Lateral magnetic anisotropy superlattice out of a single (Ga,Mn)As layer

We use lithographically induced strain relaxation to periodically modulate the magnetic anisotropy in a single (Ga,Mn)As layer. This results in a lateral magnetoresistance device where two non-volatile magnetic states exist at zero external magnetic field with resistances resulting from the orientation of two lithographically defined regions in a single and contiguous layer.Comment: 5 pages, 7 figure

Exploiting Locally Imposed Anisotropies in (Ga,Mn)As: a Non-volatile Memory Device

Progress in (Ga,Mn)As lithography has recently allowed us to realize structures where unique magnetic anisotropy properties can be imposed locally in various regions of a given device. We make use of this technology to fabricate a device in which we study transport through a constriction separating two regions whose magnetization direction differs by 90 degrees. We find that the resistance of the constriction depends on the flow of the magnetic field lines in the constriction region and demonstrate that such a structure constitutes a non-volatile memory device

Detailed transport investigation of the magnetic anisotropy of (Ga,Mn)As

This paper discusses transport methods for the investigation of the (Ga,Mn)As magnetic anisotropy. Typical magnetoresistance behaviour for different anisotropy types is discussed, focusing on an in depth discussion of the anisotropy fingerprint technique and extending it to layers with primarily uniaxial magnetic anisotropy. We find that in all (Ga,Mn)As films studied, three anisotropy components are always present. The primary biaxial along ([100] and [010]) along with both uniaxial components along the [110] and [010] crystal directions which are often reported separately. Various fingerprints of typical (Ga,Mn)As transport samples at 4 K are included to illustrate the variation of the relative strength of these anisotropy terms. We further investigate the temperature dependence of the magnetic anisotropy and the domain wall nucleation energy with the help of the fingerprint method

Comparative assessment of clinical rating scales in Wilson’s disease

Background: Wilson’s disease (WD) is an autosomal recessive disorder of copper metabolism resulting in multifaceted neurological, hepatic, and psychiatric symptoms. The objective of the study was to comparatively assess two clinical rating scales for WD, the Unified Wilson’s Disease Rating Scale (UWDRS) and the Global Assessment Scale for Wilson’s disease (GAS for WD), and to test the feasibility of the patient reported part of the UWDRS neurological subscale (termed the “minimal UWDRS”). Methods: In this prospective, monocentric, cross-sectional study, 65 patients (median age 35 [range: 15–62] years; 33 female, 32 male) with treated WD were scored according to the two rating scales. Results: The UWDRS neurological subscore correlated with the GAS for WD Tier 2 score (r = 0.80; p < 0.001). Correlations of the UWDRS hepatic subscore and the GAS for WD Tier 1 score with both the Model for End Stage Liver Disease (MELD) score (r = 0.44/r = 0.28; p < 0.001/p = 0.027) and the Child-Pugh score (r = 0.32/r = 0.12; p = 0.015/p = 0.376) were weak. The “minimal UWDRS” score significantly correlated with the UWDRS total score (r = 0.86), the UWDRS neurological subscore (r = 0.89), and the GAS for WD Tier 2 score (r = 0.86). Conclusions: The UWDRS neurological and psychiatric subscales and the GAS for WD Tier 2 score are valuable tools for the clinical assessment of WD patients. The “minimal UWDRS” is a practical prescreening tool outside scientific trials

Immunological fingerprint in coronavirus disease-19 convalescents with and without post-COVID syndrome

BackgroundSymptoms lasting longer than 12  weeks after severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection are called post-coronavirus disease (COVID) syndrome (PCS). The identification of new biomarkers that predict the occurrence or course of PCS in terms of a post-viral syndrome is vital. T-cell dysfunction, cytokine imbalance, and impaired autoimmunity have been reported in PCS. Nevertheless, there is still a lack of conclusive information on the underlying mechanisms due to, among other things, a lack of controlled study designs.MethodsHere, we conducted a prospective, controlled study to characterize the humoral and cellular immune response in unvaccinated patients with and without PCS following SARS-CoV-2 infection over 7 months and unexposed donors.ResultsPatients with PCS showed as early as 6 weeks and 7 months after symptom onset significantly increased frequencies of SARS-CoV-2-specific CD4+ and CD8+ T-cells secreting IFNγ, TNF, and expressing CD40L, as well as plasmacytoid dendritic cells (pDC) with an activated phenotype. Remarkably, the immunosuppressive counterparts type 1 regulatory T-cells (TR1: CD49b/LAG-3+) and IL-4 were more abundant in PCS+.ConclusionThis work describes immunological alterations between inflammation and immunosuppression in COVID-19 convalescents with and without PCS, which may provide potential directions for future epidemiological investigations and targeted treatments

Ferromagnetische (Ga,Mn)As Schichten und Nanostrukturen: Kontrolle der magnetischen Anisotropie durch Manipulation der Kristallverspannung

This work studies the fundamental connection between lattice strain and magnetic anisotropy in the ferromagnetic semiconductor (Ga,Mn)As. The first chapters provide a general introduction into the material system and a detailed description of the growth process by molecular beam epitaxy. A finite element simulation formalism is developed to model the strain distribution in (Ga,Mn)As nanostructures is introduced and its predictions verified by high-resolution x-ray diffraction methods. The influence of lattice strain on the magnetic anisotropy is explained by an magnetostatic model. A possible device application is described in the closing chapter.Die vorliegende Arbeit untersucht den fundamentalen Zusammenhang zwischen Gitterverspannung und magnetischer Anisotropie in dem ferromagnetischen Halbleiter (Ga,Mn)As. Die ersten Kapitel bieten eine allgemeine Einleitung in das Materialsystem und eine detaillierte Beschreibung des Wachstumsprozesses mittels Molekularstrahlepitaxie. Eine Finite-Elemente Simulation wird entwickelt, um die Verteilung der Gitterverspannung in (Ga,Mn)As Nanostrukturen zu modellieren. Die daraus abgeleiteten Vorhersagen werden mittels hochauflösender Röntgenbeugung bestätigt. Der Einfluss der Gitterverspannung auf die magnetische Anisotropie wird anhand eines magnetostatischen Modells erklärt. Das abschließende Kapitel gibt einen Ausblick auf eine mögliche praktische Anwendung der beschriebenen Phänomene

Epinephrine enhances platelet-neutrophil adhesion in whole blood in vitro.

Contains fulltext : 48287.pdf (publisher's version ) (Closed access)Previous studies showed that alpha- or beta-adrenoceptor stimulation by catecholamines influenced neutrophil function, cytokine liberation, and platelet aggregability. We investigated whether adrenergic stimulation with epinephrine also alters platelet-neutrophil adhesion. This might be of specific interest in the critically ill, because the increased association of platelets and neutrophils has been shown to be of key importance in inflammation and thrombosis. For this purpose, whole blood was incubated with increasing concentrations of epinephrine (10 nM, 100 nM, and 1 microM). To distinguish receptor-specific effects, a subset of samples was incubated with propranolol (10 microM) or phentolamine (10 microM) before exposure to epinephrine. After incubation, another subset of samples was also stimulated with 100 nM of N-formyl-methionyl-leucyl-phenylalanine. All samples were stained, and platelet-neutrophil adhesion and CD45, L-selectin, CD11b, P-selectin glycoprotein ligand-1, glycoprotein IIb/IIIa, and P-selectin expression were measured by two-color flow cytometry. Epinephrine significantly enhanced platelet-neutrophil adhesion and P-selectin and glycoprotein IIb/IIIa expression on platelets. CD11b and L-selectin expression on unstimulated neutrophils remained unchanged, whereas N-formyl-methionyl-leucyl-phenylalanine-induced upregulation of CD11b and downregulation of L-selectin were suppressed by epinephrine. beta-Adrenergic blockade before incubation with epinephrine increased platelet-neutrophil aggregates and adhesion molecule expression (CD11b, P-selectin, and glycoprotein IIb/IIIa) even further. These results demonstrate that epinephrine enhances platelet-neutrophil adhesion. The alpha-adrenergic receptor-mediated increase in P-selectin and glycoprotein IIb/IIIa expression on platelets may contribute substantially to this effect. Our study shows that inotropic support enhances the platelet-neutrophil interaction, which might be crucial for critically ill patients