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Biomedical subjects

F Leroy

Publications and source records attributed to F Leroy.

At least 145 records · Page 8Linked to original sources
PubMed1981

Regeneration of uterine epithelium after experimental ablation in the rat.

Regeneration of the uterine luminal epithelium was studied after its mechanical removal in progesterone-primed rats, leaving one control horn intact. Pulse labelling with [3H]TdR during regeneration, showed a rapid peak of labelling index in remaining glands. A differentiated and highly labelled luminal epithelium reappeared at 34 hr, thereafter showing a rapidly declining LI. After initial depletion, the glandular cell population size was restored within 64 hr, whereas luminal epithelium cell numbers became stabilized at about half normal level. Grain counts after prelabelling showed more rapid dilution in gland cells of stripped uterine horns, indicating accelerated cycling of previously dividing cells. Thymidine labelling indices also showed that, after removal of the epithelium, almost all gland cells became rapidly committed to divide. On average, less than two cell cycles were necessary to restore stable glandular and epithelial population sizes. Numbers of labelled cells were also drastically increased in myometrium and serosa of treated horns. This suggests a non-specific mechanism for stimulation of mitotic activity after ablation of epithelium.

Animals↗
PubMed1981

Transmitter role of the luminal uterine epithelium in the induction of decidualization in rats.

Ovariectomized rats were given hormonal treatment mimicking progestational ovarian secretions. At maximal uterine sensitivity, the luminal epithelium was squeezed out of one or both horn(s) transected at the isthmus. Simultaneous bilateral scratching and saline injection induced virtually no response in stripped horns while contralateral intact horns exhibited a maximal decidual reaction (DCR). The luminal epithelium regenerated after ablation and a 65% DCR was again elicited after 9 days. The inability of de-epitheliated horns to decidualize was not overcome by intraluminal injections of the supernatant or sediment of the 60 000 g homogenate of epithelium, PGF-2 alpha, PGE-2, arachidonic acid or histamine. Detachment of the epithelium without removal also prevented DCR induction. These results indicate that the luminal epithelium is an obligatory transmitter of the stimulus to DCR and cannot be by-passed by trauma. Release of the appropriate epithelial message to the stroma requires local preservation of membrane relationships between both tissues.

Animals↗
PubMed1979

Oxytocin treatment in twin pregnancy labour.

A continuous series of 483 twin deliveries was studied. In 30% of cases, intravenous oxytocic treatment was given for labour induction or to accelerate the first stage. In 13% of twin deliveries this treatment was applied only after the first twin's birth. In the group perfused during cervix dilatation, foetal mortality rate was significantly lower than in the nontreated group. In order to understand the reason(s) for this difference, the following factors were studied in relation to oxytocic treatment: parity, obstetrical complications, second stage duration, abnormal presentations, obstetrical maneuvers, and birth weight. Contrasting with mortality data, Apgar scores of first twins were significantly lower in the oxytocin-treated group. In summary, several variables indirectly linked to oxytocic treatment could have favoured or hampered foetal outcome in the treated group. Therefore, it is difficult to ascertain if the use of oxytocics is helpful in twin pregnancy management. In the majority of cases, however, it may at least be considered harmless.

Apgar Score↗
PubMed1979

Effects of actinomycin D and estrogen priming on decidual growth in ovariectomized mice.

Ovariectomized mice were primed for 2 days with estradiol and/or actinomycin D. In order to evaluate the effects of these treatments on endometrial cell proliferation, colchicine and [3H]-thymidine were administered shortly before killing groups of animals at days 4 and 5 after priming (the latter groups received 500 micrograms progesterone plus 10 ng estradiol 24 h before killing). The same priming treatments were administered 3 days before starting hormonal treatment eliciting uterine sensitivity to decidualization (incuded by intrauterine oil injection). The comparison of labeling and mitotic indices and of decidual tissue weights between experimental groups showed that under such conditions: (1) actinomycin D only partly inhibits the effects of estrogen priming: the increase in cell division obtained on day 4 after priming remains unchanged in all three endometrial components while the increase in stromal mitotic activity at day 5 and further decidual growth are reduced, (2) since the inhibition rate of these parameters is greater in non-primed than in primed animals, it appears that estrogen priming counteracts the antagonistic action of actinomycin D.

Animals↗
PubMed1979

Effects of cycloheximide on the uterine refractory state induced by 'nidatory' oestrogen in rats.

After priming with oestradiol, ovariectomized rats were given 6 days of progesterone treatment in which two doses of 50 ng oestradiol were given on Days 3 and 6. This basic treatment allows the oestradiol-induced (1st injection) disappearance of uterine sensitivity to decidual stimuli to occur. Cycloheximide could not mimic oestrogen action in the production of the uterine refractory state. However, a high dose (500 micrograms per animal) of this inhibitor given with the first injection of oestradiol allowed the uterus to remain in a neutral state and to respond to decidual induction after the second dose of oestradiol. By delaying the injection of cycloheximide after the first oestrogen treatment, protein synthesis requisite to the occurrence of uterine refractoriness would not take place within 12 h after the 'nidatory' oestrogen injection.

Animals↗
PubMed1979

3'-deoxyadenosine and implantation of delayed blastocysts in mice.

Pregnant mice were ovariectomized 3 days after mating and pregnancy was maintained by progesterone treatment. Different regimens of intraperitoneal injections of 3'-deoxyadenosine were applied 3 days after ovariectomy. Repetition of the injections at 3 h intervals induced a significant rate of implantation by delayed blastocysts. Other types of treatment with 3-deoxyadenosine as well as adenosine injections were found to be ineffective. Paradoxically, 3'-deoxyadenosine treatment had an adverse effect on the overall pregnancy rate found at autopsy.

Animals↗
PubMed1977

Effects of uterine distension and oestradiol on cell kinetics in the endometrial epithelium of ovariectomized rats.

Cell kinetics in the uterine epithelium of ovariectomized rats were studied after uterine distension and/or an oestradiol injection, by cumulative 3H-TdR labelling and percentage of labelled mitoses (PLM). With both methods it was found that distension shortens the total cell cycle at the expense of G1 more than does oestradiol. Both treatments act in a cumulative manner since the greatest reduction in T c is observed after distension plus oestradiol. PLM curves showed that distension and/or oestradiol induce a 30% reduction S phase duration. The evolution of percentages of labelled cells and colchicine-blocked mitoses after these treatments confirms their additive effects and indicates that the mitogenic action of oestradiol is delayed compared to that of distension. It is suggested that these factors stimulate epithelial cell division in the uterus through partly different metabolic channels.

Animals↗
PubMed1976

Hormonal control of pinocytosis in the uterine epithelium of the rat.

Ovariectomized rats were treated with oestradiol-17 beta and/or progesterone to mimic the hormonal parameters inducing uterine sensitivity for implantation. The degree of pinocytosis of trypan blue and ferritin in the endometrial cells was examined. Significant epithelial pinocytosis of trypan blue occurred after a 3-day treatment of progesterone, and uptake was independently increased by priming with oestrogen and by oestradiol given on the 3rd day of progesterone treatment. Progesterone treatment caused uptake of ferritin by the epithelial cells; in control animals epithelial and stromal cells were involved. Oestrogen priming enhanced ferritin absorption, while 'nidatory' oestrogen had no effect. Oestradiol given alone completely blocked pinocytosis of both intraluminally injected substances.

Animals↗
PubMed1976

Inability of actinomycin D to act upon the uterine refractory state resulting from nidatory oestrogen action in rats.

After priming with oestradiol, ovariectomized rats were given 6 days of progesterone treatment in which two doses of 50 ng oestradiol were superimposed on days 3 and 6. This basic regimen allows the oestradiol-induced (1st injection) inhibition of uterine sensitivity to decidual stimuli to appear. Actinomycin D given instead of, or together with, the first dose of oestradiol could not mimic, or prevent oestrogen action in the occurrence of the uterine refractory state. This drug was unable to interfere with the minimal 48 h progesterone treatment which is requisite to uterine sensitization. Our results together with other data from the literature, suggest that luteal hormones do not need to act at the transcriptional level to sensitize and desensitize the uterus to implantation.

Animals↗