1,540 research outputs found

    ILC2-mediated immune crosstalk in chronic (vascular) inflammation

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    Crosstalk between innate and adaptive immunity is pivotal for an efficient immune response and to maintain immune homeostasis under steady state conditions. As part of the innate immune system, type 2 innate lymphoid cells (ILC2s) have emerged as new important regulators of tissue homeostasis and repair by fine-tuning innate-adaptive immune cell crosstalk. ILC2s mediate either pro- or anti-inflammatory immune responses in a context dependent manner. Inflammation has proven to be a key driver of atherosclerosis, resembling the key underlying pathophysiology of cardiovascular disease (CVD). Notably, numerous studies point towards an atheroprotective role of ILC2s e.g., by mediating secretion of type-II cytokines (IL-5, IL-13, IL-9). Boosting these protective responses may be suitable for promising future therapy, although these protective cues are currently incompletely understood. Additionally, little is known about the mechanisms by which chemokine/chemokine receptor signaling shapes ILC2 functions in vascular inflammation and atherosclerosis. Hence, this review will focus on the latest findings regarding the protective and chemokine/chemokine receptor guided interplay between ILC2s and other immune cells like T and B cells, dendritic cells and macrophages in atherosclerosis. Further, we will elaborate on potential therapeutic implications which result or could be distilled from the dialogue of ILC2s with cells of the immune system in cardiovascular diseases

    From Teamchef Arminius to Hermann Junior: glocalised discourse about a national foundation myth

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    If for much of the nineteenth and twentieth centuries, the ‘Battle of the Teutoburg Forest’, fought in 9 CE between Roman armies and Germanic tribes, was predominantly a reference point for nationalist and chauvinist discourses in Germany, the first decade of the twenty-first century has seen attempts to link public remembrance with local/regional identities on the one hand and international/intercultural contact on the other. In the run up to and during the ‘anniversary year’ of 2009, German media, sports institutions and various other official institutions articulating tourist, economic and political interests attempted to create a new ‘glocalised’ version of the public memory of the Teutoburg battle. Combining methods of Cognitive Linguistics and Critical Discourse Analysis, the paper analyses the narrative and argumentative topoi employed in this re-orientation of public memory, with a special emphasis on hybrid, post-national identity-construction. Das zweitausendjährige Gedenkjahr der „Schlacht im Teutoburger Wald“ im Jahr 2009 bot eine günstige Gelegenheit, die bis in die zweite Hälfte des 20. Jahrhunderts dominante Tradition nationalistisch–chauvinistischer Deutungen des Sieges von germanischen Stämmen über drei römische Legionen zu korrigieren und zu überwinden. Der Aufsatz analysiert mit Hilfe diskurslinguistischer Methoden die Anstrengungen regionaler Institutionen und Medien, die nationale Vereinnahmung des historischen Gedenkens kritisch zu thematisieren sowie neue, zum eine lokal situierte, zum andern international orientierte Identifikationsangebote anzubieten. Die Analyse zeigt, dass solche „de-nationalisierten“ Identifikationsangebote zwar teilweise auch früher verwendet wurden, aber heutzutage rekontextualisiert und auf innovative Weise in den Vordergrund gestellt werden

    Critical scaling of the a.c. conductivity for a superconductor above Tc

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    We consider the effects of critical superconducting fluctuations on the scaling of the linear a.c. conductivity, \sigma(\omega), of a bulk superconductor slightly above Tc in zero applied magnetic field. The dynamic renormalization- group method is applied to the relaxational time-dependent Ginzburg-Landau model of superconductivity, with \sigma(\omega) calculated via the Kubo formula to O(\epsilon^{2}) in the \epsilon = 4 - d expansion. The critical dynamics are governed by the relaxational XY-model renormalization-group fixed point. The scaling hypothesis \sigma(\omega) \sim \xi^{2-d+z} S(\omega \xi^{z}) proposed by Fisher, Fisher and Huse is explicitly verified, with the dynamic exponent z \approx 2.015, the value expected for the d=3 relaxational XY-model. The universal scaling function S(y) is computed and shown to deviate only slightly from its Gaussian form, calculated earlier. The present theory is compared with experimental measurements of the a.c. conductivity of YBCO near Tc, and the implications of this theory for such experiments is discussed.Comment: 16 pages, submitted to Phys. Rev.

    Mobility of thorium ions in liquid xenon

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    We present a measurement of the 226^{226}Th ion mobility in LXe at 163.0 K and 0.9 bar. The result obtained, 0.240±\pm0.011 (stat) ±\pm0.011 (syst) cm2^{2}/(kV-s), is compared with a popular model of ion transport.Comment: 6.5 pages,

    Mechanical Activation of Hypoxia-Inducible Factor 1α Drives Endothelial Dysfunction at Atheroprone Sites

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    OBJECTIVE: Atherosclerosis develops near branches and bends of arteries that are exposed to low shear stress (mechanical drag). These sites are characterized by excessive endothelial cell (EC) proliferation and inflammation that promote lesion initiation. The transcription factor HIF1α (hypoxia-inducible factor 1α) is canonically activated by hypoxia and has a role in plaque neovascularization. We studied the influence of shear stress on HIF1α activation and the contribution of this noncanonical pathway to lesion initiation. APPROACH AND RESULTS: Quantitative polymerase chain reaction and en face staining revealed that HIF1α was expressed preferentially at low shear stress regions of porcine and murine arteries. Low shear stress induced HIF1α in cultured EC in the presence of atmospheric oxygen. The mechanism involves the transcription factor nuclear factor-κB that induced HIF1α transcripts and induction of the deubiquitinating enzyme Cezanne that stabilized HIF1α protein. Gene silencing revealed that HIF1α enhanced proliferation and inflammatory activation in EC exposed to low shear stress via induction of glycolysis enzymes. We validated this observation by imposing low shear stress in murine carotid arteries (partial ligation) that upregulated the expression of HIF1α, glycolysis enzymes, and inflammatory genes and enhanced EC proliferation. EC-specific genetic deletion of HIF1α in hypercholesterolemic apolipoprotein E-defecient mice reduced inflammation and endothelial proliferation in partially ligated arteries, indicating that HIF1α drives inflammation and vascular dysfunction at low shear stress regions. CONCLUSIONS: Mechanical low shear stress activates HIF1α at atheroprone regions of arteries via nuclear factor-κB and Cezanne. HIF1α promotes atherosclerosis initiation at these sites by inducing excessive EC proliferation and inflammation via the induction of glycolysis enzymes

    A Test of Rank-Dependent Utility in the Context of Ambiguity

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    Experimental investigations of non-expected utility have primarily concentrated on decision under risk (probability triangles). The literature suggests, however, that ambiguity is one of the main causes for deviations from expected utility (EU). This article investigates the descriptive performance of rank-dependent utility (RDU) in the context of choice under ambiguity. We use the axiomatic difference between RDU and EU to critically test RDU against EU. Surprisingly, the RDU model does not provide any descriptive improvement over EU. Our data suggest other framing factors that do provide descriptive improvements over EU

    Anatomy of Spin-Transfer Torque

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    Spin-transfer torques occur in magnetic heterostructures because the transverse component of a spin current that flows from a non-magnet into a ferromagnet is absorbed at the interface. We demonstrate this fact explicitly using free electron models and first principles electronic structure calculations for real material interfaces. Three distinct processes contribute to the absorption: (1) spin-dependent reflection and transmission; (2) rotation of reflected and transmitted spins; and (3) spatial precession of spins in the ferromagnet. When summed over all Fermi surface electrons, these processes reduce the transverse component of the transmitted and reflected spin currents to nearly zero for most systems of interest. Therefore, to a good approximation, the torque on the magnetization is proportional to the transverse piece of the incoming spin current.Comment: 16 pages, 8 figures, submitted to Phys. Rev.

    Identifying the anti-inflammatory response to lipid lowering therapy: a position paper from the working group on atherosclerosis and vascular biology of the European Society of Cardiology

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    Dysregulated lipid metabolism induces an inflammatory and immune response leading to atherosclerosis. Conversely, inflammation may alter lipid metabolism. Recent treatment strategies in secondary prevention of atherosclerosis support beneficial effects of both anti-inflammatory and lipid-lowering therapies beyond current targets. There is a controversy about the possibility that anti-inflammatory effects of lipid-lowering therapy may be either independent or not of a decrease in low-density lipoprotein cholesterol. In this Position Paper, we critically interpret and integrate the results obtained in both experimental and clinical studies on anti-inflammatory actions of lipid-lowering therapy and the mechanisms involved. We highlight that: (i) besides decreasing cholesterol through different mechanisms, most lipid-lowering therapies share anti-inflammatory and immunomodulatory properties, and the anti-inflammatory response to lipid-lowering may be relevant to predict the effect of treatment, (ii) using surrogates for both lipid metabolism and inflammation as biomarkers or vascular inflammation imaging in future studies may contribute to a better understanding of the relative importance of different mechanisms of action, and (iii) comparative studies of further lipid lowering, anti-inflammation and a combination of both are crucial to identify effects that are specific or shared for each treatment strategy

    A linear RFQ ion trap for the Enriched Xenon Observatory

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    The design, construction, and performance of a linear radio-frequency ion trap (RFQ) intended for use in the Enriched Xenon Observatory (EXO) are described. EXO aims to detect the neutrinoless double-beta decay of 136^{136}Xe to 136^{136}Ba. To suppress possible backgrounds EXO will complement the measurement of decay energy and, to some extent, topology of candidate events in a Xe filled detector with the identification of the daughter nucleus (136^{136}Ba). The ion trap described here is capable of accepting, cooling, and confining individual Ba ions extracted from the site of the candidate double-beta decay event. A single trapped ion can then be identified, with a large signal-to-noise ratio, via laser spectroscopy.Comment: 18 pages, pdflatex, submitted to NIM
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