247 research outputs found

    Models for the magnetic ac susceptibility of granular superferromagnetic CoFe/Al2_2O3_3

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    The magnetization and magnetic ac susceptibility, χ=χiχ\chi = \chi' - i \chi'', of superferromagnetic systems are studied by numerical simulations. The Cole-Cole plot, χ\chi'' vs. χ\chi', is used as a tool for classifying magnetic systems by their dynamical behavior. The simulations of the magnetization hysteresis and the ac susceptibility are performed with two approaches for a driven domain wall in random media. The studies are motivated by recent experimental results on the interacting nanoparticle system Co80_{80}Fe20_{20}/Al2_{2}O3_{3} showing superferromagnetic behavior. Its Cole-Cole plot indicates domain wall motion dynamics similarly to a disordered ferromagnet, including pinning and sliding motion. With our models we can successfully reproduce the features found in the experimental Cole-Cole plots.Comment: 8 pages, 6 figure

    Magnetic properties and domain structure of (Ga,Mn)As films with perpendicular anisotropy

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    The ferromagnetism of a thin GaMnAs layer with a perpendicular easy anisotropy axis is investigated by means of several techniques, that yield a consistent set of data on the magnetic properties and the domain structure of this diluted ferromagnetic semiconductor. The magnetic layer was grown under tensile strain on a relaxed GaInAs buffer layer using a procedure that limits the density of threading dislocations. Magnetometry, magneto-transport and polar magneto-optical Kerr effect (PMOKE) measurements reveal the high quality of this layer, in particular through its high Curie temperature (130 K) and well-defined magnetic anisotropy. We show that magnetization reversal is initiated from a limited number of nucleation centers and develops by easy domain wall propagation. Furthermore, MOKE microscopy allowed us to characterize in detail the magnetic domain structure. In particular we show that domain shape and wall motion are very sensitive to some defects, which prevents a periodic arrangement of the domains. We ascribed these defects to threading dislocations emerging in the magnetic layer, inherent to the growth mode on a relaxed buffer

    Correlation Functions for an Elastic String in a Random Potential: Instanton Approach

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    We develop an instanton technique for calculations of correlation functions characterizing statistical behavior of the elastic string in disordered media and apply the proposed approach to correlations of string free energies corresponding to different low-lying metastable positions. We find high-energy tails of correlation functions for the case of long-range disorder (the disorder correlation length well exceeds the characteristic distance between the sequential string positions) and short-range disorder with the correlation length much smaller then the characteristic string displacements. The former case refers to energy distributions and correlations on the distances below the Larkin correlation length, while the latter describes correlations on the large spatial scales relevant for the creep dynamics.Comment: 5 pages; 1 .eps figure include

    Engineering gene networks to emulate Drosophila embryonic pattern formation

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    Pattern formation is essential in the development of higher eukaryotes. For example, in the Drosophila embryo, maternal morphogen gradients establish gap gene expression domain patterning along the anterior-posterior axis, through linkage with an elaborate gene network. To understand the evolution and behaviour of such systems better, it is important to establish the minimal determinants required for patterning. We have therefore engineered artificial transcription-translation networks that generate simple patterns, crudely analogous to the Drosophila gap gene system. The Drosophila syncytium was modelled using DNA-coated paramagnetic beads fixed by magnets in an artificial chamber, forming a gene expression network. Transient expression domain patterns were generated using various levels of network connectivity. Generally, adding more transcription repression interactions increased the “sharpness” of the pattern while reducing overall expression levels. An accompanying computer model for our system allowed us to search for parameter sets compatible with patterning. While it is clear that the Drosophila embryo is far more complex than our simplified model, several features of interest emerge. For example, the model suggests that simple diffusion may be too rapid for Drosophila-scale patterning, implying that sublocalisation, or “trapping,” is required. Second, we find that for pattern formation to occur under the conditions of our in vitro reaction-diffusion system, the activator molecules must propagate faster than the inhibitors. Third, adding controlled protease degradation to the system stabilizes pattern formation over time. We have reconstituted transcriptional pattern formation from purified substances, including phage RNA polymerases, ribonucleotides, and an eukaryotic translation extract. We anticipate that the system described here will be generally applicable to the study of any biological network with a spatial component

    Monte Carlo Dynamics of driven Flux Lines in Disordered Media

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    We show that the common local Monte Carlo rules used to simulate the motion of driven flux lines in disordered media cannot capture the interplay between elasticity and disorder which lies at the heart of these systems. We therefore discuss a class of generalized Monte Carlo algorithms where an arbitrary number of line elements may move at the same time. We prove that all these dynamical rules have the same value of the critical force and possess phase spaces made up of a single ergodic component. A variant Monte Carlo algorithm allows to compute the critical force of a sample in a single pass through the system. We establish dynamical scaling properties and obtain precise values for the critical force, which is finite even for an unbounded distribution of the disorder. Extensions to higher dimensions are outlined.Comment: 4 pages, 3 figure

    Clinico-pathological considerations in a 48-years-old female with acute kidney injury: is it lupus nephritis, ANCA-associated vasculitis or something else?

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    BACKGROUND: The value of ANCA positivity in the setting of systemic lupus erythematous and their pathogenicity remains uncertain. CASE PRESENTATION: We report the case of a 48-year-old female with rapidly progressive kidney failure, arthro-myalgia and weight loss. Auto-immune screening showed anti-dsDNA antibodies, complement consumption and triple ANCA positivity. A first kidney biopsy done at presentation highlighted class IV-G glomerulonephritis with elective extra-capillary involvement and mainly C1q glomerular deposition at immunofluorescence study. After three months of a regimen combining steroids and cyclophosphamide, a second biopsy was performed and showed class IV-G glomerulonephritis with mainly endocapillary proliferation. CONCLUSION: This case is atypical in view of immunological profile and kidney histopathological presentation and evolution and gives rise to discussion in view of recent data on ANCA value in lupus nephritis, and suggests that different auto-immune pathways may be involved in lupus nephritis

    Creep motion in a random-field Ising model

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    We analyze numerically a moving interface in the random-field Ising model which is driven by a magnetic field. Without thermal fluctuations the system displays a depinning phase transition, i.e., the interface is pinned below a certain critical value of the driving field. For finite temperatures the interface moves even for driving fields below the critical value. In this so-called creep regime the dependence of the interface velocity on the temperature is expected to obey an Arrhenius law. We investigate the details of this Arrhenius behavior in two and three dimensions and compare our results with predictions obtained from renormalization group approaches.Comment: 6 pages, 11 figures, accepted for publication in Phys. Rev.

    Roughness at the depinning threshold for a long-range elastic string

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    In this paper, we compute the roughness exponent zeta of a long-range elastic string, at the depinning threshold, in a random medium with high precision, using a numerical method which exploits the analytic structure of the problem (`no-passing' theorem), but avoids direct simulation of the evolution equations. This roughness exponent has recently been studied by simulations, functional renormalization group calculations, and by experiments (fracture of solids, liquid meniscus in 4He). Our result zeta = 0.390 +/- 0.002 is significantly larger than what was stated in previous simulations, which were consistent with a one-loop renormalization group calculation. The data are furthermore incompatible with the experimental results for crack propagation in solids and for a 4He contact line on a rough substrate. This implies that the experiments cannot be described by pure harmonic long-range elasticity in the quasi-static limit.Comment: 4 pages, 3 figure

    Associations between viral infection history symptoms, granulocyte reactive oxygen species activity, and active rheumatoid arthritis disease in untreated women at Onset: Results from a longitudinal cohort study of tatarstan women

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    © 2017 Arleevskaya, Shafigullina, Filina, Lemerle and Renaudineau. To evaluate the effects of infectious episodes at early stages of rheumatoid arthritis (eRA) development, 59 untreated eRA patients, 77 first-degree relatives, from a longitudinal Tatarstan women cohort, were included, and compared to 67 healthy women without rheumatoid arthritis (RA) in their family history. At inclusion, informations were collected regarding both the type and incidence of infectious symptom episodes in the preceding year, and granulocyte reactive oxygen species (ROS) we re studied at the basal level and after stimulation with serum-treated zymosan (STZ). In the eRA group, clinical [disease activity score (DAS28), health assessment questionnaire] and biological parameters associated with inflammation (erythrocyte sedimentation rate, C-reactive protein) or with RA [rheumatoid factor, anticyclic citrullinated peptide (anti-CCP2) antibodies] were evaluated. An elevated incidence of infection events in the previous year characterized the eRA and relative groups. In addition, a history of herpes simplex virus (HSV) episodes was associated with disease activity, while an elevated incidence of anti-CCP2 autoantibody characterized eRA patients with a history of viral upper respiratory tract infection symptoms (V-URI). Granulocyte ROS activity in eRA patients was quantitatively [STZ peak and its area under the curve (AUC)] and qualitatively (STZ time of peak) altered, positively correlated with disease activity, and parameters were associated with viral symptoms including HSV exacerbation/recurrence, and V-URI. In conclusion, our study provides arguments to consider a history of increased viral infection symptoms in RA at the early stage and such involvement needs to be studied further

    How rheumatoid arthritis can result from provocation of the immune system by microorganisms and viruses

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    © 2016 Arleevskaya, Kravtsova, Lemerle, Renaudineau and Tsibulkin.The pathogenesis of rheumatoid arthritis (RA), similar to development of a majority of inflammatory and autoimmune disorders, is largely due to an inappropriate or inadequate immune response to environmental challenges. Among these challenges, infectious agents are the undisputed leaders. Since the 1870s, an impressive list of microorganisms suspected of provoking RA has formed, and the list is still growing. Although a definite causative link between a specific infectious agent and the disease has not been established, several arguments support such a possibility. First, in the absence of a defined pathogen, the spectrum of triggering agents may include polymicrobial communities or the cumulative effect of several bacterial/viral factors. Second, the range of infectious episodes (i.e., clinical manifestations caused by pathogens) may vary in the process of RA development from preclinical to late-stage disease. Third, infectious agents might not trigger RA in all cases, but trigger it in a certain subset of the cases, or the disease onset may arise from an unfortunate combination of infections along with, for example, psychological stress and/or chronic joint tissue microtrauma. Fourth, genetic differences may have a role in the disease onset. In this review, two aspects of the problem of "microorganisms and RA" are debated. First, is there an acquired immune deficiency and, in turn, susceptibility to infections in RA patients due to the too frequent and too lengthy infections, which at last break the tolerance of self antigens? Or, second, is there a congenital deficiency in tolerance and inflammation control, which may occur even with ordinary infection frequency and duration?
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