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Biomedical subjects

R E Oakey

Publications and source records attributed to R E Oakey.

At least 55 records · Page 3Linked to original sources
PubMed1979

Non-protein-bound oestrogens in plasma and urinary excretion of unconjugated oestrogens in men.

Unconjugated oestrone and unconjugated oestradiol-17 beta were measured in 24 h urine specimens from twenty normal men. The concentrations of non-protein-bound oestrone and non-protein-bound oestradiol-17 beta, in samples of blood obtained from these subjects during the time in which the urine was collected, were measured by equilibrium dialysis (using a correction for plasma dilution). The mean excretion of unconjugated oestrone (0.44+/- 0.36 nmol/24 h, mean +/- SD) was significantly greater (Pless than 0.01) than that of unconjugated oestradiol-17 beta (0.20 +/- 0.13 nmol/24 h). The concentrations of non-protein-bound oestrone and non-protein-bound oestradiol-17 beta in plasma were 5.52 +/- 2.69pmol/1 and 2.42 +/- 0.73 pmol/1, respectively. There was no correlation between the quantity of unconjugated oestrone excreted and the concentration of non-protein-bound oestrone in plasma (r=0.27) nor between the quantity of unconjugated oestradiol-17 beta in the urine and the concentration of non-protein-bound oestradiol-17 beta in plasma (r=0.05). Therefore in normal men, estimation of unconjugated oestrone or oestradiol-17 beta in urine provides no guide to the concentration of the corresponding non-protein-bound oestrogen in plasma.

Adult↗
PubMed1978

Comparisons of the concentrations of palmitate and cortisol in amniotic fluid for the prediction of pulmonary maturity.

The concentrations of palmitic acid, derived from lecithin, and of cortisol in samples of amniotic fluid collected during the last trimester of human pregnancy, ranged from 28 to 420 mumol/l and from 16 to 104 nmol/l, respectively. There was a weak (r = 0.43) but significant (p less than 0.01) correlation between the concentrations of cortisol and palmitate in the samples. Measurement of the cortisol concentration in amniotic fluid provided an unreliable index of pulmonary immaturity, whether this was assessed with reference to the concentration of palmitate or from subsequent development of the respiratory distress syndrome. Measurement of cortisol in amniotic fluid cannot be recommended for this purpose.

Amniotic Fluid↗
PubMed1976

Cortisol binding capacity and oestrogen concentrations in maternal and cord plasma in pregnancies with normal and anencephalic fetuses.

The cortisol binding capacity of maternal and cord plasma samples obtained at delivery from fifteen women and their normal infants and from seven women and their anencephalic infants was measured at 4 degrees C by a gel filtration technique. The concentration of oestrogen in these samples was measured by radioimmunoassay. There was no significant difference (t test) between the cortisol binding capacity of peripheral plasma from women with normal infants (1-55 +/- 0-24 mumol/1, mean +/- SD) and from those who delivered anencephalic infants (1-35 +/- 0-30 mumol/1), nor between the cortisol binding capacity of cord plasma from anencephalic infants (0-47 +/- 0-04 mumol/1) and that of normal infants (0-37 +/- 0-10 mumol/1). However, mean oestrogen concentrations in maternal and cord plasma from the pregnancies with an anencephalic fetus were significantly lower (P less than 0-01) than in the corresponding samples from normal pregnancy. It is concluded that oestrogen concentrations in maternal and cord plasma in normal pregnancy at delivery are much greater than those required to account for the increase in plasma cortisol binding capacity. Since plasma cortisol binding capacity in pregnancy with an anencephalic fetus is not diminished, the reduced excretion of corticosteroids relative to normal pregnancy in this condition is unlikely to be due to alterations in cortisol metabolism associated with a lower plasma cortisol binding capacity.

Anencephaly↗
PubMed1976

Differences in urinary excretion of steroid 21-deoxyketols by women pregnant with a normal or an anencephalic foetus.

During late pregnancy the urinary excretion of steroid 21-deoxyketols, which contain the CH3-CO-C(OH)less than side chain, was 1.16 +/- 0.50 mg/24 h (mean +/- SD n = 9). The mean excretion of these metabolites in 8 pregnancies with an anencephalic foetus showed a significant reduction (P less than 0.01, t-test) to 0.42 +/- 0.18 mg/24 h. Six untreated non-pregnant women and 7 taking oral contraceptives which contain oestrogen had steroid 21-deoxyketol excretions of 0.26 +/- 0.09 mg/24 h and 0.19 +/- 0.09 mg/24 h respectively. These results imply that the adrenal of the normal foetus makes a contribution to the secretion of those steroids which are ultimately excreted by the mother as 21-deoxyketols.

Anencephaly↗
PubMed1976

Control of oestrogen production in human pregnancy: effect of trophic hormones on steroid biosynthesis by the foetal adrenal gland in vitro.

[14C]Acetate was incorporated into dehydroepiandrosterone, pregnenolone and their sulphates and into cholesterol during incubations of adrenal tissue from three human foetuses of 10-18 weeks of gestation. No incorporation of [14C]acetate into cortisol or other 4-en-3-oxo steroids could be demonstrated. Porcine ACTH stimulated the incorporation of [14C]acetate into both dehydroepiandrosterone sulphate and cholesterol when added to incubations of adrenal tissue from foetuses of 18 weeks gestation. Such an effect was not observed with tissue from a 10-week-old foetus. Stimulation of steroid biosynthesis from [14C]acetate was also achieved by addition of human growth hormone chorionic somato-mammotrophin. These trophic hormones may therefore play some part in regulating the provision of precursors for oestrogen biosynthesis in pregnancy.

Adrenal Glands↗
PubMed1976

Corticosteroid production by the human foetus: evidence from analysis of urine from women pregnant with a normal or an anencephalic foetus.

The quantities of nine corticosteroids in 24 h urine samples collected by pregnant women (nine with normal foetuses and nine with anencephalic foetuses) were measured after hydrolysis with beta-glucuronidase and separation by paper chromatography. The excretion (mumol/24 h, mean +/- S.D.) of prenanetriol (0-85 +/- 0-17), 3 alpha, 17 alpha-dihydroxy-5 beta-pregnan-20-one (17 alpha-hydroxypregnanolone, 0-55 +/- 0-17), 3 alpha, 17 alpha, 21-trihydroxy-5 beta-pregnan-20-one (tetrahydro-11-deoxycortisol, 0-17 +/- 0-14) and tetrahydrocorticosterone (0-65 +/- 0-26) by women with an anencephalic foetus was significantly lower (P less than 0-01 or less than 0-05) than the excretion of these compounds by women with a normal foetus (pregnanetriol, 2-42 +/- 0-62; 17 alpha-hydroxypregnanolone, 2-72 +/- 0-69; tetrahydro-11-deoxycortisol, 0-56 +/- 0-37; tetrahydrocorticosterone, 1-95 +/- 0-94). These differences suggest that the adrenal of the normal foetus contributes to the quantity of pregnanetriol, 17alpha-hydroxypregnanolone, tetrahydro-11-deoxycortisol and tetrahydrocorticosterone in maternal urine. The excretion of tetrahydrocortisol, tetrahydrocortisone, tetrahydrodeoxycorticosterone, cortol and cortolone were similar in both groups of subjects. No evidence was obtained therefore to indicate the secretion of cortisol or deoxycorticosterone by the foetal zone of the adrenal of the undisturbed human foetus in late gestation.

Adrenal Cortex Hormones↗
PubMed1975

Serum cortisol binding capacity and cortisol concentration in the pregnant baboon and its fetus during gestation.

The cortisol binding capacity of serum from 11 pregnant baboons (38 samples) and from 7 baboon fetuses delivered prematurely or at term was measured after removal of endogenous steroids. Values for maternal serum collected between 60 and 120 days after mating (59.0 +/- 6.4 mug/100 ml, mean +/- SD) were greater than those for serum collected at term (42.3 +/- 4.9 mug/100 ml). The cortisol-binding capacity of fetal serum collected between 100 and 132 days' gestation was similar to that of the corresponding maternal sample, but at term was only 50% of the maternal value. The rate of clearance of cortisol from both fetal and maternal serum may therefore increase progressively during the last trimester of pregnancy. This effect is likely to be more marked in the fetus. The cortisol binding capacity of 15 serum samples from 9 non-pregnant baboons was 33.4 +/- 5.5 mug/100 ml. Mestranol2 (administered 200 mug/day im for 15 days) significantly increased the serum cortisol binding capacity. The concentration of cortisol in maternal serum from 7 pregnant baboons (10 samples) was 44.0 +/- 8.4 mug/100 ml and was independent of the state of gestation. In fetal serum the cortisol concentration was 4 mug/100 ml before 168 days' gestation and reached 49 mug/100 ml after normal delivery at term. These findings suggest that the mechanisms for production of cortisol by the fetus mature as gestation progresses. The physiological significance of the marked difference between the cortisol concentration and the cortisol binding capacity of fetal serum awaits elucidation.

Animals↗