OBJECTIVE: To determine the impact of shortened postpartum hospital stays on common clinical phenomena in a sociodemographically diverse, unselected group of general maternity patients. DESIGN: Observational cohort study in which the preapproved hospital stay duration of either 1 or 2 nights was set by third-party payers before each mother's admission. SETTING: Yale-New Haven Hospital, New Haven, Conn, from June 19 through August 10, 1995. PATIENTS: Two hundred forty-four volunteers from among 400 eligible deliveries. MAIN OUTCOME MEASURES: Readmission within 1 month of hospital discharge, report of outpatient morbidity and use of outpatient health services within 1 week of discharge, status of breast-feeding during the first post-discharge week, and patient satisfaction. RESULTS: At discharge from the hospital, the hospital stay was regarded as "too short" by 80 (47%) of 171 mothers and 19 (26%) of 73 mothers in the 1- and 2-night groups, respectively (P = .002). Although readmission rates were similar (5% vs 3%, P = .48), the 1-night group reported significantly more morbidity in the newborns (31% vs 16%, P = .03) and averaged more pediatric visits (96 vs 54 per 100 newborns, P = .002). Mothers in the 1-night group also reported more fatigue (49% vs 29%, P = .001) and more worries about their newborns' health (24% vs 11%, P = .02). They were less likely to start breast-feeding (64% vs 77%, P = .06), and, if they started, were somewhat more likely to stop prematurely (14% vs 8%, P = .43). A series of disturbing events was reported only in the 1-night group. CONCLUSIONS: In a relatively unselected group, mothers who stayed 1 night after routine vaginal delivery reported more distress and more pediatric problems and had greater use of outpatient health services than mothers who stayed 2 nights.

Adolescent↗

PubMedDate not supplied

The effects of oestrogen on hypothalamic tissue.

Oestrogens exert potent influences on hypothalamic differentiation and on sexual function throughout life. During the period in which the hypothalamus differentiates, the availability of oestrogens (or aromatizable androgens) to the hypothalamus results in a male pattern of gonadotropin secretion and in male sexual behaviour in the adult. Lack of oestrogens during this period results in a cyclic schedule of gonadotropin secretion and in female sexual behaviour. Oestrogens or their metabolites determine future sex-specific activity by facilitating synapse formation in developing target circuits. The onset of puberty may also in part reflect oestrogen-stimulated synapse formation in the hypothalamus. In contrast, oestrogen given to an adult female rat causes specific multifocal lesions in the lateral arcuate nucleus. Such animals exhibit persistent oestrus and small multicystic ovaries. Since the same anovulatory syndrome can be produced by mechanical disruption of neuronal pathways from more anterior regions to the arcuate nucleus, it would appear that oestrogen could effect a 'disconnection' of the circuit responsible for cyclic drive of gonadotropin secretion. Furthermore, old female rats spontaneously exhibit the same type of reproductive derangement as well as the arcuate lesion. Thus direct effects of oestrogens on neuronal circuitry within the hypothalamus may be responsible for (1) sexual differentiation, (2) the onset of puberty and sexual activity, and (3) cessation of reproductive function in the female rat.

Animals↗

PubMedDate not supplied

Concentration of [16 alpha-125I]iodoestradiol in human ovarian tumors in vivo and correlation with estrogen receptor content.

The gamma emitting estrogen [16 alpha-125I]iodoestradiol was administered to 11 patients with ovarian cancer and 1 patient with endometrial cancer. At specific times after the administration of the tracer, portions of the tumor and of control tissues, fat and muscle, were removed and counted. The amount of radioactivity in these tissues was compared to the cytosolic estrogen receptor content of the tumor, measured by Sephadex LH-20 gel filtration, in biopsy specimens taken before the injection of the tracer. There was a strong correlation (p less than 0.005) between the estrogen receptor concentration in the biopsied tumor and the amount of radioactivity in the tumor. There was no correlation between the isotope in the muscle and the tumor receptor, nor between the radioactivity in the tumor and that in fat or muscle. As would be expected for a steroid receptor mediated process, the bulk of the total tissue radioactivity was present in the nuclear compartment of the tumors. This pattern was not observed in the muscle. Furthermore, the nuclear radioactivity in the tumors was positively correlated with the cytosolic estrogen receptor content. These experiments demonstrate that under in vivo conditions this gamma emitting estrogen is concentrated in tumors in a manner that is dependent upon the estrogen receptor. It was also found that the concentrations of radioactivity in the blood were high, producing low tumor to blood ratios. The blood level of isotope was not due to the presence of the unmetabolized steroid, which disappeared from blood rapidly, but was caused by circulating metabolites of the injected steroid. Since the concentration of the isotope in the tumor was dependent upon the estrogen receptor level, it would appear from these experiments that it is theoretically possible to use such compounds to image and monitor tumors that contain estrogen receptors. However, rapid metabolism would seem to preclude the use of 16 alpha-iodoestradiol itself for this purpose. These studies point to the possibility that the synthesis of analogs of 16 alpha-iodoestradiol, sterically protected against inactivation by rapid metabolism, may lead to a radiopharmaceutical agent that would be useful for imaging and monitoring estrogen receptor containing tumors.

Adult↗

PubMedDate not supplied

Aromatase activity in human ovarian cancer.

Eighty-four tumor samples from 70 women with primary ovarian cancer were assayed for cytosol estrogen (ERc) and progestin (PRc) receptor concentrations and aromatase activity. In addition, 22 of the tumors were studied for their response to the aromatase inhibitor, 4-OH-androstenedione, in a soft agar clonogenic cell assay system. Although aromatase activity was detected in almost all of the primary tumors, this enzyme was barely detectable in the majority of metastatic tumor samples. There was no significant correlation between aromatase activity and either the ERc or PRc content of the tumors, or tumor grade. Of 12 tumors grown successfully in the soft agar culture system, only 1 showed a substantial (greater than 50%) reduction in colony-forming efficiency after exposure to the aromatase inhibitor. These results suggest that local estrogen biosynthesis probably does not play an important role in the majority of epithelial ovarian tumors. However, there may be a small subset of estrogen receptor-positive tumors in which aromatase could provide a local growth stimulus.

Androstenedione↗

PubMedDate not supplied

Estrogen formation in the mammalian brain: possible role of aromatase in sexual differentiation of the hippocampus and neocortex.

Recent studies suggest that sex differences in cognitive function may involve effects of circulating androgens on the developing cerebral cortex and hippocampus. The mechanism of these effects is not understood. In rhesus monkeys, aromatase activity is present in the hippocampus and several areas of the cerebral cortex during late fetal and early postnatal life. Similarly, work in rats and mice indicates that the hippocampus and cerebral cortex may be capable of estrogen biosynthesis during early development. These results are consistent with the hypothesis that the actions of androgens on the developing cerebral cortex and hippocampus may involve local estrogen-mediated effects similar to those responsible for differentiation of the hypothalamic mechanisms controlling reproductive function.

Animals↗

PubMedDate not supplied

Characterization of angiotensin II receptors in the rat fetus.

The presence of AII receptors during early and late embryonic development was studied by binding of 125I[Sar1, Ile8] AII to whole mouse blastocysts and membrane-rich fractions from rat conceptuses, 7 to 21 days in gestation. In early mouse embryos there was no detectable binding under a variety of experimental conditions. However, in late gestation rat fetuses, specific and high affinity binding was observed, with a concentration of sites similar in membranes from whole and eviscerated fetuses. Using less than 100 micrograms of membrane protein, binding was time and temperature dependent, maintaining equilibrium from 30 to 120 min at 23 degrees C and it was enhanced by addition of Mg+2 up to 5 mM, EGTA 2 mM and dithiothreitol up to 2.5 mM. Scatchard analysis of the binding data indicated Kd values ranging between 0.7 and 0.9 nM. Binding was first detectable at day 10 (14.3 +/- 2.3 fmol/mg), increasing to 104 +/- 16, 2,625 +/- 168, 5,993 +/- 152 and 5,902 +/- 92 by days 12, 15, 18, and 21 of gestational age, respectively. Since the functional significance of these binding sites depends on the availability of the agonist ligand, acid extracts from eviscerated 10-day-old fetuses were analyzed for the presence of AII. Measurement of AII by radioimmunoassay revealed immunoreactive AII-like material (845 pg/g of tissue), with an elution pattern identical to that of AII standard in a Sephadex G-50 column. This material was bioactive, as demonstrated by its ability to displace 125I[Sar1, Ile8]AII from adrenal glomerulosa membranes, an effect which was abolished by pretreatment of the extract with AII antibody.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMedDate not supplied

New insights into estrogen action on the brain.

Explore the source record for details and available documents.

Animals↗

PubMedDate not supplied

Estrogen, synaptic plasticity and hypothalamic reproductive aging.

Unlike primates who undergo ovarian failure and loss of sex steroids at the end of reproduction, aging rodents undergo constant vaginal estrus followed by constant diestrus and finally anestrus, which indicates the absence of responsive ovarian follicles. The latter state is analogous to menopause in women. The timing of the appearance of constant estrus is determined by many factors including estrogen exposure in the brain during development and the number of times that the animal gets pregnant. The chief site of this reproductive aging in rat brains is the arcuate nucleus of the hypothalamus. The transition from normal cycles to constant estrus parallels the females' gradually decreased ability to respond to administered estradiol with a cycle of inhibition followed by disinhibition of gonadotrophin-releasing hormone. Evidence has accumulated indicating this to be due to a loss of the rat's ability to respond to markedly elevated estradiol with the usual arcuate nucleus neuro-glial plasticity that supports the estrogen-induced gonadotrophin surge (EIGS). Just as male rats are not capable of an EIGS, aged females loose this ability through repeated EIGS. Experiments indicate that in male rats the hypothalamic synaptology that develops as a result of exposure to testicular androgens in the perinatal period (brain sexual differentiation) is a result of conversion of testosterone from the testes to estrogen in the brain and is therefore due to early estrogen exposure. Aging females appear to reach a synaptology similar to males and constant estrus as a result of repeated exposure to ovarian estrogens during their reproductive careers. The relative role of aging and hormonal factors remains unclear. Morphological evidence is presented that indicates the above effects of estrogen involve changes in hypothalamic arcuate nucleus neurons and glia, including changes in the organization of perikaryal membranes as well as arcuate nucleus synaptology and the load of peroxidase in the astroglia. A possible role for free radicals (reactive oxygen species) in hypothalamic reproductive aging has been proposed. Such a mechanism is supported by evidence that the anti-oxidant vitamin E delays the onset of constant estrus and the accumulation of glial peroxidase in aging female rats. However, since the synaptology and peroxidase load in constant estrus females is independent of the age at which the constant estrus occurs, it appears that the role of (repeated) estradiol exposure is more deterministic of hypothalamic failure than is aging, per se.

Aging↗