Rice washing drainage (RWD) embedded in poly(vinyl alcohol)/sodium alginate as denitrification inoculum for high nitrate removal rate with low biodiversity.

Immobilization technology with low maintenance is a promising alternative to enhance nitrate removal from water. In this study, washing rice drainage (RWD) was immobilized by poly(vinyl alcohol)/sodium alginate (PVA/SA) to obtain RWD-PVA/SA gel beads as inoculum for denitrification. When initial nitrate concentration was 50 mg N/L, nitrate was effectively removed at rates of 50-600 mg/(L∙d) using acetate as carbon source (C/N = 1.25). Arrhenius activation energy (Ea) of nitrate oxidoreductase was 28.64 kJ/mol for the RWD-PVA/SA gel beads. Temporal and spatial variation in microbial community structures were revealed along with RWD storage and in the reactors by Illumina high-throughput sequencing technology. RWD-PVA/SA gel beads has a simple (operational taxonomic units (OTUs) ã€ˆ100). Dechloromonas, Pseudomonas, Flavobacterium and Acidovorax were the most four dominant genera in the denitrification reactors inoculated with RWD-PVA/SA gel beads. This study provides an inoculum for denitrification with high nitrate removal performance and simple microbial community structures.

Polyethylenimine-Modified Mesoporous Silica Nanoparticles Induce a Survival Mechanism in Vascular Endothelial Cells via Microvesicle-Mediated Autophagosome Release.

Surface-modified mesoporous silica nanoparticles (MSNs) have attracted more and more attention as promising materials for biomolecule delivery. However, the lack of detailed evaluation relevant to the potential cytotoxicity of these MSNs is still a major obstacle for their applications. Unlike the bare MSNs and amino- or liposome-modified MSNs, we found that polyethylenimine-modified MSNs (MSNs-PEI) had no obvious toxicity to human umbilical vein endothelial cells (HUVECs) at the concentrations up to 100 µg/mL. However, MSNs-PEI induced autophagosomes accumulation by blocking their fusion with lysosomes, an essential mechanism for the cytotoxicity of many nanoparticles (NPs). Thus, we predicted that an alternative pathway for autophagosome clearance exists in HUVECs to relieve autophagic stress induced by MSNs-PEI. We found that MSNs-PEI prevented STX17 loading onto autophagosomes instead of influencing lysosomal pH or proteolytic activity. MSNs-PEI induced the structural alternation of the cytoskeleton but did not cause endoplasmic reticulum stress. The accumulated autophagosomes were released to the extracellular space via microvesicles (MVs) when the autophagic degradation was blocked by MSNs-PEI. More importantly, blockade of either autophagosome formation or release caused the accumulation of damaged mitochondria and excessive ROS production in the MSNs-PEI-treated HUVECs, which in turn led to cell death. Thus, we propose here that the MV-mediated autophagosome release, a compensation mechanism, allows the vascular endothelial cell survival when the degradation of autophagosomes is blocked by MSNs-PEI. Accordingly, promoting the release of accumulated autophagosomes may be a protective strategy against the endothelial toxicity of NPs.