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After enduring more than 2 years criticism that included evidence of contamination and misrepresentation of data, a science paper that linked a mouse retrovirus to chronic fatigue syndrome (CFS) today received its last rites: Editor Chief Bruce Alberts issued a full retraction. 13 authors of the study in September signed a partial withdrawal after one of the three collaborating laboratories have found that contamination had marred his contribution, but they could not agree on the wording of the full retraction, Alberts therefore issued without approval. " Science has lost confidence in the report and the validity of its conclusions," wrote Alberts in an "editorial" unusual retraction, which appears in the December issue 23 Science . " it is Science 's opinion that a retraction signed by all the authors is not likely to come. "

researchers from the Whittemore Peterson Institute for Neuro-immune Disease (WPI) Reno, Nevada, conducted the controversial study, teaming with researchers from the National cancer Institute (NCI) and the Cleveland clinic in Ohio. as they reported online in the issue of October 8, 09 Science , they found evidence of a mouse virus called xenotropic virus related to murine leukemia virus (XMRV) in the blood of 67% of 101 CFS patients they analyzed. alarmingly 3.7% of controls were also tested positive, leading to fears that XMRV could be widely contaminate the blood supply in many countries.

Shortly after, researchers around the world began reporting that they could not find the virus in CFS patients. One group found that XMRV was probably created in laboratory experiments with mice that have an immortalized cell line to study prostate cancer and another showed that variants of this line had evolved more isolates XMRV, exactly the opposite of what would be expected if the mouse virus infected humans and really was subjected to immune pressure. The Department of Health and Human Services United States organized a study of nine laboratory to determine if the blood supply was at risk of XMRV or related mouse retroviruses. This so-called Group which included blood work WPI and NCI researchers who co-authored the original Science study using all the tests they chose, reported online September 22 in Science that no one could reliably detect the virus into previously positive samples from patients.

Alberts said the finding of the Blood Working Group was the straw that led Science to request the complete withdrawal. "The blood of study for me was dramatic evidence of poor science," Alberts said. "He gave us absolutely no confidence in the ability of large laboratories involved for testing. I find this extremely disturbing. "Francis Ruscetti NCI, a major retrovirologist and one of the co-authors, tried to coordinate with colleagues retraction, but a dispute arose over language that suggests some of the conclusions in the original document is still valid. "We tried to get all the authors agree, but he got endless," said Alberts. "the responsibility Science magazine in the scientific community is to make a strong statement that we do not believe that anything in this document may be invoked. "

WPI, who conducted the study with Ruscetti, said she and two of his lab assistants that contribute refused to sign the retraction. the day after the publication of the study of blood working Group Mikovits presented new data at a meeting of the CFS in Ottawa, Canada, which sought to show evidence of human gamma retrovirus XMRV-the family belongs to patients. It essentially argued that the original document focused too narrowly on a variant of XMRV. (It also showed a slide in the meeting that led to Science discovered that the original document had mislabeled image, which account in the fully retracted.) "We were confident of our data," Mikovits said science Insider, explaining why they wanted to include a line in the retraction who said they still trusted their data and conclusions. Ruscetti declined to comment about the complete withdrawal.

Mikovits was fired by WPI week after the Ottawa meeting for insubordination and accused in a civil lawsuit by his former employer of embezzling laboratory notebooks and computer data on his studies. Police at the University of Nevada, Reno, then filed a warrant for his arrest in connection with the allegedly stolen material, and was briefly imprisoned. Both civil and criminal cases are being considered.

Mikovits and Ruscetti currently participating in a pathogen coordinated MultiLab study sleuth Ian Lipkin at Columbia University in New York City that will look XMRV and related viruses in many more CFS patients that were analyzed in the work group study blood. Mikovits said the study of $ 2.3 million, funded by the National Institute of Allergy and Infectious Diseases of the United States, has also taken into account in the decision not to sign the full withdrawal. "We believe it is premature to do something before it's over," said Mikovits, who believes they will have results within two months.

Alberts strongly disagree. "I think they should cancel this study, "said Alberts." It's over. They can not do the tests, so what's the point? Why should he give a different result from that of the blood group study? Maybe retracting help us to scale back how much money they spent on it. It seems like an incredible waste. "

Researchers who have closely followed this saga and invested their own efforts to find XMRV in CFS patients congratulate Science to issue a full retraction." It is very sad, but the writing is on the wall for some time and the font size got bigger during the year, "said Jonathan Stoye retrovirologist the Medical Research Council in London, who co-authored an editorial science supporting the original document. John Coffin, a retrovirologist at Tufts University in Boston, who wrote an editorial with Stoye, said the full withdrawal could have happened much earlier. "It is a bit of a surprise that it took so long," said Coffin.

Science Editor Monica Bradford said the review authors still prefer to sign retractions. "He is the work of the authors and is a very clear signal to the scientific community that can not be other charges of the agenda, "said Bradford. Alberts said they had simply been" spun "by authors too often for too long. "If our editorial retraction contributes to ending the resources to go to this useless effort, I think we have made a contribution to the scientific community," he said.

See also :. lawyer Judy Mikovits discusses developments in his criminal case

Update, 3:35 p.m. Paper co-author Robert Silverman of the Lerner College Cleveland Clinic Medicine of Case Western Reserve University has sent this statement to science Insider:

I asked for a complete withdrawal of our results this summer after finding that blood samples were contaminated. I was in favor of a withdrawal from the entire paper at the time. I am pleased that the Journal has granted a retraction of the whole paper, and I agree with that decision.

last week, the National Institutes of Health (NIH) announced that research funding success rate, a closely watched indicator of how whose investigators are doing in the fight for funds, fell to a low in 2011: 18%. At first glance, the decline appears to be due to increased competition, as evidenced by a sharp increase in applications last year. But many other factors are involved, including budgetary decisions made years ago, said the head of the extramural NIH Sally Rockey.

The success rate is the number of grants funded divided by the applications considered. 18% success rate, announced by Rockey on his blog, is down 3% compared to 2010 and is slightly higher than a preliminary estimate from last fall. It continues a rate of about 30% success ten years ago when the NIH budget has been growing. Part of the explanation is that the denominator is greater: the investigators sent a record number of grant proposals for research at NIH 49592 last year, an increase of 8%.

But not the whole story, Rockey said in a blog post today. Much of the increase is explained by a 17% increase in proposals for a specific category of R21-short-term financing grants. The mainstay of most laboratories are the largest R01, individual grant conducted at the NIH initiative, for which the success rate slipped from 22% in 2010 to 18% in 2011. Applications were up 3% R01. Another reason for the slip rate of success is that the NIH funded grants R01 copmpeting less than in 2010. This is partly because the size of the average grant increased slightly because the NIH had less to spend on global R01 (its budget was cut 1% last year).

But the most important factor, accounting for 1.5% of the decline in success rates is that most of R01 money than usual has been attached to previous grants. Because most NIH grants last 3-5 years every price creates several years of future unfunded liabilities. The amount of money needed for these ongoing grants increased from $ 189 million in 2011, reports Rockey. "This shows how careful we have to manage our funds since funding decisions in a given year have implications for years on," she wrote. She displayed a graph showing how the share of R01 NIH money committed to ongoing grants fluctuates from year to year. In 2011 it jumped to 78%, the highest level in 4 years.

A careful observer NIH, Howard Garrison of the Federation of American Societies for Experimental Biology, said the management of the off-year commitment is a delicate balancing act for the agency. If NIH gets a generous increase in a year and does not fund more grants, "People like me go mad because money does not go in the street," he said. Yet if Congress reduced the budget of the NIH few years later and NIH's commitment has increased, "You're toast," and success rates plunge

Rockey bottom line. "The success rate is complicated and it is not enough of a single factor "that animates it, she said Science Insider. She added that the success rate does not reflect "the amount of science" NIH is funding. The funded researchers basin has remained relatively stable in recent years, she said.

Although the NIH has received a modest increase of 0.8% in 2012, the agency seems to be girding for a period of austerity. Review reports today that the continuous subsidies will receive no inflationary increase in 2012 and new rewards will not receive inflationary increases in the coming years.

Yesterday, the Obama administration announced that it wants to strengthen national investment Institutes (NIH) of the health research on Alzheimer's disease with $ 80 million in new funding in the budget proposal of the President for 2013 which will be published next week. Although it is not so surprising-there are always new initiatives in the budget of NIH proposed even during the budgetary rigor-administration is also taking the unusual step of setting aside $ 50 million for the Alzheimer's studies in the budget this year. The decision, which was made at a higher level than the NIH, set off a scramble for where to find the money and how to spend it, according to officials of the NIH.

The administration reacts to the increasing number of Alzheimer's disease, which now affects as many as 5.1 million Americans and could hit 10 million by 2050, according to a press release yesterday by the Ministry of Health and social Services of the United States. "We can not wait to act," the Department of Health and Human Services (HHS) Secretary Kathleen Sebelius said. The new money above $ 458 million that NIH already planned to spend on the brain disorder this year - also meets a new law that requires the government to come up with the plan of the disease a national Alzheimer effectively prevent and treat the disease by 2025

Congress decides to approve. or not $ 80 million for next year, the officials say the NIH has not yet been allocated to specific areas within the appropriations process. (the administration also requested $ 26 million for non-program -Research as caregiver support and public awareness.)

regarding the $ 50 million budget this year, half will go to genomics studies, the Director Francis Collins NIH said yesterday. According to Richard Hodes, director of the National Institute on aging (NIA), so-called genome-wide association studies (GWAS) have found several new genetic risk factors slightly increase the risk of Alzheimer ' Alzheimer. But researchers hope to find rare variants and explore why, for example, some people who wear APOE4 gene known risk never develop the disease. The plan is to study of Exome and whole genome using DNA from the same groups of Alzheimer's patients and healthy people who were part of GWAS studies. These cohorts give the initiative "a great start from the head and is why something like this could actually be done this year," says Hodes.

But exactly where the $ 25 million for genomics come from "is actively being discussed," said Larry Thompson, spokesman for the National Institute for Human Genome Research (NHGRI). NIH has not had much time to plan, he said: '. OK, let "The Ministry [HHS] and White House said:" We would make an initiative on this, "and we said," One possibility is to add the project to the list of $ 104 million year NHGRI genome sequencing program, which supports the three major sequencing centers, and more things to do.

The other $ 25 million will be "broadly" Alzheimer funding proposals to grant NIA and other institutes which have received well in the peer review, but just missed the cutoff funding says Hodes. Some of the funding can also be assigned as supplements to existing prices. This plan is similar to how the NIH spent a lot of $ 10 billion in financing Resumption Act 2 years that the agency received in 09 and had a few months to allocate. Hodes said a group of NIH institute directors advise Collins on which specific proposals to fund.

The set-aside for Alzheimer's disease will mean less money and less funded research proposals, in fields other than Alzheimer's disease, Hodes said. He said that while $ 50 million over the $ 31.0 billion budget NIH "is not great" (it was 0.16%), at a time of historically low success rate subsidy, "he there will undoubtedly be people who will be affected. "

"This is something that should happen only in the most exceptional circumstances, and in this case, the Administration has determined that emergency Alzheimer's disease and demography be such a circumstance" , Hodes said. One reassuring point: because $ 50 million is for one year only, it should not change the basic funding level institutes, he said.

Hoping to dispel confusion about the increasing confusion of genetic testing, the National Institutes of Health (NIH ) today unveiled a new database that lists thousands of tests voluntarily submitted by companies and non-profit laboratories.

Genetic tests now exist for some 2,500 diseases, cystic fibrosis APOE, which increases the risk of Alzheimer's disease. NIH established the Genetic Testing Registry for physicians, patients and researchers after experts suggested that such a database could improve transparency on genetic testing. Led by National Center for Biotechnology Information (NIH NCBI) database can be searched by condition test, gene, and the laboratory and includes information such as whether the test sequence the entire gene for mutations and look for errors specific. Links lead to resources like GeneReviews NCBI, which are brief descriptions of specific hereditary diseases and how to test for them.

Most genetic tests should not be approved by the Food and Drug Administration as long as they are performed as a laboratory service and not marketed as a medical device. NIH does not verify the information in the registry, but the applicant must certify that the data is accurate. "It is a great resource for those who are struggling to make sense of the complex world of genetic testing," said the director Francis Collins NIH in a press release timed with the celebration of the NIH Rare Disease Day .

The tests listed so many cover essentially Mendelian diseases and genes that affect the way people metabolize drugs. Exome are missing and whole genome sequencing tests, mutations found in the tumors, and direct consumer testing, such as analysis of the entire genome of 23andMe for disease risk markers. These could come later, said NIH.

In a unanimous opinion today, the Supreme Court of the United States rejected the patents behind a diagnostic test sold by Prometheus Laboratories San Diego, California. The decision was a blow to the biotech company and a win for a test laboratory linked to the Mayo Clinic in Rochester, Minnesota, who refused to pay royalties to Prometheus.

Mayo had developed its own diagnostic blood test, and Mayo officials argued that even if it was similar to the company, it did not violate the principles of patent law and has been medically higher. Mayo has attracted the support of amicus curiae briefs from a number of medical and leading scientific societies, while Prometheus had the support of the Biotechnology Industry Organization and other industry leaders.

The opinion of the Supreme Court, written by Justice Stephen Breyer cited the basic principles to reject Prometheus patents. According to the court, Prometheus sought to claim the processes that are not very far from natural phenomena; previous court decisions clearly show that natural phenomena are "not eligible patent." Breyer explained that the court does not allow monopolies on the "scientific basis of work tools and technology" because it "might tend to impede innovation more than it would tend to promote it. " The court also noted that Prometheus allegations fell short because his invention-a thiopurine drug monitoring process in the blood a-involved "course, a routine conventional activity previously carried out by researchers in the field. "

Battle on the Prometheus drug test was closely monitored because it can foreshadow decisions on other cases of high profile biotechnology, in particular the fight whether human genes can be patented . The court has been sitting on a request to review the validity of patents on BRCA1 and BRCA2 breast cancer genes and ovarian held by Myriad Genetics of Salt Lake City, Utah. A federal district court in 2010 found these assertions invalid because they were an attempt to kind patent. This decision went to a court of appeal, which partly accepted and partly rejected the Myriad patents. Both parties appealed to the Supreme Court, which has yet to say whether it will hear arguments on the Myriad case.

Patents of invention and blogger Dennis Crouch, in comments published today in the Patently-O column, anticipates that the Supreme Court will refer the Myriad case to the lower court for reconsideration. He also speculates that the lower court "could logically find" that, in light of today's decision, the isolated DNA quoted in Myriad BRCA gene patents is "patentable".

Kill harmful bacteria in hospitals is difficult; on the ground, it can be an even bigger problem. Now researchers may have a means for remote disinfection in a "flashlight" laptop that shines a cold plasma beam to kill bacteria in minutes.

Medical scientists have high hopes for plasmas. Produced in electric shocks, have already been demonstrated that these gas of free electrons and ions to destroy pathogens, help heal wounds, and selectively kill cancer cells. Nobody knows exactly how this works, but it seems that plasmas generate reactive oxygen species called in air. These highly reactive molecules which are present in our own immune system, and oxidize cell membranes damaged DNA.

plasma devices are already in clinical trials to see if they are safe to use. But these prototypes are limited: either they need an external power source to generate many kilovolts required electrical discharge, or they need an external gas supply and regulation to maintain the plasma. Such drawbacks, it is difficult to use the devices in the field of emergency calls, the response to natural disasters or military operations.

A group led by Xinpei Lu engineer at the Huazhong University of Science and Technology in China believes it has a device with none of the drawbacks. Powered by a normal 12-volt battery and operating in the open without a gas supply, the prototype, which they call a plasma torch should be portable enough to last. "It generates the plasma is even unplugged from the wall, even using very low power," said group member Kostya Ostrikov from CSIRO science and engineering materials in Lindfield, Australia.

The battery The lamp pocket is much too small to create a plasma itself, so that researchers use a common electronic device known as a booster to intensify the DC voltage to 10 kV. an output of the amplifier is connected to the shell unit or "earth" in the technical-speak while the other goes to a network of 12 thin, stainless steel needles which create an electric discharge pulsing rapidly. the circuit includes several resistors "ballast" that limit the discharge current so that the flashlight is safe to touch.

to test the device, the Lu group grew thick films of Enterococcus faecalis , bacteria which are known to infect root canals in the mouth and are highly resistant to heat and antibiotics. The researchers used some of biofilms supposedly that of the control samples and subjected others to the plasma torch for 5 minutes at a distance of 5 mm. Thereafter, they scored all samples with two fluorescent solutions: green indicates that the living cells, and red indicates that the dead cells.

The team found that the control samples remained green, while the treated samples had turned almost entirely red-even at the bottom of biofilms, which were about 17 deep cells. The results, which are published online today in the Journal of Physics D: Applied Physics , were still better than a nonportable plasma device that Lu had previously tested group.

Making truly portable device is a great advance, said Michael Keidar, a plasma physicist at George Washington University in Washington, DC "cold plasma operation in air is difficult, [and] it seems that they were able to operate, "he said. "This is a purely technical issue that has been resolved."

Miran Mozetic Engineer of the Jožef Stefan Institute in Ljubljana, Slovenia, highlights another advantage of the plasma torch: It uses only a meager 60 milliwatts per discharge. "This is an important fact because it indicates the battery [will] not to be exchanged or refilled frequently," he said.

Like any other medical device, the plasma torch will go through rigorous clinical tests. But Ostrikov said that in addition to smaller and optimizing its efficiency, the plasma flashlight is "almost" a device already shopping.

CORRECTION: This story has been given primary affiliation Kostya Ostrikov as the University of Sydney, while in fact CSIRO Materials Science and Engineering. The article has been corrected.

good news for people who hate large needles: Researchers have invented a device that could allow diagnostics to perform with a single drop of blood. The device is a container to a few millimeters wide, which consists of a conductive core covered with an elastic layer of polydimethylsiloxane or PDMS, a silicone compound. When the liquid is drained out of the PDMS layer wraps around the droplets that result due to its surface tension the same force as the water curl up on the sides of a glass. In this configuration, the droplet can not escape. To release, the researchers simply inserting a thin electrode: Together with the conductive base, the electrode creates an electric field which causes the layer of PDMS to unpack (as above shown). The researchers believe that their container, which is described in a paper published online today in the Proceedings of the Royal Society A could allow blood tests to be performed with a single drop of blood because it would be transported droplets evaporate or become contaminated. This would reduce patient discomfort, and perhaps save time. In addition, the researchers believe that their container can provide tiny amounts of drugs to diseased cells, which avoids having to administer potentially harmful drugs for the entire body.

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castor oil can have a bad reputation among the people who were force-fed spoonfuls like children, but it is not a myth that tonic has health effects. Today, scientists have elucidated the molecular mechanism of the active ingredient in castor oil, which has been used for thousands of years as a laxative and labor spillway. ricinoleic acid, which fatty acid is about 0% oil, binds to a particular receptor in the gut and uterus, the researchers found. The discovery explains how castor oil and could lead to development of drugs less unpleasant.

While taking a daily spoonful of castor oil diluted as general assistance for health is more fashionable, alternative health stores still sell the liquid foul-tasting as a laxative. The Food and Drug Administration has classified castor oil as "generally recognized as safe and effective," but researchers do not understand its mechanism.

"When you study classic, old drugs, is almost always learn something from them," said first author of the new study Stefan Offermanns, a biologist at the Max Planck Institute for Heart and Lung Research Germany. "The biggest surprise here was how specifically castor oil worked."

Offermanns and his colleagues were screening different fatty acids for their ability to bind to certain cell receptors when they have achieved success with ricinoleic acid. Knowing extensive use of castor oil in traditional and alternative medicine, the team decided to take a closer look at the compound. The use of a large library of molecules that block the cell receptors they studied, they were able to home in two as ricinoleic acid connects to: EP ₃ and EP ₄ . Both are prostaglandin receptors, which have different roles in the body, to change the structure of neurons to control how the blood clots. In experiments on mice, the researchers showed that ricinoleic acid induces its laxative effects and inducing labor by interacting with EP ₃ . When someone swallows castor oil, ricinoleic acid on locks EP ₃ molecules in the smooth muscle cells in the walls of the small intestine and causes contractions, which explains the efficiency of castor oil as a laxative. Similarly, researchers have shown that ricinoleic acid binds to EP ₃ and in the uterus causes contractions. The team published its results today in Proceedings of the National Academy of Sciences .

"There were many theories as to how castor oil worked, including broad toxicity to intestine cells and the effects on water and electrolytes," says Offermanns. But ricinoleic acid is much more accurate than those theories suggest, acting through a single receiver. How the receiver causes contractions, however, is still not known. But the new link between EP ₃ and bowel and muscle cells of the uterus could inspire the work to find out.

"They made these experiences quite elegant and complete," says biologist Phillip Bennett from Imperial College London. "And at one level, this finding is somehow a little quaint curiosity but there is more than that. "

the knowledge that ricinoleic acid binds to EP ₃ could be used to design drugs that target the receptor, said Bennett. These drugs could be used as laxatives or working without inducing side effects such as nausea, castor oil.

a daily dose of castor oil will not keep the doctor and modern medicine n ' has not yet backed claims that he also treats skin conditions, relieves pain and heals infections. So take castor oil with a grain of salt, or a spoonful of sugar.

The researchers understand why a popular therapy for the treatment of colon cancer often eventually stops working: The tumors naturally carry genetic changes that allow certain their cells to evade the drugs and continue to grow. The good news is that doctors may be able to detect these changes in patients' blood, then stop the cancer with another drug before it can grow again to a dangerous size.

Many people with advanced colon cancer are treated with proteins called antibodies that target a weakness of the tumor, a protein that stimulates the growth of cancer cells called EGFR. Antibodies often shrink tumors, but cancer usually comes back within 18 months. To investigate how this developed resistance, a team led by geneticist Alberto Bardelli from the Institute for cancer research and cancer treatment in Candiolo, Italy, increased colon cancer cells in boxes containing a growth medium laced with cetuximab anti-EGFR antibody called. The group now reports in Nature as the cells have become resistant to the drug because of changes in KRAS , a gene encoding a protein that may reactivate the growth path of EGFR when EGFR is itself blocked. The resistant antibody producing cells had mutations in KRAS and sometimes contain additional copies of the gene. The researchers also found these changes in biopsies of six patients with tumors that were resistant to cetuximab or a similar drug called panitumumab.

The blood of a cancer patient typically contains traces of DNA of the tumor. The Italian team and a separate group led by Luis Diaz oncologist at Johns Hopkins University in Baltimore, Maryland, have now found independently that KRAS mutations are detectable in blood samples from patients whose tumors have become resistant to drugs, Bardelli technology called a "liquid biopsy." the warning signs in KRAS appeared up to 10 months before the tumors become large enough to detect various standard imaging techniques such as X-rays. This suggests that clinicians could monitor patients' blood for resistance mutations and when they appear, give patients a second drug that also blocks the path of growth of EGFR, but in a way that KRAS mutation can not replace. the combination of such a drug called a MEK inhibitor with cetuximab killed colon cancer cells in a laboratory dish that were resistant to cetuximab alone group Bardelli reports.

"The concept of liquid biopsy, both groups used, is really a step forward, and I am sure it will be widely used in the clinic," said Bardelli, named online work today in Nature and the study of the Hopkins group.

another question was how resistance mutations got there. they were present in a few cells before the patient was treated with the drug, or did they occur after treatment? to find out, the team and his Hopkins colleagues at Harvard University have developed a mathematical model of the genetic evolution of the tumor that match their data KRAS mutations in the blood. They concluded that resistance mutations resulting from spontaneous changes in DNA that cells divide are present in some tumor cells even before the treatment. The model shows that the resistance is a "done deal", Diaz and his colleagues write. It is also probably inevitable for other so-called targeted therapies, such as those for melanoma and lung cancer, which also generally work for less than a year, Diaz said.

"The lessons here that resistance mutations occur spontaneously" into a tumor, even before therapy is tried, said Diaz. In rare cases, a patient-targeted therapy lived for years without develop resistance. But these tumors may be very young when the patient is first treated, or abnormally slow growth, Diaz said.

"these results are illuminating and sobering" because they show that resistance drug against the target colon cancer is inevitable, says oncologist Neal Meropol of Case Western Reserve University in Cleveland, Ohio. The treatments will target more than one molecular pathway, he said.

But Dominik Wodarz evolutionary biologist at the University of California, Irvine, also found the Hopkins study "encouraging" because the model seems to describe drug resistance in cancer and diseases such as HIV who are "very different from each other biologically." Although cancer is complex, given that its dynamics are "relatively simple" craft will help researchers better treatments, he said.

A man working for the World health Organization (WHO) on the campaign to eradicate polio was shot dead in Karachi, Pakistan, on the evening of 20 July. Muhammad Ishaq was shot outside his clinic in a slum in Karachi rough known as Gadap. Ishaq, who was the local community, died en route to hospital.

only 3 days earlier, two gunmen killed a Ghanaian doctor working for WHO and his Pakistani driver, participating in a national campaign of vaccination against polio in their car. The doctor was shot in the stomach; the pilot suffered a grazing wound on his shoulder. The two men are recovering.

After the first shot, the WHO has canceled the rest of the vaccination campaign in Gadap and implemented increased security measures instead.

Nobody has claimed responsibility for the shooting and there is no definitive evidence linking the two events, said Bruce Aylward, WHO Deputy Director General and longtime leader of global Initiative to eradicate polio. Similarly, it is unclear whether the shooting was random or polio workers targeted specifically. Until they get more evidence, said Aylward, "Our working hypothesis is that [the shootings] may be linked, and that affects our approach to security."

is Gadap slum densely populated with a large minority and migrant population. most residents of the tribal areas along the border with Afghanistan, where opposition to a government-run or a Western program is intense rumors abound that the vaccine against polio is dangerous and is part of a US campaign to sterilize Muslim children. About a month earlier, a leader of a faction of the Taliban in North Waziristan banned vaccination against polio in its part of the tribal area to stop the US drone strikes.

Expressing deep sadness, the WHO issued a statement saying that the shooting will not distract from the state progress of Pakistan made in its fight to eradicate polio. Pakistan and Afghanistan and Nigeria, is one of three so-called endemic countries where polio transmission has never been interrupted.

The failure of treatment of pancreatic cancer, announced Wednesday by its manufacturer Amgen, is yet another sign that a class once promising treatments against cancer failed to meet expectations. The latest flop treatment called ganitumab, is a monoclonal antibody that targets the factor 1 receptor-like growth to insulin (IGF-1R), type. At Amgen, the drug all the way to a clinical Phase III trial before the company pulled the halfway taken through the trial after finding that the therapy was unlikely to help patients live longer .

IGF-1R has been considered a promising target after researchers have made a number of interesting observations. are linked to a slightly increased risk of cancer circulating levels of IGF-1 hormone in the blood of a person. The receiver is often expressed on epithelial cells, the type of cells that become cancerous, and it promotes cell survival. Finally, in cell cultures and animals overexpressing the hormone might produce something that looks like a cancer, and it would shrink when treated with an inhibitor of IGF-1R.

But in patients, drugs are "a series of failure," says Vuk Stambolic, a cancer researcher at Princess Margaret Hospital and Ontario Cancer Institute in Toronto, Canada. Other trials of this drug target in lung cancer did not work, and the effects of these drugs in colorectal cancer are also doubtful, said Stambolic.

the Achilles heel for many potential cancer drugs is biology. in short, it usually turns out to be more complicated than first thought. it may not be enough to go after only IGF-1R, and patients in these trials have very advanced disease and may be less likely to meet very targeted treatments. the work of animals and cells as real life can not fully emulate. "I think the model is probably only partially representative of what happens in cancer," said Stambolic.

Various companies are also testing a class of drugs that target both IGF-1R and the insulin receptor. The hope is that the double whammy will be more damaging to the tumor.

National Institutes of Health's new Translational Research Center (NIH) has its first head: Christopher Austin, a neurologist and former Merck researcher led drug discovery efforts at NIH for the last 10 years. The NIH Director Francis Collins announced the appointment this morning at the inaugural meeting of the Advisory Board of the 9-month-old National Centre for Advancing Translational Sciences (NCATS).

Congress signed the $ 575 million NCATS last December after months of controversy about whether the NIH tried to become a pharmaceutical company. NIH insists that NCATS will be limited to treating the bottlenecks in the drug development process.

Collins said that after "vigorous international research," NIH chose Austin, 51, who now heads the division NCATS 'preclinical innovation. "Chris has had a remarkable career with a great diversity experiences that put it in a wonderful position to lead this company, "said Collins.

A development neurogeneticist Harvard-trained Austin worked on the discovery of genome-based drugs from Merck for 7 years. In 02 he left to become advisor for translational research at the National Institute for Research on the human genome, where Collins was director. Austin helped launch the Molecular Libraries Program of the NIH, a set of testing centers of small molecules style industry in academic institutions. Until recently, he directed the intramural NIH screening center and other programs, such as the development of drugs for rare diseases. When NCATS was created, they were bent in its preclinical division.

Austin, which begins September 23 (his birthday), described the NCATS appointment today's meeting as the "culmination" of his long career efforts to bridge basic research and clinical. "This is a very difficult mission, ambitious but deeply important that we are all about," he said.

Some observers suggest that the NIH has struggled to recruit a director of NCATS outside because a scientist from the industry who moved to NIH would probably take a steep pay cut and dispose of any company stock medicines he or she belongs. Other deterrents could have been dark NIH budget outlook and the next presidential election, which could cause a change in direction of the NIH.

Steven Paul, a former head of Eli Lilly now looking at Weill Cornell Medical College in New York, who served on the search committee, declined to say if the government rules hindered research. What matters, Paul says, is that "We came with a wonderful person ... Chris is credible with both university researchers and the private sector.".

At the meeting today, leaders of the NIH and its advisers-a mixture of patients, industry experts and university-started this sort NCATS will do. (The meeting also included the board overlapping the Cures network acceleration, CAN, NCATS a component that will give grants for drug development.) US Food and Drug Administration (FDA) Commissioner Margaret Hamburg said NCATS she hopes will not only come up with specific tools to improve regulatory science, such as new trial designs but also get both basic science and clinical thinking about the steps needed to transform a potential drug a product. "We need to think about how we do research a little differently," she said.

Thomas Insel, director of NCATS acting, warned that the center, which consists mostly of existing programs at NIH, will not be much new money to work with. "We really need to be very focused," he said.

But CAN board member Tachi Yamada, Medical and Scientific Director at Takeda Pharmaceutical Co. said NCATS does not necessarily need a big budget to make an impact. "Many solutions can be very cheap if thought strategically," he said. Yamada, who also worked for the Bill & Melinda Gates Foundation, gave the example of an ongoing collaboration, he was involved in to work with the FDA to obtain approval of a cocktail of three drugs for tuberculosis, without passing through "50 years of clinical trials." NCATS, he said, will benefit from "a very serious strategic analysis when true roadblocks may be in selective areas. "

Tuberculosis (TB) continues to cause a "huge" burden of disease, according to an update released today by the World health Organization (wHO) estimates that there were 8.7 million new cases in 2011 and 1.4 million deaths. But there are high hopes that improved diagnosis and medications will, in the coming years to make a significant dent in the search for people who have the disease, the provision of appropriate treatment for their lives, and slow spread Mycobacterium tuberculosis itself.

The WHO figures Global Tuberculosis Report 2012 are similar to those published the previous year. "TB control and care is at a crossroads," said Mario Raviglione, who heads the STOP TB program of WHO, during a press conference in Washington, DC "Firstly we have existing as well as new tools on the horizon which could make a significant difference and even support dreams of elimination in some settings. But then, we are at risk of stagnation if additional resources are not mobilized urgently by governments of endemic countries first and if the international community is not ready to fill the gaps. "

the new report of 272 pages underlines that much progress has done against tuberculosis between 1995 and 2011, during which 51 million people have received a full course of treatment, which lasts a minimum of 6 month and lives 20 million were saved. But multidrug-resistant (MDR-TB) remains a huge problem, with 630,000 cases worldwide; only one in five of these people receives a proper diagnosis necessary for effective treatment.

The estimated new cases fell by 100,000, which, even taking into account the population growth is a modest decline of 2.2% between 2010 and 2011. The proportion of people with TB are co-infected with HIV remains broadly unchanged at 13%, but it is more than 50% in several countries in sub-Saharan Africa. What is clearly new to the report this year, Raviglione said, is the first estimate ever made of the burden of TB in children: half a million TB developed in 2011 and 64,000 died of the disease.

The report highlights some improvements. Many countries have begun using a new diagnosis, a machine called GeneXpert, which has a much higher accuracy than the centennial microscopy test, which is widely used and requires a lot less work. The GeneXpert test two hours can also determine if a person has MDR TB; before, it took several weeks for the culture Mr. TB , and then test the bacilli drug sensitivity. But the Xpert test is considerably more expensive: In South Africa in 2011, the government paid at least $ 15 for each test of the machine, compared to $ 3 for a microscopic test of sputum.

As noted in the report, the company that makes GeneXpert, Cepheid of Sunnyvale, California, in August agreed to sell the cartridge from the machine uses, making the chain reaction of the polymerase on sputum samples -to a discount of 41% to hit hard and countries with limited resources. June 2012, 67 countries had purchased the reduced system.

The report also highlights that for the first time in decades, two new TB drugs are about to hit the market. The drugs, which should receive regulatory approval in the coming months, will be first used to treat MDR and promise to have less toxicity and work faster than treatments currently in use. A short-term plan to cure the regular TB and a vaccine that can reliably prevent most cases of the disease are still far - although attempts to make these dreams become reality longheld intensified.

A particularly disappointing part of the report focuses on the funding of prevention, care and control, which is expected to total $ 4.8 billion in 2013 for 104 countries with 94% of cases. But these low- and middle-income and need as much as $ 3 billion more each year to effectively meet their TB epidemics. "We are facing actually the main financial risks in a scenario where efficient technologies are now available," Raviglione said. Although he acknowledged that large increases in funding from governments and multinational organizations such as the Global Fund against AIDS, Tuberculosis and Malaria, the financial deficit "means millions of unnecessary gaps in the coming years. "" history teaches us that in the fight against tuberculosis, collect achievements we have had so far as "done" is an absolutely fatal error. "

future boom in space tourism will increasingly expose members of the public or at least those lucky few able to pay the ticket price a range of ills that so far, most of the time, only the astronauts healthy superbly met. In a new analysis, the researchers surveyed previous studies of space medicine and compiled the list to alert physicians to the myriad ways that spaceflight could worsen pre-existing conditions in their patients, whether during short suborbital flights from commercial space operators (launch of Sierra Nevada Corp. 's Dream Chaser represented by an artist) to a getaway week of the international space station, or relay monthlong construction or working in hotels or orbiting laboratory commercial research. Almost no body function is spared, but most ailments could be managed with medication or with the quantities and types of exercise in proper orbit, the researchers suggest. in addition to motion sickness, headaches and sinus congestion possibly triggered by short flights, long flights could aggravate osteoporosis, back pain, acid reflux, and certain types of cancer, as well as increase the risk of infections and calculations kidney, the researchers report online today in BMJ . The new compilation is not just an abstract exercise, the researchers say: Previous studies suggest that, once the fleets of vehicles capable of space available, commercial launch companies together could expect up to 13 000 tourists space during their first decade of operation.

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nearly a year after they announced it, leading researchers flu ending a voluntary moratorium on certain types of controversial experiments involving the H5N1 avian influenza.

In a letter published online today Science and Nature , 40 researchers say the studies should restart now that scientists, government officials and public have had time to discuss the need for research and to impose new security measures. "[T] it is the voluntary moratorium have been achieved in some countries and are close to being met in others," they write, and researchers "have a public health responsibility to take this important work."

The movement essentially ended the H5N1 controversy, which began in late 2011, when two research teams showed how to redesign the virus that normally infects birds, so that it can move between the mammals. The discoveries have triggered intense global debate about whether newspapers should publish the results, some critics fear could be used by terrorists to trigger a deadly human pandemic. It also led to a discussion of whether scientists should make such studies "gain of function" at all. The results were finally published in Science and Nature , but the controversy has prompted governments in the US and elsewhere to impose increased surveillance on H5N1 research.

Today's letter comes as little surprise to those who have followed the controversy. The moratorium, which was announced January 20, 2012 in a letter signed by 39 prominent researchers H5N1, was originally intended to last only 60 days. But researchers extended it indefinitely in March 2012, when the debate intensified. Last year, however, many of those who agreed to the break began to lobby for lifting the moratorium that the United States and other nations finalized new systems of review proposals H5N1 gain function research and implemented safety guidelines for laboratories working with particularly dangerous forms of the virus. Last month, after an international meeting of two days on the issue organized by the US National Institutes of Health, which funded the two controversial studies, leading researchers and government officials said they were waiting for the moratorium to end soon .

The H5N1 research should resume in two stages, the researchers write in today's letter. scientists Influenza working in countries that have completed the safety rules and laboratory funding should now be free to resume experiments involving the re-engineering of the virus, they wrote. But "[s] Scientists are not expected to return to work in countries where, yet, no decision has been reached on the terms of the search for the transmission of H5N1. At that time, including research to United States and the United States financed conducted in other countries. "funded US researchers might not have to wait much longer to lift the moratorium, however, because officials are in the final stages of approval laboratory safety and consideration of the proposal guidelines.The Japanese government has also not yet finalized its rules for the H5N1 research, researchers say.

"There probably is not a scientific question in these time that was not so widely thrown to the public consultation that one, "one of the signatories of the letter, virologist Wendy Barclay of Imperial College London, said in a statement released by the science Media Centre in London. The moratorium was necessary, she said, because of a "reflex response from some quarters ... express the horror that scientists were preparing fatal diseases. It became clear that the public needed comfort and justification for these experiments. "

Now she and others from influenza want to return to try to understand how the H5N1 virus could become more dangerous to humans and how health officials would be able to stop a pandemic emerging. "[B] s the risk that exists in nature H5N1 virus capable of transmission in mammals may emerge," the researchers say, "the benefits of the job outweigh the risks."

in a conference call today, the main author of the letter said he does not expect researchers to be able to start the study immediately. "it takes time to stop the search, and it takes time to begin to save it, "said virologist Ron Fouchier of Erasmus MRC in Rotterdam, the Netherlands, who led a controversial studies. But Fouchier already has an idea of ​​what kind of studies he would like to do. Emphasis will determine exactly which mutations allow the H5N1 virus to move between mammals in the air or respiratory droplets. Researchers have found so far "five to nine" mutations that enable the transmission in mammals, he noted. Fouchier is also interested in whether the same mutations may make other H5N1 strains "in the air."

* Correction, 17 hours: The moratorium on H5N1 research was extended indefinitely in March 2012, not March 2011.

The World Health Organization (WHO) today released a report saying that the Fukushima nuclear disaster will cause no increase observable in cancer rates among residents of other countries and very small increased risk of cancer among residents near the plant. Workers struggled problems at the plant do not face higher risks of certain cancers.

The environmental group Greenpeace immediately condemned the report as "a political declaration to protect the nuclear industry." But at least one radiation health expert believes the report overestimate some risks.

wHO assessment of potential health effects is based on a report of May 2012, which estimated that the radiation exposure in different places around the Fukushima Daiichi nuclear plant, which released large quantities of radioactive material after having suffered several explosions and collapses in the earthquake and tsunami of 11 March 2011.

the team of 13 experts from the WHO estimated the increased risk of life of leukemia, cancer thyroid, and breast cancer in women for people living in geographical locations ranging from the most affected areas adjacent to the power plant to distant parts of the world. Beyond the areas near the plant, radiation doses were below levels known to have effects on health, the report says. "Apart from geographical areas most affected by radiation, even in areas of Fukushima Prefecture, the anticipated risks remain low and no observable increase in cancer above the natural variation of the reference rates are to be expected" reads the summary. the report notes that in the two most affected areas of Fukushima, estimated doses in the first year ranged from 12 to 25 millisieverts (mSv).

"in leukemia [sic], the lifetime risks are expected to increase by around 7% compared to the basic rate of cancer in exposed male infants, for breast cancer, the risk to estimated life increases up to about 6 % compared to the reference rate in females exposed infants, "the report concluded." [F] or all solid cancers, the risks to the estimated life increases up to about 4% from the rate reference in females exposed as infants, and for thyroid cancer, said the risk increases for life by up to 70% on the basic rate line in women exposed in infancy. "

The report explains that these are relative increases compared to the reference rate and not absolute risks. Thus, because the risk of thyroid cancer the basic life among women is just 0.75%, the additional risk due to exposure to the most affected area is 0.5%. The risks in the second most affected location are half of those in the most affected region.

Kazuo Sakai, a radiation biologist at the National Institute of Radiological Sciences in Japan, believes that the risks "are overstated." He explained that the estimates of doses used were based on preliminary data; Actual measurements showed real dose levels to be lower. He also said that the risk is based on a calculation that takes 4 months of exposure to radiation in different areas. But because of the timely evacuation, there is probably no infant females, for example, who actually received the doses estimated for the most affected area, he said.

Greenpeace, however, believes the doses are widely underestimated. "The WHO report minimizes shameless the impact of radioactive discharges beginning of the Fukushima disaster on people inside the evacuation zone of 20 km that are not able to leave quickly, "a statement quoted Rianne Teule, Greenpeace International nuclear radiation expert, as saying. The statement says the modeling by the German nuclear expert Oda Becker concluded that the people inside the 20-kilometer evacuation zone were possibly exposed to hundreds of mSv.

The WHO report said that the emergency of the central workers face a higher lifetime risks for leukemia, cancer of the thyroid, and all solid cancers.

For cancer patients, things go from bad to worse when tumor cells escape into the blood stream. Cells sometimes marauding just one among a billion blood cells can lodge anywhere in the body, the spread of cancer in a process called metastasis. Now researchers have developed a device that can detect even a single cell of any type of cancer in the blood, allowing early treatment of metastasis and new knowledge of cancer genetics.

The cancer cells that migrate into the bloodstream are called circulating tumor cells (CTC). In 07, a team led by Mehmet Toner biomedical engineer at Massachusetts General Hospital in Boston has developed a method to trap and detect CTCs on a silicon chip the size of a microscope slide etched with microchannels each no wider that 'a strand of hair. Toner pumped from whole blood samples through the channels, which have been coated with an antibody designed to trap any cancerous cell that carries a common surface protein, as far as flypaper snags annoying insects. But cancer cells without the protein, such as melanoma (a type of skin cancer), slipped unnoticed.

The new system gets around this limitation. CTC-called iChip system (the "i" is for "inertial focusing"), it targets the blood cells instead of cancer cells. Sorting by size of the cell, the first chip creams out of small cells and red blood platelets, leaving only CTCs and white blood cells flow past. Then, a second chip winds cells through curving channels, channeling the remaining cells in a single file line. Magnetic beads of the size of bacteria attach to specific surface proteins on white blood cells, and a magnetic field nudges these cells out of the flow of CTC. That leaves just the CTCs, which can be collected in a vial and analyzed individually by conventional laboratory methods.

The clinical application of this technology is clear, said lead author Emre Ozkumur, a biomedical engineer also at Massachusetts General Hospital who developed the system with toner. Early detection of CTC allows doctors to begin anti-metastatic therapies, he said, which could slow or stop final fatal attack cancer.

all CTCs not develop into metastatic tumors, however, and cancer researchers are still discovering why. Because the CTC show such large amounts of genetic variation, bulk analysis of cells will not reveal the reason, said Ozkumur. "You have to analyze one by one."

The team reports its findings online today in Science Translational Medicine is already pondering its next improvements to reduce manufacturing costs down and prepare CTC-iChip for clinical use. The researchers' task list includes the integration of the system with two current chips into one, said Ozkumur.

The group's work is "a solid lead," said the engineer Robert Langer of the Massachusetts Institute of Technology in Cambridge. Langer, who owns more than 800 biomedical patents, welcomes the improvements in this device relative previous models. other diseases, like rare LAM lung disease, also involve circulating abnormal cells, says Langer. This technology can advance research in these diseases.

The 1918 Spanish flu killed up to 40 million people. The swine flu pandemic in 09 killed about 284,000. Now scientists have discovered a substance that could help doctors save lives during future influenza pandemics. Eritoran, a compound being studied as a drug for sepsis, significantly reduces deaths due to influenza in mice. "This could open up a whole new class of anti-influenza drugs," said Michael Osterholm, a flu expert at the Research Center and policies relating to infectious diseases at the University of Minnesota, Twin Cities, which has not participated.

at present, doctors have a single class of compounds available to fight against influenza. the drugs, Tamiflu and Relenza, block neuraminidase, a surface protein that the virus influenza should leave the cell after reproduction. the drugs, taken orally, are to be given soon after infection to be effective, however, and some flu strains have developed resistance against them. some scientists have also questioned the safety and efficacy of compounds, many countries stocks during the H1N1 pandemic of 09. "Basically, if you see the arsenal available today, it is limited and could be blown over night, "said Albert Osterhaus, a virologist at Erasmus MC in Rotterdam, the Netherlands.

Instead of targeting the virus, Stefanie Vogel immunologist at the University of Maryland, Baltimore, tried to interfere with the host immune system. Scientists have long speculated that some cases of severe flu are not the direct result of the virus havoc, but due to a so-called cytokine storm, a catastrophic overactivation of the immune system that leads to many inflammatory substances being released into the whole body, which can lead to multiple organ failure. For example, immune cells and the liquid can accumulate in the lungs, airway blockage. A 08 study cell suggested that the cascade is triggered by the activation of a molecule called Toll-like receptor 4 (TLR4), which normally signals the immune system to the presence of certain bacteria in the body . If these pathogens overwhelm the body, TLR4 is also thought to trigger inflammation of the entire body known as sepsis. For this reason, blocking TLR4 was viewed as a potential treatment for patients suffering from sepsis.

Vogel and colleagues studied eritoran, a compound that blocks TLR4 and is now in clinical trials as sepsis drug. They infected mice with influenza laboratory strain called PR8 and gave half of them eritoran injections for 5 days, starting 2 days after infection. Ninety percent of the untreated mice died, against only 10% of those given the drug. If the treatment was started at 6 days after infection, 33% of the animals survived. The compound also reduced lung damage in cotton rats, a species that does not die from the influenza strain used for the study, the authors report online today in Nature .

"It is an elegant study based on assumption rather bold," says Osterhaus. But the mechanism of the disease in mice could be different from that of man, he said. "This does not disqualify the results, but that means we must be careful." Vogel said she has already submitted a grant to test the compound in ferrets, the most widely used animal influenza studies. "Since eritoran has a very good safety record in people, we hope that our preclinical studies will ultimately support clinical trials in humans for flu and perhaps other diseases that cause disease by a similar mechanism, "she wrote in an e-mail to science NOW.

For Osterholm, the paper adds to the evidence that influenza causes illness by several different mechanisms. Some strains of influenza, such as the one that caused the Spanish flu in 1918, or swine flu in 09, are more likely to cause death by activating the immune system, leading to more deaths in younger age groups he argued. "This is the case it will be demand." Osterholm but also warns that many promising drug candidates fail at later stages. "We will not know if it works until we put in people."

One day after a prominent paper in the journal Cell was reported for image duplication, the lead author and the newspaper say that problems arose from the simple mislabeling images and do not invalidate the results. They also defended the exceptionally fast examination paper, which was accepted only 4 days after the official presentation and published online 12 days later.

The work, led by Shoukhrat Mitalipov Research Center of the Oregon National Primate in Beaverton, was marked by two reasons: It is the first time anyone has used cloning to create embryonic stem human personalized (ES) cells, and it is the same result that was described in 04 and 05 by a group of south Korean scientists in what is proving to be one of the most famous cases in the world of scientific fraud .

scientists stem cells were first delighted, with a developer Science that the work was a "hard-won victory after years of painstaking research." After a commentator posted on a site called PubPeer alleging duplicate images and mislabeled in the paper, joy turned to dismay. "It is unfortunate that this important area of ​​research has come once again under control," wrote Kevin Eggan of Harvard University Science Insider in an email.

talked Mitalipov with Science Insider this afternoon and said he and the other co-authors simply neglected mistakes, partly because the images in question are intended to show that the cells are similar. "with the naked eye, it is very difficult to see if the same image or a different image." He said he is curious to know if the contributor PubPeer used the image control software to catch duplication. "I wish we had this software to run the paper through," he said.

The first series of duplications has three digits. The images are intended to show that ES cells from ' cloned embryos resemble those from IVF embryos, suggesting cloned ES cells are the real thing, but the same image seems to appear twice under a different label. once as an ES cell line derived from a cloned embryo, and elsewhere in the paper as a line of control ES cells from an embryo in vitro fertilization. another image in the same set, Figure 6, appears as a cloned cell line but also shows in an additional figure called the command line. Mitalipov, who spoke with Science Insider this afternoon, said the first author Masahito Tachibana deliberately used the images twice, but accidentally knocked the labels in Figure 6.

the second duplication appears in the supplementary Figure S6, where a cloud purporting to show similarities gene expression between cell lines was used twice. Mitalipov said the bad scatterplot was used, and the good will be published in an erratum. original microarray data are publicly available, he notes.

Mitalipov argued that the main evidence that the cell lines are derived from embryos cloned really are not affected by these errors. The most important is whether the mitochondrial DNA of ES cells matches that of the egg cell donor and the nuclear DNA is the cell that has been cloned. The researchers deliberately chose a cell line widely available for their experiments, Mitalipov said, making it easy for laboratories outside to try to confirm the results. He says he is ready to ship the ES cell lines cloned in several laboratories that have requested them, as soon as the signs of Oregon's institutional review board off of transfers, which could occur in a case days. (Restrictions prohibit federal funding of the National Institutes of Health funded laboratories working on cells because they were obtained through cloning, so that recipients must also show that they have a legal place to work with cell lines .)

cell , meanwhile, sought to defend. Newspaper editors have refused to speak with Science , but the spokesperson Mary Beth O'Leary issued a statement, noting that "it seems there were a few errors made by the authors . ... We do not believe the impact of these scientific results mistakes of the paper in any way. "

Several experts say stem cells Science Insider that the images in question are no keys to the conclusions of the paper. However, Eggan writes, "we will probably have to wait until the cell lines in question are validated by others, or reproduces the independent group [cloned ES cell] before we find know for sure. " Dieter Egli of the New York Stem Cell Foundation in New York said Science Insider that he and his colleagues are already working to reproduce the allegations Mitalipov.

Cell was not able to answer a key question before our deadline: What was the rush in securing the paper? He had an exceptionally fast turnaround, filed April 30 and accepted on May 3 "Reviewers have graciously agreed to give priority attention to examine the document in a timely manner" Cell of statement read. "It is a false statement to assimilate review by the slow peers with rigor or discipline, or use review by the timely peers to justify negligence in preparing the manuscript."

In a story by Nature Mitalipov seemed to imply that he pressed for a quick review because he wanted to present the work at a conference. But this meeting is not until mid-June, and cellular authors has already led to high-profile documents to be published in the newspaper after describing their research at a meeting.

Mitalipov said ScienceInsider that even if he mentioned the conference when he presented the document, it was not the reason for quick review or competition from another group. he says he first sent the paper to the newspaper "5 or 6 days' before April 30, the official date of submission as part of an investigation prior to approval. After Cell publishers have expressed interest, he said, he officially introduced through the website on 30 April. He said the review simply asked reviewers to look at the paper quickly, "and they did it in a day." The examiners had minor criticisms, he said, the authors were able to respond quickly. cell may have been worried about the news of the flight of paper, he says, which may have prompted the online publication shortly after acceptance. the document should be published in the June 6 printed edition of the journal.

Tachibana is "devastated" by the errors, said Mitalipov. However, the lead researcher is confident that the results will soon be confirmed. "We have the cell lines. We can show that the mitochondrial data [DNA] is, and that nuclear data, "said Mitalipov. He and his co-authors are now combing through "every point" in the paper to make sure it is no more unknown errors before submitting a formal correction.

A Japanese Ministry of Health, the panel Labour and Social Affairs has agreed a plan to carry out what would be the early clinical trials of the world involving induced pluripotent stem (iPS) cells. Acceptance opens the way for an official green light from the Ministry, which could come in early July.

The researchers from RIKEN Center Developmental Biology in Kobe plan to generate replacement pigment epithelial retinal cells from iPS cells generated from patients with macular degeneration. Research is ongoing for several years and was widely reported at conferences.

Approval for clinical trials was expected to be routine. However, the health ministry committee has cited security concerns to put off a decision at the end of May. Japanese media reported that the group meets again today and accepted additional data submitted by RIKEN. Formal approval will be up to the Ministry. RIKEN could begin recruiting patients aware of this year.

What makes some people thin and other full-figured? Besides diet and genetics, the community of microbes that lives inside of us may be partly responsible. New research on twins suggests that lean people harbor bacteria than their obese counterparts do not. And, given the chance, these bacteria may be able to prevent weight gain. But do not dig your skinny jeans closet just yet. So far the work has been done only in mice. Moreover, bacterial takeover requires a healthy, high fiber diet to work, illustrating the complex relationship between diet, microbes, metabolism and health.

Our intestines are home at least 400 species of bacteria, and the evidence is building that the balance of microbes in our internal ecosystem has a significant impact on health, including brain function and the risk of Cancer. A study last year showed that the transfer of intestinal bacteria between humans reduces insulin resistance, which is related to obesity.

To explore how microbes differ between obese and lean people, researchers at Washington University in St. Louis took the intestinal bacteria of four pairs of identical and fraternal twins; a brother in each pair was thin and the other obese. Then they transplanted the microbes in mice that had no gut microbes of their own. Mice that got the skinny twin microbes remained thin, the researchers report today Science. Those who got the obese twins microbes increased their body fat by 10% on average, though they ate the same amount of food.

What would happen if these two sets of microbes are mixed in the gut, the researchers wondered. Led by microbiologist Jeffrey Gordon and graduate student Vanessa Ridaura, the team took advantage of one of the least endearing rodent habits: They eat shit the other. After letting this happen, the researchers found that the lean twin microbes appeared to be particularly good to take hold in the ecosystems of the mouse intestine that began with microbes associated with obesity. And after moved bacteria, the mice did not gain weight. The most invasive species of microbes from animals were thin in the Bacteroidetes group, which has previously been associated with thinness in mice and humans. Obese mice seem unoccupied niches that Bacteroidetes could easily move in.

To understand what the gut bacteria could do, the researchers studied the bacterial genes that were active in both types of mice. The heavier mice had higher levels of proteins involved in stress responses and detoxification; lean mice expressed more genes involved in the breakdown of dietary fiber.

food, it turns out, was the key to the impressive properties of lean twins microbes. All mice in the first series of experiments were eating chow that was high in fiber and low in fat. The researchers then developed a mouse pellet form an unhealthy human diet, high in fat and low in fiber, and housed mice slim and heavy together again. They found that, with this scheme, the microbes associated with leanness not colonize the intestines of cage mates.

This work was carefully done and corresponds to previous findings, including the idea that Bacteroides can protect against weight gain, says Alan Walker, a microbiologist from the gut the Wellcome Trust Sanger Institute in the UK who was not involved in the study. What is new here, he said, is that researchers have begun to address the question of how this protection might work :. Species that are responsible, what genes they use, and what diet they need

"This study is important step towards ultimately answer these questions," says microbiologist Peter Turnbaugh from Harvard University. an important result of this work, they agree, is that it puts in place a way to test the effects of microbial therapies on human intestinal bacteria (even if insects live in a mouse) . the authors suggest that the next logical step is to use animals to measure the effects of foods or ingredients ecosystem of the gut in particular.

the mouse experiments also provide a way to test fecal transplants, which can cure a potentially fatal intestinal infection in humans and show a potential to treat other conditions such as inflammatory bowel disease and obesity. There is a danger inherent in this approach: Transfer of human feces in the colon of a patient at risk of pathogen transmission as well. Walker and the authors note that "the next generation of probiotic" good test compound known beneficial microbes come in pill form or another treatment could take the place of fresh faeces, and this mouse system provides a way to identify the most effective bacteria, diseases of these bacteria can be treated, and if a special diet is required.

"There is a significant way to go before you can translate these findings to humans," warns Walker. A probiotic weight loss is not just a next step, the researchers discovered when they isolated 39 of beneficial Bacteroidetes species. The mixture was unable to cause the same effects as shit mouse, maybe because Bacteroidetes not acting alone and microbial players must be identified.

Although our muscles pumping iron, our cells pump something else: the molecules that help maintain a healthy brain. But scientists have struggled to explain the mental well-known advantages of exercise, fight against depression and aging the fight against Alzheimer's and Parkinson's. Now a research team may have finally found a molecular link between a workout and a healthy brain.

Research Many exercise focuses on the parts of our body that do the heavy lifting. Muscle cells increase production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin name, cut and released into the blood, where it causes the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the wicked.)

While studying the effects of FNDC5 in muscle, cell biologist Bruce Spiegelman of Harvard Medical School in Boston arrived at some surprising findings: Mice that do not produce a so-called co-activator production FNDC5, known as PGC-1α were hyperactive and had tiny holes in certain parts of their brain. Other studies have shown that FNDC5 and PGC-1α are present in the brain, not only the muscles, and both may play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (irisin and created from it) was responsible for the benefits induced by exercise levels of an essential protein called brain-derived neurotrophic factor (BDNF), this which is essential for maintaining healthy neurons and by creating new brain in particular has increased. These functions are essential to ward off the neurological diseases, including Alzheimer's and Parkinson's. And the link between exercise and BDNF is widely accepted. "The phenomenon has been established in easily, the last decade," says neuroscientist Barbara Hempstead at Weill Cornell Medical College in New York, who was not involved in the new work. "It's just, we understand not the mechanism. "

to adjust this mechanism, Spiegelman and colleagues conducted a series of experiments on live mice and mouse brain cells in culture. first, they put the mouse over an endurance training regime of 30 days. They should not force their subjects, because the race is part of the natural feeding behavior of a mouse. "It is more difficult to get them to lift weights" Spiegelman notes. Mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from the physical differences between mice and sedentary wheels trained ones- "they just look a little more like a couch potato," says co-author Christiane Wrann, also from Harvard Medical School, figures luscious-groups of the latter also showed neurological differences. The riders had more FNDC5 in their hippocampus, a brain area responsible for learning and memory.

Using the cells of the developing mouse brain in a dish, the next group showed increased levels of the co-activator PGC- 1α stimulates production FNDC5, which in turn leads to BDNF genes to produce more of the essential protein of neurons forming BDNF. They report these findings online today in Cell Metabolism . Spiegelman said it was surprising that the molecular processes in neurons mirrors what happens in the muscles that we exercise. "What was weird is the same pathway is induced in the brain," he says, "and as you know, with exercise, the brain does not move."

So how is the brain gets the signal to BDNF? Some have hypothesized that neuronal activity during the year (as we coordinate body movements, for example) reflects changes in the brain. But it is also possible that factors outside the brain, such as proteins secreted by muscle cells, are the driving force. to test whether irisin created elsewhere in the body can still lead the production of BDNF in the brain, the group injected a virus into the . mouse blood which causes the liver to produce and secrete high levels of irisin They saw the same effect as in the exercise. increase in BDNF levels in the hippocampus This suggests that irisin might be able to spend the blood-brain barrier, or it regulates another molecule (unknown) therethrough in the brain, said Spiegelman.

Hempstead called the findings "very exciting," and believes that this research is finally beginning to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. "I think it answers the question that most of us have put us in our own heads for years."

The liver irisin effect on the brain is a "pretty cool finding and a little surprising," says Pontus Boström, researcher Diabetes at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work does not answer a fundamental question: To what extent the effects of BDNF-promoting exercise are from reaching the brain irisin from muscle cells via the bloodstream, and how many are irisin created in the brain?

although the authors stress that other important regulatory proteins may play a role in the conduct of BDNF and other brain-nourishing factors, they focus on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and improve brain health with aging.

One of the biggest vulnerabilities of infants is largely invisible: In the weeks following birth, babies are particularly susceptible to infection because their immune systems are not fully functional. There are a handful of theories to explain this responsibility, and now a research team added another to the list: immune suppression in early life may help prevent inflammation in the intestines of infants they become colonized by helpful bacteria they need to stay healthy.

Newborns are more likely than older babies to catch, and die, severe infections. The reason is fuzzy indeed, there may be more than one explanation. One theory is that as the brain, lungs, and the rest of their body, the immune system of infants have simply not yet fully matured. Another is that mothers are to their in utero and two companions suppressed the immune system, so that neither rejects the other. After birth, the thinking goes, it takes babies a month or two to boost immunity.

The search for new ways to better understand this process, Sing Sing Way, a doctor of pediatric infectious disease at the Hospital Medical Center of Cincinnati Children in Ohio, wondered whether the transfer of immune adult cells could rev their immune system. Yet when he and his colleagues injected the fight against infection of cells from adult mouse spleens in 6 days old puppies, nothing happens: The puppies were just as vulnerable to harmful bacteria than the control animals. Probing deeper into this surprise, they found that the injected cells have simply stopped work in newborn animals. Then the Way group made the transplant, they reversed the mouse newborn adult immune cells that have been inactivated in puppies and found that they "lit" in adult animals. These experiences "told us it was not a problem with the neonatal cells themselves," says Way. On the contrary, he believes the environment is a newborn body, or an adult with a guided how the cells behaved.

others in the laboratory study of the gut microbiome Way, the constellation of healthy bacteria that fills our intestines. newborn mice, just like human babies are born " clean ", with little intestinal bacteria. Very quickly it changes. Way wonders if there might be a connection between this settlement and what looked like a deliberate suppression of the immune system in its mouse.

to find out, a group focused on immune cells that eventually develop into red blood cells and which express a surface receptor called CD71, which causes immunosuppression other cells. Knocking about 60% of these cells as CD71 much that their technology could handle-was followed by severe inflammation in the intestines of mice. Way and his colleagues also found that as the mice increased, fewer cells boasted CD71 receptors, suggesting the removal was not necessary. He theorizes that this is because the gut is colonized by this point.

The work, reported online today in Nature "adds a new and very important chapter" in the history of how the immune system develops, said Mike McCune, an immunologist at the University of California, San Francisco. immunosuppression, at least in newborn mice, appears to reflect a deliberate change in the balance of immune cells. the concept is certainly plausible, accepts Heather Jaspan, a specialist in pediatric infectious diseases and immunologist at the University of Cape Town and Seattle BioMed in Washington. She wonders about other cell types in addition to those receptor CD71 that may play a role. "It would be interesting to follow this issue with other studies of cause and effect," she said, finally nailing the specific immune suppression allows bacteria to colonize the gut without harming the newborn.

Much caution is whether that Way team observed held in human babies. the baby's immune system develops differently than a mouse, and Way is interested in search of CD71 cells in babies born around their due date, as well as those born prematurely. Very premature infants often die from a disease called necrotizing enterocolitis, a massive inflammation of the intestine. Way McCune and wonder if this resulted in part from a lack of CD71 cells in these babies-if, essentially, their immune systems are still fetal, not ready for natural colonization of intestinal bacteria happens after that they were born. In theory and far into the future, the researchers say, could receive preemies immune cells that would make them immune system more like a full-term baby, allowing their guts to stay healthy.