ABSTRACT

MgO exhibits activity for the reduction of CO2 to CO under photoirradiation in the presence of H2 or CH4 as a reductant, although MgO is an insulating material. The present study clarified the mechanism of the CO2 photocatalytic reduction in the presence of H2 or CH4 over MgO. The electron paramagnetic resonance (EPR) spectra show that a CO2 molecule adsorbed on MgO was activated to a CO2 - radical under photoirradiation. In addition, it was confirmed by photoluminescence that new acceptor level built up between the valence band and the conduction band of MgO on CO2-adsorbed MgO. The CO2 - radical was reduced to a surface bidentate formate or a surface bidentate acetate by H2 or CH4 in the dark, respectively. The surface bidentate formate anchors on MgO as a photoactive species and reduces CO2 in the gas phase to CO since the CO2 photocatalytic reduction proceeded over MgO absorbing HCHO or CH3CHO and only 12CO was formed in the presence of 12CO2 over MgO modified by a 13C-labeled formate under irradiation. The active species was generated from the side-on adsorption-type bidentate carbonate selectively, although the two types of bidentate carbonates were detected by Fourier transform infrared (FT-IR) spectroscopy. On the other hand, the role of the surface bidentate acetate is under discussion. It is the first report that the substrate-modified insulating material exhibits activity in the CO2 photocatalytic reduction.

No abstract

No abstract

Recent advances in neuroblastoma (NB) research addressed that epigenetic alterations such as hypermethylation of promoter sequences, with consequent silencing of tumor-suppressor genes, can have significant roles in the tumorigenesis of NB. However, the exact role of epigenetic alterations, except for DNA hypermethylation, remains to be elucidated in NB research. In this paper, we clarified the direct binding of MYCN to Bmi1 promoter and upregulation of Bmi1 transcription by MYCN. Mutation introduction into an MYCN binding site in the Bmi1 promoter suggests that MYCN has more important roles in the transcription of Bmi1 than E2F-related Bmi1 regulation. A correlation between MYCN and polycomb protein Bmi1 expression was observed in primary NB tumors. Expression of Bmi1 resulted in the acceleration of proliferation and colony formation in NB cells. Bmi1-related inhibition of NB cell differentiation was confirmed by neurite extension assay and analysis of differentiation marker molecules. Intriguingly, the above-mentioned Bmi1-related regulation of the NB cell phenotype seems not to be mediated only by p14ARF/p16INK4a in NB cells. Expression profiling analysis using a tumor-specific cDNA microarray addressed the Bmi1-dependent repression of KIF1Bb and TSLC1, which have important roles in predicting the prognosis of NB. Chromatin immunoprecipitation assay showed that KIF1Bb and TSLC1 are direct targets of Bmi1 in NB cells. These findings suggest that MYCN induces Bmi1 expression, resulting in the repression of tumor suppressors through Polycomb group genemediated epigenetic chromosome modification. NB cell proliferation and differentiation seem to be partially dependent on the MYCN/Bmi1/tumor-suppressor pathways.