Health Meaning

The World Health Organization (WHO) works mainly to reduce the physical burden of the disease. But last week, he turned to another kind of evil insult and stigma inflicted by diseases named for people, places and animals. Among existing monikers that its new guidelines "for the name of human New infectious diseases" discourage: Ebola, swine flu, fever, Rift Valley, Creutzfeldt-Jakob and monkeypox Instead. WHO said that researchers, health officials, and journalists must use more neutral, generic terms, such as severe respiratory illness or a neurological syndrome novel.

many scientists agree that disease names can be problematic, but they are not the new rulebook is necessarily an improvement. "It will definitely lead to boring names and a lot of confusion," predicts Linfa Wang, an expert on emerging infectious diseases the Australian animal health Laboratory in Geelong. "You must not take political correctness so far that the end can not distinguish these diseases," said Christian Drosten, a virologist at the University of Bonn, Germany.

Naming diseases has long been a cumbersome process . Badly chosen names may stigmatize people, as did a gay-related immune deficiency, a first name for AIDS. They can also lead to confusion and hurt tourism and trade. called swine flu, for example, is not transmitted by pigs, but some countries still banned imports of pork or pigs slaughtered after an outbreak of 09. More recently, some Arab countries were angry that new disease caused by a coronavirus has been dubbed the Middle east respiratory syndrome.

Although "it is usually the scientists who come up with these names ... wHO gets diplomatic pressure "if someone takes action, said Drosten. The new guidelines, published May 8 are designed to facilitate the process. "WHO has to do something to get out of the firing line," said Drosten.

Since the news of a new pathogen often spreads quickly, "it is important that the name of the appropriate disease is affected by that, the first report "disease, wHO guidance notes. According to the guidelines, he added, could "minimize unnecessary negative impact of disease names on trade, travel, tourism or well-being of animals, and avoid causing offense to all cultural, social, national, regional , professional or ethnic ".

To this end, sick new names should not include geographic locations; the names of people, occupations, animals, or food; or "terms that encourage excessive fear" (as unknown, fatal and epidemic). Instead, the names should use generic descriptions of symptoms (respiratory diseases or watery diarrhea) and specific terms describing patients, epidemiology or the environment (juvenile, mother, seasonal, summer, the coast), and the names of pathogens and arbitrary identifiers (alpha, beta, 1, 2, 3).

the group that came up with the recommendations met "a few times" during a year, says Kazuaki Miyagishima, director of food safety, zoonoses and foodborne diseases of WHO, and a committee member. Among the ideas they discussed: naming diseases after Greek gods, using a system similar to that used for naming comets or by alternating male and female names as is done with hurricanes "But while the appointment of a Hurricane Katrina may not offend people if we do. for a disease, it is not only a hurricane for 1 week. it will make its way in the history of human suffering, "Miyagishima said .

The guide is well-intentioned but goes too far, says Ian Lipkin, a virologist at Columbia University. "I do not see how it will be helpful to eliminate names like monkeypox that provide an overview of the natural hosts and potential sources of infection," he said.

it could also become more difficult to easily distinguish the disease. For example, under the new rules, Marburg disease (named after a town in Germany) have been called filovirus hemorrhagic fever associated 1, while the Ebola virus (named after a river) could have been Filovirus -associated hemorrhagic fever 2. These bland names "lose something that is more than picturesque," said Howard Markel, a medical historian at the University of Michigan in Ann Arbor. Drosten added that geographical names are sometimes justified. It was clear that MERS, for example, was a partner in the Middle East. "Would it have been better if we had known this novel betacoronavirus clade C, type 1?" He asks.

The new rules are for the most difficult names, Miyagishima admits. "But we think we left a big enough space for freedom. We do not want to kill the creativity of researchers completely."

Linfa Wang knows all about the difficulty of naming diseases. There are two decades, he appointed a virus and the disease it causes after Hendra, a suburb of Brisbane, Australia; he still gets angry residents complain that calls the name hurt property values. These days its strategy is to "go small." He recently appointed a new Henipavirus isolated in a neighborhood called simply Cedar Grove Cedar virus.

virologists met other sensitivities with Norwalk virus , named after a town in Ohio. the pathogen is the only species of the genus Norovirus and usually this name is used. in 2011, however, a Japanese person has requested a change because many people in Japan bear the surname Noro. the International Committee on taxonomy of viruses has recommended "Norwalk virus" instead.

the acronyms are another good solution, says Ab Osterhaus, a virologist at Erasmus MC in Rotterdam, because they keep short names (another recommendation of the WHO) and people often forget that the letters represent. But even acronyms can become controversial. in 03, officials WHO invented the SARS (severe acute respiratory syndrome) to describe a new pneumonia spread in Asia, in part to avoid a name like "Chinese flu." SARS will not go down well in Hong Kong, however, which is officially known as Hong Kong, to the Special Administrative Region.

Leave a number of new diseases may be the only way to avoid these problems, researchers say. It precedent. Growing up in China in the late 1960s, Wang remembers that diseases had numbers. "I'm really scared of the disease Number 5," he recalls. "I do not know why, you really do not want to have a number 5. disease"

An eye-popping $ 28 billion is spent in the US each year preclinical research that can not be replicated by other researchers. This is the conclusion of a provocative analysis published today in part by economists that are based on previous studies of error rates in biomedical studies.

Meanwhile, the National Institutes of Health (NIH) today issued new criteria for the review of grants aimed at strengthening the reproducibility of research funded by the NIH.

lead author of the new price tag for the reproducibility said it is intended to stimulate discussion. "We are showing the economic cost, but we also try to promote solutions. It's really the message of the paper, "says the biologist Leonard Freedman, president of the nonprofit Organic World Standards Institute (GBSI) in Washington, DC, from the viewpoint in PLOS Biology .

One expert, however, is skeptical about the figure of $ 28 billion, saying it may exaggerate the extent of any problem.

To come up with the number, economists Freedman and Iain Cockburn and Timothy Simcoe Boston University combed the literature for two dozen studies that have attempted to quantify the number of biomedical materials are defective due to specific problems such as contaminated cell line. Looking across these data, they estimate that 53% of all pre-clinical studies have errors which means they are not reproducible. The most common reasons included problems with reagents and reference materials (36%), the design of the study (28%), data analysis and reporting (25%), and laboratory protocols (11%).

The 53% is roughly comparable to a handful of studies "top-down" that tried to reproduce a set of conclusions, says Cockburn. For example, a widely cited analysis by Amgen revealed that only 11% of the 53 documents preclinical cancer could be replicated in the laboratory of the company. Other studies have shown a rate closer to 50%.

Hence, the calculation of the economic impact was simple. Crossing the 53% to a "conservative" 50% reproducible estimate, the researchers multiplied by $ 56 billion a year that the NIH and other backers of US public and private funds dedicated to preclinical research. This provides $ 28 billion in irreproducible preclinical research.

Does this mean the money is wasted? Not exactly, say the authors. Instead, they say that the reproducibility would fight the funding goes much further. "The time has come to invest more, not less, with a relatively small share of this investment to improve the reproducibility rates," said Freedman.

Other solutions, researchers should receive better training in the design of the study, and sellers and scientists should sell and use only validated reagents, PLOS Biology commentary concludes. GBSI will encourage the research community to establish accepted standards for authentication of cell lines.

NIH also taking steps to improve reproducibility. in an announcement today, the agency describes four new criteria that grant their authors will be invited to consider starting in January . They include next the strength of the scientific premise that the proposed study is based on; the rigor of the study design; the review of the sex proposal of research animals or human subjects; and if the reagents have been authenticated.

Although he has not seen the details of the microbiologist PLOS Biology comment, a scientist who has studied why the papers are retracted said it "sounds sensational." Ferric Fang of the University of Washington, Seattle, wonders if it is possible to extrapolate from some previous studies on the reproducibility and concluded that 50% of pre-clinical research can not be reproduced. This is partly because the inability to reproduce a specific experience is not the same as not to reproduce that found in different conditions; this result is most common but does not mean the original finding was erroneous. "To say that 50% of research funds are wasted is ridiculous and unnecessary," says Fang.

There is no surprise that a sudden wave of summer heat can kill the elderly; it is dangerous for the serious public health that will only grow as the world warms. But are older survive milder winters balance the loss of life during the summers?

A new study suggests not. An increase of 1 ° C in the average temperature of 1% killed more people, whereas the same increase in average winter temperatures registered only 0.6%, according to an analysis of death records for nearly 3 million people 65 and over living in New England from 00 to 08. Not only that, but sudden temperature swings of another phenomenon that could increase with climate change in some regions were deemed killers even worse in summer winter.

"People get physically fit," says study author Joel Schwartz, an epidemiologist Environment at Harvard University. "But if [temperature] bounces back, we do not do . "

many studies have examined the immediate effect on mortality rates within days of a heat wave. But it is unclear whether some of these people with cardiovascular systems or respiratory compromise, would have died anyway. Few studies have examined the long-term effects or compare the harms of summer heat waves with the benefits of warmer winters.

so Schwartz temperatures and colleagues calculated an average summer and winter in postcodes New England for 8 years, and followed the deaths of elderly people living in them, according to Medicare data. in addition to finding that milder winters are not for warmer summers, the team discovered that the sudden changes of temperature jump from a cold winter day in a winter day warm and again, for example, was a worse killer waves from summer heat or winter or summer. Schwartz said the power to kill Jumpy temperature change is greater than that of AIDS and similar diseases such as liver cancer, which kills about 25,000 people in the US each year. The team reports its results online today in Nature Climate Change .

Highlights of work "a major public health problem," says Jonathan Patz, a public health researcher at the University of Wisconsin, Madison, who is not involved in the research. "I think that it is a very important study. "

As to why the temperature variations are so deadly, Schwartz said he do to not give people time enough for their cardiovascular systems or respiratory adaptation. in the future, he wants to see if the same trends hold in other regions, starting with the southeast United States, where people are more acclimated to warmer temperatures. he also wants to study temperature and mortality in Europe, where air conditioning is less common.

Occasionally, Congress asks federal scientific agencies to prepare a "bypass budget" expert which establishes the finance agency believes is necessary to meet an important objective. Usually those budgets are purely ambitious, and are not included in the official budget request the White House to Congress (hence the name they budget officials from the White House "by-pass"). But legislators see the documents as an opportunity to speak directly to an organization without interference from the White House. and, occasionally, budgets bypass helped build political support to shunt new funds to research in areas such as cancer and HIV.

Yesterday, the National Institutes of Health (NIH) published the first proposal as budget bypass for Alzheimer's disease is expected to triple the prevalence in 2050. distilled discussed at a series of meetings and NIH consortium, the new document request $ 1.06 billion for Alzheimer's research at during the 2017 fiscal year that begins October 1. That's $ 323.5 million more than the $ 737 million the president requested the application of formal budget. The new application, which NIH plans to update each year, identifies 66 "milestones" to separate the community of Alzheimer's, ranging from research into the molecular pathogenesis and physiology of Alzheimer's disease to new clinical trials and studies to support caregivers.

demand is far from the $ 2 billion annual government investment in research as Alzheimer's advocacy groups rights such as the Alzheimer's Association believe is necessary to meet the objectives of the national plan to treat Alzheimer's disease. It calls for treating and preventing Alzheimer's disease and related dementias in 2025. However efficiently ramp NIH regularly provides its requests for Alzheimer spending, said Walter Koroshetz, director of the National Institute of Neurological Disorders and Stroke, once it has established the basic infrastructure of new clinical trials and other projects. The first year "could be quite low load," he says, "because it is mostly planning."

better known NIH branch budget is prepared annually National cancer Institute.

He is famous for stealing Lou Gehrig's life, Stephen Hawking of its mobility and voice, but just how amyotrophic lateral sclerosis (ALS) destroys motor neurons in the brain and spinal cord remains a mystery. Now scientists converge an explanation, at least for a fraction of ALS cases caused by a mutation also associated with a kind of dementia. In cells with the mutation, the new work shows, pores in the membrane separating the nucleus and cytoplasm become blocked, preventing the vital molecules to pass through and creating a fatal cellular traffic jam. For now, the work applies only to the mutation dubbed C9ORF72 a stutter-DNA in which a short nucleotide sequence, GGGGCC is repeated hundreds of thousands of times in a gene on chromosome 9. Neither do multiple laboratories reporting results this week agree on exactly what caps the nuclear pores and how cells die. Yet many in the field call it the work of a major breakthrough, and say the findings could point to new therapies and a new mechanism of neurodegeneration.

If you head out of town on your bike or go for a relaxing cycle in the countryside, be sure not pedaling too fast. That's the advice of a group of physiologists have found that people burn more energy than necessary when pedaling furiously, except the elite cyclists. The researchers came to this conclusion by developing a new equation to describe the performance of cycling, which they say should help people in better shape

Many bikes already contain a device designed to prevent overpedaling :. Gears. Muscles contract work best when neither too fast nor too slow. To go fast, you will use less energy in a higher gear, even if you have to push harder on the pedals, because your leg muscles are much more effective at lower rate of contraction. Similarly, the gear is better to go up because they prevent you to pedal more slowly than you should.

To know exactly how the pedaling rate affects energy consumption, physiologist Federico Formenti of Oxford University in the UK and colleagues studied how 10 men of different ages and fitness levels physical performed on an exercise bike in a laboratory at the University of Auckland in New Zealand (where previously was located Formenti). Each cyclist pedaled faster and faster against the different loads while a mask monitored the amount of oxygen consumed-that a measure of metabolic rate.

Formenti and colleagues reported 0 such measures (16 per participant), and compare them with oxygen consumption rate predicted by an equation recommended by the American College of Sports Medicine (ACSM). This equation involves only two variables the mass of a cyclist and "work rate" equal to the exercise bike of the resistance force multiplied by the distance the bike would go if it was not attached to the ground

the researchers found they could get a better match to the observed values ​​of oxygen consumption by changing the equation to add a third variable: the pedaling rate, they report today in the reports physiological. estimates of the oxygen absorption ACSM equation quite well most of the time, Formenti said, because the formula for work rate already includes pedaling rate. But, he noted, the equation fails to capture the relative number imposed by the resistive force and pedaling speed. in fact, he and his colleagues found that high pedaling rate and low employment rates, test participants used up more of their energy simply spinning their legs. "The physiological response of muscles to exercise is very different if they contract slowly against a high resistance compared to contract them quickly against little resistance," he said.

The oxygen consumption during exercise is often used to measure capacity. Formenti said the new equation should improve fitness monitoring in gyms that are not equipped to analyze the breath directly. He warned that the results of his group to be confirmed by larger studies of exercisers, including women, but notes that data from previous studies totaling 50 riders gave a good match for the values ​​of consumption oxygen new equations.

Ernst Hansen, a sports scientist at the University of Aalborg in Denmark, who was not involved in the research, agrees that the equations describing the performance of the bike should include the rate pedaling. But he argues that the new equation is relatively simplistic, because it ignores individual differences in the effectiveness of muscle fibers and choice pedaling rate. Formenti recognizes that such changes are beyond the scope of his study group, but said they could explain why the cycle of effective elite cyclists, though they pedal very quickly.

As to why the so-called recreational cyclists are better pedal slower, the jury seems to be out. Formenti and colleagues believe that this is due to what they call "inner work" cyclists consume energy as they move up and down legs, as distinct from the "external work" (work rate) which propel the bicycle forward. The researchers measured the internal work during their pedaling motion tracking tests with infrared beams bounced off the body of cyclists. They found that the internal work jumped 10 times when a cyclist has increased its rate from 50 to 110 revolutions per minute pedaling, whatever external work done. Therefore, they say, a bicycle average man size at the higher rate would use about 60% of its energy just to run his legs.

Others, however, disagree with this interpretation. Steven Kautz, a biomedical engineer at the Medical University of South Carolina in Charleston, agrees that the estimates of oxygen consumption should consider the speed of pedaling, but said the reason has nothing to do with work internal. The internal and external work are "not independent quantities of additives," he said, because the first to some extent it generates. Instead, it maintains, the effect of pedaling rate is probably due to the subtleties of dynamic muscles.

Three scientists were awarded the 2015 Nobel Prize in physiology or medicine for the results of decades old that led to the "revolutionary treatment" for devastasting diseases in the developing world. William Campbell of Drew University in Madison, New Jersey, and Satoshi Ōmura of Kitasato University in Tokyo share half the price to discover avermectin, a drug to kill roundworms that cause blindness and deformities. The other half of the prize goes to Tu Youyou of the China Academy of Chinese Medical Sciences in Beijing, discovered and refined artemisinin, which has proved very effective against severe malaria.

"The overall impact of the discovery and impact on humanity is immeasurable," Hans Forssberg, a neuroscientist and member of the Nobel Assembly, which selects the winners, said today at a press conference announcing the price.

"It is extremely rewarding to know that people in the development community have been recognized for the work that really helps people," says David Molyneux, who heads the program on neglected tropical diseases in the school of tropical medicine, Liverpool, UK Molyneux believes that ivermectin, a derivative of avermectin, was given more than a billion times, preventing more than 500,000 cases of blindness.

Ōmura, a microbiologist, was in search of useful compounds from soil bacteria in Japan, and has developed methods for the large-scale cultivation and the study of these microbes. Of thousands of cultures Streptomyces identified some 50 appeared to be good candidates for antimicrobial drugs. The study of these strains, Campbell found that one was particularly effective in killing roundworms in farm animals and pets. The active component was purified and named avermectin. Later versions were so effective in curing blindness parasitic disease lymphatic filariasis and river, causing gross deformities Does diseases have been virtually eradicated .

The key results have been described in these two document , both published in 1979 Antimicrobial Agents and Chemotherapy .

The award came as a surprise to Ōmura. "I humbly accept," said the media arm of the Nobel Foundation in a telephone interview today. "I'm still not sure it is quite right for me to receive this award," at- he said later in an interview with the Japanese broadcasting company NHK. "There are a lot of talented researchers in Japan. What I do is just tedious. I'm expected a Nobel Prize. I am always proud that my work has helped people, I tried to help people. But this is different from being a Nobel Prize. "

" I'm in shock, "said Campbell science Insider. Unlike the Nobel Peace Prize, scientific Nobels can not be assigned to more than three people, he notes, "so I suppose there was no way the price could be given for it, because" it was a group effort. " Although the team's efforts are the norm in science, he said, "it was a team of teams."

The path of ö The soil sample mura to a drug used in African villages was long, Campbell said, and there were some moments of "Eureka" along the way. "We develop a very mild form of excitement," he said. "You do not suppose this will make all the way to the market or to the clinic."

Pharmacologist Tu Youyou also found an important drug from natural sources. Search if historical documents on traditional medicine Chinese, she noticed that wormwood was in hundreds of recipes for the treatment of malaria. When she tested extracts in mice, it has seen notes of an effect, but studies are inconclusive. a recipe a 1700 year book led you to a new method for extracting the active compound. This shift has led to artemisinin, which acts effectively on the early stage of the parasite life cycle. the drug "remarkably reduced the number of died over the past decades "for hundreds of millions of people infected with severe malaria, Forssberg said.

You won the Lasker Award in 2011 for his work on artemisinin first Chinese scientist to get this award. But many scientists in China were outraged that she was honored; they argued that the discovery was a mass effort involving thousands of researchers and the credit should not be you alone. The drug was increased project 523 (named for the date of its foundation 23 May 1967), an ambitious research arm of the People's Liberation Army working on orders of Chairman Mao Zedong to find a cure against malaria .

Historians say that you entered the later research project with other researchers, while many of his colleagues have been exhausted by both their work and the political struggles in progress that had swallowed China. Others have defended you during the Lasker controversy, however. She has maintained a low profile is.

With reporting by Dennis Normile, Kathleen McLaughlin, and Christina Larson.

* Update, October 5, 10:32 :. This story has been updated with new information about you and the comments of William Campbell and other researchers

Jeanne Calment is nothing on Creme Puff the cat. The oldest living human is at the ripe age of 122 not bad for a species with an average life of 71 years. But Creme Puff, a feline Texas that would have existed on the bacon, broccoli and thick cream, more than double the longevity of its kind, Surviving 38 years reported. Bluey, an Australian cattle dog, was no slouch either. At 29, he became the oldest recorded dog, living more than two times longer than the average dog.

For centuries, scientists have tried to understand the duration of human life. What sets the limits? What can we do to slow the clock? Now they are beginning to ask the same questions of our pets. As with humans, the answers were hard to find. But some interesting hypotheses emerging ideas that can help explain everything from why small dogs live longer than large why cats tend to last longer than our canine friends.

Understanding how animals age is a "fascinating problem," said Daniel Promislow, an evolutionary geneticist at the University of Washington, Seattle, and co-leader of the project Dog aging, which aims to prolong canine life. "It incorporates the behavior, reproduction, ecology and evolution. If we can understand how to improve the quality and duration of life, it is good for our pets and it is good for us. He is a winner -win. "

sCIENTISTS WERE meditating mysteries of aging for over 00 years. "The reasons why some animals are long life and other short-lived, and, in a word, causes the length and brevity of the appeal of life for investigation," wrote Aristotle 350 BCE the Greek philosopher suspected the answer had something to do with moisture: elephants survive mouse, he reasoned, because they contain more liquid and therefore take longer to dry the idea has not exactly. held water, but the observation of Aristotle that larger animals tend to live longer has. Indeed, it is the only scientific trend today agree.

"All other assumptions have fallen apart," says Steven Austad, a biogerontologist at the University of Alabama, Birmingham. One of the most popular ideas of the last 100 years has been that animals with higher metabolic rates live shorter lives because they go to their body clock more quickly. But "he did not stand up," says Austad. Parrot hearts can beat up to 0 times per minute, for example, but they survive by decades many creatures with slow tickers. Other assumptions, such as acute animals generate more free radicals damage tissue or have cells that stop dividing before, also lack solid evidence. "Many simple stories have disappeared," he said.

(chart) A. Cuadra / science (Data) Anage

Austad should know about thing about animals. He worked as a lion coach in the early 1970s, until one of the big cats tore his leg injury that persuaded him to study, rather than tame, the creatures of the world. in the mid 1980s he was observing the behavior of opossum in Venezuela as a postdoc when he began to notice how quickly marsupials older. "They're going to be in great shape for cataracts and muscle atrophy in three months, "he said. Austad also noticed something even more intriguing: possums on a nearby island free of predators appeared to age more slowly and live longer, their mainland counterparts

The observation has helped explain why a key insight Aristotle continues to be true .. large animals tend to live longer, Austad said, because they face less danger. This is not a simple matter of survival, he said, but rather the result of millions of years of evolutionary pressure. Whales and elephants can afford to take their time growing because no one will attack, he said. And that means they can invest resources in solid bodies to enable them to produce many offspring cycles. Mice and other prey heavily on small animals, on the other hand, live life in fast forward: They need to put their energy into growth and rapid reproduction, not in the development of hardy immune systems, Austad said. "You would not put a $ 1,000 crystal on a watch for $ 5."

WHEN IT COMES TO OUR ANIMALS , the largest-is-better theory turned on its ear. The cats live on average 15 years, compared to about 12 for dogs, despite being generally smaller. And the dogs can live twice as long than large.

Yet the lesson of Austad of opossums may still apply. Gray wolves, the ancestors of dogs, live up to 11 or 12 years in the wild, while feral cats can live up to 16 years. This suggests that the two species face different pressures of evolution, says Austad. The wolves are more social than cats and therefore more likely to spread infectious disease, he said; wildcats, on the other hand, keep to themselves, reducing the spread of disease, and are able to defend themselves against predators. "Cats are so incredibly well armed, they are like porcupines" -an animal who notably also a long life for its size, more than 20 years. Indeed, two other small animals that are good to avoid danger, rats and bats naked moles, can live 30 and 40 years, respectively. (Mole Rats spend most of their time underground, while bats can simply fly away.) Mice, meanwhile, only live a few years unless they eat first.

David Hedges / SWNS.com via Guinness world records

Poppy, recognized as the oldest cat in the world in 2014, lived to the ripe age of 24.

regarding why small dogs tend to survive large, the story gets a little more complicated. Large dogs like the 70-kilogram Irish Wolfhound have the chance to get to 7 years, while tiny pooches like Papillon 4 kilos can live 10 years longer. Most dog breeds are at least two hundred years the pressure, so that evolution is clearly not at work. Instead, hormones such as insulin-like growth factor 1, which inflates the dogs to great heights, can play a role; Researchers have linked short-lived protein in a variety of species, although the mechanism is unclear. Large canines also tend to grow faster, Promislow note of Aging Dog project, which could result in "jerry-built" of the body that are more susceptible to complications and diseases. Large dogs tend to have more health problems than those German shepherd children are prone to hip dysplasia, for example, and Siberian Huskies are plagued autoimmune disorders, although these could also be the result of inbreeding.

Despite differences between cats and dogs, two animals living longer than ever before. Dog life expectancy has doubled in the last 4 decades, and housecats now live twice as long as their wild counterparts. The reasons can largely be chalked up to better health care and better nutrition. Americans will spend $ 60 billion on their pets this year, with much of that going humanlike health care (think annual physicals and open heart surgery) and premium food. "The same things that allow us to live longer also apply to our pets," says João Pedro de Magalhães, a biogerontologist at the University of Liverpool in the UK Anage maintains the largest database in the world animal life covers. The trend can not continue, if :. More than half of US pets are overweight or obese, and they are exposed to the same pollutants and carcinogens that we are

All this sets only dogs and cats to solve the riddle how we age. After all, we have over medical records on them than on any other animal save man, and we are learning more about their biology and genomes every day. Perhaps they hold the clues to slow down the body clock for us all and maybe even stop it. "I do not think there's a nuts. longevity for all species. ", says Magalhães" The real question is: "How far can we go? Perhaps a thousand years from now you might have a dog that lives 300 years. "

This is good news, especially if our lifespan increase dramatically as well. After all, who wants to live forever if you can not live with your best friend

for more information on aging :?

• Feature: Death defying experiences
• Feature: the countdown

About half of Americans use marijuana at some time in their lives, and many are beginning to adolescence. Although some studies suggest that the drug could harm the adolescent brain maturing, the real risk is controversial. Now, in the first study of its kind, scientists have analyzed the consumption of marijuana long term in adolescents, comparing the IQ changes in twins siblings who either used or abstained from marijuana for 10 years . After taking environmental factors into account, the scientists found no measurable link between marijuana use and lower IQ.

"This is a very well-conducted study ... and a welcome addition to the literature," says Valerie Curran, a psychopharmacologist at University College London. She and her colleagues reached "largely the same conclusions "nontwin in a separate study of over 2,000 British teenagers, published earlier this month in the Journal of Psychopharmacology , she said. But, warning that the study has important limitations, George Patton , psychiatric epidemiologist at the University of Melbourne, Australia, added that it does not prove that the particularly heavy marijuana, or chronic use is safe for adolescents.

most studies that linked marijuana for cognitive impairments such as memory loss and low IQ, looked at a single "snapshot" in time, says statistician Nicholas Jackson of Southern California University in Los Angeles, lead author of the new job. This makes it impossible to tell which came first: drug use or poor cognitive performance. "It's a classic chicken egg scenario," he said.

To further probe whether marijuana erodes IQ or inflicts damage in other respects, scientists have begun to follow large groups of drug users among adolescents over time. The first study to do in Dunedin, New Zealand, in 2012 reported significant declines in IQ between 13 and 38 years in heavy users compared to those who used marijuana before age 18 occasionally or not at all. The document "has had a major effect on thinking about the risks of a strong early exposure to cannabis," said Patton, a co-author. Critics, however, noted that the study was not able to rule other possible explanations for the decline in IQ, such as family environment of a teenager or have dropped out.

one way "powerful" to address these concerns is to study identical twins, who share genes and education, said Jackson. in the new study, he and his colleagues looked at 789 pairs of twins teens two courses of studies in the Los Angeles, California, area and the other of Minnesota who enrolled between the ages of 9 and 11. over 10 years, the team administered five tests of intelligence and confidential surveys of marijuana. They also asked about the use of other drugs such as opioid analgesics, cocaine and excessive alcohol consumption.

Marijuana users lost about four IQ points during the study. But their brothers and twin sisters abstainers showed a similar trend of decline, suggesting that the loss of mental acuity was due to something other than pot, said Jackson. "Our results lead us to believe that this" something else "is related to something about the shared environment of twins, which would include the home, school, and peers," he said.

in the new study, adolescents who reported daily use of marijuana for 6 months or more showed no difference in how their IQ has changed, compared to teens who had tried pot less than 30 times. This is a "clear indication that cannabis is unlikely to be the cause of lower IQ," says Claire Mokryz, a PhD student in the laboratory of Curran.

But others say the new study has flaws-especially, a lack of detail on how often and how much adolescents used marijuana. Minnesota groups and Los Angeles have used various surveys on drug use. Questions of the Los Angeles group were much less extensive, Patton said. In surveys administered to this group, for example, participants were asked, "Have you ever tried marijuana?" If a 13 year old respondent answered "yes" after taking one breath, they could be considered as a drug user for each measurement result. "My feeling is that this document is not enough to dismiss the concerns of [our] Dunedin study on the effects of early intensive use of cannabis" in adolescents, Patton said.

Sarah Ewing Feldstein, a psychiatrist at Oregon Health & science University in Portland, agrees. "while it is possible that the results are quite accurate," she said the study represents a "missed opportunity to get a really detailed analysis" of the contribution of cannabis and other substances in IQ.

Although there is "new evidence" that marijuana erodes not IQ, "it does not mean that heavy use in adolescence is no problem," said Jackson. Other aspects of the daily operation might be affected, he said, adding, "we desperately need more research on the effects of marijuana on the brain."

The best way to study the cognitive effects of marijuana would be to administer the drugs to people and see how the duration, frequency and dose affect the brain, said Jackson. "Unfortunately, these types of studies are almost impossible because of federal restrictions," he said. For now, he said, "I am especially concerned about what is happening in the child's environment, who is 14, is seeking refuge in drugs. "

If you have the rare condition known as hives of vibration, you may be wary of handling trimmers and electric mixers. Rub or vibration against your skin, even dry with a towel can make you break out in hives, make your face blush, you give headaches or produce the sensation of metallic taste. The condition that runs in families, is so rare that researchers working on it have only tracked some cases over the years of research. But a genetic study on three of these unique families revealed a potential mechanism for the strange symptoms. Research published online today in The New England Journal of Medicine describes a mutation in a gene called ADGRE2 found in 22 individuals with the vibratory urticaria, but not in 14 parents are not affected. The gene codes for a receptor protein that was found on the surface of mast cells, immune cells in the skin that discharge inflammatory molecules such as histamine that increases blood flow to an area and can cause urticaria. The researchers observed that shaking the mast cells in a dish breaks apart of two subunits of the receptor protein, prompting the release of histamine. In people with the newly discovered mutation, the receiver is more likely to rupture, causing the protective immune response at the site of physical trauma to unleash.

Zika virus may be the day, but the results worrying about the latest outbreak that shook the world are continuing to emerge. At a meeting last night in Boston, researchers presented new evidence that the Ebola epidemic in West Africa has had long-term effects on many survivors, including joint pain, neurological disorders and eye damage. They also found that many men harbor the virus RNA in sperm after they recover and far longer than imagined, suggesting that new outbreaks caused by sexual transmission are always a threat and that many people may well have had Ebola unknowingly.

disappointing results the scientists also presented a clinical trial of what was once considered the most promising treatment Ebola antibody cocktail called zmapp. The study began at the end of the epidemic, registered far fewer people than the researchers had expected, and it has failed to provide statistically significant results.

The details were revealed last night during a special session at the largest annual meeting of HIV / AIDS was held in North America, the Conference on Retroviruses and opportunistic infections. The results of Ebola were decidedly off-topic, but meeting organizers have decided to make room for them because of overlap in the research community about HIV and Ebola, and because of the magnitude of the epidemic .

Eugene Richardson, an infectious disease specialist at Stanford University in Palo Alto, California, started the session with the data in an unusual study that helped the conduct in Sierra Leone. Working with health partners, a non-profit headquartered in Boston, researchers and Sierra Leone, Richardson went to a village hit hard a year after the last transmission occurred. He wanted to determine how many people may have been infected without ever being diagnosed.

During the epidemic, 34 villagers had a confirmed or probable cases of Ebola. Richardson and his colleagues visited their houses and tested blood from 207 people who had lived there, but are not known to have had Ebola. Fourteen of them had Ebola antibodies, indicating they had been infected.

Two of these people, it turned out, had had fever during the quarantine period, and the cases were suspected and whether Ebola teams had found. "We asked," Where were you when we came around the watch? ' "Said Richardson. "They said, 'Hiding in the bush." ​​The other 12 people with antibodies reported no symptoms at all. This means that overall, 25% of 48 people from the village who were confirmed to have Ebola or have was deemed probable cases had no symptoms.

Although positive antibody tests do not prove that people were infected various diseases, can trigger the production of antibodies similar looking-other findings supported the suggestion that the Ebola virus infections can occur without any symptoms. in a presentation on two vaccines tested Ebola in Liberia, scientists reported that 6.3% of those who registered had antibodies Ebola before they received the experimental products. As Fatorma Bolay, director of the Liberia Institute for biomedical research, explained, these participants had "no knowledge of previous infection of the Ebola virus."

"It is certainly possible, if not probable, that there is an asymptomatic infection," said Nancy Sullivan, Ebola researcher at the US National Institute of Allergy and Infectious Diseases ( NIAID) in Bethesda, Maryland, who co-chaired the session. small studies 15 years ago from an outbreak in Gabon have also reported high rates of asymptomatic infection.

the enormous scale of the epidemic of 2013-16, which has sickened more than 28,000 people and killed 11,316 has allowed investigators to collect the most accurate ever obtained evidence on the long-term damage Ebola, including his strange ability to persist in the body after the patient recovers. Jean-François Etard of the Institut de recherche pour le développement (INSERM) in Montpellier, France, described a study being of survivors that it leads with Guinean colleagues. to date, they examined 475 people whose blood was found on average clear the virus nearly 8 months earlier.

In clinical examinations, 83% of people reported at least one long-lasting symptom being joint or most common muscle pain, headache and fatigue. Eye examinations by specialists have shown abnormalities in about one in five patients and two children had gone blind from cataracts. The researchers obtained samples of sperm from 107 men; 6% tested positive for Ebola RNA viruses. The team found viral RNA in the sperm later than 9 months after a man had been discharged from an Ebola center.

A second study provided more details on how long the Ebola virus can remain present in semen. INSERM researcher Daouda Sissoko studied 26 men in Guinea who provided samples several times; 55 days after the onset of the disease, 73% had still Ebola RNA in their semen, and 246-day more than 8 months after getting better 27% were still positive. A man is positive to 334 days. More disappointing still, another study in 97 men in Liberia reported that the sperm of a man tested positive 18 months after his recovery, and three had Ebola-positive sperm after two previous samples have tested negative.

testing RNA positive do not mean a person is contagious; it is possible that the virus is viable or is present in minute quantities such that it is no longer a threat. However, sexual transmission of survivors considered clear of the virus have been documented, and the World Health Organization urged men who have recovered from Ebola to use condoms for at least 12 months after recovering from illness or until they have two negative RNA tests for the virus in their semen. "A single sexual transmission could restart the transmission chain," said Etard.

final presenter of the session, unveiled the highly anticipated results of a multicountry study of zmapp the frontrunning after experimental treatment saved monkeys from Ebola enormous five days after infection has occurred. Richard Davey NIAID, which co-led the study, said the trial, which enrolled patients in Liberia, Sierra Leone , Guinea and the United States had hoped to enroll 0 people. They would be receiving "optimized standard of care" -the group or control the intervention over three intravenous infusions of zmapp spaced 3 days apart. Ultimately, the waning epidemic forced the team to complete the study late last month after only 72 people registered.

One participant was "lost to" Davey said, and the remaining 71, 21 died: 37 % in the control group against 22% among those who received zmapp. "We must carefully choose its adjective," said Davey. "This is certainly suggestive of a trend in favor of containing arms zmapp." But the results are not statistically significant.

as Science reported last month in a special report , the enormous effort to test new drugs and vaccines in Guinea, Sierra Leone and Liberia has produced a thin harvest a vaccine produced by Merck is the only product that has shown positive results unequivocally Many held out some hope that the study, which zmapp used a randomized controlled design, the gold standard in. clinics deliver another bit of good news trials.

Mapp Biopharmaceutical, San Diego, California, company zmapp factory, issued a press release yesterday, quoted its CEO, Kevin Whaley, saying the company will now "vigorously pursue the development and permit application zmapp as a treatment for Ebola."

When the pharmaceutical company Eli Lilly in Indianapolis last week announced a major change his trial monitored closely for drug solanezumab Alzheimer's, some of the Community industry and the development of scientific medicine cried foul. To critics, the company's decision to eliminate changes in daily ability of an individual to function as a first measure of the effectiveness of solanezumab and focus only on a cognitive test appeared to be a last attempt to keep a drug doomed to fail his third trial. Lilly shares fell nearly 5%, apparently reflecting that feeling

Foul play :. Lilly is trying to cheat on the study midstream # Alzheimer obviously because the medicine will not work. https://t.co/dnp7C9mWYz

- Allen Frances (@AllenFrancesMD) March 16, 2016

largely lost in the line "chat", however, is that the movement Lilly reflects a growing scientific consensus on how the early stages of the progression of Alzheimer's disease, said Dennis Selkoe, a neurologist at Brigham and Women's hospital in Boston, who is not involved in the Lilly trial. "From the standpoint of a neurologist who has seen hundreds of patients, [Lilly’s decision] clinical sense," he said.

Solanezumab is an antibody designed to bind to and promote the clearance of β -. amyloid protein that forms plaques around neurons of people with Alzheimer's disease Not everyone agrees that these plaques are the cause of the disease, a concept called amyloid hypothesis, which Selkoe is a developer, but important fight is the basis of almost all current efforts in the development of Alzheimer drugs. by helping to destroy plaques in people with early stages of the disease Alzheimer's, Lilly hopes solanezumab may slow the progression of the disease.

A major challenge of these trials is how to measure the benefits of the drug, said Selkoe. Although people with early Alzheimer's disease may show impairment and problems with attention and memory of light concentration, they can often follow recipes, make a cup of coffee, or drive a car, said Selkoe. These capabilities are unlikely to change the course of a clinical trial of 18 months, and any medications to improve the daily functions is unlikely to show a difference from placebo, he said.

Regulatory bodies such as the US Food and Drug Administration (FDA) have always required and still officially stipulate that the Alzheimer drugs show efficacy in two cognitive tests and functional measures. Recognizing that functional measures might not be appropriate at an early or mild stage of the disease, however, the FDA and other agencies have begun to soften their initial standards for drugs to prevent, rather than reverse the pathology and symptoms of Alzheimer's disease, said Selkoe.

In two previous trials of solanezumab, called EXPEDITION and EXPEDITION II, Lilly used both a cognitive test and a functional measure to monitor the response of people with Alzheimer's disease in both mild and moderate . Both trials failed to show significant benefits compared to placebo in both measures. Combing through the second trial data, however, Lilly noticed that participants with mild Alzheimer's disease seemed to do better than the controls in the cognitive part of the test, said Eric Siemers, a neurologist employed by Lilly.

This led to Lilly's current play a billion dollars on a study of about 2,100 people with only mild Alzheimer's disease, which ends in October. The last-minute decision to abandon the functional measure in this third trial, EXPEDITION III, was not based on any insight into the current test data, as some have suggested, Siemers said investigators are still blind to which participants received the drug and who received a placebo.

instead, the change reflects the functional evaluation of belated recognition certainly, there is no well validated for mild Alzheimer's patients, according Siemers. "As we've done more analysis, and talked to more people in the field, we got to the point where we did not know what functional measurement is the best for this group," he said. To fill this gap, the company is still collecting operational data using two separate evaluations, and hopes to see if either is better detect subtle changes, Siemers said.

Scott Small, a neurologist at Columbia University who is not involved in all clinical trials of Alzheimer's drugs, says he finds that it is a "reasonable" explanation. "If this is the case of clinical neuroscience moves, why include [function] as an end point?" He said.

Still uncertain is how to shift Lilly clinical trial will be judged by the FDA and other global regulatory agencies during the final data become available in the course of 2017. The company did submit the changes to all relevant regulators. But because a change of setting has no effect on how the study itself was conducted before data analysis, Lilly was not required to seek formal approval from the FDA or any other regulations to make the change, says Siemers.

Selkoe believes FDA sympathetic consideration solanezumab if it shows convincing evidence of cognitive benefit without functional data especially if these positive results are matched with PET encouraging data seeking to demonstrate a reduction in amyloid plaques . "We have long known that the cardinal manifestation of the disease [in the early stages] has minor problems with every day in memory, it is a very subtle process when it starts," he said. As such, Selkoe concludes, " we have to be more sophisticated "in the treatment of test," and that's what Lilly shows evidence. "

For the last 10 years, a facility at the National Institutes of Health (NIH) in Bethesda, Maryland, HAS Housed baboons with pig hearts beating in Their abdomens. They're hand of an experiment That there Researchers hope will help pig organs Develop safe for transplant into people, about 22 of Whom die Each Day in the United States alone while waiting for human organs are in short supply That. Today, Those NIH Researchers and Their Collaborators report record-setting survival data for five transplanted pig hearts, one of qui Remained in a healthy baboon for Nearly 3 years. The results-in baboons That Kept Their original hearts and Were Given Regularly hefty doses of immune-suppressing drugs-aren't enough to justify testing pig organs in humans yet. Purpose They Come as an Encouraging piece of evidence for the long-Struggling field of cross-species organ transplants, Known As xenotransplantation.

"People used to think That this was just Some wild experiment and it Has No implications, "says Muhammad Mohiuddin, a cardiac transplant surgeon at National Heart, Lung, and Blood Institute in Bethesda, Who led the study. "I think now we're all learning that [xenotransplantation in humans] Actually can happen."

Simply moving an organ from one animal species into Reviews another provokes a violent and immediate attack from the host's immune system. In early cross-species transplants, "we Measured the survivals in minutes," says David Sachs, a transplant immunologist at Harvard Medical School in Boston, Who has Worked there for xenotransplantation Several decades. In pigs-the Most Likely candidate for replacement human tissue, in hand Because Their organs are similar in size-a carbohydrate called Expired α-1,3-galactosyltransferase (gal) on the area of ​​blood vessel cells Would prompt the human body to make antibodies That latch onto it and causes blood clots. Once scientists Developed a Genetically Engineered pig lacking the gal gene in 01, swine organs Began to survive for months in baboons and --other Nonhuman primates. Purpose thesis animals still Had To Be Kept were drug regimen That protected the foreign organ by suppressing Their immune systems, leaving em vulnerable to infections.

Mohiuddin and his colleagues-have-been experimenting with more Targeted drugs That might protect a Dramatically transplant without tamping down the whole immune system. Among the Most Promising, he says, is an antibody blocks That communication entre some immune cells by binding to a receptor on Their area called Expired CD40. In the new experiment, the group used the anti-CD40 antibody, along with the blood-thinning drug heparin, to prevent prevention clotting in five baboons with hearts transplanted from Genetically Engineered pigs. These pigs lacked the gal gene, and aussi Expressed genes for two human proteins: one that helps Regulate blood clotting, Reviews and another That blocks the signaling molecules That prompt an antibody response leading to Damaging clots

Instead of swapping out a baboon's heart original, the Researchers hooked up the pig heart to blood vessels in the baboon's abdomen. That way, They Could study immune rejection without doing a more Elaborate heart surgery-and without needlessly killing a baboon if Their approach Was a flop. The engineered hearts combined with immunosuppression soon smashed the record for Existing pig-to-baboon heart transplant-179 days. "Every [scientific] meeting, we'd go and say, 'Oh, we got the first 236-day survival, the first 1-year survival, the first 2-year survival," says Mohiuddin. "It was losing ict charm." His answer asking whether the hearings started baboons HAD Developed tolerance-whether Could They now sustain thesis hearts without high doses of immunosuppression.

So the Researchers Began to enter the baboons off the anti- CD40 antibody. That turned out to be the end of the experiments-the baboons rejected the hearts once the anti-CD40 antibodies left Their systems, the team reports online today in Nature Communications . They found in two baboons That HAD beens Who we immunosuppression for a year before tapering off, the hearts Could survive with lower doses of the drug. Goal two baboons tapered off the drugs 100 days postsurgery Began to reject Their hearts Almost time immediately. (One baboon died from an antibiotic-resistant infection about 5 months partner after the transplant.) The experiments suggest tapering That a lower "dose maintenance" might be effective, Mohiuddin says. Aim it aussi means clustering this transplant approach Would require lifelong immune suppression.

In human patients That Would confer an Increased risk of infection, says Sachs, Whose own lab is working on ways to Induce long-term tolerance after-organ transplants . "Somebody might feel [that] if you can save a person's life purpose you-have to leave 'em on long-term immunosuppression ... that's OK," says Sachs, "but that's something That HAS to be decided."

Another major caveat, says transplant immunologist and physician Daniel Salomon of the Scripps Research Institute in San Diego, California, is que la results do not Prove Would the hearts function well in the chest. "Having to pump Actually do the work to keep the animals alive ... is a big deal," he says. "Just contracting in the abdomen and doing nothing physiological is much easier." Mohiuddin and his team are gearing up for true heart replacement surgeries in a new group of baboons.

Regarding animal models of the immune system, laboratory mice as the profane own version of a song ?; they are still pretty good, but they can not capture the texture of real life. Unlike wild rodents, laboratory mice are bred, raised, and lodged in essentially sterile environments. It experimented with the easiest to reproduce and control, but it also raised serious concerns about whether or not they are realistic models for humans. Now, two new studies, researchers have proposed a way to "dirty" these mice, although some fear that the work could jeopardize future studies.

"I think these very, very important are studies," says immunologist John Wherry at the University of Pennsylvania, who was not part of the work. "They have a lot of impact on how we think of a chronic infection and global health."

The first of the new studies, published today in Nature David Masopust immunologist at the University of Minnesota, Twin Cities, Minneapolis and his team set out to create mice laboratory whose immune system more like their wild counterparts. They did this by obtaining mouse in pet stores, which have no sterile precautions facilities reserved for laboratory mice, and place them in a cage with laboratory mice. Before cohabitation, laboratory mouse has a low number and variety of memory T cells, which are specialized in the fight against a variety of foreign invaders. Their "immune profile" closely resemble that of a newborn, probably because they rarely have to deal with infections. "[Lab mice] had a very privileged life," said Masopust. "We do not live like that."

Things changed radically after 2 months with the pet mouse. Twenty-two percent laboratory mice died, but those who survived showed profound changes in their immune system. exposure to increased pathogen various components of the immune system in the blood, especially cell subsets T moving specialized immune profile closer to that of an adult human. the tests for common pathogens mice showed that laboratory mice were exposed to viruses, bacteria and parasites worm. cohousing has also changed the way the mice responded to new infections: After mixing with dirty mice, laboratory mice showed 10,000 times in their immune response against a bacterium known as Listeria monocytogenes -a reaction tied with animals mouse store themselves.

Masopust believes the experience has produced mice with immune systems more realistic kind of animal you would need, he said, to test more precisely the power and safety of new drugs and vaccines. He says that in the future, researchers could expose laboratory mice a mixture of pathogens similar to what humans might experience to get a better idea of ​​what this directory is for the immune system in general. In a perfect world, researchers could adapt this directory to match the pathogens of certain parts of the world as well.

And indeed, scientists are studying exactly the idea. In the second study, published today in Cell Host & Microbe , viral immunologist Skip Virgin of Washington University in St. Louis, Missouri and his team infected laboratory mice with herpes and influenza virus as well as intestinal worms to trace how rodents responded to a vaccine against yellow fever. "We are interested to see if we could change and, at least in theory, improve the mouse model by its exposure to more normal environmental agents," says Virgin. These pathogens were selected because they represent common infections in many parts of the world; if their presence affects how animals react to the vaccine could help explain why some vaccines seem to work better in some populations than others.

Initially, immune responses to the vaccine against yellow fever were similar between mouse and a standard laboratory co-infected with other pathogens group, but after 34 days, the group co -infecté showed signs of a reduced immune response to the vaccine, as shown by a decrease in the amount of antibodies directed against the vaccine components present in the blood of rodents. Analyses of the DNA in the blood of mice have also shown that gene expression differed between the two groups. The researchers observed changes in the fundamental genetic activation of T cells, cell death and immune response to signaling molecules, indicating that co-infection with other common pathogens modifies the immune system at the genetic level .

"[Masopust] showed that the natural state of animals is very different in nature or a pet store in a [lab]," said Mary. "We have shown that in controlled conditions, you can make substantially similar changes taking this very own mouse and giving it a range of infections. "

Exploiting this knowledge to create mice populations that closely mimic human immune systems is still far away, though. one of the biggest challenges will be to do it in a way that does not ruin the many benefits of laboratory mice. Imperfect as they may be, laboratory mice have shown an excellent model for the man in countless scientific experiments. Their sterile environment and the blank slate of immune system ensures that all scientists are working with the same models. Introducing changes to the immune system must be done in a very careful and calculated manner if it works all, Virgin said.

Wherry is also cautious, noting that apart from the issue of reproducibility, it will also be expensive and time consuming to create and house mouse populations with the desired immune profiles. "I think we'll see it used selectively in certain areas," he said. "It would be very difficult to do consistently and apply at all levels." Despite the difficulties, Wherry says he can envision a future in which scientists can select from a library of mice with defined immune profiles that reflect different human populations.

"That's the dream," Virgin said.

* Correction, April 21, 9:03 a.m. The original version of this article mentioned mice and rats. The experiments were carried out on mice only.

In the most optimistic scenario, a vaccine could Zika prove his worth at the beginning of 2018, Anthony Fauci, director of the National Institute of the United States allergy and infectious diseases (NIAID) in Bethesda, Maryland, said today.

NIAID plans to begin testing a vaccine produced in its laboratories in September to 80 people, said Fauci, who spoke at a press conference in a meeting on Zika communication challenges risks of viruses in Washington, DC If the vaccine proves safe and able to stimulate relevant immune responses, he said the NIAID plans to the first quarter of 2017 to launch what he called a phase 2b "in a country which has a very high rate of infection. "This study would enroll thousands of volunteers. "If in the first part of 2017, we still have major epidemics in South America and the Caribbean, we can show that it is effective or not in one year," Fauci said.

Several factors determine how long it takes a trial to determine the value of a vaccine, he warned the first is the way the vaccine. it is easy to see a difference between the vaccinated and unvaccinated controls whether a candidate product is 100% safe and effective, which is rarely the case

a second important factor is the speed Zika virus spreads in communities participating in studies. a higher incidence it is easier to collect data faster, but the impact, in turn, can be affected by the degree of immunity that people have naturally acquired before the start of trial. specifically, the virus spreads more slowly in people who have already been exposed to it and developed effective immune responses.

Fauci noted that at the time of NIAID set to make Ebola vaccine efficacy trials in West Africa in 2015, there was a sharp drop off in new infections, making it difficult to execute effective tests. "If this happens during the Zika vaccine efficacy trials begin," he said, "it may take 3 years to show whether it works or not." But the massive pandemic Zika being contrary to the Ebola epidemic, should not disappear from Latin America and the Caribbean in the near future.

Sylvain Aldighieri of the Pan American Health Organization in Washington, DC, who co-sponsored the conference with the US Department of Health and Social Services said, to date, the pandemic has affected 37 Zika countries and territories. "We believe that about 500 million people in the Americas are at risk of being infected by Zika virus," said Aldighieri.

Zika trigger any detectable symptoms in about 80% of people infected, but rarely cause serious damage. "It's one of the real problems we have with communication," said Fauci. "How do you communicate the danger and the threat of a disease that is basically historically sweet?"

but there is at least a real threat, "which drove him to the attention and concern worldwide," Fauci said, If the virus infects pregnant women, their babies may be born with small heads, called microcephaly and other abnormalities

Fauci said that. " we do not know exactly what the percent is "Zika infected women who give birth to babies with related problems. A small study suggested that it might be as high as 29%, but another study used a very different methodology found was only 1%.

to obtain more reliable figures, NIAID, the US centers for disease control and prevention, and Brazilian researchers plan to collaborate on a study who hopes to follow thousands of pregnant women infected Zika country. "We do not know beyond what microcephaly are the long term effects on babies might look like they were born normal, but may have defects that are more subtle hearing, vision, intellectual and others, "Fauci said." Although we know a lot about Zika, literally every week that passes, we learn more and more. "

- Four people with a family history of cancer, or who have cancer themselves, filed a complaint this afternoon with the US Department of Health and Human services (HHS). It alleges that Myriad Genetics, a genetic testing company leading, violated a federal rule retaining the genomic data that are rightfully theirs. At least one applicant wants to share information with a search database of open access, which Myriad has refused to participate.

In a twist, after the American Civil Liberties Union (ACLU) has informed journalists a press conference ahead of the issue, Myriad changed course and provided patients with information that they asked in February. Despite this movement, ACLU went ahead and helped the patients file the complaint, in part because it covers what the organization describes as a past violation.

A spokesman for Myriad, based in Salt Lake City, said the company is frustrated by the complaint and believes that it should be abandoned.

genetic testing laboratories, including Myriad normally provide customers with information on genetic variants that are known to increase the risk of disease (pathogens) may be pathogenic, or meaning uncertain. But almost everyone also has variants (often called polymorphisms) that are considered benign and companies generally do not send customers information about these variations. But researchers are pooling the data of thousands of genetic tests for cancer, some of these minor variations may be reclassified as dangerous, or can be informative in a way that was not expected. That is one reason why some of the patients involved in the complaint Myriad wanted to provide all of their genetic information, not just information on pathogenic variants.

In the complaint, the ACLU and the plaintiffs, supported by researchers in cancer genetics, that was against Myriad of new regulations promulgated by HHS this past January ". the complete information of the gene variant generated by the test "that individuals have the right to receive payment has been invited, federal officials say, by a federal law known as the law on Health Insurance Portability responsibility and (HIPAA), which among other things regulates the use of medical records and protecting patient privacy.

Myriad said he did not know about the new regulations, which was quietly posted on a blog HHS. In February, the company was surprised to receive seven letters identical terms former clients, said Ron Rogers, a spokesman for Myriad. "It was obvious to us that there was some sort of coordinated effort against Myriad for this information," says Rogers. The company receives up to 40 requests per day for the test results, and "99.9% of them, "says Rogers, are for the usual pathogenic variants or uncertain, the kind included in the reports of the company's patients. In this case, patients wanted polymorphisms-essentially, benign variants. The letters referenced settlement in January.

Following these letters, Myriad discovered the HHS rule change, Rogers said. Yet the company has no immediate information to patients, but provided results that usual tests each patient had received. With representatives of the firm LabCorp test and the American Clinical Laboratory Association, Myriad staff traveled to Washington to meet with HHS officials to better understand their obligations under the new regulations. "We tried to get a meeting ... as quickly as possible" with the office of the Department for Civil Rights, said Rogers. The office "we said how they interpreted the direction, it should include benign variants. We quickly got to work, we have compiled this information, supplemented this request yesterday and sent to all patients."

The four patients represented by ACLU is not appeased. (The organization declined to say if it had worked with the other three.) It is "my body, my blood, my data, my choice that I wish to share my information," said Annemarie Ciccarella, one of complainants, during a conference earlier today to the press. It was ten years ago, Ciccarella was diagnosed with invasive breast cancer at 49 and with a strong family history of cancer, she followed the advice of his doctor and got BRCA1 and BRCA2 tested by Myriad. Mutations in two genes are linked to an increased risk of breast cancer, ovarian and other cancers. Ciccarella results, however, were equivocal; Myriad told her that he found a "variant of unknown significance" to BRCA1 and another on BRCA2 .

Ciccarella wants all its DNA information widely available to researchers, particularly wants to donate to a database called ClinVar. ClinVar collects DNA results on as many people as possible; a separate but related database called Clingen trying to understand what these results mean. (More information on both data banks is here.)

Myriad has provoked the ire of some scientists because the company refused to present his voluminous BRCA1 and BRCA2 data to ClinVar, unlike a number of other test companies. Rogers said it because he wants to protect patient privacy. A pair of scientists has launched an effort to obtain Myriad test results of patients and providers as a substitute. One of them, Heidi Rehm, one of the leaders of Clingen and Associate Professor of Pathology at Harvard Medical School in Boston, wrote a letter of support for the complaint of the ACLU.

Coating with her was Thomas Hudson and Peter Goodhand, two leaders of the World Alliance for Genomics and Health, collaborating trying to improve the sharing of genomic data. It is running a major effort to aggregate data on BRCA genes, called BRCA Challenge. Hudson and Goodhand called the HHS Office for Civil Rights to say explicitly that the settlement "includes calls variants" -Decisions about whether a variation is mild, for example- "and the first sequencing files, giving the patients right under HIPAA to regularly access them and thus contribute to the research and improvement of health. "

" I think it's much ado about nothing, "Rogers said of Myriad complaint. He said that Myriad has already provided polymorphism data in unusual patient who asks, and will certainly do so now, if required under HIPAA.

ACLU wants more assurance than that. "We need to know there is a change in their position," said principal ACLU staff attorney Sandra Park. She says she knows of another person who has submitted a polymorphism data request before the settlement change January, she said, and that was denied by the company. "From February they took the clear position that these data were excluded from what is covered by HIPAA."

Is there a larger goal to pressure Myriad deposit their data in public databases such as ClinVar? Park is oblique. "The best solution to this issue is that Myriad fair share," she said, "and communicates this data to patients who request it."