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J Brosens

Publications and source records attributed to J Brosens.

4 recordsLinked to original sources
PubMed2003

Cyclic AMP and progesterone receptor cross-talk in human endometrium: a decidualizing affair.

During the menstrual cycle, the ovarian hormones oestradiol and progesterone control the ordered growth and differentiation of uterine cells. This remodelling process is critical for implantation of the developing embryo, the formation of the placenta, and maintenance of pregnancy. Failure of uterine tIssues to respond appropriately to ovarian hormone signalling results in defective placentation, associated with a spectrum of pregnancy disorders such as recurrent miscarriages and preeclampsia. These obstetrical disorders are a major cause of maternal and perinatal morbidity and mortality. Progesterone exerts its action on target cells, at least in part, through binding to the progesterone receptor (PR), a member of the steroid/thyroid hormone receptor superfamily of ligand-activated transcription factors. The mechanism by which progesterone controls the differentiation of human endometrial stromal cells, a process termed decidualization, in the secretory phase of the menstrual cycle is not well understood. Emerging evidence indicates that locally expressed factors and activation of the cAMP second messenger pathway integrate hormonal inputs and confer cellular specificity to progesterone action through the induction of diverse transcription factors capable of modulating PR function.

Cell Differentiation↗
PubMed2000

Regulation of platelet aggregation and adenosine triphosphate release in vitro by 17beta-estradiol and medroxyprogesterone acetate in postmenopausal women.

Clinical studies have suggested that hormone replacement therapy (HRT) may reduce the risk of coronary heart disease in postmenopausal women. Although progestins are commonly added to HRT preparations for uteroprotection, the perceived beneficial cardiovascular effects of HRT are thought to be mediated predominantly by the estrogen component. Platelets play a critical role in the pathogenesis of atherosclerosis and cardiovascular disease and, hence, it is possible that the cardiovascular effects of estrogens are mediated, at least in part, through inhibition of illicit platelet activation. The aim of this study was to examine the effects of sex steroids on adenosine diphosphate (ADP)-induced platelet aggregation and adenosine triphosphate (ATP) release in vitro in postmenopausal women. In addition, the effects of antiestrogens 14-hydroxy tamoxifen (4-OHT) and ICI 182780] and antiprogestins (RU 486 and ZK 98299) were also investigated. Preincubation of platelet-rich plasma (PRP) with antiestrogens or antiprogestins did not alter subsequent platelet aggregation or ATP release in response to ADP. However, preincubation with 17beta-estradiol (E2) significantly inhibited ADP-mediated platelet aggregation by a mean (+/-SEM) of 37%+/-6% (p = 0.02) and ATP release by 82%+/-6% (p = 0.03), an effect that was reversed by the addition of ICI 182780 or 4-OHT but not RU 486 and ZK 98299. Although the progestin medroxyprogesterone acetate (MPA) also significantly inhibited platelet aggregation (by 28%+/-5%, p = 0.02) and ATP release (by 63%+/-9%, p = 0.02), this inhibition was not reversed by the addition of antiprogestins or antiestrogens. These data show that sex steroids can modulate platelet function in vitro. Furthermore, as platelets are devoid of nuclear components, these findings indicate that estrogens may regulate platelet function through binding to a non-nuclear receptor with ligand-binding properties similar or identical to the wild-type receptor. By contrast, MPA appears to exert its effect through a mechanism that does not involve binding to the "classical" progesterone receptor.

Adenosine Triphosphate↗
PubMed1991

Conservative laparoscopic treatment of ectopic pregnancies using the CO2-laser.

OBJECTIVE: To assess the feasibility of CO2-laser-endoscopic surgical treatment for large and/or ruptured ectopic pregnancies, and to compare the results with those of microsurgical salpingotomy. DESIGN: A retrospective review of all women treated for an ectopic pregnancy during a 6-year period, 1984-1989. During 1988 and 1989 treatment was randomized by the day of admission, depending only upon the surgeon in charge, some performing a linear salpingotomy (n = 42) and some a CO2-laser laparoscopy (n = 34) in all women haemodynamically stable. SETTING: Department of Obstetrics and Gynaecology, University Hospital Gasthuisberg, Leuven. SUBJECTS: 135 women with ectopic pregnancies of whom 76 were included in the randomized series between 1988 and 1989. Overall 11 were treated by pelvic lavage, 78 by laparotomy and 46 by laparoscopic procedures. MAIN OUTCOME MEASURES: Postoperative complications, duration of hospital stay. Cumulative pregnancy rates after the procedures. RESULTS: The two groups of women analysed in the randomized series were comparable for duration of amenorrhoea, diameter of the ectopic pregnancy and prevalence of 'ruptured' ectopics, but the duration of stay in hospital was much shorter (mean 2.9, SD 1.8 days) for the 34 women treated by laparoscopy than for the 42 women treated by laparotomy (mean 6.8, SD 1.6 days). The postoperative cumulative pregnancy rate was higher in nulliparous women with a history of infertility or pelvic inflammatory disease (PID), when treated with CO2-laser-laparoscopy (P = 0.009). The recurrency rate was low (less than 5% in both groups). Overall in the women treated by laparotomy, postoperative cumulative pregnancy rates were lower following excision or adnexectomy than after a microsurgical linear salpingotomy (P = 0.01). Four women treated by laparoscopy required a second procedure. CONCLUSION: Endoscopic treatment of large and/or ruptured ectopic pregnancies is feasible and resulted in a shorter hospital stay and, in nulliparous women with a history of PID or infertility, in higher cumulative pregnancy rates, than after microsurgical salpingotomies.

Endoscopy↗