Fuel-Rich Premixed n-Heptane/Toluene Flame: A Molecular Beam Mass Spectrometry and Chemical Kinetic Study

The mole fraction profiles of major flame species and intermediates including PAH precursors are measured in an atmospheric premixed burner-stabilized fuel-rich (φ = 1.75) n-heptane/toluene/O2/Ar flame (n-heptane/toluene ratio is 7:3 by liquid volume). These data are simulated with a detailed, extensively validated chemical kinetic reaction mechanism for combustion of n-heptane/toluene mixture, involving the reactions of PAH formation. The mechanism is extended with cross reactions for n-heptane and toluene derivatives. A satisfactory agreement between the new experimental data on the structure of n-heptane/toluene flame and the numerical simulations is observed. The mechanism reported can be successfully used in the models of practical fuel surrogates for reproducing the formation of soot precursors. The analysis of the reaction pathways shows that in the flame of the n-heptane/toluene blend (7:3 liquid volume ratio) the reactions dominant for the formation of the first aromatic ring (benzene and phenyl) are as those typical for pure toluene flames. The discrepancies between the measured and calculated species mole fractions are detected as well. The steps for the mechanism improvements are determined on the basis of the sensitivity analysis performed. To our knowledge, the measurements of mole fraction profiles of PAH and intermediates reported here, are the first of its kind and represent an unique data set extremely important for validation of chemical kinetic mechanisms for combustion of practical fuels

SILENCING MICAL2 REPRESSES HUMAN CANCER CELL GROWTH AND INVASION INDUCING MESENCHYMAL TO EPITHELIAL TRANSITION

MICAL (Molecules Interacting with CasL)2 belongs to an evolutionarily conserved family of proteins that catalyze actin oxidation-reduction reactions destabilizing F-actin in cytoskeletal dynamics. Here we show for the first time that MICAL2 mRNA is significantly over-expressed in aggressive, poorly differentiated/ undifferentiated, primary gastric and renal human epithelial cancers. Immunohistochemistry showed MICAL2- positive cells on the cancer invasive front and in metastasizing cancer cells inside emboli, but not at sites of metastasis, suggesting MICAL2 expression was “on” in a subpopulation of primary cancer cells seemingly detaching from the tissue of origin, enter emboli and travel to distant sites, to be turned “off” once homing at the metastatic site occurred. In vitro, MICAL2 knock-down was clearly associated with induction of mesenchymal to epithelial transition, causing reduction of viability and loss of motility and invasion properties of human cancer cells. Moreover, expression of MICAL2 cDNA in MICAL2-depleted cells induced epithelial to mesenchymal transition. All together our data indicate MICAL2 over-expression is associated with cancer progression and metastatic disease. MICAL2 might be an important regulator of epithelial to mesenchymal transition and therefore a promising target for anti-metastatic therapy