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  • 1985-1989  (4)
  • 1989  (3)
  • 1985  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 28 (1985), S. 0 
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract The potent inhibition of the shikimate pathway enzyme 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase by the broad-spectrum herbicide glyphosate (N-[phosphonomethyl]glycine) was confirmed for the enzymes extracted from various bacteria, a green alga and higher plants. However, 5 out of 6 species belonging to the genus Pseudomonas were found to have EPSP synthases with a 50- to 100-fold decreased sensitivity to the inhibitor. Correspondingly, growth of these 5 species was not inhibited by 5 mM glyphosate, and the organisms did not excrete shikimate-3-phosphate in the presence of the herbicide.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2307
    Keywords: Bone tumors ; Osteosarcoma ; Osteonectin ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 18 bone-forming tumours and tumour-like lesions were investigated immunocytochemically for the presence of osteonectin. A group of non-bone-forming skeletal tumours (five cartilage-forming tumours, four Ewing sarcomas and five extraskeletal sarcomas) served as controls. The studies showed that osteonectin antibodies react reliably with benign and malignant bone-forming tumours (two cases of fibrous dysplasia, three osteoid osteomas, 13 osteosarcomas). This finding was supported by protein blot studies. Osteonectin is formed by cells which do not yet possess the morphological phenotype of osteoblasts and may be regarded as a “differentiation marker” of the osteoblastic lineage. Only chondroid bone (tissue in which chondrocytes were surrounded by osteoid matrix containing type I and type II collagen) showed a positive reaction. All other primary skeletal tumours and extraskeletal soft tissue tumours were completely negative.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 712-714 
    ISSN: 1432-1912
    Keywords: Insulin release ; Clonidine ; Imidazolines ; Benextramine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary As shown previously clonidine reduces glucose-stimulated insulin release and this effect is mediated by inhibitory postsynaptic α2-adrenoceptors. The present experiments demonstrate that clonidine has the additional property to also stimulate insulin release. This became evident when the a2-adrenoceptors of isolated islets were blocked by benextramine, and thus protected from being stimulated by clonidine. In the presence of benextramine, clonidine no longer reduced, but on the contrary enhanced, the release of insulin in response to glucose. In control experiments benextramine by itself failed to affect insulin release from isolated islets. These results show that the imidazoline derivative clonidine shares the property of other imidazoline compounds to enhance the insulin response to glucose. All of these agents may stimulate insulin by binding to “imidazoline-preferring” sites, that clearly differ from α-adrenoceptors.
    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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