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Anaerobic ammonium oxidation (anammox) process is regarded as a promising nitrogen removal technology to treat ammonium wastewaters in a wide concentration range. Oligotrophic anaerobic ammonia oxidation bacteria (O-AnAOB) culture has been successfully achieved from a new anammox system to treat superlow ammonium concentration wastewaters. In this work, the O-AnAOB culture was compared with the eutrophic AnAOB (E-AnAOB) culture to reveal its physiological, morphological, and ecological features. Results showed that the specific anammox activity (SAA) of O-AnAOB culture was 0.07 kgN/(kgVSS·d) with the nitrogen removal rate (NRR) of 0.20 kgN/ (m 3  d) in the reactor, while the SAA of E-AnAOB culture was 2.11 kgN/(kgVSS·d) with the NRR of 11.10 kgN/(m 3  d). The hzs gene transcription levels (hzs-mRNA) of O-AnAOB and E-AnAOB cultures were 1.32 × 10 9 copies/gVSS and 1.51 × 10 10 copies/gVSS, respectively. Morphologically, the O-AnAOB culture took on the unique brown color rather than the typical red color of E-AnAOB. The O-AnAOB cells lived in a disperse pattern in the culture. The cells were seriously deformed with deep craters on the cell wall. The size of anammoxsome and paryphoplasm compartments inside the O-AnAOB cells was smaller than that inside the E-AnAOB cells. Ecologically, the O-AnAOB culture had special microbial community with a higher bacterial diversity than the E-AnAOB. The most dominant genera in O-AnAOB were Anaerolineaceae (33.7%, fermentative bacteria), Candidatus Kuenenia (17.4%, anammox bacteria), and Nitrospira (7.3%, nitrite oxidizing bacteria). This study provided an insight into the new anammox process for deep nitrogen removal from wastewaters.

It is highly significant to investigate the toxicity of inorganic salts to denitrifying granular sludge (DGS) and its mechanism since the application of high-rate denitrification is seriously limited in the treatment of saline nitrogen-rich wastewaters. The batch experiments showed that the IC50 (half inhibition concentration) and LC50 (half lethal concentration) of NaCl, Na2SO4 and Na3PO4 on DGS were 11.46, 21.72, 7.46 g/L and 77.35, 100.58, 67.92 g/L respectively. Based on the analysis of specific denitrifying activity, the live cell percentage, the cell structure, and the DNA leakage, the toxicity of low salinity was ascribed to the inhibition of denitrifying activity and the toxicity of high salinity was ascribed to both the inhibition of denitrifying activity and the lethality of denitrifying cell., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Recent studies have established that testosterone (Tes) produces acute (nongenomic) vasorelaxation. This study examined the structural specificity of Tes-induced vasorelaxation and the role of vascular smooth muscle (VSM) K+ channels in rat thoracic aorta. Aortic rings from male Sprague-Dawley rats with (Endo+) and without endothelium (Endo-) were prepared for isometric tension recording. In Endo- aortas precontracted with phenylephrine, 5-300 microM Tes produced dose-dependent relaxation from 10 microM (4 +/- 1%) to 300 microM (100 +/- 1%). In paired Endo+ and Endo- aortas, Tes-induced vasorelaxation was slightly but significantly greater in Endo+ aortas (at 5-150 microM Tes); sensitivity (EC(50)) of the aorta to Tes was reduced by nearly one-half in Endo- vessels. Based on the sensitivity (EC(50)) of Endo- aortas, Tes, the active metabolite 5alpha-dihydrotestosterone, the major excretory metabolites androsterone and etiocholanolone, the nonpolar esters Tes-enanthate and Tes-hemisuccinate (THS), and THS conjugates to BSA (THS-BSA) exhibited relative potencies for vasorelaxation dramatically different from androgen receptor-mediated effects observed in reproductive tissues, with a rank order of THS-BSA > Tes > androsterone = THS = etiocholanolone > dihydrotestosterone >> Tes-enanthate. Pretreatment of aortas with 5 mM 4-aminopyridine attenuated Tes-induced vasorelaxation by an average of 44 +/- 2% (25-300 microM Tes). In contrast, pretreatment of aortas with other K+ channel inhibitors had no effect. These data reveal that Tes-induced vasorelaxation is a structurally specific effect of the androgen molecule, which is enhanced in more polar analogs that have a lower permeability to the VSM cell membrane, and that the effect of Tes involves activation of K+ efflux through K+ channels in VSM, perhaps via the voltage-dependent (delayed-rectifier) K+ channel.