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We present a simple method for producing SiO2-modified LiNi0.5Mn1.5O4 (LNMO) cathode materials. Manganese carbonate was directly mixed with nickel nitrate and lithium hydroxide, and a spherical structure LNMO cathode material was prepared by two-step calcination, then ethyl orthosilicate and LNMO powder were simply mixed in solid and liquid phases to prepare SiO2-coated LNMO material. The effect of SiO2 coating on the structure of LNMO was studied by diffraction of X-rays, scanning electron microscope (SEM), transmission electron microscope (TEM), and thermogravimetric analysis and differential scanning calorimetry. An amorphous SiO2 coating layer developed on the surface of the LNMO particles in the modification and this could alleviate the strike of hydrogen fluoride (HF) caused by electrolyte decomposition as well as the development of a solid electrolyte interphase. The electrochemical performance of the coated material was as follows: when the amount of SiO2 was 0 wt%, 1 wt%, 2 wt%, and 3 wt%, the initial discharge capacity of the sample was 98.2, 84.1, 101.3, and 89.8mAh/g, respectively. After 50 charge−discharge cycles, the capacity retention rates are 92.7%, 66.8%, 97.9%, and 93.8%, respectively. The cyclic stability of the samples can be significantly improved when the SiO2 coating amount is 2 wt% and 3 wt%, indicating that SiO2 coating can not only improve the discharge-specific capacity of the material but also improve its cyclic stability.

The effect of yttrium on the mechanism of oxidation film formation of the 9Cr reduced activation ferritic/martensitic (9Cr-RAFM) steel was investigated. Four alloys yttrium contents ranging from 0 to 0.065% were melted in a vacuum induction furnace and subjected to continuous isothermal oxidation experiments. The alloys were oxidized in air at 600, 700, 800 and 900 °C for 100 h. Oxidation kinetic curves were obtained and analyzed to study the effect of yttrium on the oxidation resistance of the alloys at high temperatures. The oxide films formed on the alloys were observed and analyzed by X-ray diffractometry, scanning electron microscopy and electron probe X-ray microanalysis. The results indicated that the oxidation weight gain of the samples varied with the yttrium content, with the highest gain observed in the yttrium-free alloy sample, and the least in those containing 0.065% yttrium. Adding yttrium significantly enhanced the high temperature oxidation resistance of 9Cr-RAFM alloy by promoting the formation of a selective Cr2O3oxide film. The film improved the adhesion of the oxide layer to the base metal, reduced the oxidation rate, and thereby enhanced the high-temperature oxidation resistance of the alloy.

The (111) facet of LiNi0.5Mn1.5O4CAMs exhibits a higher surface energy compared to the other two facets, resulting in increased reactivity and susceptibility to interfacial side reactions.

Objective:The endothelium plays essential roles in regulating vascular homeostasis and diseases. Endothelial cell (EC) dysfunction is associated with several pathologies including diabetes, hypertension and angiogenesis. Emerging evidences suggest that mitochondria and the contact sites between mitochondria and endoplasmic reticulon (ER), called mitochondria associated membrane (MAM), is essential for the maintenance of mitochondrial structure and EC homeostasis. Hyperglycemia leads to mitochondrial defects, subsequently endothelial dysfunction and impaired angiogenesis in diabetes. However, the precise mechanisms of MAM remodeling and EC homeostasis has not been fully elucidated.Approach and Results:In the current study we examined the role of Nogo-B, an ER membrane protein has known function of regulating ER morphology, in MAM remodeling and endothelial dysfunction triggered by hyperglycemia. Our data show that Nogo-B localized to the MAM and regulated the connection between ER and mitochondria through Mitofusin 2 (MFN2). Depletion of Nogo-B impaired high-glucose induced MAM remodeling, decreased ER-mediated mitochondria Ca2+signaling and mitochondria density, and worsened the subsequent endothelial dysfunction. In addition, increased mitochondrial fission, suppressed mitochondrial membrane potential and respiration rate were observed in Nogo-B depleted ECs under hyperglycemia conditions. Mechanistically, our results show that Nogo-B deficiency elevated JNK phosphorylation, which lead to MFN2 proteasomal degradation and MAM dysregulation.Conclusion:Taken together, our findings provide fresh insights into a new role of Nogo-B in endothelial biology. MAM localized Nogo-B facilitates and controls ER-mitochondria communication in ECs in response to hyperglycemia. The results from this study deepen our understanding on the mechanism of endothelium dysfunction in diabetes.