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As a nondegradable environmental pollutant, lead ion (Pb 2+ ) has been proven to be deleterious for environmental and health. Conveniently, quickly and accurately on-site detection of Pb 2+ is of paramount importance. Herein, an electrochemiluminescence (ECL) assay protocol using two-dimensional black phosphorus (2D BP) nanoflakes as new ECL emitter for highly sensitive and selective trace Pb 2+ was designed on the basis of Pb 2+ induced ECL resonance energy transfer (ECL-RET) between 2D BP nanoflakes and Ag/AgCl nanocubes. Anodic green ECL emission of BP nanoflakes without any coreactants was achieved. It is noteworthy that the possible ECL mechanism and the influence of coreactants on the ECL behaviour of BP nanoflakes were further investigated. Benefitting from the well match between the ECL emission spectrum of BP nanoflakes (∼510 nm) and the absorption spectrum of Ag/AgCl nanocubes (200-300 nm and 400-700 nm), effective energy transfer yielded. The introduction of Pb 2+ would lead to the detachment of Ag/AgCl nanocubes then result in an enhanced ECL emission. Based on this, the proposed method could accurately quantify the Pb 2+ in the range from 0.5 pM to 5 nM, which exhibited comparative performance to previous work. Furthermore, this study presents the example of employing 2D BP nanoflakes as ECL emitters and constructing a coreactant-free ECL sensing platform, which might open up a promising route for the potential design and implement in clinical analysis., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Vascular endothelial growth factor (VEGF) signaling promotes angiogenesis by stimulating the migration and proliferation of endothelial cells. The aim of this study was to investigate the expression of Survivin and VEGF receptor 1/2/3 (VEGFR 1/2/3) in esophageal carcinoma tissues (ECTs), and to explore the therapy effect of the suppression of VEGFR2 signaling. Here, we found that VEGFR2 and Survivin had high expressions and a significant correlation (r = 0.874, P < 0.002) in ECTs. Further, we found that VEGFR2 signaling could activate the AKT1/MDM2/Survivin pathway. The inhibition of VEGFR2 signaling with the XL184 treatment downregulated the phosphorylation of AKT1 and MDM2, and then, increased the activation of Caspase 3/7, resulting in the reduction of cell viability and the apoptosis of HUVECs. Additionally, in the esophageal tumor model, the tumor growth was significantly suppressed by blocking Survivin and the suppression of tumor growth was more effective in the combined treatment by blocking Survivin and Bcl-xl/Bcl-2. Our data thus revealed that Survivin in the signal downstream of VEGFR2 played an important role in esophageal cancer cell survival and might be a potential candidate target for the combined therapy for esophageal cancer., (Copyright © 2018. Published by Elsevier Masson SAS.)