Oekonomik der Transformation als wirtschafts- und gesellschaftspolitisches Problem

Transformation wird als Wandel einer kollektiven Identität verstanden. Daher hat diese Analyse einen wirtschaftsanthropologischen Zuschnitt: Gefragt wird nach den nicht-ökonomischen Voraussetzungen ökonomischer Entwicklung. Basis ist ein institutionalistischer, teilweise institutionenökonomischer Theorieansatz (unter Beachtung von public choice-Aspekten). Empirische Befunde aus der Entwicklungsökonomie, aus der Transitions- und aus der Integrationsforschung (etwa Europas) werden herangezogen. Es interessieren somit die polity-, politics- und policy-Voraussetzungen der Transformation als Suche nach einem (die Sozialordnung einschließenden) «Wirtschaftsstil». Als entscheidend werden die «sozialen Kosten» begriffen. Daher interessieren räumliche und inter-personelle Disparitäten infolge des Transformationsgeschehens

Menschenwürde als heilige Ordnung: Eine Re-Konstruktion sozialer Exklusion im Lichte der Sakralität der personalen Würde

Die Würde des Menschen ist unantastbar - dieses unbedingte Recht ist völker-, europa- und verfassungsrechtlich verbürgt. Dass die Würde des Menschen jedoch auch im säkularisierten sozialen Rechtsstaat letztendlich eine heilige Ordnung ist, kollektiv religiös geglaubt werden muss und sich nicht in einem rationalen Diskurs hinreichend wahrheitsfähig erweist, zeigt Frank Schulz-Nieswandt im Rekurs auf Böckenförde, Habermas, Joas und Agamben. Im Anschluss daran entfaltet er die Idee einer gottlosen Ontotheologie eines existenzialen personalistischen Humanismus, den er mit Verweis auf Paul Tillich und Romano Guardini zugleich gegen jeden Übergriff einer autoritären Theo-Dogmatik supranaturalistischer Art verteidigt.From a humanistic point of view and transcending theology and the Church, the dignity of humans as individuals is a sacred basis of the secular social constitutional state

Stationaere Altenpflege und «Pflegenotstand» in der Bundesrepublik Deutschland

Die vorliegende Arbeit skizziert den komplexen Prozeß der Präferenzbildung für stationäre Altenpflege und ihrer Inanspruchnahme. Unter Berücksichtigung des sozio-demographischen Problemdrucks sowie durch Rekurs auf ein ganzheitliches Pflegebedarfskonzept wird insbesondere der Frage der De-Institutionalisierung (Substitution stationärer durch - ambulant gestützte - häusliche Pflege) nachgegangen. Im Rahmen einer kritischen Auseinandersetzung mit den Erwartungen der neoklassischen Ökonomik hinsichtlich der Einführung einer Pflege-Sozialversicherung («moral hazard» - und «Sog»-Effekte) wird eine sozialstaatliche Lösung (Öffentliche Sicherstellung) befürwortet, die die allokativen und distributiven Mängel des bisherigen Systems der Sozialhilfe-Finanzierung beseitigen soll

Communication, social capital and workplace health management as determinants of the innovative climate in German banks

The present study aims to measure the determinants of the innovative climate in German banks with a focus on workplace health management (WHM). We analyze the determinants of innovative climate with multiple regressions using a dataset based on standardized telephone interviews conducted with health promotion experts from 198 randomly selected German banks. The regression analysis provided a good explanation of the variance in the dependent variable (RA(2)A = 55%). Communication climate (beta = 0.55; p < 0.001), social capital (beta = 0.21; p < 0.01), the establishment of a WHM program (beta = 0.13; p < 0.05) as well as company size (beta = 0.15; p < 0.01) were found to have a significant impact on an organization's innovative climate. In order to foster an innovation-friendly climate, organizations should establish shared values. An active step in this direction involves strengthening the organizations' social capital and communication climate through trustworthy management decisions such as the implementation of a WHM program

G12/13 Signaling Pathways Substitute for Integrin αIIbβ3-Signaling for Thromboxane Generation in Platelets

We have previously shown that ADP-induced TXA(2) generation requires signaling from αIIbβ3 integrin in platelets. Here we observed that, unlike ADP, protease-activated receptor (PAR)-mediated TXA(2) generation occurs independently of αIIbβ3. PAR agonists, but not ADP, activate G(12/13) signaling pathways. Hence, we evaluated the role of these pathways in TXA(2) generation.Inhibition of ADP-induced thromboxane generation by fibrinogen receptor antagonist SC57101 was rescued by co-stimulation of G(12/13) pathways with YFLLRNP. This observation suggested an existence of a common signaling effector downstream of integrins and G(12/13) pathways. Hence, we evaluated role of three potential tyrosine kinases; c-Src, Syk and FAK (Focal Adhesion Kinase) that are known to be activated by integrins. c-Src and Syk kinase did not play a role in ADP-induced functional responses in platelets. Selective activation of G(12/13) pathways resulted in the activation of FAK, in the absence of integrin signaling. Interestingly, αIIbβ3-mediated FAK activation occurred in a Src family kinase (SFK)-independent manner whereas G(12/13) pathway caused FAK activation in a SFK and RhoA-dependent manner. A FAK selective inhibitor TAE-226, blocked TXA(2) generation. However, in comparison to WT mice, Pf4-Cre/Fak-Floxed mice did not show any difference in platelet TXA(2) generation.Therefore, we conclude that differential activation of FAK occurs downstream of Integrins and G(12/13) pathways. However, the common effector molecule, possibly a tyrosine kinase downstream of integrins and G(12/13) pathways contributing to TXA(2) generation in platelets remains elusive

Cathelicidins prime platelets to mediate arterial thrombosis and tissue inflammation

Leukocyte-released antimicrobial peptides contribute to pathogen elimination and activation of the immune system. Their role in thrombosis is incompletely understood. Here we show that the cathelicidin LL-37 is abundant in thrombi from patients with acute myocardial infarction. Its mouse homologue, CRAMP, is present in mouse arterial thrombi following vascular injury, and derives mainly from circulating neutrophils. Absence of hematopoietic CRAMP in bone marrow chimeric mice reduces platelet recruitment and thrombus formation. Both LL-37 and CRAMP induce platelet activation in vitro by involving glycoprotein VI receptor with downstream signaling through protein tyrosine kinases Src/Syk and phospholipase C. In addition to acute thrombosis, LL-37/CRAMP-dependent platelet activation fosters platelet-neutrophil interactions in other inflammatory conditions by modulating the recruitment and extravasation of neutrophils into tissues. Absence of CRAMP abrogates acid-induced lung injury, a mouse pneumonia model that is dependent on platelet-neutrophil interactions. We suggest that LL-37/CRAMP represents an important mediator of platelet activation and thrombo-inflammation

Platelet GPIIb supports initial pulmonary retention but inhibits subsequent proliferation of melanoma cells during hematogenic metastasis

Platelets modulate the process of cancer metastasis. However, current knowledge on the direct interaction of platelets and tumor cells is mostly based on findings obtained in vitro. We addressed the role of the platelet fibrinogen receptor glycoprotein IIb (integrin alpha IIb) for experimental melanoma metastasis in vivo. Highly metastatic B16-D5 melanoma cells were injected intravenously into GPIIb-deficient (GPIIb(-/-)) or wildtype (WT) mice. Acute accumulation of tumor cells in the pulmonary vasculature was assessed in real-time by confocal videofluorescence microscopy. Arrest of tumor cells was dramatically reduced in GPIIb(-/-) mice as compared to WT. Importantly, we found that mainly multicellular aggregates accumulated in the pulmonary circulation of WT, instead B16-D5 aggregates were significantly smaller in GPIIb(-/-) mice. While pulmonary arrest of melanoma was clearly dependent on GPIIb in this early phase of metastasis, we also addressed tumor progression 10 days after injection. Inversely, and unexpectedly, we found that melanoma metastasis was now increased in GPIIb(-/-) mice. In contrast, GPIIb did not regulate local melanoma proliferation in a subcutaneous tumor model. Our data suggest that the platelet fibrinogen receptor has a differential role in the modulation of hematogenic melanoma metastasis. While platelets clearly support early steps in pulmonary metastasis via GPIIb-dependent formation of platelet-tumor-aggregates, at a later stage its absence is associated with an accelerated development of melanoma metastases