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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 637-643 
    ISSN: 1432-1912
    Keywords: Sympathetic nervous system ; α-Adrenoceptor blockers ; Phentolamine ; Insulin secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the effects of phentolamine and another more selective α2-adrenoceptor antagonist, rauwolscine, on insulin release in vivo (in female Wistar-rats) and in vitro (in perfused rat pancreas and in isolated perifused mouse islets). Phentolamine was found to significantly increase glucose-induced insulin release. On the other hand, rauwolscine failed to do so, when applied in a concentration that effectively antagonized the inhibitory effect of clonidine. These results demonstrate that phentolamine is capable of directly stimulating insulin release. This effect is thus not mediated by α-adrenoceptors. For this reason phentolamine is not an appropriate tool to study possible inhibitory effects of the sympathetic nervous system on insulin release. An enhanced insulin response as may be observed in animals and in man in the presence of phentolamine does not furnish evidence for a tonic inhibitory control of the islet cells by the sympathetic nervous system.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 371 (1976), S. 161-170 
    ISSN: 1432-2307
    Keywords: Giant cell granuloma ; Histochemistry ; Ultrastructure ; Cell function ; Osteoclasts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die mehrkernigen Riesenzellen des zentralen Riesenzellgranuloms entstehen durch Zellfusion aus den Pericyten der Kapillaren. In der vorliegenden Studie werden die Funktionsmerkmale der Riesenzellen durch Kombination histologischer, histochemischer und elektronenmikroskopischer Methoden untersucht. In den mehrkernigen Riesenzellen ließen sich in Übereinstimmung mit älteren Untersuchungen die lysosomalen Enzyme saure Phosphatase und Aminopeptidase nachweisen. Das lysosomale System der Riesenzellen befähigt diese zur aktiven Phagocytoseleistung. Darüber hinaus können sich die Riesenzellen neugebildeten Geflechtknochenbälkchen anlagern und osteoclastäre Funktionen übernehmen. Die enzymhistochemische und funktioneile Ähnlichkeit mit den mehrkernigen Osteoclasten wirft die Frage nach einer vergleichbaren Cytogenese beider Zellformen auf.
    Notes: Summary Multinucleated giant cells in giant cell granuloma are formed by cell fusion of capillary pericytes. In our present study we tried to analyze cell function and activity by histologic, histochemical, and electronmicroscopic examination of giant cells. Lysosomal enzymes such as acid phosphatase and amino-peptidase were found in giant cells which is in agreement with former work. By their lysosomal system giant cells are proved phagocytic. In addition, giant cells being localized at trabecular surfaces of newly formed woven bone may develop osteoclastic functions. The enzymatic and functional resemblance of giant cells and multinucleated osteoclasts points to the possibility of a similar cytogenesis of both cell types.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 370 (1976), S. 163-175 
    ISSN: 1432-2307
    Keywords: Central giant cell granuloma ; Histogenesis ; Histochemistry ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bisherige Untersuchungen an zentralen Riesenzellgranulomen des Gesichts-Kieferbereiches haben die Histogenese dieser tumorähnlichen Knochenerkrankung nicht klären können. Wir untersuchten daher zwei bioptisch gesicherte zentrale Riesenzellgranulome unter dieser Fragestellung histochemisch und elektronenmikroskopisch. Histochemisch findet sich eine enge Enzymverwandtschaft zwischen den mehrkernigen Riesenzellen und den Pericyten der Kapillaren, die das Granulom dicht durchsetzen. Elektronenmikroskopisch zeigen sich typische Membranphänomene der Zellfusion zwischen den mehrkernigen Riesenzellen und den Pericyten. Die für das Granulom charakteristischen mehrkernigen Riesenzellen entstehen daher durch Zellfusion aus den Pericyten, die als ihre Stammzellen angesehen werden müssen. Da die Pericyten das Granulom auch in Form zahlreicher blinder Kapillarsprossen durchsetzen, erklärt sich die Entwicklung einer Vielzahl von Riesenzellen. Die Ursachen, die diesem Verhalten der Pericyten aetiologisch zugrunde liegen, sind unbekannt. Ob die Cytogenese der Riesenzellen des zentralen Riesenzellgranuloms Modellcharakter hat und analog auch für die Entwicklung von Riesenzellen in anderen Gewebsneubildungen oder für die Enstehung der mehrkernigen Osteoclasten gilt, muß weiteren Untersuchungen vorbehalten bleiben.
    Notes: Summary Until now numerous studies on central giant cell granuloma of jawbones have not been able to reveal the histogenesis of this tumourlike lesion. The aim of the present investigation in two surgically proven cases was to study this question by means of histochemical and electron-microscopic methods. Rather similar histochemieal properties were shown in giant cells and pericytes of capillary sprouts penetrating the granuloma. Cell fusion occurred between both cell types as was observed by electron microscopy. The process of cell fusion is defined by characteristic interdigitations of cell membranes. Therefore pericytes are believed to be the stem cells of multinucleated giant cells in giant cell granuloma. The abundance of giant cells usually occurring in the granuloma might be explained by plenty of capillary sprouts made up by clusters of pericytes. The factors inducing the pericytic cell fusion process are still unknown. The question arises whether cytogenesis of giant cells in giant cell granuloma might be similar in other giant cell lesions or even in the development of multinucleated osteoclasts.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 321-327 
    ISSN: 1432-1912
    Keywords: Sympathetic nervous system ; α-Adrenoceptor antagonists ; Phentolamine ; Imidazolines ; Insulin secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary As we have demonstrated previously phentolamine stimulates the release of additional insulin from isolated mouse islets and raises plasma insulin levels in the whole rat. This effect was independent of the well known property of phentolamine to block α-adrenoceptors. In experiments on isolated pancreatic islets from mice we now demonstrate that tolazoline and antazoline which are chemically closely related to phentolamine, share its ability to potentiate insulin release. The following results were taken as evidence that this effect does not result from an a-adrenoceptor blocking action of imidazoline compounds. More than 10 times higher concentrations of phentolamine were required to liberate additional insulin from isolated islets than were effective in counteracting the inhibitory effect of clonidine on insulin release. The newly introduced α2-adrenoceptor antagonist BDF 8933, which is an imidazoline derivative, stimulates insulin release as well, while the irreversible α-adrenoceptor blocking agent benextramine of different structure failed to do so, even when being present in concentrations blocking the α2-adrenoceptor-mediated effects of clonidine. Antazoline shared the ability of phentolamine to stimulate insulin release despite having no or only very little α-adrenoceptor blocking activity. When used under our conditions, it almost entirely failed to alleviate the inhibition of insulin release induced by clonidine. We conclude that the response of the islet cells to imidazoline derivatives is not limited to those capable of blocking α-adrenoceptors. On the other hand, α-adrenoceptor blocking agents of different chemical structure fail to induce the release of additional insulin. We take this as evidence that in our experiments the islet cells respond to imidazoline derivatives and not to α-adrenoceptor blockade.
    Type of Medium: Electronic Resource
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