Electrical detection of spin pumping due to the precessing magnetization of a single ferromagnet.

We report direct electrical detection of spin pumping, using a lateral normal-metal/ferromagnet/normal-metal device, where a single ferromagnet in ferromagnetic resonance pumps spin-polarized electrons into the normal metal, resulting in spin accumulation. The resulting backflow of spin current into the ferromagnet generates a dc voltage due to the spin-dependent conductivities of the ferromagnet. By comparing different contact materials (Al and/or Pt), we find, in agreement with theory, that the spin-related properties of the normal metal dictate the magnitude of the dc voltage.

A solid state paramagnetic maser device driven by electron spin injection.

In response to an external, microwave-frequency magnetic field, a paramagnetic medium will absorb energy from the field that drives the magnetization dynamics. Here we describe a new process by which an external spin-injection source, when combined with the microwave field spin pumping, can drive the paramagnetic medium from one that absorbs microwave energy to one that emits microwave energy. We derive a simple condition for the crossover from absorptive to emissive behavior. Based on this process, we propose a solid-state, paramagnetic device in which microwave amplification by stimulated emission of radiation is driven by spin injection.

Unified description of bulk and interface-enhanced spin pumping.

We describe a mechanism for generating nonequilibrium electron-spin accumulation in semiconductors or metals by rf magnetic field pumping. With a semiclassical model we show that a rotating applied magnetic field (or the processing magnetization inside a weak ferromagnet) generates a dc spin accumulation. For bulk systems this spin accumulation is in general given by a small fraction of h omega, where omega is the rotation or precession frequency. With the addition of a neighboring, field-free region, and allowing for the diffusion of spins across the interface, the spin accumulation is dramatically enhanced towards h omega near the interface. The interface-enhanced spin accumulation obtained within our bulk-oriented model is surprisingly similar to predictions based on interface-scattering theory [A. Brataas, Phys. Rev. B 66, 060404(R) (2002)].

Spin polarization of CrO2 at and across an artificial barrier.

We report a systematic study of the spin polarization of epitaxial CrO2 films at and across an interface using planar junctions with a superconducting counterelectrode. By chemical modification of the CrO2 surface before the deposition of the superconductor, junctions with a wide range of barrier strength were obtained. Analysis of the conductance data on these junctions, especially under Zeeman splitting of the superconducting density of states, yields consistent, close to full spin polarization for CrO2 regardless of the barrier strength.

Inhibition of intracellular Ca2+ mobilisation by low antiproliferative concentrations of thapsigargin in human vascular smooth-muscle cells.

Low nanomolar concentrations of thapsigargin, a modulator of intracellular Ca2+ ([Ca2+]i) pools, inhibit vascular smooth-muscle cell (VSMC) proliferation. Because the mechanisms underlying this effect have not been defined, the effect of antiproliferative concentrations of thapsigargin on [Ca2+]i in fura-2-loaded VSMCs was studied by using dynamic video imaging of [Ca2+]i. After seeding on coverslips, human VSMCs were incubated for 1-48 h with thapsigargin before loading with fura-2 or during imaging. Mobilisation of [Ca2+]i was stimulated with 1 microM ionomycin in Ca2+-free medium and the increase in [Ca2+]i detected by using Ca2+ imaging techniques. Continuous exposure of cells to low concentrations of thapsigargin (which failed measurably to increase in [Ca2+]i) reduced the ionomycin response in a time- and dose-dependent manner (100% inhibition at 10 nM thapsigargin after 1 h exposure). After exposure of cells to 10 nM thapsigargin for 1 h followed by washing and further incubation for < or = 72 h, there was a time-dependent recovery of the ionomycin response. Because the concentrations of thapsigargin and exposure times are identical to those that inhibit replication in VSMCs, it is proposed that depletion of [Ca2+]i pools mediates the inhibitory effect of thapsigargin on VSMC proliferation.

Corticotrophin, cortisol, prolactin and growth hormone responses to insulin-induced hypoglycaemia in normal subjects given sodium valproate.

Plasma corticotrophin (ACTH), cortisol, prolactin and growth hormone (GH) responses to insulin-induced hypoglycaemia were measured in normal healthy subjects of both sexes before and after three weeks' treatment with sodium valproate (Epilim, 200 mg three times a day). The drug had no effect on fasting plasma glucose levels, or the extent of hypoglycaemia induced by insulin (0.15 U/kg). There was no significant difference between pre- and post-treatment values for basal or stress-induced concentrations of ACTH and cortisol (n = 12), prolactin (n = 7) or GH (n = 9). The results suggest that treatment of normal subjects with sodium valproate has no effect on the response of the hypothalamo-pituitary-adrenocortical axis to hypoglycaemia, which is in contrast to its inhibitory effects on ACTH secretion in patients suffering from Nelson's syndrome. This implies that in the disease state, there may be a unique sensitivity to GABA-ergic manipulation.