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D L Healy

Publications and source records attributed to D L Healy.

At least 127 records · Page 7Linked to original sources
PubMed1987

Mid-cavity occipitoanterior forceps delivery--Laufe and Barnes forceps compared.

Laufe forceps are divergent forceps designed to reduce compressive forces upon the fetal skull during delivery from the pelvic outlet. Here we have undertaken a retrospective matched analysis in which Laufe (N = 75) and Barnes (N = 75) forceps were used for occipitoanterior mid-cavity forceps delivery. Our aim was to compare fetal and maternal outcome following use of these 2 types of forceps in the mid-pelvis. Fetal morbidity, categorized by trauma, low Apgar score or jaundice, was present in 31 of 75 infants delivered by Laufe forceps and in 47 of 75 infants delivered by Barnes forceps (p less than 0.01). Overall, maternal morbidity was statistically similar between the 2 groups although perineal trauma was more frequent in the Laufe group (p less than 0.05). We concluded that there appeared to be an improved fetal outcome following occipitoanterior mid-cavity delivery using Laufe forceps compared with Barnes forceps. These initial findings imply that in situations of fetal compromise, where forceps delivery from an occipitoanterior position in the mid-cavity is indicated, that Laufe forceps might be chosen.

Apgar Score↗
PubMed1987

Circulating immunoreactive inhibin levels during the normal human menstrual cycle.

Serum inhibin concentrations were measured daily by RIA in six normal women throughout one menstrual cycle. The RIA was specific for inhibin, and inhibin subunits and related proteins cross-reacted minimally in it. In the early to midfollicular phase, inhibin levels changed little, while in the late follicular phase, inhibin levels rose, in parallel with estradiol (r = 0.43; P less than 0.05; n = 22), to a peak level of 714 (407-1267) U/L (geometric mean +/- 67% confidence limits) coincident with the midcycle LH and FSH surges. An inverse relationship was found between serum inhibin and FSH during the mid- to late follicular phase (r = 0.42; P less than 0.01; n = 45). Inhibin levels rose further during the luteal phase to a peak level of 1490 (1086-2028) U/L 7-8 days after the LH surge, and they correlated positively with serum progesterone (r = 0.76; P less than 0.001; n = 49) and inversely with serum FSH (r = 0.43; P less than 0.01; n = 49) throughout the luteal phase. We conclude that 1) circulating inhibin is detectable throughout the normal menstrual cycle; 2) in the late follicular phase, inhibin levels rise in parallel with estradiol, consistent with the concept that both are products of the maturing follicle; 3) in the luteal phase, the profile of inhibin suggests that it is a secretory product of the corpus luteum; and 4) the inverse relationship between inhibin and FSH in the follicular phase is consistent with the inhibin hypothesis, while at midcycle there is loss of the inhibitory effect of inhibin on FSH secretion. The inverse relationship between FSH and inhibin during the luteal phase suggests a hitherto unsuspected role for inhibin in the feedback regulation of FSH secretion.

Adult↗
PubMed1987

Corticotropin releasing hormone- and adreno-corticotropin-like immunoreactivity in human placenta, peripheral and uterine vein plasma.

The presence of corticotropin releasing hormone (CRH)-like immunoreactivity (IR) in human placenta and maternal peripheral blood has been reported by many investigators. However, its physiological role has not yet been defined. We investigated plasma and placental tissue from women at different times of pregnancy and performed peripheral and uterine vein sampling during caesarean section before and after removal of the placenta. Beside IR-CRH, IR-GRF and -GnRH as well as -ACTH and cortisol were measured. The highest content of CRH was found in placental extracts from end term (40 weeks) pregnancies and lower levels at an earlier stage (10 weeks). Plasma CRH from peripheral blood could be detected in some samples and was higher as pregnancy advanced. Thirty minutes after removal of the placenta CRH levels dropped in peripheral plasma and could not be detected in uterine vein samples. IR-ACTH plasma levels were within the range of normals, cortisol was elevated. Gel- and HPLC-chromatographie revealed that placental extracts coeluted with synthetic human CRH. The material from endterm placenta showed full bioactivity in the rat pituitary bio-assay. IR-GRF could only be detected in 10 weeks placental tissue and no IR-GnRH was measured. We conclude that CRH from the placenta is biologically active, however, cannot stimulate the maternal pituitary-adrenal-axis.

Adrenocorticotropic Hormone↗
PubMed1986

The human placenta: a novel source of inhibin.

Human placental extracts contain inhibin bioactivity and immunoactivity giving dose response curves parallel to a human follicular fluid inhibin standard. Inhibin bioactivity in vitro was neutralised by preincubation of extracts with antisera raised to pure bovine inhibin. Umbilical cord blood from term infants contained immunoactivity. Human placental inhibin differs from human ovarian inhibin in terms of its biological: immunological ratio.

Animals↗
PubMed1986

Plasma inhibin levels during gonadotropin-induced ovarian hyperstimulation for IVF: a new index of follicular function?

Human plasma inhibin was measured by radioimmunoassay in 26 women undergoing ovarian hyperstimulation for in-vitro fertilisation. Plasma inhibin rose in parallel with oestradiol during gonadotropin therapy (r = 0.79, p less than 0.001). Peak plasma inhibin levels correlated with follicle number as determined by ultrasonography (p less than 0.001) and with the number of oocytes recovered at laparoscopy (p less than 0.05). The increase in production of human ovarian inhibin by exogenous follicle stimulating hormone (FSH) is thus consistent with its proposed role in FSH regulation. Human plasma inhibin may be useful as a circulating protein marker of granulosa-cell function and may have therapeutic implications in human ovulation-induction programmes.

Chorionic Gonadotropin↗
PubMed1986

Morphologic response of endometrium to a progesterone receptor antagonist, RU486, in monkeys.

Fifteen castrate cynomolgus monkeys were assigned to one of two groups. All monkeys received estradiol (E2) capsules to mimic follicular phase E2 levels for development of a proliferative endometrium. In study I, three monkeys received RU486 on day 13 for 3 days; two others were given vehicle. On day 16, endometrium was removed. In study II, the remaining ten monkeys received progesterone capsules, beginning on day 12, to form a secretory endometrium. On day 29, six monkeys were given RU486 and four acted as controls. Endometrium was removed after 6, 18, and 32 hours. All tissue samples were prepared for light-microscopic evaluation. The results indicated that exogenous E2 alone stimulated intracellular stromal development; RU486 had weak progestational effect on proliferative endometrium, as evidenced by increase in the area occupied by glands; and RU486 had strong antiprogestational activity on secretory endometrium, illustrated by regression in the upper endometrial zones within 32 hours after a single injection of RU486.

Animals↗
PubMed1986

The stimulation of prostaglandin production by two antiprogesterone steroids in human endometrial cells.

Endometrial stromal cells and isolated endometrial glands obtained from women during days 6-26 of the ovarian cycle were cultured for 24 h in the presence of the progesterone antagonists 17 beta-hydroxy-11 beta-[4-dimethylaminophenyl]17 alpha-[1-propynyl] estra-4,9-dien-3-one (RU486) and 17 beta-hydroxy-11 beta-[4-dimethylaminophenyl] 17 alpha-[3-hydroxy-1-propenyl]estra-4,9-dien-3-one (ZK 98734). Both steroids stimulated prostaglandin F2 alpha (PGF2 alpha) production by stromal cells in a dose-dependent manner, in doses ranging from 10-1000 nM. Progesterone (100 nM) inhibited RU486 stimulation, except at the highest dose of antiprogestin. PGE2 was produced in smaller amounts than PGF2 alpha, but, when measurable, it also increased in the presence of RU486. In contrast, RU486 did not increase PG production by endometrial glands. In an experiment to determine the effect of pretreatment, stromal cells were incubated for 24 h with 1000 nM progesterone or RU486 (all with 100 nM 17 beta-estradiol) with either 30 or 6 microM arachidonic acid. These six batches of cells were incubated for a second 24 h with either progesterone or antiprogestin. Cells pretreated with the higher dose of arachidonic acid had a marked increase in PGF2 alpha production during the second 24 h only when also pretreated with progesterone. This finding suggests that progesterone allows an accumulation of PG precursor in a suitable accessible pool. Pretreatment with progesterone also allowed a greater conversion of PG to its 13,14-dihydro-15-keto metabolite. These results suggest that antiprogesterone steroids may act as menstrual regulators by: stimulating endogenous PG production within the endometrial stromal cells and inhibiting PG catabolism.

Dinoprost↗
PubMed1986

Toward removing uterine fibroids without surgery: subcutaneous infusion of a luteinizing hormone-releasing hormone agonist commencing in the luteal phase.

Intermittent sc injection of a LHRH agonist reduced uterine fibroid size in 5 women. Commencement of the LHRH agonist buserelin on day 21 of the menstrual cycle induced a marked increase in plasma LH and FSH concentrations, followed by rises in estradiol (E2) and progesterone. LH and FSH levels fell to within the normal range by 120 h after beginning buserelin, despite continuing administration of the agonist. After menstruation, marked sustained suppression of cyclical gonadotropin and steroid concentrations occurred: mean values of FSH, LH, and E2 were 4.9 +/- 0.5 (+/- SE) mIU/ml, 5.9 +/- 0.6 mIU/ml, and 47.9 +/- 10.8 pg/ml, respectively, during the 20 weeks of buserelin treatment. During treatment, E2 concentrations remained below 50 pg/ml in 98 of 116 weekly observations. Uterine fibroids shrank after 8 or 10 weeks of buserelin administration, as assessed by ultrasound or gynecological examination. Compared to their initial volume, mean uterine fibroid volume after 20 weeks of buserelin infusion decreased from 220 +/- 51 to 98 +/- 26 cm3, which was 39.4 +/- 6.9% of the pretreatment volume. We conclude that sc administration of a LHRH agonist beginning in the luteal phase markedly reduced the size of uterine leiomyomata, suppressed, but did not abolish, pituitary and ovarian function, and warrants further evaluation as an option or adjunctive therapy to uterine myomectomy or hysterectomy.

Adult↗
PubMed1986

An analysis of plasma estradiol concentrations during clomiphene citrate-human menopausal gonadotropin stimulation in an in vitro fertilization-embryo transfer program.

We report here a range of plasma estradiol (E2) concentrations suitable for use in an in vitro fertilization (IVF) program. This range was derived from nonparametric analysis of plasma E2 levels using plasma E2 measurements beginning 10 days before the anticipated day of the midcycle LH surge (midpoint), as calculated from each patient's six previous menstrual cycles, during which time the patients all received the same ovarian stimulation regimen. The regimen consisted of 100 mg clomiphene citrate/day for 5 days, beginning 10 days before the anticipated midpoint, plus 150 IU human menopausal gonadotropin, commencing the day after clomiphene. A consecutive series of 102 IVF conception cycles induced in this standardized fashion were analyzed in this study. The 5th-95 percentile envelope of plasma E2 concentrations was derived as a valid clinical indicator of satisfactory folliculogenesis during IVF treatment. Five women had plasma E2 concentrations below the 5th percentile of the E2 range on at least 3 consecutive days of ovarian stimulation, while six women had E2 levels above the 95th percentile of this range on at least 3 consecutive days. This plasma E2 range defined objectively the diagnoses of ovarian hyperstimulation and inadequate stimulation in an IVF program. These criteria should help clinicians in managing ovarian responses during IVF superovulation stimulation treatment.

Clomiphene↗
PubMed1986

Clinical aspects of LHRH analogues in gynaecology: a review.

LHRH agonists are synthetic peptide analogues of hypothalamic luteinizing hormone releasing hormone (LHRH) with superior potency and longer duration of gonadotrophin release. Paradoxically, repeated administration causes pituitary desensitization with diminished gonadotrophin and oestradiol secretion. A state of hypogonadotrophic hypogonadism is reversibly induced; plasma oestrogen can be reduced to castrate levels. LHRH agonists reliably induce anovulation but are unlikely to replace existing contraceptive methods in most normal women. By contrast these agents offer, for the first time, the prospect of inducing a reversible pseudomenopause essentially free of side-effects. LHRH analogues promise to have a profound impact upon the management of a diverse range of oestrogen-dependent gynaecological diseases both benign and malignant. In particular, they may shortly become the gynaecological treatment of choice in endometriosis, as well as becoming part of the management of common gynaecological disorders such as dysfunctional uterine bleeding and uterine fibroids.

Adolescent↗
PubMed1985

Survey of obstetric forceps training in North America in 1981.

In April, 1983, a questionnaire was sent to all 144 United States and Canadian members of the Association of Professors of Gynecology and Obstetrics to survey residency training and current use of obstetric forceps in 1981. One hundred five programs (73%), responsible for at least 283,000 births in 1981, were subsequently analyzed. All training programs used outlet forceps and all programs but one used midforceps for delivery. Hospitals with high cesarean birth rates did not perform significantly fewer midforceps operations. Hospitals with high midforceps rates did not also have high outlet forceps rates nor did these high rates closely reflect the personal attitude to obstetric forceps of the director of the obstetric training program. Simpson's forceps were most commonly used for outlet forceps and occipitoanterior midforceps operations, whereas Kielland's forceps were selected by 76% of programs for rotational midcavity deliveries. Staff obstetricians were the primary instructors of forceps technique in the delivery room in only 50% of United States programs; all Canadian respondents reported the staff obstetrician as the principal educator in obstetric residency forceps training.

Attitude of Health Personnel↗
PubMed1985

Thymic regulation of primate fetal ovarian-adrenal differentiation.

We report that fetal thymectomy inhibits oogenesis and induces abnormal ovarian differentiation in rhesus monkeys. In utero thymectomy (n = 5) elevated plasma follicle-stimulating hormone (7.8 +/- 1.1 microgram/ml vs. 4.2 +/- 0.5 microgram/ml; P less than 0.05) and decreased plasma prolactin (24.5 +/- 3.3 ng/ml vs. 76.3 +/- 11.2 ng/ml; P less than 0.05) concentrations compared with intact controls (n = 12), but did not change plasma luteinizing hormone, estradiol, cortisol, dehydroepiandrosterone sulfate, or thymosin-alpha 1 concentrations. In utero thymectomy reduced the weight of neonatal ovaries and adrenal glands, but not hepatic, renal, splenic, or total body weights. After fetal thymectomy, newborn ovaries (n = 8) contained a reduced total number of germ cells (123,926 +/- 11,651 vs. 432,034 +/- 40,311; P less than 0.001). The percentages of individual germ cell types were similar between thymectomized and intact groups (n = 11) except for an increased percentage of preantral-antral follicles in the thymectomy group (P less than 0.01). Our results indicate that the primate fetal thymus regulates antenatal ovarian follicular development, perhaps by interactions between the nascent immunologic and pituitary-ovarian systems.

Adrenal Glands↗
PubMed1985

Chronic polyhydramnios is a syndrome with a lactogen receptor defect in the chorion laeve.

Human chorion laeve contains a lactogenic hormone [prolactin (PRL), growth hormone (GH) and placental lactogen (hPL)] receptor. Here, we studied binding of the potent lactogen, human GH, to this receptor in 18 normal pregnant women, in 12 patients whose pregnancies were complicated by chronic polyhydramnios and in 13 with chronic oligohydramnios. Polyhydramnios was classified clinically as idiopathic in seven patients, and secondary and associated with various disorders in the remaining five patients. Lactogenic hormone binding was lower in association with polyhydramnios (mean 1.60, SEM 0.15%) than with normal amniotic fluid volume (mean 3.05, SEM 0.40%; P less than 0.05); Scatchard analysis indicated that a reduced number of lactogen receptors within the chorion laeve was the reason. The lactogenic hormone receptor defect in the chorion laeve was present in pregnancies complicated by either idiopathic or secondary polyhydramnios. In contrast to chronic polyhydramnios, tissue from patients with chronic oligohydramnios bound lactogenic ligands in a normal fashion. Insulin binding sites were also identified in the chorion laeve, and, in contrast to the lactogens, binding parameters were equivalent in the three patient groups. PRL resistance developing subsequent to this chorion laeve receptor defect might produce the excessive amniotic fluid volume characteristic of polyhydramnios. We propose that a chorionic PRL receptor deficiency underlies the various clinical forms of chronic polyhydramnios.

Amniotic Fluid↗
PubMed1985

Increased adrenocorticotropin, cortisol, and arginine vasopressin secretion in primates after the antiglucocorticoid steroid RU 486: dose response relationships.

The antiglucocorticoid steroid, RU 486, elevated plasma ACTH concentrations when administered im at 0700 h in a dose of 1.0 mg/kg in nonhuman primates (Macaca fascicularis; P less than 0.05). The duration, but not the magnitude, of this response increased after 5.0 mg/kg RU 486 im; release of ACTH did not rise further after 10 mg/kg. Peak ACTH elevations occurred 1-2 h after RU 486 administration. Plasma cortisol concentrations peaked 4 h after RU 486 administration and the response was significant only after 5.0 mg/kg RU 486. Plasma arginine vasopressin (AVP) concentrations also increased after RU 486 but the increase occurred only after the 10.0 mg/kg dose (P less than 0.05). The AVP elevation was greatest 4 h after 10 mg/kg RU 486 and was abolished by dexamethasone pretreatment. We conclude that: 1) RU 486 elevates plasma ACTH, cortisol, and AVP concentrations in a manner which is both dose and time dependent, 2) ACTH release occurred at an order of magnitude lower dose than did AVP release, and 3) plasma AVP changes after RU 486 are glucocorticoid dependent.

Adrenocorticotropic Hormone↗