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To measure viscosity of magnetic fluids (MFs) in adjustable magnetic field, this paper presented a novel method using a double tube and a torque measuring motor. The inner tube was fixed and the outer tube was driven by a motor. Mathematical analysis indicated that the viscosity of MFs in the gap between the two tubes could be determined by the rotational speed. A magnetic circuit constructed by some permanent magnets and yokes provided the magnetic field for the MFs in the gap. Changing the number of the magnets could adjust the magnetic density easily. Taking the temperature's influence on the viscosity into account, an extrapolation method was adopted to measure and control the MF's temperature precisely. This method was calibrated by the standard liquid with the known viscosity, which showed that the mean error was less than 0.82%. This method was used to measure the viscosity of MFs composed of MnZnFeO4 nanoparticles, oleic acid surfactants and lubricant carrier liquid in variable magnetic field at the different temperatures. [ABSTRACT FROM AUTHOR]

Background: Accumulating evidence suggests the pro-inflammatory cytokine interleukin-6 (IL-6) in tumor microenvironment may promote the development of hepatocellular carcinoma (HC). However, the underlying mechanism remains largely unknown. Methods: The expression and promoter activity of lncTCF7 were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and luciferase reporter assay. The function of the STAT3 binding site in the lncTCF7 promoter region was tested by luciferase reporter assay with nucleotide substitutions. The binding of STAT3 to the lncTCF7 promoter was confirmed by chromatin immunoprecipitation assay (CHIP) in vivo. The effects of decreasing STAT3 with small interference RNA and inhibiting STAT3 activation by small molecular inhibitor on lncTCF7 expression were also determined. Results: We demonstrate that IL-6 could induce lncTCF7 expression in a time- and dose-dependent manner, and we showed that IL-6 transcriptionally activated the expression of lncTCF7 in HC cells by activating STAT3, a transcription activator which binds to promoter regions of lncTCF7. Furthermore, knocking-down STAT3 and inhibiting STAT3 activation reduced lncTCF7 expression. Importantly, RNA interference-based attenuation of lncTCF7 prevented IL-6-induced EMT and cell invasion. Conclusion: Thus, these data provides evidence to the existence of an aberrant IL-6/STAT3/ lncTCF7 signaling axis that leads to HC aggressiveness through EMT induction, which could be novel therapeutic targets in malignancies. [ABSTRACT FROM AUTHOR]

Background: Accumulating evidence suggests the pro-inflammatory cytokine interleukin-6 (IL-6) in tumor microenvironment may promote the development of hepatocellular carcinoma (HCC). However, the underlying mechanism remains largely unknown. Methods: The expression and promoter activity of lncTCF7 were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and luciferase reporter assay. The function of the STAT3 binding site in the lncTCF7 promoter region was tested by luciferase reporter assay with nucleotide substitutions. The binding of STAT3 to the lncTCF7 promoter was confirmed by chromatin immunoprecipitation assay (CHIP) in vivo. The effects of decreasing STAT3 with small interference RNA and inhibiting STAT3 activation by small molecular inhibitor on lncTCF7 expression were also determined. Results: We demonstrate that IL-6 could induce lncTCF7 expression in a time- and dose-dependent manner, and we showed that IL-6 transcriptionally activated the expression of lncTCF7 in HCC cells by activating STAT3, a transcription activator which binds to promoter regions of lncTCF7. Furthermore, knocking-down STAT3 and inhibiting STAT3 activation reduced lncTCF7 expression. Importantly, RNA interference-based attenuation of lncTCF7 prevented IL-6-induced EMT and cell invasion. Conclusion: Thus, these data provides evidence to the existence of an aberrant IL-6/STAT3/ lncTCF7 signaling axis that leads to HCC aggressiveness through EMT induction, which could be novel therapeutic targets in malignancies. [ABSTRACT FROM AUTHOR]