Health Meaning

The 1918 Spanish flu killed up to 40 million people. The swine flu pandemic in 09 killed about 284,000. Now scientists have discovered a substance that could help doctors save lives during future influenza pandemics. Eritoran, a compound being studied as a drug for sepsis, significantly reduces deaths due to influenza in mice. "This could open up a whole new class of anti-influenza drugs," said Michael Osterholm, a flu expert at the Research Center and policies relating to infectious diseases at the University of Minnesota, Twin Cities, which has not participated.

at present, doctors have a single class of compounds available to fight against influenza. the drugs, Tamiflu and Relenza, block neuraminidase, a surface protein that the virus influenza should leave the cell after reproduction. the drugs, taken orally, are to be given soon after infection to be effective, however, and some flu strains have developed resistance against them. some scientists have also questioned the safety and efficacy of compounds, many countries stocks during the H1N1 pandemic of 09. "Basically, if you see the arsenal available today, it is limited and could be blown over night, "said Albert Osterhaus, a virologist at Erasmus MC in Rotterdam, the Netherlands.

Instead of targeting the virus, Stefanie Vogel immunologist at the University of Maryland, Baltimore, tried to interfere with the host immune system. Scientists have long speculated that some cases of severe flu are not the direct result of the virus havoc, but due to a so-called cytokine storm, a catastrophic overactivation of the immune system that leads to many inflammatory substances being released into the whole body, which can lead to multiple organ failure. For example, immune cells and the liquid can accumulate in the lungs, airway blockage. A 08 study cell suggested that the cascade is triggered by the activation of a molecule called Toll-like receptor 4 (TLR4), which normally signals the immune system to the presence of certain bacteria in the body . If these pathogens overwhelm the body, TLR4 is also thought to trigger inflammation of the entire body known as sepsis. For this reason, blocking TLR4 was viewed as a potential treatment for patients suffering from sepsis.

Vogel and colleagues studied eritoran, a compound that blocks TLR4 and is now in clinical trials as sepsis drug. They infected mice with influenza laboratory strain called PR8 and gave half of them eritoran injections for 5 days, starting 2 days after infection. Ninety percent of the untreated mice died, against only 10% of those given the drug. If the treatment was started at 6 days after infection, 33% of the animals survived. The compound also reduced lung damage in cotton rats, a species that does not die from the influenza strain used for the study, the authors report online today in Nature .

"It is an elegant study based on assumption rather bold," says Osterhaus. But the mechanism of the disease in mice could be different from that of man, he said. "This does not disqualify the results, but that means we must be careful." Vogel said she has already submitted a grant to test the compound in ferrets, the most widely used animal influenza studies. "Since eritoran has a very good safety record in people, we hope that our preclinical studies will ultimately support clinical trials in humans for flu and perhaps other diseases that cause disease by a similar mechanism, "she wrote in an e-mail to science NOW.

For Osterholm, the paper adds to the evidence that influenza causes illness by several different mechanisms. Some strains of influenza, such as the one that caused the Spanish flu in 1918, or swine flu in 09, are more likely to cause death by activating the immune system, leading to more deaths in younger age groups he argued. "This is the case it will be demand." Osterholm but also warns that many promising drug candidates fail at later stages. "We will not know if it works until we put in people."

One day after a prominent paper in the journal Cell was reported for image duplication, the lead author and the newspaper say that problems arose from the simple mislabeling images and do not invalidate the results. They also defended the exceptionally fast examination paper, which was accepted only 4 days after the official presentation and published online 12 days later.

The work, led by Shoukhrat Mitalipov Research Center of the Oregon National Primate in Beaverton, was marked by two reasons: It is the first time anyone has used cloning to create embryonic stem human personalized (ES) cells, and it is the same result that was described in 04 and 05 by a group of south Korean scientists in what is proving to be one of the most famous cases in the world of scientific fraud .

scientists stem cells were first delighted, with a developer Science that the work was a "hard-won victory after years of painstaking research." After a commentator posted on a site called PubPeer alleging duplicate images and mislabeled in the paper, joy turned to dismay. "It is unfortunate that this important area of ​​research has come once again under control," wrote Kevin Eggan of Harvard University Science Insider in an email.

talked Mitalipov with Science Insider this afternoon and said he and the other co-authors simply neglected mistakes, partly because the images in question are intended to show that the cells are similar. "with the naked eye, it is very difficult to see if the same image or a different image." He said he is curious to know if the contributor PubPeer used the image control software to catch duplication. "I wish we had this software to run the paper through," he said.

The first series of duplications has three digits. The images are intended to show that ES cells from ' cloned embryos resemble those from IVF embryos, suggesting cloned ES cells are the real thing, but the same image seems to appear twice under a different label. once as an ES cell line derived from a cloned embryo, and elsewhere in the paper as a line of control ES cells from an embryo in vitro fertilization. another image in the same set, Figure 6, appears as a cloned cell line but also shows in an additional figure called the command line. Mitalipov, who spoke with Science Insider this afternoon, said the first author Masahito Tachibana deliberately used the images twice, but accidentally knocked the labels in Figure 6.

the second duplication appears in the supplementary Figure S6, where a cloud purporting to show similarities gene expression between cell lines was used twice. Mitalipov said the bad scatterplot was used, and the good will be published in an erratum. original microarray data are publicly available, he notes.

Mitalipov argued that the main evidence that the cell lines are derived from embryos cloned really are not affected by these errors. The most important is whether the mitochondrial DNA of ES cells matches that of the egg cell donor and the nuclear DNA is the cell that has been cloned. The researchers deliberately chose a cell line widely available for their experiments, Mitalipov said, making it easy for laboratories outside to try to confirm the results. He says he is ready to ship the ES cell lines cloned in several laboratories that have requested them, as soon as the signs of Oregon's institutional review board off of transfers, which could occur in a case days. (Restrictions prohibit federal funding of the National Institutes of Health funded laboratories working on cells because they were obtained through cloning, so that recipients must also show that they have a legal place to work with cell lines .)

cell , meanwhile, sought to defend. Newspaper editors have refused to speak with Science , but the spokesperson Mary Beth O'Leary issued a statement, noting that "it seems there were a few errors made by the authors . ... We do not believe the impact of these scientific results mistakes of the paper in any way. "

Several experts say stem cells Science Insider that the images in question are no keys to the conclusions of the paper. However, Eggan writes, "we will probably have to wait until the cell lines in question are validated by others, or reproduces the independent group [cloned ES cell] before we find know for sure. " Dieter Egli of the New York Stem Cell Foundation in New York said Science Insider that he and his colleagues are already working to reproduce the allegations Mitalipov.

Cell was not able to answer a key question before our deadline: What was the rush in securing the paper? He had an exceptionally fast turnaround, filed April 30 and accepted on May 3 "Reviewers have graciously agreed to give priority attention to examine the document in a timely manner" Cell of statement read. "It is a false statement to assimilate review by the slow peers with rigor or discipline, or use review by the timely peers to justify negligence in preparing the manuscript."

In a story by Nature Mitalipov seemed to imply that he pressed for a quick review because he wanted to present the work at a conference. But this meeting is not until mid-June, and cellular authors has already led to high-profile documents to be published in the newspaper after describing their research at a meeting.

Mitalipov said ScienceInsider that even if he mentioned the conference when he presented the document, it was not the reason for quick review or competition from another group. he says he first sent the paper to the newspaper "5 or 6 days' before April 30, the official date of submission as part of an investigation prior to approval. After Cell publishers have expressed interest, he said, he officially introduced through the website on 30 April. He said the review simply asked reviewers to look at the paper quickly, "and they did it in a day." The examiners had minor criticisms, he said, the authors were able to respond quickly. cell may have been worried about the news of the flight of paper, he says, which may have prompted the online publication shortly after acceptance. the document should be published in the June 6 printed edition of the journal.

Tachibana is "devastated" by the errors, said Mitalipov. However, the lead researcher is confident that the results will soon be confirmed. "We have the cell lines. We can show that the mitochondrial data [DNA] is, and that nuclear data, "said Mitalipov. He and his co-authors are now combing through "every point" in the paper to make sure it is no more unknown errors before submitting a formal correction.

A Japanese Ministry of Health, the panel Labour and Social Affairs has agreed a plan to carry out what would be the early clinical trials of the world involving induced pluripotent stem (iPS) cells. Acceptance opens the way for an official green light from the Ministry, which could come in early July.

The researchers from RIKEN Center Developmental Biology in Kobe plan to generate replacement pigment epithelial retinal cells from iPS cells generated from patients with macular degeneration. Research is ongoing for several years and was widely reported at conferences.

Approval for clinical trials was expected to be routine. However, the health ministry committee has cited security concerns to put off a decision at the end of May. Japanese media reported that the group meets again today and accepted additional data submitted by RIKEN. Formal approval will be up to the Ministry. RIKEN could begin recruiting patients aware of this year.

What makes some people thin and other full-figured? Besides diet and genetics, the community of microbes that lives inside of us may be partly responsible. New research on twins suggests that lean people harbor bacteria than their obese counterparts do not. And, given the chance, these bacteria may be able to prevent weight gain. But do not dig your skinny jeans closet just yet. So far the work has been done only in mice. Moreover, bacterial takeover requires a healthy, high fiber diet to work, illustrating the complex relationship between diet, microbes, metabolism and health.

Our intestines are home at least 400 species of bacteria, and the evidence is building that the balance of microbes in our internal ecosystem has a significant impact on health, including brain function and the risk of Cancer. A study last year showed that the transfer of intestinal bacteria between humans reduces insulin resistance, which is related to obesity.

To explore how microbes differ between obese and lean people, researchers at Washington University in St. Louis took the intestinal bacteria of four pairs of identical and fraternal twins; a brother in each pair was thin and the other obese. Then they transplanted the microbes in mice that had no gut microbes of their own. Mice that got the skinny twin microbes remained thin, the researchers report today Science. Those who got the obese twins microbes increased their body fat by 10% on average, though they ate the same amount of food.

What would happen if these two sets of microbes are mixed in the gut, the researchers wondered. Led by microbiologist Jeffrey Gordon and graduate student Vanessa Ridaura, the team took advantage of one of the least endearing rodent habits: They eat shit the other. After letting this happen, the researchers found that the lean twin microbes appeared to be particularly good to take hold in the ecosystems of the mouse intestine that began with microbes associated with obesity. And after moved bacteria, the mice did not gain weight. The most invasive species of microbes from animals were thin in the Bacteroidetes group, which has previously been associated with thinness in mice and humans. Obese mice seem unoccupied niches that Bacteroidetes could easily move in.

To understand what the gut bacteria could do, the researchers studied the bacterial genes that were active in both types of mice. The heavier mice had higher levels of proteins involved in stress responses and detoxification; lean mice expressed more genes involved in the breakdown of dietary fiber.

food, it turns out, was the key to the impressive properties of lean twins microbes. All mice in the first series of experiments were eating chow that was high in fiber and low in fat. The researchers then developed a mouse pellet form an unhealthy human diet, high in fat and low in fiber, and housed mice slim and heavy together again. They found that, with this scheme, the microbes associated with leanness not colonize the intestines of cage mates.

This work was carefully done and corresponds to previous findings, including the idea that Bacteroides can protect against weight gain, says Alan Walker, a microbiologist from the gut the Wellcome Trust Sanger Institute in the UK who was not involved in the study. What is new here, he said, is that researchers have begun to address the question of how this protection might work :. Species that are responsible, what genes they use, and what diet they need

"This study is important step towards ultimately answer these questions," says microbiologist Peter Turnbaugh from Harvard University. an important result of this work, they agree, is that it puts in place a way to test the effects of microbial therapies on human intestinal bacteria (even if insects live in a mouse) . the authors suggest that the next logical step is to use animals to measure the effects of foods or ingredients ecosystem of the gut in particular.

the mouse experiments also provide a way to test fecal transplants, which can cure a potentially fatal intestinal infection in humans and show a potential to treat other conditions such as inflammatory bowel disease and obesity. There is a danger inherent in this approach: Transfer of human feces in the colon of a patient at risk of pathogen transmission as well. Walker and the authors note that "the next generation of probiotic" good test compound known beneficial microbes come in pill form or another treatment could take the place of fresh faeces, and this mouse system provides a way to identify the most effective bacteria, diseases of these bacteria can be treated, and if a special diet is required.

"There is a significant way to go before you can translate these findings to humans," warns Walker. A probiotic weight loss is not just a next step, the researchers discovered when they isolated 39 of beneficial Bacteroidetes species. The mixture was unable to cause the same effects as shit mouse, maybe because Bacteroidetes not acting alone and microbial players must be identified.

Although our muscles pumping iron, our cells pump something else: the molecules that help maintain a healthy brain. But scientists have struggled to explain the mental well-known advantages of exercise, fight against depression and aging the fight against Alzheimer's and Parkinson's. Now a research team may have finally found a molecular link between a workout and a healthy brain.

Research Many exercise focuses on the parts of our body that do the heavy lifting. Muscle cells increase production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin name, cut and released into the blood, where it causes the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the wicked.)

While studying the effects of FNDC5 in muscle, cell biologist Bruce Spiegelman of Harvard Medical School in Boston arrived at some surprising findings: Mice that do not produce a so-called co-activator production FNDC5, known as PGC-1α were hyperactive and had tiny holes in certain parts of their brain. Other studies have shown that FNDC5 and PGC-1α are present in the brain, not only the muscles, and both may play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (irisin and created from it) was responsible for the benefits induced by exercise levels of an essential protein called brain-derived neurotrophic factor (BDNF), this which is essential for maintaining healthy neurons and by creating new brain in particular has increased. These functions are essential to ward off the neurological diseases, including Alzheimer's and Parkinson's. And the link between exercise and BDNF is widely accepted. "The phenomenon has been established in easily, the last decade," says neuroscientist Barbara Hempstead at Weill Cornell Medical College in New York, who was not involved in the new work. "It's just, we understand not the mechanism. "

to adjust this mechanism, Spiegelman and colleagues conducted a series of experiments on live mice and mouse brain cells in culture. first, they put the mouse over an endurance training regime of 30 days. They should not force their subjects, because the race is part of the natural feeding behavior of a mouse. "It is more difficult to get them to lift weights" Spiegelman notes. Mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from the physical differences between mice and sedentary wheels trained ones- "they just look a little more like a couch potato," says co-author Christiane Wrann, also from Harvard Medical School, figures luscious-groups of the latter also showed neurological differences. The riders had more FNDC5 in their hippocampus, a brain area responsible for learning and memory.

Using the cells of the developing mouse brain in a dish, the next group showed increased levels of the co-activator PGC- 1α stimulates production FNDC5, which in turn leads to BDNF genes to produce more of the essential protein of neurons forming BDNF. They report these findings online today in Cell Metabolism . Spiegelman said it was surprising that the molecular processes in neurons mirrors what happens in the muscles that we exercise. "What was weird is the same pathway is induced in the brain," he says, "and as you know, with exercise, the brain does not move."

So how is the brain gets the signal to BDNF? Some have hypothesized that neuronal activity during the year (as we coordinate body movements, for example) reflects changes in the brain. But it is also possible that factors outside the brain, such as proteins secreted by muscle cells, are the driving force. to test whether irisin created elsewhere in the body can still lead the production of BDNF in the brain, the group injected a virus into the . mouse blood which causes the liver to produce and secrete high levels of irisin They saw the same effect as in the exercise. increase in BDNF levels in the hippocampus This suggests that irisin might be able to spend the blood-brain barrier, or it regulates another molecule (unknown) therethrough in the brain, said Spiegelman.

Hempstead called the findings "very exciting," and believes that this research is finally beginning to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. "I think it answers the question that most of us have put us in our own heads for years."

The liver irisin effect on the brain is a "pretty cool finding and a little surprising," says Pontus Boström, researcher Diabetes at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work does not answer a fundamental question: To what extent the effects of BDNF-promoting exercise are from reaching the brain irisin from muscle cells via the bloodstream, and how many are irisin created in the brain?

although the authors stress that other important regulatory proteins may play a role in the conduct of BDNF and other brain-nourishing factors, they focus on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and improve brain health with aging.

One of the biggest vulnerabilities of infants is largely invisible: In the weeks following birth, babies are particularly susceptible to infection because their immune systems are not fully functional. There are a handful of theories to explain this responsibility, and now a research team added another to the list: immune suppression in early life may help prevent inflammation in the intestines of infants they become colonized by helpful bacteria they need to stay healthy.

Newborns are more likely than older babies to catch, and die, severe infections. The reason is fuzzy indeed, there may be more than one explanation. One theory is that as the brain, lungs, and the rest of their body, the immune system of infants have simply not yet fully matured. Another is that mothers are to their in utero and two companions suppressed the immune system, so that neither rejects the other. After birth, the thinking goes, it takes babies a month or two to boost immunity.

The search for new ways to better understand this process, Sing Sing Way, a doctor of pediatric infectious disease at the Hospital Medical Center of Cincinnati Children in Ohio, wondered whether the transfer of immune adult cells could rev their immune system. Yet when he and his colleagues injected the fight against infection of cells from adult mouse spleens in 6 days old puppies, nothing happens: The puppies were just as vulnerable to harmful bacteria than the control animals. Probing deeper into this surprise, they found that the injected cells have simply stopped work in newborn animals. Then the Way group made the transplant, they reversed the mouse newborn adult immune cells that have been inactivated in puppies and found that they "lit" in adult animals. These experiences "told us it was not a problem with the neonatal cells themselves," says Way. On the contrary, he believes the environment is a newborn body, or an adult with a guided how the cells behaved.

others in the laboratory study of the gut microbiome Way, the constellation of healthy bacteria that fills our intestines. newborn mice, just like human babies are born " clean ", with little intestinal bacteria. Very quickly it changes. Way wonders if there might be a connection between this settlement and what looked like a deliberate suppression of the immune system in its mouse.

to find out, a group focused on immune cells that eventually develop into red blood cells and which express a surface receptor called CD71, which causes immunosuppression other cells. Knocking about 60% of these cells as CD71 much that their technology could handle-was followed by severe inflammation in the intestines of mice. Way and his colleagues also found that as the mice increased, fewer cells boasted CD71 receptors, suggesting the removal was not necessary. He theorizes that this is because the gut is colonized by this point.

The work, reported online today in Nature "adds a new and very important chapter" in the history of how the immune system develops, said Mike McCune, an immunologist at the University of California, San Francisco. immunosuppression, at least in newborn mice, appears to reflect a deliberate change in the balance of immune cells. the concept is certainly plausible, accepts Heather Jaspan, a specialist in pediatric infectious diseases and immunologist at the University of Cape Town and Seattle BioMed in Washington. She wonders about other cell types in addition to those receptor CD71 that may play a role. "It would be interesting to follow this issue with other studies of cause and effect," she said, finally nailing the specific immune suppression allows bacteria to colonize the gut without harming the newborn.

Much caution is whether that Way team observed held in human babies. the baby's immune system develops differently than a mouse, and Way is interested in search of CD71 cells in babies born around their due date, as well as those born prematurely. Very premature infants often die from a disease called necrotizing enterocolitis, a massive inflammation of the intestine. Way McCune and wonder if this resulted in part from a lack of CD71 cells in these babies-if, essentially, their immune systems are still fetal, not ready for natural colonization of intestinal bacteria happens after that they were born. In theory and far into the future, the researchers say, could receive preemies immune cells that would make them immune system more like a full-term baby, allowing their guts to stay healthy.

Many doctors and parents report that their autistic children have particularly serious gastrointestinal problems, such as chronic constipation or diarrhea . These observations have led some researchers to speculate that the diseased intestine contributes to the disorder in some cases, but the scientific data were insufficient. Now, a provocative study claims that probiotic treatment for gastrointestinal problems may reduce autismlike symptoms in mice, suggesting that this treatment could work for humans as well.

The frequency of bowel disease in people with autism varies widely between zero-published studies over 80% -Make it is difficult to establish how widely the two conditions go hand in hand says principal investigator Sarkis Mazmanian, a microbiologist at the California Institute of technology (Caltech) in Pasadena. Overall, however, the evidence seems to point to a connection. Last year, for example, a Centers for Disease Control and Prevention Study of thousands of children with developmental disabilities found that children with autism were twice as likely as children with other types of disorders have frequent diarrhea or colitis, an inflammation of the large intestine.

For many years, Mazmanian and his and his colleagues studied the effects of a nontoxic strain of the bacterium Bacteroides fragilis on diseases such as Crohn's disease, which causes intestinal inflammation and allows potentially harmful substances to pass on the body to escape through the junctions between cells that are normally tight. Although researchers do not understand the mechanism, the bacterium appears to restore the damaged intestine, possibly by helping fill those gaps.

"The fact that we have an organization that repairs the gut makes it a very attractive" tool to check for abnormalities of the gut may contribute to autism, said Mazmanian. To explore this issue, Mazmanian and colleagues at Caltech have used a mouse model of autism is thought to recreate about three messy stamp deficits: lack of social interaction, reduced communication (normally emit mouse ultrasonic chirps birdsonglike), and repetitive behaviors such as grooming compulsive or landfill ball.

The first step of the experiment was to determine whether the mice showed signs of gastrointestinal inflammation or other abnormalities of the intestine, said microbiologist Elaine Hsiao, a postdoctoral candidate at Caltech and lead author of the study. When the mice were 3 weeks, the researchers found that their intestines were indeed like leaky mice that had been treated with a chemical that induces colitis. Next, the researchers tested whether they can reverse the damage by feeding on mice applesauce laced with B. fragilis for a week. A second group of mice that mimic autism and a healthy group of mice ate the apple sauce that does not contain bacteria. The group then waited to see what effect the bacteria would have on rodents intestines. "We did not know what would happen-we hoped the bacteria could survive in the intestine," says Hsiao.

After 3 weeks, the team measured the levels of molecules in the intestine derivatives the blood of rodents and found that the treatment had stopped their intestinal leakage. the number of rodent poop bacteria have shown that although B. fragilis has not established lasting colonies in mice, they "shake the community," micro-organisms, approaching that of normal mice, Hsiao said. After treatment, the mice mimicking autism also resembled their normal peers in two behavioral tests, the authors report today Cell . Pets are no longer compulsively buried balls in their cages and increased their ultrasonic grinding to typical levels. They have not increased their social interactions, however, says Hsiao.

"It really is striking that any treatment, even a transient bacteria could have a lasting impact on behavior," says Hsiao. The most interesting thing about the results, she said, No. no correction of autistic symptoms in mice, but the study provided clues about how the microbial population of the gut can affect the brain and behavior. the researchers found that levels of a substance called 4 -ethylphenylsulfate that is produced by bacteria of the intestine increased 46 times in mice with autistic symptoms, but returned to normal after treatment with B. fragilis . When the team isolated this chemical and injected into healthy mice, the rodents showed anxiety increased, another autismlike symptoms, she said. While the substance did not cause the symptoms observed in the previous experiment, Hsiao said the altered response of animals suggests that the substance may play a role in the disorder. Hundreds of other metabolic byproducts have also changed in amount after B. fragilis was administered and could have an effect, it adds

By demonstrating that the mouse model widely used of autism have gastrointestinal problems, and these problems are associated with behavioral symptoms, new research. "shows us something fabulous," said Betty Diamond, an immunologist at the Feinstein Institute medical research in Manhasset, New York. It warns, however, it would be premature to use B. fragilis or other probiotic treatment as in humans. "We do not really understand" what bacterial species are important or how they colonize the intestine, she said.

Although the results are interesting, the study does not prove that changing levels of microbes and the chemicals they produce one caused behavioral changes observed in mice, says Emanuel DiCicco-Bloom, a neuroscientist at Rutgers University in New Brunswick, New Jersey. "I want to know more about the mechanism "whereby the modified bacteria behavior in mice before starting to translate the results to humans, he said. The group has also not investigated how bacteria affect a normal animal, because the microbes were only administered to mice with autism, he said. It is possible that B. fragilis could have a deleterious effect that the study did not detect, he said. Combined with the difficulty inherent in the extrapolation of human autism conclusions of a mouse, he said, "I think it is less well established than it appears."

" We propose that, after the repair of leaky gut, neurotoxic molecules do not enter the system and cause behavioral abnormalities, "says Mazmanian. But he agrees with DiCicco-Bloom there are other explanations for why the mice changed their behavior for example, "maybe the nerves are activated bacteria in the gut that are in communication with the brain, "he said. After resolving some of these issues, the group plans to launch clinical trials in humans, Hsiao said." We do not want people to start applying this to humans "for now, but "it opens the door to future research" in people.

The swine flu pandemic of late 09 had a particular impact in parts of Europe: a peak in children being diagnosed with narcolepsy, a sleep disorder incurable with symptoms including episodes of overwhelming daytime sleepiness. Researchers eventually linked a vaccine widely used to ward off the flu virus H1N1 in a small but increased risk of narcolepsy in children and adolescents. The vaccine, Pandemrix, used only in Europe, apparently triggered disorder in recipients about one in 16,000 in Finland. Sweden, Ireland and England have also found an increased risk, but not as dramatic as Finland.

Now, scientists have a clue of why that points to a new understanding of narcolepsy itself, they report this week Science Translational Medicine . They found that patients with the disease have immune cells that are pushed to the attack by hypocretin, a hormone that regulates wakefulness. Scientists knew that the neurons that produce hypocretin are missing in the narcoleptic brain, but why they go is a mystery. The work reveals "fingerprints of an immune attack," said Lawrence Steinman neuroimmunologist Stanford University in Palo Alto, California, who was not involved in the research. It suggests that autoimmune reaction perhaps triggered by Pandemrix may underlie cases related vaccines. researchers also believe that the flu itself could trigger other cases.

When the association between Pandemrix and narcolepsy showed, the vaccine manufacturer, GlaxoSmithKline funded research to investigate what, if any, in the vaccine could trigger the disease. narcolepsy researcher Emmanuel Mignot of Stanford University, which received grants, already suspected that the rogue immune cells could contribute to narcolepsy. in 09, Mignot and his colleagues found that almost all patients with narcolepsy have a particular human leukocyte antigen (HLA) type. HLA proteins present-pieces antigens abroad T cells, which then coordinate the immune attack. The method allows the immune system to distinguish between self and foreign cells and certain HLA types are associated with autoimmune diseases such as type 1 diabetes and multiple sclerosis. But there is no obvious sign of immune attack in the narcoleptic brain.

In the new work, Mignot, Stanford immunologist Elizabeth Mellins, and his colleagues have developed an immune system cell line that carries the HLA associated with narcolepsy. They combined the cell line with short pieces of protein hypocretin, is then added T cells of patients and controls in combination.

The team had access to four pairs of identical twins in which one twin had narcolepsy but the other did not. In each case, the cells of the affected double T-reacted strongly with hypocretin "epitopes" displayed by HLA-bearing cells, but the cells of the healthy twin T does not. The researchers found the same pattern when they compared cells from 10 Irish children who developed narcolepsy after receiving the Pandemrix vaccine with T cells of siblings healthy patients, who all had the same HLA type and were also vaccinated T. The T cells of patients responded to hypocretin epitope, while their siblings cells not.

They then asked if the H1N1 virus itself could provoke the same immune response. A search on the power to certain sections of a key component of the H1N1 virus, the hemagglutinin protein, which "amazingly air had the same" as the hypocretin epitopes, Mignot said. Indeed, in laboratory tests the viral protein fragment activated hypocretin-reactive immune cells that evidence high narcolepsy may be due to a process known as molecular mimicry, wherein protein fragments from an invading virus or other first pathogen immune system to respond native proteins with similar molecular structure.

results are "exactly what we expected," says Hanna Nohynek vaccine expert at the National Institute for Health and Welfare in Helsinki, which was part of the team that first identified the increased risk of narcolepsy in children who received Pandemrix.

But molecular mimicry alone can not explain the mystery. It is unclear how an immune response to hypocretin could lead to the destruction of neurons that produce, such as reactive cells in the blood would not necessarily meet those brain cells.

And it is still unclear whether the single H1N1 could trigger narcolepsy. Mignot and colleagues reported an increase in the disease in unvaccinated Chinese children who had the virus. But researchers in South Korea and Europe have found no increased risk of the disease in people who have had swine flu.

"There is a lot of work to do," said Steven Black vaccine expert medical Children's Hospital of Cincinnati in Ohio, who is studying possible links between vaccines against H1N1 and narcolepsy. But the work "is the first mechanistic explanation of the disease," which should help researchers home Pandemrix factor that could have caused problems. Identify what, he said, "is a first step" to be able to produce even safer vaccines.

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Every day, people around the world submitted them -Same? in tests, providing data for research studies, clinical diagnostics and care. But donors should have access to their raw data? By what right, for example, if a donor must download the raw output from a genetic screen of saliva? As technology allows more people to access information and makes the tests once found in expensive laboratories available and affordable for businesses, should we worry about information overload triggering uninformed decisions by consumers? Or more data always a good thing?

Join us on Thursday, January 30 at 15 pm EST on this page for a live video chat with experts as we discuss the challenges donors access to raw data.

Representatives of 26 countries are planning to hold a simultaneous meeting in Washington, DC, and Geneva today to launch a program global health security aimed at better protecting the world against infectious diseases.

Led by the United States and the World Health Organization (WHO), the new effort is an attempt to help lagging nations catch up on efforts to develop plans for face "public health emergency of international concern". In 05, 194 countries have adopted revised International Health Regulations of the WHO, which is the report of June 2012 which detailed how they had strengthened the efforts to assess and respond to outbreaks of dangerous pathogens like the new flu strains , severe acute respiratory syndrome, dengue, Middle East respiratory syndrome and Ebola. Just 40 countries, however, met the deadline.

Consequently, the world is facing "a real vulnerability to storm," said Tom Frieden, director of the Centers for Disease Control and Prevention (CDC) in Atlanta, on a conference call yesterday with journalists . "the bottom line here is that we have the ability to both our countries, the United States, and significantly more secure against infectious threats."

Frieden and other officials outlined a nine-point program, at least in outline. It includes a commitment from the United States and other governments to help low- and middle-income and better detect, prevent and respond to infectious diseases by improving laboratory capacity, the introduction of new proven technologies and building communication networks on outbreaks. Frieden said the US budget proposal President Barack Obama for 2015, which will be released early Mars will have $ 45 million in new funding to support the effort. Other high-income countries have pledged to put money on the barrelhead, too.

Laurie Garrett, senior researcher for Global Health at the Council on Foreign Relations in New York, applauded the new agenda, reflecting an idea that she advocated in October. "It just makes sense," said Garrett. "If countries can not identify new diseases, and eventually these diseases could join us." But she is worried that the United States and other donor countries will not pony enough money. "To pull this off you need to spend more than $ 100 million per year," Garrett said. "It will take 5 or 6 years of good, hard, hard work to reach everybody target knows that we must achieve."

today's meeting is closed to the media and off-the-record, but individual countries will be free to describe their contributions to the conversation.