Showing papers on "Fetus published in 1975"

Estrogens in fetal and maternal plasma of the rhesus monkey

Abstract: The quantities of estrone and estradiol were determined by radioimmunoassay in maternal and fetal plasma of the rhesus monkey from day 59 to 163 of gestation. A two way analysis of variance of data classified according to fetal sex and 3 pooled gestational ages for each hormone and for mother or fetus (4 analyses) revealed significant elevations in fetal estradiol and maternal estrone concentrations with age. All other comparisons were not significant by these analyses. The concentrations of estradiol were greater in maternal than in fetal plasma [769 +/- 64 (SE) pg/ml, N = 63 VS 57 +/- 6 (SE) pg/ml, N = 77, P less than 0.01] by a t test. Estrone, on the other hand, was similar in mother and fetus [265 +/- 30 (SE) pg/ml, N = 60 vs 318 +/- 37 (SE) pg/ml, N = 73, P greater than 0.05]. No sex differences in the concentrations of these hormones were observed except in the fetus after 150 days of gestation. At this time plasma from female fetuses contained significantly more estradiol than plasma from male fetuses [118 +/- 20 (SE) pg/ml, N = 7 vs 61 +/- 10 (SE) pg/ml, N = 19, P less than 0.01]. Except for estradiol in female fetuses, the concentrations of estrogen were significantly higher in the umbilical vein than in the umbilical artery, an indication that the placenta is a major source of fetal estrogen in this species. Estrone and estradiol were significantly correlated in both the fetal and maternal circulation, r = 0.58, P less than 0.001 and r = 0.39, P less than 0.01 respectively. The results provide quantitative data about the estrogen miliue in which the monkey fetus develops and suggest mechanisms for controlling fetal estrogen in this species.

Fetal malnutrition and postnatal immunocompetence.

Abstract: The resemblance between fetal growth retardation (FGR) and malnutrition acquired postnatally is striking. The similarities include suboptimal physical development (including retarded bone age), loss of subcutaneous fat, dry skin with reduced turgor, hypoglycemia, hypothermia, frequent and severe infections, and high mortality. In addition, restriction of growth during fetal life is. associated with perinatal asphyxia, minimal postnatal weight loss, polycythemia and elevated levels of erythropoietin, and increased incidence of congenital malformations. Increased frequency of infection in such infants is an established clinical observation. Failure or impairment of immune defense mechanisms of infants with FGR is, therefore, suspected as a basis for the susceptibility of such infants to infection. Heretofore, there have been no comprehensive systematic analyses of the effect of fetal malnutrition on postnatal immunocompetence, unlike undernutrition acquired after birth for which considerable data are now available. 1-4 The following is a summary of our recent studies relevant to this problem.

Taurine in the brain and liver of the developing human and monkey

Abstract: —The concentrations of taurine in brain and liver from human fetuses (2nd trimester) and adults and from Rhesus monkeys from mid-gestation, through birth and neonatal life to maturity have been measured. The concentration of taurine in human and monkey fetal brain was 4-5-fold higher than that in adult monkey brain. In human fetal brain the concentration of taurine decreased linearly with increasing crown-rump length (r=−0·75; P < 0·001). In fetal monkey brain, no correlation with gestational age was found. After birth, the concentration of taurine in monkey brain decreased linearly with increasing age (r=−0·96; P < 0·001) until values comparable to those found in the adult were reached 8-9 months after birth, approximately the end of weaning. The concentration of taurine in liver both from fetal humans and from fetal monkeys was approximately twice that in mature liver. Concentrations of taurine similar to those found in adult liver were reached within a few days of birth, compared to several months for brain. These results suggest that taurine may be associated with brain development in addition to any functional role it may play in the mature brain.

3,3′,5′-Triiodothyronine (Reverse T3) and 3,3′,5-Triiodothyronine)(T3) in Fetal and Adult Sheep: Studies of Metabolic Clearance) Rates, Production Rates, Serum Binding, and Thyroidal Content Relative to Thyroxine

Abstract: To examine the mechanism(s) responsible for high serum concentration of 3,3',5'-triiodothyronine (reverse T3, rT3) and low serum concentration of 3,3',5-triiodothyronine (T3) in the fetus, we studied metabolic clearance rates (MCR) and production rates (PR) of rT3, T3, and thyroxine (T4) in adult nonpregnant sheep and sheep fetuses in utero. The mean fetal MCR-rT3 was significantly lower than that in adult sheep, and the mean fetal PR-rT3 significantly higher. The mean fetal MCR-T3 was higher than, and the mean fetal PR-T3 similar to that in adult sheep. The mean fetal MCR-T4 and PR-T4 were both significantly higher than the corresponding values in adult sheep. The ratios of mean PR-rT3 to PR-T4 (rT3/T4) were similar in fetal and adult sheep. However, the ratio of mean PR-T3 to PR-T4 (T3/T4) in the fetal sheep was much lower than that in the adult sheep. The low fetal MCR-rT3 was not attributable to high serum binding of rT3. On the basis of the thyroidal content and kinetics of iodothyronines, it was estimated that whereas thyroidal secretion may account for nearly all of serum T3 (or PR-T3) in the fetus and about 50% of serum T3 in adults, it accounts for only about 3% of the serum rT3 (or PR-rT3) in both fetal and adult sheep. The results suggest a) that elevated serum rT3 in the fetus is due to its decreased clearance and increased production by mono-deiodination of T4, and b) that low serum T3 in the fetus is due to its increased clearance and decreased production by mono-deiodination of T4. In addition, on the basis of discordant changes in the production of T3 and rT3 from T4, it appears that there may exist two separate, apparently specific, iodothyronine deiodinating activities--one cleaving the iodine atom at the 5'-position and the other acting in the iodine atom at the 5-position of the T4 molecule; 5'-iodothyronine deiodinating activity is apparently reduced in the fetus.

Fetal plasma prolactin levels.

Abstract: Prolactin levels were measured by radioimmunoassay in umbilical cord plasma from fetuses, in capillary plasma from neonates, and in venous plasma from adults The concentrations of prolactin in cord plasma from fetuses having gestational ages of 16 to 19 weeks, 20 to 34 weeks, and 35 to 42 weeks were 53 ± 16 (mean and SE), 233 ± 30 and 371 ± 7 ng/ml, respectively The prolactin levels decreased to 218 ± 35 ng/ml during the first neonatal week The similarity of the patterns of prolactin levels, reported gestational estrogen levels and adrenal weights, as well as the known biological properties of prolactin, estrogen, and ACTH is consistent with the view that these three factors may be involved in the growth of the fetal adrenal cortex and its involution in the newborn

The nature and origin of the soluble protein in human amniotic fluid

Abstract: Summary 1. Amniotic fluid surrounds the human fetus and is separated from the uterus by the amnion, chorion and placenta. The ability to obtain samples of amniotic fluid from women by a simple procedure has encouraged studies on the nature and origin of the fluid, and on its use for the diagnosis of a variety of clinical conditions. The fluid contains cells, which are of fetal origin, and can be grown in a tissue culture. Cyto-genetic and biochemical analyses can therefore be used to detect chromosomal aberrations and inborn errors of metabolism in the fetus. 2. The supernatant of amniotic fluid contains many of the solutes typical of extracellular fluid. In particular, it contains a wide range of proteins and those which are of fetal origin are likely to be of use in the prenatal diagnosis of fetal disease. This review examines the nature and origin of the soluble protein in amniotic fluid, and discusses the diagnostic uses of the proteins which are of fetal origin. 3. In other mammals, the arrangement of the fetal membranes is different from that in man, and these differences are reflected by changes in the nature of the amniotic fluid. Thus data from other animals have little applicability to man. 4. Electrophoresis and immunoelectrophoresis have established that the major proteins in amniotic fluid are also present in maternal and fetal sera. Their concentrations in the fluid are influenced by their molecular weight and proteins larger than about 2.5 times 106 may be excluded. Towards term, phenotyping studies show that a number of serum proteins in amniotic fluid are of maternal origin. In the case of group-specific component (Gc) this has been shown to be so throughout pregnancy. Such proteins must enter the fluid by diffusing across either the chorion or the chorionic plate and then the amnion. 5. It has been previously claimed that various serum proteins in amniotic fluid are of fetal origin. For albumin and IgG there are data that strongly support a maternal origin. The evidence on the origin of insulin is inconclusive. The concentration of β2-microglobulin in amniotic fluid exceeds that in maternal serum and is probably too high also for fetal serum to be its major source. It has a wide tissue distribution and probably enters the fluid from surrounding structures. 6. Alpha-fetoprotein in amniotic fluid is of fetal origin as it is present in maternal serum at far lower concentrations. It is found in fetal serum, urine and yolk sac, but it is not clear how it enters the amniotic fluid of normal fetuses. The concentrations of Gc and alpha-fetoprotein have been measured in amniotic fluid and in their sera of origin. The relative concentration of Gc in amniotic fluid was found to be much greater than that of alpha-fetoprotein and the concentration gradients of these marker proteins can be compared with data for other proteins. In this way further evidence has been obtained that the albumin, α1,-antitrypsin and transferrin in amniotic fluid are mainly of maternal origin throughout pregnancy. 7. Immunological studies have shown that at least three proteins of non-serum origin are present in amniotic fluid and they have also been located in the amnion and uterine decidua. 8. The enzymes present in amniotic fluid are summarized. Many lysosomal enzymes are clearly of fetal origin since they show altered specific activities in the appropriate cases where the fetus is affected with an inborn error of metabolism. For other enzymes, analysis of specific activity gradients can help to decide the extent to which an enzyme is of serum origin, although this will not exclude the possibility of a maternal (uterine) contribution. The results of such analyses suggest that, relative to the serum protein in amniotic fluid, the greatest concentrations of the minor non-serum proteins in the fluid occurs between thirteen and eighteen weeks of pregnancy and also towards term. 9. Some inborn errors of metabolism may be diagnosed prenatally by measuring the specific activity of the respective enzyme in amniotic fluid. However, the presence of different enzymes with similar substrate specificities has prevented this in Pompe's disease. 10. In cases where the fetus is affected with anencephaly or spina bifida there is an increase in the concentration of alpha-fetoprotein in the amniotic fluid. This has provided a way of detecting these diseases early enough to allow termination of pregnancy. 11. The discovery of new proteins in fetal serum and in the tissues surrounding the amniotic cavity would seem to provide the best chance of extending the uses of amniotic fluid into the other areas of prenatal medicine.

Vitamin A Deficiency and Fetal Growth and Development in the Rat

Abstract: Studies were conducted to examine in detail the effects of vitamin A deficiency on fetal growth and development in the rat. The gradations of deficiency were examined in two studies. The first included total vitamin A depletion followed by retinoic acid supplements, and the second included three different levels of restricted intake of retinyl acetate (42, 16, or 8 mug of retinol equivalents/day/kg of body weight) in vitamin A-depleted rats. In the first study, extensive fetal resorption and death were observed in retinoic acid-fed females after day 14 of gestation. These findings confirmed the morphological studies of Thompson and associates (Proc. Roy. Soc. London, Ser. B 159, 510-535, 1964) who found the earliest Detectable histological lesions to be in the placentas at days 15-16 of pregnancy. Analyses were carried out of the total weight, the DNA, RNA, and protein contents of fetuses and placentas of different gestational ages in retinyl ester-fed and retinoic acid-fed females. Biochemical changes indicative of a reduced rate of cell division were observed in both fetus and placenta by day 14 in the retinoic acid-fed rats. The few live fetuses in this group maintained a growth rate of only 60-70% of that of the fetuses of retinyl ester-fed dams after day 14. By contrast, the growth rate of the placentas (of live fetuses) after day 14 of gestation was not as consistently affected by retinol deficiency. Restriction of retinyl acetate intake (in the second study) significantly reduced both the total litter size and the number of live pups per litter. Most of the females in the retinyl acetate-restricted groups delivered pups that had normal body weight and appeared normal on visual inspection. Significant differences from normal controls were seen only in the neonates from dams given 8 mug of retinol equivalents (per kg of body weight per day), which had smaller livers and kidneys than the control neonates. In contrast, the weights of the brains of the neonates in all three retinyl acetate-restricted groups showed no differences from control values. Vitamin A assays on maternal and neonatal sera and livers indicated that the transport of vitamin A across the placenta was well regulated, and suggested that this transport is maintained with high priority in the presence of maternal deficiency. The effects of vitamin A deficiency on fetal growth and development might reflect primary effects on the placenta, with secondary effects on the fetus, or primary direct effects on the fetus itself. The mechanisms of the observed effects remain to be explained.

Placental transfer of cadmium in rats: influence of dose and gestational age

Abstract: Placental transfer rates of cadmium were investigated in rats in relation to dose (0.1, 0.4, and 1.6 mg Cd/kg) and the gestational age (12, 15, and 20 days) when rats were treated. Pregnant rats were injected intravenously with a single dose of 109CdCl2 (approximately 20 muCi/animal), and animals were sacrificed after 24 hr. 109Cd concentrations were measured in the fetus, placenta, maternal liver, and blood. Cadmium crossed the placenta at all doses and at all gestational ages tested. However, higher percentages of administered cadmium accumulated in the fetus with increasing dose and increasing gestational age. For example, after pregnant rats were injected with low, middle, and high doses of Cd on day 12 of gestation, fetuses accumulated 0.0001, 0.0028, and 0.0095 per cent of the injected dose, respectively. Percentages of administered Cd detected in placental tissue did not change consistently with dose but Cd levels did increase with gestational age. Placental to maternal blood Cd concentration ratios increased with gestational age but not with dose. Maternal liver to fetal liver concentration ratios were 295, 137, and 27 for low, middle and high doses, respectively, 24 hr after pregnant rats were treated on day 20 of gestation. These results are discussed in relation to placental damage, metallothionein inducibility, and fetotoxicity.

Alpha-feto-protein during development and in disease.

Abstract: An alpha-feto-protein (AFP) is present in many mammals, in birds, and in sharks during development. The AFP present in different species have similar physicochemical properties and often have common antigenic determinants. Their study, both in health and disease, has provided a useful model for the understanding of other phase-specific antigens and the activation of the genes which control their synthesis. In the human fetus, the level of AFP falls with increasing maturity. The more sensitive methods of detection have disclosed that this fetal protein persists in trace amounts throughout life and its level increases in maternal blood during pregnancy. The principal sites of synthesis are the fetal liver and in some mammals, the yolk sac splanchnopleur. In humans as well as in mice and cows, it is notable that the synthesis of AFP is increased in liver cancer cells and that high levels of this protein are present in serum. Elevated values of AFP have also been detected in human subjects with undifferentiated tumours of the testis and ovary. A fall to normal levels has been noted in cases of complete remission after surgery and a return to high levels in patients who develop metastases. In some patients with hepatitis a temporary rise in the level of AFP has also been observed. In recent years, the detection of high levels of AFP in amniotic fluid has proved to be of great value for the prenatal diagnosis of neural-tube defects. Abnormal levels have also been found in the amniotic fluid or in maternal serum in cases of spontaneous abortion. Such measurements are now being assessed as a methodof monitoring abnormal pregnancy.

Zinc Deficiency during the Latter Third of Pregnancy: Effects on Fetal Rat Brain, Liver, and Placenia

Abstract: The effects of zinc deficiency during the last third of gestation on the growth and development of the fetal rat at term were investigated. Zinc deficiency resulted in anorexia and weight loss of the pregnant dams. Fetuses from such dams displayed intrauterine growth retardation when compared with fetuses from pair-fed or ad libitum-fed controls given adequate zinc. Although the brains of the zinc-deficient fetuses were smaller than those of the controls, the brain was relatively spared while the liver was severely affected. The total cell number was reduced and there was an apparent increase in cell size in the brains of zinc-deficient fetuses in comparison with the brains of the controls. The growth failure of the zinc-deficient liver resulted in a smaller complement of total DNA, RNA, protein, and lipid, and there was less incorpora tion of (3H)thymidine into DNA in the liver. The placenta appeared to be only marginally affected by the zinc deficiency. J. Nutr. 105: 1466-1475, 1975.

Cerebral metabolism in sheep: a comparative study of the adult, the lamb, and the fetus.

Abstract: The cerebral uptakes of glucose, oxygen, lactate, pyruvate, acetoacetate and beta-hydroxybutyrate were compared in the adult, the fetal, and the newborn sheep. Beginning 1-2 days after surgery, we ...

FETAL PATHOPHYSIOLOGY OF HUMAN α‐FETOPROTEIN*

Abstract: a-Fetoprotein (AFP) serves as a marker both in cancer research and in studies concerning fetal development and fetal pathophysiology. The evidence available at present indicates that, during pregnancy, fetal AFP is transmitted into the maternal circulatory system 1 . 2 and the amniotic fluid.3 In this article, an account is given of the factors affecting the AFP concentration in fetal and maternal serum and in the amniotic fluid under normal and pathological conditions of human gestation.

Successful Application of Prenatal Diagnosis in a Pregnancy at Risk for Homozygous β-Thalassemia

Abstract: A Sicilian couple whose first child had homozygous beta-+-thalassemia requiring monthly transfusion requested prenatal diagnosis during the second pregnancy. Fully informed consent was obtained. The placenta was localized by ultra-sound at the 20th week of gestation, and was aspirated with a 20-gauge needle. Samples containing fetal red cells were obtained, and studies of globinchain synthesis showed a normal beta/gamma synthesis ratio for this gestational age. The conclusion that the child was not affected by beta-thalassemia was confirmed when an infant not affected with homozygous of heterozygous beta-thalassemia was born at term. Although more experience with this approach is necessary, this study demonstrates that prenatal diagnosis or exclusion of beta-thalassemia and sickle-cell anemia is feasible.

Plasma Estetrol as an Index of Fetal Well-being

Abstract: Estetrol (15α-hydroxyestriol or E4) is considered to be a specific product of fetal liver and has been suggested as a good indicator of fetal well-being. The concentration of unconjugated estetrol (E4) was measured by rapid and specific radioimmunoassay in 1 ml of maternal plasma. E4 levels prior to the 18th week of pregnancy were often detectable (<50 pg/ml). The mean plasma E4 level at term of 1.2 ng/ml was 7-fold higher than that observed at 24 weeks of gestation, and no diurnal variations were found. E4 levels in fetal plasma at term were 12-fold higher than those in maternal plasma and no fetal arterial venous differences were found. Umbilical vein but not maternal plasma levels of patients undergoing vaginal delivery were higher than those undergoing cesarean section (P <0.05) suggesting increased adrenal output of E4precursors during labor. In patients with severe Rh-isoimmune disease plasma E4 levels were not helpful in assessing fetal well-being. However, in patients with chronic hypertension or ...

Fetal alcohol syndrome: Report of a case.

Abstract: A boy born to a known alcoholic mother demonstrated the fetal alcohol syndrome. Although considerably postterm, he weighed less than 1.5 kg (3 lb) at birth and has failed to catch up at 2 1/2 years of age. In addition to continuing prenatal and postnatal growth and developmental deficits, he has many of the other stigmata described as characteristic of this syndrome. To this list have been added other findings from our case. ( JAMA 232:1144-1147, 1975)