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Archive - Oct 13, 2011

Black Death Genome Reconstructed; Likely Ancestor of All Modern Plague

An international team, led by researchers at McMaster University in Canada and the University of Tubingen in Germany, has sequenced the entire genome of the organism causing the Black Death, one of the most devastating epidemics in human history. This marks the first time that scientists have been able to draft a reconstructed genome of any ancient pathogen, and it should allow researchers to track changes in the pathogen’s evolution and virulence over time. This new work, published online on October 12, 2011 in Nature, could lead to a better understanding of modern infectious diseases. Geneticists Hendrik Poinar and Kirsten Bos of McMaster University and Johannes Krause and Verena Schuenemann of the University of Tubingen collaborated with Brian Golding and David Earn of McMaster University, Hernan A. Burbano and Matthias Meyer of the Max Planck Institute for Evolutionary Anthropology, and Sharon DeWitte of the University of South Carolina, among others. In a separate study published recently, the team described a novel method to extract tiny degraded DNA fragments of the causative agent of the Black Death, and showed that a specific variant of the Yersinia pestis bacterium was responsible for the plague that killed 50 million Europeans between 1347 and 1351. After this success, the next major step was to “capture” and sequence the entire bacterial genome, explains Dr. Poinar, associate professor of anthropology and director of the McMaster Ancient DNA Centre and an investigator with the Michael G. DeGroote Institute of Infectious Disease Research, also at McMaster University. “The genomic data show that this bacterial strain, or variant, is the ancestor of all modern plagues we have today worldwide. Every outbreak across the globe today stems from a descendant of the medieval plague,” he says.

Schizophrenia Genetics Linked to Disruption in How Brain Processes Sound

Recent studies have identified many genes that may put people at risk for schizophrenia. But what links genetic differences to changes in altered brain activity in schizophrenia is not clear. Now, three laboratories at the Perelman School of Medicine at the University of Pennsylvania have come together, using electrophysiological, anatomical, and immunohistochemical approaches - along with a unique high-speed imaging technique - to understand how schizophrenia works at the cellular level, especially in identifying how changes in the interaction between different types of nerve cells lead to symptoms of the disease. The findings were reported online on October 3, 2011 in the Proceedings of the National Academy of Sciences. "Our work provides a model linking genetic risk factors for schizophrenia to a functional disruption in how the brain responds to sound, by identifying reduced activity in special nerve cells that are designed to make other cells in the brain work together at a very fast pace," explains lead author Dr. Gregory Carlson, assistant professor of Neuroscience in Psychiatry. "We know that in schizophrenia this ability is reduced, and now, knowing more about why this happens may help explain how loss of a protein called dysbindin leads to some symptoms of schizophrenia." Previous genetic studies had found that some different forms of the gene for dysbindin were found in people with schizophrenia. Most importantly, a prior finding at Penn showed that the dysbindin protein is reduced in a majority of schizophrenia patients, suggesting it is involved in a common cause of the disease. For the current PNAS study, Dr. Carlson, Dr. Steven J. Siegel, associate professor of Psychiatry, director of the Translational Neuroscience Program; and Dr. Steven E.

Breakthrough Approach to Allergy Treatment

Researchers from the University of Notre Dame and Harvard University have announced a breakthrough approach to allergy treatment that inhibits food allergies, drug allergies, and asthmatic reactions without suppressing a sufferer's entire immunological system. The therapy centers on a special molecule the researchers designed, a heterobivalent ligand (HBL), which when introduced into a person's bloodstream can, in essence, out-compete allergens like egg or peanut proteins in the race to attach to mast cells, a type of white blood cell that is the source of type-I hypersensitivity (that is, allergy). The new work is published as the cover article of the September 23, 2011 issue of Chemistry & Biology. "Unlike most current treatments, this approach prevents allergic reactions from occurring in the first place," says Dr. Basar Bilgicer, senior author of the paper and assistant professor of Chemical and Biomolecular Engineering and Chemistry and Biochemistry and principal investigator in Notre Dame's Advanced Diagnostics & Therapeutics initiative. Michael Handlogten, lead author on the paper and a graduate student in Dr. Bilgicer's group, explained that among the various chemical functionalities he analyzed to be used as the scaffold in HBL synthesis, ethylene glycol, an FDA-approved molecule, proved to be the most promising. Mast cells are part of the human body's defense against parasites (such as tapeworms), and, when working normally, they are attracted to, attach to, and annihilate these pathogens. But type-I hypersensitivity occurs when the cells react to non-threatening substances. More common allergies are due to ambient stimulants, and an allergic response may range from a mild itch to life-threatening anaphylactic shock. Dr.