Digestive Disease Research Center Research Articles

Transplantation of allogeneic bone marrow mesenchymal stromal cell-derived hepatocyte-like cells in homozygous familial hypercholesterolemia

These authors share senior authorship.Correspondence: Dr Hossein Baharvand, Department of Stem Cells, Cell Science Research Center, Royan Institute, ACECR, PO Box 19395–4644, Tehran, Iran. E-mail: Baharvand@RoyanInstitute.org. Professor Reza Marekzadeh, Digestive Disease Research Center, Shariati Hosp ital, North Kargar Ave, 14117 Tehran, Iran. E-mail: malek@ams.ac.ir

A Tribute to Gary M. Green (1940-2008)

From the *Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA; and †Department of Medicine, Duke University Medical Center, Durham, NC. Reprints: Joseph R. Reeve Jr, PhD, CURE: Digestive Diseases Research Center, Bldg 115 Room 117, VA Greater Los Angeles Healthcare System, 11301 Wilshire Blvd, Los Angeles, CA 90073 (e-mail: [email protected]). This article was supported by the following organizations: National Institute of Diabetes and Digestive and Kidney Diseases Grant DK-RO1-33580, CURE Digestive Diseases Research Center grants DK-41301 (J.R.R., Jr) and DK-38626 (R.A.L.), and by the Department of Veterans Affairs Research Service.

Nine New Vice-Chairs Elected to AGA Institute Council

Nine of the 12 sections of the AGA Institute Council have elected new members who will serve 2-year terms as vice-chairs of their respective sections. The 9 new vice-chairs are: Dr Prateek Sharma, University of Kansas Medical Center (Esophageal, Gastric, and Duodenal Disorders); Dr Daniel C. Chung, Harvard Medical School (Gastrointestinal Oncology); Dr Carlo Di Lorenzo, Ohio State University (Growth, Development, and Aging); Dr James R. Goldenring, Vanderbilt University Medical Center (Hormones, Transmitters, Growth Factors, and Their Receptors); Dr Jerrold R. Turner, University of Chicago (Intestinal Disorders); Dr Gregory J. Gores, Mayo Graduate School of Medicine (Liver and Biliary); Dr Kelly A. Tappenden, University of Illinois (Nutrition and Obesity); Dr Henry P. Parkman Temple University School of Medicine (Neurogastroenterology and Motility); and Dr Chris E. Forsmark, University of Florida College of Medicine (Pancreatic Disorders). “These are 4-year terms, 2 years as vice-chair, then 2 years as chair of the section, extending from DDW to DDW. They are the only positions truly elected directly by AGA members,” says AGA Council chair Dr D. Brent Polk, Vanderbilt Dean's Professor of Pediatrics. Polk explains that the council is responsible for 3 broad areas: (1) creating and implementing AGA Institute's educational program at DDW, (2) creating and conducting topical scientific symposia and clinical education programs throughout the year, and (3) developing clinical recommendations and other resources in targeted areas of practice.” A Division Director of Pediatric Gastroenterology, Hepatology, and Nutrition, and Director of the Vanderbilt Digestive Diseases Research Center, Polk says the activities related to DDW comprise the majority of the council's work every year. After the sections' individual business meetings held during DDW, each section acts on suggestions from their members about scientific programming and the abstract review process for the year leading up to the next DDW. These activities include revising/updating section descriptors for abstract submission and selecting abstract review committee members and chairs for each descriptor within the section. Collectively, these committees are responsible for reviewing the 4,500 abstracts submitted to the AGA Institute each December for presentation at DDW. “My goals for the council are to be responsive to the needs of the AGA membership, to continue to build international representation, and for our hard work and dedication to continue to be displayed at DDW each May,” says Polk. “As chair of this group, I am very grateful for the tremendous efforts of the individuals serving on AGA Institute Council and for the AGA Institute staff's support for the council's many activities.” Further details can be found at www.gastro.org.

Ligand-Induced 5-HT3 Receptor Internalization in Enteric Neurons in Rat Ileum

Release of 5-hydroxytryptamine (5-HT) from mucosal enterochromaffin cells and activation of 5-HT(3) receptors (5-HT(3)Rs) on neurons in the gut wall is important in the response of the gut to the luminal environment. Intestinal inflammation is associated with increased levels of mucosal 5-HT. The aims of the study were to determine the following: (1) if 5-HT(3)R undergoes ligand-induced internalization in myenteric neurons, and (2) the effect of long-term increase of mucosal 5-HT on 5-HT(3)Rs. Acute effects of exogenous 5-HT or endogenous release of 5-HT by luminal glucose on cellular localization of 5-HT(3)Rs was determined by immunohistochemistry and confocal microscopy. Treatment with the serotonin re-uptake inhibitor, fluoxetine, for 6 days (20 mg/kg daily orally) was used to increase mucosal 5-HT chronically in rats. Net ileal fluid movement was measured in anesthetized rats by the weight change of a 2.5% agarose cylinder. Acute increases in 5-HT induced by exogenous or endogenous 5-HT decreased 5-HT(3)R immunoreactivity at the neuronal cell membrane by 70% and 60%, respectively. Chronic fluoxetine treatment increased mucosal levels of 5-HT and decreased membrane 5-HT(3)R immunoreactivity by 27%. Net fluid absorption was decreased by a 5-HT(3)R agonist or by luminal glucose; this was attenuated 88% and 99%, respectively, by fluoxetine treatment. Long-term increase in 5-HT in the intestinal mucosa results in increased 5-HT(3)R internalization in myenteric neurons. Chronic changes in mucosal 5-HT may alter gastrointestinal secretory and motor function via ongoing loss of receptor from neuronal membrane, causing a mismatch between luminal content and absorption.

Richard M. Peek, Jr, MD

Dr Peek received his BS degree cum laude from Davidson College in 1984. Later he attended the University of North Carolina at Chapel Hill where he received his MD degree in 1988. After Internal Medicine training and Chief Residency at the University of Alabama School of Medicine, he completed a fellowship in Gastroenterology at Vanderbilt University School of Medicine in 1995. In 1996, he became an Assistant Professor at Vanderbilt, where he is now the Mina Cobb Wallace Professor of Medicine and Cancer Biology and Director of the Division of Gastroenterology, Hepatology, and Nutrition. Dr. Peek is also co-Director of the Vanderbilt Digestive Diseases Research Center at Vanderbilt. Dr. Peek has received several awards and honors and is a member of numerous professional societies. He is the recipient of the Grant Liddle Scholarship for Excellence in Clinical Research (1994), the Glaxo Institute of Digestive Health Basic Research Award (1995), the Miles and Shirley Fiterman Foundation Basic Research Award (2001), the Young Investigator Award from the American Gastroenterological Association (2002), and in 2003 he was elected to the American Society for Clinical Investigation. A charter member of the Gastrointestinal Mucosal Pathobiology Study Section at NIDDK, Dr. Peek served as co-chair of the Biology Section for the National Cancer Institute-sponsored Stomach/Esophageal Cancers Progress Review Group in 2002, and was an invited participant in the NCI-sponsored Inflammation and Cancer Think Tank Meeting June 2–4, 2004, which was organized to identify research advances and opportunities in the study and clinical applications of inflammation on cancer initiation, progression, and metastasis. He also serves as a Section Editor for Gastroenterology and is on the Editorial board of the American Journal of Physiology: Gastrointestinal and Liver Physiology. Dr. Peek’s research efforts are grounded in understanding the molecular mechanisms through which H pylori enhances the risk for gastric cancer using both in vitro and in vivo models.

Ca2+ and rho signaling pathways: Two paths to hepatic stellate cell contraction

HepatologyVolume 33, Issue 4 p. 1007-1008 EditorialFree Access Ca2+ and rho signaling pathways: Two paths to hepatic stellate cell contraction Hal F. Yee Jr. Jr., M.D., Corresponding Author Hal F. Yee Jr. Jr., M.D. M.D., Ph.D. From the Departments of Medicine and Physiology and CURE Digestive Diseases Research Center, UCLA School of Medicine, Los Angeles, CAPh.D., 675 Charles E. Young Drive South, 1-519 MacDonald Research Laboratory, UCLA School of Medicine, Los Angeles, CA 90095. E-mail: hyee@mednet.ucla.edu; fax: 310-206-7333.===Search for more papers by this author Hal F. Yee Jr. Jr., M.D., Corresponding Author Hal F. Yee Jr. Jr., M.D. M.D., Ph.D. From the Departments of Medicine and Physiology and CURE Digestive Diseases Research Center, UCLA School of Medicine, Los Angeles, CAPh.D., 675 Charles E. Young Drive South, 1-519 MacDonald Research Laboratory, UCLA School of Medicine, Los Angeles, CA 90095. E-mail: hyee@mednet.ucla.edu; fax: 310-206-7333.===Search for more papers by this author First published: 30 December 2003 https://doi.org/10.1053/jhep.2001.23901Citations: 27AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume33, Issue4April 2001Pages 1007-1008 ReferencesRelatedInformation