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Polymeric materials based on ϵ-caprolactone (CL), 1,5-dioxepan-2-one (DXO), and trimethylene carbonate (TMC) were prepared and evaluated as possible candidates for polymer-on-multielectrode (PoM) applications. CL was copolymerized with either DXO or TMC in the presence of the diol initiator 1,4-benzenedimethanol (BDM). The ring-opening polymerization experiments, carried out in bulk and using tin(II) catalysis, yielded the desired low molecular weight random copolymer diols, as evidenced by NMR, IR, MALDI-ToF MS, and DSC techniques. Upon reaction with acryloyl chloride, the corresponding diacrylate end-capped copolymers were obtained. The latter were characterized by NMR and IR spectroscopy, and their photocross-linking (in the presence of a UV initiator) was followed by ATR-FTIR spectroscopy. Transparent and soft thin films of the copoly(ether-ester) and copoly(ester-carbonate) diacrylates were prepared and cured under UV irradiation. The resulting polymeric films showed good biocompatibility properties as far as in vitro neural stem cells proliferation and differentiation to neurons and astrocytes are concerned. Noteworthy are the beneficial effects obtained upon preconditioning the copolymers by means of the cell-culture medium and the excellent properties shown particularly by the CL−TMC copolymer. Moreover, preliminary results show that microchannel formation by photocuring is possible with the synthesized polymers. [ABSTRACT FROM AUTHOR]

Insulin‐like growth factor‐I receptor (IGF‐IR) is often overexpressed in malignant tumors, and is involved in the establishment and maintenance of malignant phenotypes. Tyrosine kinase receptor endocytosis is commonly triggered by ligand binding and occurs via clathrin‐coated vescicles that transfer the receptor to the lysosome system for degradation. Our study aims at the evaluation of the mechanisms involved in IGF‐IR downregulation in neoplastic (Npl) and non‐neoplastic (non‐Npl) cells. Exposure to insulin‐like growth factor‐I (IGF‐I) of human lung adenocarcinoma cell lines (A549 and H1299) triggers IGF‐IR ubiquitination and internalization processes that require energy and are preceded by the phosphorylation of receptor tyrosines. Differently from other plasma membrane substrates of the ubiquitin system, IGF‐IR is degraded mostly by the proteasome in these tumor cell lines. The degradation is inhibited by lactacystin and unaffected by lysosomal inhibitors such as bafilomycin A1 and NH4Cl. IGF‐IR is processed in a similar manner also in fresh specimens of human lung tumors, while it requires active lysosomal functions in non‐Npl human lung tissues. These results suggest that the degradation routes of ubiquitinated IGF‐IR diverge in normal and Npl cells, and further support the involvement of IGF‐IR signaling in cancer. Such a different route for IGF‐IR processing might take place sometime during development, since both proteasome and lysosome pathways are active in fetal lung human fibroblasts, IMR90 cells. J. Cell. Physiol. 208: 354–362, 2006. © 2006 Wiley‐Liss, Inc. [ABSTRACT FROM AUTHOR]