Institut für Turnlehrerausbildung während des Das Austrofaschismus und das Hochschulinstitut für Leibesübungen während des Nationalsozialismus an der Universität Wien

Der Staat Österreich wurde in den Jahren 1934-1945 faschistisch regiert, beginnend mit dem Austrofaschismus und gefolgt vom Nationalsozialismus. Beide Regierungsformen griffen in die verschiedensten Institutionen ein. Als Ziel galten, unter anderem, die Verbreitung der jeweiligen Ideologie und die Wehrhaftmachung der Jugendlichen. Diese Arbeit setzt sich mit der Beeinflussung der beiden Staatsmächte im Hochschulbetrieb, vor allem mit dem Institut für Turnlehrerausbildung bzw. mit dem Hochschulinstitut für Leibesübungen, auseinander. Einzelne Biographien ausgewählter Lehrer und Lehrerinnen, die in dieser Zeit am Institut beruflich tätig waren bzw. das Geschehen am Institut verfolgten und teilweise mitbestimmten, werden aufgezeigt. Anhand deren Lebensläufe kann ein Einblick über die damalige Situation am Institut gegeben werden. Eine Analyse des Vorlesungs- und Personalverzeichnisses des Instituts zur Zeit der beiden faschistischen Regentschaften soll klären, inwieweit die Staatsmächte in den Universitätsbetrieb eingriffen. Die ständestaatliche Regierung verpflichtete Studenten an Hochschullagern teilzunehmen. Diese Lager fanden im Sommer 1936 und 1937 statt. Dort erwartete sie nicht nur eine intensive vormilitärische Ausbildung, sondern auch eine geistige Auseinandersetzung mit der Ideologie der Vaterländischen Front.The state of Austria was ruled by Fascist regimes in the years from 1934 to 1945, first by Austro-Fascism, then by National Socialism. Both government forms encroached various institutions. In addition to other targets the regime aimed to spread their ideology and to indoctrinate young people with it. This paper deals with the influence of both state powers in the administration of Institutes of higher learning, specifically with the Institute for Gymnastic Education and with the University College for Physical Education. Biographies of selected teachers, who either worked during this period or who observed the events, or who had a determining role in the institutes, will be pointed out. On the basis of the professors curricula vitae we gain insight into the situation at the institute at the time. An analysis of the university’s course catalog and the institute’s personnel records from the time of the Fascist regimes should clarify to what extent the state impinged on the university administration. The government of the corporative state obliged students to take part in collegiate camps. These camps were held during the summers of 1936 and 1937. At these collegiate camps students experienced not only an intensive pre-military education, but also a mental examination of the ideology of the National Front

Results from a Large, Multinational Sample Using the Childhood Trauma Questionnaire

Childhood maltreatment has diverse, lifelong impact on morbidity and mortality. The Childhood Trauma Questionnaire (CTQ) is one of the most commonly used scales to assess and quantify these experiences and their impact. Curiously, despite very widespread use of the CTQ, scores on its Minimization-Denial (MD) subscale—originally designed to assess a positive response bias—are rarely reported. Hence, little is known about this measure. If response biases are either common or consequential, current practices of ignoring the MD scale deserve revision. Therewith, we designed a study to investigate 3 aspects of minimization, as defined by the CTQ’s MD scale: 1) its prevalence; 2) its latent structure; and finally 3) whether minimization moderates the CTQ’s discriminative validity in terms of distinguishing between psychiatric patients and community volunteers. Archival, item-level CTQ data from 24 multinational samples were combined for a total of 19,652 participants. Analyses indicated: 1) minimization is common; 2) minimization functions as a continuous construct; and 3) high MD scores attenuate the ability of the CTQ to distinguish between psychiatric patients and community volunteers. Overall, results suggest that a minimizing response bias—as detected by the MD subscale—has a small but significant moderating effect on the CTQ’s discriminative validity. Results also may suggest that some prior analyses of maltreatment rates or the effects of early maltreatment that have used the CTQ may have underestimated its incidence and impact. We caution researchers and clinicians about the widespread practice of using the CTQ without the MD or collecting MD data but failing to assess and control for its effects on outcomes or dependent variables

Robo2-Slit1 dependent cell-cell interactions mediate assembly of the trigeminal ganglion

Vertebrate cranial sensory ganglia, responsible for sensation of touch, taste and pain in the face and viscera, are composed of both ectodermal placode and neural crest cells. The cellular and molecular interactions allowing generation of complex ganglia remain unknown. Here, we show that proper formation of the trigeminal ganglion, the largest of the cranial ganglia, relies on reciprocal interactions between placode and neural crest cells in chick, as removal of either population resulted in severe defects. We demonstrate that ingressing placode cells express the Robo2 receptor and early migrating cranial neural crest cells express its cognate ligand Slit1. Perturbation of this receptor-ligand interaction by blocking Robo2 function or depleting either Robo2 or Slit1 using RNA interference disrupted proper ganglion formation. The resultant disorganization mimics the effects of neural crest ablation. Thus, our data reveal a novel and essential role for Robo2-Slit1 signaling in mediating neural crest–placode interactions during trigeminal gangliogenesis

Lu/BCAM Adhesion Glycoprotein Is a Receptor for Escherichia coli Cytotoxic Necrotizing Factor 1 (CNF1)

The Cytotoxic Necrotizing Factor 1 (CNF1) is a protein toxin which is a major virulence factor of pathogenic Escherichia coli strains. Here, we identified the Lutheran (Lu) adhesion glycoprotein/basal cell adhesion molecule (BCAM) as cellular receptor for CNF1 by co-precipitation of cell surface molecules with tagged toxin. The CNF1-Lu/BCAM interaction was verified by direct protein-protein interaction analysis and competition studies. These studies revealed amino acids 720 to 1014 of CNF1 as the binding site for Lu/BCAM. We suggest two cell interaction sites in CNF1: first the N-terminus, which binds to p37LRP as postulated before. Binding of CNF1 to p37LRP seems to be crucial for the toxin's action. However, it is not sufficient for the binding of CNF1 to the cell surface. A region directly adjacent to the catalytic domain is a high affinity interaction site for Lu/BCAM. We found Lu/BCAM to be essential for the binding of CNF1 to cells. Cells deficient in Lu/BCAM but expressing p37LRP could not bind labeled CNF1. Therefore, we conclude that LRP and Lu/BCAM are both required for toxin action but with different functions. Author Summary We study a crucial virulence factor produced by pathogenic Escherichia coli strains, the Cytotoxic Necrotizing Factor 1 (CNF1). More than 80% of urinary tract infections (UTIs), which are counted among the most common bacterial infections of humans, are caused by Uropathogenic Escherichia coli (UPEC) strains. We and others elucidated the molecular mechanism of the E. coli toxin CNF1. It constitutively activates Rho GTPases by a direct covalent modification. The toxin enters mammalian cells by receptor-mediated endocytosis. Here, we identified the protein receptor for CNF1 by co-precipitation of cell surface molecules with the tagged toxin and subsequent Maldi-TOF analysis. We identified the Lutheran (Lu) adhesion glycoprotein/basal cell adhesion molecule (BCAM) as receptor for CNF1 and located its interaction site to the C-terminal part of the toxin. We performed direct protein-protein interaction analysis and competition studies. Moreover, cells deficient in Lu/BCAM could not bind labeled CNF1. The identification of a toxin's cellular receptor and receptor binding region is an important task for understanding the pathogenic function of the toxin and, moreover, to make the toxin accessible for its use as a cellbiological and pharmacological tool, for example for the generation of immunotoxins