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Simultaneous removal of NH 3 and H 2 S was investigated using two types of biofilters-one packed with wood chips and the other with granular activated carbon (GAC). Experimental tests and measurements included analyses of removal efficiency (RE), metabolic products, and results of long-term operation (around 240 days). The REs for NH 3 and H 2 S were 92 and 99.9%, respectively, before deactivation. After deactivation, the RE for NH 3 and H 2 S were decreased to 30 -50% and 75%, respectively. The activity of nitrifying bacteria was inhibited by high concentrations of H 2 S (over 200 ppm) but recovered gradually after H 2 S addition was ceased. However, the Thiobacillus thioparus as sulfur oxidizing bacteria did not show inhibition at the NH 3 concentration under 150-ppm conditions. The deactivation of the biofilter was caused by metabolic products [elemental sulfur and (NH 4 ) 2 SO 4 ] accumulating on the packing materials during the extended operation. The removal capacities for NH 3 and H 2 S were 6.0 -8.0 and 45-75 mg N, S/L/hr, respectively.

Background:Androgen ablation is the first-line therapy for patients with metastatic prostate cancer (CaP). However, castration resistance will eventually emerge. In the present study, we have investigated the role of bone morphogenetic protein-6 (BMP-6) in the development of castration-resistant prostate cancer (CRPC) in the context of bone metastases.Methods:We initially investigated the clinical course of 158 men with advanced CaP who were treated with primary androgen deprivation therapy. To elucidate the underlying mechanism of CRPC in the context of bone metastases, we examined the impact of bone stromal cells on CaP in the absence of androgens using a co-culture model.Results:In the 158 patients, we found that the median time to prostate-specific antigen progression was significantly shorter when bone metastases were present (14 months (95% CI, 10.2–17.8 months) vs 57 months (95% CI, 19.4–94.6 months)). These results suggest that bone–tumour interactions may accelerate castration resistance. Consistent with this hypothesis, in vitro co-cultures demonstrated that CaP cells proliferated under an androgen-depleted condition when incubated with bone stromal cells. Mechanistically, gene expression analysis using quantitative polymerase chain reaction arrays showed a dramatic induction of BMP-6 by CaP cell lines in the presence of bone stromal cells. Further studies revealed that WNT5A derived from bone stromal cells induced the expression of BMP-6 by CaP cells; BMP-6 in turn stimulated cellular proliferation of CaP cells in an androgen-deprived media via a physical interaction between Smad5 and β-catenin. Intracellularly, WNT5A increased BMP-6 expression via protein kinase C/NF-κB pathway in CaP cell lines.Conclusions:These observations suggest that bone–CaP interaction leads to castration resistance via WNT5A/BMP-6 loop.