Impedance of nanometer thickness ferromagnetic Co40Fe40B20 films

Nanocrystalline Co40Fe40B20 films, with film thickness tf = 100 nm, were deposited on glass substrates by the magnetron sputtering method at room temperature. During the film deposition period, a dc magnetic field, h = 40 Oe, was applied to introduce an easy axis for each film sample: one with h||L and the other with h||w, where L and w are the length and width of the film. Ferromagnetic resonance (FMR), ultrahigh frequency impedance (IM), dc electrical resistivity (ρ), and magnetic hysteresis loops (MHL) of these films were studied. From the MHL and r measurements, we obtain saturation magnetization 4πMs = 15.5 kG, anisotropy field Hk = 0.031 kG, and r = 168 mW.cm. From FMR, we can determine the Kittel mode ferromagnetic resonance (FMR-K) frequency fFMRK = 1,963 MHz. In the h||L case, IM spectra show the quasi-Kittel-mode ferromagnetic resonance (QFMR-K) at f0 and the Walker-mode ferromagnetic resonance (FMR-W) at fn, where n = 1, 2, 3, and 4. In the h||w case, IM spectra show QFMR-K at F0 and FMR-W at Fn. We find that f0 and F0 are shifted from fFMRK, respectively, and fn = Fn. The in-plane spin-wave resonances are responsible for those relative shifts

Adrenergic β2 receptor activation stimulates anti-inflammatory properties of dendritic cells in vitro

Vagal nerve efferent activation has been shown to ameliorate the course of many inflammatory disease states. This neuromodulatory effect has been suggested to rest on acetylcholine receptor (AChR) activation on tissue macrophages or dendritic cells (DCs). In more recent studies, vagal anti-inflammatory activity was shown involve adrenergic, splenic, pathways. Here we provide evidence that the adrenergic, rather than cholinergic, receptor activation on bone marrow derived DCs results in enhanced endocytosis uptake, enhanced IL-10 production but a decreased IL-6, IL-12p70 and IL-23 production. In antigen specific T cell stimulation assays, adrenergic β2 receptor activation on bone marrow DCs led to an enhanced potential to induce Foxp3 positive suppressive Treg cells. These effects were independent of IL10-R activation, TGFβ release, or retinoic acid (RA) secretion. Hence, adrenergic receptor β2 activation modulates DC function resulting in skewing towards anti-inflammatory T cell phenotypes