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Fetus

About: Fetus is a research topic. Over the lifetime, 21567 publications have been published within this topic receiving 646380 citations. The topic is also known as: foetus & fœtus.


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Journal ArticleDOI
TL;DR: In two pregnancies at risk for sickle cell anaemia and β–thalassaemia, the fetal genotypes are successfully identified and prenatal diagnosis of single gene disorders by recovering fetal cells from maternal circulation appears to be a feasible approach.
Abstract: Currently, amniocentesis, chorionic villus sampling (CVS) and fetal blood sampling are used to obtain fetal cells for genetic diagnosis. These invasive procedures pose a small but not negligible risk for the fetus. Efforts have been directed towards the enrichment of fetal cells, such as erythroblasts, from maternal blood and progress has been made in the diagnosis of some chromosomal disorders and in sex determinations. We now report the detection of point mutations in single gene disorders using this method of prenatal diagnosis by enriching fetal cells from maternal blood by magnetic cell sorting followed by isolation of pure fetal cells by microdissection. In two pregnancies at risk for sickle cell anaemia and beta-thalassaemia, we successfully identified the fetal genotypes. Thus, prenatal diagnosis of single gene disorders by recovering fetal cells from maternal circulation appears to be a feasible approach.

278 citations

Journal ArticleDOI
TL;DR: It is concluded that a large amount of CRHi is secreted by the placenta into both the maternal and fetal circulation during pregnancy and suggest that this may be an important modulator of the mothers and fetal hypothalamic-pituitary-adrenal axis during gestation.
Abstract: Corticotropin-releasing hormone immunoactivity (CRHi) was measured in the plasma of 31 pregnant women and 6 nonpregnant women as well as in the umbilical cord plasma of 40 term fetuses. CRHi was not detectable (>44 pg/ ml) in the plasma of 6 nonpregnant women or in 6 women in the first trimester of pregnancy. Mean plasma CRHi rose progressively to 58 † 18 and 270 † 68 pg/ml during the second and third trimesters, respectively, and again became undetectable within 24 h after delivery. Mean CRHi in 40 umbilical cord plasma samples was 136 † 16 pg/ml. Gel filtration of both fetal and maternal plasma showed that the majority of the CRHi eluted in the same position as synthetic human CRH. There was no significant correlation between CRHi and either /8-endorphin or ACTH in umbilical cord plasma, suggesting that this CRHi may not be primarily responsible for the release of β-endorphin and ACTH into fetal plasma at delivery. A close correlation (r = 0.82) was found between simultaneously obtained maternal and umb...

277 citations

Journal ArticleDOI
TL;DR: Ethanol-associated alterations in fetal DNA methylation may contribute to the developmental abnormalities seen in the fetal alcohol syndrome and is thought to play an important role in the regulation of gene expression during embryogenesis.
Abstract: Acute ethanol administration (3 g/kg twice a day) to pregnant mice, from the 9th thru the 11th day of gestation, resulted in hypomethylation of fetal deoxyribonucleic acid (DNA) Nuclei isolated from the fetuses of the ethanol-treated mice had lower levels of methylase activity relative to controls even in the presence of excess S-adenosylmethionine, which serves as the methyl donor for the enzyme DNA methyltransferase Acetaldehyde, at concentrations as low as 3 to 10 microM, inhibited DNA methyltransferase activity in vitro Since DNA methylation is thought to play an important role in the regulation of gene expression during embryogenesis, ethanol-associated alterations in fetal DNA methylation may contribute to the developmental abnormalities seen in the fetal alcohol syndrome

277 citations

Journal ArticleDOI
TL;DR: Parathyroid hormone (PTH)-like bioactivity, assayed as adenylate cyclase response in UMR 106-01 osteogenic sarcoma cells, was present in extracts of sheep fetal and maternal parathyroid glands and placenta and may contribute to the relative hypercalcaemia of the fetal lamb.
Abstract: Parathyroid hormone (PTH)-like bioactivity, assayed as adenylate cyclase response in UMR 106-01 osteogenic sarcoma cells, was present in extracts of sheep fetal and maternal parathyroid glands and placenta. Preincubation of extracts with PTH(1-34) antiserum inhibited approximately 40% of the bioactivity in fetal parathyroid extracts, 50% in maternal parathyroid extracts, but only 10% of the bioactivity in the placental extract. Partial purification of placental extracts by chromatography yielded fractions containing PTH-like bioactivity which were similar in behaviour to that of PTH-related protein (PTHrP) from a human lung cancer cell line (BEN). An antiserum against synthetic PTHrP(1-16) partially inhibited the bioactivity of the placental extract and synthetic PTHrP(1-34), but had no effect on the bioactivity of bovine PTH(1-34) or bovine PTH(1-84). The placental PTH-like bioactivity was higher in mid- than in late gestation. Fetal parathyroid glands contained the highest PTH-like bioactivity. Thyroparathyroidectomy of one fetal twin lamb in each of 16 ewes between 110 and 125 days of gestation resulted in decreases of the plasma calcium concentration and reversal of the placental calcium gradient that existed between the ewe and the intact fetus. Perfusion of the placenta of each twin in anaesthetized ewes was carried out sequentially with autologous fetal blood in the absence of the exsanguinated fetus. The plasma calcium concentration in the blood perfusing the placenta of each twin increased, but reached a plateau at a lower concentration in the perfusing blood of thyroparathyroidectomized fetuses than in that of the intact fetuses. Addition of extracts of fetal parathyroid glands or of partially purified PTHrP resulted in further increases in plasma calcium in the autologous blood perfusing the placentae of thyroparathyroidectomized fetuses, but addition of bovine PTH(1-84) or rat PTH(1-34) had no effect. The presence of this PTH-like protein in the fetal parathyroid gland and placenta may contribute to the relative hypercalcaemia of the fetal lamb. This protein, which is similar to PTHrP associated with humoral hypercalcaemia of malignancy, stimulates the placental calcium pump responsible for maintaining a relative fetal hypercalcaemia during gestation.

276 citations

Journal ArticleDOI
10 Mar 1983-Nature
TL;DR: It is demonstrated that fibroblast cultures established from rats 2 to 50 days of age mimic the developmental switch from IGF-II to IGF-I production observed in serum, and it is shown that placental lactogen but not GH stimulates IGF- II synthesis in fetal fibroblasts, providing a mechanism whereby PL may regulate fetal growth.
Abstract: Insulin-like growth factor-I (IGF-I) and IGF-II are chemically similar polypeptides with related receptor specificity and in vitro biological activity1. IGF-I and IGF-II have a 62% amino acid sequence identity and are 38–48% homologous with the A and B domains of human proinsulin. They can be distinguished by specific radioimmunoassays, appear to have different patterns of hormonal regulation, and presumably serve different in vivo biological functions. Plasma IGF-I levels reflect circulating concentrations of pituitary growth hormone (GH), and exogenous IGF-I substitutes for GH in inducing somatic and skeletal growth in GH-deficient rats2. Several recent observations in rats have suggested a possible role for IGF-II in fetal growth. IGF-II levels are 20- to 100-fold higher in fetal rat serum than in maternal serum and decline within days after birth3. IGF-I exhibits the reciprocal developmental pattern—low in the early neonate, rising to adult levels by approximately 4 weeks of age4,5. We recently reported6 that cultured rat embryo fibroblasts synthesize large amounts of multiplication-stimulating activity (MSA or rIGF-II), the rat homologue of human IGF-II7. We now demonstrate that fibroblast cultures established from rats 2 to 50 days of age mimic the developmental switch from IGF-II to IGF-I production observed in serum. In addition, we show that placental lactogen (PL) but not GH stimulates IGF-II synthesis in fetal fibroblasts. By contrast, both GH and PL stimulate IGF-I synthesis in fibroblasts from older rats with no effect on IGF-II synthesis. Stimulation of IGF-II synthesis in fetal fibroblasts by PL provides a mechanism whereby PL may regulate fetal growth.

276 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20249
20232,267
20224,825
2021623
2020515
2019506