Search

Background Nonalcoholic fatty liver disease (NAFLD) has become one of the leading etiologies of hepatocellular carcinoma (HCC), but risk factors for NAFLD-related HCC occurrence have not been defined. NAFLD is often complicated by metabolic abnormalities, and there is a bidirectional association of metabolic abnormalities with NAFLD progression. This study aimed to systematically evaluate the relationship between metabolic traits and HCC occurrence in patients with NAFLD. Method This study reviewed eight eligible studies that included 297,956 participants, to determine the relationship between metabolic traits and the occurrence of HCC in patients with NAFLD. Results Presence of diabetes mellitus (DM) was associated with increased risk of HCC (HR: 2.65, 95%CI: 2.02 ~ 3.49, Pheterogeneity = 0.589, I2 = 0.0%). Stratified analysis revealed that this risk was higher in NAFLD patients with advanced fibrosis/cirrhosis (HR: 4.55, 95%CI: 2.34 ~ 8.87, Pheterogeneity = 0.870, I2 = 0.0%). Nonetheless even in patients without cirrhosis, DM remained a high risk factor for HCC incidence (HR: 1.80, 95%CI: 1.05 ~ 3.06, Pheterogeneity = 0.291, I2 = 10.4%). Overweight/obesity had a slight correlation with increased risk of HCC occurrence in NAFLD patients (HR: 1.31, 95%CI: 1.00 ~ 1.71, Pheterogeneity = 0.888, I2 = 0.0%), while presence of hypertension and dyslipidemia had no correlation. Conclusion DM and overweight/obesity are high risk factors for NAFLD-related HCC. In particular, DM increases 4-fold the risk of HCC incidence in NAFLD patients with advanced fibrosis/cirrhosis. There is a need to strengthen surveillance for HCC in NAFLD patients with DM, especially in those with advanced fibrosis/cirrhosis.

Background & AimBile acids, as hydrophilicity/ hydrophobic molecules and natural ligands of bile acids receptors, are involved in the pathogenesis of liver injury and metabolic disorders. Cholestyramine acts as a bile acid chelating agent and is used to reduce cholesterol in clinic, but its hepatotoxicity and effects on metabolism are still unclear.MethodsApoE-/- mice were continuously administered with low fat diet with or without 2% cholestyramine 12 weeks to determine the hepatotoxicity and metabolic influences of cholestyramine on these mice. Serum transaminases, liver histological features and hepatic inflammatory markers expression were used to assess cholestyramine hepatotoxicity. Body weight, liver weight, serum lipids profile and liver lipid metabolism related genes expression were used to evaluate effects of cholestyramine on metabolism. Differences of endogenous bile acids composition, bile acids metabolism related genes and intestinal flora structure between groups were also analyzed by an ultraperformance liquid chromatography coupled to tandem mass spectrometry system, quantitative real time PCR and 16S rDNA sequencing.ResultsAfter 12 weeks of dietary intervention, although cholestyramine decreased ApoE-/- mice serum cholesterol level, it significantly increased the body and liver weight of these mice, and caused severe liver injury: increased serum transaminases levels, promoted liver vesicular steatosis and inflammatory cells infiltration, and enhanced the expression of lipid synthesis gene: FASN and inflammatory markers genes: TNF-α 、MCP-1、F4/80 and CD68. Moreover, cholestyramine administration caused hydrophobic transformation of bile acids pool and severe gut dysbiosis, which were characterized by decreased hydrophilic bile acids: muricholic acid (MCA) and ursodeoxycholic acid (UDCA), and increased abundance of potential pathogenic bacteria: s_Bacteroide_vulgatus.ConclusionThis study revealed that cholestyramine had the ability to induce severe liver injury and metabolic disorders. These effects might be attributed to inducing hydrophobic transformation of bile acids pool and gut dysbiosis by cholestyramine. Furthermore, our study provided a warning of hepatotoxicity and metabolic disorders for clinical application of cholestyramine, and suggested that cholestyramine was not a good scavenging tool to study the role of bile acids alternations in diseases progression.

To improve its overall performance, fast-growing poplar was modified using the vacuum-pressure-vacuum impregnation method with a urea-formaldehyde resin-sodium montmorillonite intercalation as the modification solution. The results showed that considerable amounts of urea-formaldehyde resin and montmorillonites entered the poplar tracheid, and some entered the microporous wood. These substances formed bonds with the active groups in timber, causing reduced crystallinity in the amorphous region of the poplar, a decreased level of free hydroxyl, and an enhanced association with hydroxyl and ether bonds. The density, dimensional stability, and mechanical properties of poplar were markedly improved. The best results were obtained with 14% sodium montmorillonite and 20% ureaformaldehyde resin: the bending resistance, compressive resistance, and elastic modulus increased by 19.37%, 30.24%, and 50.06%, respectively. With elevated levels of sodium montmorillonite, the impact toughness and wear rate decreased.

Woodceramics is made from bamboo powder and epoxy resin. Analysis with X-ray diffraction (XRD) shows that with an increase in sintering temperature, the degree of graphitization increases. Scanning electron microscopic (SEM) analysis also indicates that bamboo powder exists in the composite as natural plant template. The study suggests that both sintering temperature and epoxy resin content have significant effects on its basic properties. Compressive strengths of woodceramics increase as sintering temperature rises but decrease as temperature rises to 1,000°C, and Young’s modulus rises along with higher resin content. Its density increases as sintering temperature rises but decreases as temperature rises further to 1,300°C. The apparent porosity tends to increase with increasing sintering temperature. In addition, elevation of resin content and sintering temperature can reduce electrical resistance, and sintering temperature has greater impact.