Science News Headlines from ScienceNOW- The latest news from the science world. Long Life Is Still (Somewhat) in Your Genes. Will you live to 100? In 2010, scientists published a study proposing a "genetic signature" that could help answer that question. But they retracted the paper last year when critics discovered errors that invalidated the results. Now the team is back with a revamped study that proposes a different signature; it's less predictive in most people but, they say, it still underscores that your chance of living a very long life has a powerful genetic component. The flap began 18 months ago, when biostatistician Paola Sebastiani, geriatrics specialist Thomas Perls, and their colleagues at Boston University reported in Science that they had identified 150 gene variants that, taken together, could predict with 77% accuracy one's chance of becoming a centenarian.
The work was immediately criticized by geneticists who said it incorrectly inflated the importance of a number of gene variants, making the signature look more powerful than it really was. The Case of the Missing Genes. You might assume that if you're healthy, you have a normal, healthy genome. But there is no such thing as a normal genome—all of us carry a number of mutated and nonfunctioning genes. Now researchers have estimated exactly how many such genes there are in the average person: about 100, including 20 mutated and completely inactive genes. We probably don't need some of this DNA and in some cases could even be better off without it. Soon after researchers began to sequence individual genomes 5 years ago, they realized that everyone's DNA seems to have major mutations that disable the protein for which the gene codes. They found that 1285 loss-of-function gene variants are likely genuine, about 100 of which appear in the genome of the average European, MacArthur's team reports today in the 17 February issue of Science.
As more genomes are sequenced, "we know for sure that we will find a lot more" loss-of-function mutations, MacArthur says. Loss of Function Variants - MacArthur Lab. Fat Molecule Fights Weight Gain. It could be an ad in a fashion magazine: Miracle fat prevents weight-gain! Researchers aren't promising that, but they do say they've isolated a fat molecule in mice that prevents the animals from storing even more fat. The discovery could open a new front in the battle against the bulge if the molecule has the same effect in humans. The word "fat" typically evokes the image of clogged arteries or cellulite jiggling on a thigh. But fat has a good side, too. Biochemist Gökhan Hotamisligil of the Harvard School of Public Health in Boston and his colleagues wanted to understand how this process works.
The researchers then examined why the mice were accumulating less fat, suspecting that a molecular signal was in play. The idea that a fatty acid could help regulate the metabolic system is fascinating and provocative because researchers had thought only proteins could do that, says Henry Ginsberg, an endocrinologist at Columbia University. Fabricating Genetically Engineered High-Power Lithium-Ion Batteries Using Multiple Virus Genes.
Keeping Greenhouse Emitters Honest. A new study has a message for any country claiming to limit its emissions of greenhouse gasses: don't cheat. Using data gathered by sensors scattered around an urban area, researchers say they can track changes in a city's carbon dioxide output. That means that when a nation says it's complying with an emissions-limiting treaty, scientists may soon be able to see whether it's telling the truth. The Kyoto Protocol, which was adopted in December 1997, has been signed and ratified by more than 190 countries, including 37 industrial or developing nations that agreed to reduce their emissions of carbon dioxide and three other greenhouse gases by 5.2% each year, on average, between 2008 and 2012.
Although the United States signed the treaty, it stands alone as the only signatory to have not ratified the deal. But signing a treaty is one thing. Actually following through is something else. So how can nations keep each other honest? University: Research News @ Tufts. A Window into the Origin of Species Erik Dopman, PhD, joined the Department of Biology in 2009. He uses his expertise in evolutionary biology (PhD, Cornell University) and genomics and bioinformatics (postdoctoral research, Harvard University) to explore how species originate.
“The critical features that generate new species are called isolating barriers, which are traits that prevent the exchange of genetic information between organisms,” says Dopman. “The organism we study is called the European corn borer [the moth Ostrinia nubilalis], which is a major economic pest of corn and many other crops. We study it because many isolating barriers have evolved between two lineages, which are in the process of becoming new species.” Dopman and his research group identified seven isolating barriers that limit gene flow between strains of the European corn borer (ECB). Dopman breeds the E and Z strains of the ECB in his lab in Barnum Hall. A Key to Turning Off Stress. Busy lives do more than make our days a series of juggling acts. Stress has been found to cause depression, cardiovascular disease and infertility, among other disorders, so figuring out how to control stress would benefit millions.
Biomedical researchers at Tufts have made some headway—and it doesn’t involve running away to a desert island. Jamie Maguire, an assistant professor of neuroscience at the School of Medicine, and her colleagues have identified new pathways in the brain that are involved in the chemical chain reaction that leads to stress, and they have discovered that a drug used to treat male pattern baldness can tamp down that chemical response.
The work could lead to new ways to treat stress-related illnesses. Of course, stress isn’t always bad. When animals—and that includes you and me—are faced with danger, our fight-or-flight response is triggered, leading to rapid breathing and quickened heart rate. It’s All in Your Head. Keeping Drugs Potent. Researchers at Tufts University School of Engineering have discovered a way to maintain the potency of vaccines and other drugs that otherwise require refrigeration for months and possibly years at temperatures above 110 degrees F, by stabilizing them in a silk protein made from silkworm cocoons. Importantly, the pharmaceutical-infused silk can be made in a variety of forms such as microneedles, microvesicles and films that allow the non-refrigerated drugs to be stored and administered in a single device.
The Tufts findings address a serious obstacle to the effective use of life-saving pharmaceuticals: keeping them cold. Most vaccines, enzymes and antibodies and many antibiotics and other drugs require constant refrigeration from manufacture to delivery to maintain their effectiveness. International health experts estimate that nearly half of all global vaccines are lost due to breakdowns in the “cold chain.” David Kaplan with silk threads. Nanoscale Bubble Wrap. Bacteria cities cannot form on a super-slippery surface, inspired by meat-eating plants | Not Exactly Rocket Science. When bacteria start building cities, we’re in trouble. The normally free-floating cells can gather in large numbers and secrete a slimy matrix that they live within. These communities are called biofilms, and they grow wherever there is a surface to support them. Hospital catheters are prime real estate, but they’ll settle on everything from plumbing to oil refineries to ship hulls.
Within a biofilm, bacteria are extraordinarily durable. Since killing biofilms is a Sisyphean task, some scientists are trying to prevent them from forming at all. The material is called Slippery Liquid-Infused Porous Surfaces or, more aptly, SLIPS. It makes a duck’s back look like a sponge. The SLIPS consists of thousands of stacks, each a thousand times thinner than a human hair. Drops of water, blood and crude oil sit on the SLIPS as spheres. At the time, Aizenberg suggested a wide range of applications, from graffiti-proof walls to frictionless pipelines to ice-resistant windshields. Train with color to fix rapid recognition. BROWN (US) — Scientists have shown that a seemingly irreparable limitation of human perception is treatable with a small amount of training.
“Attentional blink” is the term psychologists use to describe our inability to recognize a second important object if we see it less than half a second after a first one. For example, we’ll notice that first car spinning out in our path, but maybe not register the one immediately beyond it. “Attention is a very important component of visual perception,” says Takeo Watanabe, professor of cognitive, linguistic, and psychological sciences at Brown University. “One of the best ways to enhance our visual ability is to improve our attentional function.” Watanabe and his team were at Boston University when they performed experiments described in a paper published the week of July 9 in the Proceedings of the National Academy of Sciences.
Train the brain In one set of sequences the numbers were spaced only two characters, or a fifth of a second, apart.