A new solid polymer electrolyte based on semi‐interpenetrating polymer networks (semi‐IPN) of crosslinked poly(glycidyl methacrylate‐co‐acrylonitrile)/poly(ethylene oxide) (P(GMA‐co‐AN)/PEO) was synthesized with diethylenetriamine (DETA) as the crosslinking agent and characterized. Fourier transform infrared spectroscopy (FTIR) spectra suggested the formation of semi‐IPN structure by crosslinking and revealed the interactions of Li+ ions with both the ether oxygen in PEO chain and the nitrogen atom in AN segments. Differential scanning calorimetry (DSC) and X‐ray diffraction pattern (XRD) measurements showed that crystallization of the semi‐IPN polymer electrolyte was greatly impeded. Measurement of mechanical properties revealed that tensile strength of the polymer electrolyte was increased after crosslinking. Results of electrochemistry tests suggested that the new polymer electrolyte exhibited a high‐ionic conductivity (10−4 S/cm) at room temperature, and an Arrhenius‐like behavior of the conductivity was observed. And the semi‐IPN polymer electrolyte with less content of PEO exhibited lower ion conductivity. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2008

Our findings are in agreement with those in recent publications and support the possibility that periprosthetic osteolysis and aseptic loosening in hips with a metal-on-metal articulation are possibly associated with hypersensitivity to metal debris. Prospective, comparative, randomized long-term studies are necessary to determine the cause(s) of loosening of prostheses with this particular articulation.

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ILK overexpression in BCC is implicated in tumour progression probably through the induction of an EMT-related molecular profile. Nuclear localization of E-cadherin in BCC is also associated with aggressive tumour features.

The RANK/RANKL axis emerges as a key regulator of breast cancer initiation, progression, and metastasis. RANK-c is a RANK receptor isoform produced through alternative splicing of the TNFRSF11A (RANK) gene and a dominant-negative regulator of RANK-induced nuclear factor-κB (NF-κB) activation. Here we report that RANK-c transcript is expressed in 3.2% of cases in The Cancer Genome Atlas breast cancer cohort evenly between ER-positive and ER-negative cases. Nevertheless, the ratio of RANK to RANK-c (RANK/RANK-c) is increased in ER-negative breast cancer cell lines compared to ER-positive breast cancer cell lines. In addition, forced expression of RANK-c in ER-negative breast cancer cell lines inhibited stimuli-induced NF-κB activation and attenuated migration, invasion, colony formation, and adhesion of cancer cells. Further, RANK-c expression in MDA-MB-231 cells inhibited lung metastasis and colonization in vivo. The RANK-c-mediated inhibition of cancer cell aggressiveness and nuclear factor-κB (NF-κB) activation in breast cancer cells seems to rely on a RANK-c/TNF receptor-associated factor-2 (TRAF2) protein interaction. This was further confirmed by a mutated RANK-c that is unable to interact with TRAF2 and abolishes the ability to attenuate NF-κB activation, migration, and invasion. Additional protein interaction characterization revealed epidermal growth factor receptor (EGFR) as a novel interacting partner for RANK-c in breast cancer cells with a negative effect on EGFR phosphorylation and EGF-dependent downstream signaling pathway activation. Our findings further elucidate the complex molecular biology of the RANKL/RANK system in breast cancer and provide preliminary data for RANK-c as a possible marker for disease progression and aggressiveness.