[Optimization of Dyeing Wastewater Treatment with New Eco-friendly Polysilicate Ferromanganese].

To improve the efficiency of the removal of dye wastewater, a new type of coagulant "polysilicate ferromanganese (PSFM)" has been synthesized using sodium silicate, ferrous sulfate, and potassium permanganate. Three dyes (direct red, disperse blue, and active yellow) were used for the coagulation tests. The effects of the alkalinity and turbidity on the performance of PSFM were studied. The experimental results show that PSFM performs well with respect to the coagulation of the direct red and disperse blue dyes. The color and TOC removal efficiencies reach 99.2%, 95.4% and 98.5%, and 93.8%, respectively. The coagulation performance is better than that of the conventional coagulants polysilicate iron (PSF), Al2(SO4)3, and FeCl3. The color and TOC removal rates of PSFM for the active yellow dye reach 56% and 51%, respectively. Turbidity has no significant effect on the coagulation efficiency of PSFM. The purification efficiency and alkalinity depend on the amount of dye to be removed. The best alkalinity for the direct red, disperse blue, and active yellow dyes is 50 mg·L-1, 0 mg·L-1, and 75 mg·L-1, respectively. In addition, PSFM has been characterized by scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FTIR), and X-ray diffraction (XRD). The Zeta potentials of the mixed solutions and flocs during coagulation were also determined. The main indicators of PSFM coagulation are positively charged polynuclear complexes produced by hydrolysis of Fe+ and Mn+ and the bridging polymerization of polysilicon. The adsorption of hydrated manganese dioxide and hydroxyl oxide may also be included.

[Adsorption of Tetracycline on Simulated Suspended Particles in Water].

The mechanism of adsorption of a typical antibiotic (tetracycline, TC) on particles in the aquatic environment and the parameters affecting adsorption were investigated. Experiments were conducted to elucidate the effects of pH and various cation species with different concentrations. The results show that the adsorption of TC on particles is rapid during the first four hours in the mixing stage. The adsorption process becomes slow after the first four hours. The adsorption of TC on particles can be described well by a Langmuir equation. The maximum adsorption of TC on particles occurs at pH 4.5, however it is reduced by strongly acidic (pH<4) or alkaline (pH>9) conditions. Moreover, the adsorption process is also inhibited by various cations (e.g. Na+ and Ca2+) in the range of 0.0001-0.1 mol·L-1 ionic concentrations. A special finding concerns Al3+ ions; at a low concentration of these ions (0-0.0001 mol·L-1) the adsorption of TC on particles improves, whereas at increased concentrations the adsorption is weakened. In summary, an effective removal of the particles is critical to control TC pollution in natural waters because of the rapid adsorption of TC on particles.

Scutellarin Increases Cisplatin-Induced Apoptosis and Autophagy to Overcome Cisplatin Resistance in Non-small Cell Lung Cancer via ERK/p53 and c-met/AKT Signaling Pathways.

Cisplatin, as the first-line anti-tumor agent, is widely used for treatment of a variety of malignancies including non-small cell lung cancer (NSCLC). However, the acquired resistance has been a major obstacle for the clinical application. Scutellarin is a active flavone extracted from Erigeron breviscapus Hand-Mazz that has been shown to exhibit anticancer activities on various types of tumors. Here, we reported that scutellarin was capable of sensitizing A549/DDP cells to cisplatin by enhancing apoptosis and autophagy. Mechanistic analyses indicated that cisplatin-induced caspase-3-dependent apoptosis was elevated in the presence of scutellarin through activating extracellular signal-regulated kinases (ERK)-mediated p53 pathway. Furthermore, scutellarin also promoted cisplatin-induced cytotoxic autophagy, downregulated expression of p-AKT and c-met. Deficiency of c-met reduced p-AKT level, and inhibition of p-AKT or c-met improved autophagy in A549/DDP cells. Interestingly, loss of autophagy attenuated the synergism of this combination. In vivo, the co-treatment of cisplatin and scutellarin notably reduced the tumor size when compared with cisplatin treatment alone. Notably, scutellarin significantly reduced the toxicity generated by cisplatin in tumor-bearing mice. This study identifies the unique role of scutellarin in reversing cisplatin resistance through apoptosis and autophagy, and suggests that combined cisplatin and scutellarin might be a novel therapeutic strategy for patients with NSCLC.

Norcantharidin alone or in combination with crizotinib induces autophagic cell death in hepatocellular carcinoma by repressing c-Met-mTOR signaling.

There is an urgent need for effective molecular therapies for hepatocellular carcinoma (HCC), the third-leading cause of cancer-related deaths worldwide. Norcantharidin (NCTD), a demethylated derivative of cantharidin, reportedly exhibits anticancer activity against various types of tumors, including HCC, though the mechanisms involved remain largely unknown. Here, we report that NCTD reduces viability of human MHCC-97H (97H) and HepG2 HCC cells, and induces cell death by triggering high levels of autophagy. Moreover, a significant attenuation of tumor growth was observed after NCTD treatment of HepG2 tumors in vivo, and this effect was enhanced by co-treatment with the c-Met inhibitor crizotinib. Interestingly, western blot analyses showed that the cytotoxic autophagy induced by NCTD correlates with a reduction in the phosphorylation status of both c-Met and m-TOR. These results suggest that cytotoxic autophagy resulting from inhibition of c-Met/mTOR signaling may be achieved in HCC by combined NCTD and crizotinib administration. Further studies to validate the therapeutic potential of this approach are warranted.

Characterization of a Synthetic Steroid 24-keto-cholest-5-en-3ß, 19-diol as a Neuroprotectant.

BACKGROUND: Neuroactive steroids represent promising candidates for the treatment of neurological disorders. Our previous studies identified an endogenous steroid cholestane-3ß, 5α, 6ß-triol (Triol) as a novel neuroprotectant. AIM: We aimed to identify a potent candidate for stroke treatment through a screening of Triol analogs. METHODS: Hypoxia- and glutamate-induced neuronal injury models in vitro, middle cerebral artery occlusion (MCAO)-induced cerebral ischemia model in vivo, fluorescein diacetate (FDA) for alive and propidium iodide (PI) for dead staining, LDH assay, and calcium imaging techniques were used. RESULTS: 24-keto-cholest-5-en-3ß, 19-diol (Diol) showed the most potent neuroprotective effect among the screened structurally related compounds. FDA and PI staining showed that Diol concentration dependently increased the survival rate of cerebellar granule neurons (CGNs) challenged with glutamate or hypoxia, with an effective threshold concentration of 2.5 µM. Consistently, the quantitative LDH release assay showed the same concentration-dependent protection in both models. Diol, at 10 µM, potently decreased glutamate- and hypoxia-induced LDH release from 51.6 to 18.2% and 62.1 to 21.7%, respectively, which values are close to the normal LDH release (~16-18%). Moreover, we found Diol effectively decreased MCAO-induced infarction volume in mice from ~23% to 7%, at a dose of 6 mg/kg. We further explored the underlying mechanism and found that Diol attenuated NMDA-induced intracellular calcium ([Ca(2+) ]i ) increase in cortical neurons, suggesting a negative modulatory effect on NMDA receptor. CONCLUSION: Taken together, we identified Diol as a potent neuroprotectant. It may represent a novel and promising neuroprotectant for stroke intervention.

MiR-218-targeting-Bmi-1 mediates the suppressive effect of 1,6,7-trihydroxyxanthone on liver cancer cells.

Traditional Chinese medicine is recently emerged as anti-cancer therapy or adjuvant with reduced side-effects and improved quality of life. In the present study, an active ingredient, 1,6,7-trihydroxyxanthone (THA), derived from Goodyera oblongifolia was found to strongly suppress cell growth and induce apoptosis in liver cancer cells. MicroRNAs are a group of small non-coding RNAs that regulate gene expression at post-transcriptional levels. Our results demonstrated that miR-218 was up-regulated and oncogene Bmi-1 was down-regulated by THA treatment. Further investigation showed that THA-induced-miR-218 up-regulation could lead to activation of tumor suppressor P16(Ink4a) and P14(ARF), the main down-stream targets of Bmi-1. In conclusion, THA might be a potential anti-cancer drug candidate, at least in part, through the activation of miR-218 and suppression of Bmi-1 expression.