115 bile ducts appear to bear the brunt of the reperfusion injury. The experiments described by Noack et al. can obviously be extended to other transplantable solid organs. For example, the relative susceptibility of glo-merular cells and renal tubular cells to either anoxia or reoxygenation would be of interest. Other organs affected by disease processes in which the reperfusion injury has bee...

The objective of this study was to evaluate the genotype and allelic frequencies of CYP1A2 in Chinese patients with acute liver injury induced by Polygonum multiflorum. We examined the clinical mechanism of acute liver injury induced by P. multiflorum. According to the diagnostic criteria for drug-induced liver injury (DILI), 43 cases of P. multiflorum-induced liver injury admitted to the First...

Hepatic ischemia reperfusion (IR) injury causes acute kidney injury (AKI). However, the contribution of AKI to the pathogenesis of liver IR injury is unclear. Furthermore, controversy still exists regarding the role of A(1) adenosine receptors (A(1)ARs) in AKI. In this study, we determined whether exogenous and endogenous A(1)AR activation protects against AKI with subsequent liver protection a...

BACKGROUNDS/AIMS The aim of this study was to compare operative versus non-operative management of patients with liver injury and to ascertain the differences of the clinical features. METHODS From April 2000 to July 2012, 191 patients were admitted to Seoul St. Mary's Hospital and St. Vincent's Hospital for liver injuries. Of these, 148 patients were included in this study. All patients were...

Idiosyncrasy-like liver injury occurs in rats cotreated with nonhepatotoxic doses of ranitidine (RAN) and bacterial lipopolysaccharide (LPS). Hepatocellular oncotic necrosis is accompanied by neutrophil (PMN) accumulation and fibrin deposition in LPS/RAN-treated rats, but the contribution of PMNs to injury has not been shown. We tested the hypothesis that PMNs are critical mediators of LPS/RAN-...

Mechanisms of bile acid-induced (BA-induced) liver injury in cholestasis are controversial, limiting development of new therapies. We examined how BAs initiate liver injury using isolated liver cells from humans and mice and in-vivo mouse models. At pathophysiologic concentrations, BAs induced proinflammatory cytokine expression in mouse and human hepatocytes, but not in nonparenchymal cells or...