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Although carbon dots (CDs) have been widely investigated as the fluorescence material, research on room temperature phosphorescence (RTP) CDs is still limited. In this work, diethylenetriaminepentaacetic acid (DTPA) was employed as the raw material to synthesize carbon quantum dots (denoted as CQDs-1) by a hydrothermal method. The resulting CQDs-1 inherited CO groups and N atoms from DTPA, which promoted the formation of triplet excitons under light excitation. On this basis, the CQDs-1 were dispersed in a poly-(vinyl alcohol) (PVA) matrix to prepare CQDs-1-PVA composites that exhibited an optimal emission peak at ∼466 nm and emitted the visible afterglow lasting for 8 s. Moreover, tartaric acid (TA) was combined with DTPA as the raw material to synthesize CQDs-2, which induced the formation of π–π conjugated areas in CQDs. As a result, the emission wavelength was slightly red-shifted, and the duration time of afterglow of the CQDs-2-PVA composite was increased to 9 s. Due to the ultralong-lifetime RTP properties of the CQDs-based composites, their applications in the fields of information encryption and anticounterfeiting have also been investigated. Overall, our work offered a convenient avenue for the synthesis of high-quality RTP CQDs. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a common respiratory tract disease with an incompletely understood pathogenesis. According to previous reports, miRNAs play a crucial pathophysiological role in COPD. MiR-212 was reported to be downregulated in COPD patients; however, the role of miR-212 in COPD remains unknown. In this study, the expression level of miR-212-5p and miR-223 decreased significantly in COPD patients compared to healthy controls. In vitro experiments showed that cigarette smoke extract (CSE) induced NCI-H292 cell apoptosis and inhibited cell proliferation. Inflammation and COPD related genes were also upregulated by CSE, while miR-212-5p inhibited the overexpression of these genes. Furthermore, miR-212-5p promoted cell proliferation and inhibited IGFBP3 expression which was induced by CSE. The expression of p-Akt was also inhibited by CSE, while miR-212-5p significantly promoted the phosphorylation of Akt. In summary, our data suggest that miR-212-5p exerts a protective effect in COPD, and may serve as a prognostic biomarker and potential therapeutic target for COPD.