The concentrations of hormones measured in serum from maternal blood change dramatically during pregnancy. While the relative contributions of sex steroids shift from maternal ovaries and adrenals to the fetoplacental unit, other maternal tissues such as pituitary and liver respond to increasing concentrations of estrogen and secrete increasing amounts of prolactin and sex-hormone-binding globulin. To determine longitudinal changes in circulating maternal hormones, we collected blood from 60 women on three occasions during their pregnancies. We observed a 1.7-fold increase in testosterone concentration in serum; concentrations of sex-hormone-binding globulin in serum rose 5.6-fold. The major increase (6.8-fold) in estradiol in serum occurred within the first 16 weeks, followed by a further 4.8-fold increase by term. Mean concentrations of progesterone, 17-hydroxyprogesterone, and androstenedione in serum increased 11.9-, 3-, and 1.3-fold, respectively, whereas concentrations of dehydroepiandrosterone sulfate (DHEAS) fell by 50%. Mean serum prolactin concentrations increased 3.8-fold during the first trimester and by a similar amount during the final 24 weeks of pregnancy. We used these data, obtained from a cohort of women with uncomplicated pregnancies, to construct reference intervals for hormones in maternal serum.

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The in vitro hepatic monodeiodination of L-thyroxine (T4) to triiodo-L-thyronine (T3) in rainbow trout (Salmo gairdneri) was found to be pH-and temperature-dependent, and was related to the amount of homogenate in the reaction vessel, suggestive of an enzyme-regulated event. Dithiothreitol (DTT) introduced into the reaction medium stimulated T3 production in a dose-related manner, whilst 6n-propyl-2-thiouracil (PTU) inhibited T3 production, also in a dose-related manner. The conversion was stimulated in the presence of light and depressed at buffer concentrations of less than 0.1 M.Prior treatment of fish with an intraperitoneal slow-release implant containing 17/3-estradiol (E2), at doses which are known to induce chronic mild elevations in plasma E2 levels, elicited a biphasic response to E2 as regards hepatic T3 production from T4 with a depression of T4 to T3 conversion evident within 1-2 days after implantation, and a subsequent stimulation of T3 production evident 56 days after implantation. This increased hepatic deiodinase activity after chronic exposure to E2 at physiological doses was accompanied by a 3.5 fold increase in Vmax without a significant change in Km, suggesting the presence of an increased amount of the enzyme.

Administration of 17P-oestradiol (E,) to rainbow trout, in the form of hydrogenated coconut oil implants produced a stable, long-term elevation in plasma E, levels. The elevation was doserelated (over the range I-lOmg kg-' body weight) both 4 and 8 weeks after implantation. Dose-related increases were also observed with respect to liver weight-body weight ratios and plasma protein levels. Plasma T, and total calcium levels were depressed and elevated, respectively, by E, treatment but the responses were not linearly related to the dose of E, administered;there was no significant effect of E, on plasma T, levels.E, induced a shift in the binding of T, to plasma proteins, with T3 binding to smaller molecular weight proteins; neither T, nor T, bound to vitellogenin which was present at high levels in the plasma of E,-treated fish.

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Three cases of hydrops fetalis presented in the second trimester as screen-positive for Down syndrome using multiple maternal serum markers. One case was a karyotypically normal female; one case was a monosomy X (Turner syndrome); and one case was a trisomy 21 (Down syndrome). In each case, the maternal serum human chorionic gonadotrophin (hCG) was disproportionately elevated. These cases support the contention that hydrops fetalis of any aetiology may present as screen-positive when using multiple maternal serum markers for Down syndrome. Further cases will be necessary before it can be determined whether a disproportionately elevated hCG is predictive of hydrops.

The present studies were conducted to evaluate the effects of excitatory amino acids (EAAs) on gonadotropin I1 (GtH 11) and growth hormone (GH) secretion in testosteroneprimed immature rainbow trout, Oncorhynchus mykiss. Intraperitoneal injections of N-methyl-DL-aspartate (NMA) elevated both plasma GtH I1 and GH levels. By comparison, Des Gly" [D-Ala6] LHRH-ethylamide (LHRH-A) elevated plasma GtH I1 levels but had no effect on plasma GH levels. The GtH I1 response to NMA was not evident in sexually regressing adult rainbow trout. GtH I1 secretion by perifused pituitary glands of testosterone-primed immature rainbow trout was elevated following NMA or salmon GnRH analogue (sGnRH-A) challenge. The GtH 11 response to NMA was eliminated in pituitaries previously exposed to either the NMA receptor antagonist, AP5, or a GnRH receptor antagonist (D-~G~u',D-P~~~,D-T~~~'~-LHRH), suggestingthat NMA operates by stimulating the secretion of GnRH rather than by direct actions on the pituitary gonadotropic cells. The results of these studies provide evidence of the presence of NMAspecific receptors in the hypothalamo-hypophyseal system that when activated led to the release of GtH 11. L-glutamic acid (GLU) also stimulated GtH I1 secretion from perifused pituitary glands. However, the response to GLU was only partly blocked byAP5, suggesting that GLU exerted some of its effect via non-NMA type receptors, in addition to its actions on NMA receptors. The results of these studies support the contention that EAA receptor activation may play a role in regulating the onset of sexual maturation in teleosts, as it seems to do in mammals.