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Find out if your child will be overweight

Researchers, set up an interactive website to gather information about childhood predictors of adult body mass index (BMI) from the general public.

The scientists discovered that “crowdsourcing” - everyday people asking and answering questions of each other - could zero-in on predictors of obesity. More interesting, the website visitors discovered some intriguing connections that experts hadn’t considered.

Josh Bongard, a UVM computer scientist and co-author on the new study, said that obesity is a very well-investigated subject and yet the public was able to find new angles.

He said that the non-expert might trigger the expert to think along a different line that they haven’t tried before, asserting that they’re democratizing investigation here.

Over a two-week period, 532 adults from various English-speaking countries visited the website and supplied their height and weight to determine their BMI.

Paul Hines, a co-author and professor in UVM’s College of Engineering and Mathematical Sciences, said that the most highly correlated question was: did your parents encourage you to clean your plate?, asserting that if their parents forced them to eat everything on their plate as a child, then they’re more likely to be overweight as an adult.
New breakthrough to design drugs from genome sequence

Researchers including an Indian-origin have developed a potentially general approach to design drugs from genome sequence.

Sai Pradeep Velagapudi, the first author of the study and a graduate student working in the Disney lab, said that with their program, they can identify compounds with high specificity, asserting that in the future, they hope they can design drug candidates for other cancers or for any pathological RNA.

Discovered only in the 1990s, microRNAs are short molecules that work within virtually all animal and plant cells.

In the new study, Matthew Disney, PhD, an associate professor at The Scripps Research Institute (TSRI), who led the study and team, describe their computational technique, which identifies optimal drug targets by mining a database of drug-RNA sequence (“motif”) interactions against thousands of cellular RNA sequences.

Using Inforna, the team identified compounds that can target microRNA-96, as well as additional compounds that target nearly two dozen other disease-associated microRNAs.The researchers showed that the drug candidate that inhibited microRNA-96 inhibited cancer cell growth. Importantly, they also showed that cells without functioning microRNA-96 were unaffected by the drug.

Disney added that the new drug candidate, which is easy to produce and cell permeable, targets microRNA-96 far more specifically than the state-of-the-art method to target RNA (using oligonucleotides) currently in use. 
Diabetics are at risk of microvascular complications

Researchers have made a breakthrough in understanding why patients with diabetes are at increased risk of microvascular complications, which develop when the body’s small blood vessels become diseased.

Investigators from Beth Israel Deaconess Medical Center (BIDMC) have discovered that a molecule called PGC-1alpha - which has previously been shown to spur the growth of blood vessels in muscle - has the opposite effect in the endothelial cells of patients with diabetes, impairing blood vessel growth and leading to dangerous vascular complications.

The new findings not only help explain the molecular mechanisms underlying microvascular disease in diabetes patients, they also suggest that because PGC-1alpha has opposing effects in different cell types, its role as a potential new therapeutic target should be pursued with caution.

With this new research, says senior author Zoltan Arany, MD, PhD, an investigator in BIDMC’s CardioVascular Institute and Associate Professor of Medicine at Harvard Medical School (HMS), it is apparent that high levels of blood glucose -- the hallmark of diabetes -- induces high levels of the PGC-1 alpha molecule in the endothelial cells lining the blood vessels. This, in turn, prevents endothelial cells from properly functioning, inhibiting blood vessel growth.

Through a series of cell culture experiments, as well as experiments in endothelial-specific genetic mouse models, the authors showed that PGC-1alpha in endothelial cells is induced by diabetes, which strongly inhibits endothelial migration and angiogenesis, and leads to vascular dysfunction.

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