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A novel photocatalyst was prepared by anchoring Au nanoparticles (NPs) onto one-dimensional potassium niobate (KNbO 3 ) nanowires. Photocatalytic activity towards rhodamine B degradation over Au/KNbO 3 appears to be much greater than that of KNbO 3 nanowires, nanorods and commercial Alfa Aesar. In terms of reaction rate constant (k), ultraviolet excitation (l ¼ 365 nm) is higher than that of visible-light (l > 420 nm) and increasing the size of Au NPs from 5 to 10 nm significantly improves the reactivity. Notably, Au NPs with a size of ca. 10 nm supported on KNbO 3 nanowires display the greatest photoreactivity, with k exceeding that of commercial KNbO 3 by a factor of 15. The mechanism responsible for the enhancement of photocatalytic activity was discussed, highlighting the crucial role of surface plasmon resonance as well as interband transitions on Au NPs. This study is potentially applicable to a range of low-dimensional niobate-based nanostructures combined with Au and other plasmonic NPs with promising applications in photocatalysis and relevant areas.

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A small amount of ionic liquid [bmim][BF(4)] was found to be an efficient aid for microwave heating of nonpolar dibenzyl ether in high temperature solution-phase synthesis of monodisperse magnetite nanoparticles. It was found to act as both microwave absorber and assistant stabilizer in the reactive process and was recovered and reused in successive reactions.

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Cardiac hypertrophy is closely correlated with diverse cardiovascular diseases, augmenting the risk of heart failure and sudden death. Long non-coding RNAs (lncRNAs) have been studied in cardiac hypertrophy for their regulatory function. LncRNA MEG3 has been reported in human cancers. Whereas, it is unknown whether MEG3 regulates the growth of cardiac hypertrophy. Therefore, this study aims to investigate the specific role of MEG3 in the progression of cardiac hypertrophy. Here, we found that MEG3 contributed to the pathogenesis of cardiac hypertrophy. MEG3 expression was remarkably strengthened in the mice heart which undergone the transverse aortic constriction (TAC). Moreover, qRT-PCR analysis revealed that MEG3 was upregulated in the cardiomyocytes which were treated with Ang-II. Silenced MEG3 inhibited the increasing size of hypertrophic cardiomyocytes and reversed other hypertrophic responses. Mechanically, MEG3 could affect cardiac hypertrophy by regulating gene expression. Mechanically, we found that MEG3 could be upregulated by the transcription factor STAT3 and could regulate miR-361-5p and HDAC9 by acting as a ceRNA. Finally, rescue assays were made to do further confirmation. All our findings revealed that STAT3-inducetd upregulation of lncRNA MEG3 controls cardiac hypertrophy by regulating miR-362-5p/HDAC9 axis.