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Biomedical subjects

J S Winter

Publications and source records attributed to J S Winter.

At least 73 records · Page 4Linked to original sources
PubMed1980

Cortisol, 11-desoxycortisol, and 21-desoxycortisol concentrations in amniotic fluid during normal pregnancy.

Concentrations of unconjugated cortisol, 11-desoxycortisol, and 21-desoxycortisol were measured by radioimmunoassay in amniotic fluid throughout gestation. Cortisol levels rose from a median of 6.5 nanograms per milliliter prior to 20 weeks to 13.9 ng/ml at 28 to 37 weeks. Median levels of 11-desoxycortisol and 21-desoxycortisol were 2.6 ng/ml and 0.21 ng/ml, respectively, and did not change with advancing gestation. These normal values provide a basis for the application of assays of 11-desoxycortisol and 21-desoxycortisol in amniotic fluid in the prenatal diagnosis of congenital adrenal hyperplasia.

17-Hydroxycorticosteroids↗
PubMed1980

Familial pseudohypoparathyroidism without somatic anomalies.

A family is described in which affected individuals showed pseudohypoparathyroidism, with hypocalcemia, hyperphosphatemia and increased serum levels of parathyroid hormone, but none of the somatic anomalies frequently associated with this disorder. The untreated individuals showed radiologic evidence of osteitis fibrosa. The administration of parathyroid hormone evoked only a slight increase in the excretion of cyclic adenosine monophosphate but no change in the renal tubular reabsorption of phosphate and no rise in the serum calcium level. The infusion of ethylenediamine tetra-acetic acid caused an appropriate increase in the serum level of parathyroid hormone, but again there was no apparent renal or skeletal response to the hormone. There were no associated abnormalities in calcitonin, thyrotropin or prolactin levels and no thyroid dysfunction. Therapy with vitamin D corrected the hypocalcemia but did not improve the renal and skeletal responsiveness to parathyroid hormone. The inheritance of the disorder in this family was compatible with an autosomal dominant mode with variable penetrance, but other modes could not be excluded.

Adolescent↗
PubMed1980

Adult-onset familial adrenal 21-hydroxylase deficiency.

Two sisters (28 and 30 years) were investigated for primary infertility and milk hirsutism. Both had normal puberty, were having regular menses and had normal female sexual characteristics. Studies revealed elevated urinary 17-ketosteroid levels (15.8, 18.8 mg/24 hours) and increased serum levels of 17-OH-progesterone (2,756, 1,121 ng/dl), 21-desoxycortisol (1,882, 1,090 ng/dl), progesterone (300, 346 ng/dl), dehydroepiandrosterone (DHA) (1,600, 1,700 ng/dl), and androstenedione (402, 366 ng/dl) and testosterone (100, 104 ng/dl), together with a slight increase in serum 11-desoxycortisol (1,180, 1,560 ng/dl). Blood pressure, serum sodium/potassium plasma renin and serum aldosterone, corticosterone, 11-desoxycorticosterone and cortisol levels were normal. The administration of ACTH caused a further increase in 21-hydroxylase precursors; the administration of dexamethasone normalized hormone levels and produced ovulatory cycles. Similar studies in two siblings were normal. The affected sisters were HLA identical and did not share any HLA antigens with their healthy siblings. The data suggest that these patients have a mild form of 21-hydroxylase deficiency which was insufficient to cause prenatal virilization. The gene for this disorder may be allelic with that for typical congenital adrenal hyperplasia.

Adrenal Cortex Hormones↗
PubMed1980

Aldosterone and corticosterone in amniotic fluid during various stages of pregnancy.

Concentrations of unconjugated aldosterone and corticosterone were measured in amniotic fluid (AF) at different stages of pregnancy. AT 9-20 weeks gestation the mean AF level of aldosterone was 14.4+/0.7 ng/dl, and of corticosterone 82.9 +/- 6.4 ng/dl. Both showed the same pattern during pregnancy, with a rise in AF levels in the last few weeks. At 28-40 weeks gestation the mean AF aldosterone level was 25.5 +/- 2.0 ng/dl and the mean AF corticosterone was 218.3 +/- 26.6 ng/dl.

Aldosterone↗
PubMed1980

Developmental pattern of delta 5 3 beta-hydroxysteroid dehydrogenase activity in isolated rat Leydig cells.

A direct method for determination of delta 5 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity was employed in isolated Leydig cells (LC) derived from rats on fetal day 19 (Fig) and postnatal (N) days 1, 12, 24, 34 and 45 and adults. The activity of 3 beta-HSD in the adult LC was 1.15 +/- 0.02 (mumole/microgram DNA/hr, mean +/- SEM, n = 73). Activities in the other groups, expressed as a percentage of the respective adult control, were: Fig-38%; N1-39%; N12-8%; N24-89%; N34-166%; and N45-118%. A good correlation was found between histochemical staining for 3 beta-HSD and the quantitive method employed. Using (3H)-DHA as a substrate, LC isolated from F19, N1 and N12 produced testosterone in appreciable amounts (41%, 55% and 20% of the total products respectively) whereas at advanced stages of development (N24 to adulthood) the major product was androstenedione (93 +/- 1%). These findings may be explained by the observed decrease in 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity, due to an insufficient supply of NADPH, in the older vs. earlier stages of development. This study indicates the presence of steroidogenic enzymatic activity in LC throughout development in the rat. It also provides a relatively simple in vitro model for studies of testicular regulation during development.

3-Hydroxysteroid Dehydrogenases↗
PubMed1980

Developmental pattern of testosterone production by the rat testis.

We studied the steroidogenic activity of isolated Leydig cells derived from rats on fetal day 19 (F19) and postnatal (N) days 1, 12, 24, 34, 45 and adults. Leydig cells, isolated at all ages by the collagenase method, increased in number throughout development with a doubling time of 8 days. Testicular content and serum concentrations of testosterone showed parallel changes during development. Moderate values were found at the early stages (F19 and N1), with a nadir on day 12, followed by a progressive increment to reach maximal values in adulthood. A reduction in steroidogenic activity of the testis during neonatal life was confirmed by in vitro studies with isolated Leydig cells. Maximal activity was found in group F19; testosterone production diminished after birth to reach a minimum in group N34 and rose thereafter to adulthood. Leydig cells were responsive to hCG stimulation at all ages in the following order: N1 greater than N34 greater than F19 greater than N24 greater than N45 greater than adult. The present study demonstrates the existence of an active and hCG-responsive population of Leydig cells in the rat testis from fetal life to adulthood.

Aging↗
PubMed1980

The outsider.

Explore the source record for details and available documents.

Emergency Service, Hospital↗
PubMed1979

The relationship of adrenal androgens to the secretory patterns for cortisol, prolactin, and growth hormone during early puberty.

Serum concentrations of dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHA-sulfate), cortisol, prolactin, and growth hormone were measured at half-hour intervals for 24 hr in five healthy children aged 8--13 yr. Their adolescent development was assessed by clinical staging, plus determinations of serum FSH, LH, testosterone and estradiol during both wakefulness and sleep. Correlative analysis indicates that there was synchronous secretion of DHA and cortisol, implying regulation of both by ACTH. With advancing age and sexual maturation, there was a progressive rise in mean serum DHA and DHA-sulfate levels, but no similar change in serum cortisol concentrations. There was evidence for enhanced secretion of both growth hormone and prolactin during sleep in all subjects (including one who was hyperprolactinemic), but there was no obvious relationship between levels of these pituitary hormones and the early pubertal rise in adrenal androgens.

Adolescent↗
PubMed1978

Hormonal changes in girls with precocious adrenarche: a possible role for estradiol or prolactin.

Serum concentrations of dehydroepiandrosterone, DHA sulfate, estradiol, and prolactin in 20 girls with precocious adrenarche were compared with those of healthy girls of varying age and degrees of breast and sex hair development. Production of adrenal androgens, as reflected by serum DHA and DHA-sulfate concentrations, was significantly increased in PA above that in age-matched control subjects. Surprisingly, in spite of their lack of breast growth, the patients with PA also had serum estradiol levels that were higher than in the prepubertal girls and similar to those found in girls with both breast and pubic hair development. Serum prolactin concentrations in the patients with PA were not increased over those of the age-matched (less than 8 years) prepubertal girls. In the older prepubertal ( greater than 8 years) and early pubertal girls serum prolactin levels were lower. The finding of increased estradiol levels suggests that precocious adrenarche is not a distinct endocrine entity, but merely represents a variant of early adolescence in which estrogen secretion is sufficient to influence adrenal 3beta-hydroxysteroid dehydrogenase activity with a resultant rise in DHA production, but not sufficient to produce clinically apparent breast changes. The data do not support a similar role for prolactin.

Adrenal Cortex↗