PubMed HealthSearch

SEARCH · PubMed Health

Results for “Fetal Development”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Fetal hemoglobin (HbF) synthesis in baboons, Papio cynocephalus. Analysis of fetal and adult hemoglobin synthesis during fetal development.

Fetal hemoglobin (HbF) and adult hemoglobin (HbA) synthesis was studied in fetal baboons, Papio cynocephalus, to determine the normal pattern of hemoglobin production during fetal development. Fetuses ranging from 53 to 180 days gestation (term gestation 184 days) were used. Erythroid cells were incubated with 3H-L-leucine, and the rates of globin chain synthesis and the distribution of radioactivity into hemoglobin intermediates and completed hemoglobin molecules were determined. Gamma chain synthesis accounted for approximately 97% of the total nonalpha chain synthesis up to 140 days gestation; beta chain synthesis accounted for the remainder. After 140 days gestation, approximately equal quantities of gamma and beta chain were synthesized in the bone marrow. Prior to 140 days gestation, total alpha chain synthesis was 30% greater than total non-alpha chain synthesis, while there was balanced chain synthesis after 140 days gestation. During the period of excess alpha chain synthesis, fetal erythrocytes contained a large pool of alpha-hemoglobin (alpha chain with heme attached) molecules uncombined with beta or gamma chains. In view of the possibility that alpha chains may have a lower affinity for gamma chains than beta chains, excess alpha chain synthesis may be required to maintain low levels of free gamma chains.

Animals

Hypertrophy and hyperplasia of bovine fetal tissues during development: fetal liver insulin-like growth factor I mRNA expression.

Tissue growth of crossbred fetal beef calves was examined by measuring RNA, DNA, and protein concentrations in liver, heart, and biceps femoris. Furthermore, liver insulin-like growth factor I (IGF-I) mRNA expression and mRNA species size during fetal development was observed. Tissue samples were collected from six fetuses every 42 d of gestation, from d 106 to d 274. In the liver, protein and DNA concentrations decreased, whereas RNA levels remained constant throughout fetal growth. The RNA/DNA and protein/DNA ratios in liver increased with fetal age. Heart DNA and RNA levels decreased, whereas protein concentration and protein/DNA ratios increased with fetal age. Protein and protein/DNA ratios decreased in biceps tissue, whereas DNA and RNA concentrations were constant. IGF-I mRNA was seen at 4.4, 2.5, and 1.2 kb in adult and 4.4, 2.5, and 1.7 kb in fetal bovine liver. Relative expression of liver IGF-I mRNA did not vary during fetal development. The current study shows that during the last 2 and 3 mo of gestation, heart and liver were undergoing hypertrophic growth, whereas biceps tissue did not exhibit the same trend. Elevated ratios of RNA and protein to DNA in liver above that of the heart and biceps suggest extensive hepatic cellular hypertrophy as well as increased transcriptional and translational activity. Insulin-like growth factor I mRNA levels were not related to the changes in RNA, DNA, and protein seen in hepatic tissue.

Animals

Corticotrophin-releasing factors in the hypothalamus of the developing fetal sheep.

Corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) are secreted from the hypothalamic median eminence to elicit the secretion of ACTH from the pituitary corticotrophs. During fetal development there is progressive maturation of the hypothalamic-pituitary-adrenal axis, manifest as increasing plasma ACTH and cortisol concentrations, which in species such as sheep culminates in the onset of birth. However, the precise nature of the hypothalamic signal controlling fetal pituitary ACTH secretion remains poorly understood. To investigate the ontogeny of this hypothalamic signal, the present study examined immunoreactive and bioactive ACTH-releasing factors in the developing fetal sheep hypothalamus. Immunoreactive CRH and AVP were measured by radioimmunoassay in extracts of hypothalami taken at day 70, day 100, and day 130 gestation (term = 145 days). There was a progressive and significant (P < 0.01) increase in hypothalamic CRH and AVP concentrations which was particularly marked between d100 and d130 gestation. AVP was always present in higher concentrations that CRH, although this difference was significantly reduced by day 130 gestation as the result of a large increase in the content of CRH relative to AVP. Sephadex G50 chromatography revealed that immunoreactive CRH and AVP in hypothalamic extracts existed as single molecular forms corresponding to synthetic peptides at each gestational age. In addition, these immunoreactive forms of CRH and AVP possessed significant ACTH-releasing bioactivity as measured in primary cultures of adult sheep anterior pituitary cells. Furthermore, significant bioactivity was present in high and low molecular weight fractions eluted after chromatography which did not contain any CRH or AVP immunoreactivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone

Ultrasound monitoring of fetal movements. A method for assessing fetal development?

Human fetal movements in utero have been analysed by conventional compound B-scan ultrasound techniques. With practice, movements of specific parts of the fetus can be readily recognised, and even as early as the 6th week after conception gross movements of the whole embryo are visible. Monitoring of fetal movements as an indication of normal or abnormal fetal development appears to have been neglected, and future studies in this important area of antenatal paediatrics are suggested.

Arm

Prenatal expression of the growth hormone (GH) receptor/binding protein in the rat: a role for GH in embryonic and fetal development?

Although fetal growth is generally considered to be independent of pituitary growth hormone (GH), it is possible that pituitary GH plays a modulatory role in organ development or that a GH-like substance of non pituitary origin may influence fetal growth through the GH receptor. Accordingly, we have used immunohistochemistry, northern blot analysis, the reverse transcriptase-polymerase chain reaction and solution hybridization to study the ontogeny of the GH receptor/binding protein (BP) from the 12-day-old embryo (E12) to the E18 rat fetus. GH receptor/BP immunoreactivity was observed in all major organ systems of the E18 rat fetus and was not preferentially associated with any germ layer derivative. A general increase in GH receptor/BP immunoreactivity was evident from E12 to E18, with a marked increase occurring between E16 and E18. Hemangioblastic tissue was, however, strongly or intensely immunoreactive at all stages of development, as was the placenta. Most noteworthy of the other tissues expressing GH receptor/BP immunoreactivity by day 18 were skeletal and smooth muscle, chondroprogenitor cells, epithelial lining cells, neuronal ganglia, ependymal cells and the adrenal cortex. In the placenta, the most prominent immunoreactivity was associated with decidual cells. Total RNA was isolated from E12 to E18 rat fetuses and adult rat liver. Northern hybridization with a 35S-labelled rat GH receptor cRNA probe revealed that 3.9 kb and 1.2 kb transcripts complementary to the rat GH receptor riboprobe are present from at least E16. The existence of GH receptor mRNA at E12 and E14 was demonstrated by the polymerase chain reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Gene activation of molecules with carcinoembryonic antigen determinants in fetal development and in adenocarcinoma of the colon.

"Fingerprints" of 0.9% NaCl solution extracts obtained from fetal guts and individual adenocarcinoma of the colon show a randomized pattern of expression of carcinoembryonic antigen (CEA) determinants by CEA radioimmunoassay and isoelectric focusing. All CEA-containing antigens found in a pool of 20 primary adenomas were found at some stage in fetal development. No single CEA-reacting peak was typical of any one period of fetal development. When fetal gut profiles were grouped according to trimester in utero, however, an expanded gene pool was found in the second trimester which correlates well with maximum gastrointestinal growth and differentiation. Isoelectric focusing-CEA radioimmunoassay profiles of individual primary adenomas were similar to but never identical with individual fetal gut profiles. "Fingerprints" of metastatic adenomas of entodermal origin showed quantitative and qualitative increases in molecules with CEA determinants unlike these latter categories. Such data suggest that both integrator and controller gene activities may be lost in metastatic disease. Rather than "phase-specific gene sets" on different chromosomes being activated by various oncogenic modalities, it is more probable that individual chromosomes are involved in oncogenesis. While more data are needed to confirm this idea, it is safe to say that the expression of molecules with CEA determinants need not be caused by either derepressive or reexpressive gene activation. These data point to the individuality of gene expression of molecules with CEA determinants both in fetal development and in early neoplasia. Since CEA-reacting molecules were not found in tumors of ectodermal or mesodermal origin by these methods, such products should be termed carcino-developmental antigens of entodermal or colonic origin.

Adenocarcinoma

Characterization of human alpha fetoprotein charge microheterogeneity during fetal development.

Aliquotes of human amniotic fluid (AF), fetal serum (FS), and cord blood (CB) were obtained as by-products of routine clinical diagnostic procedures at term or in the second trimester of pregnancy. When samples of CB were applied to a pH 5.5-4 chromatofocusing gradient, three isoforms of AFP could be resolved; a pl 4.57 form (isoform IA, 52% AFP), a pl 4.27 form (isoform IB, 43% AFP), and one species that was bound to the column but could be eluted with 1.0 M NaCl (isoform II, pl less than 4.00, 5% AFP). Term AF displayed a profile similar to that observed in term CB. When samples of 15-20-week gestation AF were chromatofocused, the immunoreactive AFP recovered was distributed between isoform IA and IB (60%) and isoform II (40%). FS and AF obtained from same pregnancy (23-26 weeks) displayed an identical chromatofocusing profile. Aliquotes of AF subjected to conA revealed 83% reactive variants compared with greater than 95% reactive variants for CB. FS displayed a conA profile identical to CB. When individual CB charge isoforms were isolated and subjected to conA analysis, greater than 97% of the AFP bound to conA. In contrast, when AFP isoform IA and IB were isolated from midgestation AF, approximately 22% of the AFP did not bind to the lectin while 100% of isolated AFP isoform II eluted as the reactive variant. These data suggest that human AFP exists as at least three charge and two lectin variants and that the charge profile may change during fetal development.

Amniotic Fluid

Specific binding of estrogens in different fetal tissues of guinea pig during fetal development.

Cytosol and nuclear specific estradiol binding was evaluated in the fetal uterus, kidney, lung, and brain of guinea pig during fetal development and after birth. The quantity of specific binding sites increases during fetal development and decreases after birth, particularly that of the nuclei. An exception is the binding in the cytosol fraction of lung in which the number of available binding sites continues to increase in newborn animals. In the fetal uterus the amount of specific binding of estradiol and estrone is similar. The selective uptake of radioactivity and its localization by autoradiography in cell nuclei are in accordance with the high levels of estrogen receptors, particularly at the end of gestation.

Animals

Expression of the epitope recognized by the monoclonal antibody 44-3A6 during human fetal development.

In this report we describe the expression of the adenocarcinoma associated antigen recognized by the monoclonal antibody 44-3A6, in various tissues during normal human fetal development. Conventional, formalin-fixed and paraffin-embedded sections of normal organs were examined from fetuses ranging from 9 to 42 weeks of gestation. Immunohistochemical localization of antigen-antibody complexes was accomplished using the avidin-biotin complex (ABC) method using horseradish peroxidase. The monoclonal antibody (MAb) 44-3A6 detects a cell surface 40 kD protein which is frequently expressed by adenocarcinomas and by select normal glandular tissues. Detectable expression of this protein was seen at different time periods during fetal development depending on the tissue. This expression was confined to a relatively small range of cell types and tissues; immunostaining was noted in select epithelial cells of the aerodigestive tract, exocrine pancreas, neural tissues, renal tubules, and transitional urothelium, as well as in other tissues. This immunostaining generally, but not invariably, corresponded with patterns previously reported in benign and/or malignant neoplasms of adult tissues. In most instances, once expression occurred within a tissue, it continued through gestation. These data show that this tumor associated gene product is differentially expressed in a broad range of normal developing human fetal tissues.

Adenocarcinoma

Fetal development of the pyloric muscle.

The fetal development of the pyloric muscle was studied in five human embryos (crown-rump length 5 to 31 mm) and in ten fetuses aged 3 to 9 months. Samples of pyloric muscle were obtained during operation for pyloric stenosis in two infants aged six weeks. Anatomo-radiologic, morphologic and immunohistochemical studies were made on this material, from which it emerged that the pylorus is identifiable by means of specific markers from the 40th day. Its two-layered muscular structure is described in detail. The mechanism of sphincteric function is reviewed. This study assumes clinical importance in the context of the etiopathogenesis of hypertrophic stenosis of the pylorus.

Humans

Experimental studies on the effects of aluminum on pregnancy and fetal development.

The effects of aluminum on pregnancy and fetal development were investigated. Aluminum in the form of aluminum chloride was administered intraperitoneally to pregnant rats at different dose-levels and at different stages of gestation. A high incidence of maternal death followed treatment with high dose-levels of the substance. Maternal weight gain during the entire gestational period was less in treated animals, compared to controls. In many cases, maternal liver was severely damaged as a result of the treatment. The offspring of mothers treated with aluminum chloride showed significant growth retardation as well as skeletal defects. In addition the incidence of fetal deaths and resorption was significantly increased.

Abnormalities, Drug-Induced

Expression of CYP2E1 during human fetal development: methylation of the CYP2E1 gene in human fetal and adult liver samples.

The expression and regulation of cytochrome P450IIE1 (CYP2E1) in adult and fetal human liver has been investigated. Three mRNA transcripts of 1.9, 2.7 and 3.8 kb were detected in all adult liver samples after hybridization with a full length cDNA to CYP2E1 whereas no expression was detected in 12 fetal liver samples studied. Similarly, expression of CYP2E1 was not detected in 11 placental samples (10-17 weeks gestational age) or in two full-term placental samples. CYP2E1 expression was not detected in fetal liver, kidney, lung, placenta (18 weeks gestational age) or liver (6 weeks gestational age) obtained at termination of pregnancy where maternal alcohol abuse had been established. Southern blot analysis of the cytosine methylation status of the CYP2E1 gene revealed substantial methylation of the 3' region of the gene in both adult and fetal human liver samples. No differences were observed in the methylation pattern of fetal liver samples between the gestational ages 12 and 17 weeks. Two small DNA fragments detected by the 5' end of the CYP2E1 cDNA were cleaved by the restriction enzyme HpaII in adult liver DNA but not in the fetal liver DNA samples. Methylation of specific 5' residues in the CYP2E1 gene may be responsible for the lack of transcription of the CYP2E1 gene in fetal liver.

Alcoholism

Distribution of osteonectin mRNA and protein during human embryonic and fetal development.

We investigated the temporal and spatial distribution of osteonectin during human embryonic and fetal development, using in situ hybridization and immunohistochemistry. Osteonectin gene expression was generally found in cells exhibiting high rates of matrix production/proliferation. In mineralized tissue, a strong signal was obtained in osteoblasts, odontoblasts, and chondrocytes of the upper hypertrophic and proliferative zones. Chondrocytes of the mineralized zone showed no expression throughout the different stages of development. Strong osteonectin expression was found in odontoblasts of developing teeth. In addition, osteonectin mRNA and protein were detected in several non-mineralized tissues: steroid-producing cells of the adrenal gland and the gonads, kidney (glomeruli), lung (bronchi), skin, megacaryocytes, and large vessels. Histochemistry confirmed the results and detected extracellular osteonectin in bone and in the zone of mineralized cartilage only. The localization of osteonectin in bone, cartilage, and teeth is consistent with a role in the initiation of mineralization. However, the organ-specific distribution in non-mineralized tissues suggests an important multifunction role of this protein during human development.

Abortion, Spontaneous

Rat lung polycholorinated biphenyl-binding protein: effect of glucocorticoids on the expression of the Clara cell-specific protein during fetal development.

Certain metabolites of polychlorinated biphenyls (PCBs) are retained in the Clara cells and in the airway lumen of rodent lung due to their interaction with a secretory 13-kDa protein. The expression of this Clara cell-specific, PCB-binding protein (PCB-BP) during the fetal development of the rat lung was studied by means of ligand binding and a monospecific antiserum. The PCB-BP and specific 4,4'-bis([3H]methylsulfony)-2,2',5,5'-tetrachlorobiphenyl binding was first detected on gestational Day 19 and subsequently the levels of PCB-BP and specific ligand binding increased as a function of gestational age. The start site of transcription for the rat PCB-BP gene was determined by primer extension analysis and the information thus obtained was used to develop a quantitative assay for the corresponding mRNA based on solution hybridization and S1 nuclease mapping. The appearance of PCB-BP mRNA during fetal lung development preceded the detection of immunoreactive protein and ligand binding by 1 day. By Day 21, the level of PCB-BP mRNA was 15 ng/100 micrograms total lung RNA which is approximately 30-40% of adult levels. In utero exposure to the synthetic glucocorticoid betamethasone was shown to increase specific 4,4'-bis([3H]methylsulfonyl)2,2',5,5'- tetrachlorobiphenyl binding, PCB-BP protein, and PCB-BP mRNA if administered from gestational Day 18 and onward. By Days 21-22, glucocorticoid treatment resulted in a two- to threefold increase in the levels of specific ligand binding, immunoreactivity, and mRNA, i.e., to approximately adult levels.

Animals

Pathological effects of maternal hypoglycemia on fetal development in cats.

The pathogenesis of fetal brain damage caused by acute maternal hypoglycemia was investigated experimentally in cats: profound hypoglycemia (blood glucose concentration: less than 30 mg/dl) was induced in 12 pregnant cats at various stages of gestation by intravenous bolus injections of insulin. Maximal hypoglycemia was attained within 2-3 h, although the grade and duration in individual cats varied. The EEGs of all of seven maternal cats examined showed an increased frequency of slow high-voltage waves as hypoglycemia progressed, eventually becoming flat in 3 for a maximum period of 20 min. Some fetuses showed severe neuropathological changes, such as infarction or intrauterine death. Subventricular softening, cortical hemorrhage and ischemic neuronal changes also occurred, being distributed symmetrically in the parasagittal areas of the cerebrum, basal ganglia, thalamus and tegmentum of the brainstem. In general, these pathological changes were more marked in fetuses and neonates than in the maternal cats, in which only ischemic neuronal changes were present, and may have been due to fetal systemic hypotension and cerebral ischemia induced by hypoglycemia. In maternal cats, the distribution of neurons showing ischemic changes was widest in the cerebral cortex, and some were also present in the dentate gyri of the hippocampus. Moreover, ultrastructural examination of the ischemic neurons in maternal cats, unlike those of the fetuses, showed no mitochondrial swelling. Therefore, the distribution and ultrastructural nature of the ischemic neurons found in the maternal cats were considered to be characteristic of hypoglycemia, as proposed by Agardh et al. (1980).

Animals

Progesterone secretion and fetal development during prolonged starvation in the pig.

Roles of ovarian progesterone secretion and maternal nutrition in fetal development were investigated in a species that normally experiences considerable embryonic and fetal mortality. Pregnancies were maintained in 81% of Yorkshire pigs during prolonged starvation (e.g., 40 days; 0 kcal/day, water only) in either the middle third (days 30-70) or last third (days 70-110) of gestation compared with 100% in full-fed controls (7,028 kcal/day). In spite of severe maternal deprivation, fetal survival rates averaged 65% in starved dams and 63% in controls; mean number of living fetuses was 9.9 in starved and 9.6 in control dams. Fetal growth was reduced by maternal starvation during the middle third, but not the last third of pregnancy. Placental insufficiency was the primary cause of reduced fetal growth and resulted in abortion in a few of the dams. Progesterone in peripheral serum of dams starved either during middle or late pregnancy was maintained at levels similar (P greater than 0.05) to those in controls. Abortion occurred in starved dams only when serum progesterone concentrations dropped to less than 10 ng/ml within 3 days before loss of conceptuses.

Animals

Early expression and localization of rhodopsin and interphotoreceptor retinoid-binding protein (IRBP) in the developing fetal bovine retina.

Differentiation and maturation of the photoreceptor outer segments are key steps in the development of the visual system. Morphological studies presented here show that the cow and human are nearly identical in the timing of outer segment appearance during fetal development, implying that the bovine retina is a good model system for the final stages of human photoreceptor development. To study photoreceptor maturation, rhodopsin and interphotoreceptor retinoid-binding protein (IRBP) were quantified by ELISA in a developmentally staged series of fetal bovine retinas. In addition, their localization within these retinas was determined by immunogold electron microscopy. Rhodopsin, as detected by antibodies directed against either the N- or C-terminal portions of the molecule, is first found at about 5.5 months gestation. It is first detected on the plasma membrane of the immature cilia and on the earliest emergent outer segment membrane, even before organized disk membranes are apparent. In contrast, whereas rhodopsin levels and outer segments are nearly undetectable before 5 months gestation, IRBP accumulates to a significant level (4-5% of the adult) as early as 3 months gestation. Immunogold electron microscopy confirmed this finding, with localization of IRBP predominantly in the subretinal space.

Animals