English abstract: "The wealth of nothingness - On the (im)possibility of metaphysics in Adorno and Beckett": The subject of this paper is Theodor W. Adorno's reception of Samuel Beckett and its embedding in his philosophy. Based on an interpretation of Adorno's treatment of the problem of temporality, it is shown that for Adorno Beckett's work both marks the end of time in a bad infinity and at the same time prepares the turn into a fulfilled time. As the opening of a quasi- utopian temporality, it is argued that the engagement with Beckett represents for Adorno as much as the rescue of the possibility of metaphysics and critical theory through its impossibility, moving in the semantics of gift, promise, and gratitude. Keywords: dialectics, temporality, metaphysics, gift, utopia

Genetic predisposition and exposure to alcohol and stress increase the risk for alcoholism, possibly by forming a threefold interaction. This is suggested by various aspects of alcohol-induced stress response dampening in offspring of alcoholics. We tested whether such an interaction is also revealed by prolactin secretion, which is predominantly controlled by hypothalamic dopamine. Plasma prolactin was measured during four experimental days in 26 young males with a paternal history of alcoholism (PHA) and in 22 family history negative (FHN) controls. A public speaking stress paradigm was applied on the first 2 days, and a non-stress acoustic startle experiment on the others. Before the tests, subjects drank alcohol (0.6 g/kg) or placebo in a randomized, double-blind crossover design. During placebo experiments, prolactin levels significantly increased after stress, but not after startle, and did not differ between risk groups. Alcohol administration significantly increased prolactin before stress and during startle in both groups, did not alter stress-induced prolactin stimulation in FHN, but significantly attenuated the prolactin stress response in PHA subjects. The alcohol effects on prolactin, cortisol, and adrenocorticotropin stress response were positively interrelated with each other. These data confirm that alcohol specifically dampens the stress response in PHA but not FHN subjects. Since prolactin responses to stress alone and alcohol alone were normal in PHA, we conclude that this genetic effect is not related to altered physiology of the hypothalamic dopaminergic system, but to risk-group specific alcohol effects on hierarchically higher brain areas controlling the stress response in general.

No description available.

Zugl.: Würzburg, Univ., Diss., 2005

Ziel der Arbeit ist der Beweis, dass Verschwendung in all seinen verschiedenen Formen immer ein Paradoxon aufweist. Die Analyse der Arbeit beginnt mit der Untersuchung der geschichtlichen Herkunft von Verschwendung in archaischen Gesellschaften. Soziologen des beginnenden 20. Jahrhunderts nehmen diese Ideen auf und übertragen die gewonnenen Erkenntnisse auf die aktuellen Gesellschaftsformen. Ebenso werden zeitgenössische Autoren aus Soziologie, Politik und Ökonomie zum Themengebiet Verschwendung kritisch hinterfragt. Es zeigt sich bei der Analyse, dass bisherige Interpretationen in der Soziologie, Philosophie und Ökonomie die Verschwendung jeweils entweder positiv oder negativ also einseitig bewerten. Diese einseitigen Bewertungen erweisen sich allerdings als nicht haltbar. Verschwendung ist immer von zwei Seiten zu betrachten. Jeder Verschwendungsakt beinhaltet bei Betrachtung der Makroebene immer sowohl positive als auch negative Folgen in unterschiedlichen Bereichen. Die Verschwendung erweist sich somit auf der einen Seite als grundlegender Treiber und wichtige Basis einer jeden Gesellschaft und Ökonomie. Auf der anderen Seite führt maßlose Verschwendung in die Zerstörung von Allem. Das Paradoxon der Verschwendung entsteht.

No description available.

No description available.

Genetic predisposition and exposure to alcohol and stress increase the risk for alcoholism, possibly by forming a threefold interaction. This is suggested by various aspects of alcohol-induced stress response dampening in offspring of alcoholics. We tested whether such an interaction is also revealed by prolactin secretion, which is predominantly controlled by hypothalamic dopamine. Plasma prolactin was measured during four experimental days in 26 young males with a paternal history of alcoholism (PHA) and in 22 family history negative (FHN) controls. A public speaking stress paradigm was applied on the first 2 days, and a non-stress acoustic startle experiment on the others. Before the tests, subjects drank alcohol (0.6 g/kg) or placebo in a randomized, double-blind crossover design. During placebo experiments, prolactin levels significantly increased after stress, but not after startle, and did not differ between risk groups. Alcohol administration significantly increased prolactin before stress and during startle in both groups, did not alter stress-induced prolactin stimulation in FHN, but significantly attenuated the prolactin stress response in PHA subjects. The alcohol effects on prolactin, cortisol, and adrenocorticotropin stress response were positively interrelated with each other. These data confirm that alcohol specifically dampens the stress response in PHA but not FHN subjects. Since prolactin responses to stress alone and alcohol alone were normal in PHA, we conclude that this genetic effect is not related to altered physiology of the hypothalamic dopaminergic system, but to risk-group specific alcohol effects on hierarchically higher brain areas controlling the stress response in general.

No description available.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.