Organosilica membranes were fabricated using bridged organoalkoxysilanes (bis(triethoxysilyl)methane (BTESM), bis(triethoxysilyl)ethane (BTESE), bis(triethoxysilyl)propane (BTESP), bis(trimethoxysilyl)hexane (BTMSH), bis(triethoxysilyl)benzene (BTESB), and bis(triethoxysilyl)octane (BTESO)) to produce highly permeable molecular sieving membranes. The effect of the organoalkoxysilanes on network pore size and microporous structure was evaluated by examining the molecular size and temperature dependence of gas permeance across a wide range of temperatures. Organosilica membranes showed H2/N2 and H2/CH4 permeance ratios that ranged from 10 to 150, corresponding to network pore size, and both H2 selectivity decreased with an increase in the carbon number between 2 Si atoms. Organosilica membranes showed activated diffusion for He and H2, and a slope of temperature dependence that increased approximate to the increase in the carbon number between 2 Si atoms. The relationship between activation energy and He/H2 permeance ratio for SiO2 and organosilica membranes suggested that the molecular sieving can dominate He and H2 permeation properties via the rigid microporous structure, which was constructed by BTESM and BTESE. With increased in the carbon concentration in silica, polymer chain vibration in organic bridges, which is a kind of solution/diffusion mechanism, can dominate the permeation properties. © 2017 American Institute of Chemical Engineers AIChE J, 63: 4491–4498, 2017
BACKGROUND: The responsiveness of renal cell carcinomas (RCCs) to conventional anticancer drugs is lower than those of other cancer cell lines. 15-deoxy-Δ12, 14-prostaglandin J2 (15d-PGJ2) is known as an endogenous anticancer substance. Previously, we have reported that 15d-PGJ2 activated caspase-3, condensed chromatin and induced apoptosis in RCCs independently of its nuclear receptor, peroxisome proliferator-activated receptor γ (PPARγ). However, synergistic effects of 15d-PGJ2 and various anticancer agents on RCCs have not yet been sufficiently elucidated. METHODS AND RESULTS: In the presence of serum, we examined effects of various anticancer agents on Caki-2 cells. We evaluated antitumor activities by MTT-reducing activity, caspase-3 activity, chromatin condensation and propidium iodide uptake. Anticancer activities of bortezomib (proteasome inhibitor), paclitaxel (microtubule polymer stabilizer), camptothecin (topoisomerase I inhibitor), etoposide (topoisomerase II inhibitor) and doxorubicin (topoisomerase II inhibitor) were detected in Caki-2 cells. RCCs. 15d-PGJ2 significantly enhanced the cytotoxicity of topoisomerase inhibitors (camptothecin, etoposide and doxorubicin), but not those of bortezomib and paclitaxel. 15d-PGJ2 and topoisomerase inhibitors activated caspase 3 by themselves. Combination of 15d-PGJ2 with topoisomerase inhibitors elevated the level of caspase 3 activity synergistically. In addition, 15d-PGJ2 increased the etoposide-condensed chromatin synergistically. A PPARγ antagonist, GW9662, did not block these synergistic effects of 15d-PGJ2 and topoisomerase inhibitors on Caki-2 cells. CONCLUSION: In the present study, we confirmed the antitumor effect of paclitaxel on Caki-2 cells. To our knowledge, we provided the first evidence that bortezomib induced cell death in Caki-2 cells. Furthermore, we demonstrated that 15d-PGJ2 enhanced the antitumor activity of topoisomerase inhibitors against RCC independently from PPARγ.
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