The Research Base of the CURE: Digestive Diseases Research Core Center (CURE:DDRCC) is composed of a cohesive group of physicians and basic scientists with strong independent peer-reviewed grant-supported research programs in the biology of the gut, with special emphasis on regulation of mucosal cell function, enteric neuroscience and signal transduction mechanisms. CURE, created in 1974, has grown and evolved into a broadly based gastrointestinal research organization with multiple affiliations, principally the VA and UCLA. Since 1989, a fundamental component of CURE has been the NIDDK-supported CURE: DDRCC. The research emphasis of the Center is acquisition of new knowledge about cellular, molecular and physiological processes that control the function of the digestive system and translation of this knowledge into development of therapy for patients with digestive diseases. The research programs of the CURE: DDRCC members can be broadly divided into four major areas: (1) gastroduodenal mucosal physiology and disease;(2) intestinal and pancreatic physiology and disease;(3) neural regulation of gastroenteric function and neuroenteric disease;and (4) mechanism of action of gastrointestinal peptides, including receptor regulation, signal transduction and control of cell proliferation. The Biomedical Research Cores outlined in this proposal provide ready access to technologies, and to clinical and biological materials that are essential to the programs of center members. These Cores provide access to modern cellular imaging to study signaling proteins and their functions, animal models for studying physiology and pathophysiology, molecular vectors to express a wide variety of proteins and access to a broad range of techniques and patients for clinical studies. The Administrative Core provides a wide range of administrative support for members and for center activities, including a comprehensive and multidisciplinary enrichment program. The Pilot and Feasibility Study and Named New Investigator programs have provided a successful mechanism for promoting the development of new programs in digestive diseases-related research, primarily by young investigators. The Center provides an optimal environment for cooperation and collaboration among its investigators, who have had a major impact on digestive disease research over the past three decades and promise to have an even larger impact with continued support from the Center.
CURE: DDRCC is located at both the VA Greater Los Angeles Heathcare System (VAGLAHS) and at the David Geffen School of Medicine at UCLA, Los Angeles, California. The Administrative Core, Human Studies Core, Animal Models Core and a substantial portion of the Morphology and Celllmaging Core of the CURE: DDRCC are located in Building 115 and in the adjacent Building 113 at the VAGLAHS. The laboratories of many members and associate members are housed here. CURE: DDRCC members in the Departments of Medicine, Neurobiology, Pathology, Pediatrics, Physiology and Surgery are also located on the UCLA campus. Part of the Morphology and Celllmaging Core and Molecular Vectors and Peptidomics Core are housed in laboratories at Warren Hall, the MacDonald Research Laboratories and the Center of Health Science on the UCLA campus.
|Chang, Hui-Hua; Moro, Aune; Chou, Caroline Ei Ne et al. (2018) Metformin Decreases the Incidence of Pancreatic Ductal Adenocarcinoma Promoted by Diet-induced Obesity in the Conditional KrasG12D Mouse Model. Sci Rep 8:5899|
|Pan, David Z; Garske, Kristina M; Alvarez, Marcus et al. (2018) Integration of human adipocyte chromosomal interactions with adipose gene expression prioritizes obesity-related genes from GWAS. Nat Commun 9:1512|
|Fang, Kai; Law, Ivy Ka Man; Padua, David et al. (2018) MicroRNA-31-3p Is Involved in Substance P (SP)-Associated Inflammation in Human Colonic Epithelial Cells and Experimental Colitis. Am J Pathol 188:586-599|
|Yakabi, Seiichi; Wang, Lixin; Karasawa, Hiroshi et al. (2018) VIP is involved in peripheral CRF-induced stimulation of propulsive colonic motor function and diarrhea in male rats. Am J Physiol Gastrointest Liver Physiol 314:G610-G622|
|Henström, Maria; Diekmann, Lena; Bonfiglio, Ferdinando et al. (2018) Functional variants in the sucrase-isomaltase gene associate with increased risk of irritable bowel syndrome. Gut 67:263-270|
|Soroosh, Artin; Koutsioumpa, Marina; Pothoulakis, Charalabos et al. (2018) Functional role and therapeutic targeting of microRNAs in inflammatory bowel disease. Am J Physiol Gastrointest Liver Physiol 314:G256-G262|
|Aschemeyer, Sharraya; Qiao, Bo; Stefanova, Deborah et al. (2018) Structure-function analysis of ferroportin defines the binding site and an alternative mechanism of action of hepcidin. Blood 131:899-910|
|Kaji, I; Akiba, Y; Furuyama, T et al. (2018) Free fatty acid receptor 3 activation suppresses neurogenic motility in rat proximal colon. Neurogastroenterol Motil 30:|
|Kim, Paul H; Luu, Jennings; Heizer, Patrick et al. (2018) Disrupting the LINC complex in smooth muscle cells reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome. Sci Transl Med 10:|
|Dong, Tien S; Aby, Elizabeth S; Benhammou, Jihane N et al. (2018) Metabolic syndrome does not affect sustained virologic response of direct-acting antivirals while hepatitis C clearance improves hemoglobin A1c. World J Hepatol 10:612-621|
Showing the most recent 10 out of 1097 publications