Thin films of phthalocyanine compounds formed on cleaved surfaces of muscovite by the vacuum-condensation method showed well-defined single-directional orientation when their substrates were preheated at 300°C for one hour and then kept at 150°C. Their electron diffraction patterns were fiber diagrams, the fiber period of which coincided with the unit-cell length of the b-axis of the individual compounds. When the substrates were preheated at 400°C for one hour and then kept at 150°C, the films formed on the muscovite surface were composed of discrete crystals with a different orientation. Electron-diffraction patterns from the films revealed that the b-axis of the crystal was inclined to the substrate surface. The cross-grating patterns of the (h0l) plane were obtained when the inclination of the films was properly adjusted to the incident beam. The unit-cell constants of platinum-phthalocyanine vacuum-condensed on muscovite were revealed to be as follows with the monoclinic space group C2⁄c: a=23.18 Å, b=3.818 Å, c=23.84 Å, and β=91.9 °. Films of Cu-, Co-, Fe-, Ni- and metal-free phthalocyanines exhibited an orientation similar to that of the platinum derivative. High-resolution electron-diffraction patterns revealed that all the compounds assumed a conspicuous isomorphism with one another and occurred in the metastable forms of their dimorphs.

Because selective inhibition of cyclooxygenase-2 (COX-2) suppressed the induction of skin tumors in mice by UV and as UV has been shown to induce expression of COX-2 in skin and cells, COX-2 may be crucial for photocarcinogenesis of the skin. We studied the mechanism of UVB-induced expression of COX-2 focusing on the signal transduction pathway involved. Hydrogen peroxide (H2O2) treatment of HaCaT cells induced expression of COX-2 and pretreatment with the antioxidant N-acetylcysteine (NAC) partly inhibited the UVB-induced expression of COX-2 protein in HaCaT cells, suggesting that oxidative stress contributes to COX-2 induction. To examine the signaling pathways involved in the UVB-induced expression of COX-2 in HaCaT cells, we analysed the expression of COX-2 protein after treatment with various inhibitors of signaling molecules. Inhibition of EGFR by a specific inhibitor and by a neutralizing antibody suppressed the induction of COX-2 expression by UV. Although a neutralizing antibody to transforming growth factor-alpha (TGF-alpha) suppressed COX-2 expression induced by TGF-alpha, it did not suppress COX-2 expression by UV, indicating that a direct activation of EGFR is involved. Treatment of cells at low temperature (4 degrees C) inhibited UVB-induced JNK activation, but it did not inhibit COX-2 expression by UV. Inhibitors of MEK, p38 MAP kinase and PI3-kinase, suppressed the induction of COX-2 expression by UV. In contrast, an erbB-2 inhibitor augmented the UVB-induced increase of COX-2 protein. These data indicate that oxidative stress in association with activation of EGFR, ERK, p38 MAP kinase, and PI3-kinase plays crucial roles in the UVB induction of expression of COX-2.

SynopsisThe dynamic moduli, E' and Err, and tan S for PET-CR, PET-EPDM, and PET-UR composites with unidirectional short fibers were studied as a function of temperature by using a Rheovibron. The temperature dependence of tan 6 showed three peaks for PET-elastomer composites. The peaks at the low temperature corresponded to the main dispersion of the respective matrixes and the peak at about 140°C to the adispersion of PET fiber. A small and broad peak observed at a temperature between 60 and 120°C may be caused by the relaxation of the interface region between fibers and matrix. The longitudinal storage modulus for the composite = V,. Ei + V, E A where E; and EL are the storage moduli for fiber and matrix and V, and V, are the volume fraction of fiber and matrix, respectively. In the transverse direction of fibers, the composite modulus E; was expressed by the logarithmic law of mixing as follows: log E; = V,. log E i + V, . log EL. The peak values of tan 6 from the main dispersion of the respective matrixes were given by the equation, (tan G,,,),/(tan 6,,), = 1 -fi . V , where (tan S,max)c and (tan 6, J, are the maximum values of the loss tangent for the composite and matrix, respectively, and /3 is coefficient depending on matrix's type. The fi value of PET-CR composite is the largest one among those of the composites.was given by the parallel model as

Recent studies have emphasized the important role of Stat3 activation in a number of human tumors from the viewpoint of its oncogenic and antiapoptotic activity. In this study, we examined the role and related signaling molecules of Stat3 in the carcinogenesis of human cutaneous squamous cell carcinoma (SCC). In 35 human cutaneous SCC samples, 86% showed overexpression of phosphorylated (p)-Stat3, and most of those simultaneously overexpressed p-EGFR or p-Akt. Constitutive activation of EGFR and Stat3 was observed in three SCC cell lines and four of five SCC tissues. AG1478, an inhibitor of the EGFR, downregulated Stat3 activation in HSC-1 human SCC cells. AG1478 inhibited cell proliferation and induced apoptosis of HSC-1 cells but did not inhibit the growth of normal human epidermal keratinocytes that did not show Stat3 activation. Furthermore, a PI3K inhibitor also suppressed Stat3 activation in HSC-1 cells to some degree. Combined treatment with the PI3K inhibitor and AG1478 strongly suppressed Stat3 activity and dramatically induced apoptosis of HSC-1 cells. These data suggest that Stat3 activation through EGFR and/or PI3K/Akt activation plays a critical role in the proliferation and survival of human cutaneous SCC.