The goal of this study was to gain a better understanding of the feasibility of replacing Cr(VI) in the chlorate process by Mo(VI), focusing on the cathode reaction selectivity for hydrogen evolution on steel and titanium in a hypochlorite containing electrolyte. To evaluate the ability of Cr(VI) and Mo(VI) additions to hinder hypochlorite reduction, potential sweep experiments on rotating disc electrodes and cathodic current efficiency (CE) measurements on stationary electrodes were performed. Formed electrode films were investigated with scanning electron microscopy and energy-dispersive X-ray spectroscopy. Cathodic hypochlorite reduction is hindered by the Mo-containing films formed on the cathode surface after Mo(VI) addition to the electrolyte, but much less efficient compared to Cr(VI) addition. Very low levels of Cr(VI), in the mM range, can efficiently suppress hypochlorite reduction on polished titanium and steel. Phosphate does not negatively influence the CE in the presence of Cr(VI) or Mo(VI) but the Mo-containing cathode films become thinner if the electrolyte during the film build-up also contains phosphate. For a RuO2-TiO2 anode polarized in electrolyte with 40 mM Mo(VI), the anode potential increased and increased molybdenum levels were detected on the electrode surface.

QC 20130109

BackgroundThis study aimed to investigate the mechanism of CHEK2 gene dysfunction in drug resistance of triple negative breast cancer (TNBC) cells.Material/MethodsTo perform our study, a stable CHEK2 wild type (CHEK2 WT) or CHEK2 Y390C mutation (CHEK2 Y390C) expressed MDA-MB-231 cell line was established. MTT assay, cell apoptosis assay and cell cycle assay were carried out to analyze the cell viability, apoptosis, and cell cycle respectively. Western blotting and qRT-PCR were applied for related protein and gene expression detection.ResultsWe found that the IC50 value of DDP (Cisplatin) to CHEK2 Y390C expressed MDA-MB-231 cells was significantly higher than that of the CHEK2 WT expressed cells and the control cells. After treatment with DDP for 48 h, cells expressing CHEK2 WT showed lower cell viability than that of the CHEK2 Y390C expressed cells and the control cells; compared with the CHEK2 Y390C expressed cells and the control cells, cells expressing CHEK2 WT showed significant G1/S arrest. Meanwhile, we found that compared with the CHEK2 Y390C expressed cells and the control cells, cell apoptosis was significantly increased in CHEK2 WT expressed cells. Moreover, our results suggested that cells expressing CHEK2 WT showed higher level of p-CDC25A, p-p53, p21, Bax, PUMA, and Noxa than that of the CHEK2 Y390C expressed cells and the control cells.ConclusionsOur findings indicated that CHEK2 Y390C mutation induced the drug resistance of TNBC cells to chemotherapeutic drugs through administrating cell apoptosis and cell cycle arrest via regulating p53 activation and CHEK2-p53 apoptosis pathway.

Background Successful chemotherapy of lung cancer relies largely on the use of a good drug delivery system (DDS). We successfully constructed a hybrid DDS comprised of hydroxyapatite (HAP) nanoparticles and bovine serum albumin (BSA). Material/Methods The HAP nanoparticles were selected as the core to encapsulate the anticancer drug doxorubicin (DOX), followed by surface modification of BSA as a stabilizer and shielding corona to finally prepare the hybrid DDS (BSA/HAP/DOX). Results The following characterizations revealed that BSA/HAP nanoparticles have high stability, high biocompatibility, and good DOX-loading capability to meet in vivo applications. Moreover, BSA/HAP/DOX can enhance the cellular uptake of drug in A549 cells (lung cancer cells). Most importantly, BSA/HAP had better in vivo tumor targetability than bare HAP nanoparticles, which resulted in stronger anticancer efficacy both in vitro and in vivo than free DOX or HAP/DOX, and greatly decreased the adverse effects of free DOX. Conclusions Our hybrid DDS shows potential to be applied in more advanced application of cancer therapy.