Abstract

CURE has always strived to be on the forefront of gastrointestinal research, and it has been uniquely able to translate basic cellular advances into human studies in patients with gastrointestinal diseases. The importance and significance of Gl disorders is highlighted by their national impact on quality of life and demand for health care services. In this context, the Human Studies Core is part of the CURE: Digestive Disease Research Core Center (CURE: DDRCC) since it was created in 1989. The mission of the Human Studies Core of the CURE: Digestive Disease Research Core Center (CURE: DDRCC) is to provide shared resources, personnel, services, education, and consultation to CURE: DDRCC investigators, trainees, and their collaborators for the study of patients with selected digestive disorders. The primary objective of this Core is to facilitate collaboration, education about, and performance of Gl clinical, human physiological studies, translational, and health outcomes studies in selected digestive disorders.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
5P30DK041301-24
Application #
8425029
Study Section
Special Emphasis Panel (ZDK1-GRB-8)
Project Start
Project End
Budget Start
2012-12-01
Budget End
2013-11-30
Support Year
24
Fiscal Year
2013
Total Cost
$92,993
Indirect Cost
$19,189

  Institution

Name
University of California Los Angeles
Department
Type
DUNS #
092530369
City
Los Angeles
State
CA
Country
United States
Zip Code
90095

  Publications

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
Videlock, Elizabeth J; Mahurkar-Joshi, Swapna; Hoffman, Jill M et al. (2018) Sigmoid colon mucosal gene expression supports alterations of neuronal signaling in irritable bowel syndrome with constipation. Am J Physiol Gastrointest Liver Physiol 315:G140-G157
Chen, Natalie Y; Kim, Paul; Weston, Thomas A et al. (2018) Fibroblasts lacking nuclear lamins do not have nuclear blebs or protrusions but nevertheless have frequent nuclear membrane ruptures. Proc Natl Acad Sci U S A 115:10100-10105
Larauche, Muriel; Moussaoui, Nabila; Biraud, Mandy et al. (2018) Brain corticotropin-releasing factor signaling: Involvement in acute stress-induced visceral analgesia in male rats. Neurogastroenterol Motil :e13489
Zhou, Haoming; Wang, Han; Ni, Ming et al. (2018) Glycogen synthase kinase 3? promotes liver innate immune activation by restraining AMP-activated protein kinase activation. J Hepatol 69:99-109

Showing the most recent 10 out of 1097 publications