Sozialpartnerschaftliche Arbeitsmarktpolitik in Österreich

Die Arbeitskräfteüberlassung und -vermittlung erfuhr europaweit in den letzten zehn Jahren einen enormen Aufschwung. In Staaten wie Deutschland wurde sie zu einem wichtigen Element der Arbeitsmarktpolitik, aber auch in Österreich muss, besonders seit Inkrafttreten des Konjunkturbelebungsgesetzes 2002, ein signifikanter Bedeutungsgewinn im Bereich der Arbeitsmarktverwaltung verzeichnet werden. Dem AMS Geschäftsbericht von 2007 zufolge wurden 82.409 offene Stellen von Arbeitskräfteüberlassern gemeldet. Dies entspricht einem Gesamtanteil von 22,3% aller offenen gemeldeten Stellen. Vor diesem Hintergrund untersucht diese Arbeit den österreichischen und deutschen Werdegang der Arbeitskräfteüberlassung im historischen Verlauf. Anhand eines Überblickes werden die wirtschaftlichen Transformationen nach dem Ende des 2. Weltkrieges zusammengefasst. Daran schließt eine Betrachtung der österreichischen Beschäftigungs- und Arbeitsmarktpolitik an. Im Zentrum dieser Arbeit steht auf österreichischer Seite das Arbeitskräfteüberlassungsgesetz von 1988 und der Kollektivvertrag der Arbeitskräfteüberlassung von 2002. Zur Untersuchung dieses Gebietes wurden Interviews mit ExpertInnen durchgeführt, die bei den Verhandlungen zum Arbeitskräfteüberlassungs-Kollektivvertrag eine entscheidende Rolle gespielt haben. An diesen Regelungen wird gezeigt, wie positiv sich die Einbindung der Wirtschafts- und Sozialpartnerschaft in die Arbeitsmarktpolitik auswirken kann. Im Gegensatz dazu analysiert diese Arbeit die zum Teil stark negativen Auswirkungen in Deutschland auf die überlassenen Arbeitskräfte aufgrund mangelnder oder fehlender Regelungen. Am Ende wird neben einer Zusammenfassung ein Ausblick für die Arbeitskräfteüberlassung vorgenommen, der sich besonders auf die kommenden Verhandlungen zwischen den Arbeitgeber- und den ArbeitnehmervertreterInnen konzentriert

Kindlin-2 controls bidirectional signaling of integrins.

Control of integrin activation is required for cell adhesion and ligand-induced signaling. Here we report that loss of the focal adhesion protein Kindlin-2 in mice results in peri-implantation lethality caused by severe detachment of the endoderm and epiblast from the basement membrane. We found that Kindlin-2-deficient cells were unable to activate their integrins and that Kindlin-2 is required for talin-induced integrin activation. Furthermore, we demonstrate that Kindlin-2 is required for integrin outside-in signaling to enable firm adhesion and spreading. Our findings provide evidence that Kindlin-2 is a novel and essential element of bidirectional integrin signaling

Loss of Kindlin-1 Causes Skin Atrophy and Lethal Neonatal Intestinal Epithelial Dysfunction

Kindler Syndrome (KS), characterized by transient skin blistering followed by abnormal pigmentation, skin atrophy, and skin cancer, is caused by mutations in the FERMT1 gene. Although a few KS patients have been reported to also develop ulcerative colitis (UC), a causal link to the FERMT1 gene mutation is unknown. The FERMT1 gene product belongs to a family of focal adhesion proteins (Kindlin-1, -2, -3) that bind several β integrin cytoplasmic domains. Here, we show that deleting Kindlin-1 in mice gives rise to skin atrophy and an intestinal epithelial dysfunction with similarities to human UC. This intestinal dysfunction results in perinatal lethality and is triggered by defective intestinal epithelial cell integrin activation, leading to detachment of this barrier followed by a destructive inflammatory response

Loss of talin1 in platelets abrogates integrin activation, platelet aggregation, and thrombus formation in vitro and in vivo

Platelet adhesion and aggregation at sites of vascular injury are essential for normal hemostasis but may also lead to pathological thrombus formation, causing diseases such as myocardial infarction or stroke. Heterodimeric receptors of the integrin family play a central role in the adhesion and aggregation of platelets. In resting platelets, integrins exhibit a low affinity state for their ligands, and they shift to a high affinity state at sites of vascular injury. It has been proposed that direct binding of the cytoskeletal protein talin1 to the cytoplasmic domain of the integrin β subunits is necessary and sufficient to trigger the activation of integrins to this high affinity state, but direct in vivo evidence in support of this hypothesis is still lacking. Here, we show that platelets from mice lacking talin1 are unable to activate integrins in response to all known major platelet agonists while other cellular functions are still preserved. As a consequence, mice with talin-deficient platelets display a severe hemostatic defect and are completely resistant to arterial thrombosis. Collectively, these experiments demonstrate that talin is required for inside-out activation of platelet integrins in hemostasis and thrombosis

αv-Class integrin binding to fibronectin is solely mediated by RGD and unaffected by an RGE mutation

Fibronectin (FN) is an essential glycoprotein of the extracellular matrix; binds integrins, syndecans, collagens, and growth factors; and is assembled by cells into complex fibrillar networks. The RGD motif in FN facilitates cell binding- and fibrillogenesis through binding to α5β1 and αv-class integrins. However, whether RGD is the sole binding site for αv-class integrins is unclear. Most notably, substituting aspartate with glutamate (RGE) was shown to eliminate integrin binding in vitro, while mouse genetics revealed that FNRGE preserves αv-class integrin binding and fibrillogenesis. To address this conflict, we employed single-cell force spectroscopy, engineered cells, and RGD motif-deficient mice (Fn1ΔRGD/ΔRGD) to search for additional αv-class integrin-binding sites. Our results demonstrate that α5β1 and αv-class integrins solely recognize the FN-RGD motif and that αv-class, but not α5β1, integrins retain FN-RGE binding. Furthermore, Fn1ΔRGD/ΔRGD tissues and cells assemble abnormal and dysfunctional FNΔRGD fibrils in a syndecan-dependent manner. Our data highlight the central role of FN-RGD and the functionality of FN-RGE for αv-class integrins

Silac mouse for quantitative proteomics uncovers kindlin-3 as an essential factor for red blood cell function

Stable isotope labeling by amino acids in cell culture (SILAC) has become a versatile tool for quantitative, mass spectrometry (MS)-based proteomics. Here, we completely label mice with a diet containing either the natural or the 13C6-substituted version of lysine. Mice were labeled over four generations with the heavy diet, and development, growth, and behavior were not affected. MS analysis of incorporation levels allowed for the determination of incorporation rates of proteins from blood cells and organs. The F2 generation was completely labeled in all organs tested. SILAC analysis from various organs lacking expression of β1 integrin, β-Parvin, or the integrin tail-binding protein Kindlin-3 confirmed their absence and disclosed a structural defect of the red blood cell membrane skeleton in Kindlin-3-deficient erythrocytes. The SILAC-mouse approach is a versatile tool by which to quantitatively compare proteomes from knockout mice and thereby determine protein functions under complex in vivo conditions

New U-Pb ages for syn-orogenic magmatism in the SW sector of the Ossa Morena Zone (Portugal)

The Ossa-Morena Zone (OMZ) is a major geotectonic unit within the Iberian Massif (which constitutes an important segment of the European Variscan Belt) and one of its distinguishing features is the presence of a noteworthy compositional diversity of plutonic rocks. In the SW sector of the OMZ, the tonalitic Hospitais intrusion (located to the W of Montemor-o-Novo) is considered a typical example of syn-orogenic magmatism, taking into account that both the long axis of the plutonic body and its mesoscopic foliation are oriented parallel to the Variscan WNW-ESE orientation. Another relevant feature of the Hospitais intrusion is the occurrence of mafic microgranular enclaves within the main tonalite. In previous works (Moita et al., 2005; Moita, 2007), it was proposed that: (1) the Hospitais intrusion is part of a calc-alkaline suite, represented by a large number of intrusions in this sector of the OMZ, ranging from gabbros to granites; (2) the enclaves are co-genetic to the host tonalite in the Hospitais pluton. In this study, zircon populations from one sample of the main tonalite (MM-17) and one sample of the associated enclave (MM-17E) were analysed by ID-TIMS for U-Pb geochronology. In each sample, three fractions of nice glassy, euhedral, long prismatic and inclusion free crystals were analysed. The results from the three fractions of MM-17 yielded a 206Pb/238U age of 337.0 ± 2.0 Ma. Similarly, for the enclave MM-17E a 206Pb/238U zircon age of 336.5 ± 0.47 Ma was obtained. These identical ages, within error, are in agreement with a common parental magma for the tonalite and mafic granular enclaves. Similar U-Pb ages have been reported in previous works for plutonic and metamorphic events in this region (e.g.: Pereira et al., 2009; Antunes et al., 2011). Furthermore, also in the SW sector of the OMZ, palaeontological studies (Pereira et al., 2006; Machado & Hladil, 2010) carried out in Carboniferous sedimentary basins containing intercalated calc-alkaline volcanics (Santos et al., 1987; Chichorro, 2006) have shown that they are mainly of Visean age. Therefore, magmatism displaying features typical of continental arc setting seems to have been active in this part of the OMZ during the Lower Carboniferous times

Design of the Magnet System of the Neutron Decay Facility PERC

The PERC (Proton and Electron Radiation Channel) facility is currently under construction at the research reactor FRM II, Garching. It will serve as an intense and clean source of electrons and protons from neutron beta decay for precision studies. It aims to contribute to the determination of the Cabibbo-Kobayashi-Maskawa quark-mixing element $V_{ud}$ from neutron decay data and to search for new physics via new effective couplings. PERC's central component is a 12m long superconducting magnet system. It hosts an 8m long decay region in a uniform field. An additional high-field region selects the phase space of electrons and protons which can reach the detectors and largely improves systematic uncertainties. We discuss the design of the magnet system and the resulting properties of the magnetic field.Comment: Proceedings of the International Workshop on Particle Physics at Neutron Sources PPNS 2018, Grenoble, France, May 24-26, 201