Various kinds of mutations of ATP7B cause Wilson disease. Wilson disease is a rare genetic disease that can be treated pharmacologically. Recognition and prompt diagnosis are very important, because Wilson disease is fatal if left untreated. In Pirfenidone this review, I summarize the pathogenesis and management of Wilson disease. “
“Background and Aims:  The adjuvant effects of probiotic-containing yogurt on second-line triple therapy

for Helicobacter pylori (H. pylori) infection have not been evaluated. Methods:  A total of 337 patients with persistent H. pylori infection, after first-line triple therapy, were randomly assigned to receive either triple therapy with (yogurt group, n = 151) or without (control group, n = 186) Will yogurt. Triple therapy consisted of 400 mg moxifloxacin q.d., 1000 mg amoxicillin b.i.d., and 20 mg esomeprazole b.i.d. for 14 days. Will yogurt contains Lactobacillus acidophilus, Lactobacillus casei, Bifidobacterium longum, and Streptococcus thermophilus. H. pylori eradication was evaluated by the 13C-urea breath test, histology, or the rapid urease test. Results:  The eradication rates by intention-to-treat analysis were 66.7% and 68.9% in the control and yogurt groups, respectively (P = 0.667). The eradication rates by per-protocol

selleck analysis were 78.5% and 86% in the control and the yogurt groups, respectively (P = 0.110). The adverse event rates were 25.3% and 28.5% in the control group and yogurt group, respectively (P = 0.508). Conclusions:  The addition of yogurt containing probiotics to moxifloxacin-containing second-line treatment neither improved H. pylori eradication rates nor reduced the adverse events of treatment. “
“Liver cirrhosis is a predominant risk factor for hepatocellular carcinoma (HCC). However, the mechanism underlying the progression

from cirrhosis to HCC remains unclear. Herein we report the concurrent increase of liver progenitor cells (LPCs) and transforming growth factor-β (TGF-β) in diethylnitrosamine (DEN)-induced rat hepatocarcinogenesis and cirrhotic livers of HCC patients. Using several experimental approaches, including 2-acetylaminofluorene/partial selleck kinase inhibitor hepatectomy (2-AAF/PHx) and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-elicited murine liver regeneration, we found that activation of LPCs in the absence of TGF-β induction was insufficient to trigger hepatocarcinogenesis. Moreover, a small fraction of LPCs was detected to coexpress tumor initiating cell (T-IC) markers during rat hepatocarcinogenesis and in human HCCs, and TGF-β levels were positively correlated with T-IC marker expression, which indicates a role of TGF-β in T-IC generation. Rat pluripotent LPC-like WB-F344 cells were exposed to low doses of TGF-β for 18 weeks imitating the enhanced TGF-β expression in cirrhotic liver.