Selective Photocatalytic Reduction of CO2 to CH4 Modulated by Chloride Modification on Bi2WO6 Nanosheets.

Solar-driven photocatalytic CO2 reduction into CH4 with H2O is considered to be a promising way to alleviate the energy crisis and greenhouse effect. However, current CO2 photoreduction technologies tend to overlook the role of photooxidation half reaction as well as the effect of the protons produced by water oxidation on CH4 generation, resulting in low CO2 conversion efficiency and poor CH4 selectivity. In the present study, a series of chloride-modified Bi2WO6 nanosheets were constructed in view of chloride-assisted photocatalytic water oxidation. The results show that the CH4 yield of the synthesized sample can be enhanced up to about 10 times compared to that with no Cl- modification. Besides, the selectivity of CH4 can be regulated by the loading amount of chloride, varying from 51.29% for Bi2WO6 to 94.98% for the maximum. The increase of product yield is attributed to chloride modification, which not only changed the morphology of the catalyst, but also modified the pathway of water oxidation. Further studies on intermediate products and the density functional theory calculation confirm that the Cl- ions on Bi2WO6 nanosheets not only promote H2O oxidation, but also lower the energy barrier for intermediate *CHO generation, thus facilitating CH4 production. The results gained herein may provide some illuminating insights into the design of a highly selective photocatalyst for efficient CO2 reduction.

Hint1 Overexpression Inhibits the Cell Cycle and Induces Cell Apoptosis in Human Osteosarcoma Cells.

BACKGROUND: New evidence suggests that histidine triad nucleotide-binding protein 1 (Hint1) exerts a tumor suppressor effect in various human tumors, such as colorectal cancer and gastric cancer. However, it has not been reported whether Hint1 is involved in the occurrence and development of osteosarcoma (OS). MATERIALS AND METHODS: The present study investigated the role of Hint1 in human OS cells by using cell lines, including 143B, U2OS, KHOS-240S, Saos-2 and MG-63. Cell proliferation and apoptosis were detected by flow cytometry. RESULTS: The present result revealed that Hint1 is downregulated in these cell lines. The overexpression of Hint1 by adenovirus transfection in 143B and MG63 cell lines suppressed the proliferation and cell cycle, and increased the cell apoptosis. Mechanically, it was found that Hint1 downregulated the cyclin D1 expression via FOXO1 inhibition. Furthermore, FOXO1 overexpression in the 143B and MG63 cell lines significantly blurred the effects of Hint1 on cellular proliferation and apoptosis. CONCLUSION: The present study indicates that Hint1 inhibits the development of OS by regulating FoxO1-cyclin D1, suggesting that Hint1 may be a new method for the treatment of OS.