[en] The characteristics of NOx emissions in pure hydrogen nonpremixed jet flames with coaxial air are analyzed numerically for a wide range of coaxial air conditions. Among the models tested in simple nonpremixed jet flame, the one-half power scaling law could be reproduced only by the Model C using the HO₂/H₂O₂ reaction, implying the importance of chemical nonequilibrium effect. The flame length is reduced significantly by augmenting coaxial air, and could be represented as a function of the ratio of coaxial air to fuel velocity. Predicted EINOx scaling showed a good concordance with experimental data, and the overall one-half power scaling was observed in coaxial flames with Model C when flame residence time was defined with flame volume instead of a cubic of the flame length. Different level of oxygen mass fraction at the stoichiometric surface was observed as coaxial air was increased. These different levels imply that the coaxial air strengthens the nonequilibrium effect

[en] Highlights: • SALL4 promotes stemness traits and metastatic phenotype in vitro. • SALL4 expression positively impacts PDAC-derived tumor growth. • SALL4 regulates intracellular ROS via FoxM1/Prx III by activation of ERK1/2. Pancreatic ductal adenocarcinoma (PDAC) is a major malignant phenotype in pancreatic cancer, which is one of the most death causes by cancer in the world. PDAC developed from pancreatic intra-epithelial neoplasms (PanINs) and poorly diagnosed at early stages. Beside of high drug resistance, metastasis is the great concern during pancreatic cancer treatment. SALL4 expression is inherent in the upregulations of endothelial mesenchymal transition (EMT) genes and therefore promoting cancer metastasis. Furthermore, some of evidences indicated reactive oxygen species (ROS) is also influent to metastasis and self-antioxidant capacity seems a gold standard for successful metastasis rate. In this study, we have found the role Spalt like protein 4 (SALL4) to PDAC proliferation, mobility and its regulation to mitochondrial ROS via FoxM1/Prx III axis. It is possible that SALL4 mainly induces endothelial-mesenchymal transition (EMT) phenotype and favors ROS loss to facilitate metastasis efficiency in PDAC cells. Therefore, SALL4 might be a promising marker for PDAC treatment and targeting SALL4 would benefit anti-proliferative and anti-metastasis therapies.