Health Meaning

For the first time in 27 years, researchers have published new criteria for the diagnosis of disease Alzheimer. With tests to pick up not ready for widespread use of the early stages of the disease, the new guidelines will have little immediate impact on patients, but they are intended to provide a framework for research and planning, hopefully clinicians the day the effective treatments become available.

guidelines, issued today by the Alzheimer's Association and the National Institute on Aging (NIA) and published online in of Alzheimer's disease and dementia reflect the growing understanding that the neurological damage of Alzheimer's disease starts years, even decades, before symptoms appear and future treatments probably work best when started early. They broaden the definition of Alzheimer's to include two new stages that precede dementia in their own right: a presymptomatic phase and a phase marked by mild cognitive impairment.

The new guidelines are the revised recommendations made last year.

At a press conference yesterday, Creighton Phelps NIA explained that a major revision was to clarify what recommendations relate to researchers and which relate to clinicians. In particular, the expert working groups that drafted the guidelines say that biomarker tests for Alzheimer's disease, which capture biological early signs of the disease are not yet ready for widespread clinical use. (Because the newly proposed presymptomatic stage of the disease can be detected by biomarker tests, this designation may be used by researchers at this time.)

In recent years, researchers have made considerable progress on biomarkers, including scans that detect changes in brain anatomy and physiology and tests that measure the levels of β-amyloid peptide thought to be a significant player in the disease in the brain and cerebrospinal fluid. These tests can pick up signs of Alzheimer's disease in people before memory problems appear, and they are already used in clinical trials. Many researchers believe that so many clinical trials, due to potential Alzheimer's treatments have failed in recent years is that the patients included in the trials were too far in the course of the disease. Biomarkers that can pick up early signs of the disease may enable doctors to begin treatment before too much irreversible brain damage has occurred. For now, it is only in clinical trials.

The working groups concluded that although the biomarkers are invaluable for research, more work is needed before it can be widely used by physicians. For example, the methods should be standardized so that they are used consistently from one hospital to another, and researchers need to reach a consensus on values ​​delimit the boundary between health and disease.

PARIS -After two decades of legal wrangling, a French appeals court aujourd 'hui threw excluding charges of manslaughter and other crimes against two scientists involved in a scandal of growth hormone, which led to the death of 125 children of the Creutzfeldt-Jakob (CJD) disease fatal brain. But lawyers for the victims' families say Science Insider who intend to take the case to the Court of Cassation, the highest court of appeal in France.

The verdict was a deep disappointment for the victims' families, as well as a surprise, because they felt they had an audience much fairer judges than they did at the first trial to lower court. "This time, the judges listen to us, and had a much better understanding of the case. It was a trial worthy of the name," said Jeanne Goerrian, a member of the Association for the Victims of growth hormone (AVHC ).

from 1959 to 1698 France treats children with growth disorders with hormone derived from pituitary glands taken from human corpses, a practice that has been linked to the transmission of CJD ., a prion disease prosecutors said the scientists involved should have done more to prevent infections; they also blamed the accused for the transition to the much safer hormone synthetic growth only in 1988, three years after the country as the US and the UK have done.

But the court of Appeals upheld the 09 decision of a lower court that "no fault" had been committed by biochemist Fernand Dray , who was in charge of purifying the material at the Pasteur Institute, and pediatrician Elisabeth Mugnier, in charge of collecting the pituitary glands and treatment monitoring. Dray "can not be blamed for not having the intuition of a risk of contamination no professional could have detected the moment," said the verdict. Mugnier "has no power to intervene in the management of the collection" Human glands, said the president of the court Didier Wacogne.

The case has been dragging on since the early 190s, French wheels of justice grind very slowly and two other scientists from the dock at the first trial died. Dray, 88, did not appear in court because he is weak and hospitalized.

On appeal, the prosecutor had asked for suspended sentences of 3 years and 1 year against Dray against Mugnier. It was less than four years required in the first trial for Dray, who was also accused of corruption on foreign purchases of human growth hormone. (These charges were dropped because the statute of limitations had expired.)

Today's verdict was "worse" than that of the lower court, said Toby Caroline, one of the lawyers AVHC because the court of appeal not only laid criminal charges, but said none of the defendants or their employers had any civil liability. Jean-Marc Viala, another lawyer for the victims' families, said he does not rule out continuing the French government to let the disaster happen. "This should have been done long ago," says Viala. The state has already paid € 36 million in compensation to the families of 125 CJD patients who died.

The Pasteur Institute contributed more than € 0,000 in civil damages to two families. But the institute should also have taken its scientific responsibility for young adults now living with the threat of CJD, French virologist and Nobel laureate Luc Montagnier . recently said Science Insider CJD may appear decades after infection, and more cases are expected to occur; Pasteur could fund research on the prevention, early diagnosis and treatment, Montagnier said rather. of that, "the only gesture was cash handouts from the government." During the trial, Montagnier, who could not be reached today, testified that Shepherd did not act on early indications that human growth hormone could be dangerous.

But Yves Agid, previously in charge of CJD surveillance in France and is director of the brain and spinal Institute here, welcomed the decision: "As I said in my testimony in two trials, it could not have known at the time that the material could be contaminated and transmit the disease. There were many unpredictable factors that led to this disaster. "

BERLIN- German scientists are scrambling to find the source of an outbreak of enterohemorrhagic Escherichia coli (EHEC), a dangerous intestinal pathogen That hAS Hundreds of people sent to the hospital with bloody diarrhea and killed at least one. The investigation is complicated by the fact que la outbreak HAS beens Apparently Caused by a very rare EHEC serotype O104 called Expired.

"I Hope that more patient samples will be APPROBATION today, aim it Certainly looks as if an E. Coli O104 is the case of These infections," says Klaus Stark, head of the division of gastrointestinal infections, zoonoses, and tropical infections at Robert Koch Institute (RKI) here, the German center for disease prevention and control.

RKI Researchers first Took notice last Thursday, When a clinic in Hamburg em Enable notifications of a host of Patients Suffering from hemolytic uremic-syndrome (HUS). The syndrome-caractérisé by a destruction of red blood cells and severe kidney problems-is The Most severe complication of EHEC infection year.

Selon RKI, Nearly 140 patients in Germany-have HUS Developed since the second week of May, Compared with only about 60 cases in an average year. "This is one of the biggest EHEC outbreaks in the world, the biggest one Certainly we-have ever had in Germany," says Stark.

Scientists-have-been baffled not only by the outbreak's size and rapid spread in northern Germany aussi goal by the fact That It affects mostly adults and females, an odd pattern Because EHEC usually sickens children. Of the 65 HUS cases in Germany in 2010, only six patients Were more than 18 years old.

While E. coli bacteria are hand of the human gut flora and usually not pathogenic, strains classed together as the EHEC Produce a dangerous Shiga toxin That Enters the cells in the gut and Inhibits protein synthesis by cleaving ribosomal RNA. The destruction of cells lining the gut leads to abdominal cramping, watery diarrhea, and bloody diarrhea Eventually. In about 10% of cases, the toxin attacks the kidneys aussi, leading to the Potentially fatal HUS. EHEC has-been confirmed as the causes of death in year 83-year-old woman Who HAD beens admis to a hospital in Bremen on 15 May and Who died on Saturday; Reviews another potential EHEC fatality is still under investigation.

Most EHEC infections are Caused by a notorious called Expired serotype O157: H7; Researchers Refer To That serotype and four others frequently found in Europe as the "gang of five." Aim the German reference laboratory for EHEC in Wernigerode HAS so far APPROBATION the serotype of EHEC in stool samples from five patients as O104.

That Makes the highly unusual outbreak, says Helge Karch, head of the National Consulting Laboratory on Hemolytic Uremic Syndrome in Münster. Among Karch's E. coli 588 isolates from HUS patients file Managed over the past 20 years, only two are O104. In Reviews another unusual twist, Karch HAS found the strain to be eae-negative. The gene eae codes for the protein intimin, qui the bacteria uses to attach to the intestinal wall. Most pathogenic EHEC serogroups are eae-positive.

It is still unclear whether the serotype might explain the strange pattern of infections. E. coli O104 first Emerged as a pathogen in a small outbreak in Helena in early 1994. Four people Developed abdominal cramps and bloody diarrhea. Experts at the U.S. Centers for Disease Control and Prevention (CDC) in Atlanta has APPROBATION serotype called Expired O104: H21 as the culprit. A CDC investigation later found up to 18 patients; MOST of Them Were women and the median age Was 36 years.

The source of infection in Germany is still unclear, and the uncommon serotype Could make it harder for autorités to find it. "O104 is very hard to Distinguish from normal, non-pathogenic E. Coli ," says Lothar Beutin, head of the National Reference Laboratory for E. coli at the Federal Institute for Risk Assessment here. He and --other Researchers are now try trying to Develop a more rapid and specific test for the unusual serotype.

The natural tank of EHEC bacteria are ruminants Such as cows and sheep, qui carry the pathogens In Their guts and spread Them With Their feces. It is Transmitted to humans through consumption of contaminated Primarily foods.

"When we first Interviewed patients, a lot of 'em MENTIONED eating raw vegetables, purpose That Does not mean That vegetables are the source," Stark says. RKI is using a detailed questionnaires to ask patients what They Have eaten in the days before falling ill and Comparing Their answers with Those Who of healthy controls match the characteristics in patients Such as age and sex, a common method in epidemiology.

In order to save time, HOWEVER, the Epidemiologists are not searching public records to find the matching controls. Instead, a team of 15 experts Went door to door yesterday in the areas in Hamburg Where Some patients live, looking for matching Roughly controls. "If we get a clear signal, something That 0% of the boxes purpose only 10% of the controls ate, Then We Can Be very sour That We-have found the source," says Stark.

But a first statistical analysis this morning Did not yield clear results Any. Indeed, because of the smaller MOST of the EHEC outbreaks in recent years HAS never beens Established definitely. Scientists are Hopping que le current outbreak will turn out to be unusual fait que respect as well.

Craving a snack in the afternoon? Take a drag on a cigarette, and your hunger will probably disappear. Smoking is the leading cause of preventable death in the United States and other developed countries, which causes lung cancer, heart disease, and chronic bronchitis. But smokers are, on average, thinner than nonsmokers. A new study reveals how nicotine, the active ingredient in cigarettes, works in the brain to suppress appetite smokers. The discovery also highlights a new therapeutic target for nicotine withdrawal and loss of weight.

The nicotine receptor in the brain has 15 subunits; they can be combined in a multitude of ways to form different receivers with different jobs. Nicotine can bind to each combination and stimulate a cascade of individual events; some lead to the addictive properties of cigarettes, others an increase in blood pressure or a feeling of relaxation. It has long been known that nicotine causes a drop in appetite, and scientists suspect that it worked through receptors associated with reward and reinforcement of behavior. After all, the brain considers both cigarettes and food for rewards. But the new finding suggests that appetite has its own way.

Behavioral neuroscientist Marina Picciotto of Yale University began to study whether the activation of a particular nicotine receptor, α3β4 nicknamed, had antidepressant effects in mice. But as Yale colleague Picciotto, Neurogeneticist behavioral Yann Mineur cured the mice given drugs designed to stimulate only α3β4 receptors, he noticed a side effect: mice ate less.

"Before this study, we really do not think this type of receptor would have such an important role in brain food intake," said Picciotto. She Minor and then showed that nicotine is actually binding to α3β4 receptors, which then send a signal through the rest of the brain, signaling satiety. It is impossible to distinguish the signal from the brain spreads after eating a large meal. The mice that received the drug binding to the α3β4 receptor ate half the amount of food than untreated mice within 2 hours following administration of the drug. Their body fat dropped from 15% to 20% over 30 days, the team reports online today in Science .

Because the weight gain that comes with smoking cessation is often a deterrent to smokers to quit, Picciotto suggests that the new route could be targeted by drugs to suppress appetite during the early stages of smoking cessation. In addition, such a drug could have wider application as an appetite suppressant to help in losing weight without risk to cigarette smoke-related health.

Neil Grunberg, a behavioral neuroscientist at the Uniformed University of Health Sciences Services in Bethesda, Maryland, was the first to prove by rat studies in 1982 that nicotine causes a decrease appetite. He says the new study is a step forward in understanding the phenomenon it was first observed.

"Most people have accepted that decreased appetite was caused by a dopamine reward pathway and left at that," says Grunberg. "So I think that the most important contribution of this article is to prove that there is another way that the entire nicotine works through. "

Grunberg notes, however, that the study relates only to male mice. in his previous work, he found differences in the effects of nicotine on weight between males and females. women, he said, the biggest weight loss experience when they start smoking and increased weight gain if they quit. that means the nicotine works by an additional lane, the hormone regulated in the female brain is yet to be determined.

Picciotto said his group repeated the experiments with female mice. "We are also always try back to that original question we had, "she said," is it also has antidepressant actions "

* this article has been corrected to reflect the accurate title of Yann Mineur.

Life for people with a genetic condition called Prader-Willi syndrome, which affects about one in 15,000 people can be difficult for both the patient and family. Patients have an insatiable hunger that can lead to obesity in life-threatening if access to food is not limited. And worse, they have similar behavioral problems in autism. Tantrums and tears are common because these patients have difficulty understanding the motivations of others and control their own emotions. But the treatment of brain hormone oxytocin can help bring the two emotions and eating balance, according to a new study.

Several indicators have highlighted the potential of oxytocin, often considered the "hormone of trust." Research on the brain tissue donated after death in patients with Prader-Willi showed that the hypothalamus (the thermostat of the body) shows abnormalities in nerve cells that produce the hormone. in addition, the hypothalamus releases oxytocin in response to social interaction touching, relaxation and confidence-all the things that people with Prader-Willi syndrome have problems with. And oxytocin treatments improved social skills of autistic patients. Finally, the hormone is thought to contribute to a feeling of fullness after eating, "satiety" in the language scientific.

to see if oxytocin could benefit people with Prader-Willi syndrome, endocrinologist Maïthé Tauber of the Children's Hospital of Toulouse, France, and colleagues injected oxytocin or placebo in 24 adult patients nose. The researchers monitored the patients' behavior; they also used cartoon stories to test understanding of social interactions and patients face images to see how they could recognize emotions.

For the two days that patients were studied after treatment, that were given oxytocin were significantly more confident and less sad. They were less disruptive and had fewer conflicts with others. They also had higher scores on tests assessing social understanding, compared to placebo group.

The study, which appears online today in the Orphanet Journal of Rare Diseases , focused on behavioral issues, which says Tauber "are more difficult to control than the food intake. " However, patients ate less after treatment with oxytocin, and five do not finish everything on their plates, which says Tauber is unusual in Prader-Willi syndrome.

"The search for Tauber and his colleagues is meticulous and very exciting," says Daniel Driscoll, a geneticist at the University of Florida in Gainesville. There is currently no cure for the disease except behavior modification and diet control. Driscoll said a better understanding of the role of brain chemicals like oxytocin may lead to better treatments for various stages of this complex disorder.

the authors write that although the longer-term, larger studies are needed, this work opens new perspectives for patients with Prader-Willi syndrome. "Because previous research shows abnormal secretion of oxytocin, we hope that the treatment can not only improve mood and behavior of the patient, but also help correct the underlying problem, "says Tauber.

Y are afraid of the dark penguins? Foreign moons might harbor life? And LSD may help treat painful headaches? Science Online News Editor David Grimm chats about these stories and more with Science Editor 's online Stewart Wills.

( Listen to the full Science podcast and podcasts.)

This week, the World Health Organization (WHO) criticized the use of blood tests not reliable commonly used to diagnose active TB, as well as aggressive marketing used to promote them. The first recommendation "negative" policy, the agency urged countries to ban these serological tests. "They are a waste of time, and they are a waste of money, and most importantly, they have endangered people who suffer from tuberculosis," Mario Raviglione, Director of the Stop TB Department of WHO, has said at a press conference Wednesday.

instead, WHO recommends that countries use standard microscopy or molecular test a new system called GeneXpert.

tests blood used on at least 2 million people a year are wrong 50% of the time, says the wHO, giving either positive or false negative results, both of which are dangerous.

wHO began studying in 05 blood tests after getting questions from governments and doctors who were concerned about their increasing prevalence. the tests are mainly manufactured in Europe and North America, but they are mainly used in countries where regulations is more lax but the burden of TB is the biggest development.

"It is a profitable business. It is a multi-million, which is centered on selling substandard tests with unreliable results, and we feel this must change, "Karin Weyer, Coordinator of TB diagnosis and laboratory strengthening to Stop TB Department of WHO, said at the press conference.

in a 07 assessment, WHO, with UNICEF, the United Nations development Program, and the World Bank concluded that 19 blood tests commercially available were very inaccurate and insensitive. But since then, the use of serological tests for TB has increased, prompting the wHO to make an updated review of proof. the final review, conducted by WHO and then evaluated by a panel of external experts, was delayed until yesterday Weyer said, because after the 07 report, many companies simply changed the names of their products and remarketing, which makes them difficult to track. Moreover, Weyer said, given the powerful nature of their recommendation, "we must ensure that the science behind this policy could be defended at all challenging."

The consequences of these misdiagnoses were significant. when TB is untreated, individuals are not only in danger, but also unknowingly transmit the disease to others. and when people are not properly diagnosed with tuberculosis, the underlying cause disease goes untreated and the unnecessary use of TB drugs contributes to drug resistance.

These blood tests are inaccurate because they are based on the detection of antigen-antibody produced by Mycobacterium tuberculosis (MTB), the organism that causes tuberculosis. the immune response is a poor indicator, however, because different types of actions antigens mycobacteria, and other infections raise similar antibody responses . Accordingly, blood tests may be detecting the presence of other mycobacterial infections; they can also produce false positives when antibodies remain high after the TB levels were treated.

Despite these shortcomings, manufacturers make claims of great accuracy, Weyer said, citing the instructions for a drug that said the test was 100%, although the study included only 10 topics. She also mentioned the reports of doctors who receive economic incentives to manufacturers of these tests.

Since December 2010, WHO approved / RIF test Xpert MTB, a new molecular diagnostics manufactured by Cepheid, a company based in Sunnyvale, California. The test runs on the GeneXpert system, which uses real-time polymerase chain reaction for rapid detection of MTB and rifampicin resistance, identification of patients infected with drug-resistant strains.

"The advantage of GeneXpert is that you can immediately diagnose TB [determine] if TB is drug resistant," says Weyer. It provides results in 2 hours compared to weeks required to establish a diagnosis of the cultivation of traditional TB. Unlike microscopy, instrument size to the coffee machine does not require a laboratory or trained personnel, she said. The downside is that it costs $ 20,000, expensive compared to $ 1,000 for the purchase of a microscope, although the individual test costs are similar. GeneXpert also requires constant and uninterrupted flow of electricity, lack of many developing countries, although Weyer says studies are underway to try to feed the machines with batteries and solar energy.

Several studies published in PLoS Medicine this week concluded that the MTB test / RIF is very effective in the diagnosis of tuberculosis in HIV-infected patients for HIV, which is particularly difficult, because they often have negative smear results because their disseminated or extrapulmonary tuberculosis. One study showed a 45% increase in case detection for patients with HIV using Xpert MTB / RIF test compared to smear microscopy. Last week, in
a document The Lancet , the researchers reported that GeneXpert is also effective for the diagnosis of TB in children, another population at high risk of dying tuberculosis. = "#article_upsell">

WHO still hopes a "point of care" diagnosis that will work at the bedside, but for now, Weyer says "there are many basic science still lacks image ".

Bernadine Healy, a cardiologist who was the first woman to head the National Institutes of Health (NIH) from 1991 to 1993, died Saturday in brain cancer.

Appointed by President George H. W. Bush, was a director of Healy franc NIH during a tumultuous period. She proposed initiative on women's health, $ 625 million a study that followed more than 140,000 women in part to learn more about the health effects of estrogen replacement therapy. Although some researchers questioned the cost management and top-down initiative, it proved its value a decade later, showing that taking estrogen increases the risk of stroke, heart disease and cancer of the womb of a woman.

Healy fought a powerful member of Congress, Representative John Dingell (D-MI), the scientific misconduct investigations involving laboratory of David Baltimore Nobel laureate and the role of Robert Gallo in the discovery of the AIDS virus. James Watson, the first director of the Human Genome Project, quit after clashes with Healy. But she made a smart hire by replacing it with Francis Collins, who is now director of the NIH.

Healy designed the first Strategic Plan for NIH, which went nowhere, meeting resistance. She also oversaw the transfer of mental health, alcoholism and drug addiction institutes of another NIH agency. And she became caught in a battle on fetal tissue research; as a person appointed by the administration, it supported the banning of Bush before Congress.

"She was very talented very intelligent, energetic woman, who rubbed some people the wrong way, but when she believed in something she was extremely helpful to get implemented" said Anthony Fauci, director of the National Institute of allergy and infectious diseases.

David Korn of Harvard medical School, who was dean of the Stanford medical school at the time, said Healy was " in a difficult situation, "as one of the few women in management positions at NIH. His experience as a cardiologist and the desire to "societies" NIH has attracted "hostility" basic scientists who worried their funding, said Korn. However, the strategic plan was an "overview" of the NIH director on, Elias Zerhouni, did when he created an office to analyze the NIH portfolio, said Korn. "I think he was very attentive and forethinking her," said Korn.

President Bill Clinton did not accept Healy, who later became the dean of the medical faculty of Ohio State University. She also ran unsuccessfully for the Senate and led the Red Cross during the 9/11 terrorist attacks. She worked as an editor and columnist of health US News and World Report until last year when a brain tumor that was removed in 1999 reappeared. She was 67 when she died.

PARIS -Servier, the pharmaceutical company at the heart of a massive medical scandal in France, suffered several fresh blows to its credibility this week. Yesterday, a newspaper revealed that the company is under fire from Europe's guard dog medicine for the way she studied the side effects of her medication after reaching the market. court testimony Meanwhile, leaked by two company scientists suggests that ancient Servier deleted unfavorable information from the files with which it requested regulatory approval for mediator, its drug against diabetes, in the 1970s .

the name of the Mediator, Servier brand of a drug called benfluorex-was banned in November 09 after 33 years on the french market. Although marketed as a drug against diabetes, doctors widely prescribed for people who wanted to lose weight as well. was shown mediator to cause serious heart valve problems, however, and it is now estimated to have caused up to 2,000 deaths. A French court investigating the case, and the French government announced that it will tighten regulatory oversight of drug response.

Yesterday, the French newspaper Libération reported that the European Medicines Agency (EMA) in London has set his sights on Servier as well first for problems around ranelate strontium, a drug against osteoporosis, marketed by Servier in France under the name Protelos. 30,000 French women is estimated that in France took the drug during the last 4 years.

Maraninchi Dominique, director of the French regulatory agency AFSSAPS, confirmed the EMA concerns in a telephone interview with Science Insider. In November 07, Pharmacovigilance Working Party of the EMA issued a warning that Protelos could cause serious and potentially fatal skin rash known as adverse drug with eosinophilia and systemic symptoms, and Servier ordered to correct "flaws" in his system to keep track of these adverse events, Maraninchi said.

EMA asked Afssaps carry out an inspection in December 09 to ensure Servier had followed. This inspection revealed other "critical and major findings," this time with Servier manufacturing process, and raised concerns about all drug company, said Maraninchi. Consequently, Servier was ordered to submit information about all of its drugs to the EMA, whether authorized for marketing by EMA itself or by national agencies.

EMA eventually concluded that the benefit-risk balance remains positive for Servier drug, but it instructed the company to provide additional product information for some of them, a spokesman said EMA. AFSSAPS conducted a second inspection in July this year and will present its findings at the end of this month.

Tuesday, reports in newspapers Le Figaro and Libération also expressed doubts about the integrity of Servier when regulatory application for mediator in 1973. the documents referred to the testimony of retired neurosurgeon Jean Charpentier, now 81, who prepared the regulatory file at court. Charpentier, who began working for Servier in 1968, told the judges that clinical trials have shown mediator to be a powerful appetite suppressant, but it has been minimized in its report for approved mediator as antidiabetic drug. (Diabetes was "infinitely more profitable choice" that weight loss for pharmaceutical companies, said Charpentier.)

The report did not mention that Mediator is an amphetamine derivative, Charpentier said in his testimony. "The word was amphetamine to avoid," he said.

Duhault Jacques, 78, a pharmacist who led the diabetes and obesity of the company's laboratory in the 1960s, told the judges he regretted that Servier did not shoot mediator as a precautionary measure in 1999 Libération reported. His studies have described the drug as a "powerful appetite suppressant." in January 1969, said the drug, then known under its code name S992, "causes the almost complete anorexia from day one."

Servier has denied all allegations. in press statements, the company condemned the violation of judicial secrecy on mediators testimony, reiterated that he had "deceived neither health authorities nor the patients," and denied that Carpenter studies had been falsified.

A charity family hopes to restart the search for a cause of the mysterious disease known as chronic fatigue syndrome (SFC) by funding around $ 10 million in studies by high-level research groups.

The CFS patients suffer from long-term fatigue and other symptoms such as muscle pain and cognitive problems; the cause is unknown. The New York City-based chronic fatigue Initiative (CFI), funded by the Foundation of the private Hutchins family, announced last Thursday a search for causes and treatments. The initiative plans to spend "the stadium" of $ 10 million over 3-4 years, said Executive Director of the FCI Scott Carlson. That's almost 50% of the $ 6 million per year that the National Institutes of Health ( NIH) spends CFS.

An epidemiological study funded by CFI already underway will draw on the study of health famous nurses and two health professionals study followed for 20 to 30 years Harvard School of Public Health. researchers will identify participants in these studies with CFS files and research their environmental exposures and archived blood samples for risk factors for disease. another CFI program will fund grants CFS exploring possible mechanisms based on assumptions that will be determined by scientific advisors.

the initiative will also launch a new cohort study of 0 patients and 0 controls recruited in centers across the country. Biological samples of the volunteers will be kept at Duke University and Harvard connected to a clinical database. As part of this study, Columbia University hunter Ian Lipkin of viruses and other fetch the samples for at least 20 viruses and other pathogens in the hope of finding a related to CFS.

Carlson Hutchins said the family was interested in CFS research because it is "orphaned" in relation to diseases such as Parkinson's disease, which, like CFS, affects about 1 million Americans. The family has several friends with the disease, he said.

Several characteristics are different initiative previous CFS studies, Carlson said Lipkin-the technology used, the size and the careful characterization of the cohort, the researchers involved, and approach operations. "I do not think anyone has ever taken such a comprehensive approach," he said. If the studies show promising results, the family hope the major foundations will launch in more funding.

A pathogen the study will not be tested is a mouse retrovirus called XMRV. There are two years, a report Science proposed such a link between XMRV and CFS but other groups have been unable finding the virus in CFS patients. Lipkin conducting a large study funded by NIH putative link CFS-XMRV. But that work and studies CFI "are not related in any way," says Carlson. After talking to experts, he said, "the consensus seems to be that the issue of XMRV will be completely covered."