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http://dx.doi.org/10.1016/j.jcjo.2021.03.010 | DOI Listing |
JCI Insight
December 2024
Department of Internal Medicine, University of Michigan, Ann Arbor, United States of America.
Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile duct (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, including WNT signaling, are implicated in regulating injury responses in many tissues, including the liver.
View Article and Find Full Text PDFCan J Ophthalmol
December 2021
Carver College of Medicine, University of Iowa, Iowa City, Iowa. Electronic address:
Am J Gastroenterol
December 2020
Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, P.R. China.
Surg Case Rep
August 2018
Department of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Nippon Medical School, 1-1-5 Sendagi, Bunkyo, Tokyo, 113-8603, Japan.
Background: Self-expandable metallic stent placement is a widely performed palliative procedure or bridge to surgery for obstructive colorectal cancer. However, the feasibility of this procedure for large bowel obstruction induced by effective neoadjuvant therapy is unclear.
Case Presentation: We herein report three such cases involving a 61-year-old man who underwent neoadjuvant chemoradiotherapy for lower rectal cancer, a 56-year-old woman who underwent neoadjuvant chemotherapy for lower rectal cancer, and a 63-year-old woman who underwent neoadjuvant chemotherapy for lower rectal cancer.
Peptides
July 2012
Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, China.
The objective was to determine whether protective effects of JBP485 on biliary obstruction induced by alpha-naphthylisothiocyanate (ANIT) are mediated by the organic anion transporters Oat1, Oat3 and the multidrug resistance-associated protein Mrp2. The ANIT-induced increases in bilirubin (BIL), alanine aminotransferase (ALT) and aspartate transaminase (AST) in rat serum were inhibited significantly by oral administration of JBP485. The plasma concentration of JBP485 which is the substrate of Oat1 and Oat3 determined by LC-MS/MS was markedly increased after intravenous administration in ANIT-treated rats, whereas cumulative urinary excretion of JBP485 in vivo and the uptake of JBP485 in kidney slices were decreased remarkably.
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