[Thromboembolic disease due to clinically unmanifested endoappendicitis].
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Biomedical subjects
Publications and source records attributed to P Germain.
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The acetate, hexanoate and glucose catabolisms have not repressing influence on androsta-4-ene-3,17-dione induced delta 1-steroid-dehydrogenase in Nocardia restricta during the growth on synthetic media. Methyl-perhydroindane-dione-propionic acid degradation is a limiting step of the androsta-4-ene-3,17-dione catabolism on acetate medium. On this medium induction of delta 1-steroid-dehydrogenase synthesis takes place in two steps: a first inducer is androsta-4-ene-3,17-dione; a second inducer is a so far undefined product of methyl-perhydroindane-dione-propionic acid catabolism, On hexanoate medium, during androsta-4-ene-3,17-dione degradation, this acid does not accumulate, and the synthesis of delta 1-steroid-dehydrogenase is then only induced by androsta-4-ene-3,17-dione. The degradation of this steroid on acetate at pH below 7,0 gives, with a 50% yield, 3-hydroxy-9(10)-seco-androsta-1,3,5(10)-triene-9,17-dione.
The influence of bovine serum albumin on estradiol-17 beta growth and responsiveness of human mammary cancer MCF-7 cells was studied and compared to that of dextran-coated charcoal-treated fetal calf serum and other bovine serum proteins. To reveal the protein factor role, a culture defined medium was used. It was composed of minimal essential medium without phenol red, added with human iron saturated tranferrin (10 mg/ml) and porcine insulin (5 mg/ml). An estradiol-17 beta mitogenic effect was noticed only in the present of bovine serum albumin or of dextran-coated charcoal-treated fetal calf serum. A protein concentration increase provokes a greater responsiveness of MCF-7 cells submitted to an estrogenic treatment. The obtained results suggest that serum albumin participates in the estradiol-17 beta mode of action on the target cells and modulates its effect. The culture conditions appear essential for the study of the effect of estrogens and antiestrogens on the growth of estrogen-dependent cells.