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In order to understand the ignition and combustion characteristics of tetraethylammonium dodecahydrododecaborate, laser ignition experiments were conducted on a sample with an equivalent diameter of 1.11 mm to determine its ignition and combustion parameters. Combining with the pyrolysis behaviors in both nitrogen and air atmospheres achieved by thermogravimetric analysis/mass spectrometry, the combustion mechanism of tetraethylammonium dodecahydrododecaborate was also e-valuated. The results show that tetraethylammonium dodecahydrododecaborate, which cracks at above 300°C in both nitrogen and air atmosphere, has a good thermal stability. During the cracking process, the material is oxidized simulaneously and oxidized strongly and gain weight when heated to 650°C. This compound can be ignited easily in air, and its ignition delay time is determined to be 45.8 ms with the ignition power density of 4.72 X 106 W/m², and the total burning time is 2.467 s. The surface temperature is 1 600-1 800°C during the combustion process. It is proposed that, in the combustion process of tetraethylammonium dodecahydrododecaborate, both H2 release and skeleton cracking occur, and the combustion of the gaseous hydrocarbon compounds formed from skeleton cracking could lead to obvious traces of smoke. [ABSTRACT FROM AUTHOR]

Background: Chemotherapy resistance reduces the effectiveness of chemotherapeutic drugs greatly, resulting in treatment failure. Therefore, exploring chemoresistance-related genes and the corresponding mechanism is extremely important. The central role of CD44v6 in colorectal cancer has been previously reported. However, the effects of CD44v6 gene knockdown on the chemosensitivity of colorectal cancer cells are not conclusive., Material and Methods: A stable CD44v6 knockdown cell model in HT29 cells (HT29-KD) was established via lentiviral transduction. A quantitative real-time polymerase chain reaction (PCR) was carried out to confirm the knockdown efficiency. The chemosensitivity of cells to 5-fluorouracil (5-FU) was determined by a cell counting kit (CCK)-8 assay. Cell apoptosis and the cell cycle were assessed by flow cytometry., Results: The CD44v6 knockdown cell model was successfully constructed by using lentiviral transduction. Upon treatment with 5-FU, the inhibitory rate for cell activity of HT29-KD cells was significantly higher than that of the control group (HT29-NC). CD44v6 gene knockdown did not significantly affect HT-29 cell proliferation, according to the CCK-8 assay and cell cycle analysis. The cell apoptosis assay revealed that CD44v6 gene knockdown promoted HT-29 cell apoptosis. Without 5-FU treatment, there was no significant difference in terms of the relative expression level of the autophagy-related gene BECN1 between the two groups. However, with 5-FU treatment, the relative expression level of BECN1 in HT29-KD cells was much lower than that in HT29-NC cells., Conclusion: Our study confirms that CD44v6 gene knockdown can enhance chemosensitivity in HT29 cells by promoting apoptosis and inhibiting autophagy, thus affirming the effects of CD44v6 on the chemosensitivity of colorectal cancer., (© 2019 by the Association of Clinical Scientists, Inc.)