ABSTRACT
We study the depinning of domain walls by pure diffusive spin currents in a nonlocal spin valve structure based on two ferromagnetic Permalloy elements with copper as the nonmagnetic spin conduit. The injected spin current is absorbed by the second Permalloy structure with a domain wall, and from the dependence of the wall depinning field on the spin current density we find an efficiency of 6×10{-14} T/(A/m{2}), which is more than an order of magnitude larger than for conventional current induced domain-wall motion. Theoretically we find that this high efficiency arises from the surface torques exerted by the absorbed spin current that lead to efficient depinning.
ABSTRACT
We use a pump-probe photoemission electron microscopy technique to image the displacement of vortex cores in Permalloy discs due to the spin-torque effect during current pulse injection. Exploiting the distinctly different symmetries of the spin torques and the Oersted-field torque with respect to the vortex spin structure we determine the torques unambiguously, and we quantify the amplitude of the strongly debated nonadiabatic spin torque. The nonadiabaticity parameter is found to be ß=0.15±0.07, which is more than an order of magnitude larger than the damping constant α, pointing to strong nonadiabatic transport across the high magnetization gradient vortex spin structures.
ABSTRACT
In a wide variety of cells, mitogenic factors release Ca(2+) from intracellular stores. The fall of the [Ca(2+)] within the lumen of the Ca(2+)-storing organelles triggers in many cells capacitative Ca(2+) entry (CCE). The present study was performed to elucidate the effect of insulin-like growth factor (IGF-1) on CCE in human embryonic kidney (HEK 293) cells. After depletion of Ca(2+) stores by thapsigargin, CCE was assessed by the increase in cytosolic free [Ca(2+)] (Fura-2 fluorescence imaging) when raising extracellular [Ca(2+)] from 0 to physiological concentrations. IGF-1 exposure (50 ng/ml) for 4 h in serum-free medium markedly enhanced CCE, while a 24-h exposure to IGF-1 depressed CCE profoundly. As some Ca(2+) channels are highly sensitive to the cell membrane potential, and as IGF-1 has been reported to enhance K(+) channel activity, the influence of K(+) channel blockers on the IGF-1-dependent stimulation of CCE was also tested. TEA, charybdotoxin and margatoxin decreased CCE. Similar to the total capacitative calcium entry, the fraction of CCE that was sensitive to K(+) channel blockers was increased after 4 h and decreased after 24 h exposure to IGF-1. Taken together, these data suggest that IGF-1 induces a transient increase followed by a decrease of CCE, and that these effects are at least partly dependent on IGF-1-induced K(+) channel activity.
