Search

Li-rich layered metal oxide (Li1.2Mn0.56Ni0.16Co0.08O2, denoted as LLMO) cathode materials with SiO2 coating have been successfully synthesized by using a wet chemical method combined with high temperature annealing. Scanning electron microscopy (SEM) and high-resolution transmission electron microscopy (HRTEM) analyses revealed that an amorphous SiO2 coating layer has formed on the surface of the LLMO electrode. Electrochemical analysis demonstrated that an optimal SiO2 coating amount on the surface of LLMO particles can effectively improve the cycling stability, suppress the voltage and capacity decay, and enhance the thermal stability of these electrodes. An optimal SiO2 coating amount of 0.5 wt% on an LLMO electrode (S-LLMO-0.5 wt%) improved the capacity retention to 82.6% after 200 cycles at 25 °C (67.0% for the pristine LLMO electrode) and 68.8% after 100 cycles at 60 °C (56.3% for the pristine LLMO electrode), respectively. Besides, the voltage drop of the S-LLMO-0.5 wt% sample (46.8 mV/53.6 mV) was lower than that of the pristine LLMO sample (366.1 mV/60.3 mV) after 200 cycles at 3.2 V/3.8 V, confirming that 0.5 wt% SiO2 coating can reduce the capacity loss and slower the voltage degradation rate of LLMO electrodes. In addition, the exothermic reaction of the pristine LLMO (denoted as P-LLMO from now on) electrode can be delayed by SiO2 coating while the decomposition temperature of the S-LLMO-0.5 wt% sample is significantly higher than that of the P-LLMO. These results are attributed to a uniform amorphous SiO2 coating layer that not only blocks the highly active oxygen release from the bulk material but also prevents the direct contact of the electrolyte to the positive electrodes, suppressing structural transition from a layered phase to a spinel-like one. [ABSTRACT FROM AUTHOR]

Electrolyte solutions have a vital function in lithium-ion batteries. In consideration of their toxic and harmful characteristics and widespread applications in the EVs, the treatment or recovery of the electrolyte is of concern and accurate analysis is needed for the resource and environment benefits. In this work, we present a highly-selective electrolyte recovery method―transcritical CO2 extraction―that combined the extraction and separation processes together. The use of response surface methodology helps in obtaining a simplified and optimized extraction protocol at room temperature and low pressure saving time and reagents. In order to evaluate these extracts, various techniques like GC-MS, GC-FID, FITR and NMR were applied. The GC-FID quantitative analysis and calculation formula may help with realizing the oriented control of the extraction process, and hexafluorophosphate (PF6−), fluoride (F−) and difluorophosphate (PO2F2−) detected by both 19F and 31P spectra imply the degradation pathway. [ABSTRACT FROM AUTHOR]

Background A long-term high-fat/cholesterol (HFC) diet leads to insulin resistance (IR), which is associated with inflammation, atherosclerosis (AS), cardiac sympathovagal imbalance, and cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) and nuclear factor κB (NF-κB)are involved in the development of IR-AS. Thus, we elucidated the pathological molecular mechanism of IR-AS by feeding an HFC diet to Tibetan minipigs to induce IR and AS. Methods Male Tibetan minipigs were fed either a normal diet or an HFC diet for 24 weeks. Thereafter, the minipigs were tested for physiological and biochemical blood indices, blood pressure, cardiac function, glucose tolerance, heart rate variability (HRV), and PPAR-associated gene and protein expression levels. Results HFC-fed minipigs exhibited IR through increased body weight, fasting blood glucose levels, plasma cholesterol and its composition, and insulin and free fatty acid (FFA) levels; decreased insulin sensitivity; impaired glucose tolerance; and hypertension. Increased Creactive protein (CRP) levels, cardiac dysfunction, depressed HRV, and the up-regulation of PPAR expression in the abdominal aorta concomitant with down-regulation in the heart tissue were observed in HFC-fed minipigs. Furthermore, the levels of NF-κBp65, IL-1β, TNF-α, MCP-1, VCAM-1, ICAM-1, MMP-9, and CRP proteins were also significantly increased. Conclusions These data suggest that HFC-fed Tibetan minipigs develop IR and AS and that PPARs are involved in cardiovascular remodeling and impaired function. [ABSTRACT FROM AUTHOR]

To investigate the pathogenesis of hyperlipidemia in Wistar-SD Hypercholesterolemia (WSHc) rats and clarify the genetic and biological characteristics. Six 7-8-week-old WSHc rats were fed a high-fat diet (HFD), and another six were fed ordinary feed, with age-matched Wistar rats as the control group under the same treatment. After 16 weeks, serum lipid levels were measured. A transcriptomic analysis of the differences in gene expression of the liver related to cholesterol metabolism was conducted, and 119 differentially expressed genes were discovered through bioinformatics analysis and molecular biology verification. UHPLC-Q-TOF/MS was applied for lipidomic analysis of serum samples from each group. WSHc rats developed dyslipidemia after a high-fat diet was induced. Investigation of the gene profiles using the protein-protein interaction network and one-cluster clustering analysis identified SREBF1 as a HUB gene and NR1d1 as an independent key gene. SREBF1 and NR1d1 were further validated in molecular biology experiments, which was consistent with the transcriptomic results. Lipid metabolomics analysis identified seven lipid subclasses and 84 lipid molecules. The metabolic profiles of serum lipid media of the WSHc + HFD and WSHc + SC groups were significantly different compared to that of the control group by 62 and 70 lipid molecules, respectively. Differential metabolites were produced via sphingolipid and glycerophospholipid metabolism. A stable model of hypercholesterolemia in WSHc rats can be generated by feeding on a high-fat diet, and the pathogenesis mainly involves two key genes, SREBF1 and NR1d1, and the sphingolipid and glycerophospholipid metabolism pathways.

Veronicastrum axillare is a traditional medical plant in China which is widely used in folk medicine due to its versatile biological activities, especially for its anti-inflammatory effects. However, the detailed mechanism underlying this action is not clear. Here, we studied the protective effects of V. axillare against acute lung injury (ALI), and we further explored the pharmacological mechanisms of this action. We found that pretreatment with V. axillare suppressed the release of proinflammatory cytokines in the serum of ALI mice. Histological analysis of lung tissue demonstrated that V. axillare inhibited LPS-induced lung injury, improved lung morphology, and reduced the activation of nuclear factor- κ B (NF- κ B) in the lungs. Furthermore, the anti-inflammatory actions of V. axillare were investigated in vitro . We observed that V. axillare suppressed the mRNA expression of interleukin-1 β (IL-1 β ), IL-6, monocyte chemotactic protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and tumor necrosis factor- α (TNF- α ) in RAW264.7 cells challenged with LPS. Furthermore, pretreatment of V. axillare in vitro reduced the phosphorylation of p65 and I κ B- α which is activated by LPS. In conclusion, our data firstly demonstrated that the anti-inflammatory effects of V. axillare against ALI were achieved through downregulation of the NF- κ B signaling pathway, thereby reducing the production of inflammatory mediators., Competing Interests: The authors declare that they have no competing interests.

Ethnopharmacological Relevance: Propolis is used widely in a number of cultures as a folk medicine and is gaining wider recognition for its potential therapeutic use, due to its wide range of biological properties and pharmacological activities, especially its anti-inflammatory effects. Despite an increasing number of studies focused on the biological activities of propolis together with its botanical sources, studies on Chinese propolis are insufficient. This study was designed to investigate the anti-inflammatory properties of ethanol extracts from Chinese propolis (EECP) and poplar buds (EEPB) from Populus×canadensis Moench (Salicaceae family)., Materials and Methods: Phytochemical analysis of EECP and EEPB was performed via total phenolic and flavonoid content measurements followed by high-performance liquid chromatography (HPLC) analysis. DPPH and ABTS free-radical scavenging methods were used to evaluate their anti-oxidant properties. The anti-inflammatory effects of EECP and EEPB were investigated in vitro by evaluating their modulating effects on the key inflammatory cytokines and mediators in LPS/IFN-γ co-stimulated RAW 264.7 cells and by measuring nuclear factor (NF)-κB activation in TNF-α or IL-1β stimulation HEK 293 cells using reporter gene assays. Their effects on acute inflammatory symptoms (LPS-induced endotoxemia and acute pulmonary damage) were also examined in mice., Results: EECP and EEPB exhibited strong free-radical scavenging activity and significant in vitro anti-inflammatory effects by modulating key inflammatory mediators of mRNA transcription, inhibiting the production of specific inflammatory cytokines, and blocking the activation of nuclear factor (NF)-κB. The administration of EECP and EEPB (25 and 100 mg/kg) provided significant protective effects by attenuating lung histopathological changes and suppressing the secretion of LPS-stimulated inflammatory cytokines, such as interleukin-6 (IL-6), IL-10, MCP-1, TNF-α and IL-12p70 production in endotoxemic mice., Conclusions: The results presented here reveal the potent anti-inflammatory properties of Chinese propolis and poplar buds, and provide biological information for developing suitable substitute(s) for propolis in the prevention and treatment of inflammatory diseases., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)