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VO2 affords ultrafast polysulfide adsorption on account of its oxidation potential, which matches the sulfur working window (1.7–2.8 V). Nevertheless, its nonconductive surface limits direct sulfur conversion. Herein, we gently load carbon quantum dots on VO2 to increase direct Li2S nucleation by enhanced electron conductivity. As a result, the soft-packaged lithium–sulfur pouch cell yields a capacity retention of 88.8% at 0.5C after 100 cycles and a decay rate of 0.17% per cycle over 200 cycles at 2C. The cell energy density of the multilayer cell is up to 386.1 W h kg−1. [ABSTRACT FROM AUTHOR]

VO 2 affords ultrafast polysulfide adsorption on account of its oxidation potential, which matches the sulfur working window (1.7-2.8 V). Nevertheless, its nonconductive surface limits direct sulfur conversion. Herein, we gently load carbon quantum dots on VO 2 to increase direct Li 2 S nucleation by enhanced electron conductivity. As a result, the soft-packaged lithium-sulfur pouch cell yields a capacity retention of 88.8% at 0.5C after 100 cycles and a decay rate of 0.17% per cycle over 200 cycles at 2C. The cell energy density of the multilayer cell is up to 386.1 W h kg -1 .

Background: Current studies have demonstrated that disintegrin and metalloproteinase 17 (ADAM17) plays a critical role in the pathogenesis of sepsis. MicroRNA (miR)-145 is known to control immune responses as an anti-inflammatory modulatory molecule. However, a fundamental understanding of how miR-145 regulates ADAM17 and, more broadly, sepsis-induced inflammatory response remains unknown., Methods: We used western blotting and quantitative real-time PCR (qRT-PCR) to measure expression levels of ADAM17 and miR-145. Enzyme-linked immunosorbent assays (ELISA) were performed to measure cytokine production. To determine if ADAM17 is a target gene of miR-145, bioinformatics analyses and luciferase reporter assays were conducted. The impacts of ADAM17 and miR-145 on sepsis-induced inflammatory responses were accessed in vitro using human umbilical endothelial cells (HUVECs) treated with lipopolysaccharide (LPS). Sepsis-induced inflammatory response was measured in vivo using a polymicrobial septic mouse model induced by cecal ligation and puncture (CLP) with pre-injection of a miR-145 agomir., Results: In HUVECs treated with LPS, miR-145 expression was downregulated and miR-145 negatively regulated ADAM17 expression through direct binding to the ADAM17 transcript 3'-UTR. MiR-145 overexpression markedly reduced LPS-induced inflammatory cytokine production by targeting ADAM17 in HUVECs. In comparison to CLP-induced septic mice treated with a control agomir, treatment with a miR-145 agomir significantly reduced the expression of ADAM17, numerous downstream cytokines such as IL-6, TNF-α, IL-1β and MCP-1, and the endothelial injury factors ICAM-1, VCAM-1. The miR-145 agomir also alleviated acute lung and kidney injury and improved the survival rate of septic mice., Conclusions: This study showed that miR-145, by specifically targeting ADAM17, negatively regulates sepsis-induced inflammatory responses and vascular endothelial injury, and ultimately improved organ injury and survival during sepsis. The underlying mechanism for the regulation of ADAM17 expression by miR-145 and sepsis-induced inflammatory reactions may offer sepsis patients a novel therapeutic option., Competing Interests: The authors declare no conflict of interest., (© 2024 The Author(s). Published by IMR Press.)