Transformation and fate of non-reactive phosphorus (NRP) in enhanced biological phosphorus removal process with sidestream phosphorus recovery.

Recovery of phosphorus (P) from wastewater can help establish a new P cycle. However, there are many P forms in wastewater, not always in reactive forms, which are the most suitable for direct recovery. The enhanced biological phosphorus removal process with sidestream phosphorus recovery (EBPR-SPR) is an effective way to remove and recover P resources in wastewater, but there is a lack of research on the transformation and fate of non-reactive phosphorus (NRP) in it. This study selected four model NRP to investigate their transformation and fate in an EBPR-SPR process. The transformation of NRP in pure water and activated sludge under anaerobic and aerobic conditions were compared. The effects of Ca/P ratio and pH on NRP recovery were studied, and the recovery products of NRP were characterized. It was found that NRP containing phosphoanhydride and phosphoester bonds were more easily hydrolyzed to reactive P (RP) than that containing PC bonds. NRP will be adsorbed and accumulated by activated sludge, and activated sludge will accelerate the conversion of NRP to RP. Tripolyphosphate can form complex precipitation with Ca2+. When multiform P co-existed, Ca2+ preferably complexed with polyphosphate, which harmed RP recovery. The conversion of NRP should be strengthened to recover more P in wastewater. The effect of NRP should be considered when recovering P from wastewater.

Genistein Inhibits the Proliferation of Human Lung Cancer PC14 Cells through the ERK and JNK Pathways / 中国医科大学学报

Objective To investigate the effect of genistein on the proliferation of human lung cancer PC14 cells and the underlying mechanisms. Methods Cell proliferation was examined using the MTT and colony formation assays. Western blotting was used to analyze protein expression levels. Results Genistein significantly inhibited the proliferation of PC14 cells in a concentration and time dependent manner. PD98059, SB203580, and SP100625, three specific inhibitors of the MAPK pathway, significantly inhibited the proliferation of PC14 cells. Moreover, genistein inhibited the phosphorylation of ERK and JNK in a dose dependent manner. Conclusion Genistein can inhibit the proliferation of PC14 cells, which may be related to its inhibitory effect on ERK and JNK activation.

Aspirin suppresses neuronal apoptosis, reduces tissue inflammation, and restrains astrocyte activation by activating the Nrf2/HO-1 signaling pathway.

The nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element signaling pathway plays a substantial role in preventing oxidative stress-related diseases. Aspirin has been shown to exert several pharmacological effects by inducing the expression of the heme oxygenase-1 (HO-1) protein. However, the effects of aspirin on spinal cord injury (SCI) have rarely been studied. Therefore, we sought to investigate the neuroprotective effects of aspirin after SCI. We employed a spinal cord contusion model in Sprague-Dawley rats, and aspirin was administered intraperitoneally for 7 days. Nissl staining showed that the aspirin treatment significantly reduced the loss of motor neurons after SCI compared with vehicle-treated animals. The expression of Nrf2, quinine oxidoreductase 1, and HO-1 proteins was increased in aspirin-treated animals after SCI compared with the vehicle group. In addition, aspirin simultaneously decreased the expression of inflammation-related proteins, such as tumor necrosis factor-α and interleukin-6 after SCI. Moreover, the ratio of apoptotic neurons in the anterior horn and the levels of the apoptosis-related proteins caspase-3, cleaved caspase-3, and Bax were significantly decreased in the aspirin group compared with the vehicle group. Immunofluorescence staining was used to detect the colocalization of NeuN and HO-1, and the results showed that aspirin significantly increased expression of the HO-1 protein in neurons. In addition, western blots and immunofluorescence staining showed aspirin restrained astrocyte activation. In conclusion, aspirin induces neuroprotective effects by inhibiting astrocyte activation and apoptosis after SCI through the activation of the Nrf2/HO-1 signaling pathway.

Sorafenib inhibits the proliferation of human oral cancer TCA8113 cells through the activation of p38MAPK / 实用口腔医学杂志

Objective:To investigate the effect of sorafenib on the proliferation of human oral cancer TCA8113 cells and to explore the underlying mechanisms.Methods:Mter treated with sorafenib at 2.5,5,10,20 μg/ml respectively for48 h,TCA8113 cell proliferation was examined by MTT and colony formation assay.Western blotting was employed to examine the p38MAPK expression in the cells.TCA8113 cells were pretreated with 10 μmol/L of SB203580 (a specific inhibitor of p38MAPK) for 30 min,and then by different concentrations of sorafenib for 48 h,cell proliferation was tested by MTT assay.Results:Sorafenib significantly inhibited the proliferation of TCA8113 cells in a concentration dependent fashion.Sorafenib also remarkably promoted the activation of p38MAPK of the cells.SB203580 significantly alleviated soiafenib induced TCA8113 cell viability decrease.Conclusion:Sorafenib can inhibit the proliferation of TCA8113 cells,which may be related to the activation of p38MAPK.

Genistein inhibits proliferation of human oral cancer TCA8113 cells through suppression of VEGF expression / 中国病理生理杂志

AIM:To investigate the effect of genistein on the proliferation of human oral cancer TCA 8113 cells and to explore the underlying mechanisms .METHODS:The cell proliferation was examined by MTT assay , cell counting and colony formation assay .Western blotting was employed to examine the protein levels of vascular endothelial growth fac -tor (VEGF), extracellular signal-regulated kinase (ERK) and p-ERK.RESULTS: Genistein significantly inhibited the proliferation of TCA8113 cells in a concentration-dependent fashion .Moreover , genistein dose-dependently decreased the protein levels of VEGF, ERK and p-ERK.The expression of VEGF was also blunted by U 0126, a specific inhibitor of ERK.U0126 and axitinib, a VEGF receptor antagonist , both significantly inhibited the proliferation of TCA 8113 cells. CONCLUSION:Genistein inhibits the proliferation of TCA8113 cells, which may be related to its inhibitory effect on ERK expression and activation , thus subsequently decreasing the expression of VEGF .

L-Carnitine inhibits H2 O2-mediated NFATc3 nuclear translocation / 中国病理生理杂志

AIM: To explore the effect of L-carnitine on nuclear factor of activated T-cells, cytoplasmic 3 (NFATc3) in cardiomyocytes under H2O2 stimulation.METHODS: Primary cultured neonatal rat myocardial cells were stimulated by H2 O2 at concentration of 200μmol/L for 12 h to induce oxidative stress injury.In treatment group, L-carni-tine and cyclosporin A ( CsA) , a specific inhibitor of calcineurin ( CaN) , were administered 30 min prior to H2 O2 stimula-tion.After treatment, total, cytoplasmic and nuclear NFATc3 protein levels were determined by Western blotting.The method of immunofluoresence was used to evaluate the distribution of NFATc3.RESULTS: H2 O2 treatment produced no effect on the expression of total NFATc3, but caused its translocation from the cytosolic to nuclear compartment, which was greatly blunted by L-carnitine pretreatment.CONCLUSION:L-carnitine antagonized oxidative stress injury via alleviating NFATc3 nuclear translocation.