Simultaneous recovery of ammonium and total phosphorus from toilet tail water by modified palygorskite-bentonite clay.

Suitable treatment of toilet sewage is a worldwide challenge. The anaerobic baffled reactor (ABR)-microbial fuel cell (MFC)-microbial electrolysis cell (MEC) (AMM) coupling treatment system has been constructed achieving effective removal of carbon, nitrogen, and phosphorus from toilet sewage and resource recovery; however, ammonium (NH4 + -N) and total phosphorus (TP) accumulation in tail water is a found problem of the system. In this study, acid-modified and alkali-heat modified palygorskite-bentonite (Pal-Ben) were used to recover NH4 + -N and TP from the AMM toilet tail water simultaneously. The higher adsorption capacity of the modified clay is attributed to the changes of surface structure of the material. The modified clay Pal-Ben (mass ratio 1:3) activated with alkali performed the highest NH4 + -N and TP recovery rates of 83.6% and 85.5%, respectively. The adsorption of NH4 + -N was more in line with the pseudo-second-order kinetic model and confirmed to be a chemical adsorption process, while the adsorption of TP was more in line with the pseudo-first-order kinetics and a physical adsorption process; the adsorption capacity of NH4 + -N accelerated with decrease of TP removal when pH increased. This study developed a low cost and high capacity of alkaline thermally modified clay removing/recovering NH4 + -N and TP from toilet tail water simultaneously. PRACTITIONER POINTS: A cheap composite clay was developed to recover nitrogen and phosphorus from toilet tail water simultaneously. The low costs and high capacity of alkaline thermally modified clay make it stand out in NH4 + -N and TP removal of toilet tail water. The process mechanism of simultaneous nitrogen and phosphorus recovery was clarified with characterization and kinetic model fitting. The used clay loaded with nutrients could be applied as a slow-release compound fertilizer for soil improvement.

Cullin1 regulates proliferation, migration and invasion of glioma cells.

This study was designed to explore the role of Cullin1 (Cul1) in the pathogenesis of human glioma and to investigate the role of Cul1 in the growth, migration and invasion of glioma cells. Expression of Cul1 in 191 glioma tissues, 8 normal brain tissues and 8 tumor adjacent normal brain tissues was analyzed by tissue microarray and immunohistochemistry. Cul1 expression in human glioblastoma cells was knocked down by specific siRNA to study the effect of down-regulation of Cul1 on proliferation, invasion and migration of glioma cells. Our results showed that Cul1 expression increased significantly in tissues from the benign tumor and malignant tumor in comparison with those from the tumor-adjacent normal brain (P<0.05 for both). We did not find any correlation between Cul1 expression and clinicopathological parameters. In addition, we found that knockdown of Cul1 by RNA interference markedly inhibited cell proliferation and caused cessation of cell cycle. This reduced cell proliferation was due to G1 phase arrest as cyclinA, cyclinD1 and cyclinE were diminished, whereas p21 and p27 were up-regulated. We further demonstrated that silencing of Cul1 in glioma cells inhibited the cell migration and invasion abilities, and down-regulation of MMP-2 and MMP-9 expression greatly contributed to the reduced cell invasion and migration abilities. Our data indicated that Cul1 expression significantly increased in human glioma, and it may be involved in proliferation, migration and invasion of glioma cells.