Start-up of a full-scale deammonification SBR-treating effluent from digested sludge dewatering

This study shows the start-up and operation of a full-scale sequencing batch reactor (SBR) with a volume of 550 m³ for deammonification of reject water from sludge dewatering over the first 650 days of operation. The SBR was operated with discontinuous aeration and achieved an optimum of around 85% of ammonium removal at a load of 0.17 kg m−3 d−1. The application of batch tests for activity measurement of aerobic ammonium and nitrite oxidizing bacteria and anaerobic ammonium oxidizing bacteria proved to support the identification of setbacks in reactor operation. Furthermore, the calculation of the oxygen uptake rates from online oxygen measurements helped to explain the overall reactor performance. The aeration regime is a key parameter for stable operation of such an SBR for deammonification. At aeration/non-aeration time ratios of 6–9 min, the best results with respect to turnover rates and low nitrate production were achieved. Compared to the nitrification/denitrification SBR operated in parallel with methanol as carbon source, a significant reduction in costs for energy and chemicals was achieved. The costs for maintenance slightly increased

Endomorphin-2 and endomorphin-1 promote the extracellular amount of accumbal dopamine via nonopioid and mu-opioid receptors, respectively.

Contains fulltext : 49412.pdf (publisher's version ) (Closed access)Activation of mu-opioid receptors in the nucleus accumbens (NAc) is known to increase accumbal dopamine efflux in rats. Endomorphin-2 (Tyr-Pro-Phe-Phe-NH(2); EM-2) and endomorphin-1 (Tyr-Pro-Trp-Phe-NH(2); EM-1) are suggested to be the endogenous ligands for the mu-opioid receptor. As the ability of EM-2 and EM-1 to alter the accumbal extracellular dopamine level has not yet been studied in freely moving rats, the present study was performed, using a microdialysis technique that allows on-line monitoring of the extracellular dopamine with a temporal resolution of 5 min. A 25 min infusion of either EM-2 or EM-1 into the NAc (5, 25, and 50 nmol) produced a dose-dependent increase of the accumbal dopamine level. The EM-2 (50 nmol)- and EM-1 (25 and 50 nmol)-induced dopamine efflux were abolished by intra-accumbal perfusion of tetrodotoxin (2 muM). Intra-accumbal perfusion of the mu-opioid receptor antagonist CTOP (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Phe-Thr-NH(2); 3 nmol) failed to affect the EM-2 (50 nmol)-induced dopamine release, whereas it significantly inhibited the EM-1 (25 and 50 nmol)-induced dopamine release. The EM-1 (50 nmol)-induced accumbal dopamine efflux was significantly reduced by the systemic administration of the putative mu1-opioid receptor antagonist naloxonazine (15 mg/kg, intraperitoneally (i.p.), given 24 h before starting the perfusion). Systemic administration of the aspecific opioid receptor antagonist naloxone (1 mg/kg, i.p., given 10 or 20 min before starting the perfusion) also failed to affect the EM-2 (50 nmol)-induced dopamine efflux, whereas it significantly inhibited the EM-1 (25 and 50 nmol)-induced dopamine efflux. The present study shows that the intra-accumbal infusion of EM-2 and EM-1 increases accumbal dopamine efflux by mechanisms that fully differ. It is concluded that the effects of EM-2 are not mediated via opioid receptors in contrast to the effects of EM-1 that are mediated via mu1-opioid receptors in the NAc