - a solution that forced the molecules in the liver. The molecules are designed to stop a gene called Fas , which when overactive, induces liver cells to self-destruction; Fas is also involved in human liver diseases.

The next day, the animals received an antibody that sends Fas in hyperdrive, causing liver failure. Control mice died within a few days, but 82% of the treated mice survived. About 80% to 0% of liver cells incorporated RNA molecules. In addition, RNA molecules hung around for 3 weeks, about three times longer than previous studies, the authors report online today in Nature Medicine

During this time, other mice face a distinct challenge :. Over six weeks, they received weekly injections of cells called Con, which Goad the immune system to attack the liver, producing the kind of scars seen in viral hepatitis. Some animals also received an RNA infusion during this time, and this group developed any damage to the liver. Despite the traumatic delivery method, the mouse does not seem to suffer any side effects.

"It is amazing how it worked," marvels Charles Rice of the Rockefeller University in New York City Still, he added, the delivery method is clearly problematic. In humans, the "hydrodynamic shock ... is not the way to go." Researchers have yet to determine if a more gentle approach might prove fruitful.

Related Sites
The homepage of Judy Lieberman
General Hepatitis Foundation International
Hepatitis C Information from NIH

The inherited form of Lou Gehrig disease amyotrophic lateral sclerosis -familial (FALS) - causes disintegration of the motor neurons of the spinal cord and brain, a devastating loss of control the body, and death within 2 to 5 years. A study now shows that the molecular cause of FALS is similar to other neurological diseases such as Huntington's and Alzheimer's disease, offering new hope in the search for a cure.

Fals patients with mutations in a gene called superoxide dismutase ( SOD1 ), but it is a puzzle how these mutations lead to disease. Normally, the SOD1 protein binds zinc and copper atoms and uses them to break superoxide, a destruction of cellular respiration byproduct. So it would be logical if the mutations cripple the SOD1 protein, superoxide to build to toxic levels. But this idea was discarded when the researchers found that mice lacking the SOD1 gene remain healthy. Only one mutated copy causes paralysis, indicating that mutated SOD1 is itself toxic agent behind FALS.

Because the capacity of a protein is determined by its shape, a team led by John Hart at the University of Texas Health Science Center in San Antonio used x-ray crystallography to see how the mutation alters the structure of the protein of SOD1. Reporting in May 18 issue of Nature Structural Biology , Hart and colleagues show that the mutation may cause SOD1 proteins to lose their metals, exposing patches that have just the right shape and charge for proteins to lock onto each other. These new SOD1 link interfaces always growing fibrils that can overwhelm systems degrading proteins that cells use to keep themselves tidy, known pathology other neurodegenerative disorders. With this revealed mechanism, Hart hopes to identify drugs that inhibit the destructive link.

The quality of work is "breathtaking," said Mark Gurney, Vice President of Drug Discovery at deCODE Genetics in Reykjavik, Iceland. But before seeking the drug can begin in earnest, Gurney said, it will be important to demonstrate that this aggregation mechanism occurs "inside motor neurons not only in protein crystals."

Related Sites
the homepage FALS at Imperial College London
Who was Lou Gehrig?

The AIDS virus dodges the ammunition dam immune system. researchers have now discovered one of his tricks: HIV disables a host protein that would otherwise break the virus into pieces. But the virus can not stop similar proteins in mice. The discovery, published in July 11 issue of Cell provides a new idea on why HIV only infects humans and may one day lead to better animal models of AIDS.

last year scientists discovered that a protein made by HIV, called Vif, protects the virus against the host attack. But they did not know how Vif ripped this feat. Now, AIDS researcher Nathaniel Landau of the Salk Institute for Biological Studies in San Diego, California, and colleagues report that Vif locks a human protein called APOBEC3G. In the absence of Vif in virus APOBEC3G slides and outputs the bits of its inactivating DNA. HIV Vif protects against death in human cells.

Curious how mice fight HIV so easily, Landau's group checked to see if rodents have their own version of the APOBEC3G gene. They did, but the mouse protein, the researchers found, is unrecognizable to HIV defense system. He circumvented the blockade Vif, moved into the virus, and hit it out of commission.

"It is a major breakthrough" to show that APOBEC3G plays a role in the unique sensitivity of humans to HIV, says Jeremy Luban, a virologist at Columbia University. For scientists studying drugs and vaccines against HIV, "it would be a huge technical advantage" if this information could help create laboratory mice that can support HIV infection, he said. Luban but warns that such a project is not likely to bear fruit immediately, as it is likely that many other barriers that prevent HIV from infecting other species.

Related Sites
laboratory Nathaniel Landau Jeremy Luban laboratory

An outbreak of a mild respiratory disease in two nursing homes near Vancouver, in Canada, scientists and experts puzzled and worried public health. Tests suggest that a very similar to the agent that causes severe acute respiratory syndrome (SARS) is involved, but symptoms of SARS does not look full. The results suggest that the SARS coronavirus can cause mild disease that has not been known.

The health authorities in the province of British Columbia reported that 94 residents and 49 employees at a nursing home in Surrey have fallen ill since July 1. Most had mild, coldlike symptoms, although 11 elderly patients developed pneumonia and six died of pneumonia, often accompanied by other diseases. Nine cases occurred in a second home close

In studies at Canada's National Microbiology Laboratory in Winnipeg, nine of the 19 patients had traces of the RNA of the SARS coronavirus. four of seven patients also had antibodies against the virus. Researchers still have sequenced the genome of the virus involved in the disease, but the 750 base pairs sequenced so far closely resemble extracts in the genome of the SARS coronavirus, David Patrick of the Center for Disease Control BC said yesterday in an announcement on ProMED, a list of e-mail for emerging infectious diseases

So far, the SARS virus. - The transmission of the World Health Organization (WHO) was arrested around 5 July - has not been known to cause mild disease. In its report, Patrick offered three possible explanations: Perhaps the virus was originally a benign disease unnoticed throughout; a major mutation may have rendered the SARS virus less aggressive; or the virus may be a close relative of SARS.

The results are potentially worrisome, says virologist Albert Osterhaus of Erasmus University in Rotterdam, the Netherlands, "but right now we just do not have enough data to say anything useful ". But Henry Niman, a Harvard researcher, says the results suggest that the real virus SARS is still circulating in Canada and could mutate back into the deadliest form.

The WHO sent a virologist to Winnipeg to monitor studies- -but he does not judge a health emergency because the disease is so mild. "Right now, this is just a laboratory abnormality," said spokesman Dick Thompson of the WHO. Meanwhile, Canadian authorities have isolated patients and are looking for people who might have come into contact with them.

Related Sites
More information about the epidemic
WHO SARS information

WASHINGTON, DC - Scientists reported three new animal models that could provide relatively cheap and convenient means for testing drugs and vaccines against severe acute respiratory syndrome (SARS), the disease that broke out in southern China last spring

these are not the first animal models for SARS. that honor goes to a monkey. At the height of the SARS crisis last April, virologist Ab Osterhaus and colleagues at the Erasmus University Rotterdam, the Netherlands, cynomolgus monkeys inoculated with a newly discovered coronavirus. The monkeys have developed a lung infection resembling SARS in humans, providing evidence that the new virus was indeed the culprit, and the first animal model. In Rotterdam and elsewhere, researchers are studying SARS pathogenesis and to test drug candidates in infected monkeys

But the use of monkeys raises ethical questions. Moreover, they are heavy and expensive to experiment animals, especially under strict biocontainment standards. At a meeting here last week, organized by the Institute of Medicine Board on Global Health, Kanta Subbarao of the National Institute of Allergy and Infectious Diseases said she sprayed the SARS virus in the nose of mice and found that, although the animals didn 't get sick, the virus began to replicate inside their bodies - sufficient for an animal model. "Everyone calls us to test their pet vaccine," said Subbarao, who presented the results for publication.

In an article that has been accepted by Nature , meanwhile, Osterhaus says that his group has infected two other species of SARS and found that the virus is easily reply within two . Osterhaus declined to reveal the two species pending the release, but said they are more closely related to palm civets masked Melogale - two species in which the SARS virus was found in China ( Science NOW, May 23) - than they are to mice. The results suggest that the virus may have a remarkably wide host range, says Osterhaus.

The announcement of Subbarao was one of the few concrete measures before reported during the meeting last week. With drugs and vaccine studies in childhood and flu and cold season about to hit the northern hemisphere, many wondered if the overstretched public health systems will be able to cope if SARS reappears. Summing up his feelings after the meeting, National Center for Infectious Diseases director James Hughes said: "What I have heard does not make me sleep better"

Related Sites
. paper the Lancet describing the SARS model in macaques (free registration required)
Ab Osterhaus laboratory
more on SARS

No, they are not designed as a tasty alternative low-calorie cat chow diets. But scientists have created a strain of mice that can not produce cholesterol. The animals are viable, the study shows because another fat molecule can pick up most cholesterol functions.

Despite its bad reputation, cholesterol is an important part of our lives. Cell membranes are full, enzymes to alter sex steroid, and developing embryos rely on it to grow. In cells, two biochemical pathways convert sterols cholesterol, and disruption of one or the other leads to serious diseases of the human endocrine system. Researchers had already eliminated a route in mice and found that scurriers can not live without it. Now, another group of scientists, led by Elena Feinstein Quark Biotech in Cleveland, Ohio, arrested another generation cholesterol pathway, they report in the December issue 19 Science .

team has found the gene encoding a key enzyme, desmosterol reductase, which converts desmosterol to cholesterol, and created mice lacking both copies of the gene. Compared to normal mice, the modified mice had very low levels of cholesterol both in the blood and liver; they also had about 20% to 60% less total sterols. The team found that desmosterol was the predominant sterol, suggesting that this molecule can take over in the absence of cholesterol. They also found that embryos, transgenic mice had almost normal cholesterol concentrations, probably they received from their mother and that allowed them to develop normally until birth. As they grew up, however, they developed health problems, including infertility.

The novelty of the results is that "desmosterol seems to be able to perform for cholesterol," said clinical geneticist Forbes Porter of the National Institute of Child Health and Human Development in Bethesda. The work can help researchers understand why cells bother to cholesterol instead of using its precursors, he said. metabolic clinical geneticist Hans Andersson at Tulane University Medical School says the work might not be relevant to human disease because that humans with mutations in desmosterol reductase are sick and yet have high levels of cholesterol, unlike rodents. "mice can not be the best model for human disorders of sterol biosynthesis," he said.

Related Sites
Quark biotech

Interferon a , a drug widely used to treat hepatitis C and several cancers, may also work against SARS, according to a study published online this week by Nature Medicine . Clinical studies with the drug should start as soon as possible if SARS reappears, said lead researcher Albert Osterhaus of Erasmus University in the Netherlands.

During the SARS epidemic last year, doctors have tried all kinds of treatments. A combination of an antiviral drug, ribavirin, and steroids - which attenuates the immune response and are often used in other lung infections - has quickly become the standard of care in many countries. Some studies have suggested that patients responded well, but they did, and the blind randomized controlled design that enables researchers to be sure, said Simon Mardel, a doctor working on SARS to the World Health Organization health (WHO) in Geneva. Indeed, some researchers now think the combo of drugs has done more harm than good.

Interferon a , which comes in more than a dozen varieties, is a double hammer. It blocks the replication of several viruses and also activates the immune system. It was first held in 30 of the first patients in the southern Chinese province of Guangdong, but seemed ineffective, a group of Chinese researchers reported recently. A small trial in Toronto, however, released in December, suggested some benefit.

In the new study, cynomolgus macaques received the form of interferon a chemically modified to last longer in the bloodstream. When injected 3 days before infection with the SARS virus, macaques excreted much less virus in their throat and lung damage was reduced by about 80%. When animals received compound 1 and 3 days after exposure, lung lesions was also reduced, but not as much.

This means that the compound would probably be more effective as a prophylactic for, say, family members or patients health care workers at high risk of infection, says Jindrich Cinatl Medical School of University of Frankfurt in Germany. Whether the drug might work in people with the whole SARS remains to be seen, he said.

The lead author of the small Canadian study, Eleanor Fish of Toronto General Research Institute, said she is encouraged by the new results. Already, Health Canada approved a protocol for a human trial with interferon alone, without steroids or ribavirin in SARS reappears. Several other Western countries consider the same course.

Related Sites
paper summary
laboratory Osterhaus of

has been shown in mice, fish and yeast; Now the first study of calorie restriction long term in humans suggest that if you really want to live longer, eat less.

Few people are willing to significantly reduce their caloric intake for years. But researchers from the University of Washington in St. Louis managed to locate 18 (15 of them men), aged 25-82, who spent an average of 6 years of balanced diets recommended by the Company calorie Restriction. The scientists compared 18 people with otherwise clean livers, on a "typical Western diet." On average, the subjects ate 1700 calories a day, compared to at least 2100 for controls, says lead investigator Luigi Fontana, who also works for the Italian Institute of health.

Dr. Atkins notwithstanding, the subjects lost a lot of weight while consuming 46% of their calories from complex carbohydrates. their "bad" cholesterol, blood lipids, and diabetes risk markers went down the blood pressure dropped to childhood levels the bodies of the subjects were 9% fat -.. compared to 24% for the controls and, surprisingly, with 12% for people who run 50 miles a week, said Fontana. And none of the dieters had plaque in their carotid arteries, scientists report online April 19 in Proceedings of the national Academy of science .

William Harlan, a nutrition expert and consultant clinical trials at the National Institute of Mental Health, called "provocative" study. He noted that while the study subjects were self-selected, "the differences that are present are striking. ... More studies like this [would] give us a better idea of ​​what a truly healthy diet look like. "

Related Sites
Document PNAS
Caloric restriction Society

MONTREAL, CANADA - If there is a vaccine against cancer thing developers want to know, is why only a handle patients respond strongly to their inventions. Now, during an Immunology meeting here, a team of scientists reported that a group of metastatic melanoma patients may be indicative of a response to this mysterious question.

Cancer vaccines involve the use of immune cells from a patient to initiate an attack against the cancer. Although the results of vaccine trials against cancer have often been disappointing, there is continued interest because the strategy is so logical in theory. Doctors have had the most success with vaccines to treat melanoma, a skin cancer that is often fatal if it spreads.

immunologist Nathan Martinez of the Queensland Institute of Medical Research in Australia and colleagues are testing a vaccine made from patients' dendritic cells, a type of white blood cell that normally triggers an immune response against agents pathogens. Researchers create a custom vaccine for each patient by harvesting and concentration of immune cells. At the annual Federation of Clinical Immunology companies and the annual International Union of Immunology Societies, Martinez reported that 43 patients with advanced melanoma who are receiving vaccines, seven responded completely, their tumors decreases undetectable levels. This low response rate is par for the course in terms of vaccine against cancer. Thus, the Martinez team decided to examine whether the seven wealthy patients have shared something in common.

When they analyzed blood samples of patients taken before vaccination, the researchers found that patients who responded had lower levels of a protein, S100B, compared to those who did not. S100B is normally held inside the cells, but some scientists believe that when tumors develop, healthy cells begin to die and release the protein. Martinez speculates that increased levels of S100B indicate a significant tumor burden - something that can be difficult to measure, and what can a less likely to respond to a vaccine. Equally interesting is another finding: In all stakeholders tested to date, four out of seven cells from samples of pre-vaccine CTL blood could kill the tumor cells of that patient in a petri dish . This was not the case for patients who was not helped by the vaccine.

"I've never seen such a striking correlation," said Lloyd Stoolman, an immunologist at the University of Michigan, Ann Arbor. Although skeptical about the long-term use vaccines of dendritic cells, which he thinks may be less effective than other types, it is the ability to predict success in vaccine trials against cancer is the "Holy Grail" of the field.

Related Sites
Background vaccine against the National cancer Institute cancer
cancer immunotherapy Queensland Institute of medical research

cancer researchers have long sought an alternative treatment to chemotherapy that can destroy tumors without damaging the rest of the body. A new study with mice and human tumors may put such a handy treatment.

design drugs to target cancer is a challenge because cancer cells are well camouflaged in healthy tissue. But researchers have begun to find molecular beacons unique to cancer cells. Last year, Wadih Arap and Renata Pasqualini, a husband and wife team of cancer biologists to Mr. Anderson Cancer Center D. at the University of Texas, Houston, have identified a protein called GRP78 expressed by cancer cells prostate and not healthy tissue. They knew they had found a promising therapeutic target because GRP78 is expressed on the cell surface where it is easily accessible to drugs. In addition, a targeted drug for GRP78 should be unlikely to attack healthy cells because GRP78 is a so-called stress response protein that is expressed only on the surface of cells under stressful conditions such as those that occur in the mass oxygen deficient tumor.

to test GRP78 as a target, a team led by Pasqualini and Arap designed a short chain of amino acids that binds specifically to the surface of the GRP78 protein. They then merged this system to a small protein corkscrew shape when internalized, triggers the cell to commit suicide. The team hopes that the hybrid molecule would act as a search missile tumor when injected into the bloodstream.

The missile appears to be deadly accurate. Reporting in the September issue of Cancer cell , the team shows that its localized hybrid molecule and destroys human prostate tumors transplanted into mice without harming other tissue type. He did the same for breast tumors. The next step, says Arap and Pasqualini, is a series of preclinical studies to determine its safety for clinical trials in humans.

During the last decade, Arap and Pasqualini have developed a "smart bomb" approach to cancer therapy, said Bruce Zetter, cancer researcher at Harvard Medical School in Boston. This study "shows how we are" to put the strategy into action.

Related Sites
The site of Wadih Arap
The site of Renata Pasqualini
laboratory site Bruce Zetter

as much as 117 people died in Angola during what could become the largest outbreak recorded of Marburg virus, a rare cousin of Ebola virus that also causes hemorrhagic fever, the World health organization (WHO) announced today. Also today, a Canadian team with a mobile laboratory was scheduled to arrive in the country, hoping to help quench the epidemic and learn about the mysterious disease

Marburg -. Which can cause fever, pain, diarrhea, cough, nausea and bleeding - was discovered in 1967 when a shipment of monkeys in Uganda has caused simultaneous outbreaks in the German cities of Frankfurt and Marburg and Belgrade, the capital of Yugoslavia, sickening 31 and killing seven people. Three mini-outbreaks are known to have occurred in Africa in the 1970s and 1980s, involving six. The largest outbreak to date occurred in the Democratic Republic of Congo between 1998 and 00, with 149 known cases and 123 deaths. There are no cures or vaccines against the disease.

For experts, the location of the current epidemic and its manifestation are unusual. Because Marburg had been found only in East and Central Africa, "one would think it had to be Ebola," said Thomas Geisbert of the Medical Research Institute US Army Infectious Diseases at Ft. Detrick, Maryland. According to WHO, about 75% of the victims were children until the age of 5, which is strange for a hemorrhagic fever virus, said Thomas Ksiazek of the US Centers for disease Control and Prevention (CDC) in Atlanta, Georgia, the laboratory first identified Marburg there nearly two weeks in the samples shipped from Angola. initial sequencing, however, does not suggest that it is an unusual strain, Ksiazek said.

Although some cases were identified in the Angolan capital Luanda, the current epidemic is concentrated in the northern province of Uige, the wHO, which has a team on the ground to help local authorities. logistic obstacles in a poor country, ravaged by war like Angola can be a challenge, but stopping the epidemic should not be "particularly problematic," said Ksiazek. Marburg is not very contagious (infection requires close contact), and tracing and isolation of patients in general strictly brings the virus under control.

To facilitate the diagnosis, virologist Heinz Feldmann and Allen Grolla laboratory technician of Canada's National Microbiology Laboratory left for Angola this weekend, taking with them a mobile laboratory samples test locally. While stamping disease comes first, the team hopes to do research as well, said Feldmann's colleague Steven Jones - for example, trying to find out which immune response protects some people from the disease

[ Related Sites
WHO update on the situation in Angola
CDC page on Marburg haemorrhagic fever

AIDS patients live longer and better than ever thanks to the improvement of drug therapy, but some bad luck still have their brains damaged by a devastating and fatal neurological disease called progressive multifocal leukoencephalopathy (PML). Now researchers have traced the path by which the virus that causes PML invades the brain cells. The results indicate that psychiatric drugs widely used can prolong the lives of AIDS patients with the disease.

Over 70% of adults harbor the JC virus, which causes PML. The virus is harmless in people with healthy immune systems, but up to 5% of patients with AIDS virus destroys brain cells called oligodendrocytes that provide myelin insulation that allows neurons to function. These patients develop tremors, partial blindness, and dementia and die in a year and a half.

To stop the JC virus to destroy brain tissue, Walter Atwood at Brown University and colleagues asked how she invaded oligodendrocytes first. They knew the work earlier than the JC virus sticks to the surface of cells and triggers the cell to engulf and swallow. They knew Thorazine, an anti-psychotic drug commonly prescribed, this process is blocked swallowing in other cell types, and that Thorazine receptors of the neurotransmitters dopamine and serotonin on the surface of the bound cell. So Atwood's team hypothesized that the JC virus on to one of these receptors as a prelude to invasion.

To test this hypothesis, the team added a number of drugs or chemicals that bind either dopamine or serotonin receptors Culture cells. Then they added virus. Only drugs which bind to serotonin receptors blocked infection. To confirm that the JC virus targets the serotonin receptors, they took cervical cancer cells grown in the laboratory who resisted infection with JC virus and designed them to produce oligodendrocytes serotonin receptor called 5-HT [2A] R. infected the modified cells JC virus, and antibodies to the 5HT [2A] receptor blocked the infection, the researchers report in the November issue 19 Science . The results mean that U.S. Food and Drug Administration approved drugs such as serotonin blocking and Thorazine cyproheptadine could prevent infection with the JC virus in the brain. A clinical trial is still in the works, but it could be soon, says Atwood.

"It's a fantastic study," said virologist cancer Kamel Khalili of Temple University in Philadelphia, Pennsylvania. A drug serotonin-blocking would not rid the body of the virus already hiding in the cells, he warns, but the results were nevertheless "great potential to help a therapeutic strategy for the PML."

Related Sites
PML Context of the National Institute of Neurological Disorders and Stroke
Walter Atwood laboratory homepage
Site Consortium for Research neurological AIDS PML

Researchers have eliminated metastatic cancer in mice by combining the top two candidates still in a new technique that packs a double whammy. The result - still a preliminary finding -. Illustrates the potential to improve the treatment of cancer through selling cancer killing virus on the back of an immune cell tumor targeting

Most current therapies against cancer, such as chemotherapy, can not be said of those healthy cells cancerous. Therapies based on immune cells, which target the particular tumor molecules, are more specific, but they are not effective against a variety of tumors. As a result, cancer biologists have turned to a new strategy called targeted biologic therapy, in which cancer killer virus are combined with immune cells. Once the immune cell is locked on a tumor, the virus bursts and destroys cancer cells. Find an immune cell that targets a variety of tumors and a virus that does not release too early, however, has been a challenge.

Now virologists at Stanford University led by Steve Thorne and Christopher Contag met this challenge by finding the best candidates for the job. First, they identified a type of immune cell, known as a cytokine-induced killer (CIK), which has a taste for many types of tumors. Then, for the cargo, they chose the vaccinia virus. Long used as a vaccine against smallpox, vaccinia patiently waits until 72 hours before busting. That's enough time for immune cells to find even the most hidden tumor. In other immune cells, vaccinia will pop in as little as 4 hours. The team system has another advantage: the CIK cells dig deep into tumor tissue; this means that the virus should not harm surrounding healthy cells.

When the researchers tried the system mounted on cancer mice, the cells CIK forehand for tumors. Two days after injection, the vaccine was deeply replicate inside tumor and was barely detectable in other parts of the body, today reports the team in Science . Of the eight mice that received this therapy, all fully recovered from their tumors. In a separate group of mice, injection of CIK virus without the long-term survival for another week; Only virus recovered only two of eight mice tested. That's still a small sample, but this is the first time that researchers have managed to create a system that works in a clinical setting.

"This is an excellent example of how cancer therapies in combination may have additive effects," says Inder Verma, a geneticist at the Salk Institute in San Diego, Calif. "I think this is the way to future treatments against cancer. "Although the team of Stanford believes that the vaccinia virus and the CIK cells are the best available at this time," it is possible that further investigation will produce improvements in this system, "said Contag.

Related site

• More on targeted cancer therapies

For years, the electric fields have been rumored to cause cancer. Now, there is reason to believe they could fight - and in some cases even destroy it. The researchers used low intensity, intermediate frequency electric fields to fight against an aggressive brain cancer known as glioblastoma multiforme (GBM). The strategy highlights the tumors without invasive brain surgery and more than doubled survival time in preliminary studies.

The new approach exploits a cog in the way of cell division. When cells divide, a molecular motor called the axis of microtubules helps separate the chromosomes into daughter cells resulting. Resembling a set of strings, the pin is made of electrically polar macromolecules that are sensitive to electrical fields. Previous work has shown that if a field of 0 kHz is applied to these macromolecules, the spindle can not form correctly. Consequently, cells stop dividing and eventually die.

Because cancer results from uncontrolled cell division, a team of researchers from NovoCure Limited, a biotechnology company located in Haifa, Israel, and other institutes in Israel and Europe began a clinical trial with 10 patients with GBM who was not helped by standard therapies. They gave each patient a lightweight, battery operated, called NovoTTF-100A, which generates fields 0 kHz. (Power lines, for comparison, generate about 60 Hz fields.) Then, doctors glued four sets of isolated electrodes on the scalp so as to focus the field on the tumor. The patients wore the device on the head 24 hours a day for 18 months or until the disease worsened.

In eight cases, the electric fields increased life expectancy. Although there is no control group, the researchers compared the results of volunteers in historical studies testing GBM. The median overall survival for all patients was 62 weeks compared to the average of 29 weeks of more than 800 patients at a similar stage of the disease which had been treated with chemotherapy. The tumors stopped growing in four patients and decreased in four. In one case, a patient's tumor disappeared completely and the patient remained for 2.5 years after the trial without tumor; entering the study she had an expected survival time of about six months, the doctor said Eilon Kirson of NovoCure. Tumors continued to grow in two other patients.

The device is ideal for those who GBM because it only acts on the brain and has no systemic side effects of chemotherapy, says Eric Wong, a neuro-oncologist at Beth Israel Deaconess Medical Center in Boston, Massachusetts. Because tumor cells in the brain often divide, normal brain cells are not affected by electric fields, reports online this week in the team Proceedings of the National Academy of Sciences . However, brain stimulation electric field produced seizures in laboratory rats, a phenomenon known as kindling, Wong noted, so "I would be worried if most with there would be crises [in humans]." Yet he said, no increase in foreclosures rates were observed in 10 patients.

Wong was not involved in the study, but it is part of a research team currently testing the device in a III clinical trial phase, which includes over 0 patients with glioblastoma in the United States and Europe. If it works, the researchers hope to apply the electric field therapy to other types of cancer, such as breast cancer and lung cancer non-small cell.

Related Sites

• Video of malignant melanoma cell explodes following an electrical field of 100 kHz
• More information on glioblastoma
• More information about cell division

Scientists have identified a common sexually transmitted canine tumor that can spread from dog to dog. Canine transmissible venereal tumor (CTVT) is probably the oldest cancer known and retains the same genetic structure it had when it began in a single wolf or dog there are more than 0 years. More broadly, the finding casts doubt on longstanding theory about the genetic instability in cancer cells and raises new questions about the evolution of the tumor.

CTVT is a common, usually not lethal, a cancer that affects dogs of all races worldwide. Scientists thought once it was caused by a transmissible virus, much like cervical cancer in humans, but recent studies have suggested the tumor cells themselves are spread from dog to dog, perhaps be during intercourse or oral contact with tumors.

Probing this theory, virologists led by the University College London scientist Robin Weiss took samples of tumor and blood from 16 dogs from three countries. DNA analysis revealed strong genetic similarities between tumors, evidence that tumor cells came from a common ancestral cell. In addition, there were no genetic correspondence between tumors and dogs, that would be expected if the tumors were raised by transferring clean a dog cells. After examining the genetic structures of tumors taken from 24 other dogs from five other countries, the team determined that the cancer must be from an animal, probably a wolf or an old gray dog ​​breed there are between 0 and 2500 years.

scientists suspect that CTVT arose first in one inbred herding dogs or wolves, which would have made the immune system more responsive dogs foreign tissue. Shortly after it has developed, said Weiss, cancer divided into two sub-populations, both of which are found in dogs today. The most likely cancer was more virulent in the beginning, but Weiss said, it seems to have evolved to allow the canine immune system to defeat - but not before the disease is transmitted to another dog. The work appears in August 11 issue of Cell

The conclusion -. A line of cancer cells in existence for over 0 years - challenges the notion that cancer cells become more aggressive as they evolve, eventually becoming genetically unstable and more vulnerable to drugs and the body's immune system, said Weiss. "I think this tumor tells us to think more broadly about the stability of the genome and genomic instability in cancer."

There have been no documented cases of human transmissible cancers; however, there was one case of animal. Last year, scientists in Australia released research suggesting that cancer of the face that decimated the wild Tasmanian devil population is transmissible ( Science , 18 February 05). There is no relationship between tumors, but there is a common concern for conservation biologists, said Elaine Ostrander with the American Institute National Human Genome Research in Bethesda, Maryland. "The idea that infectious tumors there is a new concern for threatened or endangered species," she said. "It would not surprise me if there are more cases of this kind that come along."

recent breakthrough skin cells reprogrammed to act like embryonic stem cells stole the show ( science NOW, December 6) cells, but adult stem prove they have advantages of their own. In December 13 number Cell Stem Cell , researchers report using stem cells from patients with a form of muscular dystrophy to correct the disorder in mice. The results suggest that this strategy might someday treat muscular dystrophy in humans and other genetic disorders.

Duchenne muscular dystrophy, which affects mainly males, is caused by a mutation in the gene for a protein called dystrophin is vital for the proper functioning of muscles. The condition leads to muscle degeneration, and patients typically die in their 30s. One particular type of stem cells found in muscle may lead to new muscle tissue, so a team led by geneticist Luis Garcia Genethon, a biotechnology company nonprofit in Evry, France, investigated whether these cells could be used to reverse problems of dystrophin.

The researchers first obtained stem cells from patients with a muscle biopsy. Then they used a virus to insert a gene into the cells which corrects the mutation in the dystrophin gene. The researchers then injected the modified stem cells in the mouse leg arteries suffering from muscular dystrophy. In just three weeks, the muscles in the foot, shin and thigh began expressing human dystrophin protein, indicating that stem cells gave rise to muscle cells that had taken up residence in mouse muscle.

The real proof came in treadmill tests. The treated mice were able to run longer, maxing out at 15 minutes, the animals untreated patients, who managed only 10 minutes before being exhausted, the researchers report.

Garcia said his team now plans to test the strategy people with muscular dystrophy. He added that the technique could be used to treat a variety of genetic diseases, including other muscle disorders and skin.

Stem cell scientist Robert Lanza of Advanced Cell Technology in Worcester, Massachusetts, called promising strategy. He added that the stem cells used in the study have benefits on skin cells reprogrammed, including the removal of delicate matter to induce the cells to become muscle cells, but noted that both cells could pose risks because the viruses used to change could cause cancer.

geneticist Kay Davies of the University of Oxford, UK, said that for the approach to be successful in humans, stem cells must be delivered to the muscles. This could prove a huge challenge, she noted, because of repeated injections and high costs.

Related Sites

• More Duchenne muscular dystrophy
• More on stem cells

BETHESDA, MARYLAND - It has been over 6 years since the first person was injected with stem cells to save a heart failure. Hundreds of patients have since followed the example of the 46-year-old German man. But experts are still divided on how the strategy works. During a 2-day symposium on cardiovascular regenerative medicine at the National Institute of Health which ended here today, cardiologists, surgeons, pathologists and other researchers have debated the future cardiac cell therapy. Clinical trials and animal studies provide a wealth of information; so far, the treatment appears safe. But it is not at all clear that stem cells should be given, or by what method -. Or, more importantly, whether patients who get them are more likely to survive

Cardiologists seized on cell therapy as a way to prevent cavities of the heart muscle immediately after a heart attack and restore the muscle long after he was dead. But three of the four largest clinical trials have failed to accomplish what they set out to do - to improve a particular measure of cardiac function, as measured by an increase in the amount of blood pumped, said ejection fraction. In other health measures, however, such as the regeneration of the heart muscle or prevent heart attacks, the tests may have been a success, argued some of those who led them. "It is sad, but it is life" that the tests have failed, said Philippe Menasche, a cardiac surgeon at the Georges Pompidou Hospital in Paris who has tried his hand at transplanting skeletal muscle cells. But "should we be discouraged? Certainly not."

A big problem, Manasseh and others have noted, is that the transplanted cells may be disappearing quickly rather than stick around to do their job. Scientists have seen this happen in animals. Joshua Hare, a cardiologist at the University of Miami in Coral Gables who also heads the Interdisciplinary Institute of stem cells, described the work in pigs showing a "cell washing" in the 8 weeks following the birth. Charles Murry , a pathologist at the University of Washington, Seattle, described how he spent 18 months frustrating trying to keep heart muscle cells derived from living human embryonic stem cells in mice after an induced heart attack. he nearly drove him out the edge, he joked, showing a slide of a white van hanging over a cliff. Finally, his lab found a cocktail of factors that kept the living cells, enabling them to preserve and transplant cardiac function in affected mice. the work appeared in the September issue of Nature Biotechnology .

A side effect could complicate how the cells are delivered. Injecting cells directly into the heart, which facilitates engraftment, may cause arrhythmias. In a speech sobering in which he chided researchers to quickly move into human trials before making comprehensive studies in large animals, Menasché a study published in May Traffic by team Great Britain, showing that rats suffered more arrhythmias if bone marrow was shot directly into the heart. (Clean cell therapy trial Menasché has been plagued by several cases of arrhythmias, which is now not sure were the result of cell therapy.)

Another hot issue: Can injected cells develop in ways that improve heart disease? Scientists working with a different stem cells hodgepodge, some better characterized than others. They understand favored mesenchymal stem cells Hare, who can become bone, muscle, and more; bone marrow cells cocktail used in German trials; and bone cells which express a marker on their surface called bone CD34. A trial in the planning stages, based at Cedars-Sinai Medical Center in Los Angeles, California, and Johns Hopkins University in Baltimore, Maryland, hopes to use a natural pool of cardiac stem cells, while groups such as Murry are interested in coaxing embryonic stem cells into heart cells more defined, but flexible. Identify what each of these cell types can be accomplished in an animal is not easy. "Right now, we are limited to throw them on the plastic" to see what they do, said David Scadden, co-director of the Harvard Stem Cell Institute in Cambridge, Massachusetts, in a speech.

stem cells from the stem is also a problem. Cardiologist Douglas Losordo of Northwestern University in Chicago, Illinois, reviewed published studies indicate that certain stem cells, such as bone marrow, may be less effective when just a heart patient than a healthy person Menasché speculates that conditions such as diabetes or atherosclerosis can alter the function of certain bone marrow stem cells using cells from patients -.. most of what has been tried so far - has other disadvantages, such as cost and complexity Hare described the first trial in cardiac patients to take a different approach and use donor stem cells.. Directed by Hare and sponsored by Osiris Therapeutics in Baltimore, the trial enrolled 53 people who received mesenchymal stem cells within 10 days of a heart attack. In spring, Hare said there were no major security problems, such as mesenchymal stem cells developing in other organs.

And then? One of the biggest fans of cell therapy, Andreas Zeiher of the University of Frankfurt, Germany, said that "it is time to embark on a clinical trial of 1,000 person" to nail once and for all if cell therapy guard heart patients alive and healthier --a challenge tests were far too small to meet. The circulatory diseases targeted by the cardiac cell therapy continues to expand: Losordo hopes to launch a trial in critical limb ischemia, which affects patients with diabetes and other and often leads to amputation and even death. Researchers are aware, too, that heart patients are desperate for new treatments. Some flock to Thailand, where a company now offers cardiac cell therapy -. At a steep cost

Cancer often strikes its final, fatal blow when a tumor spreads to other organs. A new study published online today in Science highlights this poorly understood process called metastasis. The researchers report that mutations in mitochondrial DNA may stimulate metastasis and can be reversed with drugs, at least in mice.

Mitochondria are tiny organelles the inherited from your mother used power plants of the cell. They have their own DNA, called mitochondrial DNA. It is ten years, cancer researchers noticed that mtDNA in tumor cells tends to be riddled with mutations - much more than in normal tissues. (This is partly because mtDNA are not packed in protein, which makes it more vulnerable to damage.) Some researchers believe mtDNA can cause tumors. But others suggest that the mutations are simply a byproduct of cancer; they note that people with mitochondrial diseases are not particularly susceptible to cancer, and the risk of cancer are not inherited maternally, as expected for a disease related to mitochondria.

To explore the role of mtDNA mutations in cancer, Jun -Ichi Hayashi's group at the University of Tsukuba in Japan and colleagues swapped the mtDNA of two types of tumor cells mice: one that tends to metastasize and another that does not. When they injected these hybrid cells under the skin of mice, the cells grew into tumors that eventually spread to the lungs. The mice that received the mtDNA from metastatic cells had significantly more lung tumors than mice that had mtDNA from metastases less prone to cells, suggesting that mtDNA was indeed the culprit. However, mtDNA does not seem to be involved in the formation of the primary tumor: When the group exchanged mtDNA from metastatic cells in normal cells, it did not cause these tumors to form

The metastatic mtDNA appeared to do his dirty business. with two mutations that caused the mitochondria to overproduce reactive oxygen species is known, which are molecules of DNA damaging toxic. When the researchers put a drug that sops up these molecules into the drinking water of mice that received metastatic cells under the skin, they almost not developed lung tumors.

The document is "a technical tour of strength," said Robert Taylor researcher mitochondria of Newcastle University in the UK, and the fact that antioxidants suppressed metastasis warrants further study, he said . Kornelia Polyak of Dana-Farber cancer Institute in Boston warns, however, that the antioxidants in clinical trials testing cancer prevention have had mixed results and that giving antioxidants to someone on chemotherapy could interfere with treatment.

related site

• Information about metastatic cancer

couch potato lifestyle today has been blamed for the skyrocketing rates of obesity, but the cause of this trend may have more to do with the potato as the sofa. An analysis of 20 years of published data on the daily energy expenditure of people indicates that overeating, rather than a sedentary existence, is the primary cause of the obesity epidemic in the industrialized world.

What is certain about obesity is that it is ultimately caused by an imbalance in the budgets of the energy of the people. When you take in more calories than you burn, your body squirrels the excess away as fat. The imbalance can result from too much food, too little physical activity, or a combination of both. Studies of exercise and self-reported eating habits have suggested that daily physical activity has decreased in recent decades, while the daily calorie intake remained stable. But the accounts of people of their own behavior is notoriously inaccurate.

To obtain more reliable data, Klaas Westerterp biologists from the University of Maastricht in the Netherlands and John Speakman of the University of Aberdeen in the UK turned to a technique called doubling method labeled water (DLW). Over 2 weeks, the subjects for minimal amounts of water molecules, hydrogen or oxygen atoms contain additional neutrons. The body takes on oxygen for metabolism, expelling some of them in the carbon dioxide. By tracking heavy ratio of hydrogen and oxygen in urine, scientists can estimate the overall rate of a person's metabolism.

The researchers analyzed data from a study of DLW Public Health 20 366 residents of Maastricht led Westerterp published. They compared these data with the results of published studies conducted in the United States and the developing world. DLW "is the gold standard," Speakman said, "so we gathered all available data."

The results indicate that people burn just as many calories as they ever did. The daily energy expenditure was similar in all studies throughout the period, if the subjects were in Europe, the US, or the developing world. over the same 20 year period, the prevalence of obesity doubled in the Netherlands and more than tripled in the United States. "We are not saying that exercise does not make a difference," says Speakman. "If you train for marathons, so of course you are in shape. But for people on average daily physical activity has not changed. In the time we spend watching TV today, people probably listened to the radio in the 1950s and read books in the 1920s, "he concludes. "This work suggests that the obesity epidemic has been largely driven by the increase in food intake."

"The study is provocative," says Loren Cordain, a physiologist at Colorado State University in Fort Collins. "But I wouldn 't hang my hat," he said, because the DLW studies used different experimental procedures, making them difficult to compare. Cordain also concerned that the 366 people studied in Maastricht might not be representative of the entire country. Speakman replied that "we know of no reason why they would not be representative."

Related site

• Calculate your own energy expenditure

Most of the time, doctors have a simple way to determine whether a patient needs medication against pain: They ask. But when a brain injury makes someone unable to answer questions, the right of action becomes murkier. Now a study finds that the brains of some brain-damaged patients respond to a rude shock as much as the brains of healthy people, suggesting that these patients may experience pain, even if they are unable to show.

little is known about the perception of pain in unconscious patients, says Steven Laureys, a neurologist at the University of Liège in Belgium and lead author of the new study. Therefore, we must provide medication is each doctor. Some doctors hold drugs, Laureys said, assuming that these patients are unable to feel pain. Other doctors give more liberal drugs but may turn sedating patients and missing signs of wavering consciousness.

In the new study, Laureys and colleagues used positron emission tomography (PET) to measure activity in the brains of 15 healthy volunteers; 15 patients in a "vegetative state", a famous illustrated provided by Terri Schiavo, who showed signs of awakening, but did not meet the current and its environment; and five patients in a little better condition known as a "minimally conscious state," characterized by responsiveness and limited and sporadic awareness. While few conscious patients can sometimes turn to someone calling their name, for example, vegetative patients may not respond.

In healthy subjects, a zap wrist elicits activity in the brain regions that rev in response to pain, including the thalamus, insula, somatosensory cortex and the anterior cingulate cortex. In patients who were in a vegetative state, activity in these regions has been reduced, and the time of cooking in different regions was abnormal. But little conscious patients had levels and timing of brain activity that were very similar to those of healthy people, the researchers report online this week in The Lancet Neurology . Although PET and other neuroimaging tools never reveal what people feel in fact, Laureys said the new results suggest that little conscious patients may have a greater ability to register pain compared to those in a vegetative state - and a greater need medication to treat it. The ability to feel pain can be another factor for the families of patients to consider when weighing decisions of end of life, he added.

The results are an important contribution to a little studied area, said Nicholas Schiff, a neurologist at the Hospital of New York-Presbyterian / Weill Cornell Medical College in New York. Minimally conscious patients can not speak or even wince to let the doctors know they are in pain, Schiff notes: "There is nothing to guide you without this kind of data." Although Schiff said, researchers need to study a larger sample of patients before taking specific guidelines for drug against pain.

The drug used to wean heroin kills leukemia cells, a new study shows. The researchers found that methadone treatment used in drug rehabilitation, knocks out cancer cells that previously resisted chemotherapy and done without affecting healthy cells. But critics question whether this laboratory study can lead to effective treatment in cancer patients.

Methadone works by binding to opioid receptors in the brain. It then blocks other opioids, such as heroin, reaching receivers and high production implored by addicts. The idea that methadone might act against cancer surfaced in 1999 when researchers found that methadone killed lung cancer cells in laboratory tests.

Claudia Friesen, a molecular biologist at the University of Ulm in Germany, have now discovered that it also acts on leukemia cells, triggering their death. She and her team treated bottles of leukemic cells and normal human blood cells with 30, 20, 15 and 10 micromoles per liter of methadone. After 48 hours, the highest concentration of methadone killed almost all cancer cells, but virtually none of the healthy red blood cells, which lack the specific receptor which binds to methadone. In another experiment, it was found that methadone kills leukemia cells known to resist other anticancer drugs. The researchers report their findings in the August 1 issue of Cancer Research .

Friesen said the next step is to test methadone in animal models to see if it goes against other forms of cancer and to better understand its side effects. But Scott Kaufmann, a cellular pharmacologist at the Mayo Clinic in Rochester, Minnesota, is skeptical that methadone could become a treatment. The dose that killed the leukemia cells, 30 micromoles per liter, would be toxic to humans, he said. So unless they can overcome the side effects, "it is an attractive idea, like in lung cancer, but I do not think it has any practical significance." Friesen said new experiences have shown that methadone kills tumors with lower doses administered daily.

Today, the House of Lords of the British Parliament approved the Government's proposal to reclassify cannabis as a dangerous drug Class B as well as amphetamines and speed, against the recommendations of its own Advisory Council on drug abuse (ACMD). Cannabis was previously classified as a Class C drug, one of those the government considers them less likely to cause damage.

The vote provoked an angry response from senior members of the UK scientific community.
In a letter to Guardian , the scientists wrote that "clearly ACMD recommended, for the third time in the last six years that cannabis remain a class C drug, and did so after reviewing all the available evidence and the last on the short- and long-term risks on health and social harm, public attitudes and policing priorities. "The report's recommendations ACMD, prepared at the request of the Home Office, argue against" increasing criminalization of possession, "said the letter

scientists also warn of dangers to the credibility of the drug classification system: . " Reclassification would send an ambiguous message about the dangers of the current class of drugs B "signatories to the letter include David King and Robert May, former head of government scientific advisers;. Colin Blakemore, a member of the Political Committee on Drugs UK and former Director of the medical research Council, and Gabriel Horn, president of the Academy of medical sciences Task Force on brain science, addiction and Drugs.

The Science Careers Blog has a good summary of what we know to date about the impact Bernard Madoff scandal on scientific institutions and philanthropies that give scientific research. Many organizations have invested in the Madoff hedge fund, which prosecutors allege was a scam of $ 50 billion. The blog reads:

Yeshiva University in New York, home to Albert Einstein Medical School, apparently took a major hit. Sources ... [say] that the school has lost at least $ 100 million of its endowment. ...

Technion-Israel Institute of Technology in Haifa, Israel, invested in securities of Madoff, according to the Israeli daily Ha'aretz, which estimates its losses at about 25 million NIS (6, $ 5 million). The victims of apparent fraud Madoff include foundations run by familiar names such as Nobel laureate Elie Weisel prices, Senator Frank Lautenberg, and director Steven Spielberg, and many smaller family foundations and institutions that serve Jewish communities in North America, Europe and Israel. Madoff managed most Wunderkinder Foundation investment income of Spielberg, who has donated some $ 3.3 million for medical research at Cedars-Sinai Medical Center in Los Angeles. ...

The Madoff scandal has still shaken an already nervous environment philanthropies. John Ruskay, executive vice president and CEO of the UJA-Federation of New York [said] "Already in the context of a very difficult economic environment this will present another major challenge. We do not know yet the extent of the wreckage. "

Biomedical research may be headed for a big boost of 2 years in the bill, even more than some expected stimulus lobbyists. During the debate last night, the Senate accepted by voice vote of an amendment by Republican Senator Arlen Specter of Pennsylvania that would add an additional $ 6.5 to 3.5 billion $ already proposed in the draft Senate Bill to the National Institutes of Health. The House and Senate had planned to give NIH $ 3.5 billion.

The House version would direct $ 1.5 billion of the total by NIH National Center for Research Resources for facilities and extramural equipment, while the Senate plan initial set just 300 $ million search. (Both offer $ 500 million to renovate the NIH campus facilities and the rest for extramural research.) With the amendment last night, the Senate bill would give a total of $ 10 billion for NIH of which $ 9.2 billion would go to extramural research. It passed with little debate. That many remain in the final bill is an enigma. In the past, large increases for NIH proposed Senate have reached a compromise difference division between the House and the Senate. Lobbyist Jennifer Zeitzer of Experimental Biology Federation of American Societies said it "will be difficult to keep [the Senate’s] figure" in conference with the House.

Kill 'em fast, kill' em young. This was the unofficial motto of struggle against insects for the last 50 years. But a new study suggests that, at least in the case of malaria, the strategy may be flawed. By choosing insecticides that act more slowly, or that specifically target older mosquitoes, researchers might be able to prevent the development of pesticide resistance, a problem that has long plagued efforts against malaria.

The new study, published April 6 in PloS Biology , proposes a "new thinking" on the problem of resistance, said entomologist Bart Knols of Wageningen University in the Netherlands. "You might be able to keep insecticides in business for 60, 80 years, perhaps forever," he said. Insecticides can control malaria, but only in the short term. One by one, pesticides have been abandoned because mosquitoes have developed resistance, often several years after their introduction. The reason? In areas where spraying is intense, any mutation that confers resistance, even if only partial, is extremely beneficial to mosquitoes, it spreads rapidly. Today, insecticide resistance is a major problem for malaria control worldwide. This could have been prevented, medical entomologist Andrew Read of Pennsylvania State University, University Park, and colleagues say.

This is their idea. Insecticides that kill mosquitoes early in their life cycle continue to reproduce, creating an enormous selective pressure to become resistant. But if you want to fight against malaria, it is good to let mosquitoes breed; the trick is to prevent them from transmitting malaria. - They are only in middle age from 10 to 14 days

In their paper, the team present models that show that targeting these older mosquitoes could delay the emergence of resistance decades - and still reduce the number of infectious bites by 95%. Some of the same authors co-author of an article on a late killer fungus slow action in Science in 05. But other candidates exist, and existing insecticides spray doses lower, maybe in smart combinations, can also be a way to target older mosquitoes, they write.

knols applauded the idea but said there would also disadvantages. People who have sprayed their home, for example, would not be the immediate advantage of being rid of their problem of mosquitoes. "You'd have to explain that they will still have mosquitoes, and they will still be bitten, but malaria will go down," says Knols. "This could be a tough sell."

President Barack Obama tapped Jeffrey Crowley today to fill the top slot of the Office of National AIDS Policy (NAPO).

The move comes amid growing concern that the United States does not have a national plan against HIV / AIDS. Crowley, a public health specialist at Georgetown University in Washington, coordinate HIV / AIDS policy at the national and international levels. Between 1994 and 00, Crowley has worked at the National Association for People with AIDS from a deputy executive director.

The Director of NAPO, once given the high nickname the "Czar of AIDS," has lost the cachet than the end of the Bush administration-not even fill the position for the last 2 years.

"it is an excellent choice for this work. it certainly comes with all the right background and experience, and on top of that, it is one of the hardest working people I know in my life, "said Georgetown University expert on health policy Tim Westmoreland.

Journalists like to go directly to the source, and a group of journalists covering health care say a change in federal policy the help make their jobs better.

Scientists working for the US government in general can not speak with reporters until they are approved by the press office of their agency, which sometimes insists on monitoring interviews . On February 26, the Association of Health Care Journalists wrote President Barack Obama and urged him to change the policies behind these requirements, which argues AHCJ "impede newsgathering and interfere with the public's right to know."

Journalists health are particularly concerned about the impact of policies on the various branches of the Department of Health and Human Services, including the National Institutes of Health, the Centers for Disease Control and Prevention, and the Food and Drug administration. AHCJ argues that these restrictions have increased in the administrations of Presidents George W. Bush and Bill Clinton, raising the chances "of incorrect or incomplete information being transmitted to the public."

Although AHCJ said the public affairs officers can help journalists do their job, he feared that too often they "are used to inhibit the flow of information to the public rather than encouraging . " the letter asks that federal employees authorized to speak to reporters without receiving prior approval or having to report the interaction.

administration has not responded to the letter.

AHCJ, which has over 1000 members, with headquarters at the University of Missouri School of Journalism in Columbia. the National Association of Science Writers, which has nearly three times more members (including myself), said he plans to send the Obama administration a similar letter requesting that the policy change applies to all federal agencies that science journalists cover.

Senator Arlen Specter (R-PA) said to the US National Institutes of Health billion more is not enough to strengthen biomedical research. On Saturday at a Clinical Research meeting in Chicago, he proposed a new independent agency to get the bench to the bedside discoveries. And he wants your money to help him keep his seat.

Specter led a push to give NIH $ 10.4 billion in the recent stimulus package. It is now drafted a bill to be introduced this week that would allow NIH to receive funding as part of its base budget, bringing the total to $ 40 billion.

He explained his plan to a website, specterforthecure.com, which also invites visitors to contribute to his campaign, he is facing a primary battle hard to hold his seat in 2010 draft law would also create what he calls Cures network acceleration, an independent federal agency, financed $ 2 billion per year, it would try to fill the so-called valley of death between the discovery of a potential drug and test the patients.

The objective of the agency is to "transform biomedical research discoveries into better health for the American people," said Specter, a cancer survivor twice. Biotechnology companies, universities and patient groups could all apply for scholarships, Specter said.

at least one prominent scientist think that the network is a great idea. Former Director National Institute for Human Genome Research Francis Collins, who was at the same meeting, said Science Insider that Specter's proposal is a "bold step" and that "... the medical community should line up and try to understand how to get there."