Photochemical Ammonia Synthesis over Reduced Polyoxovanadate-Intercalated Defective ZnAl Layered Double Hydroxide Nanosheets.

The exploration of efficient and stable N2 fixation photocatalysts featuring a broad absorption spectrum and N2 fixation active sites has become specifically conspicuous. Herein, a series of reduced polyoxovanadates (POVs) were intercalated into copper-induced ZnAl layered double hydroxide (0.5%-ZnAl LDH) nanosheets with oxygen vacancies via an anion exchange strategy toward green ammonia production. The intervalence charge transfer arising from mixed-valence POV materials is responsible for its light-harvesting behavior, and the LDHs lay the foundation for the chemical adsorption and activation process of nitrogen molecules; both contributions facilitate the nitrogen photofixation performance of such composite materials. As predicted, the catalytic efficiency of V34/0.5%-ZnAl is 7.0 times higher than 0.5%-ZnAl LDH. Therefore, such an all-inorganic system exhibits an apparent quantum efficiency of 0.3137% at 500 nm. The strategy of "working in tandem" established by POV-based light-absorber species and oxygen vacancies as the sites for N2 activation is extremely vital for enhanced ammonia formation. This work opens up a versatile insight for the rational design of an efficient photo-driven nitrogen-reduction composite catalyst toward sustainable ammonia production compared to the industrial Haber-Bosch process.

Isoflurane inhibits occludin expression via up-regulation of hypoxia-inducible factor 1α.

UNLABELLED: The blood-brain barrier (BBB) is a functional structure which regulates and restricts the transfer of circulating molecules and immune cells into the central nervous system. The barrier is formed by the presence of tight junctions (TJ) between the specialized brain endothelial cells. The volatile anesthetic isoflurane may affect the permeability of the BBB. Previous studies have proven that isoflurane alters hypoxia-inducible factor-1α (HIF-1α) expression, which may affect the TJ proteins; however, the mechanism of how TJ proteins are affected by isoflurane is still unclear. Primary human brain vascular endothelial cells (HBVEC) were exposed to isoflurane at various concentrations (0-2.5%) and different time periods (0-6 h). The cell viability, occludin expression, paracellular permeability, VEGF expression, TGF-ß3 expression and occludin protein endocytosis were quantified. Isoflurane treatment induced a time- and concentration-dependent decrease in occludin mRNA and protein levels in HBVEC. This effect was partially abrogated by silencing the HIF-1α expression. Isoflurane could activate HIF-1α, and the overexpression HIF-1α up-regulated the level of VEGF and TGF-ß3, VEGF decreased the expression of occludin and TGF-ß3 accelerated the endocytosis of occludin. RNA interference targeting HIF-1α reduced both VEGF and TGF-ß3 expression after isoflurane treatment. CONCLUSION: This study provides direct evidence in vitro that exposing isoflurane to HBVECs can trigger HIF-1α activation, leading to lower protein levels of occludin, and increased permeability of the BBB.