pubmed-article:147913 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:147913 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:147913 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:147913 | lifeskim:mentions | umls-concept:C0042149 | lld:lifeskim |
pubmed-article:147913 | lifeskim:mentions | umls-concept:C0002844 | lld:lifeskim |
pubmed-article:147913 | lifeskim:mentions | umls-concept:C0033306 | lld:lifeskim |
pubmed-article:147913 | lifeskim:mentions | umls-concept:C0034804 | lld:lifeskim |
pubmed-article:147913 | lifeskim:mentions | umls-concept:C2346501 | lld:lifeskim |
pubmed-article:147913 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:147913 | pubmed:dateCreated | 1978-6-17 | lld:pubmed |
pubmed-article:147913 | pubmed:abstractText | The inhibitory effect of some gestagens and calusterone on the binding of oestradiol-17beta to its specific uterine receptors has been investigated in intact rats. Progesterone, medrogestone, clogestone, medroxyprogesterone acetate and calusterone reduce the specific oestradiol-receptor interaction in vitro; this effect is dose-dependent and does not differ significantly from one drug to the other. A more relevant decrease in the amount of oestradiol-17beta bound to specific receptors has been observed with calusterone. Progesterone, clogestone, medrogestone, medroxyprogesterone acetate and calusterone given orally induce a marked decrease (between 30 and 70% depending on the dose) in the binding capacity of oestradiol-17beta to specific uterine receptors in vivo. Results from a Scatchard plot analysis suggest that the interference with the binding of oestradiol-17beta caused by both progestogens and calusterone is due to a non-competitive interaction. | lld:pubmed |
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pubmed-article:147913 | pubmed:language | eng | lld:pubmed |
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pubmed-article:147913 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:147913 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:147913 | pubmed:month | Apr | lld:pubmed |
pubmed-article:147913 | pubmed:issn | 0022-0795 | lld:pubmed |
pubmed-article:147913 | pubmed:author | pubmed-author:Di CarloFF | lld:pubmed |
pubmed-article:147913 | pubmed:author | pubmed-author:ContiGG | lld:pubmed |
pubmed-article:147913 | pubmed:author | pubmed-author:ReboaniCC | lld:pubmed |
pubmed-article:147913 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:147913 | pubmed:volume | 77 | lld:pubmed |
pubmed-article:147913 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:147913 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:147913 | pubmed:pagination | 49-55 | lld:pubmed |
pubmed-article:147913 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:147913 | pubmed:otherAbstract | PIP: The inhibitory effect of some gestagens and calusterone on the binding of estradiol-17beta to its specific uterine receptors has been investigated in intact rats. Progesterone, medrogestone, clogestone, medroxyprogesterone acetate and calusterone reduce the specific estradiol-receptor interaction in vitro; this effect is dose-dependent and does not differ significantly from 1 drug to the other. A more relevant decrease in the amount of estradiol-17beta bound to specific receptors has been observed with calusterone. Progesterone, clogestone, medrogestone, medroxyprogesterone acetate and calusterone given orally induce a marked decrease (between 30 and 70% depending on the dose) in the binding capacity of estradiol-17beta to specific uterine receptors in vivo. Results from a Scatchard plot analysis suggest that the interference with the binding of estradiol-17beta caused by both progestogens and calusterone is due to a noncompetitive interaction. | lld:pubmed |
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pubmed-article:147913 | pubmed:year | 1978 | lld:pubmed |
pubmed-article:147913 | pubmed:articleTitle | Interference of gestagens and androgens with rat uterine oestrogen receptors. | lld:pubmed |
pubmed-article:147913 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:147913 | pubmed:publicationType | In Vitro | lld:pubmed |