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Abstract
Recently, inhibin-A has been shown to be a useful new prenatal marker of Down's syndrome, significantly increasing detection rates. While the placenta is believed to be the major source of inhibin in pregnancy, there are actually very limited data available on specific inhibin dimers in pregnancy. Using a sensitive and specific ELISA we have measured the inhibin-A content of amniotic fluid (AF) to investigate further the biology of inhibin-A in chromosomally normal and abnormal pregnancies. AF from 51 Down's syndrome and 161 chromosomally normal pregnancies between 16 and 19 weeks of gestation were analysed, blinded as to whether the sample was from a Down's syndrome or normal pregnancy. There were no sex differences in inhibin-A content in either the control or Down's syndrome pregnancies. The median (10th–90th percentiles) inhibin-A level in the control pregnancies increased from 339·6 (175·2–649·1) pg/ml at 16 weeks to 592·9 (256·4–1027·3) pg/ml at 19 weeks of gestation. The median (95% confidence interval) inhibin-A in the Down's syndrome pregnancies, expressed as multiples of the median (MoM) to correct for gestation, was 0·77 (0·68–0·89) MoM, significantly lower than the controls (P<0·001, Mann–Whitney U test).
We believe that these data are compatible with more than one source of inhibin-A in pregnancy and suggest that the fetal membranes may be contributing significantly to AF inhibin-A content. Further, our data would suggest that the endocrine function of the placenta and the other inhibin source(s) are differentially regulated.
Journal of Endocrinology (1997) 152, 109–112
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The aim of the study was to investigate maternal thyroid function in pregnancy by monitoring the circulating concentrations of thyroid stimulating hormone (TSH), free thyroxine (fT(4)) and human chorionic gonadotrophin (hCG) in multifetal pregnancies before and after embryo reduction. We studied two groups of women: group 1 comprised singleton (n=12) and twin (n=12) pregnancies achieved after superovulation and in vitro fertilisation and embryo transfer (IVF-ET), and group 2 were multifetal pregnancies (n=39) undergoing selective fetal reduction to twin pregnancies. Blood samples were obtained initially at 10-12 weeks gestation (before fetal reduction) and then 4 and 8 weeks afterwards. Before fetal reduction, the circulating concentrations of fT(4) in multifetal pregnancies were significantly greater than those in singleton or twin pregnancies (singleton, mean 16.49 pmol/l (interquartile range 14.09-18.13 pmol/l); twins, 15.84 (15.36-16.95 pmol/l); multifetal, 21.08 (16. 64-26.29 pmol/l); P<0.005 for singleton and twins), and in a multiple regression analysis, fT(4) was significantly related to the number of fetuses (F=23.739, P=0.0001), but not to hCG. After fetal reduction to twins, the circulating concentrations of fT(4) in multifetal pregnancies decreased progressively towards those in control twin pregnancies, but remained significantly greater at both 4 (P=0.003) and 8 weeks (P=0.050). This pattern of change in the concentrations of fT(4) is similar to, but lags behind, that of hCG, which attains twin levels 4 weeks after fetal reduction. This may represent a delayed thyroid response to the decreasing concentrations of hCG, but the alternative is that the maternal thyroid function is controlled by a fetal factor in addition to hCG.
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We investigated the cellular mechanisms responsible for the inability of 8-month-old previously malnourished (PM) females to adapt their beta-cell mass during pregnancy. The evolution during pregnancy of beta-cell fraction, size and proliferation was studied. At day 21 of pregnancy beta-cell fraction increased less in PM than in control females, compared with their non-pregnant values. A slight beta-cell hypertrophy was observed during pregnancy in both groups. In control females, beta-cell 5-bromo-2'-deoxyuridine (BrdU) labelling index (LI) increased from 0.07+/-0.04% before pregnancy to 1.13+/-0.20% at day 12 and decreased thereafter to reach again basal levels at day 21. In PM females, beta-cell proliferation rate was decreased at day 12 (0.74+/-0.15%, P<0.05) but similar to controls at all other stages studied. Separate analysis of the head and tail parts of the pancreas in control animals revealed that the beta-cell fraction during pregnancy increased more in the head than in the tail; similarly, BrdU LI increased 20-fold in the head and 10-fold in the tail, compared with non-pregnant values. In PM females, no adaptation of beta-cell fraction could be observed in the head, where BrdU LI was decreased by half at day 12 of pregnancy. In PM females the lactogenic activity was twice that of controls at day 12 whereas all beta-cells expressed the prolactin receptor. In conclusion, perinatal malnutrition impairs subsequent adaptation to pregnancy by decreasing beta-cell proliferation in the head of the pancreas at a critical time during pregnancy.
Department of Biological Sciences, Allergan Inc., Irvine, California, USA
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Department of Biological Sciences, Allergan Inc., Irvine, California, USA
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Department of Biological Sciences, Allergan Inc., Irvine, California, USA
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Department of Biological Sciences, Allergan Inc., Irvine, California, USA
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Department of Biological Sciences, Allergan Inc., Irvine, California, USA
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the stable thromboxane mimetic U46619 ( Abramovitz et al. 2000 ) in the mouse uterus taken during different reproductive stages of the oestrous cycle and during pregnancy. This work is part of a larger on-going project and is running concurrently
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ABSTRACT
Mammary tissue from goats had significantly higher aromatase activity at 148-149 days of pregnancy than earlier in pregnancy or during lactation. Aromatase activity was determined by production of 3H2O from [1 β–3H]androstenedione that was inhibited by 4–hydroxyandrostenedione. The time of maximum aromatization was during peak mammary output of oestradiol–17β described previously in vivo in the same species. Aromatase activity in the mouse mammary gland was low and no peak was observed in late pregnancy. It is concluded that the oestrogens produced by the mammary gland in the late–pregnant goat are formed by aromatization of androgens.
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SUMMARY
1. Aminoguanidine sulphate can inhibit in vitro the histaminase of rat placental extracts; given subcutaneously, it can also inhibit in vivo the placental and uterine histaminase of pregnant rats.
2. Aminoguanidine sulphate given subcutaneously to pregnant rats in doses producing more than about 50% inhibition of the maternal placental histaminase leads to a general disturbance of the course of pregnancy. The foetuses are more sensitive than the mother.
3. The results provide evidence that the great increase of placental and uterine histaminase during rat pregnancy plays an important part in maintaining pregnancy and bringing it to a successful conclusion.
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SUMMARY
A method is described for reducing the maintenance of frogs used for the diagnosis of pregnancy by enforced hibernation.
Fifty males (Rana esculenta) were stored in a domestic refrigerator; twenty were removed at the end of 5 months, and thirty at the end of 7 months, and all survived and were healthy.
Examination of the frogs' urine after injection of 1 ml. of untreated pregnancy urine, known to contain between 8 and 16 i.u. of chorionic gonadotrophin, showed that all fifty animals shed uncountable numbers of sperm.
It is suggested that in addition to the use of these animals for pregnancy work, they are always available for dissection and physiological experiments.
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SUMMARY
1. Rabbit-skin homografts transplanted to recipients that are between 20 and 24 days pregnant survive for about twice as long as do homografts transplanted to pregnant rabbits early or late in pregnancy or to normal males or females.
2. Pregnancy does not interfere with the manifestation of a pre-existing immunity to a donor's skin.
3. The results are taken to provide evidence that the production of corticosteroids is increased during pregnancy. Possible sources of such increased production are discussed.
4. It is suggested that adrenocortical hormones may help to protect the foetus from the immunological consequences of its genetic incompatibility with the mother.
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SUMMARY
Ovariectomy on day 17 of pregnancy in rats that normally give birth on day 23 induced lactogenesis and foetal resorption but did not alter the pattern of change in pituitary or plasma prolactin concentration. Plasma prolactin levels increased significantly in both ovariectomized and sham-operated animals from days 18–22 of pregnancy. This suggests that factors other than ovarian products control the rise in late pregnancy of plasma prolactin in the rat. The results support earlier reports that progesterone withdrawal may be the lactogenic trigger in the rat.
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ABSTRACT
Changes in concentration of human atrial natriuretic peptide (hANP) in normal and toxaemic pregnancy were examined. The maternal plasma concentration of hANP increased gradually during normal pregnancy to a maximum of 20·0±2·4 pmol/l (mean ± s.e.m.) after week 36 of pregnancy. From week 20, the plasma concentrations of hANP were significantly higher than those in non-pregnant women (9·3±2·0 pmol/l). In toxaemia with hypertension, maternal plasma hANP levels were increased after week 26 of pregnancy (37·7±6·0 pmol/l) compared with those in normal gravida at the same time (17·1±1·6 pmol/l). Maternal plasma hANP levels in toxaemia only with oedema were not different from those in normal gravida.
J. Endocr. (1987) 114, 325–328
