miR-19b was expressed differently between quiescent and activated HSCs, using comparative analysis of microRNA (miRNA) expression. As is well known, comparative analysis is the gold standard approach for detecting dys-regulated miRNAs. This same approach has been used on HSC in 4 other studies related to the topic.2-5 The profiles of dys-regulated miRNAs in activated HSCs are summarized in Table 1. The same protocol was executed with the following steps in these studies: step 1, quiescent HSCs were isolated from normal rat liver; step 2, activated HSCs were acquired by culturing quiescent HSCs in vitro for 10 or 14 days until activated; step 3, the different miRNA expression HM781-36B in vivo patterns of activated and quiescent

HSCs were analyzed by comparative analysis. However, there was an interesting phenomenon shown in Table 1, which was that the profiles of dys-expressed miRNAs in activated HSCs varied greatly across the studies. The issue remains why the same protocol for detecting

dys-regulated miRNAs in activated HSCs resulted in such different miRNA profiles. Shao-Long Chen M.D.*, Ming-Hua Zheng M.D.*, Tao Yang M.D.*, Mei Song ATM/ATR inhibitor M.D.*, Yong-Ping Chen M.D.*, * Department of Infection and Liver Diseases, Liver Research Center,The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, China. “
“Bariatric surgery is an increasingly popular approach for effecting significant weight reduction in obese patients with comorbidities, including hepatic steatosis. Here we report a novel case of advanced nonalcoholic steatohepatitis (NASH) fibrosis

with portal hypertension after duodenal switch bariatric surgery, resolving histopathologically with partial reversal of the malabsorptive procedure.1 BPD/DS, biliopancreatic diversion with duodenal switch; CPT, Childs-Pugh-Turcotte; DM, diabetes mellitus; JIB, jejunoileal bypass; MELD, model for endstage liver disease; NASH, nonalcoholic steatohepatitis. A 50-year-old male with a history of morbid obesity and no alcohol prior to presentation presented to the Hepatology Clinic with cirrhosis secondary to NASH. Three years prior, the patient underwent biliopancreatic MCE公司 diversion with duodenal switch (BPD/DS). Two years postsurgery he had lost 188 pounds with resolution of hypertension and diabetes mellitus (DM). At presentation the patient was noted to have extensive bridging fibrosis on percutaneous liver biopsy with trichrome staining (Fig. 1) complicated by portal hypertensive ascites and mild hepatic encephalopathy. Computed tomography (CT) of the abdomen noted diminished size with nodular contour of the liver and moderate ascites. His initial model for endstage liver disease (MELD) was 19 (international normalized ratio [INR] 1.50, total bilirubin 1.9 mg/dL, creatinine 1.8 mg/dL; weight = 193 lbs; body mass index [BMI] = 29.3; albumin = 3.4 gm/dL [after albumin infusions]) and he was Childs-Pugh-Turcotte (CPT) Class B.