An Ultrafast and Room-Temperature Strategy for Kilogram-Scale Synthesis of Sub-5 nm Eu3+ -doped CaMO4 Nanocrystals with a Photoluminescence Quantum Yield Exceeding 85.

Rare earth-doped metal oxide nanocrystals have a high potential in display, lighting, and bio-imaging, owing to their excellent emission efficiency, superior chemical, and thermal stability. However, the photoluminescence quantum yields (PLQYs) of rare earth-doped metal oxide nanocrystals have been reported to be much lower than those of the corresponding bulk phosphors, group II-VI, and halide-based perovskite quantum dots because of their poor crystallinity and high-concentration surface defects. Here, an ultrafast and room-temperature strategy for the kilogram-scale synthesis of sub-5 nm Eu3+ -doped CaMoO4 nanocrystals is presented, and this reaction can be finished in 1 min under ambient conditions. The absolute PLQYs for sub-5 nm Eu3+ -doped CaMoO4 nanocrystals can reach over 85%, which are comparable to those of the corresponding bulk phosphors prepared by the high-temperature solid state reaction. Moreover, the as-produced nanocrystals exhibit a superior thermal stability and their emission intensity unexpectedly increases after sintering at 600 °C for 2 h in air. 1.9 kg of Eu3+ -doped CaMoO4 nanocrystals with a PLQY of 85.1% can be obtained in single reaction.

Room-Temperature, Ultrafast, and Aqueous-Phase Synthesis of Ultrasmall LaPO4:Ce3+, Tb3+ Nanoparticles with a Photoluminescence Quantum Yield of 74.

LaPO4:Ce3+, Tb3+ nanoparticles with a particle size of 2.7 nm are prepared by a facile room-temperature ligand-assisted coprecipitation method in an aqueous solution. Short-chain butyric acid and butylamine are used as binary ligands and play a critically important role in the synthesis of highly luminescent LaPO4:Ce3+, Tb3+ nanoparticles. The absolute photoluminescence quantum yield as high as 74% can be achieved for extremely small LaPO4:Ce3+, Tb3+ nanoparticles with an optimal composition of La0.4PO4:Ce0.13+, Tb0.53+, which is different from La0.4PO4:Ce0.453+, Tb0.153+ for bulk phosphor. The energy transfer from Ce3+ ions to Tb3+ ions is investigated in sub-3 nm LaPO4:Ce3+, Tb3+ nanoparticles, and Ce3+ ion emission is almost completely suppressed. This room-temperature, ultrafast, and aqueous-phase synthetic strategy is particularly suitable for the large-scale preparation of highly luminescent LaPO4:Ce3+, Tb3+ nanoparticles. LaPO4:Ce3+, Tb3+ nanoparticles (110 g) can be synthesized in one batch, which is perfectly suited to the needs of industrial production.

Room-temperature and ultrafast Eu3+ ion doping for highly luminescent and extremely small CaMoO4 nanocrystals.

We developed a room-temperature and ultrafast Eu3+-ion doping approach for the synthesis of highly luminescent Eu-doped CaMoO4 nanoparticles. Firstly, CaMoO4 nanoparticles with a particle size of 3.9 nm are rapidly prepared using a room temperature co-precipitation approach. Subsequently, Eu-doped CaMoO4 nanoparticles with a photoluminescence quantum yield of up to 75% are synthesized by a post-cation exchange reaction at room temperature. This facile and room-temperature synthetic strategy enables us to prepare highly luminescent and extremely small rare earth ion-doped metal oxide nanocrystals.

Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-ß1/Smads signaling pathway by targeting TRPM6.

MicroRNAs (miRNAs) have been found to act as key regulators in the pathogenesis of myocardial ischemic-reperfusion (I/R) injury. In this study, we explore the role and mechanism of microRNA-202-3p (miR-202-3p) in regulating cardiomyocyte apoptosis, in respective of the TGF-ß1/Smads signaling pathway by targeting the transient receptor potential cation channel, subfamily M, member 6 (TRPM6). The targeting relationship between miR-202-3p and TRPM6 was verified by a dual-luciferase reporter gene assay. Sprague-Dawley rat models of myocardial I/R injury were initially established and treated with different mimics, inhibitors and siRNAs to test the effects of miR-202-3p and TRPM6 on myocardial I/R injury. The levels of inflammatory factors; IL-1ß, IL-6, TNF-α as well as the degree of myocardial fibrosis and cardiomyocyte apoptosis were determined in rats transfected with different plasmids. TRPM6 was found to be the target of miR-202-3p. Up-regulated miR-202-3p or knockdown of TRPM-6 alleviated oxidative stress and inflammatory response, reduced ventricular mass, altered cardiac hemodynamics, suppressed myocardial infarction, attenuated cell apoptosis, and inhibited myocardial fibrosis. MiR-202-3p overexpression activates the TGF-ß1/Smads signaling pathway by negatively regulating TRPM6 expression. Taken together, these findings suggest that miR-202-3p offers protection against ventricular remodeling after myocardial I/R injury via activation of the TGF-ß1/Smads signaling pathway.

ABCG1--a potential therapeutic target for atherosclerosis.

Cholesterol efflux from macrophage foam cells, the initial step of reverse cholesterol transport, is assumed to be the most relevant step with respect to atherosclerosis. As one of the ATP-binding cassette transporter (ABC) family members, ABCG1 plays a critical role in the process of cholesterol efflux. It has been recently identified to export cellular cholesterol to large HDL particles. For mature HDL constitutes the bulk of the plasma HDL, ABCG1 is responsible for the majority of the cholesterol efflux from macrophage foam cells to serum. Overexpression of ABCG1 improves HDL function through stimulating cholesterol export. Therefore, it could be hypothesized that ABCG1 would be a new target for the treatment of atherosclerosis.