ABSTRACT
The secondary effluent of urban sewage treatment plants contains many opportunistic pathogens (OPs), which pose a potential threat to human health. In this study, the slow filtration technique is employed as the advanced treatment procedure, with the secondary effluent as the treatment object. The effectiveness of the operating conditions of the slow filtration process (filtration rate and Ca2+ concentration) in removing OPs (Pseudomonas aeruginosa, Legionella and Mycobacterium avium) and Escherichia coli from water, as well as the dynamic deposition process of pollutants on the surface of the slow filtration biofilm, was investigated. The results showed that under different filtration rates and different Ca2+ concentrations, biofilm slow filtration was more effective in removing OPs than slow filtration. The optimal filtration rate of biofilm slow filtration was 5 cm/h, and the optimal inlet Ca2+ concentration was 60 mg/L. When the filtration rate was 5 cm/h, the deposition of pollutants in the secondary effluent on the surface of biofilm slow filtration was mainly dominated by the physical adhesion of extracellular polymeric substances (EPS). When the concentration of Ca2+ was 60 mg/L, the adsorption of microorganisms was the primary method.
Subject(s)
Environmental Pollutants , Legionella , Water Purification , Humans , Filtration/methods , Biofilms , Extracellular Polymeric Substance Matrix , Water Purification/methodsABSTRACT
BACKGROUND: Pyroptosis refers to programmed cell death associated with inflammation. Emodin has been reported to alleviate lung injuries caused by various pathological processes and attenuate ischemia-reperfusion (I/R) injuries in diverse tissues. METHODS: Lewis rats were assigned into the sham, the I/R, and the I/R + emodin groups. Emodin and phosphate-buffered saline were intraperitoneally injected into rats of the emodin group and I/R group for 30 min, respectively. These rats were then subjected to left thoracotomy followed by 90-min clamping of the left hilum and 120-min reperfusion. Sham-operated rats underwent 210-min ventilation. Lung functions, histological changes, lung edema, and cytokine levels were assessed. Protein levels were measured by western blotting. Immunofluorescence staining was conducted to evaluate pyroptosis. RESULTS: Emodin alleviated the I/R-induced lung dysfunction, lung damages, and inflammation. Protective effects of emodin against I/R-mediated endothelial pyroptosis was observed in vivo and in vitro. Mechanistically, emodin inactivated the TLR4/MyD88/NF-κB/NLRP3 pathway. CONCLUSION: Emodin attenuates lung ischemia-reperfusion injury by inhibiting GSDMD-mediated pyroptosis in rats.
