Syndicate content

Archive - Nov 10, 2017


Distinct Molecular Signatures (miRNAs) Identified in Spinal Fluid of Patients with Gulf War Illness and Chronic Fatigue Syndrome

Researchers at Georgetown University Medical Center (GUMC) have found distinct molecular signatures in two brain disorders long thought to be psychological in origin -- chronic fatigue syndrome (CFS) and Gulf War Illness (GWI). In addition, the work supports a previous observation by GUMC investigators of two variants of GWI. The disorders share commonalities, such as pain, fatigue, cognitive dysfunction, and exhaustion after exercise. The study, published online on November 10, 2017 in Scientific Reports, lays groundwork needed to understand these disorders in order to diagnose and treat them effectively, says senior investigator James N. Baraniuk, MD, Professor of Medicine at Georgetown University School of Medicine. Narayan Shivapurkar, PhD, Assistant Professor of Oncology at the medical school worked with Dr. Baraniuk on the research. Their open-access article is titled “Exercise-Induced Changes in Cerebrospinal Fluid miRNAs in Gulf War Illness, Chronic Fatigue Syndrome and Sedentary Control Subjects.” The changes in brain chemistry -- observed in levels of miRNAs that turn protein production on or off -- were seen 24 hours after subjects rode a stationary bike for 25 minutes. "We clearly see three different patterns in the brain's production of these molecules in the CFS group and the two GWI phenotypes," says Dr. Baraniuk. "This news will be well received by patients who suffer from these disorders who are misdiagnosed and instead may be treated for depression or other mental disorders." Chronic fatigue syndrome (also called myalgic encephalomyelitis, ME/CFS) affects between 836,000 and 2.5 million Americans, according to a National Academy of Medicine report.

How “Flipped” Gene Helped Butterflies Evolve Mimicry: Rare Genetic Inversion 2 Million Years Ago Helped Asian Swallowtail Butterflies Develop Different Wing Patterns to Disguise Themselves from Predators

Female swallowtail butterflies do something a lot of butterflies do to survive: they mimic wing patterns, shapes and colors of other species that are toxic to predators. Some - but not all - swallowtail species have evolved several different forms of this trait. But what kind of genetic changes led to these various disguises, and why would some species maintain an undisguised form when mimicry provides an obvious evolutionary advantage? In a new study published online on November 7, 2017 in Nature Communications, scientists from the University of Chicago analyzed genetic data from a group of swallowtail species to find out when and how mimicry first evolved, and what has been driving those changes since then. The open-access article is titled “Tracing the Origin and Evolution of Supergene Mimicry in Butterflies.” It's a story that started around two million years ago, but instead of steady, progressive changes, one chance genetic switch helped create the first swallowtail mimics. And it has stuck around ever since. "In butterflies with one color pattern, we have a gene in a normal orientation on the chromosome. In the butterflies with the unusual, alternate color pattern, that gene was spliced out, flipped, and then spliced back into the chromosome at some point," said Marcus Kronforst, PhD, Associate Professor of Ecology and Evolution at U Chicago and the senior author of the study. "That flip, or inversion, keeps the two genes from recombining if those two different kinds of butterflies mate, so they've kept both copies of the gene over evolutionary time, because they split from their common ancestor two million years ago," Dr. Kronforst said. For a long time, scientists thought that butterfly mimicry was controlled by "supergenes," groups of several tightly linked genes that were always inherited as a group.

Former NFL Football Players Twice As Likely to Have Enlarged Aortas; Health Risk Currently Unknown

Former NFL players were more likely to have enlarged aortas, but further study is needed to determine whether that puts them at greater risk for life-threatening aneurysms, researchers found. The former National Football League players were twice as likely to have enlarged aortas as those in a control group, even after adjusting for their typically larger size and other factors, said researchers with the Dallas Heart Study at UT Southwestern Medical Center, from which the control group was drawn. “Whether that translates to the same risk for these former elite athletes as a dilated, or enlarged, aorta does for the general population is unclear,” said cardiologist Dr. Parag Joshi, Assistant Professor of Internal Medicine and one of the study’s authors. “Is this a normal adaptation from having trained at the elite level throughout their youth, or is this a bad adaptation that puts them more at risk for problems?” Former linemen – players who tend to be larger and engage in more strength training than non-linemen – were more likely to cross the threshold into the enlarged aorta range, suggesting that increased aortic diameter is an adaptation to the demands placed on a player’s heart during his career, said co-author and fellow cardiologist Dr. James de Lemos, Professor of Internal Medicine and Medical Director for the Dallas Heart Study. Nearly 30 percent of the former NFL players studied had enlarged aortas compared with less than 9 percent in the comparison group from the Dallas Heart Study, a one-of-a-kind population-based study to identify new genetic, protein, and imaging biomarkers that can detect cardiovascular disease at its earliest stages, when prevention is most effective.