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

Rare mutations in SQSTM1 modify susceptibility to frontotemporal lobar degeneration

Mutations in the gene coding for Sequestosome 1 (SQSTM1) have been genetically associated with amyotrophic lateral sclerosis (ALS) and Paget disease of bone. In the present study, we analyzed the SQSTM1 coding sequence for mutations in an extended cohort of 1,808 patients with frontotemporal lobar degeneration (FTLD), ascertained within the European Early-Onset Dementia consortium. As control dataset, we sequenced 1,625 European control individuals and analyzed whole-exome sequence data of 2,274 German individuals (total n = 3,899). Association of rare SQSTM1 mutations was calculated in a meta-analysis of 4,332 FTLD and 10,240 control alleles. We identified 25 coding variants in FTLD patients of which 10 have not been described. Fifteen mutations were absent in the control individuals (carrier frequency < 0.00026) whilst the others were rare in both patients and control individuals. When pooling all variants with a minor allele frequency < 0.01, an overall frequency of 3.2 % was calculated in patients. Rare variant association analysis between patients and controls showed no difference over the whole protein, but suggested that rare mutations clustering in the UBA domain of SQSTM1 may influence disease susceptibility by doubling the risk for FTLD (RR = 2.18 [95 % CI 1.24-3.85]; corrected p value = 0.042). Detailed histopathology demonstrated that mutations in SQSTM1 associate with widespread neuronal and glial phospho-TDP-43 pathology. With this study, we provide further evidence for a putative role of rare mutations in SQSTM1 in the genetic etiology of FTLD and showed that, comparable to other FTLD/ALS genes, SQSTM1 mutations are associated with TDP-43 pathology

Asymmetric magnetization reversal in exchange-biased hysteresis loops

This article may be downloaded for personal use only. Any other use requires prior permission of the author and the American Institute of Physics.Polarized neutron reflectometry is used to probe the in-plane projection of the net-magnetization vector M of polycrystalline Fe films exchange coupled to twinned (110) MnF2 or FeF2 antiferromagnetic (AF) layers. The magnetization reversal mechanism depends upon the orientation of the cooling field with respect to the twinned microstructure of the AF, and whether the applied field is increased to (or decreased from) a positive saturating field; i.e., the magnetization reversal is asymmetric. The reversal of the sample magnetization from one saturated state to the other occurs via either domain wall motion or magnetization rotation on opposite sides of the same hysteresis loop

Автоматизированная система управления технологическими процессами производства гексафторида урана: диссертация на соискание учёной степени кандидата технических наук: спец. 05.13.06

The exchange bias coupling at ferromagnetic/antiferromagnetic interfaces in epitaxially grown Co/CoO layers can intentionally be increased by a factor of up to 3 if the antiferromagnetic CoO layer is diluted by nonmagnetic defects in its volume part away from the interface. Monte Carlo simulations of a simple model of a ferromagnetic layer on a diluted antiferromagnet show exchange bias and explain qualitatively its dilution and temperature dependence. These investigations reveal that diluting the antiferromagnet leads to the formation of volume domains, which cause and control exchange bias