Clinical Focus

• Neurogastroenterology and Gastrointestinal Motility
• Gastroparesis
• Abdominal Pain
• Chronic Pancreatitis
• Esophageal Achalasia

Administrative Appointments

• Chair, NIDDK Gastroparesis Clinical Research Consortium (2006 - present)
• Member, National Commission on Digestive Diseases (2006 - present)
• Chief, Division of Gastroenterology and Hepatology (2007 - present)

Honors and Awards

• Best Doctors in America, Best Doctors (2001-present)
• America's Top Doctors, Castle Connolly (2003-present)

Professional Education

Postdoctoral Advisees

Laren Becker , Cuiping Li

Industry Relationships

Stanford is committed to ethical and transparent interactions with our industry partners. It is our policy to disclose payments of $5,000 or more, equity valued at $5,000 or more in a publicly traded company, or any equity in a privately held company, to physicians and scientists employed by Stanford University from companies or other commercial entities with which they interact as part of their professional activities. View Full Information

Current Research Interests

THE ENTERIC NEUROMUSCULAR DISORDERS AND PAIN (END PAIN) LABORATORY AT STANFORD
The defining theme in my research is the translation of fundamental knowledge to clinical solutions in neurogastroenterology. My laboratory focuses on exploring the molecular mechanisms of disorders of the enteric nervous system (the autonomous nervous system that controls gastrointestinal physiology) and visceral sensory nerves. Within this broad area, we are pursuing several themes, outlined as follows. Our techniques encompass behavioral, electrophysiological (single nerve fiber recordings, patch clamp) as well as molecular approaches.
VISCERAL PAIN. Work in this laboratory represents a systematic approach to uncover the neurobiology of visceral pain in chronic pancreatitis, irritable bowel syndrome and functional dyspepsia and has provided a framework for designing novel treatments for pancreatic, gastric and colonic pain including targeting PAR-2, TRPV1, 5-HT4 and trkA receptors, Kv ion channels and neurotransmitters such as BDNF.
GASTROINTESTINAL DYSMOTILITY. We study models of diabetic and idiopathic gastroparesis. We are focusing on two major questions- what is the biological basis of the gender bias seen in gastroparesis (80% of patients are women) and what are the mechanisms responsible for loss of nitric oxide/nNOS dysfunction including the role of advanced glycation end products (RAGE).
NEURAL STEM CELLS. Our laboratory has been exploring the use of neural stem cells into the gut for restoring function ine cure for this condition. We have shown proof of principle that neural stem cells isolated from the brain can indeed restore function when transplanted into the gut of a mouse with genetically determined dysmotility. We are now working on manipulating a specific signaling pathway (GDNF-RET) to produce an optimal long-term outcome after transplantation. In addition we are attempting to identify the nature of the neural stem cell in the post-natal gut.
CLINICAL...

Publications

• Gastroparesis and gastroparesis-like syndrome: response to therapy and its predictors. Anaparthy R, Pehlivanov N, Grady J, Yimei H, Pasricha PJ. Dig Dis Sci. 2009; 54 (5): 1003-10
• P2X receptor-mediated visceral hyperalgesia in a rat model of chronic visceral hypersensitivity. Xu GY, Shenoy M, Winston JH, Mittal S, Pasricha PJ. Gut. 2008; 57 (9): 1230-7
• Transient receptor potential vanilloid 1 mediates hyperalgesia and is up-regulated in rats with chronic pancreatitis. Xu GY, Winston JH, Shenoy M, Yin H, Pendyala S, Pasricha PJ. Gastroenterology. 2007; 133 (4): 1282-92
• Gastroparesis and functional dyspepsia: excerpts from the AGA/ANMS meeting. Parkman HP, Camilleri M, Farrugia G, McCallum RW, Bharucha AE, Mayer EA, Tack JF, Spiller R, Horowitz M, Vinik AI, Galligan JJ, Pasricha PJ, Kuo B, Szarka LA, Marciani L, Jones K, Parrish CR, Sandroni P, Abell T, Ordog T, Hasler W, Koch KL, Sanders K, Norton NJ, Hamilton F. Neurogastroenterol Motil. 2010; 22 (2): 113-33
• Tetrahydrobiopterin (BH4), a cofactor for nNOS, restores gastric emptying and nNOS expression in female diabetic rats. Gangula PR, Mukhopadhyay S, Ravella K, Cai S, Channon KM, Garfield RE, Pasricha PJ. Am J Physiol Gastrointest Liver Physiol. 2010