Health Meaning

Billions of dollars have been spent on clinical trials for Alzheimer's drugs that target amyloid plaques, tangles of proteins that clog stamp brain cells in people with the memory-stealing disease. So far, all have failed, leading some frustrated researchers say it is time to move on to other drug targets. Others say that the drugs are not tested enough because they were administered too late, after brain damage is irreversible. Yesterday, the National Institutes of Health (NIH) announced that it gave $ 33 million to a study that researchers hope or reliving the amyloid hypothesis, or to bed

The new cost-trial is estimated to be at least $ 100 million overall, with most of the remaining funds provided by partners in the pharmaceutical industry will be part of the Prevention Initiative Alzheimer's disease, a large consortium of researchers trying to identify biomarkers and treatments that can slow or stop the disease. The lead researchers Eric Reiman and Pierre Tariot Institute Banner Alzheimer Phoenix plan to provide a drug that is yet to be identified anti-amyloid, or a placebo, 650 people who carry two copies of APOE4 general a double whammy gene that confers increased 10 risk factor for developing late Alzheimer's disease in life. All participants will be aged between 60 and 75 and in good health, including recognized Alzheimer's symptoms. About a third probably will not be much amyloid in their brains again, allowing researchers to track whether the drug affects its accumulation, Reiman said.

The Banner trial "is a very reasonable approach" to determine whether anti-beta amyloid drugs can effectively prevent Alzheimer's disease, said Gary Landreth, a neurologist who studies the disease at Case Western Reserve University in Cleveland, Ohio. He notes, however, that it is quite unusual that the drug be used has not yet been identified, given the size of the grant. since no anti-amyloid / drugs Alzheimer yet shown any clinical efficacy, "I think it really reflects the state of despair felt in the scientific community and the public that we have no effective therapeutic in the face of an epidemic over AD, "he said." They take a gamble. "

The APOE4 test is based on another test of an anti drug -amyloid in 300 members of a Colombian family who carry a mutation of the gene that puts them at high risk of developing a form of early onset Alzheimer's disease. Rather than wait for the results of this study, Reiman said he and his colleagues decided to conduct two trials simultaneously to ensure that the positive results of the Colombian study can be rapidly tested in a representative population-drugs working for those early-onset Alzheimer's may not necessarily help people with late-onset Alzheimer's, he said.

Maria Carrillo, vice president of medical and scientific relations for the Alzheimer's Association, an advocacy group, applauded NIH to give the green light Trial: Targeting APOE4 people will "increase the possibility that the trial participants become symptomatic during the period of the study so that the scientists can assess whether the intervention of the drug is having an impact on delaying or preventing Alzheimer's disease symptoms without having to wait 10 or 15 years or more, "she said.

the US government has placed a high priority on the fight against Alzheimer's disease, which is expected to hit 10 million Americans in 2050, according to the US Department of Health and Human Services (HHS). The Act on the draft 2011 National Alzheimer's, for example, demanded that HHS develop a national plan to prevent or effectively treat Alzheimer's disease in 2025. The new APOE study will use to share the lion of the $ 45 million that Francis Collins, NIH director, has set aside for Alzheimer's research during fiscal 2013. (total of $ 45 million includes a contribution of $ 5 million of the Institute National on aging [NIA]). According to Neil Buckholtz, director of the NIA Division of Neuroscience, the investment reflects a move towards trying to prevent the disease before it ravages the brain, rather than reverse its effects, and a commitment to test the hypothesis that amyloid correctly . "We believe that this has not been sufficiently tested," he said. He acknowledged, however, that putting so many dollars of research into one basket is a strategy "high risk"

NIH also announced funding for five additional grants to Alzheimer's research, with a sixth reward waiting :.

• $ 1,5 M test test three new anti-amyloid treatments of gantenerumab-beta drugs, solanezumab, and a third drug in indefinite volunteers with an inherited form of early onset Alzheimer's disease. Directed by Randall Bateman from the University of Washington St. Louis, international trial has the potential to earn $ 6 million in funding over 4 years.

• Phase A $ 2.4 million, 12 weeks 1 test test safety and tolerability of allopregnanolone steroids for the treatment of mild cognitive impairment and Alzheimer's disease, led by Roberta Brinton and Lon Schneider of the University of Southern California in Los Angeles. Animal studies have shown that the drug can lower amyloid levels, restore cognitive function, and stimulate the production of new neurons.

• A $ 1.7 million drug discovery effort to identify genetic and molecular risk factors and new therapeutic target for cognitive decline and Alzheimer's disease, on the religious study database Order and memory and aging Project Rush. Led by Philip De Jager Brigham and Women's Hospital, Broad Institute and Harvard University, and David Bennett of the Rush University Medical Center in Chicago, the study will focus on drugs that have completed Phase 1 trials , and may be granted $ 7.9 million over 5 years.

• A $ 1.6 million effort to study the complex mechanisms of the disease and to identify existing drugs that might be able to be used for treatment or prevention of Alzheimer's disease, led by Eric Schadt of Mount Sinai School of Medicine in New York. The study has the potential to be granted $ 8.2 million over 5 years.

• A $ 1.6 million study of the role of the immune system and inflammation of the brain in Alzheimer's disease directed by Todd Golde of the University of Florida in Gainesville. The study has the potential to be granted $ 7.7 million over 5 years.

The spinal cord is the nerve of highway that connects the brain to the body. A car accident or a bad fall can partially or completely sever the spinal cord and paralyze the person below the injury site. In the US, more than 10,000 people are injured spinal cord each year, but the treatment of these lesions is mainly based on intensive rehabilitation usually providing modest improvements. Many experimental therapies are being tested on animals and in some patients in Phase I clinical trials. These include stem cell transplantation, the administration of growth factors or antibodies directed against growth inhibitors, electrostimulation of the injury site of the spinal cord and deep brain stimulation of brain centers controlling the movement. None of these experimental treatments have been approved for the treatment of patients with spinal cord injury, and many questions remain unanswered. Where and how should be delivered treatments? If the combinations of these treatments are used in conjunction with an extensive refurbishment? And how soon will these therapies available in the clinic?

Please join Science Translational Medicine and special guests neurosurgeon Michael Fehlings, president of neural repair and regeneration at University Health Network in Toronto, Canada, and researcher Martin Schwab co-director of the Brain Research Institute at the University of Zurich in Switzerland, Thursday, October 24, at 15 pm EDT on this page for our first live video chat. We will discuss the many barriers to treatment for spinal cord and take your questions, so please be sure to let your requests for our customers in the comment box below.

The first new drug in half a century to target malaria parasites in one of their best hiding showing encouraging results. Researchers in drug development, called tafenoquine, said today that data from a recently completed phase II trial were promising enough that they will soon begin a III-final stage Phase before seeking drug regulatory approval.

tafenoquine kills the malaria parasite when it hides in the liver cells, in a form called hypnozoite, or "dormant parasite." hypnozoites not cause any symptoms and are impossible to detect by blood tests. But when it is triggered by signals that are not fully understood, they can reactivate to cause another bout of malaria, which can then be picked up by mosquitoes and transmitted to new victims. Five species of Plasmodium can cause malaria in humans. Two of them- Plasmodium vivax , which is widespread, and relatively rare P -Can hypnozoites oval shape. This ability to hide is one of the things that makes P. vivax so hard to eliminate a region.

Now, the only treatment that can cure malaria parasites hiding vivax and everything is within 14 days of a drug called primaquine, which was developed in the 1940s works well enough, but it is difficult for people who do not feel ill to complete 2 full weeks. "Compliance with the current regime is really a problem," said JP Kleim, director of clinical development for the pharmaceutical company GlaxoSmithKline (GSK). "The acute malaria disappeared after a few days [of treatment]," so motivation patients continue to take medication is low. that is why GSK has decided to develop tafenoquine and the medicines for Malaria Venture, a nonprofit based in Geneva. the partners launched a lawsuit in 2011 to test whether a single dose of tafenoquine might work as well as the 2-week course of primaquine.

the data, presented today at the American Society of Tropical Medicine and Hygiene annual Meeting in Washington, DC, suggest that a single dose works fine. the trial involved 329 patients in Brazil, India, Thailand and Peru. in patients who received either 300 mg or 0 mg dose of the drug, 0% had no relapses after 4 month. The partners will now move forward with a Phase III trial testing the safety and efficacy of 300 mg in 0 patients, said Marcus Lacerda of Fundação de Medicina Tropical Dr. Heitor Vieira Dourado in Manaus, Brazil, who helped coordinate the study and presented the results at the meeting today.

a single-dose drug would be a huge advantage in the fight against vivax malaria, said Ric Price from the Menzies School of Health Research in Darwin, Australia, and the University of Oxford UK. "One of the biggest challenges we face is how do we deal adequately and reliably hypnozoite stage."

While the world mourns the passing of Nelson Mandela some observers are mindful of the crucial role he played in promoting science at the heavy AIDS crisis in South Africa. protected and Mandela's successor as president of South Africa Thabo Mbeki rejected the scientific consensus and married the discredited view that HIV does not cause AIDS, popularized by the University of California, Berkeley, biologist molecular Peter Duesberg. Mbeki's refusal to bring government resources to bear against the disease is responsible for 300,000 unnecessary deaths, the researchers estimated.

In first public break with Mandela's African National Congress, which he had belonged to and taken over a period of 65 years, in 01, he denounced Mbeki's failure to fight against the epidemic . "We must not continue to debate, argue, when people die," Mandela said, reports Stephanie Nolen The Globe and Mail , which was based in South Africa from 03 to 08. D ' Meanwhile, a revered veteran, Mandela has the immense power of his moral authority to the need to change the policies of his country.

Mandela, however, "were late" in the fight against the disease, according to The Globe and Mail . During his presidency, he has relatively little attention to the epidemic growing rapidly and has supported Mbeki to deal with it. This approach allowed the infection to spread. Mandela was to give priority to even the most critical issues in the first crucial days of the establishment of non-racial democracy in the country long troubled his supporters argue.

When Mandela came out on the side to accept and act with vigor science, however, it has become a powerful and effective advocate, help reverse the trend of opinion and politics in his own country and elsewhere. In 05, Nolen reports, Mandela struck a blow against the huge social stigma of the disease in South Africa by announcing that his own son, Makgatho, "died of AIDS", as did the woman Makgatho . "Let us give publicity to HIV-AIDS and not hide it, because the only way to make it appear like a normal illness like TB, like cancer, is always to come out and say that someone died because of HIV. And people will stop regarding it as something extraordinary, "Mandela said at the funeral of Makgatho.

The life of Mandela showed the value of forgiveness and reconciliation in human affairs, but also the importance of political leadership in embracing and acting on the best science.

staph infections represent one of the most serious microbial threats to people. Yet efforts to prevent with vaccines have always failed, even though the bacteria responsible is becoming increasingly resistant to antibiotics. Now, an experimental vaccine with new ingredients was very protective in rabbits against staphylococcal pneumonia, one of the most dangerous results from bacterial infection. The inventor hopes to take human studies soon.

Staphylococcus aureus is thought to colonize the nose of about one third of the human being at some point, but it also causes about half a million hospitalizations and 20,000 deaths each year in the United States. The strains of the bacteria that are resistant to most antibiotics, particularly MRSA doubled varieties (methicillin-resistant S. Aureus ), have become a major threat, emphasizing the need for a vaccine against the microbe.

However, a series of vaccines has undergone dramatic failures in recent years. A candidate of Nabi Biopharmaceuticals of Rockville, Maryland, flopped in two trials in dialysis patients in the United States, and a Merck vaccine was abandoned in 2012 after millions of dollars were spent testing.

microbiologist Patrick Schlievert of the University of Iowa in Iowa City believes that pharmaceutical companies were under way on a vaccine against the wrong direction. Previous staphylococcal vaccines have attempted to provide protection including protein or carbohydrates in the natural capsule that surrounds the cell wall of the bacterium staphylococcus and allows it to evade the immune system. This approach was successful for vaccines against other bacteria as Haemophilus influenzae type B and Streptococcus pneumoniae , but did not work with S. aureus. Other vaccines that failed included simple proteins from the cell wall of S. aureus bacteria.

In an article published online this month The Journal of Infectious Diseases, Schlievert and colleagues took a new approach. The strategy involves an entirely different class of substances extracted from S. aureus bacteria. These included so-called superantigens and cytolysins proteins that are produced by S. aureus internal structures and play a major role in diseases caused by bacteria. Researchers vaccinated 88 rabbits, divided into several groups with different combinations of these substances. All but two of the animals survived when S. aureus bodies were sprayed into their lungs. 88 unvaccinated rabbits exposed to the same bacteria, only one survived.

In another experiment, the researchers found evidence that typical vaccines can actually make those immunized more vulnerable to a staph infection. They vaccinated five rabbits neutralized with proteins from the cell surface S. aureus -the type of substances used in most previous and current candidate vaccines. All five of these animals died within 6 hours of exposure to a common MRSA strain; however, five non-vaccinated animals survived at least 4 days after exposure.

results against-intuitive The studies are consistent with previous research by Schlievert indicating that the cell surface antigens, which are frequently used to create bacterial vaccines are poor choice for prophylactic to S. aureus because of particular way the body to cause disease, he said.

"One of the ways Staphylococcus works is to create aggregations of bacteria which block blood vessels and airways," said Schlievert. Therefore, vaccines that stimulate the creation of antibodies against antigens of cell surface can be more dangerous than no vaccine at all, he said, because in connection with these antigens, they created molecular complexes that intensify the phenomenon of agglutination.

Schlievert also believes that its results are more relevant to humans than other animal studies with staphylococcal vaccines. While other researchers tested S. aureus vaccines in mice and non-human primates, supports the immune system of the rabbit is more similar to that of humans, at least in terms of how it responds to this bacteria. Staph researchers say the new study Schlievert is provocative, but not entirely convincing. "It shows that superantigens are more protective than the antigen-bunnies area undergoing experimental infection," said Robert Daum, a pediatrician and microbiologist at the University of Chicago in Illinois. It remains to be seen whether the same is true in humans, he says. "Many people have used surface antigens [in vaccines] for a long time. it was not a great success, but there is little evidence to suggest that vaccines are worse. "

Daum considers the suggestion that rabbits were better than mice as experimental animals to be interesting. It is true that mice are not particularly good models in S. aureus , he said, but then, rodents are inexpensive and well studied. "If it is true that rabbits are a better model, it Roil the field, because they are much more expensive and difficult to work with. I think rabbits have not yet been studied enough to conclude that they are better . "most of the data come from group Schlievert this.

Daum argued that failures in previous vaccines have shown that defeat S. aureus requires more basic science before new vaccine antigens are debited. Too little is understood about the human immune response to S. aureus , which can cause fatal infections, but often live in and on us without causing disease at all. "We do not want to eliminate all staphylococci. We want to eliminate the bad ones that cause the disease. So we need to understand immunology, and we are not yet there," said Daum.

Schlievert said that unpublished data from his group show that its also superantigen-based vaccines prevent skin infections in rabbits. It then intends to ask the Food and Drug Administration to allow it to conduct safety studies of the vaccine base man.

For some children, even traces of peanuts can be fatal. But until now, children with allergies to peanuts not have other treatment options that avoid legumes completely. The results of a new clinical trial may change that. The scientists found that feeding small children allergic amounts of peanut protein each day, an approach known as immunotherapy by mouth, can help them lead a normal life.

"This is a very important first step," said Gideon Lack, a pediatric allergist at King's College London, who has not participated. "But I do not think he is ready to go into clinical practice."

About 1% of children in high-income countries like the United States and the United Kingdom suffer from a peanut allergy. Their immune system reacts to proteins found in nuts and in severe cases the reaction can cut breathing or lead to sudden drop in blood pressure, the oxygen starved bodies. The condition puts a lot of stress on families, because even the children who reacted moderately to peanuts in the past may suddenly have an incident of life-threatening, said Andrew Clark, a pediatric allergist at Cambridge University Hospitals NHS Foundation Trust in the UK and one of the researchers involved in the trial. Some studies have shown that exposing children to increasing doses of peanut can desensitize, but some great tests were performed. Some studies in the 190s attempted injecting the antigen into the skin. But the side effects were serious and in a study of one patient died due to dosing errors. "Because of this, people have not touched it 10, 20 years and are now approaching again," said Clark.

Clark and his colleagues started with 49 old allergic children from 7 to 16 years. meals children included a small amount of peanut flour, slowly increasing the dose of 2 milligrams to 800 milligrams (equivalent to about five peanuts). a group of 46 children who had an allergy to peanuts avoided the control nuts. After 6 months, 24 of 39 children in the treatment group who completed the study could tolerate 1400 mg of peanut protein not show a reaction, but no one in the control group might, the authors report today the Lancet . many children suffered from nausea or vomiting, but in general, these side effects were mild and occurred in the first days after a dose increase. "We think we found a diet that works very well, "said Clark, who hopes to offer treatment as part of a" patient program named "within a year. These programs allow doctors to use therapies that are not approved for patients if no other treatment exists. "I think we have an obligation to act on our results," he said.

A group led by Kirsten Beyer, a pediatrician at the Medical University of Berlin Charity, recently completed a test and similar is to analyze the critical results. Beyer study for not using a placebo treatment in the control group. "But it is a big step in the right direction," she said. "We need urgently to other studies on the treatment of peanut allergy. "

Lack also praises the study to be larger and more rigorously conducted than previous tests. But the benefits of treatment are likely to be short term, he warns. "If you stop eating peanuts for a few weeks or even days, and you are re-exposed, you may have a serious allergic reaction." Because of this hazard, avoiding peanuts may still be the best option, he said. But Clark said that the participants seemed to tolerate short gaps, and he hopes to change some of the children who have now been in therapy for 2 years at a weekly dose.

Hugh Sampson, a researcher allergy Mount Sinai Hospital in New York, said that further studies are needed to address unanswered questions. For example, the optimal dose is, if there are chemicals that can make the treatment safer, and if long-term negative consequences of therapy. "Although this study adds to growing data on the potential utility of oral immunotherapy for the treatment of food allergy," he wrote in an email, "I'm not sure this study brings us closer to the answers. "

The Middle East Respiratory Syndrome (MERS) first made headlines the world when it was discovered in 2012. But the new research shows that the virus was probably lurking in camels in Saudi Arabia since 1992 or even longer, and it is very common in animals today. The study suggests that undiscovered human cases may also have occurred in the last 2 decades.

MERS is caused by a coronavirus, a class of high pathogens on scientific watch list because another member, severe acute respiratory syndrome (SARS) virus spread around the world in 03 killing more than 700 people. The syndrome has sickened 182 and killed 80 people so far, but it does not spread from one person to another as easily as SARS did. This suggests that most patients have contracted the virus from animals. SARS probably originated in bats and transmitted to humans through civets. But scientists studying SEAS finding more and more evidence showing camels as a source.

Last summer, researchers reported finding antibodies against the virus signaling either a past or current infection in the blood of retired racing camels Oman, but not in cows, goats or sheep. Since then, studies have also reported such antibodies in camels from Qatar, Jordan and Egypt. One study found antibodies against MERS in samples of camels kept cold blood in the United Arab Emirates since 03. At least one team as antibodies found in recent samples of camels in Saudi Arabia, the country that saw the most human cases. But many scientists are frustrated by the lack of information emerged from this important country so far.

The study of MERS virus was fraught with other difficulties too. For example, import samples of camels and other animals in the United States is hampered by fears FMD, a highly infectious disease that infects cloven-hoofed animals such as cattle and pigs; Meanwhile, research resources in affected countries in the Middle East are limited. To address these problems, Columbia University virologist Ian Lipkin built a mobile laboratory and sent to Saudi Arabia late last year. "Two thermal cyclers, a nucleic acid extractor robotics, tools for serology, all this equipment went there in six cases Pelican," he said.

with Saudi colleagues, researchers equipment used to test 203 camels from different parts of Saudi Arabia. They found antibodies against the MERS virus in 150 of them. They also found the virus RNA in the rectal or nasal sampling 51 animals, a sign that they harbored the virus at the time of testing. the viral sequences closely match those of human patients. Because the nasal swabs gave most viruses, the most likely scenario is airborne agent pathogen, the authors write in MBIO today.

the researchers also examined more than 100 camel serum samples from an archive dating back to 1992 and found antibodies against MERS in almost all. "This virus has clearly been camels since at least 1992," says Lipkin.

The document adds to the evidence increasingly on the animal reservoir of MERS, said Marion Koopmans, a researcher in infectious diseases at the National Institute of Public Health and the Environment in Bilthoven, in the Nederlands. "It is now indisputable that these viruses circulate among the camels," she wrote in an email.

Bart Haagmans, a virologist at Erasmus MC in Rotterdam, the Netherlands, says he is surprised that viral RNA could be found in a large number of animals. "you do not expect to find a virus from a respiratory infection in nearly one in four animals," he said. he suggested that the virus known to remain in the camel population very well. it is not known if the virus actually makes camels sick, but it seems to infect many camels at a young age, said Haagmans. most scientists agree that studies of camels infected over time are needed to know how long they can harbor the virus.

Find antibodies in samples of 22 years raises the question of why the first known date human patients from 2012, Koopmans said. "Having human cases has failed before, or has something changed in the making camels virus transmitted to humans?" To address this issue, scientists would have to look older samples from Middle East patients with respiratory disease and those who are not available, she wrote.

What MERS was infective for 2 decades or 2 years, there is still a real danger that it will begin broadcasting between people more quickly and trigger a pandemic, said Michael Osterholm, director of the Center for research on infectious diseases and politics at the University of Minnesota, Twin Cities. "We are now at the second level of concern", he said, because MERS is not only a dangerous virus in animals but overflows into the human population, again and again. "The third level could happen tomorrow."

in June 2012, three men remove slag of abandoned copper mine in southwest China fell ill severe pneumonia and died. Six months later, the researchers in the mine cave-an artificial cave carved from a research hillside in pathogens. After anal swabs bats, rats and shrews musk living in the cave, the team found what it says is a new virus that could have shot the workers.

The alleged pathogen looks like a kind of virus known as henipaviruses, two of which are fatal: Hendra virus, discovered 20 years ago in Australia when he started killing horses-from four people who have been in contact with infected horses died and Nipah virus, the cause of periodic outbreaks among people in Southeast Asia since 1998. the third Henipavirus confirmed, Cedar virus was first reported in Australia in 2012; it does not infect humans. For all three species, animals that harbor the virus in the wild-state natural reservoir appear to be the fruit bats called flying foxes.

The new virus, paramyxovirus appointed Mojiang (MOJV) after the county of Yunnan province, where he was found, joins a growing list of species which share genetic similarities with henipaviruses and family members of Paramyxoviridae comprising henipaviruses. Bats and shrews in Yunnan cave tested negative for the new virus the Henipa-like; three out of nine rats were infected. "It is not entirely surprising to find sequences Henipa as rodents," as rats are the natural reservoir for some paramyxovirus, said Lin-Fa Wang of the Australian Animal Health Laboratory in Geelong, which has not participated in Mojiang. MOJV study "could be a bridging virus" among those bats and rodents, "said Wang, one of the team leaders who discovered Cedar virus.

the three victims in Yunnan have succumbed long before scientists arrived on the scene, so "it has not established a direct relationship between human infection and MOJV" says Jin Qi, director of the State Key Laboratory of molecular Virology and genetic engineering in Beijing, and head of the new work, reported in the June issue of emerging infectious diseases . The new virus and parents, if they exist, are keeping a low profile. Jin team sampled bats in the cave Mojiang again and empty newcomer. More recently, he says, a "systemic viral investigation" in 38 of bat species across China led his team failed to implement henipaviruses. He believes the rodents should be studied in more as potential wildlife reservoirs Henipavirus. But for now, said Jin MOJV is "more likely a curiosity."

* Correction, March 21, 11:28: The original version of this article does not contain a link to the research paper. We have corrected this.

A document 2012 on the human heart regeneration powers was removed from the magazine Traffic amid a compromised data survey. The American Heart Association, which publishes the newspaper published a retraction on April 8 for the paper, which was the corresponding author Piero Anversa, a cardiologist at Brigham and Women's Hospital in Boston. The retraction states that "a permanent institutional review by the Harvard Medical School and Brigham and Women's Hospital has determined that the data are sufficiently compromised that a withdrawal is justified."

Another author circulation 's editor in chief, Joseph Loscalzo, who is chairman of the Department of Medicine Brigham. the newspaper received a letter last week from Harvard University dean for faculty and integrity search calling for the retraction, Rose Marie Robertson, chief science and doctor at the American Heart Association, said science Insider. She said the letter mentioned problems with data in multiple figures the paper. A Brigham representative declined to give details of the current review. Robertson said that, based on the Harvard letter she has no concerns about the role of Loscalzo in the newspaper and that he -even challenged both the review process and retraction.

* Harvard and Brigham sent a second letter raising concerns about another document involving Anversa, this one published in The Lancet . See the update below for more.

The document is part of a series of group Anversa defending the controversial idea that the human heart regenerates quickly muscle cells, and this regeneration increases with age. Some wondered if the heart muscle cells can be renewed as adults at all. A 09 document Science conducted by researchers in Sweden used a new technique to estimate that the cells are renewed at a rate of about 1% per year in 25 years, falling by 0.45% year 75. But Anversa and colleagues have challenged these estimates in the document 2012 and others, saying the renewal is much more dramatic, 7% per year from 20 to 40 years and that the rate increases with age, as much as 19 % in 80 years.

"They were rather lonely with this view," said Jonas Frisén , a researcher on stem cells at the Karolinska Institute in Stockholm, who led the work in 09 . He and his colleagues measured the age of cardiac muscle cells by matching the amount of carbon-14 in their DNA to carbon-14 in the atmosphere at the time they were formed. The group of Anversa used this technique, among others, the Traffic 2012 paper, and Frisén said he contacted the group to understand why their two efforts had reached different conclusions.

After the authors have shared more data Frisén said he began to suspect that the samples used by the Anversa group had been contaminated with other carbon sources, such as in that the cell proteins or chemicals used for reactions. He also raised other concerns about how the data were processed. Anversa did not respond to a request of Science Insider for comments

* Update, April 11, 4:57 p.m. :. Harvard and Brigham sent another letter raising concerns about the work of Anversa, this one about high level of clinical trial results published in The Lancet . On April 11, the newspaper published an "expression of concern" on paper, on which Anversa is the last author. He cites the Harvard Brigham letter saying that the medical school and the hospital "examine concerns the integrity of certain data generated in a laboratory at BWH, "and adds:" the purpose of this investigation is on two additional digits published online (figures 2A and 3). For all we know, the investigation is limited to work performed at BWH. "

When the document was published in November 2011, it was announced as the first study in humans to test the therapy of cardiac stem cells in the fight against heart failure. the authors reported an improved ability to pump blood and decrease the amount of dead heart tissue in patients severe heart failure after an infusion of stem cells.

The letter of concern to The Lancet was first reported by Retraction Watch.

The intimidation cast a shadow. Children who are bullied are more prone to depression and suicidal tendencies, even when they grow up; they are also more likely to get sick and have headaches and stomach aches, the researchers found. A new study may have found the underlying cause: A specific indicator of disease, called C-reactive protein (CRP), is higher than normal among bullied, even when they get older. However, the bullies, the same size, appear to be healthier.

The researchers focused on the CRP because it is a common marker of inflammation easily tested, the runaway immune system activity which is a characteristic of many chronic diseases including cardiovascular disease , diabetes, chronic pain and depression, says lead author William Copeland, a psychologist and epidemiologist at the medical Center of Duke University in Durham, North Carolina.

to link inflammation to bullying, the researchers asked 1420 young people between the ages of 9 and 16 if, and how many times they had been bullied or have bullied others . Interviewers asked participants whether they felt teased, bullied or treated miserably by siblings, friends and peers than other children and if they had upset or hurt others on purpose, tried to get others in trouble, or people to do something forced by threatening or hurting them. The researchers took blood tests finger stick for each evaluation. The interviews were held annually until the participants were 16 and again when they were 19 and 21. The children were interviewed participants in the larger study Great Smoky Mountains, where some 12,000 children NC were evaluated to monitor the development of psychiatric conditions.

short term, the effect of bullying on victims was immediate. CRP levels increased and the number of cases of intimidation reported, and more than doubled in those who said they had been bullied three or more times in the previous year, compared to children who had never been bullied. No changes were seen in the bullies, or in children who had not been involved in bullying in one form or another, the researchers report online today in the Proceedings of the national Academy of sciences .

the revelation, Copeland said, was the change of CRP in the 19- and 21. The levels of protein increased over time in all groups, which is normal. But the increase was greater in bullying victims: Even 10 years later, average CRP levels were even higher (more than 1.5 mg / L) than in those who had never been bullied ( about 1 mg / L). In bullies, levels were about 0.5 mg / L, a little less than half of the victims. The differences in CRP between bullies and victims remained even when the researchers accounted for potential confounding factors, such as mental disorders, substance abuse and other forms of stress.

high CRP can be a specific way that childhood stress leads to health problems down the road, the researchers conclude. Adults who were abused as children also show increased inflammation, as measured by CRP levels in some studies.

Despite the implied health benefits of intimidation, Copeland does not advocate picking on people to improve your health. The advantage probably lies not in the attack itself, but rather in the more control, power and social status that bullies like, he believes.

The advantages of bullying are daunting but not surprising, said biological anthropologist Thomas McDade of Northwestern University in Evanston, Illinois. The increase slower than normal CRP in bullies supports a growing mound of research showing that those at the top have better, he said.

A key strength of the new study, McDade said, is that it focuses on a specific measure, checked repeatedly over time. "CRP is clearly one way in which the social environment can get under his skin" -affecting health for better or worse, he said.

Because inflammation is an underlying factor in many chronic diseases, the fact that people in their early 20s already show signs of inflammation is an alarm bell, Copeland adds . Using data from the larger study, his team will examine other measures of adversity, such as cortisol, the stress hormone, and epigenetic changes in which environmental factors affect how genes are turned on . Scientists will also look for biomarkers to more positive methods as intimidation through which children can increase their confidence and social status.

Ideally fight against bullying programs, in addition to protect potential victims, should help the most aggressive children find ways to improve their social status "without wreaking havoc on others" said Copeland.

The animal that kills humans worldwide most are not the shark, lion or grizzly bear: He is the mosquito. In 2012, about 0 million people have developed malaria after being bitten by the insect; about 0,000 deaths, 0% of them in Africa and most of the children under 5 slippery parasite that causes the disease has long defied the efforts to develop a vaccine. But a study of the children of resistant malaria in Tanzania has turned to an antibody that will stop the infection in its tracks. Based on the action of this antibody, scientists have developed a preliminary vaccine shows promise in mice.

The parasite that causes malaria is a single-celled organism called Plasmodium . He might as well have been designed by an evil mad scientist, said Jonathan Kurtis, an immunologist at Brown University and lead author of the new study. When an infected mosquito bites a human female, the microbe enters the blood of the victim and made to the liver, where it multiplies by tens of thousands. By the liver, it rises in the blood, to infect and multiply within red blood cells. Finally, he broke again in a form called schizont - infect more blood cells and re-enter the bloodstream to infect the next hungry mosquitoes, in whose body it requires a more complex cycle. Step bursting-out, which occurs about every 24 hours, produces fever, chills and pain that make the patient miserable. "It's like the worst flu you've ever had," said Kurtis.

Because different proteins are produced at each stage of the microbe cycle Plasmodium presents a moving target potential vaccines. So far, the most promising candidate is dubbed RTS, S. in a clinical trial phase III reported at the end of 2012, this vaccine, which works by reducing the amount of infected liver cells, has led to a 50% decrease in the number of severe symptoms and parasite blood levels in children aged 5 months to 17 months.

But even in areas where malaria is hit, some people symptoms or not mild at all, and they can show only minimal levels of parasite in blood samples. to see why, Kurtis and his colleagues compared the blood of people who are resistant to those that are not. with National Institutes of Health colleagues, Harvard Medical School and the University of Washington, the team examined a group of children in Tanzania who had been studied since shortly before birth. First researchers collected blood samples from 23 2-year-old children (the age at which resistance to malaria usually develops); 12 were resistant to the disease, as evidenced by the small number of parasites in their blood. To see if these 12 had unique antibody protection, the team checked the-plasma, the liquid containing the antibodies clear the blood of all the children against a set of Plasmodium genes known to be activated when the parasite infects the blood.

Among the proteins produced by about 3 million possible genes, antibodies in the blood of children locked without symptoms only three, the team announced today online science . A gene produces a protein known to assist the parasite infects red blood cells and is already being investigated as a target for a vaccine. When another gene, previously unknown to investigators worked on the structure of its proteins and studied in tissue culture has proved to be just the opposite. The protein helped the schizont leave cell infected blood

"At first it did not make sense. We checked the results three times, "says Kurtis. Apparently, the antibodies against this protein protected against malaria by trapping inside the schizont erythrocyte - and not preventing it from infecting new. The researchers checked the largest group of participants in the study. From about 450 infants from about 6% had antibodies against the protein; none of these children developed severe malaria (defined as difficulty breathing, convulsions, high fever, blood sugar, or severe anemia). When the researchers checked blood samples from a group of teenagers in an unrelated study in Kenya, they found that the blood containing the antibody were only about half as many parasites as have samples made without it.

Finally, Kurtis and his colleagues used antibodies to develop a vaccine candidate that gave mice infected with a particularly deadly form of malaria. Vaccinated animals lived almost twice as long, and in one case, had about a quarter as many parasites untreated mice. Kurtis said a vaccine that exploits the ability of the antibody to imprison Plasmodium in the blood cells would have more time to work with than trying to block re-infection. "The parasite infects a new cell in about 15 seconds, so a vaccine to prevent this action would have to work immediately," he said. Infected blood cells are eliminated by the immune system, he said.

" it is a very elegant approach, "said David Lanar, parasitology at Walter Reed Army Institute of research in Silver Spring, Maryland. After the few seconds Plasmodium takes to invade a red blood cell infected earlier, it is hidden from antibodies, he said. When the new cell is infected, however, the membrane becomes leaky for several hours before schizonts erupt again, giving larger molecules, such as an antibody or vaccine a chance to get. A vaccine that keeps them trapped schizonts shift the chronology in favor of the patient, he said.

A vaccine based on this approach would need to work in tandem with others to different parts of the cycle Kurtis warns. The strategy would not eliminate the parasite, only reduce to levels that can relieve the symptoms, he says.

"At this stage of the game, which is a good thing," said Lanar. No treatment breaks the cycle of infection between humans and mosquitoes, he said. The best thing is to reduce the number of clinical symptoms. "The number of parasites in the blood determines sick, you will be."

A vaccine would be particularly effective in people who have never been exposed to the disease before, or who have lost their immunity from childhood, leaving malaria affected areas, Lanar said, because these groups are more vulnerable to very serious forms of the disease than those who are partially immunized. As a next step, the group of Kurtis conducting a study of the vaccine in non-human primates. If it is successful, the team will start clinical trials in humans

* Update, May 23, 12:12 :. This article has been updated to clarify that the red blood cell membrane leaky push to allow Schizonts escape, it provides an opportunity for treatments to enter

* Correction, May 27, 4:57 p.m. :. An earlier version of the caption of this article incorrectly described the image. The malaria parasite takes most of the red blood cell; dark, rod-shaped forms are bits of hemoglobin that has digested.

Imagine if people in Kansas and California were genetically distinct from each other as someone from Germany is someone from Japan. That's the kind of remarkable genetic variation that scientists have now found in Mexico, thanks to the first detailed study of human genetic variation in this country. This local diversity could help researchers trace the history of the different indigenous peoples of the country and help them develop better diagnostic and medical treatment tools for people of Mexican origin living around the world.

The team has done a "tremendous job" creating a "map of all the genetic diversity in Mexico," said Bogdan Pasaniuc, population geneticist at the University of California (UC), Los Angeles, who was not involved in the research.

Mexico contains 65 different indigenous ethnic groups, 20 of which are represented in the study, said Andres Moreno Estrada, a geneticist of the population in Stanford University in Palo Alto, California, and lead author of the study. Working with Carlos Bustamante, a geneticist other population Stanford, the team sampled the genomes of indigenous people throughout Mexico, in the desert of northern Sonora in the Chiapas jungle in the south. over the centuries of life so distant and often in isolation because of mountain ranges, vast deserts, or other geographical barriers, these people have developed genetic differences from one other, Bustamante said. Many of these variants are what he calls "rare in the world, but locally common." In other words, a genetic variant is widespread in an ethnic group, as the Mayans, may almost never occur in people of different ancestry as people of European descent. If you study the genomes of Europeans alone, you'd never catch the Maya variant. and that's a big problem for people with Mayan descent if this variant increases their risk of disease or changes how they react to different types of drugs. "All politics is local, right? what we are beginning to find is that many of genetics is local, too," Bustamante said.

When the team analyzed the genomes of 511 indigenous people from across Mexico, they found a remarkable amount of genetic diversity. The most divergent indigenous groups in Mexico are as different from each other that Europeans are East Asians, they report online today in Science . This diversity maps the geography of Mexico itself. Most ethnic groups live distant from each other, more various of their genomes appear to be.

But most people in Mexico or of Mexican origin these days are not indigenous, but mestizo, which means they have a mix of native ancestry, European and African. Is their genomes also vary by which region of Mexico where they come from or whatever the local variation was smoothed by centuries of various group meetings, mixing, and having babies?

To answer this question, the team collaborated with the Mexican National Institute of Genomic Medicine, which was genetic data collection mestizos for many years. Somewhat surprisingly, they found that mestizos in a given part of Mexico tend to have the same genetic variants "rare" than their native neighbors. The genomes of mestizo "track so well with Aboriginal groups that we could use genetic diversity in mestizos to make inferences about [their native] ancestors," said Pasaniuc. Strong genetic markers of Mayan descent, for example, appear in the genomes modern people living in the Yucatan Peninsula and the northern part of the Gulf coast of Mexico in the modern state of Veracruz, which probably reflects a trade or way of pre-Columbian Maya migration. "this gives us an understanding of history what these people were up to, "says Christopher Gignoux, a postdoc in the group of Bustamante at Stanford.

Even more important are the clinical implications of the study. to determine whether genetic variation Mexico could influence the risk of disease and the accuracy of diagnostic tools, Esteban Burchard, a lung specialist at UC San Francisco, analyzed how a common measure of lung function tracks with the genetic variation of Mexico. It found that people with common genetic variants in the east of the country have had different results on the lung function test compared with people with western variants. This means that doctors probably should not use the same criteria to diagnose lung diseases in both populations, he said. "What we have shown that, depending on the type of Amerindian descent you have, it can significantly influence the diagnosis of lung disease, in a good or bad way," says Burchard.

The function lung is just one example of how fine-scale genetic variation of Mexico could affect the disease and diagnosis, the team said. for Bustamante, this wealth of potential clinical applications has been particularly exciting study to be a part of. "let's move beyond the issues that we tend to focus on population genetics and really try to address how we will think about the translation of this" so that modern people can benefit.

* Correction, June 13, 11:28: Mexico contains 65 different indigenous ethnic groups, not 55, as was previously indicated. This has been corrected.

As red blood cells zip through the vessels, they provide oxygen to almost every nook and cranny of your body. But oxygen is not anything they can tote around. By orchestrating the red blood cells to have 'sticky' proteins on their surface, a team of researchers gave the cells the ability to transport anything from drugs to treat immune disorders or cancer to radioactive molecules used in the imaging of blood vessels.

"This is really a great idea, and a very new approach," said biochemist Vladimir Muzykantov of the University of Pennsylvania, who was not involved in the new work.

red blood cells represent a quarter of all human cells in the body and survive for an average of 4 months. Their ubiquity and durability makes it an ideal vehicle to transport therapeutic throughout the body, said Hidde Ploegh immunologist at the Massachusetts Institute of Technology in Cambridge. Previously, researchers have loaded red blood cells with drugs by pushing the molecules through the cell membrane in its interior, but the process weakens the cell, and the molecules are released when the cell reaches its final destination.

Ploegh and colleagues wanted instead of attaching molecules outside the red blood cells. Because red blood cells are not nuclei and therefore lack of genetic material that can be modified to make new proteins, the researchers turned to erythroblasts, the precursors of red blood cells that still contain DNA. Scientists added to erythroblasts modified versions of the genes are known to code for proteins present on the surface of red blood cells. The sequences of the introduced genes, however, had changes so that the erythroblasts produce surface proteins with an additional marker that is recognized by a protein called sortase.

These modified proteins remained erythroblasts matured in red blood cells. When the researchers added sortase mixtures of mature cells, the protein cut off the ends of all proteins, the researchers genetically modified, leaving teams of "sticky" trailers for freight. Any molecule with a label corresponding sortase would then bind to the surface protein of the red blood cell. To show that the coupling could work, team Ploegh attaches the vitamin biotin to red blood cells and infused into mice. The cells of biotin-toting survived for at least 28 days outstanding and do not harm the mice, they report online today in the Proceedings of the National Academy of Sciences .

Ploegh considering the technical being used to create a new type of personalized therapy in the cells of the future of your own could be isolated, used to create stem cells that differentiate into erythroblasts, genetically modified to carry a molecule and injected back into your body. Any molecule that has spread through the circulatory system could be the cargo. When the cells have matured into new red blood cells, they will have lost their DNA, eliminating the risk of changes in progress or dissemination of genetic material. "Payloads that you can install are unlimited," says Ploegh. "But many of the applications are still, for the moment hypothetical."

Muzykantov, who developed other approaches to the use red blood cells as molecular vehicles, said the importance of the new method "beyond just drug delivery. "It could be used to track the red blood cells to diagnose blood diseases, the spread of imaging agents through the body to visualize atherosclerotic plaques or blocked arteries, or counteract the immune system before transplantation by blocking antibodies that enter the bloodstream.

"But there are many issues to be addressed in animal models," he added. "I would love to see a real demonstration that a drug binds to a red blood cell using this approach always works. "

A syringe full of harmful bacteria sounds like the last thing a cancer patient needs. But a new study of dogs with tumors, and even a human cancer patient, shows that the injection of some bacteria directly into tumors may reduce or even eliminate. The results strengthen the case that the use of bacteria to treat cancer, an approach that performed poorly in some clinical trials, will work.

Doctors first noticed bacterial infections sometimes slowed or eradicated tumors there are more than 0 years. William Coley, a surgeon in New York, was the first to run with the idea. In the 180s, he began injecting cancer patients with living Streptococcus bacteria to fight against their tumors. After two recipients died from infections, it passed to the administration of dead bacteria and eventually treat more than 1,000 patients with so-called Coley toxins. Coley sometimes injected bacteria into tumors and sometimes in blood, and many of his patients survived. But treatments such as radiotherapy, chemotherapy and soon pushed approach Coley surgery in the history books. Yet a new analysis of some of its business in 1999 suggested his success rate was about the same as for modern cancer therapies.

Recent attempts to revive the treatment of cancer bacteria have run into obstacles. For example, a clinical trial in which patients received intravenous doses of weakened Salmonella bacteria found that the treatment was safe but had little impact on tumors. For over a decade, geneticist Bert Vogelstein cancer at Johns Hopkins University in Baltimore, Maryland, and colleagues studied a different bacterium, -dweller the ground Clostridium novyi , a relative of the microbe responsible for botulism. Oxygen is the rare tumor inside, and these bacteria "of love of low oxygen zones," said Saurabh Saha, a cancer researcher at BioMed Valley Discoveries Inc. in Kansas City, Missouri, and a co-author of the new study, which appears online today in science Translational Medicine . "They grow and divide and kill cancer cells," says Saha. The researchers speculated that the bacteria release enzymes that destroy tumor cells, and then they feast on the remains.

Inject the spores of the bacteria in brain tumors in rats extended the survival of animals, the researchers found. But the treatments that work in laboratory rodents have a bad habit of not in people, so the researchers wanted to test the bacteria in animals that more closely resemble human patients with cancer. They chose dogs. Like humans, dogs are genetically more diverse than laboratory rodents. And as human tumors, canine tumors grow spontaneously, unlike tumors induced by researcher of laboratory rodents.

Saha and his colleagues injected C. novyi spores in dog tumors 16 animals whose owners have run out of options to treat them. In six dogs, the tumors shrank or disappeared, and tumors stopped growing in five animals. Several dogs needed surgery to erase the injuries that tumors have disintegrated.

Encouraged by the results of animal studies, researchers have begun a trial of treatment with the security people. The first person who received the bacteria was a woman whose abdominal tumor had metastasized to several parts of his body, including his right shoulder. Although the researchers injected within 1% of the bacterial dose dogs had received in the shoulder metastases, growth began to decline. However, treatment stimulated an unusual side effect. The tumor had burst into the humerus bone in the arm, and was apparently provide physical support. Destruction of cancer cells leads to bone breaking, which required surgery to repair. Finally, the patient died of his other metastatic tumors.

The bacteria not only destroy tumor cells, but they also stimulate immune cells to attack the cancer, researchers have shown. And because microbes survive only in low oxygen environment of a tumor, the treatment is specific, said Saha. "It distinguishes tumor from normal cells." The researchers plan to continue their safety trial and want to determine which types of tumors respond to bacterial therapy, he said.

Saha and colleagues altered their bacteria to be less harmful to people and the microbes die when they contact oxygen, limiting their ability to spread. However, some dogs and human patients in the trials received antibiotics, and doctors and other caregivers used anti-infection standard measures such as wearing protective gowns and gloves.

The study is important because it provides "proof of concept that this particular approach can have antitumor activity in" real tumors, "" rather than only in induced tumors of laboratory rodents, said Douglas Thamm, a biologist and cancer researcher in veterinary oncology at the cancer Center Flint animals of the Colorado State University in Fort Collins. doctors may need to combine treatment with other therapies, such as radiation to mop up all tumor cells that escape the bacteria, he said.

"There is a very good very important paper," says biologist cancer Robert Hoffman of AntiCancer Inc., a biotechnology company California based San Diego ,. He and his colleagues have shown that a different strain of Salmonella bacteria than that used in previous clinical trials could eradicate various types of mouse tumors, but they are not carried out studies on human patients .

One concern about the new approach is that most cancer patients are not killed by the original tumor, but metastasis. Thamm and Hoffman fear that the injection C. novyi directly into tumors will leave intact these fatal metastases. "If the bacterial therapy will be widely available and effective," says Hoffman, "it needs to target metastatic disease."

* Correction, August 14, 1445: The researchers genetically modify bacteria to mitigate; they used the heat.

The Ongoing Ebola virus disease outbreak is Taking an appalling toll on health workers in West Africa. More than 240-have-been infected and more than 0-have died. At Kenema Government Hospital (KGH) in Sierra Leone, Where the country's first case Was Diagnosed, more than 2 dozen nurses, doctors, staff and media-have died of Ebola. KGH Is Where Were Many of the samples file Managed for a paper published online today in Science That Analyzes the genetics of the virus responsible for the disease. Highlighting the hazard To Those caring for infected people, five of the paper's co-authors-all Experienced members of the hospital's Lassa fever team-died of Ebola ict before publication. (A sixth co-author, uninfected, aussi Recently died as well.)

Mbalu Fonnie , a licensed nurse midwife and the nursing supervisor of the KGH Lassa Ward, was "matron of nursing at KGH," says Robert Garry, a study co-author and virologist at Tulane University in New Orleans, Louisiana. Mrs. Fonnie HAD more than 30 years of experience Treating Lassa fever, a hemorrhagic illness with symptoms similar to Ebola Many, and Specialized in the management of severe Lassa cases in pregnant women. She Began her career working at Nixon Memorial Methodist Hospital in Segbwema, Sierra Leone, and participated there in Lassa fever research trials Conducted by the Centers for Disease Control and Prevention. "Aunty Mbalu Was a mother to face the Entire staff," Garry says. She Had survived Lassa fever. She Was infected with Ebola while caring for one of her fellow nurses, Who Was pregnant and HAD Ebola.

Alex Moigboi , a registered nurse with more than 10 years of experience caring for Lassa fever patients, Was aussi la même Treating infected while colleague. Mr. Moigboi "loved to interact and raise everyone's spirits with His great sense of humor," says Garry. "Always with a smile on His face ... the last one off the dance floor."

Alice Kovoma Was helping Mrs. Fonnie treat the pregnant nurse When She, too, est devenu infected. A Lassa Ward nurse for more than 6 years, Ms. Kovoma was "a wonderful person ... very dedicated and professional with a devotion to the patient and her teammates," Garry says.

Mohamed Fullah , a laboratory technician Who Helped on the study, was an instructor at Eastern Polytechnic College in Sierra Leone, Where he served for more than 10 years. Extremely popular with His students, Mr. Fullah HAD Worked part time in the Lassa fever laboratory for 6 years. Was Mr. Fullah intense, disciplined, and very hard-working, says Garry. He was "very dedicated and serious about the laboratory and in general science." He lost Several de son close family members to Ebola and presumably contracted the disease from one of Them.

Sheik Humarr Khan Was the director of the National Lassa fever program for the Ministry of Health and Sanitation in Sierra Leone and an expert on viral hemorrhagic fevers like Lassa Treating fever and Ebola disease. He Studied medicine at the University of Sierra Leone and completed a residency in internal medicine at Korle Bu Teaching Hospital in Ghana. He Worked with the African Centre of Excellence for Genomics of Infectious Disease, the Human Heredity and Health in Africa Initiative, and Was a founding member of the Viral Hemorrhagic Fever Consortium. Khan HAD Treated Lassa fever patients for more than 10 years. At the time de son death, He Was helping coordinate His country's response to the Ebola outbreak. Widely respecté by colleagues, President Ernest Bai Koroma hailed _him_ as a "national hero." His death Sparked Widespread debate about whether he shoulds-have-been Treated with the untested drug zmapp. "I will miss His smile and good nature and will always admire His exceptional bravery, loyalty, and strength," writes Pardis Sabeti of the Massachusetts Institute of Technology, Who led the study published genetics, in a tribute page dedicated to Dr. Khan .

Sidiki Saffa , Who died of a stroke unrelated to Ebola while the paper in press was, was a laboratory technician Who file Managed blood samples and processed em. Mr. Saffa HAD more than 20 years of experience collecting blood samples from Lassa fever patients. "Very well organized and great with the record keeping ... [he was] always on the move from the clinic to the laboratory and back," Garry says. . "He Was the Lifeblood of the operation"

* The Ebola Files: Given the current Ebola outbreak, Unprecedented in terms of number of people killed and rapid geographic spread, Science and Science Translational Medicine -have made a collection of research and news items on the viral disease freely available to Researchers and the public generally.

Bruce Aylward is used to mobilize armies of health workers A Deputy Director General at the World Health Organization (. WHO) in charge of poliomyelitis and emergency situations, leading the massive global effort to eradicate polio. But Aylward said he never met a challenge as big as the Ebola epidemic in Africa West, which has infected more than 4,000 people and killed over 00. Margaret Chan, who leads wHO Aylward asked to help with the response in August and since he was running operations and helped develop Ebola response WHO Roadmap, published August 28 He spoke with Science September 4. (This interview has been edited for clarity and brevity.)

Q: Margaret Chan said that all organizations involved in the outbreak, including WHO, underestimated the complexity and scale. How did this happen

A: I did not live through it, but as I went back and asked what was going on, clearly these guys [in the response effort] were flat on it for 6 months. And they put 450 people on the ground. These are incredible numbers to respond to Ebola. But the virus got past them.

Could the answer have been scaled faster? Maybe they were out of 2 weeks to a point here or there. As Margaret said, you are still a few weeks behind the virus, and there are so many reasons. It is a dangerous pathogen. Foreign medical teams and NGOs [nongovernmental organizations] are used to treat trauma and primary health care; they are not trained to deal with pathogens

Q :. I have heard that there are tensions between WHO and Médecins Sans Frontières (MSF), the organization has treated more patients than any other. They criticized the WHO for being too slow and do too little

A :. Probably at the local level, there is some tension in some places, but certainly not here in Geneva to senior levels. There is great respect for the organization. MSF is great at two things: They are fantastic in their field operations and to tell the rest of us how we are to them. Of course, people will go out and say, "Oh, that's unfair," You need a thick skin you're in the World Health Organization; you deal with a major international threat, and our job is to.. . be responsible if MSF considers that this is a public responsibility, it is their right

. Q: Why stop this epidemic so hard compared to control polio

a: the polio program is really difficult because of the level of programmatic perfection you need you must reach every single child with the vaccine over a vast geography and environments. very difficult. But even if you do not, you still have a level of control over the virus. Now, when I look Ebola, you need a whole new level of perfection.

you have make perfect contact tracing because contact can blow open a new chain of transmission. You must get your perfectly safe burials. You must get your right to laboratory tests. There is not much capacity in the world about it. You must get your right social messages. You must be perfectly safe and protect the health of workers. And you have to do it all at incredibly low environments in three countries that are near the bottom of the development index, and also deal with the embers landing in Nigeria or Senegal. Wow, that is really hard

Q:.? Do you think it is still possible to contain the epidemic with standard procedures, patient isolation, contact tracing, bury the dead safely

A: Absolutely. But with one important difference. What happened is that you have a workload that far exceeds the capacity of standard Ebola strategies to manage them, so you need to innovate on these strategies. Each infected person is having a lot of contacts because they are essentially left to their communities for long periods of time. What you have to do is first shot spread outward from each patient, which means you have to get many new Ebola treatment centers up. And you have to adapt your strategies in a way that communities can play a much larger role and help them increase their own Ebola Community Care units. This is absolutely essential and must be done in September.

Will it be done? Well, that will depend on whether the international community will put money on the table, help people in, and understand the conditions they need to operate

Q :. WHO Ebola road map calls for the epidemic to finish in 6-9 months. Is it not too optimistic

A: I do not know, because no one has ever had to do something of this magnitude. What I know is that if the roadmap is not implemented, you're not going to stop in 6 to 9 months. In a month, you need at least 10 new operational facilities with an additional capacity of bed and teams on the ground, and money for people who do such things are paid, and a means evacuate stakeholders who get medical trouble. You must begin to implement the roadmap today.

But the usual relief organizations are not rushing to do so. These are not bad people and they are not cowards. These are people who go to wars operating environments and the most dangerous natural disasters. But they do not normally deal with dangerous pathogens

Q:.? So you need more people and you need more money, but it's just not coming

A: Not yet, but I'm optimistic. I think it is time the world struggling with this. It is so new, and he plays the deepest fears of the people and their greatest uncertainties. People will learn MSF will remain on the ground there. And then one or two NGOs will go and run an installation, and they will do very well. And then it will degenerate. The world does not want to be beaten by a pathogen. But the question is: will they do it fast enough

Q :? So who are the players you hope come to build and manage treatment centers

A: many foreign medical teams are linked to governments, and some affected countries have deep relations with the United States Liberia; the U.K. with Sierra Leone; France with Guinea. Now these countries are keen to look at what they can do and how to do, but they are struggling to mobilize. They might be able to set up a field hospital, but can they provide? Because a field hospital that does not have just a building, it is not an Ebola treatment center

Q :. Two vaccine candidates will soon be tested in Phase I studies and can be deployed later this year. How important do you think they will and drug candidates to end the epidemic

A: You want to have as many tools as possible to help lower the number of breeding where you can manage with traditional strategies. Want to do both in parallel and go flat-out. Vaccines and treatments would be extremely helpful-they help get the stakeholders and keep the players that are there healthy. This can give us an advantage to close this thing faster. But if we say that we have these drugs and vaccines, then you are yourself the establishment of defeat because you can not get them. And then you also have the risk of people saying, "There will be a vaccine or med, we'll wait," and a lot of people will die. I will not sit twiddling my thumbs waiting to find, and neither is my organization

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

A week after strong criticism met the announcement of the US military that it plans to help Liberia fight the Ebola epidemic with a "deployable hospital" which has only 25 beds, tomorrow plans US President Barack Obama to unveil major new efforts to help the West African country besieged by illness.

(Update: The White House Tuesday morning issued a fact sheet outlining its planned response He will be coordinated by a US army general. stationed at a new command center in Monrovia with an estimated 3,000 soldiers. the Ministry of Defence has requested "reprogramming" $ 500 million for the effort.)

Obama will visit the US Centers for Disease Control and Prevention in Atlanta to discuss the response of the United States, at the same time, a US Senate hearing on Ebola will also take place with the testimony of key officials and Ebola survivor Ken Brantly .

Nicole Lurie, assistant secretary for preparedness and response at the US Department of Health and Human Services (HHS), spoke with science Insider Friday and said she expected there would be "a substantial increase" in aid of the US government. It wants to see particular attention to providing people infected with good care. "There is a very, very great variability in what is delivered in clinical care, "said Lurie, noting that Case fatality rates are substantially different in different places." We know that simple interventions can save as lives. "

Lurie points out that, in the absence of adequate basic care, it becomes exceedingly difficult to determine whether biomedical interventions actually work. zmapp , an experimental cocktail of Ebola antibody, was given seven people (two of whom died) and have received considerable attention in spite of a complete absence of clinical data that suggests the treatment helped. A familiar researcher with blood tests of two recipients of five zmapp survivors who spoke with Science Insider, but asked not to be identified, said the declines in Ebola virus levels mirrored what we saw in monkey experiments with the antibody cocktail. But without being able to compare the clinical care they received, leaving aside the fact that there was no untreated control group data has little meaning.

Michael Callahan, a clinician at Massachusetts General Boston Hospital who consults HHS about Ebola and responded to past epidemics, said that "many" people die of Ebola even if their natural immune responses are driving down viral levels. Callahan notes that they do not die of Ebolavirus itself, but succumb to what he calls "side events", such as low potassium levels, wasting vomiting and diarrhea and bacterial infections. And many clinics in West Africa lack the simple devices that exist and can safely monitor blood electrolytes, organ failure, and acid-base balances. "The point is very important for the current epidemic," said Callahan, who believes care will drive reported rates higher than 75% lethality "down in the lower range of 40%."

What Lurie says will be a "substantial surge" in the response of the US government will probably also include sending staff to train more people in how to care safe for patients Ebola. One idea under consideration is to teach people who survived an Ebola infection to assist in providing care because they will probably immune to a second infection. "It is a very important issue and something we have had many discussions about," said Lurie, who said she spoke with a Liberian public health officer who is establishing a register of survivors. "It is very difficult for them to return to their communities," says Lurie. "I am very intrigued by the idea of ​​setting up a training program with people who are otherwise a difficult time." She notes that jobs are hard to find in Liberia, and it could give under-employed people additional skills.

In a widely discussed op-ed on New York Times ran September 11, epidemiologist Michael Osterholm University of Minnesota, Twin Cities, argued that on top of more support, the global response to the epidemic of Ebola much better coordination necessary. "Many countries have committed medical resources, but donations will not lead to an effective treatment system if no group is responsible for coordinating," Osterholm wrote, formerly a bioterrorism adviser at HHS.

Osterholm suggested in the op-ed that the United Nations coordinated response, but he said science Insider he was just floating an idea and hoped that the international community would find a leader who included not only medical, but the supply chain, and logistics and tactical movement. "I do not want the world's best treatment doctor to Ebola," says Osterholm. "You must have a responsible person who can take command decisions and be the spokesperson really tell what is necessary and not necessary."

Osterholm said that for now, the government of the United States and every other country well-to-d or nongovernmental organization to try to help battle operates without a master plan. " we do not need 50 sergeants in the room trying to run D-Day, "says Osterholm. "Right now, everything moves at the speed of water in a Minnesota winter. This is exactly what we can not do. We must be able to move quickly and together, we walk. This is a fast marathon. This was completely missing "

* 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.

* update, September 16th, 11:45 :. This article has been updated to provide a link to the information sheet of the white House