Status Report of the DPHEP Study Group: Towards a Global Effort for Sustainable Data Preservation in High Energy Physics

Data from high-energy physics (HEP) experiments are collected with significant financial and human effort and are mostly unique. An inter-experimental study group on HEP data preservation and long-term analysis was convened as a panel of the International Committee for Future Accelerators (ICFA). The group was formed by large collider-based experiments and investigated the technical and organisational aspects of HEP data preservation. An intermediate report was released in November 2009 addressing the general issues of data preservation in HEP. This paper includes and extends the intermediate report. It provides an analysis of the research case for data preservation and a detailed description of the various projects at experiment, laboratory and international levels. In addition, the paper provides a concrete proposal for an international organisation in charge of the data management and policies in high-energy physics

Aufbau eines Bibliotheksverbundsystems in Schleswig-Holstein: Vorunters

Available from Bibliothek des Instituts fuer Weltwirtschaft, ZBW, Duesternbrook Weg 120, D-24105 Kiel C 148032 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

Snakes, Ladders, and Isolas of Localized Patterns

Stable localized roll structures have been observed in many physical problems and model equations, notably in the 1D Swift–Hohenberg equation. Reflection-symmetric localized rolls are often found to lie on two “snaking” solution branches, so that the spatial width of the localized rolls increases when moving along each branch. Recent numerical results by Burke and Knobloch indicate that the two branches are connected by infinitely many “ladder” branches of asymmetric localized rolls. In this paper, these phenomena are investigated analytically. It is shown that both snaking of symmetric pulses and the ladder structure of asymmetric states can be predicted completely from the bifurcation structure of fronts that connect the trivial state to rolls. It is also shown that isolas of asymmetric states may exist, and it is argued that the results presented here apply to 2D stationary states that are localized in one spatial direction

Resveratrol Impairs the Release of Steroid-Resistant Inflammatory Cytokines from Human Airway Smooth Muscle Cells in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) therapy is complicated by corticosteroid resistance of the interleukin 8 (IL-8)dependent and granulocyte macrophage-colony stimulating factor (GM-CSF)-dependent chronic airway inflammation, for whose establishment human airway smooth muscle cells (HASMCs) might be crucial. It is unclear whether the release of inflammatory mediators from HASMCs is modulated by cigarette smoking and is refractory to corticosteroids in COPD. Resveratrol, an antiaging drug with protective effects against lung cancer, might be an alternative to corticosteroids in COPD therapy. Vascular endothelial growth factor (VEGF) might offer protection from developing emphysema. We tested the following hypotheses for HASMCs: 1) smoking with or without airway obstruction modulates IL-8, GM-CSF, and VEGF release; and 2) corticosteroids, but not resveratrol, fail to inhibit cytokine release in COPD. Cytokine release from HASMCs exposed to tumor necrosis factor alpha (TNF alpha), dexamethasone, and/or resveratrol was measured via enzyme-linked immunosorbent as-say and compared between nonsmokers (NS), smokers without COPD (S), and smokers with COPD (all n = 10). In response to TNF alpha, IL-8 release was increased, but GM-CSF and VEGF release was decreased in S and COPD compared with NS. Dexamethasone and resveratrol inhibited concentration-dependently TNF alpha-induced IL-8, GM-CSF, and VEGF release. For IL-8 and GM-CSF efficiency of dexamethasone was NS > S > COPD. That of resveratrol was NS = S = COPD for IL-8 and NS = S = COPD for GM-CSF. For VEGF the efficiency of dexamethasone was NS = S = COPD, and that of resveratrol was NS = S > COPD. All resveratrol effects were partially based on p38 mitogen-activated protein kinase blockade. In conclusion, smoking modulates cytokine release from HASMCs. Corticosteroid refractoriness of HASMCs in COPD is cytokine-dependent. Resveratrol might be superior to corticosteroids in COPD therapy, because it more efficiently reduces the release of inflammatory mediators and has limited effects on VEGF in COPD

Simvastatin requires activation in accessory cells to modulate T-cell responses in asthma and COPD

T-cell-dependent airway and systemic inflammation triggers the progression of chronic obstructive pulmonary disease (COPD) and asthma. Retrospective studies suggest that simvastatin has anti-inflammatory effects in both diseases but it is unclear, which cell types are targeted. We hypothesized that simvastatin modulates T-cell activity. Circulating CD4+ and CD8+ T-cells, either pure, co-cultured with monocytes or alveolar macrophages (AM) or in peripheral blood mononuclear cells (PBMCs), were ex vivo activated towards Th1/Tc1 or Th2/Tc2 and incubated with simvastatin. Markers for Th1/Tc1 (IFN gamma) and Th2/Tc2 (IL-5, IL-13) were measured by ELISA; with PBMCs this was done comparative between 11 healthy never-smokers, 11 current smokers without airflow limitation, 14 smokers with COPD and 11 never-smokers with atopic asthma. T-cell activation induced IFN gamma, IL-5 and IL-13 in the presence and absence of accessory cells. Simvastatin did not modulate cytokine expression in pure T-cell fractions. beta-hydroxy-simvastatin acid (activated simvastatin) suppressed IL-5 and IL-13 in pure Th2- and Tc2-cells. Simvastatin suppressed IL-5 and IL-13 in Th2-cells co-cultivated with monocytes or AM, which was partially reversed by the carboxylesterase inhibitor benzil. Simvastatin suppressed IL-5 production of Th2/Tc2-cells in PBMCs without differences between cohorts and IL-13 stronger in never-smokers and asthma compared to COPD. Simvastatin induced IFN gamma in Th1/Tc1-cells in PBMCs of all cohorts except asthmatics. Simvastatin requires activation in accessory cells likely by carboxylesterase to suppress IL-5 and IL-13 in Th2/Tc2-cells. The effects on Il-13 are partially reduced in COPD. Asthma pathogenesis prevents simvastatin-induced IFN gamma up-regulation. Simvastatin has anti-inflammatory effects that could be of interest for asthma therapy. (C) 2016 Elsevier B.V. All rights reserved

Oeffentliche Versorgungsunternehmen in Berlin ihre Strukturen und ihre Beziehungen zum Kunden

UuStB Koeln(38)-870106349 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman