The sulfate assimilation and reduction of marine microalgae and the regulation of illumination.

To examine the sulfate assimilation and reduction process and the regulation of illumination, diatom Phaeodactylum tricornutum and dinoflagellate Amphidinium carterae were selected for continuous simulation incubation under different photon flux densities (PFDs) (54, 108 and 162 µmol photons m-2 s-1), and concentration variations of related sulfur compounds sulfate, dimethylsulfoniopropionate (DMSP), dimethylsulfide (DMS) and acrylic acid (AA) in the culture system were observed. The optimal PFD for the growth of two microalgae was 108 µmol photons m-2 s-1. However, the maximum sulfate absorption occurred at 162 µmol photons m-2 s-1 for P. tricornutum and at 54 µmol photons m-2 s-1 for A. carterae. With the increase of PFD, the release of DMSP by P. tricornutum decreased while A. carterae increased. The largest release amount of DMS was 0.59 ± 0.05 fmol cells-1 for P. tricornutum and 2.61 ± 0.89 fmol cells-1 for A. carterae under their optimum growth light condition. The sulfate uptake of P. tricornutum was inhibited by the addition of amino acids, cysteine had a greater inhibitory effect than methionine, and the absorption process was controlled by light. The intermediate products of sulfur metabolism had an up-control effect on the sulfate uptake process of P. tricornutum. However, the addition of amino acids had no obvious effect on the sulfate absorption of A. carterae.

Heat shock protein: a double-edged sword linking innate immunity and hepatitis B virus infection.

Heat shock proteins (HSPs), which have a variety of functions, are one of the stress protein families. In recent years, They have been reported to play a dual role in hepatitis B virus (HBV) which as persistent infection which is associated with, cirrhosis and liver cancer. In this article, we have summarized the regulatory mechanisms between HSPs and viruses, especially HBV and associated diseases based on HSP biological functions of in response to viral infections. In view of their potential as broad-spectrum antiviral targets, we have also discuss current progress and challenges in drug development based on HSPs, as well as the potential applications of agents that have been evaluated clinically in HBV treatment.

Production of volatile fatty acid from fruit waste by anaerobic digestion at high organic loading rates: Performance and microbial community characteristics.

This study examined the performance and microbial community dynamics of an anaerobic volatile fatty acid (VFA) production reactor for treating fruit waste by stepwise increasing organic loading rates (OLRs) from 8 to 24 g volatile total solids (VTS)/(L·d). Results showed that higher VFA concentrations of 52.25-61.90 g chemical oxygen demand (COD)/L can be maintained at each OLR, thereby resulting to a production of 0.70-0.76 g chemical oxygen demand (COD)VFA/g VTS. Notably, an increase in OLR from 8 to 14 g VTS/(L·d) was beneficial for achieving higher VFA concentrations and yields. Moreover, an increase in OLR affected the VFA distribution significantly; acetate and butyrate became dominant in the fermentation liquid at OLRs ≥ 14 g VTS/(L·d). Microbial community dynamics analysis revealed that phyla Firmicutes and Actinobacteriota were predominant at each OLR, and the genera Lactobacillus, Clostridium_sensu_stricto_12, and Caproiciproducens were closely related to anaerobic VFA production.

Interfering RNA against PKC-α inhibits TNF-α-induced IP3R1 expression and improves glomerular filtration rate in rats with fulminant hepatic failure.

We have reported that tumor necrosis factor-α (TNF-α) is critical for reduction of glomerular filtration rate (GFR) in rats with fulminant hepatic failure (FHF). The present study aims to evaluate the underlying mechanisms of decreased GFR during acute hepatic failure. Rats with FHF induced by d-galactosamine plus lipopolysaccharide (GalN/LPS) were injected intravenously with recombinant lentivirus harboring short hairpin RNA against the protein kinase C-α ( PKC-α) gene (Lenti-shRNA-PKC-α). GFR, serum levels of aminotransferases, creatinine, urea nitrogen, potassium, sodium, chloride, TNF-α, and endothelin-1 (ET-1), as well as type 1 inositol 1,4,5-trisphosphate receptor (IP3R1) expression in renal tissue were assessed. The effects of PKC-α silencing on TNF-α-induced IP3R1, specificity protein 1 (SP-1), and c-Jun NH2-terminal kinase (JNK) expression, as well as cytosolic calcium content were determined in glomerular mesangial cell (GMCs) with RNAi against PKC-α. Renal IP3R1 overexpression was abrogated by pre-treatment with Lenti-shRNA-PKC-α. The PKC-α silence significantly improved the compromised GFR, reduced Cr levels, and reversed the decrease in glomerular inulin space and the increase in glomerular calcium content in GalN/LPS-exposed rats. TNF-α treatment increased expression of PKC-α, IP3R1, specificity protein 1 (SP-1), JNK, and p-JNK in GMCs and increased Ca2 + release and binding activity of SP-1 to the IP3R1 promoter. These effects were blocked by transfection of siRNA against the PKC-α gene, and the PKC-α gene silence also restored cytosolic Ca2+ concentration. RNAi targeting PKC-α inhibited TNF-α-induced IP3R1 overexpression and in turn improved compromised GFR in the development of acute kidney injury during FHF in rats.

[Significance of serum level of NO and IL-8 in Helicobacter pylori associated gastric diseases].

OBJECTIVE: To investigate the relation between serum level of interleukin-8 (IL-8), nitrogen monoxide (NO) and Helicobacter pylori (HP) infection, as well as the possible molecular mechanism of HP infection causing the imbalance of apoptosis and proliferation in gastric epithelial cells, which may lead to oncogenesis in stomach. METHODS: Serum IL-8 level was detected with enzyme-linked immunosorbent assay (ELISA). Serum NO was detected with chrome reduction method using plated copper. RESULTS: Serum level of IL-8 were 22.50 +/- 1.87 pg/ml in the normal tissue, 34.99 +/- 7.89 pg/ml in superficial gastritis, 65.27 +/- 10.60 pg/ml in atrophic gastritis and 94.84 +/- 11.09 pg/ml in gastric cancer (P < 0.01). Serum level of NO in the atrophic gastritis group (39.93 +/- 5.43 micromol/L) was significantly higher than that in the gastric cancer group (37.02 +/- 4.13 micromol/L) (P < 0.05). The differences in the other groups were not significant. IL-8 and NO levels in the HP(+) group were significantly higher than those in the HP(-) group (77.30 +/- 20.92 pg/ml vs 39.16 +/- 14.40 pg/ml, P < 0.01; 39.77 +/- 5.57 micromol/L vs 35.35 +/- 5.24 micromol/L, P < 0.01). Serum levels of IL-8 and NO in the cytotoxin-associated gene A protein (CagA)(+)HP group were significantly higher than those in the CagA(-)HP group (83.45 +/- 16.92 pg/ml vs 66.24 +/- 23.21 pg/ml, P < 0.01; 40.97 +/- 4.59 micromol/L vs 37.62 +/- 6.58 micromol/L, P < 0.05). Serum levels of IL-8 and NO showed positive correlation between superficial gastritis and atrophic gastritis groups (r = 0.881, r = 0.995), whereas no correlation was found in the normal or gastric cancer groups. CONCLUSION: Serum levels of IL-8 and NO are correlated with CagA(+)HP strain infection. Combined detection of serum level of IL-8, NO and HP-CagA will contribute to the early diagnosis of precancerous lesion in the stomach.