Health Meaning

In a report published today, the Institute of Medicine recommends that men who suffer from brain injury traumatic (TBI) in the battlefield must receive adequate protein and calories immediately after the injury and for at least 2 weeks to help reduce inflammation and minimize brain damage. The report was commissioned by the Ministry of Defence, who wanted a review of the potential role of nutrition to minimize the impact of a brain injury, injury to the signing of the wars in Iraq and Afghanistan.

The panel of experts who wrote the report noted that although the current guidelines for the treatment of TBI recommend early feeding, the details vary.

They recommended the army develop standard nutritional guidelines for soldiers with studies on injuries and the conduct of the brain to determine the levels of sugar in the blood and optimal diets to minimize the impact of brain damage.

The committee also reviewed the scientific literature on the various nutritional supplements, including choline, creatine, fish oil and antioxidants, but concluded that there is insufficient evidence for beneficial effects in patients with brain injury to recommend their use for that time.

Can robots evolve altruism? What is hidden behind a visual battle of the sexes in dogs? And can you get leprosy from an armadillo? Science s Online News Editor David Grimm discusses about these stories and more with Science Podcast host Robert Frederick.

( Listen to the full Science podcast and podcasts.)

German researchers suspect cucumbers from Spain were the cause of a massive enterohemorrhagic Escherichia coli (EHEC) outbreak which hit the northern regions of the country. According to the Robert Koch Institute (RKI), so far 214 patients developed hemolytic uremic syndrome (HUS), a potentially fatal complication of EHEC infection, characterized by destruction of red blood cells and severe kidney problems. At least two patients died.

Local authorities in Hamburg today announced that they had isolated the bacteria EHEC four cucumbers. Three of the samples came from a big market in Hamburg selling shops as well as restaurants and caterers of fruits and vegetables. These cucumbers from two organic producers in Spain. Scientists have speculated in recent days that manure from infected animals used on an organic farm could have spread the bacteria to vegetables. A fourth sample was from a restaurant, and it was not immediately clear where the cucumber was grown. After the announcement, the stores have started taking Spanish cucumbers on the shelves.

Consumers were already hesitant about vegetables since scientists at RKI and the Federal Risk Assessment Institute announced the results of a first case-control study Wednesday: Women who had become EHEC infection were significantly more likely to have eaten raw tomatoes, cucumbers and lettuce in the days before falling ill than women who were not sick.

The scientists used a detailed questionnaire to ask 25 women EHEC patients and 96 women living in the same areas of what they had eaten in the days before hatching. Only women were included in the study because they got sick more often than men in the home. "It also strengthened the results of the study, because it meant that we could ignore all the sex-specific differences in eating habits," says Gérard Krause, head of the department of infectious disease epidemiology at RKI.

statistical analysis revealed that 92% of women who had been infected already had eaten tomatoes. only about 60% of healthy women did. "for something that people eat so often, it is a big difference "said RKI expert Klaus Stark. The results for cucumbers and lettuce were similar, but slightly smaller. These three results are statistically significant. Experts invited Germans, especially in the north, not to eat it raw tomatoes, cucumbers, lettuce or until further notice.

This advice remains in place. "It is certainly possible that more than one of these foods is responsible," said Reinhard Burger, president of RKI. Scientists also want to be sure that the results of Hamburg are confirmed in another laboratory.

New idea of ​​the nature of the bacteria could help. scientists of the National reference Laboratory on hemolytic uremic syndrome in Münster have samples of all 42 cases of EHEC that occurred among patients HUS in Germany since 1996. They . have identified the strain of the current epidemic as HUSEC41, the type of sequence ST678 in common serotype classification which means the pathogen is a E. coli O104: H4

according to Helge Karch, head of the laboratory of Münster, O104: H4 has not a single documented outbreak in his name "that's why we were very surprised that this strain can cause severe illness in a short time," he said. -he.

Karch and others are now working on sequencing the entire genome of HUSEC41 and establish a new and easy way to diagnose this particular strain of EHEC. This is important because the bacterium is difficult to distinguish from normal, non-pathogenic E. coli .

The strain is also eae-negative, which is unusual for a pathogen E. coli . The gene eae encodes intimin protein that bacteria use to attach to the intestinal wall. "This has been shown to be particularly important to infect children, so it could be an explanation, why we mostly see adult patients in this epidemic," said RKI expert Stark.

Meanwhile the epidemic continues in full force. "he looked a little, as there was a dip in the numbers, but in particular in Hamburg many patients are still present in the hospital with bloody diarrhea" said Stark. the next few days will show whether the warning about eating cucumbers, tomatoes and lettuce had an impact on the epidemic.

* This article has been corrected . June 3 An earlier version of this story incorrectly reported that researchers had isolated the strain EHEC O104 H4 :. cucumbers

A new analysis of the literature confirms that from the scientific cells have been saying for some time: studies induced pluripotent stem cells (iPSCs), which are presented as an ethical alternative to embryonic stem cells (hESCs), often involve hESCs as well. Therefore, research that limits funding of hESC would also harm the iPSC research.

hESCs are derived from human embryos, whereas iPS cells are made by reprogramming adult cells. In a study in the June 10 issue of cell , Stanford University bioethicist Christopher Scott Thomas and colleagues analyzed 2,086 publications on hESCs and iPSCs from 1998 to 2010. Although the number of publications using iPSCs climbed since the first report on these cells in 07, 100 of the 161 iPSC documents (62%) published last year used the two cell types. especially established researchers tend to include hESCs, which are often used as controls.

Many researchers are worried that a lawsuit claiming hESC research funded by the federal government violates a ban on research that destroys human embryos could thwart their work. The authors say that any decision by the courts or legislators to limit funding of hESC "will also have disastrous consequences for [iPSC funding] because research using two different types of cell lines is deeply, perhaps inextricably , related."

- The two sides in a high-stakes legal battle over the expanded stem cells on their arguments in the briefs filed today a case being heard by the judge Royce Lamberth chief of the US district court for the district of Columbia.

The case, Sherley v. Sebelius , was brought by two researchers who argue that the National Institutes of Health (NIH) 09 restrictions guidelines on research funded by the federal lifting government on human embryonic stem cells (hESCs ) violate a law prohibiting research funded by the federal government that destroys human embryos. Last August, Lamberth issued a preliminary ruling for the plaintiffs who briefly interrupted funding of hESC research.

April 29 in a 2-1 decision, the Court of Appeal set aside the injunction, finding that the NIH "seems reasonably have concluded that" the law prohibits the derivation of hESCs, but does not obstacle to fund research that uses cells. This decision sent the suit back to Lamberth to rule on the merits of the case.

the plaintiffs then requested a chance to respond to the court decision call. (they initially asked that they take turns and get a chance to respond to the memory of the Government ;. Lamberth decided instead both parties must file a single brief 10 pages of June 24)

the both parties spend most of their memories in a second argument made by the complainants has not been taken into consideration by the court of appeal that the guidelines "encourage" the destruction of embryos, creating a demand for more of hESC lines

de plaintiffs memory.

the hESC research sponsored by the federal government that the guidelines inevitably argue creates a risk indeed important, certainty that more virtual human embryos will be destroyed in order to derive more hESCs for research purposes.

As evidence, the memory includes a declaration by the applicant James Sherley who notes that researchers are increasingly developing new lines in order to study the genetic and ethnic diversity .

The counters of the Government in its submission:

The theory of the applicants that the guidelines "encourage" the future embryo donation throws doubt if NIH had reasonably interpreted the law both because future donors would not be engaged in "research in which" an embryo is subjected to risk of injury, and because it is not plausible to claim that researchers funded by NIH "knowingly" creating the incentive for future donation.

plaintiffs also argue that the NIH did not follow proper procedures when it developed the guidelines. The two sides both asked Lamberth for summary judgment, meaning they want to decide the case quickly without trial. Spectators predict Lamberth could exclude at any time between autumn and the end of the year.

UPDATE: A decision Lamberth could come very soon, according to professor Hank Greely Stanford Law School. He noted that last summer after a decision of the appeal court granting legal status to the plaintiffs reached a court Thursday Lamberth issued a preliminary injunction, the following Monday, August 23 This suggests that if Lamberth did not order oral arguments or call for a trial (which seems unlikely, says Greely), it could not rule on summary judgment within 2 to 4 weeks. If Lamberth ordered argument, it would probably take place in August with a decision soon after, says Greely.

If Lamberth is in favor of the plaintiffs and ordered a permanent injunction (which end funding of hESC again), the Court of Appeal should remain rapidly (suspend) the injunction until that it hears the case.

A drug already widely used in massive campaigns to help control two parasitic diseases, river blindness and elephantiasis, could also reduce malaria, a new study has found. The compound, called ivermectin, shortens mosquito spans the lives and makes them less likely to transmit the malaria parasite.

Ivermectin is known worldwide primarily developed as a drug to treat head lice in children and heartworm in animals. It also kills several tropical parasites, including those transmitted by mosquitoes that cause lymphatic filariasis, a disease also known as elephantiasis for members horribly swollen suffered by patients and those worn by black flies that cause river blindness, blindness rivers.

many countries use ivermectin in a strategy called mass drug administration (MDA), which means that the entire population in an affected area is given the drug once or twice a year. Merck, which produces ivermectin under the brand name Mectizan, provides free to treat river blindness and elephantiasis; the company promised to do as long as necessary.

But Brian Foy, who studies insect vectors at Colorado State University in Fort Collins (and became a minor internet celebrity last year after the sexual transmission of the virus to his wife Zika and the publication of a study on this), is interested in another effect of ivermectin: it kills mosquitoes. Laboratory studies have shown that when mosquitoes bite a person recently treated with the drug, they swallow a dose which is sometimes fatal to them. To see if the drug could thwart malaria transmission, Foy and colleagues studied mosquito populations in a region in southern Senegal where ivermectin is used in annual MDAs to stop river blindness. In a study published last year, the team showed that MDA has greatly reduced the lifespan of mosquitoes that feed on treated.

In the new study, Foy and colleagues wanted to know if the insecticide effect of ivermectin translates into less infectious mosquitoes, which could slow the spread of malaria. In theory it should, because Plasmodium falciparum , the malaria parasite, takes about 2 weeks to develop inside the body of the mosquito, which is the life of the insect. So the team took the mosquitoes in three villages who participated in a MDA and three others nearby who do not. Indeed, they found that in treated villages, the proportion of mosquitoes with fully developed P. falciparum in their saliva fell by 79% in 2 weeks. But in the villages of control, the proportion increased by 246%, the ratio of online research today The American Journal of Tropical Medicine and Hygiene .

The discovery suggests the mass ivermectin treatment would be a new weapon against malaria, in addition to insecticide spraying, bed nets and other drugs, said Foy. But ivermectin should be given more often than once a year, he said, perhaps monthly, because the effect of the drug on the mosquito population will not last long. Merck will donate the extra amount needed Ivermectin is clear.

Brian Greenwood of the London School of Hygiene & Tropical Medicine paper called an "interesting pilot study," but he is "not very impressed" by the evidence in the document. He says the number of mosquitoes tested by researchers was small, and the paper leaves some unanswered questions such as why mosquitoes in treatment villages had much higher rates of malaria at the beginning of the study, or why rates rose in the control villages.

Peter Hotez, head of the Sabin Vaccine Institute in Washington, DC, and the current president of the American Society of Tropical Medicine and Hygiene in Deerfield, Illinois, agrees that much more study of the antimalarial activity ivermectin is necessary but calls the idea of ​​Foy "exciting" and "potentially very important." Hotez helped create the global Network for neglected tropical diseases, advocating the widespread use of a set of cheap drugs, including ivermectin, to target the seven tropical diseases less well known. "Now we have the proof possible that this package can also have an impact on other infections, including malaria," says Hotez.

Hotez sees a pattern emerging. In 09, a study published in the Journal of the American Medical Association showed that the mass administration of antibiotics in Ethiopia to treat trachoma, a bacterial eye infection, had huge additional benefits. For reasons still under discussion, it has reduced infant mortality by half. "We are only beginning to understand the enormous potential impact of MDAs on diseases for which they are not intended," said Hotez.

The human brain is great, and it is powerful, able to imagine innovative solutions to complex problems. Yet, our brains do not age well: As we grow older, they tend to shrink and become increasingly vulnerable to cognitive impairments such as memory loss and dementia. A new magnetic resonance imaging (MRI) study comparing humans and chimpanzees found that chimps brains maintain their size as they age. slowly lose our minds, it is, perhaps the price changes we pay for having bigger brains and longer life.

Regarding the researchers can tell, humans are the only animals subjected to specific brain diseases such as Alzheimer's disease, which affects the United States nearly 50% of people aged over 85. But even normal, apparently healthy human brains showed the effects of aging, such as the accumulation of amyloid-beta plaque deposits and loss of neural connections, particularly in areas related to learning and Memory. And previous studies of human brains have suggested that these brain regions, which include the frontal lobe and the hippocampus, are especially prone to shrinkage with age.

Although few similar studies of other primates were conducted, recent research rhesus monkeys have shown that the very limited shrinkage with age. Nonetheless, the evolutionary lineages leading to humans and rhesus monkeys diverged there are about 30 million years, leaving scientists in the dark when the human model brain aging could have started.

For a better idea, a team led by Chet Sherwood, an evolutionary neuroanatomist at George Washington University in Washington, DC, directly compared the brain-shrinking chimps and humans schemes, which have diverged are only about 5000000 to 7000000 years. The study sample consisted of 87 humans ranging from ages 22-88, and 69 chimpanzees from 10 years to 51. As chimpanzees rarely live more than 45 years in the wild, although some in captivity survived in their 60s represents the sample at the normal lifetime of these two species.

The team used MRI scanners to measure the size of a number of brain regions in humans and chimpanzees. The differences are striking: Although chimpanzees showed no significant age-related shrinkage in one of the measured regions, all regions of the human brain have shown dramatic effects of age, reports the online team this week in the Proceedings of the national Academy of sciences . Some regions have decreased to 25% in 80 years. Furthermore, the tendency was somewhat different for the human gray matter, which contains the body of the nerve cells and their nuclei, as well as auxiliary cells such as microglial cells and human white matter, which consists of long axons neural and making connections between the various brain regions.

For example, the gray matter of the human frontal lobe shrank on average by about 14% between the ages of 30 and 80, and gray matter in the hippocampus by about 13% in the same period. But the withdrawal of the white matter was even more severe. The white matter of the frontal lobe decreased by approximately 24%, similar to white decrease in the volume of the material in most other brain regions measured

In addition, unlike the gray matter, which showed a gradual withdrawal over time, the decline in white matter was steepest between the ages of 70 and 80. Thus, although the average decline in the frontal lobe was 24% at 80 years, it was only about 6% to 70 years.

Why are chimpanzees throughout their normal life cover without significant shrinkage of the brain, whereas the human brain seems to wither with age?

"This is the question a million dollars," said Sherwood. In the paper, the team points out that the greatest human brain, which is more than three times larger than that of a chimpanzee, also energy demand much higher. Thus, the human brain uses up to 25% of the total available energy of the body when we are at rest, compared to no more than about 10% for other primates.

the record track with what energy supplies, the team argues, appears on the cellular and molecular levels in the human brain. this includes a decline in mitochondrial efficiency, energy storage of living cells, as well as damage caused by oxidative stress, the result of molecules containing oxygen that are produced during cellular metabolism.

"My guess is that our neurons essentially do the best they can to keep the maximum operating for as long as possible, "said Sherwood. "But they have the chance really stacked against them after years of high energy consumption."

Dean Falk, an anthropologist at the Advanced Research School in Santa Fe find the differences between gray and white matter material models particularly interesting withdrawal. White matter, humans have relatively more as chimpanzees and other primates, "is particularly important for complex cognition Homo sapiens ," Falk said, because it makes the connections between brain regions involved in the transmission of information in problem solving and other complex tasks.

Nevertheless, Peter Rapp, a neurobiologist at the National Health Laboratory of Experimental Gerontology Institute in Baltimore, Maryland, who conducted some of the earlier brain imaging studies in rhesus monkeys, indicates that the new study does not distinguish between brain shrinkage as a result of normal aging in humans and that the withdrawal could be due to the neuro-degenerative disease of the brain of a subset of subjects. "Is what distinguishes humans and chimpanzees susceptibility to disease, or a qualitative difference in the brains of aging in good health?"

Bruce Yankner, a neurologist at Harvard Medical School in Boston, agrees. to test the hypothesis of the authors that the narrowing of the human brain is the result of greater longevity, Yankner said, "it would be interesting" to see if similar brain shrinkage occurs in other species with extreme longevity, "as turtles and tortoises that live for more than 100 years, elephants can live for 70 years, and parrots that can live for 80 years. "

A dozen plaintiffs filed a complaint against Duke University and administrators, researchers and doctors there, claiming they engaged in fraudulent behavior and neglect when they registered cancer patients in a clinical trial compromised by incorrect data. The lawsuit, filed Wednesday before a North Carolina court is 14 months after a scandal erupted at Duke who finally exposed the extent of testing problems in July 2010, Duke oncologist Anil Potti, whose job was the trial center, admitted he had embellished his resume and later resigned.

The complainants - cancer patients who were in the tests and the families of trial participants who are no longer alive - Duke officials say the long knew that the work Potti and Joseph Nevins , a cancer geneticist who was director of the Center for Applied Genomics at Duke & Technology, was "very suspicious", but launched clinical trials based on it anyway. (A series of co-author pair of documents was retracted during the past year.) "In May 07, after being placed on notice of the flawed science behind its cancer studies as mentioned above, Duke University and / or Duhs [Duke University Health System] nevertheless began their first clinical trial, "the lawsuit says. the trial assigned patients lung cancer to certain treatments based on gene expression profiles now discredited Potti and Nevins said that they had identified in tumor cells.

the prosecution is scathing in his assessment of how Duke handled the growing concern expressed by foreigners, especially the two biostatistician at MD Anderson Cancer Center in Houston, Texas.

the applicants argue that the answer of the Duke "to the charge of the invalid and fraudulent science was deceptive, misleading and fraudulent conduct to protect its reputation and interests of owners. .. rather than to protect the safety of patients involved in clinical trials. "The trial continues: This" reduces the likelihood that the plaintiffs to survive his / her cancer or the likelihood of experiencing a positive response to chemotherapy "

The plaintiffs want at least $ 30,000 each in. damages and a jury trial. Duke University said it can not comment on active litigation. Meanwhile, the Institute of medicine studies how gene expression profiles are used in medicine and hope conclude the project next year.

Two groups of scientists working independently of each other have discovered a genetic mutation that causes amyotrophic lateral sclerosis (ALS) known as the disease of Lou Gehrig. Both teams found that mutations of the same gene can also cause a common type of dementia called frontotemporal dementia (FTD). The results add to the growing evidence that these devastating disorders have more in common than meets the eye.

ALS robs patients of the ability to control their bodies. The first symptoms can be subtle, a tic, some muscle stiffness, or speech, but then occasionally mumbled paralysis spreads throughout the body. Most patients die of respiratory failure within 5 years. FTD is a very different beast. The most common type of dementia after Alzheimer's disease, it triggers a strange and inappropriate behavior, particularly in social situations, and difficulty with decision making, language, and other cognitive functions.

Despite these differences, there are overlapping signs. Clinicians have observed that people with a disorder may have symptoms of the other, and some families seem to have more than their share of both. In 06, researchers have linked a region of chromosome 9 in both ALS and FTD. The results suggest that a gene mutated in this region was responsible for many cases of the two conditions, but scientists PinPoint a specific gene.

The race that followed to find the gene was "very intense," said Rosa Rademakers, Neurogeneticist at Mayo Clinic Florida in Jacksonville, who led one of several teams that joined the lawsuit. "In areas of ALS and FTD, it was a result that everyone expected."

In papers published online today Neuron , the team of Rademakers and another group led by Bryan Traynor, a neurologist specializing in ALS at the National Institute on aging in Bethesda, Maryland, identified the same genetic culprit, mutations in an obscure gene called C9ORF72 . Do virtually nothing is known about its function . both teams found that repeated string of six-nucleotide building blocks of DNA that make up the "letters" of the genetic code in this gene can cause ALS or FTD. While healthy people in both studies had no more than 20 repetitions, those with ALS or FTD often were hundreds if not thousands.

the team reviewed hundreds Traynor patients and control subjects in Finland, where the SLA is almost twice as common as in other Caucasian populations. They found that C9ORF72 mutations accounted for 46% of familial ALS cases and about 21% of cases "sporadic" in which the patient reported no family history of the disease. In comparison, the proximate cause genetic most common of ALS gene mutations SOD1 , is responsible for about 15% of familial cases in other European populations, says Traynor.

Rademakers team studied patients in several clinics in the United States and Canada. They found that C9ORF72 mutations accounts for about 22% of familial ALS cases and 12% of familial cases of FTD, far more than any of a handful of other genetic risk factors they examined in the same patients. C9ORF72 mutations accounted for 3% to 4% of sporadic cases of both disorders.

"This is a great step forward because it is such a common mutation," said John Trojanowski, studying neurodegenerative disorders at the University of Pennsylvania. His group found that ALS and FTD share common cellular features, including a misfolded protein called TDP-43 which form clusters inside neurons. Trojanowski said that the new points working in a similar direction. "These results add another convincing proof that the concept ... and ALS [FTD] are mechanistically related disorders at both ends of a clinical and pathological spectrum."

Yet, many important questions remain. No team has found an explanation for why some people C9ORF72 ALS mutations while others get FTD. And it is unclear how mutations cause the disease is. It may be that the protein encoded by C9ORF72 performs an essential function that is yet to be discovered, that gets disturbed, says Traynor. Or perhaps the function of C9ORF72 does not matter. Alternatively, Traynor said, is that repeated nucleotides cause toxic accumulation of messenger RNA, a key player in the cellular machinery for the reading of the DNA for the manufacture of proteins.