Predictors for efficacy of combination therapy with a nucleos(t)ide analogue and interferon for chronic hepatitis B.

This study aims to explore the efficacy of interferon-α (IFN-α) combined with either entecavir (ETV) or adefovir (ADV) therapy versus IFN-α mono-therapy for chronic hepatitis B (CHB) patients, and to identify the factors associated with treatment outcomes. Totally, 159 CHB patients receiving interferon-based treatment for 48 weeks were enrolled in this retrospective study, including IFN-α mono-therapy group (group A, n=44), IFN-α plus ADV group (group B, n=53) and IFN-α plus ETV group (group C, n=62). The primary measures of efficacy assessments were the changes in HBsAg.

Prdx1-encoded peroxiredoxin is important for vascular development in zebrafish.

Genetic signaling and redox homeostasis are required for proper growth of blood vessels. Here, we report a novel function of peroxiredoxin1 (Prdx1) in vascular development in zebrafish. Knockdown of prdx1 impairs the growth of intersegmental vessel and caudal vein plexus (CVP), and reduces the expression of vascular markers, thus suggesting a role for prdx1 in vasculature and indicating that the antioxidant function of prdx1 is important.

Prognosis of acute-on-chronic liver failure patients treated with artificial liver support system.

Aim: To establish a new model for predicting survival in acute-on-chronic liver failure (ACLF) patients treated with an artificial liver support system.

Methods: One hundred and eighty-one ACLF patients who were admitted to the hospital from January 1, 2012 to December 31, 2014 and were treated with an artificial liver support system were enrolled in this retrospective study, including a derivation cohort (n = 113) and a validation cohort (n = 68). Laboratory parameters at baseline were analyzed and correlated with clinical outcome.

Recombinant adeno-associated virus-mediated transfer of shRNA against Notch3 ameliorates hepatic fibrosis in rats.

Liver fibrosis, a wound healing process following all kinds of liver injuries, is characterized by excessive deposition of extracellular matrix (ECM). Our previous study revealed that Notch3 might participate in liver fibrogenesis by regulating the activation of hepatic stellate cells (HSCs). The aim of this study was to assess the effects of Notch3 shRNA on hepatic fibrosis in a rat model induced by carbon tetrachloride (CCl4) and to clarify the mechanisms underlying those effects.

[Effect of Notch signaling on the activation of hepatic stellate cells].

Objective: To investigate whether Notch signaling is activated in hepatic stellate cells (HSCs), and to determine whether manipulation of the Notch signaling pathway can effect the activation of HSCs.

Methods: The expression of Notch signaling components in unactivated or TGF-b1-activated HSC-T6 cells was detected by Taqman Probe-based gene expression analysis. Differential expression of Notch3 and Jagged1 was detected by immunofluorescence analysis.

Notch3 regulates the activation of hepatic stellate cells.

Aim: To investigate whether Notch signaling is involved in liver fibrosis by regulating the activation of hepatic stellate cells (HSCs).

Methods: Immunohistochemistry was used to detect the expression of Notch3 in fibrotic liver tissues of patients with chronic active hepatitis. The expression of Notch3 in HSC-T6 cells treated or not with transforming growth factor (TGF)-β1 was analyzed by immunofluorescence staining.

[Enhancement of antiviral immunity in HBV mouse model by blocking PD-1/PD-L1 signaling pathway].

Objective: To establish a mouse model for human chronic HBV infection, and to investigate the role of PD-1/PD-L1 signaling pathway in antiviral immunity.

Methods: A mouse model was established by hydrodynamic injection of the plasmid pAAV/HBV1.2-GFP into the tail vein of C57BL/6 mice, HBV markers were assayed at different time points after injection.

Programmed death-1 expression is associated with the disease status in hepatitis B virus infection.

Aim: To define the potential role of programmed death-1/programmed death-ligand (PD-1/PD-L) pathway in different hepatitis B virus (HBV) infection disease status; we examined the expression of PD-1 on antigen specific CD8+ T cells in peripheral blood of patients with chronic hepatitis B (CHB) and acute exacerbation of hepatitis B (AEHB) infection.

Methods: The PD-1 level on CD8+ T lymphocytes and the number of HBV specific CD8+ T lymphocytes in patients and healthy controls (HCs) were analyzed by staining with pentameric peptide-human leukocyte antigen2 (HLA2) complexes combined with flow cytometry. Real-time quantitative polymerase chain reaction (PCR) was used to measure the serum HBV-DNA levels.

Inhibition of hepatitis B virus replication by pokeweed antiviral protein in vitro.

Aim: To explore the inhibitory effects of pokeweed antiviral protein seed (PAP-S) and PAP encoded by a eukaryotic expression plasmid on hepatitis B virus (HBV) replication in vitro.

Methods: HepG2 2.2.

Analysis of prognosis on patients with severe viral hepatitis using the model for end-stage liver disease.

Aim: To study the practical use of the model for end-stage liver disease (MELD) on clinic and assess its validity by the concordance (C)-statistic in predicting the prognosis of the patient with severe viral hepatitis.

Methods: One hundred and twenty-one patients were divided into plasma exchange group and non-plasma exchange group, and were graded with MELD formula. The death rate was observed within 3 mo.