Health Meaning

a computer could predict the next pandemic? -

The use of a computer to predict an epidemic of infectious disease before it starts may seem a bit of Philip K. Dick's science fiction, but scientists are approaching. In a new study, the researchers used machine learning and computer education to recognize patterns in large data sets to make accurate forecasts on which the animals can harbor dangerous viruses, bacteria and fungi. Better predictions could help experts to improve the way they and prevent epidemics.

"I can not stress enough how exciting this paper. I think it will really resonate with the scientific community," says Lynn Martin, a conservationist of the disease to the University of Florida South, Tampa, who was not involved in the study.

Almost all new infectious disease outbreaks occur when a virus, a bacterium, a fungus or jumps from one animal to be human. accurately predict when and where these species infections called zoonotic diseases could stifle cross-epidemics before they become epidemics. But maintaining active surveillance of the disease worldwide is costly and takes time.

to help narrow the search, a team of scientists have built a computer program to analyze massive database habits and habitats of mammals, including geographical distribution and reproductive strategies for hundreds of species. Their program evaluated 86 variables such as body size, lifespan and population density, hunting for common patterns in animals known to be carriers of zoonotic diseases. "I'm really surprised that no one had. It seemed like a natural approach, "says team leader Barbara Han, an environmental disease in Cary Institute of studies of the ecosystem in Millbrook, New York.

To simplify the results, Han and his colleagues restricted their analysis to Rodents- a group that bears an abnormally high number of zoonotic diseases. Rodents carrying zoonotic infections tend to have "live fast, die young" lifestyle, said Han. They have large geographic areas, early sexual maturity, large litter sizes, and shorter periods of gestation. Scientists are not certain why this lifestyle is common in rodents carriers of zoonotic diseases, but they suggest that the pace reproduction cycle can allow animals to pass on their genes successfully before the disease kills. "Even if it kills you in 6 months, you'll be able to put out as five litters," says Han.

Han and his team first used their program to identify common lifestyles rodent harboring diseases such as plague, rabies virus and the haunted and found that their model had a 0% accuracy. After the machine had "learned" the warning signs, researchers sought new rodent who fit the profile, but no one previously thought to be carriers. So far, the model has identified more than 150 new animal species that might harbor zoonotic diseases, the researchers report online today in the Proceedings of the national Academy of sciences . the computer program also predicted 58 new infections in rodents that were already known to carry a zoonotic disease.

based on its findings, the team was also able to identify hot spots where a disease was more likely to jump from rodents to humans in the Middle East, Central Asia, and the US Midwest. Rodents living near the man were also more likely to be carriers of zoonotic diseases. But even as low population densities than 50 people per square kilometer have been associated with increased chance for zoonotic diseases in animals-a threshold that was surprising to Han. "I thought the tanks to be in areas where there are a lot of people," she said, "but it seems that if you have an average level of the man in your range that is enough."

As exciting as it is to predict new zoonotic diseases, it is another thing to prevent. "I think all the work is ahead of us," said Han It is difficult to know what the rodent distinguished by the study to focus on;.. Many rarely interact with humans, if at all behaviors humans such as deforestation, urbanization, and increased carbon emissions could all influence where and when an illness made the jump from animal to person, but exactly how and when this might occur is difficult to predict. Finally once the disease is cross species, health workers and epidemiologists will be challenged to contain and treat infections never seen before. "They can really we of whether a kind door a parasite, "says Martin. really understand how it is likely to cross to humans will require further study.

But Han said the work of his team has yet to make this job easier. He also talks about the importance of basic research, she said. Without the information from the database, much of which had no obvious application as it was being developed, the study would never have been possible. "I kind of worry if we stop to appreciate the contributions of basic science then we will not be able to do these types of breakthroughs in the future," she said . "One will not be able to predict anything if we do not have the back story. "

Making contact -

Push China Tissue Engineering - push China in Tissue Engineering

weight problem of liver -

drug antibody to stir hope and Alzheimer doubts -

The development of drugs for Alzheimer's disease is a cemetery for clinical trials, with over 0 failures over the past 20 years. The handful of approved treatments provide only a modest and temporary relief to symptoms such as memory loss; no stopping the progression of the disease.

In this gloomy context come the provocative results of two clinical trials highly publicized, presented today at the International Conference of the Alzheimer Association in Washington, DC Both trials tested antibodies that latch onto amyloid β, a protein that forms sticky masses in the brain of people with Alzheimer's disease. It was reported that treatment slowed cognitive decline; another found that the antibody reduces amyloid levels, many scientists have argued is the heart of the Alzheimer's brain.

The results, presented at the meeting by the biotech companies Biogen and Eli Lilly, provide some of the first "clear" evidence that the targeting of the β-amyloid protein is a promising approach for treatment Alzheimer's disease, said Dennis Selkoe, a neuroscientist at Harvard University and a leading proponent of the hypothesis called amyloid. But small and cognitive benefits that a trial showed no reduction of amyloid in the brains of people have left plenty of room for skepticism.

antibody, solanezumab Eli Lilly had failed to show a benefit over placebo in a previous trial in people with mild to moderate Alzheimer's and Lilly's own study in 2012. today, however, the company said the drug appeared to slow cognitive decline in a standard measure of about 34% in a subset of patients with mild Alzheimer's disease, which Lilly allowed to continue taking the drug after the trial has ended, 2012. A control group in the original trial which was then launched on the drug later showed similar improvements

However, the study did not Lilly actually measure the decline of amyloid Selkoe rating :. "It could go down, but we don 't know that." Participants in the Lilly trial also failed to show significant benefits in two other trials, cognitive important result that "guarantees caution to draw firm conclusions from these analyzes," the company acknowledged in a statement. hoping to see clearer benefits, the company is currently running, IIIa much phase, which will end in October 2016, only in people with mild Alzheimer's disease.

antibody adumanucab Biogen, also a record mix. He had put the effervescence in the Alzheimer community when the company announced positive results of an early study. After administering several different doses of the drug in 166 patients who had been diagnosed with early stage Alzheimer's disease, the company said that 27 people who had received the maximum dose of 10 mg per kg showed significant cognitive benefits compared to controls and reduced levels of protein.

But this dose caused brain swelling and microscopic hemorrhages in some cases, so the company decided to try a smaller dose, 6 mg. Today, the company said deflate the results of a monitoring test: Over 54 weeks the 6 mg dose showed no significant effects on cognition, although it has reduced levels of amyloid in the brain. The stock market, for one, found the results hard, first sending the stock price Biogen low after the data were released. Despite the setback, this year the company will launch a Phase III trial of 18 months with 2,700 participants in the US, said company representative Jeff Sevigny.

Much rides on the success of these monitoring tests, said neurologist Rakez Kayed from the University of Texas Medical Branch in Galveston, Texas. "If they do not arrive later and we get another black eye, it will be difficult."

Selkoe argued that new data suggests Biogen although other approaches to reducing amyloid, such as drugs that block the production and transport of molecules that contribute to amyloid accumulation and as vaccines that prime the immune system to break down the plaques should be "vigorously" pursued.

But Kayed warns that mouthwatering results should not obscure other approaches for the treatment of Alzheimer's disease. Although many researchers now agree that the amyloid β is an important trigger for Alzheimer's disease, most also think that secondary processes, such as the accumulation of another protein called tau, drive the disease in its later stages. "If we're all going in the β-amyloid and ignore other therapeutic approaches, it will be devastating," he said.

Feature: Revealing the hidden dangers of dietary supplements -

P ieter Cohen brush with death came at a most inopportune time. as he was about to nail another ingredient lurking in a dietary supplement

hike last August in New Hampshire with his wife and three children, Cohen, an internist at Cambridge Health Alliance in Massachusetts, stumbled and fell. A rock pierced his left calf. "It was a small cut, but deep," recalls his wife, Lauren budding. The next day, the bacteria were coursing through the bloodstream of Cohen. The leg became red and swollen. His blood pressure dropped precipitously. Cohen was taken to a community hospital and soon after by ambulance to a trauma unit in Boston.

Doctors worked feverishly to stabilize and stop the spread of infection. In the coming days, the threat of death receded, while the risk that he would never walk normally stayed. Cohen, meanwhile, frets on the same issues he did in general consumers, including patients, which could be swallowed up food supplements enriched with medication. And confined to bed burning pain, he asked his computer. His wife refused.

"I'm like, 'I'm sorry, that person needs to sleep," she told the hospital staff. So Cohen had his mother smuggled into the laptop, and data sets hidden inside the Boston Globe . "I could work on the manuscript when Lauren was not looking," he reasoned.

Eleven days after the accident, and after the fourth of what would be five surgeries, Cohen and two colleagues presented their document Drug Testing and Analysis . The report was unnerving: At least a dozen supplements sold in the United States for weight loss, improved brain function, and improve athletic performance contained a synthetic stimulant. The compound, which Cohen and his co-authors cited DMBA, resembled its chemical structure called a stimulant dimethylamylamine or DMAA. It has never been tested in people, in two animal studies of the 1940s "Its efficacy and safety are entirely unknown," they wrote

Now installed in a bed hospital in his living room and waiting for skin grafts to heal, Cohen appealed to the review :. "I can not walk, I am totally available. Can you Crank guys agree?" The paper was published online a month later, last October. In April this year, the US Food and Drug Administration (FDA) has issued warning letters to 14 companies that sell products containing DMBA. "FDA believes that these food supplements adulterated," he wrote. And boom, Cohen was on his next project.

Since 05, when he found his patients were sickened by a Brazilian against supplement containing -Depressants weight loss and thyroid hormones, Cohen become something of a mix of Indiana Jones and Sherlock Holmes in the world supplement. Chemist with colleagues in the United States, Brazil and Europe, hunting for drugs illegally buried in supplements. Then it goes public. His unorthodox public relations strategy is to publish the Quick Search low profile, journals, reaching out to a network of journalists handpicked, and he hopes eventually inspire new regulations. It has virtually no funding, nor aspire to guarantee all. "I have total freedom," he said. . So far, he and his collaborators have identified three stimulant drugs hidden in supplements

Cohen discoveries point to a larger problem, he and others argue: a dys-functional system for maintenance of order food supplements. "It comes to this," said Paul Offit, director of the Vaccine Education Center at Children's Hospital of Philadelphia, who published a book entitled Do you believe in magic? on alternative medicine. "Basically a citizen [is] take the test to make sure that what is on the label is in the bottle. ... It is absurd. "

But this citizen has an impact. Actions by the FDA cited the work of Cohen and monitoring its publications, like the warnings of DMBA did. He also drew the attention of supplement manufacturers, y included in a lawsuit filed against him in April looking for $ 0 million in damages. "Everything I write gets such a review" it creates enormous pressure, he said. "I want our science to be bulletproof."

THE AGE OF MODERN SUPPLEMENT started in 1994, when Congress passed the Education Act of health, or DSHEA and Dietary Supplement (pronounced duh-shay-uh). in the decades that preceded it, the supplement industry has been heavily concentrated on vitamins and minerals. much of the regulation based daily allowances . recommended products such as vitamin C, iron and calcium

DSHEA established the first general framework for the regulation of supplements It also gave supplements a legal definition. power as for substances "to supplement the diet," containing "food ingredients" such as herbs, plants, or vitamins

at the same time, the law greatly reduced the FDA .. companies are not required to notify the FDA provided food ingredient was a law before the use of history was adopted. For the first time, DSHEA has allowed them to make claims on supplement labels suggesting affect the structure or function of the body for example, by stimulating the immune system or the protection of the health of the prostate. DSHEA and codifies a loose arrangement: Under the law, as noted by the FDA on its website, "unlike pharmaceuticals that must be proven safe and effective for their intended use before marketing, there is no provisions in the law of the FDA to "approve" dietary supplements ... before they reach the consumer. "The agency can act only after a supplement is on the market and the evidence shows that it is dangerous.

Whereas consumers from industry and much celebrated DSHEA to expand access to supplements, the act was skewered by doctors, journalists and consumer protection groups. in an editorial shortly before DSHEA passed, the New York Times called the "snake oil protection law "suggesting that it was" the right unscrupulous companies and individuals to maximize profits by making fraudulent claims. "Meanwhile, the industry has grown exponentially: since 1994, the number of supplements food marketed in the United States has swelled from about 4,000 to more than 75,000. about $ 36 billion were sold last year.

the ink was barely dry on DSHEA when trouble began . Within 2 years, a Chinese herb called ma huang or ephedra, the companies promoted as a legal alternative to ecstasy, was under control. Although a natural product, the plant contains the chemical ephedrine, which stimulates the nervous system and constricts blood vessels. In early 1996, he had been linked to at least 15 deaths. Meanwhile, the FDA regularly published warnings on the liver, kidneys and other health risks associated with supplements.

"There are food authentic multivitamin-supplements, calcium, iron which supplement the diet" and can help many people, says rheumatologist and immuno-logist Donald Marcus Baylor College of Medicine in Houston, Texas, an early critic of the supplement industry. But other supplements, such as "St. John's wort, echinacea ... are used as drugs," he said. Partly because "botanicals are complex mixtures of chemicals," supplements in this category present "a serious and growing public health problem," Marcus and colleague, pharmacologist Arthur Grollman of the State University of New York at Stony Brook, wrote in the New England Journal of Medicine in 02 how great problem was unclear, however, because the FDA hears a tiny fraction of the effects adverse business, they noted.

Meanwhile, concerns about ephedra continued to rise. commissaries army stopped selling after he was involved in the death of soldiers; after 16 years of taking the supplement died in Illinois, the state halted sales of ephedra, too. FDA banned ephedra in 04 after a 23-year-old Major League baseball pitcher collapsed and died during practice and was found to be the grass.

The initiation of supplementation Cohen came to work. After finishing at Yale School of Medicine, he started his residence and then work at Cambridge Health Alliance, a network of neighborhood clinics and community hospitals. Many of Cohen's patients were Brazilian immigrants who settled nearby.

Before long, patients of the clinic developed mysterious symptoms. A woman came "with palpitations, sweating, anxiety, but also feel very tired," recalls Daniel McCormick, primary care internist in the same practice, mentor Cohen residence and shares a small office with him. Another rolled up in the emergency room with kidney failure. A man has lost his job after his urine tested positive for amphetamines

Cohen made the connection :. patients were all weight loss pills taking called diet arc pills, imported in bulk from Brazil. He sent the capsules to a private laboratory for testing. the results shocked the doctors. the tests revealed amphetamines, thyroid hormones, diuretics, benzodiazepines and antidepressants such as fluoxetine. "It was a Pharmacopoeia in a pill," says McCormick. "It became clear to many of us that you could explain the symptoms diet pills."

McCormick, Cohen and three colleagues conducted a survey of 307 Brazilian patients in their clinic and two neighboring churches. They found that 18% in clinical and 9% in churches reported taking the pills, and two-thirds reported side effects. The paper was published online in 07 in the dark Journal of Immigrant and Minority Health .

"Less than 10 people will read that," Cohen admitted to himself, because the magazine is so specialized. "I knew that if I wanted more ... I had to do some outreach." He contacted a local journalist who had recently NPR ran a story on Latino bodegas selling antibiotics without prescription, thinking he might be interested. The journalist invited to an interview in the studio. Folha de S.Paulo , a major Brazilian newspaper, contacted Cohen and published an article on the front page. a few years later, diet pills rainbow were banned in Brazil, though Cohen does not know if his work had something to do with it.

Cohen thought the enriched supplements were limited anomaly Brazilian neighborhoods. But then he received a call an official of the division of drugs to the FDA. "what you found in these diet pills shipped from Brazil," the official said, "are actually found in supplements weight loss in the US and is a major problem. "

" wE WERE WORRIED on contaminated food supplements for ages, "said Amy Eichner Agency US Anti-doping in Colorado Springs, Colorado. In 03 and 08 two elite swimmers have lost the chance to compete in the Olympics after testing positive for performance-enhancing drugs they said they did not know were in their supplements. A similar fate two best cyclists. "This is our nightmare scenario," said Eichner.

Another concern is longtime Patricia Deuster at the Uniformed Services University of the Health Sciences in Bethesda, Maryland, which estimates that between 15% and 20% of soldiers swallow supplements she and others worry about most.. the products marketed for bodybuilding, weight loss, and athletic performance another worrying category includes products for sexual enhancement

So in 2013, she and Eichner started the systematic analysis of additional ingredients. preliminary results, not yet published, show that of the 169 products tested at high risk so far, 107 "contained at least a banned substance in sport, "said Eichner, and often it did not clearly included on the label. In many cases, she said, the ingredients are "either Schedule III substances on the Controlled Substances Act, which is quite large and they have been specifically declared illegal by the FDA."

About this time Cohen had an electrifying telephone conversation. a scientific laboratory that tests supplements for the companies told Cohen he was deeply troubled by the prevalence of a substitute for ephedra, DMAA, which kept appearing in products despite increasing concerns about its safety. this conversation was "the catalyst that opened a new world to me," says Cohen.

with diet pills in the sky, he was focused on prescription drugs. Although DMAA had appeared in nasal sprays there decades before being removed from the market, it was now more like a "research chemical," Cohen said, some companies claimed came plants but Cohen and others challenged. It began to look dangerous additives in the supplements. FDA said the supplements containing DMAA illegal shortly after, in 2013, but as Cohen quickly learned there was no shortage of other targets.

"It is a situation Sherlock Holmes," he said with relish. "There is a crime scene, there are hints fight, people die after taking the supplements.? ... What really happens"

He found a ideal partner to more than 5000 kilometers, near Utrecht, the Netherlands: Bastiaan Venhuis, medicinal chemist who also analyzes the ingredients supplement. One of their first joint publications, in collaboration with NSF International, which tests foods, supplements, and other consumer products, appeared online in the fall of 2013 Drug Testing and Analysis . It considered a popular workout supplement called Craze. When Venhuis diluted powder and ran through his analyzer, revealing peaks indicated DEPEA, an analog of methamphetamine.

To collect advertising, Cohen has expanded the strategy he had followed with Brazilian supplements. He sought a final manuscript of the newspaper on a week in advance and sent personal emails to rise three dozen journalists, carefully selected for their coverage or the relationship he had fed them before.

boyfriend office McCormick Cohen acknowledges that these media awareness, which he made himself, can feel awkward. It is often considered "as self-promotion," says McCormick. "At first I felt this intense and it was very uncomfortable. ... But the number of hours that go into reflection on a research project, write, is simply wasted "if it stops there, especially when it could have an impact on health policy.

Cohen has attracted the attention not only of journalists but a myriad of the supplement industry, too. In late April, a company called Hi-Tech Pharmaceuticals has applied for $ 0 million in damages against Cohen and two colleagues, after researchers published a paper suggesting Hi-Tech supplements and other companies were marketing that contained a stimulant amphetaminelike, BMPEA they mislabeled as Acacia rigidula , a shrub that grows in Texas and south into Mexico.

company vigorously denies that BMPEA not part of the plant. "A true scientist concerned with objectivity would have taken steps to ensure they are not disparaging products before they did it to the public," said Edmund Novotny, a lawyer in Atlanta who represents Hi-Tech .

Cohen was not alone in singling BMPEA: His study was approximately 18 months after FDA scientists reported detecting BMPEA in supplements, also noting that nowhere could -they find evidence that BMPEA was a natural component of plants. Shortly after the publication of Cohen, the FDA sent warning letters to five companies that sell BMPEA-laced supplements, including Hi-Tech.

Like others, Cohen agrees that the FDA police extra powers are too limited. But this does not mean that the agency has no muscle. "There are so many things that could FDA they do not, "he said, for example, the removal of stores shelves supplements when companies do not fully pass FDA inspections. The agency, Cohen believes, is overwhelmed by the volume of supplements and discouraged by the political forces to act aggressively. When it comes to take an extra ingredient, the attitude of the FDA is "show us the bodies," he said.

FDA officials would not put it that way, but they strongly disagree not. " Under current law, the FDA faces a strong charge before taking enforcement action on a food supplement, "wrote spokeswoman Lyndsay Meyer in an email. The agency has its own frustrations. "... The supply chain is highly fragmented," wrote Meyer. "Individuals and companies that sell these products can run on residential homes, and distribute via internet, small shops, and email ... We recognize that more can and should be done."

Near a year after his terrible ordeal while hiking, Cohen has resumed full function of his leg, but he still has a low black compression. Sitting in his office in June, surrounded by pictures of his three children and a pell -mêle bottles of patients supplements given to him for testing, Cohen shows little fatalism of those who fought against the supplements for years. the reform movement "certainly has the momentum," he said. "I think we'll look back 50 years from now and say" How could supplements were regulated like that? "

In anticipation of that day, Cohen now works for nail two other drugs that appear in supplements. He also studied yohimbine, a prescription drug that can be extracted from the bark of a tree species Evergreen West Africa and sometimes appears in bodybuilding capsules. Like ephedrine, yohimbine "comes from a plant, but is pharmaceutically active," he said, blurring the line between the drug and the supplement.

His dream is an informed population with businesses required to fork over revenues and risks of their products. "Whenever possible, we should have the freedom to be able to buy everything we want to put in our bodies," says Cohen. "People should be able to buy echinacea. It's just, when they buy echinacea, they must know what they are getting"

* Correction, September 3, 11:37 :. This article has been corrected to reflect that the DMBA structure resembles that of a stimulant called DMAA, not methamphetamine.

Melatonin may help treat multiple sclerosis -

insomniacs and world travelers use both melatonin a hormone that regulates the body's internal clock to help them fall asleep and get some extra shuteye. Now, a new study shows that the "sleep hormone" may also provide relief to patients with multiple sclerosis (MS), a debilitating neurological disorder that can quickly morph remission in attacks that the last days, months, even years.

MS is a rare disease in which the immune own body cells attack neurons by eating away their protective layer, fat. This layer, the "myelin sheath" -insulates the portion of the neuron that transmits signals, such as flexible plastic protects the telephone cables. In patients with multiple sclerosis, the damaged sheath off the cell-cell communication, knocking out the vision, balance and muscle coordination, while altering the thinking and memory. The cause of MS is still unknown, and scientists suspect that environmental factors such as low vitamin D, obesity and viral infections could contribute.

Another environmental factor could be changes in the seasons. Mauricio Farez, a neurologist at the Institute Raúl Carrea for Neurological Research in Buenos Aires, and colleagues suspected as much when they noticed that fewer multiple sclerosis relapses occurred in the fall and winter time of year that melatonin production is at its peak.

melatonin levels depend on sun exposure, so that seasonal changes cause hormone fluctuate; less sunlight in fall and winter increases melatonin, while more sun in spring and summer decreases.

To test the "seasonal" effect of melatonin on MS patients, researchers followed 139 MS patients for a year, monitoring the rates and levels of a small molecule in melatonin relapse called SM-6. They saw that during the fall and winter, relapse rates of patients was 32% lower than in the rest of the year, when melatonin levels naturally plunge.

Think of the immune system probably played a key role, scientists hypothesized that the increase in melatonin has led to increased advocacy organizations called regulatory T cells, which work by secreting proteins protective that prevent rogue immune cells in check. At the same time, the active melatonin a protein that blocks the production of harmful T cells. The researchers then confirmed their hypothesis in mice: When animals dosed with melatonin, rodents increased production of protective T cells and reduced their levels of harmful cells. The team has seen similar effects on human cells in the laboratory, it makes online account today Cell . "Our research explains something that has not been experienced before in terms of how MS is modulated by the environment," says co-author Francisco Quintana, a neurologist at Ann Romney Centre for disease neurological at Brigham and Women's hospital in Boston.

Although the results are a step in the right direction, the link between melatonin and the immune system still lacks some important details. Researchers have yet to identify, for example, how helper T cells protect the myelin sheath misguided immune attack. Farez said he and his colleagues plan to explore this process in the future.

But other researchers caution against too absorbed in a single mechanism of an extremely complicated disease. "This group is enthusiastic about the role of [rogue cell] Th17, and me too, but it is only part of the story," said Lawrence Steinman, a neurologist at Stanford University in Palo Alto, California who specializes in MS.

Monitoring of clinical research should target a larger population, more inclusive, experts say. The current study included only patients in Buenos Aires. Farez said a diversified geographic sample is important to ensure melatonin has the same effects on patients in locations with different amounts of the light of day season.

But the main concern of the team has not to do with the experimental setup. It must give way to training on the effects of the publication of this research. Melatonin is widely available as a helper over-the-counter sleep, and they fear that some MS patients can use the hormone as an additional treatment. "We do not want patients to see the study and misinterpret our results," says Farez. "It's a neat and big data study, but we still need to do much work."

Learn more about melatonin and MS remission on Science Signaling site.

The links between health problems and endocrine disrupting chemicals now stronger, the statement argues -

The list of health problems that scientists can confidently link exposure to endocrine disrupting chemicals has grown to include diabetes, cardiovascular disease and obesity, a new scientific statement suggests. The statement, released today by the Endocrine Society, also adds support for the somewhat controversial idea that even small doses of these chemicals can interfere with the activity of natural hormones, which play a major role in regulation of the physiology and behavior.

But the report, which updates a similar report published in 09, is the criticism of drawing the chemical industry.

a summary of the new report, which summarizes 1300 studies on endocrine disruptors, postulates that scientists are more confident than ever to tie these substances to a host of known health problems, including reproductive and development problems, thyroid deficiency, certain cancers of the reproductive and neurodevelopmental problems such as reduced IQ. But studies suggest these links can now be extended to heart and weight problems and diabetes, explains the first author of the abstract, Andrea C. Gore, professor of pharmacology and toxicology at the University of Texas, Austin. It was six years ago, scientists could not make such a case for these strong ties, Gore said, because there was not enough good studies. "But it really was an emerging area where there is evidence much stronger now," said Gore reporters today a conference call.

Yet some toxicologists and industry groups have long disputed the assertion that endocrine disruptors can trigger effects in small doses; this idea can be difficult to test in laboratory animals, which are generally exposed to high doses in toxicology studies. And critics of the new report say it does not seem to clarify the vagueness of the 09 version of what it means for an endocrine disruptor to cause a "negative effect".

The summary of the new report "is broad, unsupported claims about the relationship between chemicals and disease," the American Chemistry Council, the largest trade group for the industry chemicals, argued in a statement. Regulatory agencies such as the Environmental Protection Agency (EPA) has still not accepted the idea that minute doses of endocrine disruptors can cause health problems, the industry group based in Washington, DC, said. And the Endocrine Society failed to specify when a chemical causes a "negative effect" scientifically proven counsel argues (against only show endocrine activity).

The National Research Council has launched a multi-year review whether the current EPA chemical assessment practice properly capture endocrine effects at low doses. Meanwhile, Gore rejects the criticism that the Endocrine Society has not adequately defined the "negative effects". It notes that, in studies on laboratory animals, some toxicologists believe wrongly that endocrine disruptors must-related health problems show immediately. But these health problems can take years or even decades to manifest in men, she said, and months in laboratory animals. And the specific disease that chemicals can induce in animals is often not always known from the beginning of the study, she added. "I think the problem has been solved for many endocrinologists and toxicologists," she said.

The Endocrine Society summary strongly emphasizes studies of bisphenol A (BPA), phthalates, persistent organic pollutants such as polychlorinated biphenyl ethers, and flame retardants such as polybrominated diphenyl ethers. "These chemicals have the greatest depth and breadth of information available," says the summary.

But the summary adds that most industrial chemicals released into the environment numbering in the tens of thousands-have never been tested for potential endocrine disruptor. in addition, Gore said, scientists are increasingly finding that some chemical alternatives to BPA and other EDCs suspected endocrine disruptor potential display themselves. These findings the summary said, highlighting the need to test chemicals before entering the trade and to better educate the public and policy makers on how to prevent exposures.

emerging test methods such as high-throughput screening assays could help researchers identify which of the thousands of chemicals in the environment now need more scientific control, the summary suggests. (EPA currently studying the use of these methods for prioritizing chemicals deserves animal testing for the full effects of endocrine disruptors.)

The Endocrine Society also calls for more research funding endocrinology, general, arguing that the benefits the company will far outweigh the costs. Funding agencies should focus on projects "science team", and not just individual studies by individual scientists, the summary submitted.

The company recommends several expansion of research areas. Researchers should increase the range of studied hormone-receptor proteins that receive chemical signals from hormones to see how endocrine disruptors may affect them. And future research could target more specific responses to gender and the effects of mixtures of several endocrine disruptors, the summary said.

Designer antibodies can rid the body of the AIDS virus -

Anti-HIV drugs have prolonged millions of lives, but they have not eliminated the virus from person. Indeed, HIV integrates its genetic material in the chromosomes of certain white blood cells, helping him to escape the attention of the immune system. Two new studies show that artificial antibodies could "redirect" the immune response to these latently infected cells and help drain the HIV reservoirs in the body. But this creative strategy also carries risks.

"The reason is sound, and data are exciting, but we need to move cautiously," said Steven Deeks, a clinical HIV / AIDS at the University of California, San Francisco (UCSF) , which tests the healing strategies. "There's really no room for error."

Several previous studies have investigated whether drugs can shock the cells that are infected with latent HIV to make new virus, setting them up for the kill by the natural immune response. But this new work ups the ante by developing so-called bispecific antibodies that both promise to reverse the lag and do the job of raking. "the dual activity makes this interesting new approach," said Sharon Lewin, a researcher cure HIV who heads the Peter Doherty Institute for Infection and Immunity in Melbourne, Australia. "It's exciting."

The two new documents that appear only online to date, mainly involving experiments test tubes. One, described in Nature Communications today ' hui, was conducted by a team from the vaccine research Center at the US National Institute of allergy and infectious diseases (NIAID) in Bethesda, Maryland. the second study was published last month in the Journal of Clinical Investigation ( JCI ) and involved a collaboration between three universities and a biotechnology company.

both groups artificial versions designed antibodies, the molecules form Y performed by the immune system to target pathogens. In natural antibodies, the two "arms" of the Y enclose the same target. However, the antibody arm bispecific each capture a unique protein. In this case, the two teams their antibodies designed to hug an HIV protein and CD3, a receptor present on the surface of white blood cells.

The bispecific antibodies focus on CD3 receptor for two reasons. The first is that the HIV hides within the DNA of white blood cells or T lymphocytes, which have CD3 receptors. The other is that a second type of CD3-studded lymphocytes cells known as killer T name destroys cells infected with HIV.

The bispecific antibody binds to CD3 first on cells harboring latent HIV. This prompts the cells to divide, a process of "activation" that awakens the virus of sleep. new proteins by HIV are then produced that migrate to the cell surface.

However, the bispecific antibody captures a killer T cell that has a CD3 receptor and with its second arm, is a newly activated cell that HIV proteins on its surface. Bring the killer T cell near the infected cell effectively shoves prey in the lion's mouth. "The molecule works the way you want to hope that it would be in several trials," said John Mascola, director of the NIAID Vaccine Research Center and leader of the group reporting of Nature Communications study.

But no team has yet shown that their bispecific antibodies can effectively reduce HIV reservoirs in monkeys, which are commonly used to study the AIDS virus. These studies are ongoing, and it will take at least a year before either team tests concepts in people infected with HIV. David Margolis, a virologist at the University of North Carolina, Chapel Hill, and co-author of the study JCI , said drain a reservoir ultimately may require combination with bispecific antibodies other reversing latency approaches and immune system stimulators such as HIV vaccines.

Deeks of

UCSF warns that anti-CD3 antibodies can cause too much activation of T cells, leading to a massive inflammatory reaction that damages organs and can even cause death. Indeed, in a 1999 study of anti-CD3 antibodies used for purging the tanks of three people infected with HIV, severe side effects, including kidney failure and seizures surface quickly. But the anti-CD3 antibody in the previous study were the two arms, Mascola ratings, which leads to the activation much more than the single arm in the new bispecific antibodies. It also emphasizes that two bispecific antibodies cancer on both the market have anti-CD3 arms. "The key is to find the right balance between activation and toxicity CD3" said Mascola. "That's the real challenge here."

Vitamin C kills the tumor cells with difficult to treat mutation -

Maybe Linus Pauling was on to something after all. There decades chemist Nobel Prize has been relegated to the periphery of medicine after defending the idea that vitamin C could fight against a host of diseases, including cancer. Now a study published online today in Science reports that vitamin C can kill tumor cells that carry a mutation common cancer-causing and - mice can slow growth of tumors with the mutation.

If the results hold in people, the researchers could find a way to treat a wide band tumors that lacked effective drugs. "This [could] be an answer to everyone fighting for," says molecular biologist Channing Der, University of North Carolina, Chapel Hill, one of many researchers who are trying to target cancers with mutation. The study is also rewarding for the handful of researchers who pursue vitamin C or ascorbic acid as a drug against cancer. "I'm encouraged. Maybe people will finally pay attention, "says vitamin C researcher Mark Levine of the National Institute of Diabetes and Digestive and Kidney Diseases.

In 1971, Pauling began collaborating with a Scottish doctor who had successful treatment of cancer patients with vitamin C. But the failure of two clinical trials of vitamin C pills, carried the late 1970s and early 1980s at the Mayo Clinic in Rochester, Minnesota reported, dampened enthusiasm for the idea of ​​Pauling. Studies conducted by Levine's group later suggested that vitamin must be administered intravenously to reach high enough doses to kill cancer cells. Some recent small trials over the five years - to pancreatic and ovarian cancer - suggested that the treatment of IV vitamin C combined with chemotherapy can prolong survival Cancer. But skeptics are not influenced. "The atmosphere was poisoned" by previous failures, says Levine.

there

A few years Jihye Yun, a graduate student at Johns Hopkins University in Baltimore, Maryland, found that colon cancer cells whose growth is driven by mutations in the gene KRAS or less frequently mutated gene, BRAF , make exceptionally large quantities of a protein which transports glucose across the cell membrane. The carrier, GLUT1, provides the cells with high levels of glucose they need to survive. GLUT1 also carries the oxidized form of vitamin C, dehydroascorbic acid (DHA) in the cell, bad news for cancer cells, because Yun found that DHA may deplete the supply of a cell of a product chemical that sops free radicals. Because free radicals can harm a variety of ways cell, the conclusion suggested "vulnerability" if the cells were flooded with DHA, says Lewis Cantley at Weill Cornell Medicine in New York City, where Yun is now a postdoc.

[1945018laboratoireetcollaborateurs] Cantley found that high doses of vitamin C actually kill colon cancer cells cultured with BRAF or KRAS mutations by increasing levels of free radicals, which in turn inactivates an enzyme needed to metabolize glucose, depriving the energy cells. Then they gave daily injections of high doses - equivalent to a person eating 300 orange - to modified mice to develop KRAS focused on tumors colon. Mice developed fewer and smaller tumors colon compared to control mice.

Cantley hopes to soon start clinical trials that select patients with cancer based on KRAS or BRAF mutations and possibly GLUT1 state. New research from his group "indicates you should get the drug and who should not," he said. Bert Vogelstein cancer geneticist at the University Johns Hopkins, in whose laboratory Yun GLUT1 noticed the connection, is excited about the therapy of vitamin C, not only as a possible treatment for KRAS -mutated colon tumors, which account for about 40% of all colon cancers, but also for pancreatic cancer, a usually fatal cancer caused by KRAS . "No KRAS -targeted therapeutic emerged despite decades of effort and hundreds of millions of dollars [spent] industry and academia," says Vogelstein.

D others warn that the effects observed in mice may not hold up in humans. But because the high dose vitamin C is already known to be safe, says the researcher Vuk Stambolic cancer of the University of Toronto, Canada, oncologists "can quickly move forward in the clinic."

a disadvantage is that patients have to come to a clinic for infusions of vitamin C, ideally every day for months because vitamin C seems to take this time to kill cancer cells, Levine notes But Cantley said, it may be possible to make an oral formulation that reaches high levels in the blood -.. can be a way to get companies interested in sponsoring testing

How agriculture has changed the European - genome

When the first farmers plowed the Middle East in Europe 8500 years ago, they brought with them more than one style life, they also set in motion changes in genes that have changed the way Europeans looked digested food, and adapted to the disease. In a new study published in Nature today, an international team to sequence ancient DNA from 230 people who lived there 3000 years 8500 in Europe, Siberia, and Turkey. Their sample included the first ever sequenced DNA of the first farmers in the Middle East, as it buried in Barcin Höyük northwest of Anatolia, in Turkey today. The team reported earlier this year how natural selection has favored the spread of genes of white skin, tallness and digest the sugars in milk. In today's paper, the same researchers sequenced the DNA of more skeletons and found that the transition to agriculture also promoted the genes for digesting fat and immune genes that protect against disease infectious diseases, such as tuberculosis and leprosy. Interestingly, the team also found the spread of two variants of genes associated with celiac disease. These variants may have been favored because they help to compensate for a deficiency associated with certain regimes-in an amino acid called agricultural ergothioneine. But variants also have the secondary effect of stimulating Crohn's disease and other celiac disease.

Campaign against tuberculosis is intensifying its ambitions -

Your poor diet could hurt the bowels of your grandchildren -

Here's another reason to eat your vegetables. Trillions of microbes in the large intestine known as the human microbiome-dependent fiber prosper and give us energy. As the consumption of fibers decreases, so, too, is the range of bacteria which can survive in the intestine. Now a new study of several generations of mice fed a diet low in fiber indicates that this diversity dives deeper with each generation, a hint of what might occur in the human intestine as we continue to eat a diet of contemporary refined foods. The work may also help explain the rise in many Western diseases, such as inflammatory bowel disease and obesity.

"This is a seminal study," said Jens microbial ecologist Walter of the University of Alberta in Canada. "The extent by which the weak [fiber] supply depletes the microbiome in mouse experiments is striking."

For much of human history hunter-gatherer and early agricultural times, the daily fiber intake was probably at least three or four times the officially recommended today (something like 100 grams against 25 grams) -and several times higher than the average consumption in the United States today (15 g). the tendency has led many researchers, including Erica Sonnenburg microbiologist from Stanford University in Palo Alto, California, to suspect that the low well documented diversity of gut microbes in people in developed countries, 30 % less diverse than modern hunter-gatherers- is in part a product of considerably reducing the consumption of fibers.

the new study confirms this relationship in rodents. Sonnenburg and his colleagues raised mice in a germ-free environment, then fed them human faeces, giving them the human intestinal bacteria. When fed a diet low in fiber (about 30% less fiber than the chow control high fiber), animals experienced a significant dip in the gut microbial diversity (with about 60% of microbes lose at least half their populations). The mice then maintained on the food poor in fiber and have helped raise the offspring produced with a diversity even lower, the team announced today online Nature . And subsequent generations of mice fed low fiber continued to lose whole groups of microbes such as bacteria have reached these reduced numbers in the parents that they could not be transmitted through birth, nursing, or even tend to eat'S mouse droppings on the other.

by the fourth generation, mouse microbiota seemed to have reached a new normal, low steady microbiota diversity, accommodation only over a quarter of the diversity enjoyed by the first generation. In particular, no low generations fiber could be "saved" by reintroducing foods rich in fiber. To reach the bacterial variety of their grandparents, mice need a fecal transplant group rich in fiber and a diet rich in fiber.

The results raise questions about how our diet affects our own offspring. "As we move relatively little change in our human DNA for each generation, this study indicates that we potentially pass on huge changes in our gut microbiome," Sonnenburg said. Because the mice in this study started with microbes of a Westerner, the microbiome was already low in diversity, the study also suggests that "it may be possible for Western microbiota to lose the extra diversity," she adds. Microbiologist Eric Martens, University of Michigan Medical School in Ann Arbor, amazed by the extent of the loss. "The surprise is that the proportion of organizations can actually be driven to extinction," he said.

The researchers have yet to prove that the same rapid reduction of microbial diversity occurs on rights generations and if it is, what it means for health. "in these complex ecosystems, it is very difficult to know the exact result of the loss of biodiversity," said Sonnenburg. But, she notes, "it is likely that these extinctions in the microbiota have big effects." For example, other research has shown that obese people are more likely to have the lowest microbial diversity in their guts that their lean peers. and our more macroenvironments studies teach us that a diverse ecosystem is heartier and quicker to bounce to another less diversified.

Meanwhile, as Martens suggests in an accompanying commentary in Nature , "you might consider choosing a salad ... or an additional portion of beans."

Zika virus: Answers to Your Questions -

Where the Zika virus come from

First isolated in 1947 and first described in an article? 1952 Zika has long been known to occur in Africa and South Asia, but until there ten years, less than 15 cases have been described in the scientific literature. In 07, the virus caused a large outbreak in Yap, a group of islands in the western Pacific that is part of the Federated States of Micronesia; since then it has made a major tour of other Pacific islands before he landed in Brazil, where he began to spread quickly to other parts of South America, Central America, Mexico and the Caribbean.

Why has it exploded so suddenly

there may have been large epidemics in Africa and Asia in the past that was not detected ?; scientists did not pay much attention. But the current epidemic is a massive event waiting to happen. Latin America has a large number of A. aegypti , also known as the yellow fever mosquito, an important vector for Zika. (The tiger mosquito, A. albopictus , which is on the rise around the world, is considered a vector as well.) In addition, in the Americas had immunity to the virus. Travel makes things worse. Aedes mosquitoes do not fly more than a few hundred meters during their life; Zika moves from city to city and country to another when infected people receive on cars, buses, trains and planes.

These factors combined mean that the virus has the ability to spread far and fast once he had arrived.

Will Zika across the United States and Europe?

the United States and Europe have already seen "imported cases" -the people who arrived a Zika affected countries carrier of the virus. This was widely expected given the size of the epidemic in Latin America. The key question is whether there will be local homes-that is, the mosquitoes spread the virus from person to person. There is certainly a chance; A. albopictus occurs in several countries in Southern Europe (and it can move to the north), while the southern and eastern United States have populations of both A . aegypti and A. albopictus .

If so, scientists expect epidemics to be much lower than anywhere else on the basis of past experience with diseases transmitted by mosquitoes. Recent outbreaks of dengue fever in Florida, Texas and Hawaii were not sickened more than a few hundred people, for example; an outbreak of a disease transmitted by mosquitoes called chikungunya in northern Italy in 07, which began when a man infected with the virus arrived from India-ended after 197 cases. One reason that the epidemics in these countries tend to be smaller may be that people spend less time outdoors and live in homes that are harder for mosquitoes to enter; the size of mosquito populations may play a role as well.

Do we know for certain that Zika is causing an increase in birth defects?

No. There are strong indications that the areas in Brazil hit hard by Zika experienced a sharp increase in the number of babies born with microcephaly, a condition in which the head is much smaller than normal because the brain fails to develop properly. But it will take at least several months before results of the first case-control studies of pregnant women infected with Zika are available. Doctors in Brazil first noticed the increased cases of microcephaly for ultrasounds for pregnant women in June and July, months after the surge of Zika infections. expert in fetal medicine Manoel Sarno, who works at the Federal University of Bahia, said the pattern of brain damage he sees now appears separate from microcephaly caused by other infections, such as cytomegalovirus (CMV) or rubella. He and his colleagues began a study in August following Zika infected women during pregnancy; the results could come out late summer. Similar studies are underway elsewhere in Brazil and Colombia.

Are there other pressing issues that the scientists involved?

Plenty. Scientists are struggling to determine who was infected and who is not because the diagnostic tests have limitations. The tests, which detect the most accurate of the viral RNA in the blood of patient work within a week of the first symptoms appear. After this period, researchers can test the antibodies in the blood. But current testing for Zika antibodies cross-react with antibodies to dengue, which is so widespread in Brazil and much of the rest of Latin America-that almost all adults have antibodies to it. It is therefore difficult to say whether the mother of a baby born with microcephaly has been infected by Zika earlier in her pregnancy.

The researchers would also like to know how often Zika is transmitted through sexual contact. American scientist who caught the virus in Africa adopted his wife after getting home in 08, and a second case of alleged sexual transmission arrived in French Polynesia in 2013. But researchers have no idea what that risk is . ( "If I'm a man and I'm symptoms Zika, I wait a few months before having unprotected sex," virologist Scott Weaver of the University of Texas Medical Branch in Galveston recently said The New York Times .)

What drugs are available against Zika?

None. Until last year, Zika was so rare, and believed to be so sweet, that nobody cared to look for drug candidates. Even now that the virus is surging, it is not obvious that there is a large market for an antiviral drug, because the vast majority of infected people have very . few symptoms or none at all and it is not known that a drug could prevent birth defects when women Zika contract during pregnancy when they become infected and develop symptoms, it may be too late to avoid such damages. A vaccine against Zika can offer more hope to prevent microcephaly.

And when can we expect a vaccine?

It will take years. Several groups have started making vaccine candidates Zika, a process that will take at least several months. Most of these vaccine approaches are piggybacking on existing vaccines. For example, many vaccines are made by assembling proteins from the surface of a pathogen in a harmless virus or vector; who is now with Zika tried using these vectors. Once a candidate is made, it should be tested in animals before humans.Human tests start with small safety studies and move on to larger studies that verify if the product candidate is working. All it usually takes 10 to 15 months. Given the urgency, the time may be compressed, but even so, Anthony Fauci, director of the US National Institute of Allergy and Infectious Diseases, said STAT he can be at least 5 to 7 years before that a Zika vaccine is commercially available.

So what can we do to stop the spread of the virus?

stop mosquitoes from biting people. Countries and communities can try to reduce mosquito populations by eliminating small reservoirs such as water flower pots, empty bottles, and scrap tires that Aedes mosquitoes like to breed. People can also reduce their especially significant personal exposure for women who are or may become pregnant by putting screens on windows, covering their skin, and using insect repellent. However, history has shown that the impact of the fight against mosquitoes on epidemics is modest at best, and they are difficult to maintain.

There must be better ways to fight against mosquitoes?

Not yet, but they are in the works. A British biotech called Oxitec, which was recently bought by Intrexon, a US company, has developed synthetic biology A. aegypti mosquitoes containing a gene construct that will kill their offspring before they reach the age adult. When a substantial number of males of this strain are released into the wild, they will mate with local females produce offspring that are not viable, which has been shown to make a dent in the population.

In another line of research, scientists infect A. aegypti with a bacterium called Wolbachia , which reduces the ability of mosquitoes to transmit diseases. developing the researchers, these approaches were mostly thinking about dengue, but the rise of Zika is to give their efforts a new sense of urgency. But again, it will take several years before these strategies are ready for prime time.

Microbes in the gut right help children grow -

Why high "good" cholesterol may be bad news -

The 67-year-old woman had sky-high high-density lipoprotein (HDL) cholesterol to form long considered as protective against heart disease, yet his arteries were lined plate. His paradoxical cases helped motivate a team of scientists to show how high HDL can sometimes be a signal not of heart health, but the opposite :. A system incapable of siphoning fatty particles from circulation cholesterol

In the past 10 years, HDL particles have confounded scientists. The normal role of these beams of protein and lipid is to transport cholesterol in the liver rest of the body, which eliminates from the body. More something good should mean better health, and people naturally have higher HDL levels are usually better. But drugs that increase HDL cholesterol have flopped in clinical trials, and the genes that help raise does not seem to follow with less heart disease. "Nothing ever single HDL" said Jay Heinecke, a biochemist at the University of Washington, Seattle, who has studied for years.

In this week's issue of Science Daniel Rader, a geneticist and lipidologist at the University of Pennsylvania, and colleagues suggest that the amount of HDL is less important than the way it is effectively moved the arteries in the liver. the inspiration of Rader was a model mouse developed by Monty Krieger at the Massachusetts Institute of Technology in Cambridge there about 20 years. the mouse developers had deleted a gene called SCARB1 , resulting in animals with surprisingly high HDL and, just amazingly arteries severely blocked. "the mice actually receive heart attacks," said Heinecke. Indeed, the cholesterol displacement system outside the body is broken in these mice.

particles Normally HDL cholesterol gather immune cells that line the arteries, then deposit their load in the liver so that the cycle can begin again. The protein made by the SCARB1 gene, known as SR-B1, helps make this deposit occurs. Mice without SR-B1 have HDL particles swollen with cholesterol, struggling to attract more away from the arterial wall.

Rader wondered if the same could occur in some people. He and his colleagues began by sequencing the gene in 852 people with high HDL and 1,000 controls. They found a person of 67 years, women who had no copies of operation of SCARB1 gene and had more plaque on the arteries mean that a woman of her age. His HDL was 152 mg / dL, well above the average of about 62 mg / dl in women in her age group. Eighteen others were just a functional copy SCARB1 instead of the usual two, and most of them also had higher HDL. Detailed studies of nine people with SCARB1 mutations, including women, have suggested that in mice, their abundant HDL failed to effectively carry cholesterol throughout the body.

Rader then spread to his colleagues who had collected the DNA of hundreds of thousands of people for studies of lipids and heart disease. Among them, he found another 284 people who have had a single copy operation SCARB1 . (No one else was like the first woman with two missing copies.) Most of these people were also higher than average HDL. They were also 80% more likely than the witnesses CHD-roughly the same increase in risk seen traditional risk factors such as diabetes and hypertension.

"This is a key indication of what people have suspected from animal studies," says Alan Tall, an HDL researcher at Columbia University. It seems that HDL is higher "because the flow is blocked, "not because HDL excels in maintaining cholesterol on arteries.

Yet because Rader could find so few people without fully operational SCARB- 1 and because the potential effects of mutations on heart health appeared modest, the link between transport defective HDL and heart disease is still fragile, he and others say. and HDL behavior in a box Petri does not necessarily reflect what it does to the body, suggests Kuivenhoven Jan Albert, who studies the genetics of lipid metabolism at the University Medical Center Groningen in the Netherlands. "We have no good ways do the tests with HDL that can really say what happens "in a person, said Kuivenhoven.

HDL remains extraordinarily complex, and Rader Kuivenhoven say. It is possible that the collection of HDL drugs failed in clinical trials because of the type of HDL-products detected drugs doctors larger HDL particles than expected. Overall, however, there is little doubt that high HDL always follows with a healthier heart for most people, except, Rader said, when it does not.

Ultimately, he said, we would be able to say, "Your HDL is high because X which is good," and someone else, "Your HDL is high because of Y, which is a bad thing. "now, he and others want to nail down exactly what these factors might be and, potentially, how to run them off.

Local immunity goes -

Parasitic worms may prevent Crohn's disease by modifying the bacterial balance -

Parasitic worms that hide in the intestines of some people may be revolting, but they seem to prevent disease Crohn and other types of inflammatory bowel disease (IBD). A new study may explain how revealing that to allow beneficial microbes in the gut to supplant the bacteria that promote inflammation. The findings could lead to new ways to treat diseases of the gut by mimicking the effects of parasites.

"It is a beautifully made paper," says immunologist Joel Weinstock of Tufts University in Boston, who was not connected to the work. "It has not been shown previously that one of the mechanisms [of IBD] is through changes in the intestinal flora."

In people with IBD, inflammation in the results of digestive symptoms such as diarrhea and bleeding and can sometimes lead to bowel obstructions or other serious complications. Because parasitic worms, or helminths, can be harmful, they seem to be unlikely allies against these diseases. "They are called parasites for a reason," says immunologist Ken Cadwell of the New York University School of Medicine in New York City, co-author of the new study. However, the EIA is rare in parts of the world where helminths are prevalent, and it is surging in most developed countries, where few people now carry intestinal intruders. This difference suggests, the researchers say they are protective.

to determine how to could be our frenemies, Cadwell and his colleagues tested mice with the same genetic defect found in many people with Crohn's disease. mucus secreting cells in the bowel dysfunction in animals, reducing the amount of mucus that protects the intestinal mucosa of harmful bacteria. the researchers also detected a change in the microbiome rodents, the natural microbial community in their guts. The abundance of a microbe, an inflammation-inducing bacteria in the Bacteroides rises in mice with the genetic defect.

The researchers found that feeding rodents a type of intestinal worms restored their mucus-producing cells to normal. At the same time, the levels of both indicators of inflammation decreased in the intestines of animals. In addition, the range of bacteria in the intestines of displaced rodents, the team announced today online Science . Bacteroides numbers have plunged, while the prevalence of species in a different microbial group, Clostridiales increased. A second species of worm also trigger similar changes in the intestines of mice, the team confirmed

To check whether helminths cause the same effects in people, the scientists compared two populations in Malaysia :. Urban population living in Kuala Lumpur, which harbor some intestinal parasites, and members of indigenous groups, the Orang Asli who live in a rural area where worms are common. One type of Bacteroides proinflammatory microbes, predominated in the people of Kuala Lumpur. It was rarer among Orang Asli, where a member of Clostridiales group was plentiful. Orang Asli treat with drugs to kill their intestinal worms reversed this trend, favoring Bacteroides species on Clostridiales species, the team documented.

Cadwell and his colleagues also asked whether Clostridiales and Bacteroides microbes disagreed with others. They analyzed two sets of data on the frequencies of different gut microbes, which include results for American healthy residents and children in North America who have IBD. They saw the same relationship when Clostridiales species are in place Bacteroides varieties are down, and vice versa.

The findings of the study suggest that parasitic worms deliver their benefits indirectly through their impact on the microbial mix in the intestines. Worms are "having an anti-inflammatory effect by kicking something that is inflammatory," said Cadwell. Clostridiales group members can get a boost when worms are around, he said, because the intestines produce more mucus, bacteria feed on.

"This is a good proof of concept," says Gabriel Nunez immunologist at the University of Michigan, Ann Arbor, who was not connected to the research. It supports "the principle that some of these diseases may be related to changes in the microbiome. "But he warned that researchers still need direct evidence that Bacteroides species are responsible for Crohn's disease.

turn the results into a treatment for IBD could be difficult. Two recent clinical trials helminth treatment for Crohn's disease, in which participants drank a solution containing worm eggs, stopped early because the results been disappointing. These studies may not be the last word, however. Cadwell said the worm therapy might work in more or less 30% of Crohn's patients who have the same genetic defect as mice. and Weinstock noted that if researchers can determine how parasites trigger the change in the composition of microbe, "we may be able to bypass and develop a small molecule drug to achieve the effect of a safe manner."