0056). Additionally, female carriers of the CCKAR haplotype C-T-C-T (rs2071011-rs915889-rs3822222-rs1800855) had a reduced risk of gallbladder cancer (odds ratio = 0.61, this website 95% confidence interval: 0.43–0.86) compared with those with the G-C-C-A haplotype; the association also remained significant after Bonferroni correction. These findings suggest that variants in the CCKAR gene may influence the risk of gallbladder cancer in women. Additional studies are needed to confirm our findings. “
“Background and Aim:  To investigate

the therapeutic effect of ligustrazine on hepatic veno-occlusive disease (HVOD) induced by Gynura segetum and the possible mechanism of it. Methods:  Female Kunming mice (115) were randomly divided into four groups, gavaged with 30 g/kg per day Gynura segetum (group A), 30 g/kg per day Gynura

segetum + 100 mg/kg per day ligustrazine (group B), 30 g/kg per day Gynura segetum + 200 mg/kg per day ligustrazine (group C) or 30 mL/kg per day phosphate-buffered saline (PBS) (group D). Thirty days later, all of the mice were killed. Blood samples and livers were harvested. Histological changes were evaluated by light microscopy. Liver function learn more was measured, and the expression of tissue factor (TF), early growth response factor-1 (Egr-1) and nuclear factor-KBp65 (NF-KBp65) were determined by reverse transcription-polymerase chain reaction and Western blot. Results:  A total of 24 mice in group A developed HVOD. Compared with the controls, they had increased liver ratio, serum total bilirubin (TBIL), check details direct

bilirubin (DBIL), transaminase and decreased albumin (ALB) (P < 0.05). Administration of ligustrazine improved the clinical signs and biochemistry parameters in a dose-dependent manner. Compared with group A, the expression of TF, Egr-1 and NF-KB p65 decreased in groups B and C (P < 0.05). Conclusion:  Ligustrazine has a therapeutic effect on HVOD, improving clinical manifestations and liver function. The possible mechanism may be that ligustrazine could reduce the expression of TF by downregulating the expression of transcription factors: Egr-1 and NF-KB p65. "
“Background & Aims: Antiviral therapy may eradicate hepatitis C viral replication, but its long-term impact on the reduction of hepatocellular carcinoma (HCC) remains unclear. This large clinical cohort study aimed to evaluate the predictors of sustained virological response (SVR) and assess the efficacy to reduce HCC post-treatment in Taiwanese chronic hepatitis C patients. Methods: This multicenter study enrolled 1778 anti-HCV-positive patients who were treated with peg-interferon plus ribavirin (PR) for 6-12 months. All of the patients were ≧30 years old and seronegative for HBsAg. The treated patients were followed from the date starting PR therapy to the date of HCC diagnosis, death, or the end of 2011, whichever came first.