Hydrogen Evolution Reaction at Anion Vacancy of Two-Dimensional Transition-Metal Dichalcogenides: Ab Initio Computational Screening.

The catalytic activity for the hydrogen evolution reaction (HER) at the anion vacancy of 40 2D transition-metal dichalcogenides (TMDs) is investigated using the hydrogen adsorption free energy (Δ GH) as the activity descriptor. While vacancy-free basal planes are mostly inactive, anion vacancy makes the hydrogen bonding stronger than clean basal planes, promoting the HER performance of many TMDs. We find that ZrSe2 and ZrTe2 have similar Δ GH as Pt, the best HER catalyst, at low vacancy density. Δ GH depends significantly on the vacancy density, which could be exploited as a tuning parameter. At proper vacancy densities, MoS2, MoSe2, MoTe2, ReSe2, ReTe2, WSe2, IrTe2, and HfTe2 are expected to show the optimal HER activity. The detailed analysis of electronic structure and the multiple linear regression results identifies the vacancy formation energy and band-edge positions as key parameters correlating with Δ GH at anion vacancy of TMDs.

In Situ Spectroscopic and Computational Studies on a MnO2-CuO Catalyst for Use in Volatile Organic Compound Decomposition.

In situ near-edge X-ray absorption fine structure (NEXAFS) spectroscopy and density functional theory calculations were conducted to demonstrate the decomposition mechanism of propylene glycol methyl ether acetate (PGMEA) on a MnO2-CuO catalyst. The catalytic activity of MnO2-CuO was higher than that of MnO2 at low temperatures, although the pore properties of MnO2 were similar to those of MnO2-CuO. In addition, whereas the chemical state of MnO2 remained constant following PGMEA dosing at 150 °C, MnO2-CuO was reduced under identical conditions, as confirmed by in situ NEXAFS spectroscopy. These results indicate that the presence of Cu in the MnO2-CuO catalyst enables the release of oxygen at lower temperatures. More specifically, the released oxygen originated from the Mn-O-Cu moiety on the top layer of the MnO2-CuO structure, as confirmed by calculation of the oxygen release energies in various oxygen positions of MnO2-CuO. Furthermore, the spectral changes in the in situ NEXAFS spectrum of MnO2-CuO following the catalytic reaction at 150 °C corresponded well with those of the simulated NEXAFS spectrum following oxygen release from Mn-O-Cu. Finally, after the completion of the catalytic reaction, the quantities of lactone and ether functionalities in PGMEA decreased, whereas the formation of C=C bonds was observed.

Structure of amorphous GeSe9 by neutron diffraction and first-principles molecular dynamics: Impact of trajectory sampling and size effects.

The structure of glassy GeSe9 was investigated by combining neutron diffraction with density-functional-theory-based first-principles molecular dynamics. In the simulations, three different models of N = 260 atoms were prepared by sampling three independent temporal trajectories, and the glass structures were found to be substantially different from those obtained for models in which smaller numbers of atoms or more rapid quench rates were employed. In particular, the overall network structure is based on Sen chains that are cross-linked by Ge(Se4)1/2 tetrahedra, where the latter are predominantly corner as opposed to edge sharing. The occurrence of a substantial proportion of Ge-Se-Se connections does not support a model in which the material is phase separated into Se-rich and GeSe2-rich domains. The appearance of a first-sharp diffraction peak in the Bhatia-Thornton concentration-concentration partial structure factor does, however, indicate a non-uniform distribution of the Ge-centered structural motifs on an intermediate length scale.

Polymorphic porous supramolecular networks mediated by halogen bonds on Ag(111).

Intermolecular structures of porous two-dimensional supramolecular networks are studied using scanning tunnelling microscopy combined with density functional theory calculations. The local configurations of halogen bonds in polymorphic porous supramolecular networks are directly visualized in support of previous bulk crystal studies.

Effect of protopanaxadiol derivatives in high glucose-induced fibronectin expression in primary cultured rat mesangial cells: role of mitogen-activated protein kinases and Akt.

A lot of anti-diabetic agents using natural plants have been extensively studied. Ginsenosides are known to be used as a remedy for diabetes in Asian countries and American Societies. Diabetic nephropathy is a major complication of diabetes mellitus. Extracellular matrix in mesangial cells is mainly composed of fibronectin and the increase of fibronectin is a hallmark of diabetic nephropathy. Protopenaxadiol (PPD) is a major component of total ginseng. Thus, we examined the regulatory mechanism of PPD derivatives-induced preventive effect of fibronectin expression in mesangial cells cultivated under diabetic condition. In present study, ginsenoside Rb1 prevented the high glucose-induced increase of fibronectin expression in mesangial cells. Ginsenoside Rb2 and Rg3 also mildly inhibited it. However, ginsenoside Rc and Rd did not prevent the high glucose-induced increase of fibronectin expression in mesangial cells. In addition, ginsenoside Rb1 prevented high glucose-induced phosphorylation of p44/42 mitogen activated protein kinase (MAPK), p38 MAPK, JNK/SAPK, and Akt. These results suggest that ginsenoside Rb1 is the most powerful component of PPD derivatives. In conclusion, ginsenoside Rb1 prevented high glucose-induced increase of fibronectin expression via the inhibition of MAPK-Akt signaling cascade.

Both B1R and B2R act as intermediate signaling molecules in high glucose-induced stimulation of glutamate uptake in ARPE cells.

Bradykinin (BK) is a potent modulator of biological processes in the retina, and retinal pigment epithelial cells (RPE) and the regulation of glutamate are believed to be important in the pathogenesis of diabetic retinopathy. However, the mechanism by which BK regulates glutamate uptake in RPE cells in diabetic retinopathy is unknown. Here, we examined the involvement of BK receptors in high glucose-induced dysfunction of glutamate uptake in human ARPE cells. High glucose stimulated glutamate uptake and the expression of excitatory amino acid transporter-4 (EAAT4) mRNA, and these were blocked by treatment with small interfering RNA (siRNA) for BK1 receptor (B1R) and BK2 receptor (B2R), but not scrambled siRNA, supporting an involvement of B1R and B2R in this process. High glucose-stimulated glutamate uptake was also blocked by the B1R antagonist [des-Arg(10)]-HOE 140 and the B2R antagonist HOE 140. High glucose increased B1R and B2R mRNA and protein expression in a time-dependent manner, increased B1R and B2R translocation from the cytosol to the nucleus, and stimulated kininogen, kallikrein, and kininase I mRNA expression. We examined whether BK receptors were involved in high glucose-induced signaling pathways. High glucose stimulated arachidonic acid release, cytosolic phospholipase A(2) and cyclooxygenase-2 proteins, nuclear factor-kappaB activation, and inhibitor-kappaB activation; these events were blocked by treatment with B1R and B2R siRNAs, but not scrambled siRNA. In addition, high glucose-induced stimulation of glutamate uptake was blocked by the cyclooxygenase-2 inhibitors arachidonyl trifluoromethyl ketone, mepacrine, 5-bromo-2-(4-fluorophenyl)-3-[4-(methyl-sulfonyl)phenyl]-thiophene, and N-[2-cyclohexyloxy-4-nitrophenyl] methane-sulfonamide, and by the nuclear factor-kappaB inhibitors pyrrolidine dithiocarbamate and SN-50.

Bradykinin stimulates glutamate uptake via both B1R and B2R activation in a human retinal pigment epithelial cells.

AIMS: We were to examine the effect of bradykinin (BK) in the regulation of glutamate transporter and its related signaling molecules in a human retinal pigment epithelial (ARPE) cells, which are important cells to support retina. MAIN METHODS: d-[2,3-(3)H]-aspartate uptake, western immunoblotting, reverse transcription polymerase chain reaction, [(3)H]-arachidonic acid release, and siRNA transfection techniques were used. KEY FINDINGS: BK stimulated glutamate uptake as well as the mRNA expression of excitatory amino acid transporter 4 (EAAT4) and excitatory amino acid carrier 1 (EAAC1), which was blocked by treatment with bradykinin 1 receptor (B1R) and bradykinin 2 receptor (B2R) siRNA, suggesting the role of B1R and B2R in this process. The BK-induced stimulation of glutamate uptake was also blocked by [des-Arg(10)]-HOE 140, a B1R antagonist, and HOE 140, a B2R antagonist, as well as by the tyrosine kinase inhibitors genistein and herbimycin A. In addition, the BK-induced stimulation of glutamate uptake was blocked by treatment with the phospholipase A(2) inhibitors mepacrine and AACOCF(3), the cyclooxygenase (COX) inhibitor indomethacin, and the COX-2 inhibitor Dup 697. Furthermore, the BK-induced increase in COX-2 expression was blocked by the PI-3 kinase inhibitors wortmannin and LY294002, Akt inhibitor, and the protein kinase C (PKC) inhibitors staurosporine and bisindolylmaleimide I, suggesting the role of PI-3 kinase and PKC in this process. BK stimulated Akt activation and the translocation of PKC activation via the activation of B1R and B2R. SIGNIFICANCE: BK stimulates glutamate uptake through a PKC-Akt-COX-2 signaling cascade in ARPE cells.