Induced four fold anisotropy and bias in compensated NiFe/FeMn double layers

A vector spin model is used to show how frustrations within a multisublattice antiferromagnet such as FeMn can lead to four-fold magnetic anisotropies acting on an exchange coupled ferromagnetic film. Possibilities for the existence of exchange bias are examined and shown to exist for the case of weak chemical disorder at the interface in an otherwise perfect structure. A sensitive dependence on interlayer exchange is found for anisotropies acting on the ferromagnet through the exchange coupling, and we show that a wide range of anisotropies can appear even for a perfect crystalline structure with an ideally flat interface.Comment: 7 pages, 7 figure

Metastable Random Field Ising model with exchange enhancement: a simple model for Exchange Bias

We present a simple model that allows hysteresis loops with exchange bias to be reproduced. The model is a modification of the T=0 random field Ising model driven by an external field and with synchronous local relaxation dynamics. The main novelty of the model is that a certain fraction f of the exchange constants between neighbouring spins is enhanced to a very large value J_E. The model allows the dependence of the exchange bias and other properties of the hysteresis loops to be analyzed as a function of the parameters of the model: the fraction f of enhanced bonds, the amount of the enhancement J_E and the amount of disorder which is controlled by the width sigma of the Gaussian distribution of the random fields.Comment: 8 pages, 11 figure

Gene expression differences in peripheral blood of Parkinson's disease patients with distinct progression profiles

The prognosis of neurodegenerative disorders is clinically challenging due to the inexistence of established biomarkers for predicting disease progression. Here, we performed an exploratory cross-sectional, case-control study aimed at determining whether gene expression differences in peripheral blood may be used as a signature of Parkinson's disease (PD) progression, thereby shedding light into potential molecular mechanisms underlying disease development. We compared transcriptional profiles in the blood from 34 PD patients who developed postural instability within ten years with those of 33 patients who did not develop postural instability within this time frame. Our study identified >200 differentially expressed genes between the two groups. The expression of several of the genes identified was previously found deregulated in animal models of PD and in PD patients. Relevant genes were selected for validation by real-time PCR in a subset of patients. The genes validated were linked to nucleic acid metabolism, mitochondria, immune response and intracellular-transport. Interestingly, we also found deregulation of these genes in a dopaminergic cell model of PD, a simple paradigm that can now be used to further dissect the role of these molecular players on dopaminergic cell loss. Altogether, our study provides preliminary evidence that expression changes in specific groups of genes and pathways, detected in peripheral blood samples, may be correlated with differential PD progression. Our exploratory study suggests that peripheral gene expression profiling may prove valuable for assisting in prediction of PD prognosis, and identifies novel culprits possibly involved in dopaminergic cell death. Given the exploratory nature of our study, further investigations using independent, well-characterized cohorts will be essential in order to validate our candidates as predictors of PD prognosis and to definitively confirm the value of gene expression analysis in aiding patient stratification and therapeutic intervention

TBK1 mutation spectrum in an extended European patient cohort with frontotemporal dementia and amyotrophic lateral sclerosis

We investigated the mutation spectrum of the TANK-Binding Kinase 1 (TBK1) gene and its associated phenotypic spectrum by exonic resequencing of TBK1 in a cohort of 2,538 patients with frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), or FTD plus ALS, ascertained within the European Early-Onset Dementia Consortium. We assessed pathogenicity of predicted protein-truncating mutations by measuring loss of RNA expression. Functional effect of in-frame amino acid deletions and missense mutations was further explored in vivo on protein level and in vitro by an NFB-induced luciferase reporter assay and measuring phosphorylated TBK1. The protein-truncating mutations led to the loss of transcript through nonsense-mediated mRNA decay. For the in-frame amino acid deletions, we demonstrated loss of TBK1 or phosphorylated TBK1 protein. An important fraction of the missense mutations compromised NFB activation indicating that at least some functions of TBK1 are lost. Although missense mutations were also present in controls, over three times more mutations affecting TBK1 functioning were found in the mutation fraction observed in patients only, suggesting high-risk alleles (P = 0.03). Total mutation frequency for confirmed TBK1 LoF mutations in the European cohort was 0.7%, with frequencies in the clinical subgroups of 0.4% in FTD, 1.3% in ALS, and 3.6% in FTD-ALS

Domain state model for exchange bias. I. Theory

For a model system consisting of a ferromagnetic layer coupled to a diluted, antiferromagnetic layer extensive Monte Carlo simulations are performed. Exchange bias is observed as a result of a domain state in the antiferromagnetic layer which develops during field cooling, carrying an irreversible domain state’s magnetization. In agreement with recent experimental observations on Co/CoO bilayers a strong dependence of the exchange bias field on dilution of the antiferromagnet is found and it is shown that a variety of typical effects associated with exchange bias, such as positive bias, temperature, and time dependencies as well as the dependence on the thickness of the antiferromagnetic layer can be explained within our model

Size and shape dependence of the exchange-bias field in exchange-coupled ferrimagnetic bilayers

Exchange biasing was studied in an exchange-spring system consisting of two ferrimagnetic films with different coercivity. Magnetite and Co-Fe ferrite were chosen as the soft and hard magnetic bilayer components, respectively. The samples were epitaxially grown on MgO single crystal substrates by pulsed laser deposition. The exchange-bias field was investigated as a function of system size and shape, magnetic field direction and magnetization reversal in the hard layer. A clear dependence of the exchange-bias field on the sample size and shape was found. This was attributed to an interplay between exchange and dipolar energies. Micromagnetic simulations agree with the experimental results. Copyright EDP Sciences/Società Italiana di Fisica/Springer-Verlag 2005