Effect of Composition Ratios on the Performance of Graphene/Carbon Nanotube/Manganese Oxide Composites toward Supercapacitor Applications.

Herein, we describe the preparation and characterization of graphene/carbon nanotube (CNT)/MnO v composites and the effects of chemical composition and phase transformation on the properties of the corresponding electrode film. In general, the effect of graphene-to-CNT ratio (G/C ratio) and the manganese (Mn) content on the morphology, chemical state, crystallization properties, and microstructure of the composite material was examined by scanning electron microscopy, X-ray photoelectron spectroscopy, X-ray diffraction, and selected area electron diffraction. The bonding mechanism between MnO v and graphite-based materials, that is, graphene and CNTs, is discussed. The influence of the composition of the composites on the performance of the electrode was investigated using charge-discharge curves. The faradically active MnO v also functioned as a considerable cobinder and allowed for a reduced amount of polymeric binder, which enhanced the conductivity and capacitance of the electrode. The optimized electrode composition was obtained based on our present graphene and CNT specifications. In summary, the results discussed in this article provide significant background information for future applications of graphene/CNT/MnO v composite electrodes.

Emodin represses TWIST1-induced epithelial-mesenchymal transitions in head and neck squamous cell carcinoma cells by inhibiting the ß-catenin and Akt pathways.

Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer deaths worldwide. In recent studies, a crucial link has been discovered between the acquisition of metastatic traits and tumour-initiating abilities in cancer cells during the epithelial-mesenchymal transition (EMT). Herein, we demonstrated that the ectopic expression of TWIST1, the EMT regulator, in HNSCC FaDu cells triggered EMT and resulted in the acquisition of a mesenchymal phenotype. Moreover, FaDu-pFLAG-TWIST1 cancer cell populations that were induced to EMT displayed an increased proportion of cells with the CD44 marker, which is associated with tumour initiation. Interestingly, we found that emodin treatment reduced the tumour-initiating abilities and inhibited cell migration and invasion in FaDu-pFLAG-TWIST1 cells. Emodin directly inhibited TWIST1 expression, upregulated E-cadherin mRNA and protein expression, and downregulated vimentin mRNA and protein expression. Moreover, we found that emodin inhibited TWIST1 binding to the E-cadherin promoter and repressed E-cadherin transcription activity. We also found that emodin inhibited TWIST1-induced EMT by inhibiting the ß-catenin and Akt pathways. More interestingly, emodin significantly inhibited TWIST1-induced invasion in vivo. Therefore, emodin might be applicable to anticancer therapy and could be a potential new therapeutic drug for HNSCC.