Javascript must be enabled to use this form.

View Profile	Home Browse Faculty Facility Research Consortia Training Grants Courses Search Support About rSp Help and FAQ's Contact Us	GCC Home
Faculty Profile Last Modified Time: 09:33:11 AM Mon, 23 Jul 2018   Contact Information John H. Winston Associated Profiles  Associate Professor, Gastroenterology and Hepatology, UT Medical Branch at Galveston     jhwinsto@utmb.edu    Web Link    Colon, Hypersensitivity, Inflammation, Spinal Ganglia, Irritable Bowel Syndrome, Nerve Growth Factor, Neurons, Ulcerative Colitis    Associated Profiles Professional Preparation Research and Expertise Affiliations Appointments  Professional Preparation  Degree Major Institution Year  PhD   UT Southwestern Medical School 1990  BS   Louisiana State University 1983  Research and Expertise Research Interests   Although pain is a cardinal feature of pancreatitis, the underlying biological mechanisms are poorly understood. The vanilloid receptor (TRPV1) is an ion channel that is activated by heat and by various inflammatory mediators and functions as a molecular transducer of noxious stimuli into nerve impulses in primary sensory afferent neurons. This channel is expressed on 80% of pancreatic afferent neurons. Capsaicin activated current is increased 2 to 4 fold in rats with acute necrotizing pancreatitis, but there is no increase in TRPV1 expression. Recent findings indicate that increased production of nerve growth factor in pancreatitis may be linked to increased TRPV1 activity. Further experiments are in progress to define the molecular mechanisms responsible for this increase in TRPV1 function in pancreatitis. Additional studies address the efficacy of various TRPV1 antagonists in the treatment of pain and inflammation in pancreatitis. Irritable Bowel Syndrome (IBS) is a functional bowel disorder of unknown etiology defined by symptoms including abdominal pain and alterations in bowel habits that occur in the absence of detectable ongoing organic disease. Human studies demonstrate that IBS is associated with a state of chronic visceral hypersensitivity suggesting that processing of visceral sensory information is altered. However, little is known about changes in the processing of visceral information occur. Our long-term objective is to identify key molecular events responsible for the perpetuation of the sensitized state and provide targets for new pharmacological approaches to the treatment of this syndrome. To attain this goal, we have developed a rat model of chronic visceral hyperalgesia produced by irritation of the colon of neonatal rats. We have identified gene expression profiles in the colon, sensory neurons and spinal chord associated with chronic visceral hyperalgesia. There are an ongoing collaborative studies with clinicians to determine whether any of the genes identified in the colon can serve as biological marker (s) of post-infectious IBS. Gene expression profiles in colon show alterations in genes that regulate smooth muscle contractility; studies are in progress to determine whether there is an increase in smooth muscle contractility in this model.  Publications/Creative Works Click here to search for this faculty member's publications on PubMed.  Affiliations  Research Consortia Gulf Coast Consortium for Translational Pain Research  Appointments Title Department / School Institution Associate Professor Gastroenterology and Hepatology UT Medical Branch at Galveston

powering - The Partnership
Important Disclaimer: The responsibility for the accuracy of the information contained on these pages lies with the authors and user providing such information.