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Carbon–polymer nanocomposites with good dielectric properties have potential applications in the electronic and electrical industry because of their good mechanical properties and low cost. The morphology, structure, dielectric properties, and mechanical strength of reduced-graphene oxide nanosheet/poly(vinylidene fluoride-co-hexafluoropropylene) nanocomposites (rGO/PVDF-HFP) were investigated. The rGO nanosheets were well dispersed and strongly oriented in the matrix, thanks to the unique spin-assistant preparation process. A dielectric constant of 54 (100 Hz) which was four times higher than that of pure PVDF-HFP was obtained when the concentration of rGO was 0.7 vol % and the dielectric loss was as low as 0.27. The good dielectric performance of the nanocomposites was attributed to the homogeneous dispersion and good alignment of rGO. The shear force provided by spin-coating, the thickness decreasing process, and thickness control were assumed to be key factors in the alignment of rGO nanosheets in the nanocomposite films. At the same time, the aligned rGO sheets increased the percolation threshold of the composite which shed light on the mechanism for obtaining low loss materials.

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Background/Aims: Bile duct cancer, although not among the most common tumors, still accounts for more and more worldwide deaths each year. By attempting to verify an overexpression of ALDOA in cholangiocarcinoma tissues and cells and explore the underlying molecular mechanism regulated by miR-122-5p, this study was designed to provide a potential molecular target in bile duct cancer treatment. Methods: Western blot and immunohistochemistry were performed to detect the ALDOA protein level in duct carcinoma tissues. The transfection efficiency was confirmed by western blot and/or RT-qPCR assay. The proliferation of bile duct carcinoma cells was determined by MTT and colony formation assay. The invasion ability of bile duct carcinoma cells was evaluated with Transwell invasion assay. Flow cytometry detected cell apoptosis of bile duct carcinoma cells. The miRNAs which modulate ALDOA were filtrated from bioinformatics software and clinical specimens. The target relationship was confirmed by dual luciferase reporter assay. Furthermore, a xenograft model was completed to verify the impact of miRNA on inhibition growth of bile duct carcinoma cells. Results: ALDOA was found up-regulated in bile duct carcinoma tissues and cells. Knockdown of ALDOA promoted the apoptosis of cells and inhibited the proliferation and invasion of bile duct carcinoma cells. Bioinformatics and clinical specimens indicated the negative correlation and targeted regulation between miR-122-5p and ALDOA. By down-regulating ALDOA, overexpression of miR-122-5p appeared to promote cell apoptosis and significantly inhibit cell proliferation, invasion in vitro and suppress the tumor growth in vivo. Conclusion: miR-122-5p inhibited proliferation and invasion of bile duct carcinoma cells and promoted cell apoptosis by targeting ALDOA expression.

Metabolic reprogramming and immune escape play a major role in tumorigenesis. Increasing number of studies have shown that reprogramming of glutamine metabolism is a putative determinant of the anti-tumor immune response in the tumor microenvironment (TME). Usually, the predatory uptake of glutamine by tumor cells in the TME results in the limited utilization of glutamine by immune cells and affects the anti-tumor immune response. The cell-programmed glutamine partitioning also affects the anti-tumor immune response. However, the reprogramming of glutamine metabolism in tumors modulates immune escape by regulating tumor PD-L1 expression. Likewise, the reprogramming of glutamine metabolism in the immune cells also affects their immune function. Additionally, different types of glutamine metabolism inhibitors extensively regulate the immune cells in the TME while suppressing tumor cell proliferation. Herein, we discuss how metabolic reprogramming of tumor and immune cells regulates anti-tumor immune responses, as well as functional changes in different immune cells in the context of targeting tumor glutamine metabolism, which can better explain the potential of targeting glutamine metabolism in combination with immunotherapy for cancer.

Compounds of styrene-butadiene rubber (SBR) filled with bamboo charcoal powders (BCPs) were prepared with a laboratory-sized two-roll mill. The effects of the BCP loading on the curing characteristics and mechanical and thermal properties were investigated. The results indicate that the addition of BCP resulted in a longer curing time and a higher Mooney viscosity in the SBR materials. The incorporation of BCP into SBR improved the mechanical properties and dynamic properties. Furthermore, the mechanical properties of the vulcanizates after thermal aging were also studied, and the experimental results indicate that most of the mechanical properties improved after thermal aging. The overall results indicate that BCP could be used as a cheaper filler for SBR materials.

Histone deacetylase 9 (HDAC9) regulates hepatic gluconeogenesis by deacetylating Forkhead box O 1 (FoxO1). HDAC9 upregulation is involved in hepatitis C virus (HCV)-associated exaggerated gluconeogenesis. Herein, we found in addition to FoxO1, HDAC9 also regulates other gluconeogenic transcription factors, including peroxisomeproliferator-activated receptor-γ coactivator-1α (PGC-1α), cyclic AMP-responsive element-binding protein (CREB), and glucocorticoid receptor (GR). Unlike FoxO1, which is regulated by post-translational modification responses to HDAC9, HDAC9 regulates PGC-1α, CREB and GR by altering gene expression. Similar to PGC-1α, CREB and GR were found to be novel regulatory targets of FoxO1 by examination of the FoxO1 binding site in their promoter. PGC-1α, CREB and GR were upregulated in response to HDAC9 via FoxO1 deacetylation. These findings indicate that HDAC9-FoxO1 signalling contributes to gluconeogenesis by modulating the expression of gluconeogenic transcription factors. In particular, metabolic profiling demonstrated a clear shift towards gluconeogenesis metabolism, and HDAC9-FoxO1 signalling can be strongly induced to upregulate gluconeogenic transcription factors following HCV infection. The positive correlation between HDAC9 and gluconeogenic transcription factor expression levels in the livers of both HCV-infected patients and normal individuals further emphasizes the clinical relevance of these results. Thus, HDAC9-FoxO1 signalling axis is involved in regulating gluconeogenic transcription factors, gluconeogenesis, and HCV-induced type 2 diabetes.

A highly dispersed nickel catalyst supported on alumina with an NiO loading of 40 wt % has been prepared from Ni­(NO3)2·6H2O and NaAlO2 as precursors through a novel cation–anion double-hydrolysis strategy. The product has been tested for its efficacy in CO methanation. The preparation process can be considered as a time-saving and green synthetic technique that does not require the use of a basic precipitation agent. The resulting Ni/Al2O3 catalyst shows a high dispersion of NiO with small particle size (<5 nm), in spite of the high metal loading. Various promoters, namely Zr, Fe, and Ce, were further added to regulate the catalytic properties of the Ni/Al2O3 catalyst, and 40Ni-5Zr/Al2O3 showed the optimal CO methanation activity. The improved catalytic performance could be mainly due to the high degree of Ni dispersion and the abundance of oxygen vacancies, which enhanced the adsorption and dissociation of CO.