Monday, September 5, 2011

News in Brief: Genes & Cells

Bacterium’s DNA mostly unused, the death of Black Death and more in this week’s newsWeb edition : Friday, September 2nd, 2011

Life’s essentials
Most of the DNA in the bacterium Caulobacter crescentus really isn’t necessary. Researchers used genetic tricks to map out the pages of the bacterium’s genetic instruction book that are essential to life in the lab. Of Caulobacter’s 3,876 genes, only 480 are essential, Stanford microbiologist Lucy Shapiro  and her colleagues report online August 30 in Molecular Systems Biology. Also necessary are 402 pieces of DNA that govern activity of genes and 130 pieces of DNA that don’t encode proteins. Of the 130 “non-coding” bits, “90 don’t fit any of the categories we know about, and we don’t have a clue what they do,” Shapiro says. —Tina Hesman Saey

Black Death bacterium is extinct
Fear not. A version of the plague bacterium that wiped out at least 30 percent of Europe’s population between 1347 and 1351 is a goner. Scientists have debated whether the plague bacterium Yersinia pestis really caused the Black Death because that plague had different symptoms than modern outbreaks of bubonic or pneumonic plague. Now scientists from the University of Tübingen in Germany and McMaster University in Canada and colleagues have found traces of Y. pestis in skeletons of Black Death victims. The team reports online August 29 in the Proceedings of the National Academy of Sciences that the Black Death bacterium was genetically different from modern plague strains and probably no longer exists. —Tina Hesman Saey

Yellow eyes get less sleep
Elderly people’s sleeping problems may be due to a natural yellowing of the eyes with age, a new study suggests. Researchers at the University of Copenhagen examined 970 Danish people between 30 and 60 years old. The team found that as people age, the lenses of their eyes yellow slightly, blocking out blue light wavelengths that help synchronize the body’s daily rhythms. The less blue light that got through to the retina, the more likely people were to have sleep disturbances, the researchers report in the Sept. 1 Sleep. Yellowing is sped up in smokers and people with diabetes and heart disease. —Tina Hesman Saey

Ancient antibiotic resistance
People have been fighting bacteria with antibiotics for more than 70 years, but a new study finds that the microbes have had at least a 30,000-year head start on building resistance. The finding, published online August 31 in Nature, contradicts the idea that resistance to antibiotics is a modern phenomenon brought about by misusing the drugs. Researchers at McMaster University in Hamilton, Canada, and colleagues isolated ancient DNA about 30,000 years old from the permafrost near Dawson City, Canada, and found genes for proteins that work together to inactivate the antibiotic vancomycin. Resistance to that antibiotic was previously thought to have first arisen in the late 1980s. —Tina Hesman Saey


Found in: Genes & Cells

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Tuesday, August 30, 2011

News in Brief: Genes & Cells

A family without fingerprints and the long-term harm of sleep skimping in this week’s news Web edition : Friday, August 19th, 2011

No fingerprints
Members of a Swiss family who lack fingerprints have a mutation in a gene called SMARCAD1, Eli Sprecher of Tel Aviv University in Israel and colleagues report. The mutation, which also reduces the density of sweat glands in the hands, leads to a problem with a version of the gene’s protein that is made only in the skin, the team writes in the August 12 American Journal of Human Genetics. The researchers don’t yet know whether the gene is involved in creating the pattern of fingerprints or just in building the skin ridges that make up the print. —Tina Hesman Saey

Chronic sleep loss can cause permanent harm
Repeatedly skimping on sleep can add up to permanent health damage, a new study in rats suggests. Carol Everson and Aniko Szabo of the Medical College of Wisconsin in Milwaukee restricted rats’ sleep in repeated 10-day bouts, with two days in between to rest up. The rats lost weight despite chowing down on far more food and water than usual. The animals’ hormones were messed up, and they developed other problems as well, the researchers report August 11 in PLoS ONE. Even after four months of recovery, the rats still had hormone imbalances and were eating 20 percent more and drinking 35 percent more than rested rats. —Tina Hesman Saey


Found in: Genes & Cells

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Monday, August 29, 2011

Antidepressants show signs of countering Alzheimer’s

Mice and human data link treatment to less plaque in the brainWeb edition : Monday, August 22nd, 2011

Widely used antidepressants may reduce the ominous brain plaques associated with Alzheimer’s disease, a new study in mice and humans finds.

Brain scans of people who have taken antidepressants reveal fewer clumps of the protein amyloid-beta, a target of Alzheimer’s prevention strategies, when compared with people who have not taken the drugs.

Many in the field voiced caution about the results. But if borne out by further study, the findings may point to a new, relatively safe way to treat and prevent Alzheimer’s disease, which is the sixth leading cause of death in the United States.

“I think this is a wonderful piece of news, and I think there’s going to be a lot of excitement about this,” says internist Michael Weiner, who leads the Alzheimer’s Disease Neuroimaging Initiative at the Veterans Affairs Medical Center campus of the University of California, San Francisco. “It points the way towards a possible approach to treating Alzheimer’s disease that people have not been talking about very much.”

In the study, mice genetically engineered to overproduce amyloid-beta, or A-beta, were given one of three selective serotonin reuptake inhibitors, a class of antidepressants that boost circulating levels of the chemical messenger serotonin in the brain. After a single dose of the antidepressants, A-beta levels dropped in the fluid that surrounds mouse brain cells, researchers report online the week of August 22 in the Proceedings of the National Academy of Sciences. A full day after receiving the drug, the mice’s A-beta levels fell by nearly a quarter.

Long-term, chronic administration of the drug had a larger effect. Engineered mice that took the SSRI citalopram for four months had about half the A-beta plaques in their brains as mice that hadn’t had the drug. This reduction seems to happen through a protein called ERK, which serves as the middleman between brain cells’ serotonin-sensing proteins and A-beta production.

Figuring out the details of this process may open the door for developing new ways to prevent A-beta buildup, says study coauthor John Cirrito of the Washington University School of Medicine in St. Louis.

To see if a similar effect might be happening in people, the scientists scanned the brains of 186 cognitively normal elderly people and looked for signs of A-beta plaques. The team used a compound called PIB that binds to big clumps of A-beta in the brain and glows on a PET scan.

Of these participants, 52 reported that they had taken an antidepressant in the last five years. These people, researchers found, had about half the A-beta load in their brains as the people who hadn’t taken an antidepressant. What’s more, the length of time the participants took the drugs correlated with the density of A-beta plaques in the brain — the longer the antidepressant dose, the less plaque.

“We think there are influences going in two opposite directions,” says study coauthor and psychiatrist Yvette Sheline, also of Washington University. “We think depression pushes you toward dementia, but antidepressant treatment pushes you toward protection.”

Finding similar results in mice and humans lends the study credibility, Weiner says. “When you have animal data and human data coming together, then you start to get really excited,” he says.

Still, Weiner and others caution that it would be premature to conclude that antidepressants protect against A-beta buildup or that fewer plaques necessarily translate into less disease.

The study uncovered an association — not a clear-cut cause and effect, Weiner notes. “We cannot say with certainty that the reason why people who took the SSRIs have lower cortical amyloid is due to the fact that they took SSRIs,” he says.

And molecular neuroscientist Heather Snyder of the Alzheimer’s Association in Chicago points out that even if antidepressants are shown to reduce A-beta, scientists still don’t know how A-beta levels affect the brain. “We don’t really know what modulating amyloid will do to cognition,” she says. “And we don’t know if we need to reduce it by 10 percent or 20 percent, or if it needs to be completely reversed.”

Another confounding factor is that A-beta can take several forms in the brain, from small molecules to large, sticky clumps, and some forms may be more dangerous than others. Interpreting the A-beta clumps that PIB detects in human brain scans remains challenging.

“We’re being very cautious,” Cirrito says. “There are a lot of people on these drugs and we don’t want to get anybody overly excited without reason.” He and his colleagues plan to test whether acute doses of SSRIs change A-beta levels in the cerebrospinal fluid of healthy human subjects.

Even if the new findings are replicated in larger studies, a major question about Alzheimer’s and antidepressants remains, Sheline says. “The real question is — which this paper sheds no light on — does that mean that long-term, they [SSRI-treated people] will have less of a risk of dementia? And that’s exactly the big study that needs to be done.”


Found in: Body & Brain and Genes & Cells

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News in Brief: Molecules/Matter & Energy

Metamaterial warp drives, secrets of coffee rings and more in this week's newsWeb edition : Sunday, August 21st, 2011

Toy warp drive proposed
A physicist who previously created a toy universe out of metamaterials that bend light in unusual ways has now dreamed up a way to use those materials to build a warp drive. Simulations by Igor Smolyaninov at the University of Maryland in College Park show that moving faster than light is still impossible in toy universes, just as it is in the real one. But the right material should allow superspeed travel at up to one-quarter light speed — by riding in a moving spacetime bubble, he reports in an upcoming issue of Physical Review B. —Devin Powell.

Butterflies sip like sponges
To sip nectar, a butterfly uses a proboscis that looks like straw but also works like a sponge. At the small scales of butterfly existence, liquid is just too thick to be slurped, a team led by researchers at Clemson University in South Carolina reports. X-ray images of butterfly feeding tubes reveal pores that draw fluid upward by capillary action, the same process that pulls water through a paper towel. This anatomy may help butterflies dine on a greater variety of foods, and its principle could be borrowed to design probes that sample the liquid inside cells, the researchers report online August 17 in the Journal of the Royal Society Interface. —Devin Powell.

Coffee ring regulation
Starbucks tables everywhere rejoice: There’s a way to prevent the coffee ring effect. The quiet drying of spilled coffee on a countertop produces a crusty edge because round particles flee in a frenzy from the center of the spill. But oblong particles in the liquid can’t flee that well and end up spreading out uniformly, University of Pennsylvania scientists report in the Aug. 18 Nature. Upping the number of elongated particles compared to spherical ones can prevent ring formation, suggesting that particle shape influences fluid interactions. The finding could help in designing better inks, paints and even foams and lotions.—Rachel Ehrenberg


Found in: Matter & Energy and Molecules

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Sunday, August 28, 2011

News in Brief: Body & Brain

Leukemia gene therapy, the brain tickle of beautiful voices and more in this week's newsWeb edition : Thursday, August 18th, 2011

Gene therapy for leukemia
Tweaking immune cells to attack cancer cells in leukemia patients can bring about remission, a small study shows. Scientists at the University of Pennsylvania genetically altered immune T cells to target malignant cells in chronic lymphocytic leukemia patients and mass produced the T cells before injecting them into three patients. The modified cells gravitated to bone marrow, where they killed malignant cells. In two of three patients tested the cancer went into remission, and a portion of the genetically modified T cells persisted, possibly as a cadre of defenders on standby. The researchers report the findings in the Aug. 10 Science Translational Medicine. —Nathan Seppa

Gout drug lessens flares
A drug approved in 2010 for treatment of gout has proved its worth, reducing symptoms over six months in many people who had failed to get relief from standard medications. The routine therapy for gout fails in about 3 percent of the 5 million to 6 million people in the United States who have it. A drug called pegloticase, which is given by intravenous infusion over two hours, gained approval last year for chronic gout. Two clinical trials in the United States, Canada and Mexico of people who had failed to improve? on standard drugs now show that of 65 of 169 patients getting pegloticase (Krystexxa) every two or four weeks for six months had reduced uric acid in the blood, a standard measure. The biweekly group had better symptom reduction. —Nathan Seppa

Live longer with exercise
Just 15 minutes of moderate daily exercise seems to extend life. A team of U.S. and Taiwanese researchers kept track of physical activity levels in more than 400,000 adults age 20 and older in Taiwan using questionnaires. Compared with sedentary people who didn’t exercise, those putting in 92 minutes a week — 15 minutes a day on average — were 14 percent less likely to die over an average follow-up period of eight years. The benefits applied to both sexes and to all age groups, the researchers report online August 16 in the Lancet.  —Nathan Seppa

Granddaddy’s stress changes grandson’s brain
What your grandfather experienced in the womb may change your brain. Grandfather mice who were stressed out in utero went on to produce grandsons with more feminine brains, a study in the Aug. 17 Journal of Neuroscience shows. In male descendents of stressed-out grandfathers, genes important for brain development switched their behavior to become more like the gene activity in female mice’s brains. These results may offer a way to link stress and neurological disorders that strike males and females differently, such as autism spectrum disorders, Christopher Morgan and Tracy Bale of the University of Pennsylvania write in the study. —Laura Sanders


Beautiful voices tickle the brain
From Laura: Attractive voices tickle the part of the brain that normally handles visual input, a new study finds. In the study, participants listened to different voices saying “had” and later rated how attractive the voices were. Voices rated more attractive were associated with greater brain activity in a region near the part of the brain that responds to faces, an international team of scientists reports in an upcoming Cerebral Cortex. That the brain detects and responds to vocal beauty suggests that people may be tuned in to hidden, nonverbal forms of communication. —Laura Sanders

Why autistic brains confuse pronouns
The brains of people with autism behave abnormally when grappling with pronouns such as “you” and “I.” While answering a question that contained the word “you,” adults with autism had a weaker connection between two key brain regions than unaffected participants, Akiko Mizuno of Carnegie Mellon University in Pittsburgh and colleagues report in an upcoming Brain. This weak brain connection vanished when the question omitted pronouns and instead used people’s names. The results help explain why children with autism often have trouble with the concept of self-identity, sometimes referring to themselves as “you.” —Laura Sanders


Found in: Body & Brain

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News in Brief: Humans

Prehistoric assembly lines, a trigger for riots and more in this week's newsWeb edition : Monday, August 22nd, 2011

Early start for advanced tools
Large-scale production of sophisticated stone tools, using standardized assembly steps, emerged a surprisingly long time ago. Between 400,000 and 200,000 years ago, unidentified members of the genus Homo regularly made slender, sharp-edged blades and other animal-butchery implements at Qesem Cave in what’s now Israel, say archaeologist Ron Shimelmitz of Tel Aviv University and his colleagues. Analyses of thousands of Qesem stone artifacts, and experimental reproductions of these finds, indicate that the implements were made in stages requiring as much planning as Neandertal tools that didn’t appear until 200,000 years ago, the researchers will report in the Journal of Human Evolution.  —Bruce Bower

A fate worse than death
Patients in persistent vegetative states often get tagged as having less mental capacity than the dead. Ending up in biological limbo is also regarded as a fate worse than death, say psychologist Kurt Gray of the University of Maryland in College Park and his colleagues. Religious and non-religious participants alike attributed less mental activity to vegetative patients than to the dead, due to afterlife beliefs and a tendency to assume that deceased but unseen people still have minds, the scientists will report in Cognition. Religious people also usually advocated life support for vegetative patients despite regarding such states as worse than death. —Bruce Bower

Food fights
Violent protests in North Africa and the Middle East in 2008 and 2011 coincided with large spikes in global food prices, a new study shows. The analysis, which spans January 1990 to May 2011, suggests that high global food prices are a precipitating condition for social unrest, say Yaneer Bar-Yam and colleagues at the New England Complex Systems Institute in Cambridge, Mass. Their study, posted at arXiv.org on August 11, also calculates a food price threshold above which vulnerable populations typically find themselves in desperate straits. This indicator could help guide policy interventions.—Rachel Ehrenberg


Found in: Humans

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Saturday, August 27, 2011

Science & the Public: Blacks far less likely than whites to land NIH grants

Among minority scientists applying for National Institutes of Health research grants, blacks alone face a substantially lower likelihood of being successful than whites, a new study finds. This investigation, which was prompted by the research agency itself, will catalyze further probes and a host of changes, promises NIH director Francis Collins.

The findings emerge from a study published online Aug. 18 in Science. Donna Ginther of the University of Kansas in Lawrence and her colleagues probed the success rates of Ph.D. investigators working at U.S. institutions in winning NIH grants between 2002 and 2006. Over that time, more than 40,000 individuals submitted a total of 83,188 applications. Each hoped for the opportunity to dip deeply from a pool of funds averaging about $1.4 billion annually.

Researchers who described themselves as Hispanic had grant success rates comparable to whites. Initially, Asians appeared to have a 4 percentage-point lower success rate than whites. But when Ginther’s group reanalyzed the data, restricting the applicants to U.S. citizens, the Asian disadvantage vanished. (Says Collins, this suggests that applicants who didn’t fare well here might have been non-native English speakers with a language barrier to articulating their ideas cogently.)

But nothing erased the black disadvantage, Ginther’s team found.

“These data are deeply troubling,” Collins says. “Even after controlling for all of the factors that were considered to be important for predicting success” — like education and NIH training, the labs in which they ended up working, the number of research papers they’ve authored — “black applicants were 10 percentage points less likely than white applicants to receive research grants.”

Numerically, he told reporters, that translates to about 27 percent of white researcher’s grant applications winning funding, compared to only about 17 percent of those submitted by blacks.

“It is certainly a situation that we all agree is unacceptable and requires intervention,” Collins says.

On the drawing board
He and Lawrence Tabak, the principal deputy director of NIH, broadly outline an action plan to deal with the problem in a report that also appears online in Science. Details, however, await the findings of a pair of new advisory groups that Collins created.

Tabak co-chairs one of these: a diversity in biomedical research working group. He reports that in its initial teleconference, the group discussed how to probe obstacles to the recruitment of first-rate applications from minority scientists and to ensure that those proposing the best science have an equally high chance of landing NIH funds.

“This is a committee that is not designed to produce a glossy report that will sit on shelves,” Tabak says, but rather to provide Collins “tangible action items” by next June.

One issue NIH plans to take on immediately: how to adequately “blind” grant reviewers to applicants so that any chance of bias is minimized — without also eliminating important details that might reflect the quality of a scientist’s research or resources.

NIH already strips off a researcher’s stated race or ethnicity from a grant proposal before reviewers judge its merit. However, names and the background of the principal investigator remain — which in some instances may offer clues. Such as a first name like Kwame or L’Shaniqua, or perhaps reference to an applicant having attended a historically black college.

In an experiment set to begin soon, Collins promised to investigate whether further blinding is needed. His agency will simultaneously subject some collections of grant applications to two review panels, then compare their results. One panel will receive applications that contain the same information as in the past; the other will receive proposals from which all names and identifying characteristics have been removed.

Boosting help, enriching opportunities
While the magnitude of the black disadvantage might have surprised NIH, the agency has long known that blacks play a bit role in biomedical research. They constitute 10.2 percent of the U.S. population, Collins notes, yet only 1.2 percent of researchers leading projects financed by NIH (through investigator-led — or RO1 — grants).

The newly quantified disadvantage highlighted by Ginther’s team might reflect weaker training of black researchers on how to craft a winning application, less access to mentoring on research design, some subtle bias on the part of grant-review committees — or a combination of all these. Collins vows his new advisory groups will look into each.

For instance, not all grant applications are scored for quality. Those that reviewers feel will fall within the lower half are just rejected.

Ginther’s group now reports that among grant proposals that were scored highly, race and ethnicity had no impact on funding success. This suggests that blacks may face some disadvantage in drafting a compelling proposal.

Collins now promises NIH will soon offer extra assistance to inexperienced grant applicants and be “supporting innovative approaches to encourage more extensive and effective local mentoring of junior faculty” by the academic institutions at which they work. He adds that his new advisory groups will also consider how NIH might encourage researchers who weren’t successful the first time around to reapply for a grant (since most successful applicants have to try a few times before they land a grant — and blacks are less likely to do that).

Sitting in on grant deliberations should help young faculty of all ethnic backgrounds get a better taste of how research proposals are judged and what’s most likely to wow their peers. Scientists recruited to review grants, however, tend to be older, more experienced individuals. Collins aims to change this by actively recruiting “promising junior faculty” to become reviewers: “We aim to have 50 of these early career reviewers assigned to each of NIH’s three rounds of grant reviews in the 2012 fiscal year, which begins Oct. 1."

At a briefing for reporters, Tabak noted that NIH has already begun sharing what it’s learned with officials at the National Science Foundation, Department of Defense, Energy Department and Education Department. From those discussions, he says, it sounds like these agencies are also open to investigating whether racial or ethnic disparities may exist among applicants for their grants.


Found in: Biomedicine and Food Science

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