Two-dimensional stable metallic 1T-MoSe with expanded interlayer spacing of 10.0 Å in situ grown on SWCNTs film is fabricated via a one-step solvothermal method. Combined with X-ray absorption near-edge structures, our characterization reveals that such 1T-MoSe and single-walled carbon nanotubes (abbreviated as 1T-MoSe/SWCNTs) hybridized structure can provide strong electrical and chemical coupling between 1T-MoSe nanosheets and SWCNT film in a form of C-O-Mo bonding, which significantly benefits a high-efficiency electron/ion transport pathway and structural stability, thus directly enabling high-performance lithium storage properties. In particular, as a flexible and binder-free Li-ion anode, the 1T-MoSe/SWCNTs electrode exhibits excellent rate capacity, which delivers a capacity of 630 mAh/g at 3000 mA/g. Meanwhile, the strong C-O-Mo bonding of 1T-MoSe/SWCNTs accommodates volume alteration during the repeated charge/discharge process, which gives rise to 89% capacity retention and a capacity of 971 mAh/g at 300 mA/g after 100 cycles. This synthetic route of a multifunctional MoSe/SWCNTs hybrid might be extended to fabricate other 2D layer-based flexible and light electrodes for various applications such as electronics, optics, and catalysts.

Design of high performance multilayer microwave absorbers using fast Pareto genetic algorithm Science in China Series E-Technological Sciences 52, 2749 (2009); A new solution to enhance cuttings transport in mining drilling by using pulse jet mill technique SCIENCE CHINA Technological Sciences 62, 875 (2019); Mining rice new germplasm containing S 5 n gene by functional molecular marker and sequencing Chinese Science Bulletin 54, 3258 (2009);. RESEARCH PAPER. SCIENCE CHINA Information Sciences

No abstract

No abstract

No abstract

No abstract

No abstract

Toll-like receptor 4 (TLR4) and myeloid differentiation protein 2 (MD-2) are the main lipopolysaccharide (LPS) binding receptors that respond to inflammatory stimuli and mediate NF-kappa B (NF-κB) signaling pathway in macrophages. We have previously shown that plasminogen activator inhibitor-1 (PAI-1) deletion increased lung injury induced by intratracheal instillation of LPS through downregulation of TLR4 negative regulators. However, the mechanisms by which PAI-1 regulates lung inflammation are largely unknown. The aim of this study is to assess the relationship between PAI-1 and TLR4 signaling pathways in LPS-induced NR8383 cells inflammatory reaction. The results showed that the levels of PAI-1, TNF-α, and IL-1β protein were increased remarkably in NR8383 cell supernatants after LPS stimulation. PAI-1 gene knockdown reduced TNF-α and IL-1β levels in cell supernatants and inhibited the NF-κB p65 protein expression in NR8383 cells. The upregulated mRNA and protein expressions of TLR4, MD-2, and myeloid differentiation protein (MyD88) induced by LPS were attenuated after PAI-1 gene knockdown. Conversely, overexpression of PAI-1 in NR8383 cells not only resulted in additional mRNA and protein production of PAI-1, TLR4, MD-2, and MyD88, it also aggravated the inflammatory response induced by LPS. In conclusion, PAI-1 contributes to the regulation of LPS-induced inflammatory response in NR8383 cells, likely by affecting the TLR4-MD-2/NF-κB signaling transduction pathway.