ABSTRACT
Anaerobic ammonia oxidation (ANAMMOX) process is an efficient and low-cost biological nitrogen removal process. However, it still faces some challenges in mainstream applications due to the limitation of substrate types and nitrate accumulation. In recent years, the combined process of anammox has been widely studied to solve the above problems. In this paper, the combined processes of anammox developed in recent years are reviewed, and discussed from the process principle, advantages and disadvantages, influencing factors, process extensibility and the key bottlenecks existing in the promotion and application, as well as the relevant work of the subject group. Finally, we take an outlook on the development of the combined anaerobic ammonia oxidation process in municipal domestic wastewater treatment.
Subject(s)
Ammonium Compounds , Anaerobiosis , Bioreactors , Denitrification , Nitrogen , Oxidation-Reduction , Sewage , WastewaterABSTRACT
Objective To investigate the role of Heme oxygenase-1 in the effect of hyperbaric oxygen preconditioning (HBOP) against the brain edema formation after experimental intracerebral hemorrhage in rats.Methods The study was carried out by animal experiment in two steps by using 54 Spradgue-Dawley rats weighting from 300-350 g.In the first step,rats were treated with HBOP (HBOP group,n =3) or with sham pre-conditioning (Sham pre-conditioning group,n =3).All the rats were sacrificed 24 h after the preconditioning,and basal ganglion of brain tissue was taken for detect HO-1 level by using western blot analysis.In the second step,rats were divided into 4 groups (n =12 in each group):HBOP +ZnPP group,in which rats had a micro-pump intra-peritoneally implanted containing a specific HO-1 inhibitor ZnPPⅨ (Zinc protoporphyrin IX,0.01 mg/kg),Sham pre-conditioning + Znpp group,HBOP + DMSO group,in which rats with a intra-peritoneal micro-pump containing 2 mL Dimethyl sulfoxide (DMSO,a solvent vehicle) and Sham pre-conditioning + DMSO group before HBOP.At 24 hours after the pre-conditioning,rats received an infusion of 100 μL autologous blood into the caudate nucleus to form a simulated intracerebrum hemorrhage (ICH),and were sacrificed 72 h later for brain water content measurements.All data were analyzed by using Stata 7.0 software and statistical analyses were carried out by two-tailed Student t test.Results Compared with the Sham pre-conditioning group,the HBOP group had significant higher level of HO-1.Compared with the Sham pre-conditioning + DMSO group,the HBOP + DMSO group had a significant lower level of water content in the ipsilateral basal ganglion [(81.4 ± 0.9) ％ vs.(82.6 ± 0.8) ％ (P ＜ 0.05)],however,peritoneal infusion of ZnPP Ⅸ before HBOP abolished HBOP-induced protection against brain edema formation after experimental ICH [(82.8 ± 0.9) ％ vs.(82.6 ± 0.7) ％ (P ＞ 0.05)].Conclusions Hyperbaric oxygen preconditioning attenuate brain edema formation after experimental ICH in rats,and this protection is attributed to the activation of HO-1.
ABSTRACT
Objective To investigate the effects of hyperbaric oxygen preconditioning (HBOP) on brain edema, inflammatory reaction and neuronal cell apoptosis induced by experimental hemorrhage in rats. Method Eighteen male Spraque-Dawley rats, weighing 300 - 350 g,received five successive sessions of HBOP with 3 atmosphere absolute pressure and 100% O2 one hour daily for five successive days, and other eighteen rats received five successive sessions of pretreatment with one atmosphere absolute pressure, air, one hour daily for five successive days. Twenty-four hours after the final pre-conditioning, rats received an infusion of 100 μL autologous blood into the basal ganglion. Seventy-two hours later, rats were sacrificed for brain edema measurements in 12 rats of each group. The histopathological changes around the hematoma were observed microscopically, and the neuronal cell apoptosis was detected by using the terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) in six rats of each group. Data of brain water content were analyzed by using Stata 7.0 software and statistical analysis was carried out by two-tailed Student t -test. Results Compared with the control group, HBOP significantly attenuated brain edema 72 hours after intra-cerebral hemorrhage in experimental rats (81. 6± 0. 7% vs. 82. 8± 0.9%, P < 0.01). Inflammatory cell infiltration and neuronal cell apoptosis were also significantly decreased in the HBOP group. Conclusions HBOP protects the rats against brain edema formation, and quells inflammatory reaction and neuronal cell apoptosis following intra-cerebral hemorrhage in experimental rats.