Hepatoprotective drugs for prevention of liver injury resulting from anti-tuberculosis treatment: A meta-analysis of cohort studies.

Background: The incidence of liver injury caused by anti-tuberculous (TB) drugs is very high. However, owing to a lack of sufficient evidence, preventive use of hepatoprotective drugs is not yet recommended. Therefore, we aimed to assess the protective effect of hepatoprotective drugs for anti-TB drug-induced liver injury.

Identifying potential biomarkers of nonalcoholic fatty liver disease via genome-wide analysis of copy number variation.

Background: The prevalence of Non-alcoholic fatty liver disease (NAFLD) is increasing and emerging as a global health burden. In addition to environmental factors, numerous studies have shown that genetic factors play an important role in the development of NAFLD. Copy number variation (CNV) as a genetic variation plays an important role in the evaluation of disease susceptibility and genetic differences.

[Temporal and Spatial Characteristics of Total Phosphorus in the Middle and Lower Yangtze River Mainstem Under New Water and Sediment Conditions].

After the completion of the Three Gorges Reservoir and the upstream reservoir group of the Yangtze River, new water and sediment conditions appeared in the middle and lower reaches of the Yangtze River, and its influence on the phosphorus concentrations in water has attracted much attention. Therefore, the spatial and temporal distributions of total phosphorus (TP) concentrations in the middle and lower reaches of the mainstem under the new water and sediment conditions were studied. The results show that:① after the construction of the Three Gorges Reservoir, the concentrations of TCP (samples were allowed to settle for 30 min) in the middle and lower reaches of the Yangtze River fluctuates between 0.

The role of hepatitis B infection in anti-tuberculosis drug-induced liver injury: a meta-analysis of cohort studies.

Drug-induced liver injury (DILI) is a common adverse drug reaction leading to the interruption of tuberculosis (TB) therapy. We aimed to identify whether the hepatitis B virus (HBV) infection would increase the risk of DILI during first-line TB treatment. A meta-analysis of cohort studies searched in PubMed, Web of Science and China National Knowledge Infrastructure was conducted.

Microcystin-LR promotes necroptosis in primary mouse hepatocytes by overproducing reactive oxygen species.

Microcystin-LR (MC-LR) is a type of cyclic heptapeptide toxin produced by cyanobacteria during bloom events. MC-LR-induced cell death is critically involved in its potent specific hepatotoxicity. Many studies have demonstrated that prototypical apoptosis as a form of programmed cell death after MC-LR is associated with liver injury.

Dose-response association between physical activity and non-alcoholic fatty liver disease: a case-control study in a Chinese population.

Aim: Physical activity plays an important role in the development of non-alcoholic fatty liver disease (NAFLD).However, the optimal intensity and dose of physical activity for the treatment of NAFLD have yet to be found. In the present study, we aimed to provide a dose-response association between physical activity and NAFLD in a Chinese population.

Hepatitis B Virus X Protein Increases 8-Oxo-7,8-Dihydro-2'-Deoxyguanosine (8-Oxodg) Level via Repressing MTH1/ MTH2 Expression in Hepatocytes.

Background/aims: Chronic hepatitis B virus (HBV) infection markedly increases the risk of development of hepatocellular carcinoma (HCC). Among the seven viral proteins that HBV encodes, HBV X protein (HBx) appears to have the most oncogenic potential. The mitochondria-associated HBx can induce oxidative stress in hepatocytes, leading to the production of abundant reactive oxygen species (ROS).

Multiple MicroRNAs Ameliorate Hepatocyte Steatosis and Injury by Suppressing FABP1 Expression.

Background/aims: Liver fatty acid-binding protein (FABP1) is a key regulator of hepatic lipid metabolism. MicroRNAs (miRNAs) are thought to be involved in nonalcoholic fatty liver disease (NAFLD), and the underlying mechanism is largely unclear. We investigated whether miRNAs influence hepatocyte steatosis by regulating the FABP1 gene.

Deubiquitylation of hepatitis B virus X protein (HBx) by ubiquitin-specific peptidase 15 (USP15) increases HBx stability and its transactivation activity.

Hepatitis B virus X protein (HBx) plays important roles in viral replication and the development of hepatocellular carcinoma. HBx is a rapid turnover protein and ubiquitin-proteasome pathway has been suggested to influence HBx stability as treatment with proteasome inhibitors increases the levels of HBx protein and causes accumulation of the polyubiquitinated forms of HBx. Deubiquitinases (DUBs) are known to act by removing ubiquitin moieties from proteins and thereby reverse their stability and/or activity.

[Temporal and Spatial Variation Characteristics of the Heavy Metals Content in the Surface Sediment and the Potential Ecological Risk Trends in the Three Gorges Reservoir Area].

With the construction progress of the Three Gorges Project, the hydrological situation of Three Gorges Reservoir changes greatly, which causes the changes of suspended solids precipitation conditions and surface sediment traits. This research analyzed the temporal and spatial variation of the heavy metal pollution in the surface sediment and the potential ecological risk trends during the years from 2000 to 2015 in the trunk stream of the Yangtze River from Jiangjin to the Three Gorges Dam area and some major tributaries, such as Jialing River, Yulin River, Wujiang River, Xiaojiang River, Xiangxi River. The results showed that the average content ranges of heavy metals (including Cu, Pb, Mn, As, Hg etc.

Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein.

Unlabelled: Hepatitis B virus (HBV) has been implicated as a potential trigger of hepatic steatosis although molecular mechanisms involved in the pathogenesis of HBV-associated hepatic steatosis still remain elusive. Our prior work has revealed that the expression level of liver fatty acid binding protein 1 (FABP1), a key regulator of hepatic lipid metabolism, was elevated in HBV-producing hepatoma cells. In this study, the effects of HBV X protein (HBx) mediated FABP1 regulation on hepatic steatosis and the underlying mechanism were determined.

Association of a Human FABP1 Gene Promoter Region Polymorphism with Altered Serum Triglyceride Levels.

Liver fatty acid-binding protein (L-FABP), also known as fatty acid-binding protein 1 (FABP1), is a key regulator of hepatic lipid metabolism. Elevated FABP1 levels are associated with an increased risk of cardiovascular disease (CVD) and metabolic syndromes. In this study, we examine the association of FABP1 gene promoter variants with serum FABP1 and lipid levels in a Chinese population.

Transcriptional regulation of the apolipoprotein F (ApoF) gene by ETS and C/EBPα in hepatoma cells.

Apolipoprotein F (ApoF) inhibits cholesteryl ester transfer protein (CETP) activity and plays an important role in lipid metabolism. In the present study, the full-length human ApoF promoter was cloned, and the molecular mechanism of the regulation of ApoF was investigated. The ApoF promoter displayed higher activities in hepatoma cell lines, and the -198 nt to +79 nt promoter region contained the maximum promoter activity.

Hepatitis B virus core protein inhibits Fas-mediated apoptosis of hepatoma cells via regulation of mFas/FasL and sFas expression.

Hepatitis B virus core protein (HBc) has been implicated in hepatocarcinogenesis through several mechanisms. Resistance of hepatitis B virus (HBV)-infected hepatocytes to apoptosis is considered one of the major contributors to the progression of chronic hepatitis to cirrhosis and ultimately to hepatocellular carcinoma. The Fas receptor/ligand (Fas/FasL) system plays a prominent role in hepatocyte death during HBV infection.

Hepatitis B spliced protein (HBSP) promotes the carcinogenic effects of benzo [alpha] pyrene by interacting with microsomal epoxide hydrolase and enhancing its hydrolysis activity.

Background: The risk of hepatocellular carcinoma (HCC) increases in chronic hepatitis B surface antigen (HBsAg) carriers who often have concomitant increase in the levels of benzo[alpha]pyrene-7,8-diol-9,10-epoxide(±) (BPDE)-DNA adduct in liver tissues, suggesting a possible co-carcinogenesis of Hepatitis B virus (HBV) and benzo[alpha]pyrene in HCC; however the exact mechanisms involved are unclear.

Methods: The interaction between hepatitis B spliced protein (HBSP) and microsomal epoxide hydrolase (mEH) was confirmed using GST pull-down, co-immunoprecipitation and mammalian two-hybrid assay; the effects of HBSP on mEH-mediated B[alpha]P metabolism was examined by high performance liquid chromatography (HPLC); and the influences of HBSP on B[alpha]P carcinogenicity were evaluated by bromodeoxyuridine cell proliferation, anchorage-independent growth and tumor xenograft.

Results: HBSP could interact with mEH in vitro and in vivo, and this interaction was mediated by the N terminal 47 amino acid residues of HBSP.

The roles of HBV infection and host factors in ultrasound-diagnosed fatty liver: a case-control study.

Background/aims: The present study is to evaluate the roles of HBV infection, host factors and their interactions in the development of ultrasound-diagnosed fatty liver in Fujian province of China, a highly HBV endemic area.

Methodology: From June 2007 to May 2008, 527 ultrasound-diagnosed fatty liver patients and 1042 controls were ultrasonically diagnosed in this hospital-based case-control study. Their demographic, anthropometric, biochemical, behavioral factors and HBV markers were compared, and factors associated with fatty liver were determined by multivariate logistic regression analysis.

Epigenetic silencing of NAD(P)H:quinone oxidoreductase 1 by hepatitis B virus X protein increases mitochondrial injury and cellular susceptibility to oxidative stress in hepatoma cells.

NAD(P)H:quinone oxidoreductase 1 (NQO1) is a phase II enzyme that participates in the detoxification of dopamine-derived quinone molecules and reactive oxygen species. Our prior work using a proteomic approach found that NQO1 protein levels were significantly decreased in stable hepatitis B virus (HBV)-producing hepatoma cells relative to the empty-vector-transfected controls. However, the mechanism and biological significance of the NQO1 suppression remain elusive.

Genetic variants in PNPLA3 and risk of non-alcoholic fatty liver disease in a Han Chinese population.

We investigated the possible association between genetic variants in the Patatin like phospholipase-3 (PNPLA3) gene and nonalcoholic fatty liver disease (NAFLD) in a Han Chinese population. We evaluated twelve tagging single-nucleotide polymorphisms (tSNPs) of the PNPLA3 gene in a frequency matched case-control study from Fuzhou city of China (553 cases, 553 controls). In the multivariate logistic regression analysis, the rs738409 GG or GC, and rs139051 TT genotypes were found to be associated with increased risk of NAFLD, and a significant trend of increased risk with increasing numbers of risk genotype was observed in the cumulative effect analysis of these single nucleotide polymorphisms.

Interaction of the hepatitis B spliced protein with cathepsin B promotes hepatoma cell migration and invasion.

Hepatitis B spliced protein (HBSP) is involved in the pathogenicity and/or persistence of hepatitis B virus (HBV). Chronic HBV infection is one of the most important risk factors for the development of hepatocellular carcinoma (HCC). However, whether or not HBSP contributes to the progression of HBV-associated HCC remains unknown.

Hepatitis B virus X protein blocks filamentous actin bundles by interaction with eukaryotic translation elongat ion factor 1 alpha 1.

Hepatitis B virus (HBV)-encoded X protein (HBx protein) is a multi-functional regulatory protein. It functions by protein-protein interaction and plays a pivotal role in the pathogenesis of HBV-related diseases. However, the partners in hepatocytes interacting with HBx protein are far from understood fully.

Two genetic variants in FABP1 and susceptibility to non-alcohol fatty liver disease in a Chinese population.

Liver fatty acid-binding protein (FABP1) serves as a key regulator of hepatic lipid metabolism, and polymorphisms within the FABP1 gene have been associated with several metabolic traits. To investigate the association between FABP1 polymorphisms and the risk of non-alcohol fatty liver disease (NAFLD) in a Chinese population, the genotypes and haplotypes of FABP1 (rs2241883 T/C and rs1545224G/A) were determined in 553 patients with NAFLD and 553 healthy controls. The results showed that individuals with at least one copy of the rs2241883 C allele (TC or CC genotype) had an elevated risk for developing NAFLD (odds ratio [OR]=1.

Human liver fatty acid binding protein (hFABP1) gene is regulated by liver-enriched transcription factors HNF3β and C/EBPα.

The human liver fatty acid binding protein (hFABP1) participates in cellular long-chain fatty acid trafficking and regulation of lipid metabolism and changes in hFABP1 are associated with an increased risk for type 2 diabetes, cardiovascular disease (CVD), and metabolic syndromes. Gene regulation of hFABP1 is not fully understood. Therefore, in the present study, the full length hFABP1 promoter (nucleotides -2125 to +51) and a series of truncated promoter regions were cloned.

Hepatitis B spliced protein (HBSP) generated by a spliced hepatitis B virus RNA participates in abnormality of fibrin formation and functions by binding to fibrinogen γ chain.

Hepatitis B spliced protein (HBSP) encoded by a 2.2 kb singly spliced hepatitis B virus (HBV) pre-genomic RNA (spliced between positions 2447 and 489 nt) is involved in the pathogenesis of HBV infection, whereas the exact mechanism is far from being fully elucidated. In this study, a yeast two-hybrid system using HBSP as bait was employed to screen binding partners for HBSP from a human liver cDNA library.

Spectroscopic studies on the interaction between CdTe nanoparticles and lysozyme.

Nanoparticles of cadmium telluride (CdTe) coated with thioglycolic acid (TGA) were prepared in the water phase. The interaction between CdTe nanoparticles (NPs) and lysozyme (Lyz) was investigated by fluorescence and circular dichroism (CD) spectroscopy at pH 7.40.

Determination of lysozyme at the nanogram level by a resonance light-scattering technique with functionalized CdTe nanoparticles.

Nanoparticles of cadmium telluride coated with mercaptoacetic acid were prepared in the water phase. Further, an assay of lysozyme with a sensitivity at the nanogram level is proposed. At pH 7.