The U(VI) complex with a pentadentate Schiff base ligand (N,N'-disalicylidenediethylenetriaminate = saldien(2-)) was prepared as a starting material of a potentially stable U(V) complex without any possibility of U(V)O(2)(+)...U(V)O(2)(+) cation-cation interaction and was found in three different crystal phases. Two of them had the same composition of U(VI)O(2)(saldien) x DMSO in orthorhombic and monoclinic systems (DMSO = dimethyl sulfoxide, 1a and 1c, respectively). The DMSO molecule in both 1a and 1c does not show any coordination to U(VI)O(2)(saldien), but it is just present as a solvent in the crystal structures. The other isolated crystals consisted only of U(VI)O(2)(saldien) without incorporation of solvent molecules (1b, orthorhombic). A different conformation of the coordinated saldien(2-) in 1c from those in 1a and 1b was observed. The conformers exchange each other in a solution through a flipping motion of the phenyl rings. The pentagonal equatorial coordination of U(VI)O(2)(saldien) remains unchanged even in strongly Lewis-basic solvents, DMSO and N,N-dimethylformamide. Cyclic voltammetry of U(VI)O(2)(saldien) in DMSO showed a quasireversible redox reaction without any successive reactions. The electron stoichiometry determined by the UV-vis-NIR spectroelectrochemical technique is close to 1, indicating that the reduction product of U(VI)O(2)(saldien) is [U(V)O(2)(saldien)](-), which is stable in DMSO. The standard redox potential of [U(V)O(2)(saldien)](-)/U(VI)O(2)(saldien) in DMSO is -1.584 V vs Fc/Fc(+). This U(V) complex shows the characteristic absorption bands due to f-f transitions in its 5f(1) configuration and charge-transfer from the axial oxygen to U(5+).
The receptor for advanced glycation end products (RAGE) is associated with cancer progression in several human cancers. In this study, we examined the roles of RAGE in the angiogenesis of oral squamous cell carcinoma (OSCC). RAGE concentration was examined in 20 OSCC tumors by enzyme-linked immunosorbent assay (ELISA). The microvessel density (MVD) and lymph vessel density (LVD) were examined by immunostaining. Concentrations of vascular endothelial growth factor (VEGF) and VEGF-C were examined in tumor tissues by ELISA. Tumoral RAGE concentration was associated with higher tumor MVD (P = 0.0123) and tumor VEGF concentration (P = 0.0344), but not with LVD and VEGF-C concentration. Treatment with RAGE ligand, high-mobility group box (HMGB)-1 increased the secretion of VEGF but not that of VEGF-C in human OSCC cell lines, HSC-3 and HSC-4. The effect of HMGB-1 was abrogated by RAGE down-regulation by antisense S-oligodeoxynucleic acid. These results suggest that RAGE expression is closely associated to angiogenesis in OSCC.
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