158 research outputs found

    Magnetic Domain Patterns Depending on the Sweeping Rate of Magnetic Fields

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    The domain patterns in a thin ferromagnetic film are investigated in both experiments and numerical simulations. Magnetic domain patterns under a zero field are usually observed after an external magnetic field is removed. It is demonstrated that the characteristics of the domain patterns depend on the decreasing rate of the external field, although it can also depend on other factors. Our numerical simulations and experiments show the following properties of domain patterns: a sea-island structure appears when the field decreases rapidly from the saturating field to the zero field, while a labyrinth structure is observed for a slowly decreasing field. The mechanism of the dependence on the field sweeping rate is discussed in terms of the concepts of crystallization.Comment: 4 pages, 3 figure

    Theory of Hysteresis Loop in Ferromagnets

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    We consider three mechanisms of hysteresis phenomena in alternating magnetic field: the domain wall motion in a random medium, the nucleation and the retardation of magnetization due to slow (critical) fluctuations. We construct quantitative theory for all these processes. The hysteresis is characterized by two dynamic threshold fields, by coercive field and by the so-called reversal field. Their ratios to the static threshold field is shown to be function of two dimensionless variables constituted from the frequency and amplitude of the ac field as well as from some characteristics of the magnet. The area and the shape of the hysteresis loop are found. We consider different limiting cases in which power dependencies are valid. Numerical simulations show the domain wall formation and propagation and confirm the main theoretical predictions. Theory is compared with available experimental data.Comment: RevTex, 13 pages, 8 figures (PostScript), acknowledgements adde

    Stochastic Hysteresis and Resonance in a Kinetic Ising System

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    We study hysteresis for a two-dimensional, spin-1/2, nearest-neighbor, kinetic Ising ferromagnet in an oscillating field, using Monte Carlo simulations and analytical theory. Attention is focused on small systems and weak field amplitudes at a temperature below TcT_{c}. For these restricted parameters, the magnetization switches through random nucleation of a single droplet of spins aligned with the applied field. We analyze the stochastic hysteresis observed in this parameter regime, using time-dependent nucleation theory and the theory of variable-rate Markov processes. The theory enables us to accurately predict the results of extensive Monte Carlo simulations, without the use of any adjustable parameters. The stochastic response is qualitatively different from what is observed, either in mean-field models or in simulations of larger spatially extended systems. We consider the frequency dependence of the probability density for the hysteresis-loop area and show that its average slowly crosses over to a logarithmic decay with frequency and amplitude for asymptotically low frequencies. Both the average loop area and the residence-time distributions for the magnetization show evidence of stochastic resonance. We also demonstrate a connection between the residence-time distributions and the power spectral densities of the magnetization time series. In addition to their significance for the interpretation of recent experiments in condensed-matter physics, including studies of switching in ferromagnetic and ferroelectric nanoparticles and ultrathin films, our results are relevant to the general theory of periodically driven arrays of coupled, bistable systems with stochastic noise.Comment: 35 pages. Submitted to Phys. Rev. E Minor revisions to the text and updated reference

    Time-Lapse Imaging of the Dynamics of CNS Glial-Axonal Interactions In Vitro and Ex Vivo

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    Myelination is an exquisite and dynamic example of heterologous cell-cell interaction, which consists of the concentric wrapping of multiple layers of oligodendrocyte membrane around neuronal axons. Understanding the mechanism by which oligodendrocytes ensheath axons may bring us closer to designing strategies to promote remyelination in demyelinating diseases. The main aim of this study was to follow glial-axonal interactions over time both in vitro and ex vivo to visualize the various stages of myelination.We took two approaches to follow myelination over time: i) time-lapse imaging of mixed CNS myelinating cultures generated from mouse spinal cord to which exogenous GFP-labelled murine cells were added, and ii) ex vivo imaging of the spinal cord of shiverer (Mbp mutant) mice, transplanted with GFP-labelled murine neurospheres. We demonstrate that oligodendrocyte-axonal interactions are dynamic events with continuous retraction and extension of oligodendroglial processes. Using cytoplasmic and membrane-GFP labelled cells to examine different components of the myelin-like sheath, we provide evidence from time-lapse fluorescence microscopy and confocal microscopy that the oligodendrocytes' cytoplasm-filled processes initially spiral around the axon in a corkscrew-like manner. This is followed subsequently by focal expansion of the corkscrew process to form short cuffs, which then extend longitudinally along the axons. We predict from this model that these spiral cuffs must extend over each other first before extending to form internodes of myelin.These experiments show the feasibility of visualizing the dynamics of glial-axonal interaction during myelination over time. Moreover, these approaches complement each other with the in vitro approach allowing visualization of an entire internodal length of myelin and the ex vivo approach validating the in vitro data

    Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

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    Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

    Endothelial proliferation and adhesivity

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