Suchergebnisse

AbstractA modified anaerobic/aerobic (A/O) bioreactor that simultaneously removed carbon, nitrogen (
‐N) and phosphorus (
‐P) was continuously run and debugged. After 34 days of reactor operation, the removal efficiencies of
‐N, carbon (glucose) and
‐P reached 99.26, 95.81 and 94.35%, respectively. Notably, the ammonium removal with no accumulation of nitrite (
‐N) and nitrate (
‐N) in the anaerobic part supported the occurrence of simultaneous nitrification and denitrification and no
‐P was released during the removal process of phosphorus. Moreover, the principal component analysis and response surface methodology based on the Box–Behnken design were applied to determine the optimal removal conditions for volatile suspended solids (VSS) (335 mg/L),
‐N (60 mg/L), glucose (900 mg/L) and pH (7). Finally, phylogenetic analysis of the bacterial consortium was conducted by denaturing gradient gel electrophoresis, which demonstrated that Clostridium and Proteobacteria were the potential functional groups in the anaerobic tank of the A/O bioreactor.

Cordycepin, or 3′-deoxyadenosine, is a derivative of the nucleoside adenosine. Initially extracted from the fungus Cordyceps militaris, cordycepin exhibits antitumor activity against certain cancer cell lines; however, the mechanism by which cordycepin counteracts colorectal cancer (CRC) remains poorly understood. The aim of the present study was to explore the underlying mechanisms of cordycepin against human CRC. To investigate the molecular mechanisms of cordycepin against colon cancer and in driving apoptosis, p53 and Bcl-2-like protein 4-null (Bax−/−) colon cancer HCT116 cell lines were used. Cell viability and growth were repressed in a dose-dependent manner in cells treated with cordycepin. Treatment with cordycepin resulted in increased apoptosis in HCT116 cells; however, flow cytometic analysis demonstrated that apoptosis was notably decreased in the Bax−/− HCT116 cell lines, but not in the p53−/− HCT116 cell lines. Furthermore, cordycepin exposure resulted in the translocation of Bax from the cytosol to the mitochondria and the subsequent release of cytochrome c from the mitochondria. Results from the present study demonstrated that cordycepin inhibited colon cancer cell growth in vitro and this appears to be through the endogenous Bax-dependent mitochondrial apoptosis pathway, which suggested a molecular mechanism for cordycepin against human colon cancer. These results indicated the possibility of cordycepin as a novel drug for the prevention of colon cancer.