Intrinsic Domain Wall Resistance in Ferromagnetic Semiconductors

Transport through zincblende magnetic semiconductors with magnetic domain walls is studied theoretically. We show that these magnetic domain walls have an intrinsic resistance due to the spin-orbit interaction. The intrinsic resistance is independent of the domain wall shape and width when the latter is larger than the Fermi wavelength. For typical parameters, the intrinsic domain wall resistance is comparable to the Sharvin resistance and should be experimentally measurable.Comment: Final versio

Asymmetry of charge relaxation times in quantum dots: The influence of degeneracy

Using time-resolved transconductance spectroscopy, we study the tunneling dynamics between a two-dimensional electron gas (2DEG) and self-assembled quantum dots (QDs), embedded in a field-effect transistor structure. We find that the tunneling of electrons from the 2DEG into the QDs is governed by a different time constant than the reverse process, i.e., tunneling from the QDs to the 2DEG. This asymmetry is a clear signature of Coulomb interaction and makes it possible to determine the degeneracy of the quantum dot orbitals even when the individual states cannot be resolved energetically because of inhomogeneous broadening. Our experimental data can be qualitatively explained within a master-equation approach

External Control of a Metal-Insulator Transition in GaMnAs Wires

Quantum transport in disordered ferromagnetic (III,Mn)V semiconductors is studied theoretically. Mesoscopic wires exhibit an Anderson disorder-induced metal-insulator transition that can be controlled by a weak external magnetic field. This metal-insulator transition should also occur in other materials with large anisotropic magneto resistance effects. The transition can be useful for studies of zero-temperature quantum critical phase transitions and fundamental material properties.Comment: Major revised final versio

Look who is calling: a comparison of genotype calling algorithms

In genome-wide association studies, high-level statistical analyses rely on the validity of the called genotypes, and different genotype calling algorithms (GCAs) have been proposed. We compared the GCAs Bayesian robust linear modeling using Mahalanobis distance (BRLMM), Chiamo++, and JAPL using the autosomal single-nucleotide polymorphisms (SNPs) from the 500 k Affymetrix Array Set data of the Framingham Heart Study as provided for the Genetic Analysis Workshop 16, Problem 2, and prepared standard quality control (sQC) for each algorithm. Using JAPL, most individuals were retained for the analysis. The lowest number of SNPs that successfully passed sQC was observed for BRLMM and the highest for Chiamo++. All three GCAs fulfilled all sQC criteria for 79% of the SNPs but at least one GCA failed for 18% of the SNPs. Previously undetected errors in strand coding were identified by comparing genotype concordances between GCAs. Concordance dropped with the number of GCAs failing sQC. We conclude that JAPL and Chiamo++ are the GCAs of choice if the aim is to keep as many subjects and SNPs as possible, respectively

ACPA: automated cluster plot analysis of genotype data

Genome-wide association studies have become standard in genetic epidemiology. Analyzing hundreds of thousands of markers simultaneously imposes some challenges for statisticians. One issue is the problem of multiplicity, which has been compared with the search for the needle in a haystack. To reduce the number of false-positive findings, a number of quality filters such as exclusion of single-nucleotide polymorphisms (SNPs) with a high missing fraction are employed. Another filter is exclusion of SNPs for which the calling algorithm had difficulties in assigning the genotypes. The only way to do this is the visual inspection of the cluster plots, also termed signal intensity plots, but this approach is often neglected. We developed an algorithm ACPA (automated cluster plot analysis), which performs this task automatically for autosomal SNPs. It is based on counting samples that lie too close to the cluster of a different genotype; SNPs are excluded when a certain threshold is exceeded. We evaluated ACPA using 1,000 randomly selected quality controlled SNPs from the Framingham Heart Study data that were provided for the Genetic Analysis Workshop 16. We compared the decision of ACPA with the decision made by two independent readers. We achieved a sensitivity of 88% (95% CI: 81%-93%) and a specificity of 86% (95% CI: 83%-89%). In a screening setting in which one aims at not losing any good SNP, we achieved 99% (95% CI: 98%-100%) specificity and still detected every second low-quality SNP

X-ray detection of a nova in the fireball phase

Novae are caused by runaway thermonuclear burning in the hydrogen-rich envelopes of accreting white dwarfs, which leads to a rapid expansion of the envelope and the ejection of most of its mass1,2. Theory has predicted the existence of a ‘fireball’ phase following directly on from the runaway fusion, which should be observable as a short, bright and soft X-ray flash before the nova becomes visible in the optical3,4,5. Here we report observations of a bright and soft X-ray flash associated with the classical Galactic nova YZ Reticuli 11¿h before its 9¿mag optical brightening. No X-ray source was detected 4¿h before and after the event, constraining the duration of the flash to shorter than 8¿h. In agreement with theoretical predictions4,6,7,8, the source’s spectral shape is consistent with a black-body of 3.27+0.11-0.33¿×¿105¿K (28.2+0.9-2.8¿eV), or a white dwarf atmosphere, radiating at the Eddington luminosity, with a photosphere that is only slightly larger than a typical white dwarf.Peer ReviewedPostprint (author's final draft

Treatment with an Anti-CD44v10-Specific Antibody Inhibits the Onset of Alopecia Areata in C3H/HeJ Mice

A murine CD44v10-neutralizing antibody has been reported to impair delayed-type hypersensitivity reactions. Because alopecia areata is characterized by a delayed-type hypersensitivity-like T cell mediated immune response, we addressed the question whether an anti-CD44v10-antibody influences the onset of alopecia areata. Therefore, we used the C3H/HeJ mouse model with the induction of alopecia areata in unaffected mice by the grafting of lesional alopecia areata mouse skin. Six grafted mice were injected (intraperitoneally) with anti-CD44v10, six grafted mice with anti-CD44standard, and six with phosphate-buffered saline only. After 11 wk phosphate-buffered saline injected animals on average had developed alopecia areata on 36.8% of their body. The onset of hair loss was slightly delayed and its extent reduced to 17.2% of their body in anti-CD44standard-treated mice. By contrast, five of six anti-CD44v10-treated mice did not show any hair loss and one mouse developed alopecia areata on only 1% of the body. Immunohistochemical examination revealed a marked reduction of perifollicular CD8+ lymphocytes and, to a lesser degree, CD4+ cells as well as a decreased expression of major histocompatibility complex class I on hair follicle epithelium in anti-CD44v10-treated mice as compared with phosphate-buffered saline or anti-CD44 standard-treated mice. Our data show that anti-CD44v10 is able to inhibit the onset of alopecia areata in C3H/HeJ mice. This might be accomplished by an anti-CD44v10-triggered impairment of immune cell homing (e.g., CD8+ T cells), resulting in a decrease of their number in target tissues

Wohnungseinbruchdiebstahl als Verbrechen : was nützen die Neuregelungen zum Wohnungseinbruch?

akzeptierte Manuskriptversio

Inhibition of Inducible Nitric Oxide Synthase Prevents IL-1β-Induced Mitochondrial Dysfunction in Human Chondrocytes

Interleukin (IL)-1β is an important pro-inflammatory cytokine in the progression of osteoarthritis (OA), which impairs mitochondrial function and induces the production of nitric oxide (NO) in chondrocytes. The aim was to investigate if blockade of NO production prevents IL-1βinduced mitochondrial dysfunction in chondrocytes and whether cAMP and AMP-activated protein kinase (AMPK) affects NO production and mitochondrial function. Isolated human OA chondrocytes were stimulated with IL-1β in combination with/without forskolin, L-NIL, AMPK activator or inhibitor. The release of NO, IL-6, PGE2 , MMP3, and the expression of iNOS were measured by ELISA or Western blot. Parameters of mitochondrial respiration were measured using a seahorse analyzer. IL-1β significantly induced NO release and mitochondrial dysfunction. Inhibition of iNOS by L-NIL prevented IL-1β-induced NO release and mitochondrial dysfunction but not IL-1β-induced release of IL-6, PGE2 , and MMP3. Enhancement of cAMP by forskolin reduced IL-1β-induced NO release and prevented IL-1β-induced mitochondrial impairment. Activation of AMPK increased IL-1β-induced NO production and the negative impact of IL-1β on mitochondrial respiration, whereas inhibition of AMPK had the opposite effects. NO is critically involved in the IL-1β-induced impairment of mitochondrial respiration in human OA chondrocytes. Increased intracellular cAMP or inhibition of AMPK prevented both IL-1β-induced NO release and mitochondrial dysfunction