CD40 ligand inhibits endothelial cell migration by increasing production of endothelial reactive oxygen species

Background— The CD40/CD40 ligand system is involved in atherogenesis. Activated T lymphocytes and platelets, which express high amounts of CD40 ligand (CD40L) on their surface, contribute significantly to plaque instability with ensuing thrombus formation, leading to acute coronary syndromes. Because reendothelialization may play a pivotal role for plaque stabilization, we investigated a potential role of CD40L on endothelial cell (EC) migration

Relevance of monocytic features for neovascularization capacity of circulating endothelial progenitor cells

Background— Transplantation of ex vivo expanded circulating endothelial progenitor cells (EPCs) from peripheral blood mononuclear cells improves the neovascularization after critical ischemia. However, the origin of the endothelial progenitor lineage and its characteristics have not yet been clearly defined. Therefore, we investigated whether the phenotype and functional capacity of EPCs to improve neovascularization depend on their monocytic origin

Nicotine strongly activates dendritic cell-mediated adaptive immunity - potential role for progression of atherosclerotic lesions

Background - Antigen-presenting cells (APCs) such as monocytes and dendritic cells (DCs) stimulate T-cell proliferation and activation in the course of adaptive immunity. This cellular interaction plays a role in the growth of atherosclerotic plaques. Nicotine has been shown to increase the growth of atherosclerotic lesions. Therefore, we investigated whether nicotine can stimulate APCs and their T cell–stimulatory capacity using human monocyte–derived DCs and murine bone marrow–derived DCs as APCs. Methods and Results - Nicotine dose-dependently (10-8 to 10-4 mol/L) induced DC expression of costimulatory molecules (ie, CD86, CD40), MHC class II, and adhesion molecules (ie, LFA-1, CD54). Moreover, nicotine induced a 7.0-fold increase in secretion of the proinflammatory TH1 cytokine interleukin-12 by human DCs. These effects were abrogated by the nicotinic receptor antagonist -bungarotoxin and mecamylamine, respectively. The effects of nicotine were mediated in part by the phosphorylation of the PI3 kinase downstream target Akt and the mitogen-activated kinases ERK and p38 MAPK. Nicotine-stimulated APCs had a greater capacity to stimulate T-cell proliferation and cytokine secretion, as documented by mixed lymphocyte reactions and ovalbumin-specific assays with ovalbumin-transgenic DO10.11 mice. In a murine model of atherosclerosis, nicotine significantly enhanced the recruitment of DCs to atherosclerotic lesions in vivo. Conclusions - Nicotine activates DCs and augments their capacity to stimulate T-cell proliferation and cytokine secretion. These effects of nicotine may contribute to its influence on the progression of atherosclerotic lesions

Microscopy of a scalable superatom

Strong interactions can amplify quantum effects such that they become important on macroscopic scales. Controlling these coherently on a single particle level is essential for the tailored preparation of strongly correlated quantum systems and opens up new prospects for quantum technologies. Rydberg atoms offer such strong interactions which lead to extreme nonlinearities in laser coupled atomic ensembles. As a result, multiple excitation of a Micrometer sized cloud can be blocked while the light-matter coupling becomes collectively enhanced. The resulting two-level system, often called "superatom", is a valuable resource for quantum information, providing a collective Qubit. Here we report on the preparation of two orders of magnitude scalable superatoms utilizing the large interaction strength provided by Rydberg atoms combined with precise control of an ensemble of ultracold atoms in an optical lattice. The latter is achieved with sub shot noise precision by local manipulation of a two-dimensional Mott insulator. We microscopically confirm the superatom picture by in-situ detection of the Rydberg excitations and observe the characteristic square root scaling of the optical coupling with the number of atoms. Furthermore, we verify the presence of entanglement in the prepared states and demonstrate the coherent manipulation of the superatom. Finally, we investigate the breakdown of the superatom picture when two Rydberg excitations are present in the system, which leads to dephasing and a loss of coherence.Comment: 7 pages, 5 figure

Low-energy shock wave for enhancing recruitment of endothelial progenitor cells: a new modality to increase efficacy of cell therapy in chronic hind limb ischemia

Background— Stem and progenitor cell therapy is a novel approach to improve neovascularization and function of ischemic tissue. Enhanced tissue expression of chemoattractant factors such as stromal cell–derived factor 1 and vascular endothelial growth factor is crucial for the recruitment of circulating endothelial progenitor cells (EPCs) during acute ischemia. In chronic ischemia, however, expression of these chemoattractants is less pronounced, which results in insufficient EPC recruitment into the target tissue. Therefore, we investigated the effect of targeted extracorporeal shock wave (SW) application in order to facilitate EPC recruitment into nonischemic and chronic ischemic tissue

Die Wohlfahrt von Kindern in europäischen Ländern. Einführung in den Themenschwerpunkt

Mit der COST2 Aktion 19 "Children\u27s Welfare" wurde 2001 ein europäisches Wissenschaftler-Netzwerk initiiert, das es sich zur Aufgabe gemacht hatte, das Wissen und das Verständnis in Bezug auf die intergenerationale Verteilung materieller, zeitlicher und räumlicher Ressourcen in den beteiligten europäischen Ländern zu verbessern. In den jährlich zwei Treffen ging es um die Wohlstandsbeteiligung von Kindern im europäischen Vergleich und um die theoretische und methodologische Konzeptualisierung der Erforschung von Wohlstand im Generationenverhältnis. Die COST Aktion 19 endete nach fünfjähriger Kooperation mit einer Abschlusskonferenz im Sommer 2006. (DIPF/Orig.