Die Cultural Theory of Risk als Erweiterung des systemtheoretischen Konfliktanalyserahmens für transdisziplinäre Forschungsprojekte

Transdisziplinäre Forschungsprojekte beschäftigen sich häufig mit Problemkomplexen wie dem anthropogenen Klimawandel, dem Umgang mit seinen Folgen sowie den Möglichkeiten zur Mitigation. In der Regel geht damit der Anspruch einher, die gesellschaftliche Wirklichkeit in Richtung nachhaltiger, sozial-ökologischer Transformation mitzugestalten. Infolgedessen treffen innerhalb solcher Projekte unterschiedliche Handlungsorientierungen und Risikowahrnehmungen aufeinander, was zu Konflikten führen kann und einen Konfliktanalyserahmen erforderlich macht. Einen solchen stellt der vorliegende Beitrag vor. Hierbei wird an einen bestehenden systemtheoretischen Konfliktanalyserahmen angeknüpft, welcher mithilfe der Cultural Theory of Risk erweitert wird, um identifizierte Leerstellen zu schließen. Bei diesen Leerstellen handelt es sich um die Nichtberücksichtigung der Binnenheterogenität in gesellschaftlichen Teilsystemen und das Fehlen von Verfahren, um akzeptanzfähige Entscheidungen in transdisziplinären Forschungsprojekten zu treffen. Um diesen Leerstellen zu begegnen, wird sich für eine Synthese der beiden theoretischen Perspektiven in Form eines kombinierten Analyserahmens ausgesprochen.  Transdisciplinary research projects often deal with complex problems such as anthropogenic climate change, how to deal with its consequences and the possibilities for mitigation. This is often accompanied by the goal of helping to shape society in the direction of sustainable, socio-ecological transformation. As a result, different risk perceptions and ideas on how to deal with risks come together within such projects. This can lead to conflicts and makes a conflict analysis framework necessary. This paper presents such a conflict analysis framework. It builds on an existing systems-theoretical conflict analysis framework, which is extended with the help of the Cultural Theory of Risk. This extension is intended to fill identified gaps. These gaps are the disregard of internal heterogeneity in social subsystems and the lack of procedures to make acceptable decisions in transdisciplinary research projects. To address these gaps, a synthesis of the two theoretical perspectives in the form of a combined analytical framework is advocated. circumstance; second, they indicate different localizations of the locus of control of transformation processes. (peer reviewed

Learning for sustainability

The 'Deutsche Bundesstiftung Umwelt' (DBU) financed for a period of three years the introduction and evaluation of new a complex Workshop in high Schools concerning electronic waste Recycling and material Efficiency. We report about the results

A study of the origin of chloramphenicol isomers in honey

Due to the unexpected detection of chloramphenicol isomer residues in honey, we have studied the hypothesis of unauthorized or unintended use of unregistered veterinary drug preparations. First, we have investigated honey samples in which a discrepancy was observed between the results of the immunological screening methods and the confirmatory liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. In all samples, previously identified to be contaminated with the banned antibiotic chloramphenicol according to LC-MS/MS only, the presence of dextramycin (SS-para isomer of chloramphenicol) was detected by chiral LC-MS/MS. The source of dextramycin in honey was investigated by studying the preparations utilized in apiaries from which the above non-compliant honey samples have been received. In all these preparations (beehive strips applied against the mite Varroa destructor) chloramphenicol was detected in the concentrations ranging from 33 to 34,400 μg kg-1. Chiral LC-MS/MS demonstrated the presence of chloramphenicol and dextramycin in different ratios, and it was concluded that these preparations can be the source of chloramphenicol and dextramycin residues in honey. These preparations were of foreign production and are not officially registered in accordance with current legislation

Erk5 activation elicits a vasoprotective endothelial phenotype via induction of Kruppel-like factor 4 (KLF4)

The MEK5/Erk5 MAPK cascade has recently been implicated in the regulation of endothelial integrity and represents a candidate pathway mediating the beneficial effects of laminar flow, a major factor preventing vascular dysfunction and disease. Here we expressed a constitutively active mutant of MEK5 (MEK5D) to study the transcriptional and functional responses to Erk5 activation in human primary endothelial cells. We provide evidence that constitutive Erk5 activation elicits an overall protective phenotype characterized by increased apoptosis resistance and a decreased angiogenic, migratory, and inflammatory potential. This is supported by bioinformatic microarray analysis, which uncovered a statistical overrepresentation of corresponding functional clusters as well as a significant induction of anti-thrombotic, hemostatic, and vasodilatory genes. We identify KLF4 as a novel Erk5 target and demonstrate a critical role of this transcription factor downstream of Erk5. We show that KLF4 expression largely reproduces the protective phenotype in endothelial cells, whereas KLF4 siRNA suppresses expression of various Erk5 targets. Additionally, we show that vasoprotective statins potently induce KLF4 and KLF4-dependent gene expression via activation of Erk5. Our data underscore a major protective function of the MEK5/Erk5/KLF4 module in ECs and implicate agonistic Erk5 activation as potential strategy for treatment of vascular diseases

Inhibition of VCAM-1 expression in endothelial cells by CORM-3: The role of the ubiquitin-proteasome system, p38, and mitochondrial respiration

Carbon monoxide (CO) abrogates TNF-alpha-mediated inflammatory responses in endothelial cells, yet the underlying mechanism thereof is still elusive. We have previously shown that the anti-inflammatory effect of CO-releasing molecule-3 (CORM-3) is not completely mediated via deactivation of the NF-kappa B pathway. In this study, we sought to explore other potential mechanisms by which CORM-3 downregulates VCAM-1 expression on TNF-alpha-stimulated HUVECs. By genome-wide gene expression profiling and pathway analysis we studied the relevance of particular pathways for the anti-inflammatory effect of CORM-3. In CORM-3-stimulated HUVECs significant changes in expression were found for genes implicated in the proteasome and porphyrin pathways. Although proteasome activities were increased by CORM-3, proteasome inhibitors did not abolish the effect of CORM-3. Likewise, heme oxygenase-1 inhibitors did not abrogate the ability of CORM-3 to downregulate VCAM-1 expression. Interestingly, CORM-3 inhibited MAPK p38, and the p38 inhibitor SB203580 downregulated VCAM-1 expression. However, downregulation of VCAM-1 by CORM-3 occurred only at concentrations that partly inhibit ATP production and sodium azide and oligomycin paralleled the effect of CORM-3 in this regard. Our results indicate that CORM-3-induced downregulation of VCAM-1 is mediated via p38 inhibition and mitochondrial respiration, whereas the ubiquitin-proteasome system seems not to be involved. (C) 2011 Elsevier Inc. All rights reserved