Syndicate content

Archive - Sep 13, 2013


New "Urzyme" Findings Challenge “RNA World” Assumptions on Origin of Life

Before there was life on Earth, there were molecules. A primordial soup. At some point a few specialized molecules began replicating. This self-replication, scientists agree, kick-started a biochemical process that would lead to the first organisms. But exactly how that happened — how those molecules began replicating — has been one of science's enduring mysteries. Now, research from University of North Carolina (UNC) School of Medicine biochemist Charles Carter, Ph.D., and colleagues, appearing in the September 13, 2013 issue of the Journal of Biological Chemistry, offers an intriguing new view on how life began. The paper was selected as one of the JBC’s papers of the week. Dr. Carter's work is based on lab experiments during which his team recreated ancient protein enzymes that likely played a vital role in helping create life on Earth. Dr. Carter's finding flies in the face of the widely-held theory that ribonucleic acid (RNA) self-replicated without the aid of simple proteins and eventually led to life as we know it. In the early 1980s, researchers found that ribozymes — RNA enzymes — act as catalysts. It was evidence that RNA can be both the blueprints and the chemical catalysts that put those blueprints into action. This finding led to the "RNA World" hypothesis, which posits that RNA alone triggered the rise of life from a sea of molecules. But for the hypothesis to be correct, ancient RNA catalysts would have had to copy multiple sets of RNA blueprints nearly as accurately as do modern-day enzymes. That's a hard sell; scientists calculate that it would take much longer than the age of the universe for randomly generated RNA molecules to evolve sufficiently to achieve the modern level of sophistication.

New Research Points to Promising Treatment for Macular Degeneration

Researchers at the University of North Carolina (UNC) School of Medicine, together with colleaguesat other institutions, have published new findings in the hunt for a better treatment for macular degeneration. In studies using mice, a class of drugs known as MDM2 inhibitors proved highly effective at causing the regression of the abnormal blood vessels responsible for the vision loss associated with the disease. “We believe we may have found an optimized treatment for macular degeneration,” said senior study author Sai Chavala, M.D., director of the Laboratory for Retinal Rehabilitation and assistant professor of Ophthalmology and Cell Biology & Physiology at the UNC School of Medicine. “Our hope is that MDM2 inhibitors would reduce the treatment burden on both patients and physicians.” The research was published online in an open-access article on September 9, 2013 in the Journal of Clinical Investigation. As many as 11 million Americans have some form of macular degeneration, which is the most common cause of central vision loss in the western world. Those with the disease find many daily activities such as driving, reading, and watching TV increasingly difficult. Currently, the best available treatment for macular degeneration is an antibody called anti-VEGF that is injected into the eye. Patients must visit their doctor for a new injection every 4-8 weeks, adding up to significant time and cost. “The idea is we’d like to have a long-lasting treatment so patients wouldn’t have to receive as many injections,” said Dr. Chavala. “That would reduce their overall risk of eye infections, and also potentially lower the economic burden of this condition by reducing treatment costs.” Dr. Chavala practices at the Kittner Eye Center at UNC Health Care in Chapel Hill and New Bern.