Anthropogenic activity shapes the assemble and co-occurrence pattern of microbial communities in fishing harbors around the Bohai Economic Circle.

This study aimed to elucidate the effects of coastal environmental stress on the composition of sediment bacterial communities and their cooccurrence patterns in fishing harbors around the Bohai Economic Circle, China. Compared with the natural sea area, fishing harbors contained higher levels of organic pollution (organic pollution index = 0.12±0.026) and considerably reduced bacterial richness and evenness. The distributions of sediment microbial communities clustered along the pollutant concentration gradients across fishing harbors. Betaproteobacteria dominated (76%) organically polluted fishing harbors, which were mostly disturbed by anthropogenic activities. However, the harbors also revealed the absence of numerous pathogenic (Coxiella and Legionella) and photosynthetic (Synechococcus and Leptolyngbya) bacteria. Abundant genera, including Thiobacillus and Arenimonas, exhibited a positive correlation with total phosphorus and a negative correlation with total nitrogen in sediments. Meanwhile, Sulfurovum, Psychrobacter, and Woeseia showed the opposite trend. Pollutant accumulation and anthropogenic activities caused the decrease in the sediment microbial diversity and dispersal ability and promoted convergent evolution. Severely polluted harbors with simplified cooccurrence networks revealed the presence of destabilized microbial communities. In addition, the modularity of bacterial networks decreased with organic pollution. Our results provide important insights into the adjustment mechanism of microbial communities to community organization and functions under environmental pollution stress. Overall, this study enhanced our understanding of how microbial communities in coastal sediments adapted and survived amidst anthropogenic activities like oily effluent discharges from large ships, wash water, domestic sewage, garbage, and fisheries wastes. It also examined their resilience to future contamination.

Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells.

Melanoma is a common type of cutaneous tumor, but current drug treatments do not satisfy clinical practice requirements. At present, mitochondrial uncoupling is an effective antitumor treatment. Triclosan, a common antimicrobial, also acts as a mitochondrial uncoupler. The aims of the present study were to investigate the effects of triclosan on melanoma cells and the underlying mechanisms. Mitochondrial membrane potential (MMP), mitochondrial morphology, mitochondrial reactive oxygen species (mito-ROS), intracellular superoxide anion and [Ca2+]i were measured using confocal microscopy. It was found that triclosan application was associated with decreased A375 cell viability in a dose- and time-dependent manner and these effects may have cell specificity. Furthermore, triclosan induced MMP depolarization, ATP content decrease, mito-ROS and [Ca2+]i level increases, excessive mitochondrial fission, AMP-activated protein kinase (AMPK) activation and STAT3 inhibition. Moreover, these aforementioned effects were reversed by acetylcysteine treatment. Triclosan acute treatment also induced mitochondrial swelling, which was reversed after AMPK-knockdown associated with [Ca2+]i overload. Cell death was caused by STAT3 inhibition but not AMPK activation. Moreover, triclosan induced autophagy via the ROS/AMPK/p62/microtubule-associated protein 1A/1B-light chain 3 (LC3) signaling pathway, which may serve a role in feedback protection. Collectively, the present results suggested that triclosan increased mito-ROS production in melanoma cells, following induced cell death via the STAT3/Bcl-2 pathway and autophagy via the AMPK/p62/LC3 pathway.

[Association of activated CD4+ cell and HBeAg with liver damage and cirrhosis in patients with chronic hepatitis B].

OBJECTIVE: To study the association of the CD4+ cell counts and HBeAg with liver damage and cirrhosis in patients with chronic hepatitis B (CHB). METHOD: To measure the lymphocytes both CD4 and HLA-DR positive of 58 patients with CHB and 18 patients with HBsAg negative but HBcAb positive. The Platelets (PLT) were counted and the ALT and AST were measured, meanwhile, AST/PLT values were calculated. RESULTS: The CD4+ cell counts of the three types patients were lower than those of healthy controls significantly,and those of HBcAb positive patients without CHB were higher than those of HBeAg negative patients with CHB which were higher than those of HBeAg positive patients significantly (P < 0.05). And the ALT, AST and AST/PLT levels of both HBeAg negative and positive patients were much higher than the three indicators of both HBcAb positive patients without CHB and healthy controls significantly (P < 0.02), meanwhile, the three indicators of HBeAg negative patients were much lower than those of HBeAg positive ones. In addition, the CD4+ cell counts of the two types patients were negatively correlative with the three indicators(P < 0.05). CONCLUSION: Decreased CD4+ cell count can be used as the indicator to predicate the progress of liver damage in patients with CHB, and it is also useful for HBeAg to evaluate the development degree of liver damage and fibrosis in CHB patients.

[The clinical significance of interferon-gamma and its receptor in patients with schistosomiasis].

OBJECTIVE: To study the expression of interferon-gamma (IFN-gamma) and type I interferon-y receptor (IFN-gammaRI) in the chronic and advanced patients of schistosomiasis japonica, and to discuss its clinical relationship with hepatic fibrosis. Methods IFN-yR1 in the peripheral blood lymphocytes was detected by ELISA, and the hyaluronic acid (HA) , collagen type IV (C-IV), procollagen type III (PC III), laminin (LN) were detected by radio-immunoassay (RIA) in schistosomiasis patients. The level of IFN-y, IFN-gammaR1 and serum markers of hepatic fibrosis were observed, and the relationship with each other was analyzed by statistical method. RESULTS: There was no difference in the expression of IFN-gamma and IFN-gammaR1 between the patients with chronic schistosomiasis and the normal group (P > 0. 05 ), the IFN-gammaR1 in advanced cases without splenectomy was low (P <0. 05) , but IFN-y was high (P < 0. 01). The two indicators in the advanced schistosomiasis patients with splenectomy returned to normal. There was no corresponding relationship between the two indicators and HA, C-IV, PC III, LN with a r value of 0. 19, 0.20, 0. 14, and 0.21 respectively. CONCLUSION: There is a corresponding relationship between IFN-gamma and IFN-gammaR1; the expression of IFN-gammaR1 is related to the course of schistosomiasis, and the relationship with hepatic fibrosis needs further study.