Trapping lithium polysulfides of a Li–S battery has been successfully demonstrated by forming lithium bonds in a polymer matrix.

The electrical conductivity and the specific surface area of conductive fillers in conductor-insulator composite films can drastically improve the dielectric performance of those films through changing their polarization density by interfacial polarization. We have made a polymer composite film with a hybrid conductive filler material made of carbon nanotubes grown onto reduced graphene oxide platelets (rG-O/CNT). We report the effect of the rG-O/CNT hybrid filler on the dielectric performance of the composite film. The composite film had a dielectric constant of 32 with a dielectric loss of 0.051 at 0.062 wt% rG-O/CNT filler and 100 Hz, while the neat polymer film gave a dielectric constant of 15 with a dielectric loss of 0.036. This is attributed to the increased electrical conductivity and specific surface area of the rG-O/CNT hybrid filler, which results in an increase in interfacial polarization density between the hybrid filler and the polymer.

Melatonin influences sleep and circadian rhythm, and it has anti-inflammatory functions. However, the mechanism of its anti-inflammatory roles is not well understood. In our studies, we show that melatonin blocked lipopolysaccharide (LPS)-induced CCL2 (monocyte chemotactic protein-1; MCP-1), CCL5 (Regulated upon Activation, Normal T-cell Expressed, and Secreted), and CCL9 (macrophage inflammatory protein-1γ) chemokine mRNA expression in BV2 murine microglial cells. Melatonin markedly inhibited LPS-induced Akt phosphorylation and NF-κB activation. Furthermore, melatonin inhibited LPS-induced STAT1/3 phosphorylation and interferon-gamma activated sequence (GAS)-driven transcriptional activity. Interestingly, these effects were not associated with reactive oxygen species scavenging effects of melatonin or melatonin receptor signal pathways. Taken together, our results suggested that melatonin has anti-inflammatory functions through down-regulation of chemokine expression by inhibition of NF-κB and STAT/GAS activation in LPS-stimulated BV2 murine microglial cell line.

No abstract

Methylglyoxal (MGO) is a reactive dicarbonyl metabolite of glucose, and its plasma levels are elevated in patients with diabetes. Studies have shown that MGO combines with the amino and sulphhydryl groups of proteins to form stable advanced glycation end products (AGEs), which are associated with vascular endothelial cell (EC) injury and may contribute to the progression of atherosclerosis. In this study, MGO induced apoptosis in a dose‐dependent manner in HUVECs, which was attenuated by pre‐treatment with z‐VAD, a pan caspase inhibitor. Treatment with MGO increased ROS levels, followed by dose‐dependent down‐regulation of c‐FLIPL. In addition, pre‐treatment with the ROS scavenger NAC prevented the MGO‐induced down‐regulation of p65 and c‐FLIPL, and the forced expression of c‐FLIPL attenuated MGO‐mediated apoptosis. Furthermore, MGO‐induced apoptotic cell death in endothelium isolated from mouse aortas. Finally, MGO was found to induce apoptosis by down‐regulating p65 expression at both the transcriptional and posttranslational levels, and thus, to inhibit c‐FLIPL mRNA expression by suppressing NF‐κB transcriptional activity. Collectively, this study showed that MGO‐induced apoptosis is dependent on c‐FLIPL down‐regulation via ROS‐mediated down‐regulation of p65 expression in endothelial cells.