Promoted diffusion mechanism of Fe2.7wt.%Si-Fe10wt.%Si couples under magnetic field by atomic-scale observations.

Diffusion behavior of newly designed Fe2.7wt.%Si-Fe10wt.%Si couples at 1100 °C for up to 12 h has been investigated under the 0, 0.8 and 3 T magnetic fields. Diffusion thickness of solid solution layer and weight percent of Si on Fe2.7wt.%Si side increase significantly under a magnetic field. Application of a magnetic field promotes the diffusion of solid solution layer through the possible diffusion of vacancies mainly due to the appearance of defects, which has been demonstrated by the increased dislocation density and broadening of the typical XRD peaks. Replacement of Si sits by Fe atoms in the crystal structure leads to the appearance of Fe diffraction peaks, which has been confirmed by the increased interplanar spacings under a magnetic field. The magnetic field benefits the depinning of dislocations and leads to higher dislocation density because of the magnetoplastic effect which has been confirmed by the significantly reduced thickness of Fe2.7wt.%Si. Nano-sized Fe3Si particles precipitate in the matrix with an orientation relationship on Fe10wt.%Si side as {220}Fe3Si || {220}matrix & < 1-10 >Fe3Si || < 1-10 >matrix. Fe3Si particles pin dislocation moving and lead to higher dislocation density.

Non-monotonic changes in critical solidification rates for stability of liquid-solid interfaces with static magnetic fields.

We report the magnetic field dependence of the critical solidification rate for the stability of liquid-solid interfaces. For a certain temperature gradient, the critical solidification rate first increases, then decreases, and subsequently increases with increasing magnetic field. The effect of the magnetic field on the critical solidification rate is more pronounced at low than at high temperature gradients. The numerical simulations show that the magnetic-field dependent changes of convection velocity and contour at the interface agree with the experimental results. The convection velocity first increases, then decreases, and finally increases again with increasing the magnetic field intensity. The variation of the convection contour at the interface first decreases, then increases slightly, and finally increases remarkably with increasing the magnetic field intensity. Thermoelectromagnetic convection (TEMC) plays the role of micro-stirring the melt and is responsible for the increase of interface stability within the initially increasing range of magnetic field intensity. The weak and significant extents of the magneto-hydrodynamic damping (MHD)-dependent solute build-up at the interface front result, respectively, in the gradual decrease and increase of interfacial stability with increasing the magnetic field intensity. The variation of the liquid-side concentration at the liquid-solid interface with the magnetic field supports the proposed mechanism.

Growth-inhibiting and apoptosis-inducing activities of Myricanol from the bark of Myrica rubra in human lung adenocarcinoma A549 cells.

Myrica rubra (Lour.) Sieb. Et Zucc. is a myricaceae Myrica plant. It is a subtropical fruit tree in China and other Asian countries. The bark of M. rubra is used in Chinese folk medicine because of its antibacterial, antioxidant, anti-inflammatory, and anticancer activities. However, the mechanisms underlying such activities remain unclear. This study investigated whether or not Myricanol extracted from M. rubra bark elicits anti-cancer effects on human lung adenocarcinoma A549 cells by inducing apoptosis in vivo. Myricanol was extracted from M. rubra bark through system solvent extraction and silica gel layer column separation. The results of tritiated thymidine assay, colony formation assay, and flow cytometry indicated that Myricanol inhibited the growth of A549 cells. The effects of Myricanol on the expression of key apoptosis-related genes in A549 cells were evaluated by quantitative PCR and Western blot analyses. Myricanol significantly inhibited the growth of A549 cells in a dose-dependent manner, with a half maximal inhibitory concentration of 4.85 µg/ml. Myricanol significantly decreased colony formation and induced A549 cell apoptosis. Myricanol upregulated the expression of Caspase-3, Caspase-9, Bax, and p21 and downregulated the expression of Bcl-2 at the mRNA and protein levels. These changes were associated with apoptosis. Based on these results, we propose that Myricanol elicits growth inhibitory and cytotoxic effects on lung cancer cells. Therefore, Myricanol may be a clinical candidate for the prevention and treatment of lung cancer.