First-principles study of the discharge electrochemical and catalytic performance of the sulfur cathode host Fe0.875M0.125S2 (M = Ti, V).

Lithium-sulfur batteries (LSBs) are one of the most promising energy storage devices with high energy density. However, their application and commercialization are hampered by the slow Li-S redox chemistry. Fe0.875M0.125S2 (M = Ti, V), as the sulfur cathode host, enhances the Li-S redox chemistry. FeS2 with Pa3̄ is transformed into Li2FeS2 with P3̄m1 after discharge. The structure changes and physicochemical properties during Fe0.875M0.125S2 discharge process are further investigated to screen out the sulfur cathode host materials with the best comprehensive properties. The discharge structure of Fe0.875M0.125S2 is verified by the thermodynamic stability of Li-deficient phases, voltage and capacity based on Monte Carlo methods. Fe0.875M0.125S2 with Pa3̄ is transformed into Li2Fe0.875M0.125S2 with P3̄m1 after discharge. Using the first-principles calculations, the physicochemical properties of Li2Fe0.875M0.125S2 are systematically investigated, including the formation energy, voltage, theoretical capacity, electrical conductivity, Li+ diffusion, catalytic performance and Li2S oxidation decomposition. The average redox voltage of Li2Fe0.875V0.125S2 is higher than that of Li2Fe0.875Ti0.125S2. Li2Fe0.875M0.125S2 shows metallic properties. Li2Fe0.875V0.125S2 is more beneficial to the reduction reaction of Li2S2 and Li2S oxidation decomposition. Fe0.875V0.125S2 has more potential as the sulfur cathode host than Fe0.875Ti0.125S2 in LSBs. A new strategy for the selection of the sulfur cathode host material for LSBs is provided by this work.

Global Gene Expression Profile of the Hippocampus in a Rat Model of Vascular Dementia.

Vascular dementia (VD) has been one of the most serious public health problems worldwide. It is well known that cerebral hypoperfusion is the key pathophysiological basis of VD, but it remains unclear how global genes in hippocampus respond to cerebral ischemia-reperfusion. In this study, we aimed to reveal the global gene expression profile in the hippocampus of VD using a rat model. VD was induced by repeated occlusion of common carotid arteries followed by reperfusion. The rats with VD were characterized by deficit of memory and cognitive function and by the histopathological changes in the hippocampus, such as a reduction in the number and the size of neurons accompanied by an increase in intercellular space. Microarray analysis of global genes displayed up-regulation of 7 probesets with genes with fold change more than 1.5 (P < 0.05) and down-regulation of 13 probesets with genes with fold change less than 0.667 (P < 0.05) in the hippocampus. Gene Ontology (GO) and pathway analysis showed that the up-regulated genes are mainly involved in oxygen binding and transport, autoimmune response and inflammation, and that the down-regulated genes are related to glucose metabolism, autoimmune response and inflammation, and other biological process, related to memory and cognitive function. Thus, the abnormally expressed genes are closely related to oxygen transport, glucose metabolism, and autoimmune response. The current findings display global gene expression profile of the hippocampus in a rat model of VD, providing new insights into the molecular pathogenesis of VD.

Yifei Xuanfei Jiangzhuo formula, a Chinese herbal decoction, improves memory impairment through inhibiting apoptosis and enhancing PKA/CREB signal transduction in rats with cerebral ischemia/reperfusion.

Apoptosis and the dysfunction of the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-responsive element binding protein (CREB) signaling pathway have a key role in memory impairment in vascular dementia (VaD), a challenging clinical problem. Yifei Xuanfei Jiangzhuo formula (YXJF), a Chinese herbal decoction, has been used to treat VaD in clinical practice and has produced positive outcomes; however, convincing evidence is currently lacking. The present study aimed to investigate the effects of YXJF on memory impairment in rats with cerebral ischemia/reperfusion and to explore the underlying mechanism. YXJF ameliorated memory impairment in rats with cerebral ischemia/reperfusion, inhibited hippocampal apoptosis in a dose-dependent manner and attenuated increases in the protein expression of B-cell lymphoma 2 (Bcl-2)-associated X protein as well as c-Jun and a reduction in Bcl-2 protein expression in the hippocampal tissue of the rats. Furthermore, administration of YXJF significantly increased the protein expression of PKA C-α and CREB, and promoted CREB phosphorylation. The results indicated that YXJF improves memory impairment through inhibiting apoptosis and enhancing PKA/CREB signal transduction in rats with cerebral ischemia/reperfusion.

[Synthesis and spectra of transition metals complexes RE3L6(NO3)6(H2O)2].

Schiff base 4-(p-dimethylaminobenzaldehydeamino)-4H-1,2,4-triazole(L) was synthesized from 4-amino-1,2,4-triazole and p-dimethylaminobenzaldehyde using acetic acid as the catalyst. The solid complexes RE3L6(NO3)6(H2O)2 (RE = Cu, Co, Zn, Cd; x = 3-6) were synthesized with 4-(p-dimethylaminobenzaldehydeamino)-4H-1,2,4-triazole and nitrate of transition metals in ethanol and characterized by elemental analysis, infrared spectroscopy, UV spectrum, and fluorescence spectrum. Experimental results showed that the free ligand is a thermally stable material, and its ethanol solution emitted intense blue fluorescence at the peak wavelength of 416 nm. The absorption band at about 406 nm can be assigned to the intrinsic absorption of C==N. Compared with the fluorescence emission of free ligand in ethanol solution, the emission of the complex of RE3L6 (NO3)6(H2O)2 was red-shifted to 445 nm and narrow in solution. RE(II) was coordinated with N atomy of triazole in 4-(p-dimethylaminobenzaldehydeamino)-4H-1,2,4-triazole.

[Synthesis, characterization and fluorescence of Zn3 (NCS)6 (L1)6 (NO3)2 and Ni3(NCS)6(L2)6(NO3)2].

The complexes of Zn2+, Ni2+ with 4-amino-3,5-dimethyl-1,2,4-triazole and 4-amino-1,2,4-triazole were synthesized in water, respectively. By elemental analysis, coordination titration and molar conductivities studies, the compositions of the complexes were suggested as Zn3 (NCS)6 (L1)6 (NO3)2 and Ni3 (NCS)6 (L2)6 (NO3)2 respectively. The ligands and coordination compounds were studied by means of IR spectra, UV and fluorescence excitation and emission spectra. The IR spectra studies indicate that triazolate was bonded with RE (II) through nitrogen atoms in the heterocyclic ring. The fluorescence spectra showed that the fluorescence emission intensity of Ni3 (NCS)6 (L2)6 (NO3)2 was stronger than that of Zn3 (NCS)6 (L1)6 (NO3)2.

[Synthesis and fluorescence property of new La3+ complex].

The solid complex of lanthanum nitrate hydrate with 4-(p-dimethylaminobenzaldehydeamino)-4H-1,2,4-triazole (L) LaL3 (NO3)3 x (H2O)2 x (C2 H5 OH)2 was synthesized in dry N2 atmosphere and absolute alcohol. The composition of the complex was determined by chemical and elemental analyses. The crystal structure showed that La3+ was coordinated by ten oxygen atoms with three nitrate, two water and two alcohol molecules. Characterized by elemental analysis, infrared spectroscopy, and solid fluorescence, the experimental results showed that the free ligand is a thermally stable material, and emitted intensive blue fluorescence at the peak wavelength of 451 nm. Compared with the fluorescence emission of free ligand in solid-state, the emission of complex of LaL3 (NO3)3 x (H2O)2 x (C2H5 OH)2 red-shifted to 464 nm and exhibited stronger blue fluorescence.