Nonuniform current density and spin accumulation in a 1 {\mu}m thick n-GaAs channel

The spin accumulation in an n-GaAs channel produced by spin extraction into a (Ga,Mn)As contact is measured by cross-sectional imaging of the spin polarization in GaAs. The spin polarization is observed in a 1 \mum thick n-GaAs channel with the maximum polarization near the contact edge opposite to the maximum current density. The one-dimensional model of electron drift and spin diffusion frequently used cannot explain this observation. It also leads to incorrect spin lifetimes from Hanle curves with a strong bias and distance dependence. Numerical simulations based on a two-dimensional drift-diffusion model, however, reproduce the observed spin distribution quite well and lead to realistic spin lifetimes

'Theory for the enhanced induced magnetization in coupled magnetic trilayers in the presence of spin fluctuations'

Motivated by recent experiments, the effect of the interlayer exchange interaction $J_{inter}$ on the magnetic properties of coupled Co/Cu/Ni trilayers is studied theoretically. Here the Ni film has a lower Curie temperature $T_{C,\rm Ni}$ than the Co film in case of decoupled layers. We show that by taking into account magnetic fluctuations the interlayer coupling induces a strong magnetization for T\gtsim T_{C,\rm Ni} in the Ni film. For an increasing $J_{inter}$ the resonance-like peak of the longitudinal Ni susceptibility is shifted to larger temperatures, whereas its maximum value decreases strongly. A decreasing Ni film thickness enhances the induced Ni magnetization for T\gtsim T_{C,\rm Ni}. The measurements cannot be explained properly by a mean field estimate, which yields a ten times smaller effect. Thus, the observed magnetic properties indicate the strong effect of 2D magnetic fluctuations in these layered magnetic systems. The calculations are performed with the help of a Heisenberg Hamiltonian and a Green's function approach.Comment: 4 pages, 3 figure

Stationary Properties of a Randomly Driven Ising Ferromagnet

We consider the behavior of an Ising ferromagnet obeying the Glauber dynamics under the influence of a fast switching, random external field. Analytic results for the stationary state are presented in mean-field approximation, exhibiting a novel type of first order phase transition related to dynamic freezing. Monte Carlo simulations performed on a quadratic lattice indicate that many features of the mean field theory may survive the presence of fluctuations.Comment: 5 pages in RevTex format, 7 eps/ps figures, send comments to "mailto:[email protected]", submitted to PR

Spin dynamics in the diluted ferromagnetic Kondo lattice model

The interplay of disorder and competing interactions is investigated in the carrier-induced ferromagnetic state of the Kondo lattice model within a numerical finite-size study in which disorder is treated exactly. Competition between impurity spin couplings, stability of the ferromagnetic state, and magnetic transition temperature are quantitatively investigated in terms of magnon properties for different models including dilution, disorder, and weakly-coupled spins. A strong optimization is obtained for T_c at hole doping p << x, highlighting the importance of compensation in diluted magnetic semiconductors. The estimated T_c is in good agreement with experimental results for Ga_{1-x}Mn_x As for corresponding impurity concentration, hole bandwidth, and compensation. Finite-temperature spin dynamics is quantitatively studied within a locally self-consistent magnon renormalization scheme, which yields a substantial enhancement in T_c due to spin clustering, and highlights the nearly-paramagnetic spin dynamics of weakly-coupled spins. The large enhancement in density of low-energy magnetic excitations due to disorder and competing interactions results in a strong thermal decay of magnetization, which fits well with the Bloch form M_0(1-BT^{3/2}) at low temperature, with B of same order of magnitude as obtained in recent squid magnetization measurements on Ga_{1-x}Mn_x As samples.Comment: 13 pages, 14 figure

Clinical and genetic analysis of 29 Brazilian patients with Huntington’s disease-like phenotype

Huntington’s disease (HD) is a neurodegenerative disorder characterized by chorea, behavioral disturbances and dementia, caused by a pathological expansion of the CAG trinucleotide in the HTT gene. Several patients have been recognized with the typical HD phenotype without the expected mutation. The objective of this study was to assess the occurrence of diseases such as Huntington’s disease-like 2 (HDL2), spinocerebellar ataxia (SCA) 1, SCA2, SCA3, SCA7, dentatorubral-pallidoluysian atrophy (DRPLA) and choreaacanthocytosis (ChAc) among 29 Brazilian patients with a HD-like phenotype. In the group analyzed, we found 3 patients with HDL2 and 2 patients with ChAc. The diagnosis was not reached in 79.3% of the patients. HDL2 was the main cause of the HD-like phenotype in the group analyzed, and is attributable to the African ancestry of this population. However, the etiology of the disease remains undetermined in the majority of the HD negative patients with HD-like phenotype. Key words: Huntington’s disease, Huntington’s disease-like, chorea-acanthocytosis, Huntington’s disease-like 2

Primary skin fibroblasts as a model of Parkinson's disease

Parkinson's disease is the second most frequent neurodegenerative disorder. While most cases occur sporadic mutations in a growing number of genes including Parkin (PARK2) and PINK1 (PARK6) have been associated with the disease. Different animal models and cell models like patient skin fibroblasts and recombinant cell lines can be used as model systems for Parkinson's disease. Skin fibroblasts present a system with defined mutations and the cumulative cellular damage of the patients. PINK1 and Parkin genes show relevant expression levels in human fibroblasts and since both genes participate in stress response pathways, we believe fibroblasts advantageous in order to assess, e.g. the effect of stressors. Furthermore, since a bioenergetic deficit underlies early stage Parkinson's disease, while atrophy underlies later stages, the use of primary cells seems preferable over the use of tumor cell lines. The new option to use fibroblast-derived induced pluripotent stem cells redifferentiated into dopaminergic neurons is an additional benefit. However, the use of fibroblast has also some drawbacks. We have investigated PARK6 fibroblasts and they mirror closely the respiratory alterations, the expression profiles, the mitochondrial dynamics pathology and the vulnerability to proteasomal stress that has been documented in other model systems. Fibroblasts from patients with PARK2, PARK6, idiopathic Parkinson's disease, Alzheimer's disease, and spinocerebellar ataxia type 2 demonstrated a distinct and unique mRNA expression pattern of key genes in neurodegeneration. Thus, primary skin fibroblasts are a useful Parkinson's disease model, able to serve as a complement to animal mutants, transformed cell lines and patient tissues

Genotype-Specific Differences between Mouse CNS Stem Cell Lines Expressing Frontotemporal Dementia Mutant or Wild Type Human Tau

Stem cell (SC) lines that capture the genetics of disease susceptibility provide new research tools. To assess the utility of mouse central nervous system (CNS) SC-containing neurosphere cultures for studying heritable neurodegenerative disease, we compared neurosphere cultures from transgenic mice that express human tau with the P301L familial frontotemporal dementia (FTD) mutation, rTg(tauP301L)4510, with those expressing comparable levels of wild type human tau, rTg(tauwt)21221. rTg(tauP301L)4510 mice express the human tauP301L variant in their forebrains and display cellular, histological, biochemical and behavioral abnormalities similar to those in human FTD, including age-dependent differences in tau phosphorylation that distinguish them from rTg(tauwt)21221 mice. We compared FTD-hallmark tau phosphorylation in neurospheres from rTg(tauP301L)4510 mice and from rTg(tauwt)21221 mice. The tau genotype-specific phosphorylation patterns in neurospheres mimicked those seen in mice, validating use of neurosphere cultures as models for studying tau phosphorylation. Genotype-specific tau phosphorylation was observed in 35 independent cell lines from individual fetuses; tau in rTg(tauP301L)4510 cultures was hypophosphorylated in comparison with rTg(tauwt)21221 as was seen in young adult mice. In addition, there were fewer human tau-expressing cells in rTg(tauP301L)4510 than in rTg(tauwt)21221 cultures. Following differentiation, neuronal filopodia-spine density was slightly greater in rTg(tauP301L)4510 than rTg(tauwt)21221 and control cultures. Together with the recapitulation of genotype-specific phosphorylation patterns, the observation that neurosphere lines maintained their cell line-specific-differences and retained SC characteristics over several passages supports the utility of SC cultures as surrogates for analysis of cellular disease mechanisms

Curcuminoid Binding to Embryonal Carcinoma Cells: Reductive Metabolism, Induction of Apoptosis, Senescence, and Inhibition of Cell Proliferation

Curcumin preparations typically contain a mixture of polyphenols, collectively referred to as curcuminoids. In addition to the primary component curcumin, they also contain smaller amounts of the co-extracted derivatives demethoxycurcumin and bisdemethoxycurcumin. Curcuminoids can be differentially solubilized in serum, which allows for the systematic analysis of concentration-dependent cellular binding, biological effects, and metabolism. Technical grade curcumin was solubilized in fetal calf serum by two alternative methods yielding saturated preparations containing either predominantly curcumin (60%) or bisdemethoxycurcumin (55%). Continual exposure of NT2/D1 cells for 4–6 days to either preparation in cell culture media reduced cell division (1–5 µM), induced senescence (6–7 µM) or comprehensive cell death (8–10 µM) in a concentration-dependent manner. Some of these effects could also be elicited in cells transiently exposed to higher concentrations of curcuminoids (47 µM) for 0.5–4 h. Curcuminoids induced apoptosis by generalized activation of caspases but without nucleosomal fragmentation. The equilibrium binding of serum-solubilized curcuminoids to NT2/D1 cells incubated with increasing amounts of curcuminoid-saturated serum occurred with apparent overall dissociation constants in the 6–10 µM range. However, the presence of excess free serum decreased cellular binding in a hyperbolic manner. Cellular binding was overwhelmingly associated with membrane fractions and bound curcuminoids were metabolized in NT2/D1 cells via a previously unidentified reduction pathway. Both the binding affinities for curcuminoids and their reductive metabolic pathways varied in other cell lines. These results suggest that curcuminoids interact with cellular binding sites, thereby activating signal transduction pathways that initiate a variety of biological responses. The dose-dependent effects of these responses further imply that distinct cellular pathways are sequentially activated and that this activation is dependent on the affinity of curcuminoids for the respective binding sites. Defined serum-solubilized curcuminoids used in cell culture media are thus suitable for further investigating the differential activation of signal transduction pathways