A series of semialicyclic polyimides (PIs) have been successfully prepared by the polycondensation of two alicyclic dianhydrides, 1,2,3,4-cyclobutanetetracarboxylic dianhydride (CBDA) and 1,2,4,5-cyclohexanetetracarboxylic dianhydride (CHDA) with two sulfur-containing aromatic diamines, 4,4′-thiobis [(pphenylenesulfanyl)aniline] (3SDA) and 2,7-bis(4-aminophenylenesulfanyl)thianthrene (APTT), respectively, by a two-step polymerization procedure via the soluble poly(amic acid) (PAA) precursors. Flexible and tough PI films were obtained with a tensile strength greater than 82 MPa and elongation at breaks higher than 12%. The films showed good thermal and thermal-oxidative stability without significant weight loss up to 400 °C, both in air and nitrogen. The glass-transition temperatures of the PIs ranged from 236.5 to 274.1 °C. Good optical transparency, including the cutoff wavelengths lower than 350 nm and transmittances higher than 80% at 400 nm, was achieved for all the PI films. The refractive indices of the PI films were in the range of 1.6799-1.7130 measured at 632.8 nm, which agreed well with the values calculated by the time-dependent density functional theory (TD-DFT). In addition, PAA-II a (CHDA-3SDA) showed a good affinity with silica-modified TiO 2 nanoparticles. The hybrid system with 45 wt % load of TiO 2 nanoparticles, combined with the photobase generator N-{ [(4,5-dimethoxy-2-nitrobenzyl)oxy]carbonyl}2,6-dimethylpiperidine (DNCDP) exhibited good photolithographic characteristics. A fine negative pattern with a resolution of approximately 4 µm was successfully printed on the hybrid film. The cured PI-II a -TiO 2 hybrid film exhibited a refractive index of 1.8100 at 632.8 nm.

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Ovarian cancer remains the most lethal gynecologic cancer and new targeted molecular therapies against this miserable disease continue to be challenging. In this study, we analyzed the expressional patterns of Interleukin-6 (IL-6) and its receptor (IL-6R) expression in ovarian cancer tissues, evaluated the impact of these expressions on clinical outcomes of patients, and found that a high-level of IL-6R expression but not IL-6 expression in cancer cells is an independent prognostic factor. In in vitro analyses using ovarian cell lines, while six (RMUG-S, RMG-1, OVISE, A2780, SKOV3ip1 and OVCAR-3) of seven overexpressed IL-6R compared with a primary normal ovarian surface epithelium, only two (RMG-1, OVISE) of seven cell lines overexpressed IL-6, suggesting that IL-6/IL-6R signaling exerts in a paracrine manner in certain types of ovarian cancer cells. Ovarian cancer ascites were collected from patients, and we found that primary CD11b+CD14+ cells, which were predominantly M2-polarized macrophages, are the major source of IL-6 production in an ovarian cancer microenvironment. When CD11b+CD14+ cells were co-cultured with cancer cells, both the invasion and the proliferation of cancer cells were robustly promoted and these promotions were almost completely inhibited by pretreatment with anti-IL-6R antibody (tocilizumab). The data presented herein suggest a rationale for anti-IL-6/IL-6R therapy to suppress the peritoneal spread of ovarian cancer, and represent evidence of the therapeutic potential of anti-IL-6R therapy for ovarian cancer treatment.

The prolongation of progression-free survival (PFS) in patients with advanced ovarian cancer by antiangiogenic therapy has been shown in several clinical trials. However, although an anti-VEGF antibody (bevacizumab) is the only option currently available, its efficacy is limited and it is not cost effective for use in all patients. Therefore, the development of a novel antiangiogenic drug, especially composed of smallmolecule compounds, could be a powerful armament for ovarian cancer treatment. As NF-kB signaling has the potential to regulate VEGF expression, we determined to identify whether VEGF expression is associated with NF-kB activation and to investigate the possibility of a novel IKKb inhibitor, IMD-0354 (IMMD Inc.), as an antiangiogenic drug. Tissue microarrays from 94 ovarian cancer tissues were constructed and immunohistochemical analyses performed. We revealed that IKK phosphorylation is an independent prognostic factor (PFS: 26