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We construct a kind of structure of silver oxide capped silver nanoparticles (AgNPs) by cost-efficient air plasma irradiation, and study its visible-light driven photocatalytic activity (PA). By controlling the oxidization time, the relationship between the intensity of the localized surface plasmon resonance (LSPR) and the PA is well established. The PA reaches the maximum when the LSPR of AgNPs is nearly completely damped (according to absorption spectra); however, under this condition, the LSPR still works, confirmed with the high efficient selective transformation of p-Aminothiophenol (PATP) to p, p′-dimercaptoazobenzene (DMAB) under visible light. The mechanism of the LSPR damping induced PA improvement is discussed. We not only provide a cost-efficient approach to construct a LSPR strong damping structure but also promote the understanding of LSPR strong damping and its relationship with photocatalysis.

Background: Regulatory T cells (Tregs) have shown to be protective against the development of atherosclerosis, a major pathological cause for cardiovascular events. Here, we aim to explore the roles of Tregs-related genes in atherosclerosis deterioration.Methods and Results: We downloaded the gene expression profile of 29 atherosclerotic samples from the Gene Expression Omnibus database with an accession number of GSE28829. The abundance of Tregs estimated by the CIBERSORT algorithm was negatively correlated with the atherosclerotic stage. Using the limma test and correlation analysis, a total of 159 differentially expressed Tregs-related genes (DETregRGs) between early and advanced atherosclerotic plaques were documented. Functional annotation analysis using the DAVID tool indicated that the DETregRGs were mainly enriched in inflammatory responses, immune-related mechanisms, and pathways such as complement and coagulation cascades, platelet activation, leukocyte trans-endothelial migration, vascular smooth muscle contraction, and so on. A protein-protein interaction network of the DETregRGs was then constructed, and five hub genes (PTPRC, C3AR1, CD53, TLR2, and CCR1) were derived from the network with node degrees ≥20. The expression patterns of these hub DETregRGs were further validated in several independent datasets. Finally, a single sample scoring method was used to build a gene signature for the five DETregRGs, which could distinguish patients with myocardial infarction from those with stable coronary disease.Conclusion: The results of this study will improve our understanding about the Tregs-associated molecular mechanisms in the progression of atherosclerosis and facilitate the discovery of novel biomarkers for acute cardiovascular events.

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