Complexes of cis-dioxomolybdenum(VI) and oxovanadium(IV) with a tridentate ONS donor ligand: synthesis, spectroscopic properties, X-ray crystal structure and catalytic activity.

New cis-dioxomolybdenum(VI) and oxovanadium(IV) complexes of the Schiff base, derived from S-methyl dithiocarbazate and 2,3-dihydroxybenzaldehyde (H2dhsm), have been synthesized. The complexes of the type cis-[MoO2(dhsm)] (1a), cis-[MoO2(dhsm)(D)] (1b-1d) [D=neutral monodentate ligand; EtOH, pyridine (py) or imidazole (imz)], [VO(dhsm)(NN)] (2a, 2b) [NN=2,2'-bipyridine (bipy) or 1,10-phenanthroline (phen)] and [VO(dhsm)] (2c) have been isolated, characterized by (1)H NMR, IR, UV-Vis and EPR spectral studies and investigated by cyclic voltammetry. The X-ray crystal structure of cis-[MoO2(dhsm)(EtOH)] (1b) has been determined and shows that the complex has a distorted octahedral geometry in which the H2dhsm behaves as a dianionic ONS tridentate ligand coordinating via phenoxide oxygen, hydrazinic nitrogen and thiolate sulfur. The oxomolybdenum(IV) complex [MoO(dhsm)] (1e) has obtained from dioxomolybdenum(VI) complex (1b) by oxo abstraction with PPh3. The reactivity of the complexes toward catalytic oxidation of alcohols in the presence of H2O2 and t-BuOOH as co-oxidants under solvent free conditions is reported.

Gravin gene expression in acute myeloid leukemia.

Acute leukemias are caused by genetic and epigenetic mechanisms involving tumor suppressor genes and oncogenes. Aberrant DNA methylation patterns are the most frequent molecular alterations detected in acute myeloid leukemia (AML). Gravin is down-regulated in several solid tumors and is implicated in tumorigenesis. To explore its role in the molecular pathogenesis and its possible prognostic importance in AML, we have evaluated the expression levels of the gravin gene in 83 acute myeloid leukemia patients as compared with controls using quantitative real-time polymerase chain reaction (qRT-PCR). Mean gravin expression was 0.53 ± 1.34 and 8.81 ± 11.6 for patients and controls, respectively, and was found to be about 16-fold lower than controls. Gravin gene expression was lower than controls in 83.1 % (69/83) and was similar to controls in 16.9 % (14/83) of cases (p < 0.0001). It was found that there was no significant correlation between gravin expression and laboratory prognostic markers (p > 0.05). Gravin expression was highest in complete remission (1.065 ± 1.79) and lowest in relapse (0.019 ± 0.03) with a statistical difference (p = 0.004). Patients with gravin expression below median level had higher risk to develop relapse (OR = 8.689, 95 % CI = 2.464-30.638; p < 0.0001). No statistical correlation was reported between gravin expression and survival times (OS, DFS) (p = 0.482, 0.409, respectively), and this was confirmed in multivariate analysis. Gravin gene expression was found to be decreased in acute myeloid leukemia, and the degree of its decreased expression has been found to be correlated with poor prognosis.