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Roger T. Worrell, PhDAssistant Professor Department of Molecular and Cellular Physiology
Dr. Worrell’s research interest is focused on epithelial ion absorption and secretion. Increased levels of blood ammonia can cause brain malfunction, referred to as hyperammonemia-induced encephalopathy. Liver disease is often the cause of hyperammonemia, however treatment regimes are targeted to the intestine in an effort to minimize ammonia absorption. Current treatments may have uncomfortable or severe side effects. The long-term goal of Dr. Worrell’s research is to identify improved treatment options for hyperammonemia. A second focus of Dr. Worrell’s laboratory uses Real-Time RT-PCR to characterize the intestinal microbiome in wild type and various transporter null mice, which have varying degrees of intestinal inflammation. These studies aim to better understand the interaction of intestinal ion transport status with intestinal microbiome representation and subsequent associated inflammation. The long-term goal is to establish more targeted prebiotic or probiotic therapy as well as target ion transport processes to strategically manipulate the endogenous microbiome. Additionally, Dr. Worrell investigates capsaicin (the “hot” in pepper) effect on colonic Cl–/HCO3– secretion. The effects of capsaicin on gut thus far have been attributed to a neuronal action. However in colonic secretory cells, capsaicin acts directly and results in an attenuation of subsequent cAMP-stimulated Cl- secretion. Dr. Worrell seeks to determine the physiological mechanism and relevance of this direct capsaicin effect on epithelial cells.
Dr. Worrell collaborates with Dr. Montrose in the projects related to the grant listed above, with Dr. Shull examining transgenic mouse models for epithelial ion transport, and with Dr. Zavros examining barrier function integrity. Anticipated Core use: Integrative Morphology Core, Gene and Protein Expression Core.
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Intracellular pH (pHi) response to ischemia with subsequent reperfusion (IR). B: time course of 1 representative experiment, showing pHi in response to short ischemia and reperfusion. C: time course of pHi after long ischemia (~40 min) and reperfusion. During reperfusion, pHi was restored in one-third of the villi (open circle represented by villus 2), whereas the other villi remained acidified (closed triangle represented by villus 1). Figure from Am J Physiol Gastrointest Liver Physiol, 2009;297:G187-196.
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