Health Meaning

Thousands of researchers, physicians, and patient advocates gathered this morning in downtown Washington, DC, park, urging Congress and the White House to support federal funding for biomedical research. Scroll down to see what the event looked like. More details soon on Science Insider.

David Malakoff

David Malakoff

David Malakoff

David Malakoff

David Malakoff

David Malakoff

David Malakoff

David Malakoff

David Malakoff

David Malakoff

After weeks of worrying about how in-mandatory budget map-2013 cuts known as sequestration will play the National Institutes of Health (NIH), the biomedical research community of the now final figures. The bottom line is as dark as expected: the overall budget of the agency will decrease by $ 1.71 billion compared to 2012, to $ 29.15 billion, a decline of about 5%, according to an NIH review today ' hui. That's basically what the NIH predicted within the 5.1% sequestration. (Including transfers to other organizations and other adjustments in the bill on spending NIH funding in 2013, the total reduction of $ 1.71 billion or 5.5% compared to 2012 ).

Accordingly, NIH plans to fund 8283 new and competing research grants this year, down from 703, according to this table. This number strengthens the "hundreds less" price makers warned NIH earlier this year. Including (already assigned) ongoing grants that end, the total number of research grants will decrease 1357-3402 prices. The decline "reflects the fact that the budget of NIH has shrunk because of the new budget and the political reality, which is bad news for researchers and patients that they are trying to help," said Tony Mazzaschi of the Association of American Medical Colleges in Washington, DC

NIH will try to keep the size of the average grant in line with 2012; it will not grant inflationary increases for the coming years the agency also plans to cut subsidies. permanent. the subsidies that have been cut up to 10% earlier this year due to budgetary uncertainty "can be partially restored," but probably not at the level of the initial commitment, notice NIH said.

individual institutes have also begun to sequester announce their plans. The National Cancer Institute (NCI) is effectively reduced by 5.8% to $ 4.78 billion due to transfers to other departments, NCI Director Harold Varmus said beneficiaries yesterday. Varmus wants to keep new and stable competitive grants, and NCI plans to 1006 prices, a decline of only 79. But to do this, NCI cut current subsidies of about 6%, the 6.5% centers, contracts 8.5%. Similar cuts will be made to or more intramural programs, Varmus wrote. Success rates, currently around 14%, "may refuse a small degree," wrote Varmus. "Needless to say, the person NCI is pleased with these reductions, but they are now inevitable for fiscal 2013."

At the National Institute of General Medical Sciences (NIGMS), which is lined with about 5% to $ 2.3 billion, subsidies and current centers will have a more modest 3.5% hit. But NIGMS provides only fund 758 new grants, a slide of 210 awards. 18% success rate.

As for how these cuts will affect individual companies, which may not be known for some time that the award notice trickle to recipient. However, the NIH director Francis Collins is already looking for stories of the impact of sequestration by a twitter debate he launched yesterday by using the hashtag #NIHSequesterImpact. "I'll share some of your stories to try to turn this mess around," he wrote in a follow-up tweet. An answer sampling appears below.

Young lab grant that would . was funded last year to unfunded day Firing talented ppl slows future progress NIHSequesterImpact #

. - DeWayne Townsend (@Dr_dtown) May 7, 2013

I was told 3 times that despite being qualified for the job, the laboratory has not hiring because of instability in #NIHSequesterImpact funding

- Travis Chapman (@ travischapman) May 7, 2013

My department has a T32 training grant Slots keep being empty. - laboratories do not feel stable enough to add a free * postdoc #NIHsequesterImpact.

- D. 'Beauty' Bancroft (@beautybancroft) May 7, 2013

#NIHSequesterImpact will only worsen the situation. I quit looking when I finish my thesis. No money and no cares.nexus.od.nih.gov/all/wp-content...

- clausti (@prettyflysci) May 7, 2013

If we can not reactive please / borrow / steal other laboratories to our medical school. Other schools are simply screwed. #NIHSequesterImpact

- Laura Mariani (@lauramariani) May 8, 2013

* Updated at 11:45 on May 10: The original l article said the NIH budget will be reduced by $ 1.55 billion in 2013, but it is only with the kidnapping. Including $ 156 million in transfers to other organizations and other adjustments to the NIH budget in fiscal 2013 continuing resolution, the overall reduction of $ 1.71 billion, or 5.5%.

tens of thousands of new compounds will be screened for efficacy against severe disease

Japan joined the global efforts to contain malaria, tuberculosis, and a variety of tropical diseases a big way. A public-private partnership has recently formed on Saturday will officially announce the agreements on the screen tens of thousands of drug candidates from Japanese banks public and private sectors compounds for treatments for diseases that mainly afflict the poor in developing countries.

The first 11 agreements are the first fruits of a newly formed public-private Global Health Fund Innovative Technology (Ghit Fund). It was created in April and brings together Foreign Affairs of Japan and the ministries of health and well-being, a consortium of five pharmaceutical companies, and the Bill & Melinda Gates Foundation. The Japanese government is a little more than half of the $ 100 million that is committed to Ghit over the next five years; drug manufacturers and the Gates Foundation are contributing the rest. Funding could increase if more companies join the consortium, said BT Slingsby, the fund's CEO and Executive Director.

Slingsby said Japan was a bit behind other nations contributing to global health R and D efforts Although Japan is a major producer of new pharmaceutical products, Japanese companies have not the size and global recognition of US and European pharmaceutical giants. Although Japan was one of the biggest contributors to development aid in recent years, little of this money has already spent in R & D for global health. And major non-governmental organizations dealing with global health concerns are based in the US or Europe, leaving Japan out of the picture.

Returning to the game, looked Ghit a new model rather than creating new nonprofit organizations focused on specific diseases, said Slingsby. "We try to be additive and does not reproduce what is there," he said. They work with nonprofit-World Alliance established goal for TB Drug Development, the Medicines for Malaria Venture (MMV ), and drugs for Neglected Diseases initiative (DNDi) -to help develop drug candidates.

Ghit funding will allow researchers to test compounds from libraries of Japanese drugmakers Eisai, Daiichi Sankyo, Shionogi and Takeda Pharmaceutical, and non-profit institute based in Tokyo of Microbial Chemistry private. the TB Alliance and MMV are looking for drugs to increase current treatments for TB and malaria are losing their effectiveness. DNDi hope to find treatments for three neglected tropical diseases, leishmaniasis, Chagas disease and sleeping sickness. Astellas Pharma is also involved in the initiative.

Let the fundraising begin! At a press conference today, the Oregon Health & Science University (OHSU) authorities have announced plans to raise $ 500 million for cancer research over the next 2 years to win a grant equivalent consideration. The challenge of $ 500 million was offered last Friday in a surprise move by philanthropists Phil and Penny Knight. The campaign of $ 1 billion "is a moment of transformation" for the university and the war against cancer, said OHSU President Joe Robertson.

The Knights had donated $ 100 million to create a research institute on cancer at OHSU, led by Brian Druker, who led development of the drug Gleevec against cancer. Their latest commitment was made after Druker has recently pressured the couple for $ 1 billion to take ideas to Gleevec, and other so-called molecularly targeted therapies, and develop more early tumor detection tools. Call the current methods of cancer detection "technology relatively crude," Druker said, "we must do better."

OHSU officials did not provide details of how they intend to spend the potential $ 1 billion, although Druker said it plans to hire about 20 scientific elite and give them sufficient funds to take risks, a strategy he compared to what the Howard Hughes medical Institute did. "We are trying to release the investigators of our current constraints of writing grant," he said.

Phil Knight was a co-founder Sports giant Nike shoes and is now a major contributor to academia. In 06 he gave the Business School of Stanford University which was, at that time the largest donation in its history, $ 105 million.

Two new genetic studies of a parasite that causes malaria suggest that it may evolve new ways of invade human blood cells. The development could make some more dangerous parasite strains for people who have some natural immunity. Now about 95% of people in sub-Saharan Africa, where the malaria burden is highest are considered resistant to the parasite in question, Plasmodium vivax . If the parasite was to overcome their genetic defense against disease, it would potentially threaten hundreds of millions of people than it does today.

Vivax malaria is widespread in Asia and South America. Although less deadly than its cousin Plasmodium falciparum , which causes most malaria deaths, P. vivax beginning to be recognized as an important cause of serious diseases worldwide. To enter human blood cells, the parasite usually uses said protein Duffy blood group, a protein on the surface of red blood cells. But because up to 95% of the population across sub-Saharan Africa has the protein a genetic trait called "negative Duffy" -They have long been thought to be protected against infection. However, reports have emerged in recent years of Duffy-negative people who are still infected with vivax malaria. Peter Zimmerman of Case Western Reserve University in Cleveland, Ohio, and colleagues found, for example, that nearly 10% of Duffy-negative patients in Madagascar that have clinical malaria were infected P. vivax .

Now Zimmerman and his colleagues found a genetic clue that may help explain clinical observations. They sequenced the genomes of several P. vivax strains from patients in Madagascar and found that they had two copies of the gene that encodes the protein binding Duffy. Duplication occurred at higher rates in areas where relatively Duffy-negative patients vivax malaria, researchers reported this morning at the American Society of Tropical Medicine and Hygiene annual meeting in Washington, DC

Because P. vivax can not be grown in the laboratory, it is difficult to test how the extra copy of the gene could change the behavior of the parasite. But Zimmerman thinks that duplication can somehow help the parasite to invade blood cells Duffy-negative. It's still just an association, he said, but "two things happen in Madagascar that are unusual in the world," Duffy-negative infections and gene duplication. The genetic signature of the additional copy suggests that it may be a relatively new mutation, he said.

In a second study presented at the meeting this morning, David Serre of the Institute of Genomic Medicine of the Cleveland Clinic said that he and his colleagues have discovered a previously unidentified gene in P. vivax strain of Cambodia seems encode another protein that helps the parasite invades the blood cells. The gene is present in strains from around the world, but it lacks the first strain of P. vivax sequencing, which provided the "reference strain" for the species. It was a strain that had adapted to infect laboratory monkeys, because the parasite can not be grown in the laboratory. Serre says the parasite tamed laboratory may have lost the gene, which is why it was not found in the sequence reference. the gene may also play a role in the Duffy-negative infections, he said.

This is "biologically plausible," says Kevin Baird of the clinical research Unit Eijkman-Oxford in Jakarta . But it is not yet clear whether the Duffy-negative infections are an emerging phenomenon or have been present undetected, all along. "it is certainly cause for concern and merits further investigation," he said.

allergy sufferers rejoice. Two new studies suggest that your sneezing and wheezing may actually protect you. The researchers report that mice that develop an allergic reaction to the venom in bee stings are more likely to survive potentially lethal doses of the same poison later. The results show that allergy can be beneficial and reveal some of the molecular machinery at work, but experts say that the implications for humans are still unclear.

In humans and other mammals, the immune system pushes unknown and potentially harmful substances such as viruses or toxins, in one of two ways. Said reaction "type 1" responds to viruses, bacteria and other microbes by destroying them, while reaction "type 2" uses an array of symptoms, including sneezing, coughing and diarrhea to expel allergens in the body.

Because type 2 response and the antibody it produces immunoglobulin E (IgE), were associated with resistance to worm infections, many scientists believe that they have evolved to protect against parasites (contrary to germs), but that they have no purpose of modern protection. In the developed world without parasite, they are rampant in response to benign substances such as pollen or peanuts with boring or, in the case of anaphylactic shock (an extreme allergic reaction that can cause severe swelling and difficulty breathing) the consequences of the life threatening. Or the prevailing theory goes.

But pathologist Stephen Galli of the School of Medicine of Stanford University in Palo Alto, California, the type of thinking 2 replies had gotten a bad reputation. To explore the effects and unravel the benefits-potential type 2 reactions, he and his colleagues exposed mice to a common allergen: bee venom. They administered a dose of venom about the same as found in one or two bee stings in both mouse strains: type 1 strain response and subject to subject like response deformation 2. Two control groups of same strains received no injection.

Regardless of their predisposition to type 1 or 2 reactions, both groups of mice "bitten" showed a response type 2, the rise of production of specific IgE antibodies to the venom. Then, three weeks later, the researchers gave all the mice a potentially lethal dose of venom and waited to see what would happen.

"It was a response to an allergist would not expect," said Galli. "The second time, the mice were protected."

Eighty-six percent of type 1-prone mice that had had an allergic reaction survived the dose, against only 7% of the mice that were not allergic. Among mice prone 2 standard, 80% of allergic mice survived, while only 28% of non-allergic mice did. Scientists have seen a similar protective effect when they repeated the experiment using snake venom, which contains some of the same allergens present in bee venom.

The antibodies protected mice even when the rodents were not produced. Injecting mice with deficient IgE-specific IgE rich blood serum the poison was sufficient to confer protection, said Galli. And repeat the experiment in mice lacking IgE or the ability to respond showed no protective effect.

The results suggest that type 2 responses may have evolved to protect against venoms as well as parasites and they still serve that function, reports the team today in the journal immunity .

defense mechanism could help humans survive in the difficult conditions in which we evolved, said Galli. "We spent a lot of time meeting with insects and venomous reptiles, and it is likely that this defense mechanism has made this possible."

In a separate study also published today in Immunity immunologist Ruslan Medzhitov of medical school and his colleagues at Yale University confirm that mice with type 2 previous response to bee venom have greater resistance to potentially lethal doses of the substance and later the mice lacking IgE miss this protective effect. in addition, the team found the venom ingredient that triggers the allergy an enzyme called PLA2 as cell membranes and damage is found in snake venoms, spiders, and many other creatures. the researchers worked at each stage of the chain of events that led to the reaction type 2. the immune system sends a wave of chemical messengers called cytokines to repair damage PLA2 and activates the type 2 response, Medzhitov said.

"As far as I know, this is the first direct evidence that IgE-mediated responses may be protective and beneficial," said Medzhitov. "It is like the feeling of pain. It is very unpleasant, but very important for our protection"

"They are very convincing, excellent education," said immunogeneticist Kathleen Barnes of Johns Hopkins University in Baltimore, Maryland, who was not involved in either study, "but we must be cautious in applying these results in humans." human type 2 responses are a number of mysteries, they say it. it is unclear, for example, that people with severe type 2 responses, which are prone to allergies, enjoy a greater resistance to poisons than the rest of us, or why type 2 response can cause life-threatening symptoms in some people. the studies provide important new information, but leave these questions unanswered, she said.

Fred Finkelman immunologist at the University of Cincinnati College of Medicine in the Ohio agrees. "Together, these studies complement our understanding of the evolution of the allergic response," he said. "But what is the beginning of the story at the end of it."

This week, researchers described an ambitious project to explore 1,000 years of the disease and the health of people buried since the year 1039 in a cemetery along with a wellness pilgrimage route known in Tuscany, Italy. By studying the skeletons of farmers, peasants, monks and nobles, paleopathologists hope to discover what diseases killed people from medieval times to the present day and how their general health has fluctuated during the famine, war, climate change and other challenges. They also use new tools, such as the ancient DNA to trace the origins and evolution of deadly pathogens that cause plague, tuberculosis, cholera and other diseases. Why is it important to study the health of our ancestors? What we learn from the study of ancient diseases? And what impact can study the evolution of pathogens have the treatment or prevention of modern epidemics?

Join us on Thursday, December 12, at 15 pm EST on this page for a live video chat. Our guests will be two experts on the study of ancient diseases with two different methods, using ancient DNA, or the study of fossil bones. Make sure you let your requests for them in the comment box below.

fiber consumed in fruits and vegetables appears to help calm the activity of overzealous immune system which leads to conditions such as irritable bowel syndrome, Crohn's disease, and perhaps even colon cancer. Now it seems that a diet rich in fiber can also repel asthma, an inflammatory disease that constricts the airways of the lung, changing how certain immune cells are produced in bone marrow.

When we eat abundant fruit and vegetables, the bacteria that occur naturally in our intestines help us to digest the fiber. Microbes are fiber "soluble" such as pectin found in apples, pears, berries, citrus fruits and onions and simmer in specific types of fatty acids that interact with immune cells, helping to keep the inflammation under control. This anti-inflammatory effect extends beyond the gastrointestinal tract is less clear. But fatty acids in question are able to circulate through the bloodstream, may clash with the immune cells throughout the body.

This could mean that the influences of dietary fiber other inflammatory diseases such as asthma. It is known that asthma has increased in westernized countries since the 1960s, in which the amount of fiber consumed also decreased. In addition, asthma is not as common in less developed areas, such as Africa, where fruit and vegetables are a big part of the diet.

To test a possible link, Benjamin Marsland immunologist at the University of Lausanne in Switzerland and colleagues put one group of mice a diet low in fiber. After 2 weeks, the researchers sniff the animals a derivative of dust mite allergen (a key trigger allergy and asthma human). These mice showed exaggerated asthmatic responses, including inflammatory compounds in the lungs and narrowed airways causing wheezing and shortness of breath so familiar to asthmatic patients.

Moreover, mice that ate a diet rich in pectin for 2 weeks to obtain the extract of dust mites showed reduced inflammatory response. The levels of immune cells called eosinophils and immunoglobulin E antibodies, both generally increased in allergy and asthma have been almost halved, and the mice showed less constricted their airways.

To see if intestinal bacteria were responsible for the benefits of fiber to mediation, the scientists analyzed the mouse droppings on a normal diet, low and high fiber. In animals given pectin types of bacteria most able to produce anti-inflammatory fatty acids were about twice as common than other most common bacteria in a diet low in fiber. A closer examination, the researchers found proportionately higher amounts of fatty acids not only in the stools of pectin-eat mice, but also in their blood.

were the fatty acids in the blood tells the immune system to reverse, and this message was enough to call trigger an asthma attack? To find out, the researchers injected mice with propionate, one of these fatty acids. After 2 weeks, the rodents again showed reduced inflammatory markers and less airway constriction in response to treatment of dust mites, the team announced today online Nature Medicine . In addition, the key immune cells called dendritic cells behave differently. The dendritic cells can either reduce the activity of the immune system or rise of the response, depending on the signals they send to other types of immune cells. In mice on a diet rich in fiber, dendritic cells were less able to turn on cells called effector, which are key players in allergic asthma in mice and humans.

In the final phase of the experiment, the researchers found that the mice that received propionate were actually produce more immature cells "precursors" that develop into dendritic cells that protect against asthma . "Our study is the first to show that diet can influence the production of immune cells in the bone marrow, which could have important implications as the precursors of immune cells leave the bone marrow and spread to tissues throughout the body including the lungs, "Marsland said.

by Gary Huffnagle, an immunologist at the University of Michigan, Ann Arbor, researchers predicted that if compounds produced by bacteria influence the asthma, they would in the lung tissue. the channel connection events dietary changes, altered metabolism of the intestinal bacteria, a change in the production of immune cells in the bone marrow, and the relief of inflammation asthma is an exciting development, he said. "No one has ever put that together before. The study is a great convergence of observations. "

rigorous scientific work must be done, Marsland believes, to check whether dietary supplements, including purified propionate, or similar fatty acid, may be beneficial for people with asthma or those who do not have access to fruits and vegetables. at the same time, he said, a balanced diet high in fiber is the best way to get the anti-inflammatory benefit.

Johnson & Johnson announced an unusual partnership today with Yale University, where he will share the raw data most of its clinical trials. The project of Yale University Open Data Access (aptly nicknamed YODA) will "review requests from investigators and physicians seeking access to anonymous data on clinical trials of Janssen Pharmaceutical Companies of Johnson & Johnson" wrote the company in a press release. YODA The team will then decide that researchers can access the information for their own studies.

The announcement caused a small explosion of new. Forbes wrote that "First, it will only include products division of drugs, but it will be expanded to include devices and consumer products." Janssen Pharmaceuticals extend the range, including pills for acid reflux, schizophrenia, pain, and birth control, among others. the data to share with YODA go well beyond the study design and results, and include de-identified information on each volunteer. YODA is led by Harlan Krumholz, a cardiologist who has long pushed for more access to data in clinical research. (in 2010, Forbes named him "the Doctor stronger you never heard of. ")

Johnson & Johnson, of course, will get to decide what it sends to New Haven, even if it is put into wide release pledge. It's a bit in contrast to a brewing controversy in Europe where drug regulators hope to release the same kind of raw data submitted to it by pharmaceutical companies. This effort has been met with repression and prosecution. But it is part of a broader change in the US and Europe, where some researchers and regulators are increasingly frustrated by the secrecy surrounding many drug trials, and want to get the information outdoors.

It is called the Middle East Respiratory Syndrome, or MERS, after the region where almost all patients have been reported. But the name can prove to be a misnomer. A new study has found the virus in camels from Sudan and Ethiopia, suggesting that Africa, too, hosting the pathogen. This means more MERS can sicken humans than previously thought and perhaps already the most likely to trigger a pandemic.

MERS has sickened 183 people and killed 80, most of them in Saudi Arabia. If a couple have occurred in countries outside the region, such as France and the UK, but these clusters all started with a patient who had traveled to the Middle East before becoming ill.

Scientists have found more evidence implicating camels in the spread of the disease. They found that a large percentage of camels in the Middle East have antibodies against MERS in their blood, while other animals, such as goats and sheep, do not. The researchers also isolated RNA from MERS virus camel nose levies in Qatar, and earlier this week, they showed that the virus was circulating in the camels to Saudi Arabia for at least 2 decades.

Malik Peiris, a researcher in infectious diseases at Hong Kong University, and colleagues have expanded the research in Africa. In an article published last year, they showed that camels in Egypt made antibodies against MERS. For the new study, they took samples from four slaughterhouses around Egypt; Again they found antibodies against MERS in the blood of 48 of 52 camels they were tested. But the most interesting results came from making 110 camels nose samples. They found MERS RNA in four animals that had been shipped from Sudan and Ethiopia

Peiris warns that it is unclear whether the camels infected picked up the virus in Sudan and Ethiopia or their last trip in Egypt. Slaughterhouses could help MERS spread as live poultry markets are for influenza, he said. "You can not point the finger on exactly where these viruses came," he said. "But I would be very surprised if you can not find the virus in large parts of Africa."

If so, it changes the picture considerably MERS. No human cases of MERS were reported from Egypt or elsewhere in Africa, but if camels are infected, they may very well happen, said Marion Koopmans, a researcher of infectious diseases at Erasmus MC in Rotterdam, the Netherlands. "It would be important to examine systematically in this," she wrote in an email. "The health authorities really need to test patients with severe pneumonia throughout Africa for MERS," Peiris said.

the researchers were able to sequence the virus of one of the camels almost completely, and it is more than 99% identical to viruses found in people. "I would be very surprised if this virus can not infect humans," said Christian Drosten, a virologist at the University of Bonn in Germany. But the virus also shows some interesting differences from samples of known camels, he said. "We have to analyze carefully in the coming days, but it seems that this sequence expands the viral directory found in camel," he said. If the virus found in camels show more genetic variation than those isolated from man, who is a strong new evidence that camels infect humans, not the reverse.

Anthony Mounts, the point person for MERS at the World Health Organization in Geneva, Switzerland, said it is very likely that human MERS cases occur in Africa. "Wherever we find [infected] camels, there is a good chance that we will find [human] case if one looks closely," he said. And humans can be exposed to camels in Africa much more often as in the Middle East: There were about 260,000 camels in Saudi Arabia in 2012, but nearly one million in Ethiopia and 4.8 million in Sudan, according to the UN Food and agriculture the UN. human cases are, the more the risk that the virus will one day learn to become easily transmissible among people, which could trigger a pandemic.

the researchers also looked at the blood of 179 people working in slaughterhouses camels for antibodies against the MERS virus, but found none. This shows that the virus is rarely able to infect humans, Peiris said. "what we now know is the result of these rare transmissions."

When an article published on March 17 asked if the fats from fish oils or vegetables are healthier than meat or butter, he quickly made headlines around the world; after all, the study seemed to demystify the cornerstone of many dietary guidelines. But a new version of the publication was to be published shortly after his appearance on the site of Annals of Internal Medicine to correct several errors. And although the first author of the study held by the findings, a number of critical scientific paper and even calling the authors to retract.

"They have done a huge amount of damage," says Walter Willett, chairman of the nutrition department at the Harvard School of Public Health in Boston. "I think the withdrawal to promoting similar release should be considered. "

health officials have long argued that so-called saturated fats, found in butter, meat, chocolate and cheese, increase the risk of heart disease, and that people should instead eat more unsaturated fatty acids, the type that dominates in fish, nuts, and vegetable oils.

in the new study, a meta-analysis, scientists from Europe and the United States together 72 individual studies to assess how different fats influence the risk of heart attack or other cardiac events such as angina. These included trials in which participants were assigned randomly to different diets, as well as observational studies in which the consumption of fatty acids of participants was determined by asking them about their diet or measuring fatty acids circulating in the blood.

When the researchers compared those with the highest and the lowest saturated fat intake, they found no significant difference between the risk of heart disease or other cardiac events. Similarly, they found no significant difference between those who consume high or low amounts of supposedly healthy unsaturated fats. "Current data do not clearly taking guidelines that encourage high consumption of polyunsaturated fats and low intake of saturated total fat," the authors conclude.

But even before the document was published , other scientists began to report the errors, said first author Rajiv Chowdhury, an epidemiologist at the University of Cambridge in the UK. for example, the authors took a study on omega-3 fats, a type of unsaturated fats, to show a slightly negative effect, while in fact he showed a strong positive effect. the correction means that the meta-analysis now shows the people who report eating a lot of this particular fat have much less heart disease ; previously, he said there was no significant effect

critics have also pointed out two major studies on omega-6 fatty acids that the authors missed.. Errors "demonstrate research of poor quality and are wondering if there is more that has not been detected," wrote Jim Mann, a researcher at the University of Otago, Dunedin, New Zealand, writes in an e-mail. "had I been the referee I would have recommended rejection."

Mann and others say the paper has other problems, too. for example, it does not deal that people who reduced their consumption of saturated fats consumed instead. a 09 study concluded that replacing saturated fats with carbohydrates was no benefit, while replacing them with polyunsaturated fatty acids reduced the risk of heart disease. Many scientists say that should have been mentioned in the new document.

Chowdhury said the conclusions of the paper are valid, however, even after the corrections. randomized clinical trials are the "hard "such evidence, he says, and they do not show a significant effect of saturated and unsaturated fats. But even one of the authors of the article, Dariush Mozaffarian of Harvard School of Public Health, admits he is not happy with the main conclusion that the evidence does not benefit from polyunsaturated fats. "Personally, I think the results suggest that fish and vegetable oils should be encouraged," he said. But the document was drafted by a group of authors, he says. "And science is not a dictatorship . "

another study author, Emanuele Di Angelantonio from the University of Cambridge, said the main problem is that the paper was" misinterpreted by the media. "" We are not saying the guidelines are false and people can eat as much saturated fat as they want. We say that there is no strong support for the guidelines and we need more good tests. "

Willett said the correct paper is not enough." It is good that they set the record, but it has caused massive confusion and the public has not heard about the correction. "the paper should be removed, he said.

the controversy should serve as warning about the meta-analyzes, Willett says. These studies compile data from many individual studies to get a clear result. "it looks like a summary of scanning all the data it receives much attention," says Willett. "But these days meta-analyzes are often made by people who are not familiar with the field, who do not have primary data or do not make the effort to get it." And while the drug trials are often very similar in design, making it easy to combine their results, nutritional studies vary greatly in how they are implemented. "Often the strengths and weaknesses of the individual studies are lost," says Willett. "He is dangerous."

After taking an antibiotic or catching an intestinal bug, many of our belts down probiotic drinks restore the "natural balance" of bodies in the intestines. Probiotics are one of the food industry's most dynamic products now added to yoghurts, drinks and baby food. Still, not everyone needs to stay healthy. A new study of the gut bacteria of hunter-gatherers in Africa found that they completely lack a bacterium that is a key ingredient in most probiotics and considered healthy food. In addition, the Hadza are not suffering from colon cancer, colitis, Crohn's disease, or other diseases of the colon that are found in humans eating modern diets in western countries.

The new study is the first to report on the gut bacteria of hunter-gatherers who hunt and forage for most of their food, just as our ancestors did before invention of agriculture 10,000 years ago. So far, studies on intestinal bacteria have focused on people living in industrialized countries, many eat diets rich in sugar, salt and fat. These regimes have changed the type of bacteria in our guts, known as the microbiome. Gut bacteria react quickly to changes in the diet of their hosts, and humans who live in rural areas and eating less processed foods have more diverse microbiomes. Conversely, the researchers also found an association between less diversity in the microbiome and disease of the colon, such as Crohn's disease and colon cancer.

In the new study, an international team worked together to collect and analyze bacteria in stool samples from one of the last hunter-gatherers of the remaining communities in the world, the Hadza of Tanzania. As part of his thesis project, Stephanie Schnorr, a graduate student at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, had the unenviable task of asking the Hadza for fecal samples. But when the interpreter explained what she wanted, she got lucky when one elder, named Panda, said: "We normally give ground. We will give him instead. "

Once Schnorr had samples of 27 Hadza, aged 8 to 70, she sent them in frozen or dried at the University of Bologna in Italy, where a specialized team and extraction sequencing the DNA of bacteria. the team identified the bacteria using the DNA of the Hadza and also analyzed the type of nutrients in feces, including microbial metabolites, which are fatty acids that microbes use in the gut to get their energy. when they compared the DNA from the Hadza with those of the Italians, the team found that the Hadza have an intestinal ecosystem more diverse microbe. in addition, when they also examined these bacteria in two groups of farmers in Africa, they found that the Hadza were the only people who did not have a type of bacteria commonly added to probiotic drinks known as Bifidobacterium - Perhaps because it is associated with dairy products, the Hadza do not consume. The Hadza also had high levels of bacteria as Treponema , which is considered a sign of disease in Western populations because different types are associated with systemic lupus and periodontitis, and the syphilis. Yet Hadza experience almost no autoimmune diseases, obesity or diabetes, which are associated with imbalances in the various types of intestinal bacteria.

"We must redefine our notions of what is considered healthy and unhealthy, since these distinctions are clearly addicted to food," says Alyssa Crittenden, nutritional anthropologist at the University of Nevada, Las Vegas, and lead author of the study, which appears online today in Nature Communications .

other surprise is that Hadza men and women had significant differences in the type and amount of intestinal bacteria a sex difference ever observed before. the disparity reflects the sexual division of male Hadza hunting work and eat meat and honey, while women primarily dig tuberous plants. both sexes eat more what they see, and women eat more fibrous tubers. "We think that bacteria women are particularly good at digesting fiber," said Amanda Henry palaeobiologist of Max Planck. The team is currently testing the Hadza intestinal bacteria in laboratory studies to see if they are more efficient to break the fiber that Westerners of gut bacteria.

Other researchers also note that previous studies suggested that humans had less diversity in their gut microbiome on average than other primates. But this may be partly because researchers have not collected stool samples of human subjects eating different diets and living in a wide range of habitats. "This is a really important study because it helps us to find the range of variation in the microbiome in humans," says Steven Leigh biological anthropologist at the University of Colorado, Boulder.

This information will help researchers understand how our ancestors adapted to new habitats and diets that spread around the world because their intestinal bacteria co-evolved with them as their diet has changed. and it can be essential to understand that the spectrum diversity and how different species of bacteria interact with each other (and, perhaps, resist antibiotics) before consuming probiotic products on an "industrial scale", as if a single type, Leigh said.

Every day our cells produce small amounts of a molecule which, in higher doses, could be the key to lead a longer and healthier life. A team of researchers has discovered that this molecule increases the lifespan of worms over 50%, raising the possibility that it will increase human longevity.

"I think the data is really compelling," says molecular geneticist William Mair of the Harvard School of Public Health in Boston. "They have a strong effect of lifetime use the [compound]."

The way a long life does not lead through the kitchen. Researchers have known for decades that when animals eat considerably less than undergo what is known as caloric restriction or dietary restriction they live longer and delay or prevent age-related problems such as cardiovascular disease and diabetes. But if you intend to try at home, there are a few catches. On the one hand, scientists have not confirmed the benefits of calorie restriction in primates, including humans. While eating less helps monkeys age, it is difficult to know whether calorie restriction increases their lifespan. And survive on far fewer calories is no picnic. "The problem is that this requirement is so strict that almost no one can do it," says Jing Huang of the University of California, Los Angeles.

Therefore, the researchers tested other ways to slow aging and prolong life, such as resveratrol grape extract and immunosuppressive drug rapamycin. Although both have shown promise in experimental animals rapamycin increases the life of middle-aged mice-they've disadvantages also represented. Rapamycin, e.g., blends sugar metabolism and can lead to diabetes. Huang and his colleagues concluded that because aging depends on the metabolism, the compounds produced in the cells by metabolic reactions known as metabolites, may also increase the lifetime.

The researchers tested their idea on nematodes, worms long millimeter commonly used in longevity studies. They hit the jackpot with the first molecule they tried, α-ketoglutarate (α-KG), an intermediate in a metabolic cycle that helps a cell extract energy from food. When the researchers added the compound to the culture dishes worms, the animals survived up to 70% longer than normal, the team announced today online Nature . Animals transported about 50% of α-KG in their cells than to witnesses. As caloric restriction, the α-KG supplement postponed the physical deterioration of worms.

To understand how α-KG works, Huang and his colleagues used a technique they developed that identifies proteins in human cells that interacts with a-KG. The results showed that the compound binds to the ATP synthase, an enzyme that makes ATP, main carrier molecule of the cell's energy. ATP synthase lies in the power generation structures called mitochondria. By studying the mitochondria of cow heart cells, the researchers found that the α-KG blocks ATP synthase, turning down the metabolism of the cell.

When the researchers tracked more cellular effects of α-KG, they discovered that indirectly inhibits a protein called TOR which measures the supply of nutrients and scientists suspect, to determine how speed we age. Alpha-KG "can be an inner fountain of youth, if you like, which can be adjusted to counteract aging," says Huang. Caloric restriction causes side effects in animals such as reduced reproduction, but researchers not see these problems in the worms that ate α-KG.

mitochondrial biochemist Michael Ristow of the Swiss federal Institute of technology in Zurich said that the molecular mechanism of this effect took him by surprise. He noted that d other studies have shown that calorie restriction increases the synthesis of ATP by making more efficient mitochondria, so you had predicted that α-KG would do the same. "that's what makes it interesting," he said. "It is unexpected."

Dietary supplements that contain α-KG and supposedly strengthen the muscles are already on the market. The study drops a barbell on their use, however, suggesting that α-KG inhibits TOR, thus counteracting muscle growth. "If people take this as a muscle builder, one might think that this does not cause the desired effect," says Mair.

There is no guarantee that α-KG will have the same effects on aging in people that's in worms. and before researchers can not even answer that question, they will need to determine if the compound also extends the life of laboratory organisms such as flies and mice. However, Mair said, researchers have long hoped to identify small molecules that slow human aging and the study "is the next step towards this goal."

an opinion column in the edition today of New York Times addresses a long tension in the world of clinical trial: the reluctance to include older individuals, even if they 're most of the population to take medication. bar regularly tests the elderly in their ranks, in part because researchers and regulators fear that medication older you are, the more likely you are to have complicated health conditions that are testing new drugs more difficult. The opinion cites an article in The Journal of the American Medical Association in 07, which revealed that nearly 40% of trials in big name magazines between 1994 and 06 excluded over 65

It is time to change the system, say the authors. "Older Americans are our patients, too. We can not leave them out," write doctor Donna Zulman and psychologist Keith Humphreys, working at Stanford University School of Medicine in California, and the health care system for veterans . Extrapolating the results of young people to older is risky, because biology is moving with age. Moreover, "old age is not a reliable proxy for poor health," Humphreys Zulman and support. Researchers can even exclude voluntary test if they have certain conditions, but health "not only on their age."

university pushed a cautious sigh of relief when the European Medicines Agency (EMA) announced yesterday that he would soften project controversial rules to open the clinical trial data to public scrutiny. In particular, the agency said it will allow researchers "to download, save and print the test data for academic research purposes and not commercial." A previous plan would have allowed only to view the data on their computer screens.

last month, researchers and the European Ombudsman criticized the proposed agency policy for data sharing as too restrictive and impractical. Today, they welcomed the announced changes, but sounded a note of caution, like other controversial elements are likely to remain in the final text.

"This is a good thing. It means the researchers will be able to review, compare and share information on clinical trials. To allow researchers access to information on clinical trials on the screen only have obstructed their work, "said Síle Lane, director of campaigns in the UK pressure group Sense about science, in a statement today.

But in an email sent to science Insider today, European Ombudsman Emily O'Reilly said she did not know if the agency responded to its remaining concerns and "consider carefully" the final text. The draft rules "imposed broad legal requirements" on data access and use, and a "limited only authorized access to clinical trial data by expunge important information," says O'Reilly.

"The Ombudsman remains puzzled as to why EMA has abandoned its original policy the Disclosure Project in 2012 and replaced by a different political project, more in line with industry wishes pharmaceutical, "his email statement added.

spokesman EMA Martin Harvey-Allchurch said the policy stems from a long consultation process." We listened and we tried to come what we think is a viable solution, "he said. the final text should be adopted in mid-July, before the new rules are implemented in October.

An effort at the US National Institutes of Health (NIH) to diagnose mysterious ailments is expanding. Representatives of the Undiagnosed Diseases Program (UDP), administered by the Institute (NHGRI) of the NIH National Human Genome Research, announced today that six medical centers will join the program, the formation of a network of clinical sites to investigate on refractory cases of patients across the country. The program aims to provide patients with a diagnosis and treatment as sometimes waited while building data for scientists studying the genetic basis of rare diseases

The new sites-Baylor College of Medicine. Harvard teaching hospitals (Boston children, of Brigham and Women, and the Massachusetts General); Duke University; Stanford University; the University of California, Los Angeles; and the Centre will Vanderbilt University Medical each receive a 4-year grant of approximately $ 7.2 million to participate. As the NIH Clinical Center in Bethesda, Maryland, who served as a pilot site, the centers host the patients for about a week at a time, performing many clinical tests and genetic sequencing to search for an explanation of their symptoms.

Harvard Medical School in Boston, who received an award of $ 9 million in January to act as a "focal point" facilitate collaboration between researchers and will make the data widely available to patients through public deposits such as the NIH database of genotypes and phenotypes, said Anastasia Wise, director of the genomic medicine NHGRI Division, at a press conference today .

since the program launched in May 08, he received requests for about 30 patients, 750 who were selected for the study. "There was never a shortage of references to the program," said UDP Director William Gahl today. (Indeed, in 2011, the program temporarily stopped accepting applications to catch the flood of inquiries.) The roadmap program for medical sleuthing depends on how you define a diagnosis, Gahl said. Between 25% and 50% of cases are considered "solved" based on clinical diagnosis, molecular, biochemical or so about a quarter are closed without reply. "You can see that this is hard work, in which we fail sometimes," he added.

The program now admits about 150 patients a year at the NIH Clinical Center, but plans to host 50 per year to each of the seven sites by summer 2017.

Behind the epidemic without previous Ebola in West Africa is a species with an incredible power to exceed its host. Zaire ebolavirus and the filovirus family to which it belongs must virulence mechanisms that first disarm the immune response and then dismantle the vascular system. The virus progresses so rapidly that researchers are struggling to unravel the precise sequence of events, especially in the midst of an epidemic. Much is still unknown, including the role of some of the seven proteins that the virus RNA, AOS is diverting the machinery of host cells and the type of immune response needed to defeat the virus before it spreads throughout the body. But researchers can test how different live virus attacks cells in culture and can observe the progression of disease, AOS in primates, AIA nonhuman model almost identical to humans.

Here are some basic things that we understand how Ebola and humans interact.

What do the Ebola virus for the immune system?

Once the virus enters the body, it has several types of immune cells that are the first line of defense against invasion. The virus infects dendritic cells, which normally have signals of an infection on their surfaces to activate lymphocytes, Äîthe T white blood cells that can destroy other infected cells before the virus replicates further. With defective dendritic cells not giving the right signal, the T cell donation, AOT respond to infection, and do the antibodies that depend on them for activation. The virus can begin replicating immediately and very quickly.

Ebola, like many viruses, works in part by inhibiting molecule type interferon, AIA that cells use to prevent further viral reproduction. In a new study published today in Cell Host & Microbe , the researchers found that one of the Ebola protein, AOS, called VP24 binds to and blocks a transport protein on the surface of immune cells that plays an important role in the pathway of interferon.

Curiously, themselves donation lymphocytes, AOT be infected, but a series of other lack factoring, AIA stimulation of certain cells and toxic to others signals Äîprevent these primary immune cells to a fight.

How Ebola cause of bleeding?

As the virus moves into the bloodstream to new sites, other immune cells called macrophages eat up. Once infected, they release proteins that trigger the coagulation, forming small clots through the blood vessels and reducing blood supply to the organs. They also produce other inflammatory signaling proteins and nitric oxide, which damage the wall of blood vessels, causing a leak. Although this damage is one of the main symptoms of infection, all patients will exhibit hemorrhaging, external Äîbleeding eyes, nose or other orifices.

Does the target of some of the organs virus?

Ebola triggers inflammation and system fever and can also damage many types of tissue in the body, either by tricking the immune cells such as macrophages to release inflammatory molecules or by direct injury : invade cells and consume in. But the consequences are particularly deep in the liver, where Ebola erases cells necessary to produce coagulation proteins and other important components of plasma. Damaged cells in the gastrointestinal tract lead to diarrhea which often puts patients at risk of dehydration. And in the adrenal gland, the virus paralyzes the cells that make steroids to regulate blood pressure and causes circulatory failure that can starve the oxygen of organs.

What finally kills Ebola patients?

damage to the blood vessels leads to a drop in blood pressure, and patients die of shock and multiple organ failure.

Why do some people survive infection?

patients fare better with supportive care, including rehydration orally or intravenously that can buy time for the body to fight infection. But studies on blood samples from patients during the outbreak in 00 of a different Ebola strain in Uganda have also identified genes and other markers that seem to be a predictor of survival. Patients who have recovered higher levels of activated T cells in the blood, and there was some variants of a gene coding for surface proteins as white blood cells use to communicate. Earlier this year, researchers found a new association between survival and levels of sCD40L, a protein produced by platelets that could form part of the body attempt, AOS to repair damaged blood vessels. The authors note that the markers as sCD40L could suggest new therapies that increase the most important mechanisms for the repair of survival

* Correction, August 15, 1:51 p.m. :. This article has been corrected to note that nitric oxide, nitrous oxide does, damages blood vessels

* Ebola files :. Given the current Ebola epidemic, unprecedented in terms of the number of people killed and the rapid geographic spread, science and Science Translational Medicine made a collection of research articles and news on the viral disease available for researchers and the general public.

When President Barack Obama spoke about the US military helping fight the Ebola epidemic on Meet the Press NBC News this past Sunday, Tim Flanigan, an American clinician working in Monrovia, said he was "ecstatic". It was exactly what most people who run the Ebola efforts in Liberia, the hardest hit country, had hoped. But joy turned to dismay the next day when Flanigan has learned the details of the Pentagon's plans.

Obama promised "to get military US assets just to set up, for example, isolation units and equipment there to ensure security for the public health workers outbreak everywhere. "on Monday, a representative of the Pentagon said the army planned to send only field hospital with 25 beds for $ 22 million in Monrovia, Liberia's capital." He will not make a dent in the treatment of Ebola for the people of Liberia, "Flanigan warns." It is such a small number of beds and they can thus be directed to non-Liberians. "

Flanigan, who works at Brown University 1999-2012 and headed the Division of Infectious Diseases, he arrived in Monrovia on September 1 and plans to stay for two months. A Catholic deacon, he also works with faith-based groups focused on health and blogging about his experience.

Flanigan said Liberia and officials and international workers, he spoke with the US military had planned to set up field hospitals that have the ability to help up to 400 people. there is a great shortage of beds for patients with Ebola in the nation, and standard care is the same shortage for people who are admitted to what is called Ebola treatment units. News that just one small facility would come was disheartening, he said, given the expectations.

"the US military has the capacity and know -How and training and infectious disease experts are incomparable to come and establish an Ebola treatment unit that would be able to take care of a large number of patients, "he insists.

for the US military, it is "a top priority" for the "deployable field hospital" in Monrovia and "we expect to get there quickly," wrote Navy Cmdr. Amy Derrick-Frost, a spokesman for the US Department of Defense (DOD), in an e-mail to Science Insider. The Army is also working with partner agencies, including centers for the US Agency for International Development- Disease Control and "to assess the situation in affected areas to determine what other needs and necessary or required resources "Derrick-Frost wrote.

A deployable field hospital can be moved on pallets by air and quickly implemented, which plans to do before replacing the Liberian government DOD. "The purpose of this piece of equipment is to provide an installation that health workers in the affected area can use for themselves if they become sick or injured," writes Derrick-Frost.

Flanigan said a US military stronger response could help solve another problem coming the health care system badly fractured Liberia can not answer. There is a pressure to treat patients Ebola with the blood of people who survive disease and perhaps give people infected untested medicines, as well as a separate effort that can offer experimental Ebola vaccine to health workers and other first responders. But hospitals and clinics are not not currently the ability to collect blood samples and tissue necessary to study the impact of these interventions, Flanigan said. "we will not learn what we desperately need to know about the treatment and prevention of this disease" he said. "It is not in the best interest of the Liberian people, West Africa, or the Americans."

* Ebola files: Given the current Ebola epidemic, unprecedented in terms of the number of people killed and rapid geographic spread, science and science Translational Medicine made a collection of research articles and news on the viral disease available for researchers and the general public.

Marc September 16, 2014 as the day the United States declared all-out war on the Ebola epidemic raging in West Africa.

As President Barack Obama said in remarks he made today to the US Centers for Disease Control and Prevention (CDC) in Atlanta, the world is looking to the US for 'help. "It is a responsibility that we embrace," said Obama. "We are ready to take leadership on this to provide the kinds of capabilities that only America has, and mobilize the world so that only America can do. this is what we are doing as we speak. "

at the same time, Obama spoke in Atlanta, the uS Senate held an Ebola audience who presented the testimony of senior officials of public health and can -being the most famous survivor of the world Ebola, Kent Brantly, who fell ill with the disease while treating patients in Liberia in July. "We must take the dangerous threat of deadly Ebola outbreak as seriously as we take ISIS [Islamic State in Iraq and Syria]," said Senator Lamar Alexander (R-TN).

The centerpiece of what Obama called "a significant increase in our response" is in fact the US military, which in cooperation with the Liberian government will put up a command center in Monrovia run by US army Maj. Gen. Darryl Williams. As explained by Obama, the army will set up a command and control, logistics and engineering support for civil society organizations working in the region. "Our armed services are better that any organization on Earth," Obama said.

The US response will focus on providing beds for patients who Ebola are almost non-existent in Liberia-isolation areas to keep people when Ebola treatment units not to space, more trained health care workers, an airlift to move people and equipment in West Africa faster, and kits to help families with infected people in the house at the time of care for a sick person and protect themselves against infection. "We can not dawdle on this one," said Obama, who urged global communities to dramatically step response, too. "International organizations just have to go faster than they up to this point. "(this fact sheet explains the details of the response of the United States overhauled.)

in the 3-hour-long Senate hearing-which, an unusual move, was organized jointly by a subcommittee of the appropriations and the health Committee, education, labor and pensions, topics ranged from financing the efforts of the need for a greater sense of urgency, health public and scientists, and personal experiences issues. Beth Bell, who heads CDC's National Center for emerging and zoonotic infectious diseases, described the epidemic in Liberia, Sierra Leone and Guinea as "fierce and spread exponential, "so severely crippling the health care systems in some places that malaria can not be treated and infants can be safely delivered.

report the current situation of the World Health Organization estimated that there were nearly 5,000 cases, almost half of them died, but Bell said CDC estimates that "the actual numbers would be two to three times higher." She pointed out that we have the tools to end this epidemic, but the window of opportunity closes. "If we do not react now to stop the Ebola virus we could be dealing with it for years to come affect larger areas of Africa," she said.

The senators asked repeatedly Anthony Fauci, director of the US National Institute of allergy and infectious diseases, if the Ebola virus could mutate into a more dangerous form and even spread in the air. "We see that carefully," Fauci said. He explained that, as all the RNA viruses, one that causes Ebola made many mistakes when it copies itself, but most of these mutations do nothing. "It is an unusual situation where a mutation will completely change the way a virus spreads," said Fauci, stressing that it was impossible, but very unlikely. "What is likely is that if we do not do what we do now, in the direction of a main ramp of infection control capacity, including what we mean to get heavily involved in all military things they bring to the table ... it will get worse, "Fauci said. "A virus does not replicate can not mutate."

The Ministry of Defense of the United States hopes to reschedule $ 500 million to Ebola efforts. The Obama administration has asked Congress to pass a continuing resolution that will give $ 30 million dollars more to the CDC for use until 11 December, and $ 58 million to the Department of Health and Human Services to support the development of experimental vaccines and treatments. The continuing resolution passed the House of Representatives, and Senator Tom Harkin (D-IA), who chaired the hearing of the Joint Committee, said he hopes the Senate to pass the "the next day or two." But Harkin and others stressed that more money will be needed for the budget for year 2015. "I hate to say this, but Ebola will not be defeated within 10 weeks of the continuing resolution."

Harkin and other senators were surprised by the lack of a clear leader for American global effort against Ebola. "I'm a little surprised to see that," said Harkin. Senator Barbara Mikulski (D-MD) said this was a matter that the Senate should take with Obama. "We need someone points," said Mikulski. "If we wanted to meet on responsible person who would on person in charge?"

The hearing ended with testimony and questions Brantly, an American physician with Samaritan's purse was airlifted to Monrovia to Atlanta for care state-of-the-art and is well today. Brantly, who met Obama in the Oval Office this morning, spoke of the many people he treated who have died of Ebola virus and the urgent need for other countries health workers to go help in Africa Where is.

"Many, including one of the senators today, used the analogy of a fire out of control to describe this epidemic of unprecedented Ebola," said Brantly. "Indeed, there is a fire. It is a straight line to the fire pit of hell. We can not deceive us into thinking that the great moat from the Atlantic Ocean to protect us against the flames of this fire. instead, we must act quickly and immediately to deliver the promises that were made and to be open to innovative practices interventions. this is the only way to keep whole nations to be reduced to ashes "

* Ebola files :. Given the current Ebola epidemic, unprecedented in terms of the number of people killed and the rapid geographic spread, science and Science Translational Medicine made a collection of research articles and news on the viral disease available for researchers and the general public.