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Four GSBS Students to Receive Presidents’ Research Award

January 10, 2013

Tracey Barnett


It’s a new year and with it The University of Texas Graduate School of Biomedical Sciences is proud to announce the newest group of Presidents’ Research Scholarship Awardees who will be honored at a luncheon on January 24 at the Mitchell Building. 

The awards are sponsored by the presidents of UTHealth and UT MD Anderson Cancer Center and provide a one-year scholarship in the amount of $5,000 which is awarded to outstanding students who have advanced to Ph.D. candidacy and who have achieved distinction in research while a GSBS student. 

This year’s awardees are: 

Deepavali Chakravarti: (Advisor: Elsa Flores, Ph.D.) Roles for p63 in the microRNA Biogenesis Pathway: Effects on Metastasis and Pluripotency: MicroRNAs have been shown to play roles in various biological processes such the formation of tumors, the spread of cancer cells through the body and the potential for stem cells to differentiate cellular layers also known as pluripotency. Interestingly, my thesis work has demonstrated roles for p63, a gene that has a complex structure and multiple isoforms in the upstream regulation of microRNA biogenesis, or the production of new living organisms. The p63 gene can be classified into two categories: TAp63 isoforms, which have been demonstrated to have tumor suppressive activities in vitro; and ΔNp63 isoforms, which has been shown to have tumor causing properties in vitro. Through my work, I found that TAp63 suppresses metastasis and ΔNp63 transcriptionally activates DGCR8 by binding to its promoter, resulting in a miRNA profile that is critical to reprogram cells to pluripotency.  This work is significant because it demonstrates that iPS (induced pluripotent stem) cells can be generated by the deletion of a single gene. 

Christopher Conner: (Advisor: Nitin Tandon, M.D.) Spatio-temporal Dissociations of Auditory and Visual Naming Networks in Human CortexEpilepsy is a debilitating disorder with some sufferers seeking surgical treatment for a possible cure, but surgery runs the risk of disrupting normal brain function. Therefore, there is a constant drive for new, more accurate mapping of brain activity so that critical functions, such as language, can be preserved. Using neuroimaging and electrophysiology recordings from epilepsy patients, my research investigates the existence of separate networks for semantic processing of different sensory channels and parts of speech that converge before linguistic development. 

Jessica Galloway-Pena: (Advisor: Barbara Murray, M.D.) Defining the Role of WxL Proteins in Enterococcus faecium: Treatment of Enterococcus faecalis infections have become particularly difficult and costly because of multiple intrinsic and acquired resistances to commonly used antibiotics; therefore, the design of novel treatment strategies is pertinent. Recently, researchers have indicated the probability of a new cell wall binding motif, designated the WxL domain. Proteins containing this domain have been implicated as important in peritonitis infections caused by E. faecalis. In this study, I will determine if WxL proteins are antigenic during natural infection and if antibodies to the WxL proteins confer a protective role. 

Callie Kwartler: (Advisor: Dianna Milewicz, M.D., Ph.D.) The Myh11 R247C Rare Variant Alters Smooth Muscle Cell Phenotype and Increases Risk of Aortic Disease:  Thoracic aortic aneurysms and dissections (TAAD) are life-threatening cardiovascular conditions that affect more than 30,000 Americans each year. People predisposed to this condition have mutations in a number of genes, including MYH11, a smooth muscle myosin – a motor protein that plays a role in muscle contraction. Based on the identified mutations in MYH11 and other contractile genes in patients with inherited forms of TAAD, my research suggests a common pathogenic process for TAAD originating from disrupted contractility of the smooth muscle cells in the vessel wall. The goal of this study is to determine if and how a rare variant in MYH11 could increase risk and contribute to the pathogenesis of vascular disease.