Angular dependence of domain wall resistivity in SrRuO3_{{\bf 3}} films

${\rm SrRuO_3}$ is a 4d itinerant ferromagnet (T$_{c}$ $\sim$150 K) with stripe domain structure. Using high-quality thin films of SrRuO$_{3}$ we study the resistivity induced by its very narrow ($\sim 3$ nm) Bloch domain walls, $\rho_{DW}$ (DWR), at temperatures between 2 K and T$_{c}$ as a function of the angle, $\theta$, between the electric current and the ferromagnetic domains walls. We find that $\rho_{DW}(T,\theta)=\sin^2\theta \rho_{DW}(T,90)+B(\theta)\rho_{DW}(T,0)$ which provides the first experimental indication that the angular dependence of spin accumulation contribution to DWR is $\sin^2\theta$. We expect magnetic multilayers to exhibit a similar behavior.Comment: 5 pages, 5 figure

Assessing the risk of central post-stroke pain of thalamic origin by lesion mapping

Central post-stroke pain of thalamic origin is an extremely distressing and often refractory disorder. There are no well-established predictors for pain development after thalamic stroke, and the role of different thalamic nuclei is unclear. Here, we used structural magnetic resonance imaging to identify the thalamic nuclei, specifically implicated in the generation of central post-stroke pain of thalamic origin. Lesions of 10 patients with central post-stroke pain of thalamic origin and 10 control patients with thalamic strokes without pain were identified as volumes of interest on magnetic resonance imaging data. Non-linear deformations were estimated to match each image with a high-resolution template and were applied to each volume of interest. By using a digital atlas of the thalamus, we elucidated the involvement of different nuclei with respect to each lesion. Patient and control volumes of interest were summed separately to identify unique areas of involvement. Voxelwise odds ratio maps were calculated to localize the anatomical site where lesions put patients at risk of developing central post-stroke pain of thalamic origin. In the patients with pain, mainly lateral and posterior thalamic nuclei were affected, whereas a more anterior-medial lesion pattern was evident in the controls. The lesions of 9 of 10 pain patients overlapped at the border of the ventral posterior nucleus and the pulvinar, coinciding with the ventrocaudalis portae nucleus. The lesions of this area showed an odds ratio of 81 in favour of developing thalamic pain. The high odds ratio at the ventral posterior nucleus-pulvinar border zone indicates that this area is crucial in the pathogenesis of thalamic pain and demonstrates the feasibility of identifying patients at risk of developing central post-stroke pain of thalamic origin early after thalamic insults. This provides a basis for pre-emptive treatment studie

Die Beeinflussung der zentralen Schmerzverarbeitung beim Menschen durch konkurrierende Aufmerksamkeitsleistung mit einer Stroop-Aufgabe

Im Schmerzerleben spielt die gerichtete Aufmerksamkeit auf die schmerzende Körperstelle und die Schmerzen selbst eine zentrale Rolle. Je nach Ausrichtung der Wahrnehmung kann die subjektive Schmerzempfindung unterschiedlich stark ausfallen. In der vorliegenden fMRT-Studie wurde die Schmerzverarbeitung auf akut einwirkende Hitzereize, sowie deren Veränderung durch eine kognitiv interferierende Stroop-Aufgabe untersucht. Die Beeinträchtigung führte zu einer signifikanten Abnahme der subjektiven Empfindung für Schmerzunangenehmheit und Schmerzintensität. Ziel der Untersuchung war die Identifikation von Hirnstrukturen, die für eine dämpfende Modulation und Regulation nociceptiver Signale bedeutsam sind. Auf neuronaler Ebene drückte sich die reduzierte Schmerzwahrnehmung einerseits in einer verminderten Aktivierung sensorisch und affektiv verarbeitender Hirnregionen aus, andererseits in einer vermehrten Aktivierung des orbitofrontalen Cortex, des posterioren Thalamus und des PAG. Die Kovariationsanalyse zeigte eine Kommunikation zwischen orbitofrontalem Cortex und PAG/posteriorem Thalamus, die nur während der attentional beeinflussten schmerzhaften Reizung auftritt. Evidenzen aus anderen Forschungsarbeiten deuten auf das gleiche Netzwerk hin, welches sowohl bei Opiatanalgesie wie auch bei Placebo induzierter Analgesie aktiviert wird. Da PAG oder posteriorer Thalamus Schaltstellen höherer Top-Down Einflüsse darstellen, scheint nach den vorliegenden Ergebnissen der orbitofrontale Cortex die Top-Down Modulation auszuüben. Für zusätzliche Bildgebungsstudien erscheint die weitergehende Untersuchung des Zusammenspiels dieser Strukturen wesentlich. Außerdem ist die Überprüfung der Aktivierung dieses Netzwerks bei anderen Schmerzmodulationsstrategien (z.B. emotional, hypnotisch, autosuggestiv) von hohem Interesse. Die dargestellten Befunde erweitern das Verständnis von Schmerzmodulationsmechanismen und bieten möglicherweise Ansatzpunkte für die Entwicklung selektiver Pharmazeutika oder chirurgisch interventioneller Maßnahmen mit Wirkung auf orbitofrontaler Ebene zur therapeutischen Beeinflussung zentral vermittelter chronifizierter Schmerzen

The Gut Microbiota Regulates Intestinal CD4 T Cells Expressing RORγt and Controls Metabolic Disease

SummaryA high-fat diet (HFD) induces metabolic disease and low-grade metabolic inflammation in response to changes in the intestinal microbiota through as-yet-unknown mechanisms. Here, we show that a HFD-derived ileum microbiota is responsible for a decrease in Th17 cells of the lamina propria in axenic colonized mice. The HFD also changed the expression profiles of intestinal antigen-presenting cells and their ability to generate Th17 cells in vitro. Consistent with these data, the metabolic phenotype was mimicked in RORγt-deficient mice, which lack IL17 and IL22 function, and in the adoptive transfer experiment of T cells from RORγt-deficient mice into Rag1-deficient mice. We conclude that the microbiota of the ileum regulates Th17 cell homeostasis in the small intestine and determines the outcome of metabolic disease

Neurometabolic correlates of depression and disability in episodic cluster headache

A close association between pain, depression and disability has been shown. However, the neurometabolic correlates of this association have been barely investigated in disease states. Episodic cluster headache is a severe headache syndrome and represents a suitable disease model for the investigation of episodic pain. The aim of this study was to explore the relationship between depression and disability as well as pain scores and brain metabolism in patients with cluster headache during the disease period with repetitive pain attacks, but outside an acute attack. Thirteen patients with cluster headache underwent 2-[fluorine-18]-fluoro-2-deoxy-d-glucose positron emission (FDG-PET) and completed questionnaires on depression and disability as well as a pain visual analogue rating scale (VAS). A positive correlation between the depression scores and glucose metabolism was observed in the insular cortex. A positive correlation between the pain disability scores and brain metabolism was detected in the amygdala. The same applied to the pain visual analogue rating scores. Our data underline the association between severe episodic pain, depression and disability. In addition to this clinical observation, our results stress the importance of the insula and amygdala in pain processing and suffering

Interactive analysis of systems biology molecular expression data

Peer reviewedPublisher PD

Interaction of hyperalgesia and sensory loss in complex regional pain syndrome type I (CRPS I)

Sensory abnormalities are a key feature of Complex Regional Pain Syndrome (CRPS). In order to characterise these changes in patients suffering from acute or chronic CRPS I, we used Quantitative Sensory Testing (QST) in comparison to an age and gender matched control group

Local and Systemic Cytokine Expression in Patients with Postherpetic Neuralgia

Background Postherpetic neuralgia (PHN) is the painful complication of a varicella zoster virus reactivation. We investigated the systemic and local gene expression of pro- and anti-inflammatory cytokine expression in patients with PHN. Methods Thirteen patients with PHN at the torso (Th4-S1) were recruited. Skin punch biopsies were obtained from the painful and the contralateral painless body area for intraepidermal nerve fiber density (IENFD) and cytokine profiling. Additionally, blood was withdrawn for systemic cytokine expression and compared to blood values of healthy controls. We analyzed the gene expression of selected pro- and anti-inflammatory cytokines (tumor necrosis factor-alpha [TNF] and interleukins [IL]-1β, IL-2, and IL-8). Results IENFD was lower in affected skin compared to unaffected skin (p<0.05), while local gene expression of pro- and anti-inflammatory cytokines did not differ except for two patients who had 7fold higher IL-6 and 10fold higher IL-10 gene expression in the affected skin compared to the contralateral unaffected skin sample. Also, the systemic expression of cytokines in patients with PHN and in healthy controls was similar. Conclusion While the systemic and local expression of the investigated pro- and anti-inflammatory cytokines was not different from controls, this may have been influenced by study limitations like the low number of patients and different disease durations. Furthermore, other cytokines or pain mediators need to be considered

How to treat an asymptomatic carotid stenosis? The view of the neurologist

SummaryThe optimal treatment strategy for patients with asymptomatic carotid artery stenosis (ACS) is still a matter of debate. Based on a simplistic view, all stenosed vessels should be cleaned, and the earlier the better. Due to the improvements of medical management in patients with high-grade ACS, there is uncertainty as how to best manage these patients. Consequently, the cost-effectiveness of CEA in patients with ACS has been questioned. Therefore, the question arises how best medical treatment changes the risk of stroke in patients with ACS. This overview discussed the therapeutic options for ACS from a neurological point of view

Funktionell-bildgebende Untersuchungen zur zerebralen Verarbeitung von Schmerz und Juckreiz

Die kumulative Habilitation beschäftigt sich mit zerebralen Prozessen der Schmerz- und Juckreizverarbeitung bei gesunden Menschen und Patienten mit chronischen Schmerz- und Juckreiz-Erkrankungen. Mit Methoden der funktionellen Neurobildgebung (fMRT, VBM, PET) wurden insbesondere die Mechanismen von Modulation und Sensitivierung bei Schmerz- und Juckreizzuständen näher erforscht. Die Untersuchungen zur Modulation von Schmerzen ergaben, dass eine verminderte Schmerzempfindung durch kognitive oder pharmakologische Interventionen in Zusammenhang mit einer reduzierten zerebralen Aktivierung in sensorisch und affektiv verarbeitenden Hirnregionen und einer verstärkten Aktivierung von schmerzmodulierenden Hirnstrukturen (präfrontaler Cortex, Hirnstamm) steht. Ebenso konnten durch weitere Arbeiten Einblicke in pathophysiologische Mechanismen der Schmerzsensitivierung und Schmerzchronifizierung gewonnen werden. Hierbei wurden sowohl funktionelle als auch strukturelle Veränderungen des Gehirns gefunden, die sowohl nach kurzzeitigen repetitiven Schmerzstimulationen wie auch bei lange bestehenden Schmerzsyndromen nachweisbar waren. Weiterhin wurden zerebrale Mechanismen chronisch anhaltender Juckreizzustände erforscht, bei der zerebrale Veränderungen für die Aufrechterhaltung der Erkrankung mit angenommen werden