Estrogen and progesterone receptor proteins in breast cancer.
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The effects of a single, variable dose (5 to 200 mg) of RU38486 (RU486) (Roussel-Uclaf, Paris, France) in the first half of the luteal phase of the menstrual cycle were studied in 30 normal fertile volunteers. Quantitative histologic techniques were employed, and the results were compared with normal ranges derived from a separate, normal, fertile population. It was found that RU486 inhibited glandular secretory activity, accelerated degenerative changes, induced various vascular changes, increased stromal but not glandular mitotic activity, and did not affect the predecidual reaction. The superiority of morphometric analysis over traditional dating criteria was demonstrated in this study of endometrial responses to an exogenously administered agent. In addition, it was found that temperature drop occurred in 56%, menstrual induction in 43%, luteolysis in 24%, mood change in 23%, and thirst sensation in 3% of women studied. Both menstrual induction and changes in hypothalamic function after the administration of RU486 occurred independently of luteolysis and so were likely to be the direct result of progesterone receptor blockade in these organs. Menstrual induction was significantly related to the dose given and the day on which RU486 was administered. Mood change was significantly related to the day on which RU486 was given. Most of the effects of RU486 occurred around 48 hours after its administration.
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Event-related potentials (ERPs) and behavioral ratings were collected from 30 female subjects who were exposed to picture slides. The slides belonged to five affective categories whose content was babies, dermatological cases, ordinary people, male models, and female models. Based on the day of testing relative to their menstrual cycle, the subjects were grouped according to their expected levels of androgens, estrogen, or progesterone. The data were examined to determine whether any ERP component or behavioral rating (non-erotic/erotic, unpleasant/pleasant, simple/complex, and low arousal/high arousal) varied as a function of subjects' hormone defined menstrual phase. Only the P3 component was sensitive to menstrual phase. The P3 to babies and male models was largest when progesterone levels were high. High progesterone was also associated with a decrease in the complexity and eroticism of all slide categories. An increase in the pleasantness of all categories was evident when estrogen levels were high. The results are interpreted as support for an "adaptive context updating" theory of the P3 component of ERPs.
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The most common oral manifestation of elevated levels of ovarian hormones, as seen in pregnancy or oral contraceptive usage, is an increase in gingival inflammation with an accompanying increase in gingival exudate. This gingivitis can be avoided or at least minimized by establishing low plaque levels at the beginning of pregnancy or the beginning of oral contraceptive therapy. It would appear that bacteria are not solely responsible for the gingivitis seen during these times, nor are the ovarian hormones solely responsible for the condition. Data from numerous studies suggest that the ovarian hormones alter the microenvironment of the oral bacteria so as to promote their growth and shifts in their populations. The present article reviews the current state of knowledge concerning the relationship of gingivitis to elevated levels of ovarian hormones, and describes the role that these hormones may play in the gingivitis associated with pregnancy or oral contraceptive usage.
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Ovariectomy increases the percentage of total lipids in liver, kidney and uterus of intact cyclic rats. Estrogen and progesterone, when administered individually to ovariectomized rats, caused a decrease in the total lipid content of all tissues. Th effect of progesterone in estrogen-primed rats is not significant. Triglyceride and cholesterol content increases after ovariectomy; treatment with estrogen in ovariectomized rats led to a decrease in the concentration of these lipids. Progesterone has no significant effect on these lipids but showed an antagonistic action when given in estrogen-primed ovariectomized rats. The proportions of ethanolamine, choline and inositol phospholipids decreased after spaying and increased when estrogen was given to spayed rats. Progesterone alone had effect only on the uterus whereas progesterone administered to estrogen-primed rats showed an antagonistic effect in all tissues.
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Many women appear to experience menstrual disturbances after tubal sterilization. In this study the ovarian function in such women was investigated. Serial measurements of FSH, LH, estradiol and progesterone were performed throughout the study cycle in 23 previously sterilized patients, 14 with menstrual disturbances (group I--symptomatic) and 9 with normal cycles (group II--asymptomatic). A group of 28 parous women served as controls. Among 23 patients, luteal phase progesterone was elevated in 19, and in 4 it was undetectable (anovulatory). All four anovulatory patients belonged to group I. Anovulatory cycles were also characterized by tonic elevated LH levels. Mean midluteal progesterone values were lower in group I (8.5 ng/ml) than in group II (13.8 ng/ml) and in the controls (16.5 ng/ml). Mean midluteal progesterone was lower than 10 ng/ml in 78% of group I, 44% of group II and 15% of the control patients.
In a 36-year-old woman taking an oral contraceptive containing 50 mug of ethinyloestradiol each day, a pulmonary arterial thrombosis and a monoclonal gammapathia were associated. The monoclonal IgI lambda Mai... was prepared. When purified, this IgG lambda binds ethinyloestradiol with strong affinity (Ka= 2.7 times 10(7)M-1) and also 17-beta-oestradiol with a little less affinity (Ka = 0.4 times 10(7)M-1. For those ligands each IgG lambda Mai... molecule has two sites of same affinity and specificity so that a Scatchard plot of the experimental values gives a straight line. It is likely that the antibody sites of the IgG lambda Mai... are the binding sites. These facts support the hypothesis of an immunological mechanism of the thromboembolic disease which may be induced by oral contraceptives.
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