679 resultados para Herzog
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Mode of access: Internet.
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Errata: p. [xv].
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Mode of access: Internet.
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v.1. Geschichte von Griseldis.--v.2. Alte und neue Lieder.--v.3. Schöne Melusina.--v.4. Schildbürger.--v.5. Schöne Magelone.--v.6. Octavianus.--v.7. Sieben Schwaben.--v.8. Genoveva.--v.11. Drei Schwestern: Drei Rolandsknappen.--v.12. Wiederstandner Eulenspiegel.--v.13-14. Tristan und Isolde.--v.15-17. Reineke der Fuchs.--v.18. Wigolais vom Rade.--v.19-20. Deutsche Lieder.--v.21. Hirlanda.--v.22. Fortunat.--v.23. Fortunat's Söhne.--v.25. Unschätzbares Schloss.--v.26. Robert der Teufel.--v.27. Schnurren.--v.30-31. Sieben weise Meister.--v.32. Armer Heinrich.--v.33. König Eginhard.--v.34. Herzog Ernst.--v.35. Senfkörner.--v.36. Schwanenritter.--v.37. Geduldige Helena.--v.38. Deutsches Fabelschatz.--v.39. Maerkischer Eulenspiegel.--v.40. Schlesischer Ruebezahl.--v.41-43. Weiser Ritter, Herpin von Bourges.--v.45. Lustiger Kirmesbruder.--v.46. Zauberer Virgilius.--v.47. Joachim und Anna.--v.48. Leben Jesu Christi.--v.49-50. Dorfgespräche.--v.51. Volksmärchen.--v.53. König Apollonius. Zwergenburg. Deutsches Räthselbuch.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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Thesis (doctoral)--Universitat Freiburg in der Schweiz.
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Thesis (doctoral)--
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l. T. Herzog Theodor van Gothland. Scherz, Satire, Ironie und tiefere Bedeutung.--2. T. Nannette und Maria. Marius und Sulla. Don Juan und Faust.--3. T. Die Hobenstaufen. Barbarossa im Kyffhäuser. Aschenbrödel.--4. T. Napoleon. Hannibal. Der Cid. Die Hermannsschlacht. Kleinere dramatische Fragmente.--5. T. Aufsätze. Rezensionen und Vermischtes. Briefe I.--6. T. Briefe II.
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Mode of access: Internet.
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Bd. 1. Fliegende Blätter ; Frühlingslieder ; Der Zecher ; Sehnsucht ; Das Steinbild am Dome ; Anhang -- Bd. 2. Ritter Wahn ; Ahashver -- Bd. 3. Heinrich der Finkler, König der Deutschen ; Kaiser Otto III ; Cola Rienzi, der letzte Volkstribun der Römer -- Bd. 4. Wendelin und Helene ; Die Bräute von Florenz ; Johann von Österreich ; Herzog Bernhard ; Der Sohn des Fürsten ; Cromwell -- Bd. 5-6. Der Congress von Verona -- B. 7. Bilder im Moose -- Bd. 8. Studien zur Kunst der Malerei ; Über Goethe's Faust ; Das neuere deutsche Drama und die deutschen Theaterzustände ; Erinnerungen ; Georg Venlot, eine Novelle mit Arabesken.
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Leptin and Y2 receptors on hypothalamic NPY neurons mediate leptin effects on energy homeostasis; however, their interaction in modulating osteoblast activity is not established. Here, direct testing of this possibility indicates distinct mechanisms of action for leptin anti-osteogenic and Y2(-/-) anabolic pathways in modulating bone formation. Introduction: Central enhancement of bone formation by hypothalamic neurons is observed in leptin-deficient oblob and Y2 receptor null mice. Similar elevation in central neuropeptide Y (NPY) expression and effects on osteoblast activity in these two models suggest a shared pathway between leptin and Y2 receptors in the central control of bone physiology. The aim of this study was to test whether the leptin and Y2 receptor pathways regulate bone by the same or distinct mechanisms. Materials and Methods: The interaction of concomitant leptin and Y2 receptor deficiency in controlling bone was examined in Y2(-/-) oblob double mutant mice, to determine whether leptin and Y2 receptor deficiency have additive effects. Interaction between leptin excess and Y2 receptor deletion was examined using recombinant adeno-associated viral vector overproduction of NPY (AAV-NPY) to produce weight gain and thus leptin excess in adult Y2(-/-) mice. Cancellous bone volume and bone cell function were assessed. Results: Osteoblast activity was comparably elevated in oblob, Y2(-/-), and Y2(-/-) oblob mice. However, greater bone resorption in oblob and Y2(-/-) oblob mice reduced cancellous bone volume compared with Y2(-/-). Both wildtype and Y2(-/-) AAV-NPY mice exhibited marked elevation of white adipose tissue accumulation and hence leptin expression, thereby reducing osteoblast activity. Despite this anti-osteogenic leptin effect in the obese AAV-NPY model, osteoblast activity in Y2(-/-) AAV-NPY mice remained significantly greater than in wildtype AAV-NPY mice. Conclusions: This study suggests that NPY is not a key regulator of the leptin-dependent osteoblast activity, because both the leptin-deficient stimulation of bone formation and the excess leptin inhibition of bone formation can occur in the presence of high hypothalamic NPY. The Y2(-/-) pathway acts consistently to stimulate bone formation; in contrast, leptin continues to suppress bone formation as circulating levels increase. As a result, they act increasingly in opposition as obesity becomes more marked. Thus, in the absence of leptin, the cancellous bone response to loss of Y2 receptor and leptin activity can not be distinguished. However, as leptin levels increase to physiological levels, distinct signaling pathways are revealed.
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Reduction in levels of sex hormones at menopause in women is associated with two common, major outcomes, the accumulation of white adipose tissue, and the progressive loss of bone because of excess osteoclastic bone resorption exceeding osteoblastic bone formation. Current antiresorptive therapies can reduce osteoclastic activity but have only limited capacity to stimulate osteoblastic bone formation and restore lost skeletal mass. Likewise, the availability of effective pharmacological weight loss treatments is currently limited. Here we demonstrate that conditional deletion of hypothalamic neuropeptide Y2 receptors can prevent ongoing bone loss in sex hormone-deficient adult male and female mice. This benefit is attributable solely to activation of an anabolic osteoblastic bone formation response that counterbalances persistent elevation of bone resorption, suggesting the Y2-mediated anabolic pathway to be independent of sex hormones. Furthermore, the increase in fat mass that typically occurs after ovariectomy is prevented by germ line deletion of Y2 receptors, whereas in male mice body weight and fat mass were consistently lower than wild-type regardless of sex hormone status. Therefore, this study indicates a role for Y2 receptors in the accumulation of adipose tissue in the hypogonadal state and demonstrates that hypothalamic Y2 receptors constitutively restrain osteoblastic activity even in the absence of sex hormones. The increase in bone formation after release of this tonic inhibition suggests a promising new avenue for osteoporosis treatment.