Health Meaning

Exactly how much and which parts of the two controversial H5N1 studies will be published could be decided today and tomorrow during a meeting in Geneva. The World Health Organization (WHO) invited 22 experts from around the world to discuss and debate-whether and how to publish research that describes how scientists have made the avian H5N1 flu transmissible between ferrets, a mammal model common to the flu. The meeting is closed to the public and journalists, and the WHO has kept the guest list under wraps until now.

The final list has some surprises and is dominated by influenza experts. The only real stranger seems Jerome Singh, an expert on ethics and health law of the School R. Mandela Medical University of KwaZulu Natal in Durban, South Africa. Singh studied apartheid biological weapons program in South Africa, called Project Coast, which was active in the 1970s and 1980s

Also present were Ron Fouchier of Erasmus MC in Rotterdam, the Netherlands, and Yoshihiro Kawaoka of the University of Wisconsin, Madison, who led both studies and want to publish them in their entirety; Paul Keim, acting chairman of the Scientific Advisory Board for the National Biosecurity (NSABB), the panel that recommended to leave the key new details; Publishers Nature and Science , the two journals considering publishing the documents; and representatives of the five WHO collaborating centers for the study of influenza. Three representatives participate Indonesia, one of the hardest hit by H5N1 country. Indonesian lab would have given Fouchier virus he used as a starting material. There is a representative of the Vietnamese laboratory collaborates with which Kawaoka, and from which he received the sample of influenza used in its study.

In the late 1950s and early 1960s, Mao Zedong of China proposed the "Great Leap Forward" campaign which was supposed to increase the production of steel and propel his country in the higher ranks of industrialized nations. But the leaders were scrambling to find ways to make more steel, grain production has fallen. Tens of millions of Chinese died. A new study finds that the famine also had demographic consequences: A significantly higher proportion of girls born after the famine in the years leading up to it.

Evolutionary biology predicts that when times are tough, it is advantageous to give birth to girls. The reason may be that inferior men are not more likely to get opportunities to mate the males stronger. Shige Song, a social demographer at Queens College of the City University of New York, wanted to see if this effect occurred in people suffering from famine. Other researchers have sought a ratio sex change after two other famines, the Dutch Hunger Winter 1944-1945 and famine in 1942 associated with the siege of Leningrad in the former Soviet Union, but they have found results contradictory.

Song went after more famine: the Great Leap Forward. More than 30 million people died during this event. This is several times the number who died in the two smaller European famines. Chinese famine had many causes. Among them was the emphasis on making more steel took the job away from agricultural work, such as harvesting grain. The disaster began in the fall of 1958 in some areas and was widespread in China by January 1959.It lasted 3 years, until the end of 1961.

song used in a data survey of 310.101 elderly Chinese women aged 15 years 1982-67, which collected information on all of their children. He found that, before the famine, the proportion of male births has increased slowly. (We do not know why this is happening, but the song has used the trend as a baseline to examine changes in the sex ratio associated with starvation.) The sex ratio reached a peak of "masculinity" around 1958, then began to change, falling from 521 men per thousand births in April 1960 to 510 males per thousand births in October 1963. the sex ratio has not begun to swing back toward a higher proportion of men until nearly 2 years after the famine ended, reported online today in the song Proceedings of the Royal Society B.

song think the long duration of the famine may explain why other studies have failed to show similar results. The Dutch famine and Leningrad may have been too short, 7 months and 6 months respectively, to affect the number of baby girls born. "It's not like you skip breakfast for 1 or 2 days, then you influence the sex ratio," he said. "It is a cumulative process. The body has to learn that it is real. "

Tessa Roseboom, a biologist at Academic Medical Center in Amsterdam who studies the Dutch famine, recognizes seven months of famine may simply not long enough to cause change in sex ratio. It also emphasizes that it has birth records for only 2500 babies while studying the song covers more than 830,000. It is not surprising that other researchers have managed to find a consistent effect of sex ratio with the Dutch data, she said, "just because the effect, if there is not very big."

But other research has found that even the short-term fasting can influence the sex, says Douglas Almond, an economist at Columbia University who also studied the famine of the Great Leap forward. He analyzed the women who fast during Ramadan and found that babies which have been designed near the time of fasting are relevant and most skewed female sex change in the ratio is greater than the song found. "I think there is an immediate effect," said Almond. He agrees with the song on the base point, though. "Sex respond to maternal condition and nutrition is a major factor . "

The big push in the nowadays cancer treatment is to sample the tumor of a person, the test for mutations, and give the patient a medicine for genetic weak point in the tumor. A new study suggests one reason why this strategy of targeted drugs do not always work. A solid tumor, it turns out, is not a mass of identical cancer cells, but a mosaic of genetically different cells that are not captured with a single biopsy. Some of these different cells may be resistant to targeted drugs, which allows a tumor persist or grow.

The conventional view of how cancer develops is a single, normal cell accumulates mutations that allow or possibly force it to divide uncontrollably. This "clone" then grows into a tumor of identical cells, which can also sow seeds of cells in the blood that can take root somewhere else in the body, or metastasize. The hypothesis that tumors develop from a single clone has sparked a rush to find drugs that block one of the weak points genetic clone. But although the strategy has led to some very effective drugs, Iressa for lung cancer and a new melanoma drug called Zelboraf, for example, these drugs often stop working in a year or two. One reason might be that already house some solid tumors cells, or clones with "resistance" mutations that take over when the cells targeted by the drug are destroyed.

Now, British researchers confirmed this idea by using the new generation of DNA sequencing to explore the genetic landscape in unprecedented detail tumors. Charles Swanton of the UK London Cancer Research Institute Research and University College London, James Larkin of The Royal Marsden Hospital in London and colleagues took samples from nine locations within 10 centimeters wide primary tumor of the kidney of a patient and certain tumor metastases patient. The researchers then put these biopsies through a battery of genomic tests, including sequencing all genes encoding proteins in each sample.

The researchers found a huge amount of variation within tumors than patients. Only 34% of the 118 mutations detected they showed in all samples. Several genes of key cancer were mutated in the primary tumor, but in different ways in different areas. When the researchers examined which genes in the tumor were active-these so-called gene expression signatures are designed to predict whether the prognosis for a kidney patient is poor or good results differ depending on the part of the tumor, they tested.

The team then created a family tree of how these clones evolved from a single clone. The good news, Swanton said, is that this analysis revealed that certain mutations in the "trunk" of the tree persisted that cancer has evolved, which means that all the patient's tumor cells had these weaknesses. Therefore, drugs targeting these mutations should work even on tumors that heterogeneous could explain the initial success of Iressa and Zelboraf. However, other resistance mutations to existing drugs in the branches of the tree could possibly block the drugs work, Swanton said. His team reports its results today The New England Journal of Medicine .

Carlo Maley University of California, San Francisco, who studies the evolution of cancer, warns that the study was small in total, the UK team tested only four tumors and two patients in detail . Yet it is "highly suggestive that intratumoral heterogeneity should be expected," he said. "It adds a great level of noise and uncertainty that everybody does," says Maley. Swanton said bottom line of the study is that the researchers develop new therapies against cancer, they should be aware that the single biopsies can be deceiving. "We must think about the sequencing of tumors means more thoroughly"

last month, a third of the US National Science Advisory Board for Biosecurity (NSABB) disagreed with the recommendation of the group to publish full two studies that describe how the bird flu virus transmissible in mammals. Now, one of the six dissidents, flu epidemiologist Michael Osterholm of the University of Minnesota, Twin Cities, wrote a scathing critique of the meeting that led to the decision. In a letter sent yesterday to Amy Patterson, an official at the US National Institutes of Health, headquartered oversees NSABB, Osterholm charged that the meeting was "designed to produce the result that occurred."

Osterholm and other dissidents in particular have had strong concerns about a study by Ron Fouchier of the Erasmus MC in Rotterdam, Netherlands, which is being considered in Science. The seven-page letter to Osterholm, obtained by Science , tells many arguments he has made publicly before the need to redact details of the experiments in ferrets Fouchier group, a model used to study how flu viruses behave in humans. But the letter adds Osterholm new scientific detail its concerns and also specifies why he believes the meeting a bad precedent for future NSABB deliberations. "Although I do not claim that there was a sinister motive by the [U.S. government] regarding either the agenda or guest speakers, I think there was a bias towards finding a solution which was much less of a science- and solid policy basis of the analysis of risk-benefit and more on how to get us out of this difficult situation, "Osterholm wrote.

Scientifically, Osterholm revealed that Fouchier new data, which is not in his manuscript in progress, which makes it even easier for others to create a mutated version of avian flu H5N1 transmits in ferrets. He argues that attempts to publish these works raise all the same problems as the group struggled with for the last 6 months, and he predicted that the paper "will prove to be the straw that breaks the camel." The current decision NSABB, he complained, "just launched the can down the road to another manuscript."

The 2-day meeting itself, Osterholm argued, did not constitute an "objective examination provided by an expert in the field of selfless purpose" about the ease with which groups of bad intentions could learn to engineer a H5N1 transmits humans. experts at the meeting that dealt with these scientific, costs Osterholm, "have a real conflict of interest that their laboratories are involved in the same type of work and the results of our deliberations affect them directly, too. "He called a meeting of information that NSABB members received intelligence experts" one of [the] most incomplete and, dare -I say, unnecessary briefings small security that I have ever attended. "

Susan Ehrlich, a retired judge and NSABB member who also voted against the manuscript publishing Fouchier in full, the letter says Osterholm of "this thoughtfully very valid points, those who deserve and serious discussion."

the letter Osterholm is available in its entirety.

Researchers in California today unveiled what they describe as the largest repository in the world for cancer genomes . The database will be easier for scientists to analyze large amounts of sequencing data spilling genome projects (NCI) of the National Institute of United States cancer.

Cancer Genomics Hub (CGHub) built by a team from the University of California, Santa Cruz (UCSC), will hold the first sequencing data from The Cancer Genome Atlas (TCGA). The atlas is the enormous effort of NCI to sequence the DNA of normal cells and tumor cells than 10,000 people with 20 types of cancer. (In some cases, the project is the sequencing of entire genomes;. In other cases, only 1% of the genome that code for proteins) CGHub projects also contain data on the genome associated with cancer and childhood- HIV NCI. He will take over for the NIH for Biotechnology Information National Centre, which had been collecting cancer sequencing data by last August

Physically based at the San Diego Supercomputer Center, the computer system is ready to store CGHub 5 petabytes of data DNA and RNA from cancer patients. (TCGA generates 10 terabytes of data per month, and will eventually produce 10 petabytes [10,000 terabytes] data.)

TCGA built a catalog of genetic modifications cancer key driving that researchers can use to develop treatments suitable for genetic tumor of an individual. A central database will allow researchers to compare the changes and not connected paths through the types of cancer, said UCSC bioinformatics David Haussler, director of the project financed by a $ 10.3 million contract from the NCI: "What is very important is to gather the data in one place and make it easy for researchers to make comparisons between the data sets. "CGHub not hold data from other international projects on cancer genome, however.

for now, researchers will be able to only download data. But sending genome data through the Internet is more convenient than the balloon data sets in size (see our 2011 story "Will Computers crash genomics?"). Haussler said finally, researchers will be able to work on remote data servers CGHub through cloud computing, as NIH did with Amazon for data from its 1000 Genomes Project.

Connective tissue holds our body together, but in a condition called fibrosis, an overabundance of material devastates organs such as the liver, heart and lungs . A new study suggests that the fragments of a promising cancer drug may inhibit fibrosis, which is currently incurable.

Fibrosis occurs when cells pump the excess collagen and other connective tissue proteins, which affect the organs. Pulmonary fibrosis, for example, stiff lungs, eventually stifle patients unless they receive a lung transplant. In people with cirrhosis, connective tissue piles up in the liver. Heart and kidney disease can also be caused by fibrosis. So far, no drug to stop or reverse fibrosis won approval in the US.

cell and molecular biologist Carol Feghali-Bostwick of the University of Pittsburgh School of Medicine in Pennsylvania and his colleagues decided to test whether endostatin, a drug in clinical trials as a treatment for various cancers, has also an effect on fibrosis. Endostatin is one of angiogenesis inhibitors supposedly a group of drugs vaunted blocking the formation of new tumor blood vessels in need of growth. Endostatin also occurs naturally in the human body, and patients with pulmonary fibrosis up to 20 times their normal levels in blood or lungs. This finding raised the possibility that the protein is a natural defense against the proliferation of connective tissue, said Feghali-Bostwick.

To test this hypothesis, she and her colleagues studied samples of human skin they fed in the laboratory. They assayed the skin with TGF-β, a cellular signal that promotes fibrosis and causes the skin to thicken the connective tissue accumulates. Adding endostatin prevented patches of skin become thicker, the team found.

Because endostatin counteracts the growth of blood vessels, an undesirable quality for the treatment of fibrosis, the researchers then tested three fragments of the molecule, or peptides. After a few tweaks to improve stability, one of the peptides by itself reverse fibrosis stimulated by TGF-β in the skin patches, the researchers report online today in Science Translational Medicine . In addition, this part of endostatin had little effect on the growth of blood vessels in the culture dish, the team showed.

The peptide also worked in mice, which reduces skin fibrosis caused by TGF-β and the drug bleomycin. After a dose of bleomycin, the peptide also reduced lung fibrosis in animals.

"It makes a lot of sense that the body would try to mount an opposite process to fibrosis," said Feghali-Bostwick. Scientists believe that endostatin produced naturally can not fight against the connective tissue accumulation in fibrosis patients, perhaps because another molecule inhibits. But the peptide may be able to do the job, and it could overcome some of the limitations that have cut down on the use of endostatin in the treatment of cancer, such as the rapid deterioration of the body. The researchers now want to nail down how their fibrosis shorting peptide and to determine if they can make it more powerful, said Feghali-Bostwick.

"I think the peptides are a new approach to target the TGF-β pathway," says immunologist Thomas Wynn of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, which has not was involved in the research. However, he warns that until now, other compounds that block this pathway in mice are not panned in clinical trials, and he would like to see further research with different versions of fibrosis mice. "It is not clear how generally applicable the results will be."

A popular program that provides patients with mysterious illnesses to the National Institutes of Health (NIH) campus in Bethesda, Maryland, so the experts can try identify the cause of their disease develops in universities.

The 4-year-old NIH Undiagnosed Diseases Program (UDP) evaluated 500 patients who come to the Clinical Center of the NIH for clinical and genetic testing. About 10%, or 50 patients were fully diagnosed with a genetic disease and about 30% have a partial diagnosis, says Director William Gahl UDP National Institute for Research on the human genome. Often they have "rare disease" incredibly with only a few dozen cases in the world, said Gahl. UDP found two diseases that are new to science-a neurological disorder and a condition that causes arteries calcify. Another 15-20 cases can be genetic disorders news, said Gahl.

UDP now sees over 150 patients a year and has a budget of $ 3.5 million. The program, a media favorite, received thousands of inquiries. There is one year, the NIH has temporarily stopped accepting applications for catching up.

NIH could expand the intramural program, but he wanted to "let others engage in this" and to create centers which would be located near the patient says Gahl. NIH plans to finance five or six extramural centers at $ 145 million over 7 years. Researchers will be trained to UDP methods for screening patients, clinical studies and genetic tests, which may include sequencing the DNA encoding the protein of the patient's family. Each center will see about 50 patients a year, which, combined with the Bethesda patients will bring the total to 450.

The expansion comes from the NIH Common Fund, a $ 557 million program for cross-initiatives turns on a little money each year than the wind projects down or move to the NIH institutes. Another new launch Common Fund initiative in 2013 will focus on the RNA molecules that cells secrete to communicate with each other. The extracellular RNA Communication program will receive $ 130 million over 5 years.

Too often, the cancer seems to have been erased by the processing returns. Some scientists have blamed so-called cancer stem cells, a subset of cancer cells that may be able to remain dormant, evading chemotherapy or radiation to form months or years, new tumors later. The idea was controversial but today published three documents to prove that in certain brain, skin and intestinal tumors, cancer stem cells are the source of tumor growth.

The model of cancer stem cells is different from the traditional idea that tumor growth is equality of opportunity which is all and all cancer cells can divide and cause a tumor to grow and propagate. The stem cell model assumes that the growth of the tumor is hierarchical, mainly driven by a subset of cells that can make new copies of themselves and give rise to other types of tumor cells contains. Some of the first evidence for cancer stem cells come from leukemia studies in the 190s showing that only a small part of cancerous blood cells could spread the disease in mice. But it was difficult to determine whether cancer stem cells fuel the growth of tumors in other tissues.

In the new study, three independent groups used genetic cell labeling techniques to trace the proliferation of certain cells in the tumors to grow. The method gives researchers a glimpse of "what happens in the real life of a tumor," explains Cédric Blanpain, stem cell researcher at the Free University of Brussels in Belgium. He and his colleagues report online Nature that in tumors papilloma mouse, a precursor of skin cancer, most of the tumor growth came from a few cells, which in some ways resembled the stem cells that maintain healthy skin.

In a second article, also published online today in Nature , developmental biologist Luis Parada and his colleagues at the University of Texas Southwestern Medical Center (UTSMC) show in Dallas than in mice that develop glioma, a form of brain cancer, the growth of the tumor appears to be from a small subset of cells in the tumor. They found that the cells may remain dormant for chemotherapy that kills most cancer and may give rise to new tumors after drug treatment stops.

And in the third paper, published online today in Science , developmental biologists and researchers on stem cells Snippert Hugo, Arnout Schepers, Hans Clevers, and their colleagues the Hubrecht Institute in Utrecht, Netherlands, used mice with multicolored intestines watching the cell types that form the intestinal adenomas, a precursor to intestinal cancer. Rodents, scientists have nicknamed confetti mice are genetic markers that can label the intestinal cells blue, green, red or yellow according to the cell where they come from. The team reports that adenomas develop from cells that express a gene called LGR5 ⁺ , which is also active in normal intestinal stem cells. "The tumor is really like a caricature of normal tissue," said Snippert.

These cell tracing techniques are the right approach to test the model of cancer stem cells, said Sean Morrison, who studies stem cells and cancer UTSMC and has not been involved in any studies. There is now enough evidence to be pretty sure that the model explains at least some types of cancer, he said. Morrison warns, however, that studies of papilloma and adenoma looked precancerous tumors. Indeed, when Blanpain and colleagues examined mice with squamous cell carcinoma, a malignant growth papilloma, they found that most of the cells were actively dividing, not just a small subset of stem cell-like cells .

Understanding cancers that can develop from or simply harbor-cancer stem cells is key to more effective treatments, researchers say. This is not an easy task, however. Morrison notes that the growth of tumors differs even in patients with the same cancer. Still, says Parada, with three examples where tumors appear to harbor cancer stem cells suggests that there will be more. "I hope will strengthen and stimulate community" to understand how to better study the model of cancer stem cells, he said. "We will bring this level of control in all solid tumors."

National Cancer Institute (NCI) Director Harold Varmus says his agency budget problems do not just slow progress in fight against cancer; they can also affect the "accuracy" of papers by increasing the pressure to publish quickly. With his usual frankness, he also told reporters yesterday about his concerns about a bill that set aside funding for specific cancers.

In a speech at the National Press Club titled "What Prevents Cancer Research," the Nobel laureate and former National Institutes of Health (NIH) Director (1993-1999) considered a range obstacles on the ground, including the complex biology of cancer and science budgets have not kept pace with inflation since 01, despite a wealth of new knowledge and tools, "the pace of research is slower than it could be and should be, "Varmus said.

in addition, the grant of 17% to 14% NIH and NCI are having" side effects, "including" a serious sense of competition and stress "that discourages young scientists and foreign researchers planning to historically low success a move to the United States.

In addition, Varmus said, financial pressures can influence the "accuracy", referring to reports that the industry has been unable to reproduce the university research studies. "The need to get things published and get your work out there has probably decreased the accuracy of the work is published," Varmus said.

He also accuses the pressure to publish in journals such as Cell Nature and Science when important results are also shown in d other journals. One solution, he pushes at the NIH is to have biosketch an investigator, a statement on background and research achievements of the investigator, discuss how its work has contributed in the field and rely less on whether they have published in high impact journals.

Varmus also discussed a bill that was recently passed by the House of Representatives and a companion bill in the Senate that both require NCI pay particular attention to the "recalcitrant cancers." The House bill would initially set aside funds specifically for pancreatic cancer and make funding decisions in the hands of lawyers. Varmus has agreed with a speaker that these bills are "a slippery slope" that could lead to a proliferation of narrowly targeted funding. If a targeted bill passes, "Very soon all the other groups will say:" I also want. "" But he noted that progress in basic science is difficult to predict, and studies in an area often contribute to great advances in another

other remarks Varmus.

• on the "sequestration" or imminent, federal budget cuts across-the-board if Congress and the Obama administration can not agree on how to reduce the deficit, "I do not like and I guess that will not happen." Varmus said that although $ 5 billion budget NCI would be reduced by 8%, because much of the money is set aside for ongoing subsidies, cutting could reduce by 40% the funds available for new and competing grants.

• On the lack of discussion of biomedical research in the presidential campaign. "I do not think it's the fault of the candidates that there was not much said about medical research "He would like to see the questions in future debates on issues such as research on stem cells and the balance of basic and applied research.

• On a Sunday story first page in The New York Times that critics say hype the importance of NCI project cataloged genetic changes in breast cancer: the conclusion that breast cancer breaks into four subtypes is "no real breakthrough in this direction" because researchers had already identified the four types. Instead, the importance of the study is that it gave "a much denser genetic landscape that genetic abnormalaties are" that could eventually lead to better diagnosis and treatment.

• On a "moon shot" plan announced last week by the MD Anderson Cancer Center Director Ronald DePinho to dramatically improve the survival of eight cancers: "We encourage our directors cancer centers to be ambitious, "Varmus said. He added, however, that" I will not comment on his particular decision about it. "

Texas Governor Rick Perry (R) yesterday asked embattled $ 3 billion research agency on the state to stop cancer grants until it addresses concerns about its procedures. The Institute of Prevention and Cancer Research of Texas (CPRIT) responded by announcing a moratorium on new subsidies.

problems CPRIT went public in May, when then-scientific director Alfred Gilman, a Nobel Prize, left to protest against the proceedings of scientific review of the agency. Two other top agency officials, including the executive director of CPRIT, have left in recent weeks amid new allegations-and-investigations in civil and criminal matters how the agency has made certain marketing functions.

In a letter received yesterday, Perry and two other heads of state have asked CPRIT to "fully meet the concerns that have been raised about its processes and operations before future subsidies are granted." The committee monitoring CPRIT replied that he "accepts" and impose "a moratorium on CPRIT grants. ... These issues must be resolved to restore public confidence in CPRIT. "Current grants are not affected, the agency said.

spokesman CPRIT Ellen Read said staff the agency seeking "clarification" about what the moratorium proposals already in the pipeline. this includes those of a request for applications for the first translational price which closed on December 14.

CPRIT funded 502 grants totaling $ 841 million for research, commercialization and prevention since 09. the legislature of the state of Texas is scheduled to hear testimony today about whether the agency should be funded in 2014 2015, according to The Texas Tribune .

a tonic of gut microbes may be the secret recipe to treat a common hospital scourge. The researchers revealed the exact combination of microbes necessary to cure mice with a chronic infection with a bacterium that causes difficult to treat bloating, pain and diarrhea in people. A similar bacterial cocktail may one day be able to replace a controversial treatment involving the consumption of feces to restore the balance of microbes in the gut.

Clostridium difficile is a threat in hospitals and nursing homes, causing nearly 336,000 infections and 14,000 deaths annually in the United States. Antibiotics can temporarily drop the bacteria, but about 25% of infected people relapse, often several times, because the germ produces spores that hand sanitizers and hand washing do not kill. Antibiotics can also turn against because they kill normal microbial community in the gut, opening the way to C. difficile to resettle.

In desperation, some doctors have turned to an unpleasant Contact: successfully treat patients by inserting a tube into the stomach containing ground up, filtered faecal a person healthy subjects containing a dose of beneficial microbes. But this treatment is controversial and in some places illegal, because of the risk of introducing other pathogens.

In search of alternatives, microbiologist Trevor Lawley Wellcome Trust Sanger Institute in Hinxton, U.K., and colleagues examined Clostridium infection in mice. Lawley and his colleagues first demonstrated that the spores of the germ can cause any infection recurrences after antibiotic treatment and fecal therapy cures the problem. They then cultured feces used to cure mice, the isolation of 18 types of bacteria. Finally, they began to mix and match, infecting mice with different combinations of bacteria. Among the various combinations tested, only one, a mixture of six very different types of bacteria, cured the mice, they report online today in PLoS Pathogens .

"It is an excellent paper, avant-garde," says Brendan Wren, a microbiologist at the London School of Hygiene & Tropical Medicine, who was not involved in the study of the mouse. It works now with Trawley to determine if they can find an appropriate bacterial cocktail that will heal humans. If they succeed, Wren said one day "single suppository of the bacteria could prevent C. difficile reinfection and avoid need antibiotics, which can make the problem worse "

* Correction, 05:20 pm.. patients Some doctors have successfully treated for C. difficult with ground up, the filtered fecal matter inserted into the stomach with a tube, not through an enema.

Some well-funded biomedical researchers may have to tighten their belts in a new funding policy announced yesterday by the National Institutes of Health (NIH). The agency plans to give further consideration to the proposals of researchers receiving more than $ 1 million per year in direct support grants and can not finance such research is superimposed on what they already do.

After years of flat budgets and lower subsidies success rate, the NIH has been looking for ways to stretch its funding further research. An idea which floated last fall was to limit the amount of grant money the principal investigator (PI) might hold. While some fear that it would hamper the production laboratories, in February the agency announced it was moving forward: high quality researchers applications with at least $ 1.5 million in total annual funding would get a layer additional examination of the scientific council of the Institute funding. The council would ensure that the research is "very promising" and "separate from" the other IP projects.

After piloting the plane during its May round of grant reviews, the NIH has made some changes. A big problem was that because the indirect costs vary from school, those who have a higher overhead rate would be disproportionately affected. So the final policy will cover IPs with at least $ 1 million in direct costs. This adds about 19 grants to about 70 to be revised in September using the threshold of $ 1.5 million, writes the NIH Deputy Director for Extramural Research Sally Rockey in his blog Rock Talk. NIH will not require large multi-PI grants to undergo special examinations unless all individual IPs are on the threshold of $ 1 million. And tips can make exceptions, for example for clinical trials, which tend to be more expensive than laboratory research.

Last fall, the NIH has estimated that about 1,0 IP, 6% of the total funds it would be above the threshold of $ 1.5 million of total costs. But with the restrictions in the final policy, less than 1% of all proposals will get additional advice examination, said NIH Scienc eInsider. And because politics is not a cap, it is unclear how much money it will eventually release. (The driver in May was intended to gather input ;. It has not resulted in funding decisions)

Howard Garrison of the Federation of American Societies for Experimental Biology, who last year wrote the NIH to support the policy, said it is important anyway. "It will not necessarily solve all our problems. But people have found it an appropriate measure, "says Garrison. A blogger, however, is disdainful of politics: "It will do nothing to feed all the hungry mouths," wrote DrugMonkey

A gunman or gunmen shot and killed up to 11 people this morning in two health clinics in Kano State in northern Nigeria. The shootings follow closely on the heels of the targeted killing of nine polio workers and other humanitarian workers in Pakistan in December and January. Several media reported that the victims were in Kano polio vaccinators as well and have speculated that the terrorist group Boko Haram is involved.

Details are murky, and it is unclear who and how many people were killed, said Oliver Rosenbauer, spokesperson of the Global Initiative to eradicate polio with headquarters in Geneva , Switzerland, the World health Organization (wHO), which is closely following events.

The picture that has emerged to date is that at 9:30 this morning, local time, one or more gunmen attacked two health clinics in quick succession. No one has claimed responsibility.

The government of Kano investigation and, as a precaution, he interrupted all immunization activities against polio that could be underway. WHO has also drawn its members polio field staff and asked them to work from home.

Nigeria is one of the three remaining countries, as well as Afghanistan and Pakistan, where polio remains endemic. The government and international agencies to the eradication initiative intensified campaigns there in recent months to eliminate the virus. As part of these efforts, vaccinators go door to door drops of oral polio vaccine to children. The latest campaign in Kano ended February 5, but sometimes the polio workers continue "mop up" activities for several days.

"Our sympathy goes to the victims and families," says Rosenbauer, who calls the "tragic" and "scandalous" events.

Analysis of queries made to Google, Bing and other search engines can reveal potentially dangerous consequences of mixing requirements before they are known to the Food and Drug administration (FDA), according to a new study. This data mining could even expose the medical risks that slip through undetected clinical trials.

Pharmaceuticals often have side effects that go unnoticed until they are already available to the public. This is especially true of the side effects that occur when two drugs interact, largely because drug tests attempt to identify the effects of a drug at a time. Doctors have few ways to drive these hidden risks, such as reports to the FDA of doctors, nurses and patients. A study in 2011, the data extracted from these reports and FDA discovered a hidden drug interactions: When taken together, the antidepressant paroxetine and pravastatin cholesterol suppressor because hyperglycemia or high blood sugar. After checking that research experiments, the researchers behind the study asks what other sources of information have been left unexploited.

Enter the search engines. Just as Google Flu Trends reveals influenza outbreaks by tracking search terms related to influenza, search queries on combinations of drugs and possible side effects say, "Paroxetine", "pravastatin" and "hyperglycemia" -might enable researchers to identify unforeseen drawbacks to drugs, said researcher Nigam Shah bioinformatics from Stanford University in Palo Alto, California. "If a lot of people are concerned about a symptom, which in itself is valuable information."

Although many bad drug reactions are never reported to doctors, people talk about what bothers them all the time on an occasional basis to friends or online, says the biologist Nicholas Tatonetti calculation of Columbia University, who was also involved in the study. "They do not really know," he said. "They are just reports of their symptoms, which is just a normal thing that humans love to do."

Thus, researchers have turned to Microsoft, which gets permission many Internet Explorer users to collect Google, Bing and Yahoo! search queries for research. Microsoft has provided a database containing 82 million queries search engines from 6 million unique users as of 2010. The research team looked for users interviewed "paroxetine" and "pravastatin" or each drug alone, to determine if the same users also sought "hyperglycemia" or other terms describing hyperglycemic symptoms. for example, they may have looked "dry mouth" or the technical term "xerostomia."

Before anyone knew the side effects of the drug combination, one in 10 people looking for both drugs also looked for terms related to hyperglycemia, or about twice what people looking paroxetine or pravastatin alone, reports the team today in the Journal of the American Medical Informatics Association . The researchers then looked for another 62 pairs of drugs, half known to cause high blood sugar and half unknown. They found that the data mining procedure correctly predicted whether the combo drug did or did not cause hyperglycemia about 81% of the time.

The results add yet another resource for scientists to find clues about the risks of drugs, Shah said, and it can be followed in real time. Hope, he notes, is that companies search engine could analyze data and send the results to the FDA, which would then track down information and alert doctors to potential new risks. "This is information we have access. As a society, we're sitting on it," he said. "We could use it to help the FDA, which is currently based on sources reported."

The new study is "exciting" because the field is so new, said researcher Hojjat Salmasian Biomedical Informatics at Columbia University, who has not participated. "We do not know how much it has potential," he said. "But based on the results that have been published so far in this study and other similar studies, it seems that this is a very important area explore. "

thousands of scientists and advocates for paid patients in a square in downtown Washington, DC, today to hold what organizers billed as the largest ever rally to demand more funds for biomedical research. The event, as reported earlier today with a slide show Science initiated and organized in conjunction with the annual meeting of the American Association for Cancer Research (AACR) with the support of over 0 organizations , aiming to draw attention to the 5% reduction for the National Institutes of Health budget $ 31 billion (NIH) imposed by Congress last month by sequestration, as well as the flat growth of NIH budget over the last decade. "The continued erosion of funding for the largest institute of medical research in the world, the National Institutes of Health, must end," said CEO AACR Margaret Foti.

AACR and other participants listened for nearly 2 hours unusually hot weather in April that more than a dozen legislators, patient advocates, and celebrities have spoken in support of the NIH. Emcee Cokie Roberts of ABC News and NPR stated that "it could not be a stupid time to cut funds for medical research." Representative Rosa DeLauro (D-CT), a survivor of ovarian cancer, said "is cut lifesaving cancer research because of ideology, and it's wrong." President of the Rockefeller University and former Genentech framework Marc Tessier-Lavigne said he worried most that young people are discouraged from careers in research. "You can ruin our scientific community. If we continue on this path, we will kill the goose that lays golden eggs, "he said, drawing cheers.

Dressed in white T-shirts and an occasional hot pink boa, participants in the rally chanted "more progress, more hope, more life." They raised their cell phones with actress . Maura Tierney of the television series ER to send a mass text message asking Congress to reverse the cuts to NIH

one of the scheduled speakers was missing: NIH Director Francis Collins. Although federal employees can not participate in lobbying activities, Collins was first going to speak as a private citizen, the sources said, but eventually canceled. (NIH spokesperson John Burklow refused to comment on the reasons for Collins, saying only, "Dr. Collins could not attend the rally, however, supports the participants effort to shine a light on the importance of biomedical research.") However, Foti read a message from President Barack Obama, who said he has sent "greetings" and that he also supports "a serious and sustained effort to advance medical research."

Although probably only a few thousand the AACR 18,000 participants left the conference center to the streets to participate, the organizers deemed their event which included tuning supporters via YouTube success. He was "truly historic and unprecedented," said Foti. For a time, tweets with the tag #RallyMedRes of the rally were second only tweets about the death of former Prime Minister Margaret Thatcher U.K., Foti said afterwards.

It's time to go back on a ticker aging. Drawing on a bizarre experimental technique invented there more than a century, but rarely now, researchers have found that a protein in the blood makes the old mouse hearts appear young and healthy again. It is not yet known if humans react the same way, but scientists hope that this discovery may help treat one of the most frustrating ailments of the heart.

"This is probably the first round we have about what makes the heart young and making the old," said cardiologist Deepak Srivastava of the Gladstone Institute of Cardiovascular Disease in San Francisco, California who was not involved in the work.

As the heart muscles age, they grow thicker. The thickened heart can still pump blood on normally, but he can not relax enough to fill between the pumps. The condition is called diastolic heart failure, named after the rest of the heart, or diastolic phase. There is currently no treatment to reverse the thickening of the heart and restore normal function.

But researchers continue to seek such a heart fountain of youth. One approach has been to apply a technique of 150 years to infuse young blood in older mice. Parabiosis called heterochronic the method involves surgically connect the systemic circulation of two different ages mouse, opening a flap of skin on the side of each mouse and sewing the two together, so that the pumps of the same blood through the two creatures. (There are more than a century, the technique was developed to study the exchange of nutrients between animals.) Previous studies have found better muscle health and strongest healing in older mice receiving the blood of a younger counterpart. But the heart tissue is not known to be as strong as the skeletal muscles and skin. The effect can work both ways-young mouse stem cells lose power in the old blood.

stem cell biologist Amy Wagers and cardiologist Richard Lee, both of the Harvard Stem Cell Institute, wonders if all the factors that circulate in young blood, such as hormones, may affect the aging hearts. Wagers, Lee and their colleagues used parabiosis yoke together on February 5 years mouse (downright ancient in mouse years) with 2-month-old counterparts. The team also joins 12 pairs aged mice and young mice 10 pairs, as witnesses. The first result was "evidently positive," said Lee, who also practices at Brigham and Women's Hospital in Boston. After 4 weeks of access for young mouse heart tissue of five older mice had thinned and softened, looking as spry and flexible as the 2-month-olds. " Older mice had now young hearts, while young mice hearts remained strong.

But the team has spent years trying to understand why; it was often the subject of Lee and weekly bike in paris. "There had found factors that are proposed for the aging factors," said Lee, "but it was not the identification of a circulating factor that can go the other way, to transform old tissue in the youngest tissue. "the team began to examine the factors in the blood, including 69 amino acids and more than a hundred fat. with the help of SomaLogic, a company-protein analysis Boulder, Colorado, the team has made a breakthrough, narrowing down the suspects likely to only 13 factors.

one of the suspects, growth differentiation factor 11, or GDF-11 appears explain the miraculous rejuvenation heart. GDF-11, which regulates the growth of (smell) receptors and olfactory spinal column is produced in abundance in young mice, but production decreases with age. other experiences team on cultured heart cells confirmed that GDF-11 stops the growth of thickening observed with age.

In addition, the researchers report online today in Cell , old mice injected with this protein for 30 days developed younger, stronger heart tissue. GDF-11, they say, directly counteracts the genes responsible for the thickening of the muscle.

"It is conceivable that this is just a story of interesting mice," says Lee, "but we're hoping to get data that could tell us that respect for man . "GDF-11 also appears in human blood, he said, although his role in the aging of the human heart is still uncertain. Then the team will study how GDF-11 affects other age-sensitive organs such as the tissues of the bone marrow.

Srivastava adds that GDF-11 appears to be effective against heart disease due to age, but he hopes that the protein could one day help patients hearts, stiffened by attacks heart, to relax.

This study is a validation of the parabiosis modern science of the 18th century using the molecular biology of the 21st century, says Gerald Dorn cardiologist at the University of Washington in St. Louis . However, the use of technology gives the research a gothic macabre flavor, he said. "I was looking to see if Tim Burton or Vincent Price were a part of the experimental design."

Neanderthals living 0,000 years ago in what is now Croatia has not been exposed to industrial chemicals, and they ate a diet without processed foods. Yet, this did not spare our modern diseases. Scientists have discovered the first known case of a tumor in the rib of a Neanderthal man dating back to there are more than 0,000 years. The oldest known human tumor is there are less than 4,000 years.

"relatively little is known about [tumor] prevalence in ancient times," said forensic anthropologist Douglas Ubelaker of the Smithsonian Institution in Washington who was not involved in the new work. This result " is very useful to understand the roots of this disease. "

the bone-portion of an upper left rib of an adult male Neanderthal-was initially uncovered between 1899 and 105 during the excavation Krapina, a cave in the north of Croatia, who gave hundreds of ancient human remains. But the coast was misfiled and ignored for nearly a century until, in 1999, he was briefly described in a list of specimens. recently, anthropologist David Frayer of the University of Kansas, Lawrence, and colleagues began studying the bone pathologies in Krapina collections. It was immediately clear that the rib fragment- 0.17 in the normal specimen collection, wasnt. "The bone is broken away so that you can look into the room of the cord, where even a child, you expect to see the cancellous bone," says Clearing. "But in this side, instead of have a bone mesh there, it is completely empty. "

Even to the naked eye, scientists have recognized that the blank area of ​​the bone indicated a tumor had once sat there. But to get more details on its size and shape, the researchers turned to the X rays and CT scans. These studies revealed that physical standard characteristics and location of the missing bones were consistent with dysplastic neoplasm fibrous vacuum, a tumor caused by a bone growth disorder, scientists report online today in PLOS oNE . Now fibrous dysplasia neoplasms are one of the most common causes tumors in the ribs and can lead to bone fractures and pain.

"Unfortunately, we do not have more of this particular skeleton," says Clearing. As a result, the researchers can not determine more details about the individual with the tumor, as if his bones had other tumors and if he had symptoms of systemic diseases that can occur alongside the tumors. Researchers also can not draw conclusions from a single sample on the incidence of tumors in the Neanderthal population, he said.

"There is always a temptation to try to read more into a lesion that can be interpreted with confidence," said Ubelaker. "But these authors have done a splendid job and prudent to take proof that insofar as it will go in terms of differential diagnosis. "

the causes fibrous dysplasia neoplasms are not now included. Knowing that they were present in the human family since the prehistoric times could shed light on how tumors co-opt an ancient molecular pathway in our cells to grow. But it will take more than old bone tumors examples to draw broader conclusions, say the researchers.

Boston- A heated discussion broke out today at the annual meeting of the American Society of Human Genetics on a hot topic -button: When will we know enough about the risk of rare cancer genes begin to systematically test for them in patients with a family history of cancer

on one side of debate was a team led by geneticist Mary breast cancer -Claire king, who discovered the first risk gene for hereditary breast cancer, BRCA1 . The King group now wants to regularly test some women for other genes linked to cancer. Other researchers, however, have argued that it is premature to test these other genes, which are less well understood.

Physicians often offer women with breast cancer in their family to test for mutations in BRCA1 and a related gene, BRCA2 . If the tests are positive, some women can take preventive measures. Earlier this year, for example, actress Angelina Jolie drew widespread attention for his decision to have a double mastectomy because she inherited a version of BRCA1 which carries a risk of developing breast cancer by 87%

Many women with breast cancer in their family, however, do not test positive for the BRCA mutations ,. At the meeting, Tomas Walsh of the University of Washington, Seattle, reported a test he and King developed, called Broca, as sequences not only BRCA genes, but also about 38 other genes cancer risk. They ran the test on BROCA nearly 2,300 women from 743 families with breast cancer. In 77 families, they were not BRCA mutations, but find changes in other genes they say are definitely linked to breast cancer, such as TP53 and CHEK2 . Another 41 families carried mutations in a larger set of genes whose role in cancer is "emerging," said Walsh.

King and Walsh are not just using their BROCA test in research, however, the university is also offering it as a clinical test for patients. And doctors also can order the commercial test.

This did not sit well with other researchers in the meeting today. "It is irresponsible and unacceptable" in the clinical trial for other genes that BRCA for which the risks are not well established, said Nazneen Rahman of the Institute for Research on Cancer in Sutton , United Kingdom do is "harmful" she said science Insider, because it could cause women to take drastic measures such as having their breasts removed. the King team "mixed research clinical "tests, she said.

King defended their test group in a discussion with reporters. Doctors receive results for 12 genes that evidence suggests can double or quadruple the risk of cancer; this means a chance of a woman developing breast cancer of 25% to 50%, Walsh said. When the team detects these genes, they did not recommend surgery, but screening at regular place with imaging.

King emphasizes that screening BRCA1 was controversial before the community consensus in 1997. "I have a sense of déjà vu," she said science Insider. She said her critics mistakenly think the returns BROCA clinical test results for 40 genes, not just 12. "We are comfortable on those where we already have data," on the basis of their own studies and literature, she said. "We were extremely careful not to report variants" of uncertain significance, she said.

Surgeon Greta Bernier, King group added that during the test only BRCA genes is recommended by the National Comprehensive cancer network, which issues guidelines for the treatment of cancer, his team is confident that the network will soon add other genes on their list. it stresses also doctors can already order tests for the genes on the list of gene-testing companies around.

Melissa Southey from the University of Melbourne in Australia believes that while it is important to test all the cancer risk genes in the research, evidence for clinical trials is strong enough for a small number of genes, and even then only for some specific variants. The problem, she says, is that most other variants are so rare that it may never be possible to study enough people to identify risks. Instead, researchers have to rely on other evidence that mutations are harmful, such as laboratory studies of the proteins encoded by genes.

The same difficulty confronting geneticists as they discover other genetic variants of risk rare, Southey says. "This is the edge, where we are," she said. "We have a lot of information, but not enough to offer advice."

virologist Ron Fouchier suffered a loss of a legal battle with the Dutch government on the publication of his controversial research on H5N1 . On Friday, a Dutch district court ruled that the government was right to ask Fouchier to obtain an export license before sending two documents hotly debated for publication. The decision, published yesterday (Dutch), could provide new dams for research Fouchier in the future.

The issue is hotly debated document Fouchier of showing that some mutations may H5N1, a virus that normally infects birds, transmitted through the air between ferrets, which was published in science in June 2012. the fight also involved a companion paper published in the same issue in which Fouchier and others have tried to assess the likelihood that these viruses arise spontaneously in nature.

The Dutch government considered sending the documents to science a form of "export" and Fouchier necessary to formally ask the first official authorization. In doing so, the government has correctly interpreted E.Ü. regulations aimed at preventing the proliferation of weapons of mass destruction and the technology called "dual-use" which could be used for good or evil, the court of Haarlem said.

The decision means that the future studies- H5N1 transmissibility Fouchier which resumed after a worldwide moratorium ended in January-would require an official stamp of approval as well. The same could be true for similar studies involving H7N9, a strain that emerged in China this spring, because the government could consider studies that give the virus to new capabilities as providing results dual use.

Fouchier was available for comment today, but he has said in previous interviews that the Dutch government infringes on academic freedom and he and other scientists in the Netherlands putting at a disadvantage compared with scientists from other countries.

Working H5N1 Fouchier triggered an outcry around the world at the end of 2011, with a similar study by Yoshihiro Kawaoka of the University of Wisconsin, Madison and the University of Tokyo, when the US National science Advisory Board for biosecurity (NSABB) ruled that he should not be released without hitting the most sensitive details. In the wrong hands, the reasoned NSABB, studies could be used to turn H5N1 into a bioweapon. The board reversed that decision in March 2012 and gave the papers a green light.

But while Kawaoka paper was published online in Nature in early May 2012, the study Fouchier was retained longer because of the position of the Dutch government.

Fouchier requested an export license subject and received April 27, 2012, to allow the paper to finally be published. But Erasmus MC has also filed an appeal against the decision of the Government; when the government rejected, he took the matter to the District Court.

The government based its decision on E.Ü. regulations issued in 09 aimed at preventing the spread of nuclear, chemical and biological weapons. These rules impose limits on exports, trade and transfer of a range of materials, including the dangerous flu virus and are also valid for the technical expertise that could be used to make such weapons .

Erasmus MC and Fouchier argued that the rules do not apply to paper Fouchier as an annex of the document carves exceptions for "basic scientific research" and for the information already "in the public domain . "ferrets studies were fundamental scientific research, counsel for Fouchier argued, because researchers have sought to better understand the transmissibility of mammal a strain of influenza; Meanwhile, the methods used in study to generate mutants have been described previously and were well known.

the court, which heard arguments in the case on August 29, do not buy this line of reasoning. Make H5N1 airborne was not only basic research, but was a "practical purpose," the judges said, and while the methods previously described, the researchers had to avoid hollowing out "took action and made choices that led to completely new results." the regulations, any exception "must be interpreted strictly," the court said, adding that he is not the researchers to decide if their work is basic research.

the court recognized that its decision could result in delays in the dissemination of scientific information, but said that "disadvantage" is outweighed by the importance of the prevention of proliferation.

Fouchier and Erasmus MC have six weeks to take their case to the Amsterdam Court of Appeal.

Here are some lousy news for parents of children biting head: Lice eggs can take 2 weeks to hatch in the hair humans, which makes the standard 7 days treatment delousing ineffective in some cases. New research shows that if the conditions are good, eggs, called nits, can sit dormant for treatment, only to appear later and re-infest the scalp. A third application may be necessary after 14 days to remove nits hatch slow, they say.

Lice do lay their eggs directly on the skin instead, they lay nits at the base of the hair stems. The timing of the outbreak louse on a human head is difficult to follow because adult lice lay eggs continuously, obscuring earlier hatches, and the effectiveness of traditional insecticides on eggs varies. Previous estimates of how long remain viable nits only to 14 days, but most of this work from the 1920s and 1930s, when researchers reared body lice inside boxes attached to the arm or ankle of a person. More recent work is based on head lice raised in laboratory incubators, which are more stable than the wide range of temperatures and cleanliness found on a human scalp.

For a more reliable estimate, medical entomologist Ian Burgess of Insect Research & Development Ltd. in Cambridgeshire, UK, analyzed data from 20 previous studies on treatments that kill lice by physical means, such as lotions that suffocate insects, but do not kill the eggs. They do not include insecticide treatments for lice across the UK have developed resistance to standard drugs, Burgess said, leading more doctors to try a brute force approach that does not rely on insecticides.

1895 Data patients revealed cases where newly hatched found technicians lice nymphs on the 14th day after the start of treatment, even if the second application the scalp was held seven days before. "Some [nymphs] had emerged just an hour or two before checking," said Burgess. To exclude cases where reinfestation of another child had occurred, or when adults had escaped little lice treatment, it excluded cases with lice that have emerged over the number of days since the last treatment. Nearly two dozen cases have remained-enough to check a handful of nits may last longer than standard treatment protocols, Burgess reported in an upcoming issue of Medical and Veterinary Entomology.

Although the treatments themselves may play a role, the temperature of a person's scalp is likely to be the most important factor in the time it takes to hatch eggs, Burgess said. Location and hair issues as: Lice grow faster in warmer temperatures, so they will hatch more quickly when on the warm, thick hair at the nape as the thinner hair on top and in front of the scalp

analysis is the most rigorous yet to quantify the outbreak louse times, said Rich Pollack, an entomologist of public health at Harvard University. "It must be considered by those trying to make a management decision process," said Pollack, noting that only a small number of patients may need a third dose.

New insecticides oral may make the issue of time of incubation theoretical, Pollack notes. These drugs now available by prescription in the United States, are up to 85% effective in killing lice and eggs with a dose sparing spraying scalp's parents several times a child squirms.

With all the recent talk about how gut bacteria affect health and disease, it begins to seem like they could be in charge of our body. But we can have our say by what we eat. For the first time in humans, the researchers showed that a radical change in diet can quickly change the microbial composition in the gut and also change what these bacteria do. The study takes a first step to identify how these microbes, collectively the intestinal microbiome, can be used to keep us healthy.

"It is a landmark study," said Rob Knight, a microbial ecologist at the University of Colorado, Boulder, who was not involved in the work. "It changes our view of the speed of the microbiome may change."

Almost every month, a new study suggests a link between bacteria living in the gut and diseases ranging from obesity to autism, at least in mice. Researchers have struggled, however, immobilizing the links between health and the microbes in humans, in part because it is difficult to make people change their diet for weeks and months that researchers thought need to change the gut microbes and see a health effect.

But in 09, Peter Turnbaugh, a microbiologist at Harvard University, demonstrated in mice that the change in diet affected the microbiome in a day. So he and Laurent David, now a biologist calculation at Duke University in Durham, North Carolina, decided to see if the diet could have an immediate effect in humans too. They recruited 10 volunteers to eat only what the researchers provided for 5 days. Half ate only animal bacon and eggs for breakfast; spareribs and chest for lunch; salami and a selection of cheese for dinner with pork rinds and string cheese as snacks. The other half consumed a high-fiber, plant-only diet with grains, beans, fruits and vegetables. For the few days before and after the experiment, the volunteers recorded what they ate so that the researchers could evaluate how dietary intake differed.

The scientists isolated DNA and other molecules, as well as bacteria from stool samples from before, during and after the experiment. This way they could identify bacterial species were present in the intestines and what they produced. The researchers also examined the activity of genes in microbes.

Within each diet group, the differences between microbiomes volunteers began to disappear. The types of bacteria in the intestines do not change much, but the abundance of these different types have, especially in meat eaters, David Turnbaugh, and colleagues reported online today in Nature . In 4 days, the bacteria known to tolerate high levels of bile acids increased significantly in meat eaters. (The body secretes more bile to digest meat.) The activity of genes, which reflects how the bacteria were metabolizing food, has also changed a little. In eating meat, genes involved in protein degradation have increased their activity, while in food plants, other genes that help digest carbohydrates resurfaced. "What was really surprising is that the gene [activity] profiles conform almost exactly what [is seen] in herbivores and carnivores," David said. This same rapid change has occurred in the long-term vegetarian who switched to meat for the study, he said. "I'm really surprised how quickly it happened."

From the perspective of evolution, that intestinal bacteria can contribute to mitigating the effects of a rapid change in diet food, reviving quickly different metabolic capabilities based on meal consumed, may have been useful to early humans, said David. But this flexibility also has possible implications for health today.

"this is a very important aspect of a very hot area of ​​science, "writes Colin Hill, a microbiologist at University college Cork in Ireland, which has not participated. "Perhaps by adjusting diet, we can shape the microbiome in ways that can promote health," added Sarkis Mazmanian, a microbiologist at the California Institute of Technology in Pasadena, also affiliated with the study.

But how it should be shaped is still in the air. "We are not yet at the point where we can make significant dietary recommendations to" improve "the microbiota (and host)" wrote Hill. He and others are cautious, for example, on the consequences of the increase in any bacterium, Bilophila wadsworthia , in meat eaters than in mice is associated with inflammatory bowel disease and diets high in fat. Knight said, "There is still a long way to go before causation is established"

So Hill best advice for today. "People should ideally consume a varied diet with nutrients and micronutrient-whether derived from appropriate animal or plant or a mixed system. "

A trust fund created by billionaire shipping magnate Daniel K. Ludwig ends today with a bang and donated for research. Six US medical centers will receive $ 540 million- $ 0 million each-funds to provide cancer studies in perpetuity, or until the cancer is no longer a problem, as specified in the will left by Ludwig, who is died in 1992. in all, his estate gave $ 2.5 billion in cancer research since the 1970s

new money goes to Ludwig centers already located six elite research institutions: . Harvard Medical School in Boston; Johns Hopkins University in Baltimore, Maryland; Massachusetts Institute of Technology in Cambridge; Cancer Center Memorial Sloan-Kettering in New York; Stanford University in Palo Alto; and the University of Chicago. Ludwig had established trust the same centers in 06.

Financing by the Ludwig Trust was "sort of under the radar," said oncologist Kenneth Kinzler, who with Bert Vogelstein, co-directs the Ludwig Center at Hopkins. These are among the most coveted awards in the biomedical field, said Kinzler. The money is held for endowment and comes with few strings attached just a mandate to investigate cancer and find ways to stop it. There is no progress reports or renewal requests to write, Kinzler said, which "allows you to focus on what you think give the most important results without worrying about respect artificial intermediate deadlines."

the Ludwig group seeks clinical outcomes, Kinzler said, a goal that he and Vogelstein heavily. Without money Ludwig, the Hopkins group was not able to make cancer genetic studies, they are famous for, he notes, for example, the duo used surveys of Exome to identify genes associated with colon and breast cancer.

size Ludwig endowments makes a difference, says Jedd Wolchok cancer immunologist at Memorial Sloan-Kettering ". It allows a budget of respectable research "Wolchok figures that the budget of his group for Cancer Immunology Research will double this year, an increase of" several million dollars "and will continue to grow, thanks to the money earned by staffing. For Wolchok, this means that "we can go from concept to clinical research very, very quickly." For example, he expects his group to launch a clinical trial in two months to test a therapeutic antibody developed by a Japanese company that could be used to modulate the T cells that regulate the immune response. The team Memorial Sloan-Kettering also has a number of ongoing clinical trials to monitor immune system reactions to various cancer therapies, including radiation.

Ludwig, a friend of President Richard Nixon, was a supporter of Nixon unconditional "war against cancer" that has been linked to the Congressional legislation that restored National Cancer Institute of the United States in 1971. this year, the shipping magnate has created an independent in New York, the Ludwig Institute for cancer research. The organization now has an endowment of more than $ 1.2 billion and employs more than 0 people, including scientists in six countries outside the United States, according to the institute CEO Edward McDermott Jr.

the philosophy behind this research network, McDermott said, is that which led Ludwig McDermott adds "in its to personal business enterprises find the best people and resources as well". "We are investing in science, not science special. ... We are not in the area of ​​discovery, because of the discovery. It is a means to an end, which is improved patient outcomes. So we are very committed to infrastructure ... allow us to take our patient's bedside to the laboratory findings. "McDermott said that the institute has sponsored more than 100 clinical trials and eight during this time. these are focused on cancer immunotherapy.

MADRID A Spanish researcher HIV / AIDS is facing a hefty fine for violating the regulation of clinical trials. An appeals court upheld most of the verdict of a lower court against Vicente Soriano, a doctor at the Hospital Carlos III here and well known clinical investigator with hundreds of publications to his name.

Soriano is responsible for € 210,000 to conduct a clinical trial without the approval of the Spanish Agency of medicines and health products, failing to get insurance for the trial, and inform the meeting that he had his hospital ethics approval when he did not, according to the decision, which was released on January 14. But the court overturned a € 6,000 fine for obstructing the original investigation, which took place in 2010.

The clinical trial phase IV, Soriano registered on ClinicalTrials.gov in July 09, sought to determine whether HIV patients with undetectable virus in their blood levels can replace so-called protease inhibitors in their treatment of cocktail with a new potent compound, raltegravir, the first in a class called inhibitors integrase, which has fewer side effects. Soriano's team divided patients into three groups with different treatment regimens; a group raltegravir once daily instead of twice the standard. (Simplifying a treatment regimen may help patients adhere.) The study included 311 patients, 222 completed 24 weeks of follow-up; an article in HIV Clinical Trials in 2010 showed that raltegravir successfully removed the virus in all but 13 of them.

An anonymous tipster told the Madrid health service that the trial lacked the proper regulatory and ethical approvals, according to the court decision, and between 24 and 29 November 2010, the Department sent inspectors to examine the records of Soriano. In October 2011, a Madrid court issued a fine of € 216,000

Soriano appealed the fines on various points. the core of its defense, however, supported by three witnesses Spanish experts was that the study was retrospective and observational, and that treatment changes were in the normal range of what doctors might recommend for any patient.

One of the seven judges hearing the case in the Superior Court of Justice of Madrid agreed but the majority did not. They wrote in the verdict that "the call is to avoid that the proposed project not only a change in dose, but also a change in medicine." One of the expert witnesses seem to obscure the fact that patients have was put on a new type of drug by asserting without proof that they were already raltegravir, the court added. fines, two for "very serious" offenses and one for a "serious" offenses, has was the lowest allowed by law.

"This study was undoubtedly a clinical trial," which would need the appropriate ethical approval, said bioethicist Ruth Macklin of Albert Einstein College of Medicine in New York. After reviewing the study protocol Soriano, Macklin said that they are incompatible with observational studies.

Soriano refused to be interviewed about the trial or appeal, but in an e-mail to Science Insider, he said that he and his group are victims of "harassment" related to a dismantling plan of the infectious diseases group at Carlos III. The hospital is in the midst of a merger with the Hospital La Paz in Madrid; both are owned by the Madrid regional government and coins were scheduled for privatization until this week, when a court ordered the cancellation of plans.

It is not known if the hospital will take action against Soriano. While his appeal was pending, he continued his medical practice, but the ethics committee did not approve all clinical trials of its since March 2011, said Rafael Pérez-Santamarina Feijoo, CEO of the hospital La Paz. Now that the final decision of the Court is available, the hospital will assess how to proceed, says Pérez-Santamarina. A spokesman of the Medical College of Madrid said Science Insider that it has taken no formal disciplinary action against Soriano.