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Guang-Yin Xu, M.D., Ph.D.
Assistant Professor, Division of Gastroenterology and Hepatology



Guang-Yin Xu, M.D., Ph.D.

Guang-Yin Xu, M.D., Ph.D.
Assistant Professor
Department of Internal Medicine

University of Texas Medical Branch
301 University Blvd.
Galveston, TX 77555-0655
Phone: 409.772.1501
gyxu@utmb.edu

Biosketch

Dr. Xu is an Assistant Professor with Tenured Track of the Division of Gastroenterology and Hepatology in the Department of Internal Medicine at The University of Texas Medical Branch (UTMB) in Galveston. He earned his medical degree in 1986 from Nantong University, master degree of Science in 1992 from Soochow University and a Ph. D degree in 1998 from Shanghai Institute of Neuroscience of Chinese Academy of Sciences. In 1998, he came to UTMB as a visiting scientist and postdoctoral fellow in the Department of Neuroscience and Cell Biology. In 2004, Dr. Xu was recruited as an Instructor at the Division of Gastroenterology in the Department of Internal Medicine and was promoted to Assistant Professor in 2005.

He has been funded by the NIH for research in gastrointestinal science. He has served on the editorial boards of numerous medical and scientific journals. He was a Contributing Associate Editor-in Chief of the World Journal of Gastroenterology. He has authored and co-authored over 20 peer-reviewed journal articles, book chapters, review and editorial.

Research Interests

Dr. Xu's current research areas include the neuropathogenesis of chronic visceral pain associated with inflammation and neuropathy, such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), functional dyspepsia, chronic pancreatitis and gastric ulcers. He has been focused on: (1) How neural excitability changes and what ion channels (both voltage- and ligand-gated ion channels) contribute to the chronic pain; and (2) How inflammatory/neurogenetic mediators (e.g., growth factors and H2S) modulate the ion channel activity (function and expression); and (3) how intracellular signaling transduction molecules (such as CaMKII and p38MAPK) involve in the neuronal sensitization of peripheral and central nerve systems and thus contribute to the chronic visceral pain; and (4) How electroacupuncture treatment improves pain and other symptoms of functional gastrointestinal disorders. His research efforts include in establishment of animal models, in evaluation of currents of voltage-gated ion channels and ligand-gated receptor channels, and in measurement of protein and gene expression of the same, using whole cell patch clamp techniques, advanced optical imaging system, and laser capture microdissection and RT-PCR or combinations.

His recent studies demonstrated that the excitability of organ-specific sensory neurons was greatly enhanced in the rat models of IBS and chronic pancreatitis, which may be mediated by the reduction in currents of voltage-gated potassium channels. He also demonstrated that TRPV1 and P2X receptors were sensitized in these diseases and that these key molecules may play important roles in the development and maintenance of chronic visceral hyperalgesia. It is hoped that these studies and ongoing projects will provide valuable insight into the potential therapeutic value of drugs in the management of inflammatory and neuropathic pain.

Selected Publications

  1. Xu G-Y, Wang F, Jiang XH, Tao J. Aquaporin 1, a potential therapeutic target for migraine with aura. Molecular Pain, 6:68, 2010
  2. Winston JH., Xu G-Y and Sarna, SK. Adrenergic Stimulation Mediates Visceral Hypersensitivity to Colorectal Distension following Heterotypic Chronic Stress. Gastroenterology, 138(1): 294-304, 2010
  3. Xu G-Y*, Winston JH and Chen J D Z. Electroacupuncture attenuates visceral hyperalgesia and inhibits the enhanced excitability of colon specific sensory neurons in a rat model of irritable bowel syndrome. Neurogastroenterology and Motility, 1302-e125, 2009.
  4. Xu G-Y*, Winston JH, Shenoy M, Zhou S, Chen JDZ and Pasricha PJ*. The endogenous hydrogen sulfide producing enzyme cystathionine-β synthase contributes to visceral hypersensitivity in a rat model of irritable bowel syndrome. Molecular Pain, 5:44, 2009
  5. Xu G-Y*, Shenoy M, Winston JH, Mittal, S. and Pasricha PJ. P2X receptor-mediated visceral hyperalgesia in a rat model of chronic visceral hypersensitivity. GUT, 57(9):1230-1237, 2008.
  6. Xu G-Y, Winston J H, Shenoy M, Yin H and Pasricha P J. Transient Receptor Potential Vanilloid 1 Mediates Hyperalgesia and Is Up-Regulated in Rats With Chronic Pancreatitis. Gastroenterology, 133(4):1282-1292, 2007.
  7. Xu G-Y, Winston J H, Shenoy M,.Yin H. and Pasricha PJ. Enhanced excitability and suppression of A-type potassium current of pancreas specific afferent neurons in a rat model of chronic pancreatitis. Am J Physiol-Gastrointest Liver Physiol, 291:424-431, 2006.
  8. Xu G-Y and Huang L-Y M. Calcium/calmodulin-dependent protein kinase II potentiates ATP responses by promoting trafficking of P2X receptors. Proc. Natl. Acad. Sci. U. S. A. 101(32):11868-11873, 2004.
  9. Xu Y, Gu Y-P, Xu G-Y, Li G-W, Wu P and Huang L-Y M. Adeno-associated viral transfer of opioid receptor gene to primary sensory neurons: A strategy to increase opioid antinociception. Proc. Natl. Acad. Sci. U. S. A. 100: 6204-6209, 2003.
  10. Xu G-Y and Zhao Z-Q. Cross-inhibition of mechanoreceptive inputs in peripheral inflammatory cat. Brain Research, 970 (1-2):188-194, 2003.
  11. Xu G-Y and Huang L-Y M. Peripheral inflammation sensitizes P2X-receptor mediated responses in rat dorsal root ganglion neurons. Journal of Neuroscience, 22(1):93-102, 2002.
  12. Xu G-Y and Zhao Z-Q. Changes in excitability and phenotype of substance P and its receptor in cat sensory neurons following peripheral inflammation. Brain Research, 923(1-2): 112-119, 2001.
  13. Xu G-Y, Huang L-Y M and Zhao Z-Q. Activation of silent mechanoreceptive cat C and A-delta sensory neurons and their SP expression following peripheral inflammation. Journal of Physiology (Lond.), 528:339-348, 2000.

»Pub Med Search

The department of internal medicine is developing evidence based clinical protocols which will be available in EPIC (as order sets) for use when admitting patients with these diagnoses. Their AIM is to standardize care and decrease length of stay and readmission rates.

Currently available protocols are:
  • CAP - Community Acquired Pneumonia Orderset
  • Congestive Heart Failure (CHF)
  • Chronic Obstructive Pulmonary Disease (COPD)
  • Diabetic Ketoacidosis Adult, ICU
  • General Medicine Admission
  • Immunodeficiency Flow Panel
  • MICU/CCU Admission Order Set
  • Oral Analgesic Medicaitons
  • Parenteral Opioids
  • Sepsis, Adult ICU
  • 111 - Stroke Alert
  • 112 - Stroke Activation
  • 300086 - Stroke Floor Admission
  • 3000000001 -  Stroke Critical care without tPA
  • 300088 Stroke - Transfer from Critical care to floor
  • 3004002 - Stroke Discharge

All protocols can be found in the EPIC order set section.

» For more information

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