Possible mechanism for the activation of PS by MIL-88A involves heterogeneous and homogeneous reaction.

In this work, a novel effective heterogeneous catalyst metal-organic framework MIL-53(Fe) has been synthesized for the purpose of activating persulfate (PS). Catalytic performance of MIL-53(Fe) activated under different vacuum conditions was investigated; stability and reusability of the catalyst were evaluated, and the activation mechanism was also investigated. The results indicated that vacuum activation could cause variation of the FeII/FeIII relative amount ratio of the catalyst, and thus would change the catalytic activities of MIL-53(Fe), because FeII or FeIII CUS (coordinative unsaturated metal site) are alternative active sites. It was found that MIL-53(Fe)-2 exhibits good performance for PS activation and could be used for multiple cycles. A removal rate of 98% for Orange G was obtained within 120min (95.7% mineralization efficiency), and 94.3% was attained in the fifth cycle. The mechanism of the activation of PS by MIL-53(Fe) was also suggested, which involves a predominant heterogeneous reaction and an auxiliary homogeneous reaction. The findings of this study provide new insight into the application of the reactive metal-organic frameworks in activating persulfate for the degradation of environmental contaminants.

Renal cell carcinoma (RCC) is one of the most drug-resistant malignancies, and an effective therapy is lacking for metastatic RCC. Anisomycin is known to inhibit protein synthesis and induce ribotoxic stress. The aim of this study was to explore whether anisomycin enhances the cytotoxic effects of mapatumumab, a human agonistic monoclonal antibody specific for death receptor 4 (DR4), in human RCC cells. We examined the cytotoxicity of anisomycin alone and in combination with mapatumumab in human RCC cell lines and primary RCC cell cultures. RCC cells treated with anisomycin showed cytotoxicity in a dose-dependent manner. Anisomyin in combination with mapatumumab showed a synergistic effect not only in two human RCC cell lines but also in five primary RCC cell cultures. The synergy between anisomycin and mapatumumab for cytotoxicity was also observed for apoptosis. Interestingly, anisomycin significantly increased DR4 expression at both the mRNA and the protein level. Furthermore, the combination-induced cytotoxicity was significantly suppressed by a human recombinant DR4:Fc chimeric protein. The combination of anisomycin and mapatumumab also enhanced the activity of caspases 8 and 3, the downstream molecules of death receptors. These findings indicate that anisomycin sensitizes RCC cells to DR4-mediated apoptosis through the induction of DR4, suggesting that combinational treatment with anisomycin and mapatumumab might represent a novel therapeutic strategy for the treatment of RCC.