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A constructed rapid infiltration (CRI) system is a new type of sewage biofilm treatment technology, but due to its anaerobic zone it lacks the carbon sources and the conditions for nitrate retention, and its nitrogen removal performance is very poor. However, a shortcut nitrification–denitrification process presents distinctive advantages, as it saves oxygen, requires less organic matter, and requires less time for denitrification compared to conventional nitrogen removal methods. Thus, if the shortcut nitrification–denitrification process could be applied to the CRI system properly, a simpler, more economic, and efficient nitrogen removal method will be obtained. However, as its reaction process shows that the first and the most important step of achieving shortcut nitrification–denitrification is to achieve shortcut nitrification, in this study we explored the feasibility to achieve shortcut nitrification, which produces nitrite as the dominant nitrogen species in effluent, by the addition of potassium chlorate (KClO3) to the influent. In an experimental CRI test system, the effects on nitrogen removal, nitrate inhibition, and nitrite accumulation were studied, and the advantages of achieving a shortcut nitrification–denitrification process were also analysed. The results showed that shortcut nitrification was successfully achieved and maintained in a CRI system by adding 5 mM KClO3 to the influent at a constant pH of 8.4. Under these conditions, the nitrite accumulation percentage was increased, while a lower concentration of 3 mM KClO3 had no obvious effect. The addition of 5mM KClO3 in influent presumably inhibited the activity of ammonia-oxidizing bacteria (AOB) and nitrite-oxidizing bacteria (NOB), but inhibition of nitrite-oxidizing bacteria (NOB) was so strong that it resulted in a maximum nitrite accumulation percentage of up to over 80%. As a result, nitrite became the dominant nitrogen product in the effluent. Moreover, if the shortcut denitrification process will be achieved in the subsequent research, it could save 60.27 mg CH3OH per litre of sewage in the CRI system compared with the full denitrification process.

Constructed rapid infiltration system (CRI) is a new type of sewage biofilm treatment technology, but due to its anaerobic zone lacks of the carbon sources and the condition for nitrate retention, its nitrogen removal perfomance is very poor; However, shortcut nitrification-denitrification process presents distinctive advantages, as it saves oxygen, requires less organic matter and needs less time for denitrification compared to conventional nitrogen removal method. Thus, if the shortcut nitrification-denitrification process could be applied to CRI system properly, the simpler, more economic and efficient nitrogen removal method will be obtained. But, as its reaction process shows that the first and the most important step of achieving shortcut nitrification-denitrification is to achieve shortcut nitrification. Thus, in this study, we explored the feasibility to achieve shortcut nitrification, which produces nitrite as the dominant nitrogen species in effluent, by addition of potassium chlorate (KClO3) to the influent. In an experimental CRI model system, the effects on nitrogen removal, nitrate inhibition and nitrite accumulation were studied, and the advantages of achieving shortcut nitrification-denitrification were also analysed. The results showed that shortcut nitrification was successfully achieved and maintained in a CRI system by adding 5 mM KClO3 to the influent at a constant pH of 8.4. Under these conditions nitrite accumulation rate was increased, while a lower concentration of 3 mM KClO3 had no obvious effect. The addition of 5 mM KClO3 in influent presumably allowed sufficient activity of ammonia-oxidizing bacteria (AOB) but inhibited nitrite-oxidizing bacteria (NOB) strongly enough to result in a maximum nitrite accumulation rate of up to over 80%. As a result, nitrite became the dominant nitrogen product in the effluent. Moreover, if the shortcut denitrification will be achieved in the subsequent research, it could save 60.27 mg carbon source (CH3OH) consumption when treatment of per liter sewage in CRI system compared with full denitrification process.

Sepsis-induced blood vessel dysfunction is mainly caused by microvascular endothelial cell injury. However, the mechanism underlying sepsis-induced endothelial cell injury remains unclear. The present study hypothesized that sepsis-induced inflammatory injury of endothelial cells may be the first step of endothelial barrier dysfunction. Therefore, the present study aimed to uncover the mechanism underlying the inflammatory effects of sepsis. A rat model of cecal ligation and puncture-induced sepsis was established, and septic serum was collected. Subsequently, human umbilical vein endothelial cells (HUVECs) were treated with the isolated septic or normal serum. HUVEC viability was assessed using a Cell Count Kit-8 assay. Furthermore, transmission electron microscopy and reverse transcription-quantitative PCR (RT-qPCR) analysis were carried out to observe the cell morphology and determine the mRNA expression levels in septic serum-induced HUVECs. The protein expression levels were evaluated by western blot analysis, and the secretion of the inflammatory factors interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α was determined by ELISA. Additionally, reactive oxygen species (ROS) generation and nuclear factor (NF)-κB nuclear translocation were observed under a fluorescence microscope. The results of the present study demonstrated that HUVEC viability was significantly decreased following 12- or 24-h treatment with septic serum. In addition, chromatin condensation, mitochondrial vacuolization and endoplasmic reticulum degranulation were observed following treatment with septic serum. Furthermore, the secretion levels of IL-1β, IL-6 and TNF-α were increased in septic serum-stimulated HUVECs. Septic serum treatment also enhanced superoxide anion generation, promoted extra-cellular signal regulated kinase 1/2 (ERK1/2), N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) phosphorylation, and increased NF-κB levels in the nuclei of HUVECs. Finally, pre-treatment of HUVECs with the antioxidant N-acetylcysteine, the ERK1/2 inhibitor PD98059, the p38 inhibitor SB203580, the JNK inhibitor SP610025 or the NF-κB inhibitor pyrrolidine dithiocarbamate restored the septic serum-induced IL-1β, IL-6 and TNF-α expression. In conclusion, the results of the current study suggested that the septic serum-induced endothelial cell injury may be mediated by increasing ROS generation, activation of mitogen-activated protein kinases and NF-κB translocation.

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