Flow-Dependent Mass Transfer May Trigger Endothelial Signaling Cascades

It is well known that fluid mechanical forces directly impact endothelial signaling pathways. But while this general observation is clear, less apparent are the underlying mechanisms that initiate these critical signaling processes. This is because fluid mechanical forces can offer a direct mechanical input to possible mechanotransducers as well as alter critical mass transport characteristics (i.e., concentration gradients) of a host of chemical stimuli present in the blood stream. However, it has recently been accepted that mechanotransduction (direct mechanical force input), and not mass transfer, is the fundamental mechanism for many hemodynamic force-modulated endothelial signaling pathways and their downstream gene products. This conclusion has been largely based, indirectly, on accepted criteria that correlate signaling behavior and shear rate and shear stress, relative to changes in viscosity. However, in this work, we investigate the negative control for these criteria. Here we computationally and experimentally subject mass-transfer limited systems, independent of mechanotransduction, to the purported criteria. The results showed that the negative control (mass-transfer limited system) produced the same trends that have been used to identify mechanotransduction-dominant systems. Thus, the widely used viscosity-related shear stress and shear rate criteria are insufficient in determining mechanotransduction-dominant systems. Thus, research should continue to consider the importance of mass transfer in triggering signaling cascades

An atomic model calculation of exchange anisotropy and uncompensated spin element in antiferromagnetic layer: An effect of exchange coupling with various ferromagnetic materials

An atomic model of the direct exchange coupling in an antiferromagnetic (AF) and ferromagnetic (FM) bilayer has been investigated. Exchange anisotropy is achieved by different mechanisms in the body-centred-cubic and face-centred-cubic FM layers. For the former, the formation of an AF domain wall directly causes the exchange anisotropy. For the latter, a cooperative effect in the AF domain wall and the asymmetric form of the uncompensated AF spins produces the exchange anisotropy