At operation, he had a contracted gallbladder and a fistula between

the fundus of the gallbladder and the transverse colon. A frozen section of the bile duct showed chronic inflammation with stenosis of the duct lumen, mucosal necrosis, granulation tissue and fibrosis in the bile duct wall (Figure 2A). The appearance was consistent with sclerosing cholangitis. An operative liver biopsy showed a mixed inflammatory infiltrate in portal tracts (Figure 2B), hepatocellular edema with cholestasis (Figure 2C) and NVP-BEZ235 datasheet degenerative changes in bile duct epithelium (Figure 2D). He was treated by cholecystectomy and prolonged T-tube drainage and is currently asymptomatic. There are now several case reports of sclerosing cholangitis in critically ill patients who required long-term treatment in intensive care units. The mechanism may be arterial hypoperfusion of the peribiliary vascular plexus that

causes ischemic injury to the bile duct. In some patients, this appears to be a progressive disease, perhaps because of infection or activation of immunological mechanisms. In the patient described above, inflammatory changes involved both the intrahepatic and extrahepatic bile ducts although the major radiological changes involved the common hepatic duct. It also seems likely that he had coexisting acalculous cholecystitis that resulted in the formation of a fistula between the gallbladder and colon. The optimal management of selleck inhibitor “ischemic” sclerosing cholangitis remains unclear. Some patients improve after endoscopic extraction of intrahepatic biliary casts while others may improve with endoscopic stents. Those with progressive disease will need to be considered for liver transplantation. Contributed by “
“Although a cancer cell line has limitations in modeling medchemexpress the physiological complexity in human

cancer, it has shown to be useful as a convenient tool to interrogate the molecular mechanism of action of cancer therapeutics.[1] Finn et al.[2] tested an intriguing idea to use a human hepatocellular carcinoma (HCC) gene signature to probe genomic profiles of hepatoma cell lines to evaluate sensitivity to a molecular targeted agent, dasatinib, although more work is needed to determine its mechanism of action. The authors identified two groups of cell lines according to the presence of a gene signature of “progenitor/HB” subtype linked to a distinct median inhibitory concentration (IC50) profile as well as cell cycle arrest and apoptosis induced by dasatinib. Of note, the classification looks concordant with positivity of alpha-fetoprotein (AFP), which has been repeatedly reported as the major determinant of global transcriptome landscape in hepatoma cells.[3, 4] We previously annotated the AFP-based subtypes of hepatoma cell lines with various molecular features and clinical phenotypes by using the gene signature assessment.