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At least 343 records · Page 19Linked to original sources
PubMed1995

Uteroglobin gene expression in the rabbit uterus throughout gestation and in the fetal lung. Relationship between uteroglobin and eicosanoid levels in the developing fetal lung.

Uteroglobin (UG) gene encodes a cytokine-like, multifunctional, antiinflammatory protein, with potent phospholipase A2-inhibitory activity. It has been suggested that during implantation this protein protects the embryos from maternal immunological assault, facilitates the maintenance of quiescence in the uterus throughout pregnancy, prevents the onset of premature labor, and helps maintain an inflammation-free respiratory organ. This latter function of UG is suggested to be accomplished by preventing hydrolysis of surfactant phospholipids by a lung-specific phospholipase A2. Using reverse transcription polymerase chain reaction, in situ hybridization, immunofluorescence, and radioimmunoassay, we studied UG gene expression in the rabbit uterus throughout gestation and in the fetal lung. Here, we report that: (a) contrary to previous reports, UG gene expression in the rabbit uterus occurs throughout gestation with a precipitous decline just before parturition; (b) this gene expression is dramatically increased in the fetal lung with increasing gestational age; and (c) while there is an inverse relationship between the levels of UG, PGE2, and PGF2 alpha, a positive correlation was found in that of UG and leukotriene C4 in the fetal lung. Our results raise the possibility that dysregulation of UG gene expression, at least in part, may contribute to the onset of premature labor and the development of inflammatory lung disease in premature neonates.

Animals↗
PubMed1981

Reproduction and fetal development in mice chronically exposed to enflurane.

Reproductive indices and developmental toxicity were evaluated in Swiss/ICR mice chronically exposed to a subanesthetic (0.01 or 0.1 per cent) or an anesthetic (0.5/1.0 per cent) concentration of enflurane. Pregnant mice (443) and fetuses (4743) were examined. In one experiment, groups of females were exposed to 0.01, 0.1, or 0.5/1.0 per cent enflurane for 4 hours per day, 7 days per week for 3 weeks; they were then mated with unexposed males. Exposure of females was continued daily throughout pregnancy. No adverse effects on fertility were observed at any dosage. At the highest dosage, 1.0 per cent, minor developmental variations occurred (i.e., lumbar ribs and increased renal pelvic cavitation). In a second experiment, groups of mice were exposed to 0.01, 0.1 or 1.0 per cent enflurance only on days 6 through 15 of pregnancy for 4 hours per day, after having been mated with untreated males. Abnormalities (i.e., increased incidence of cleft palate, minor skeletal and visceral anomalies, and developmental variants) were again seen only at the highest dosage. In a third experiment, male mice were exposed to 0.01, 0.1 or 0.5/1.0 per cent enflurane for 11 weeks for 4 hours per day, 5 days per week, prior to mating with unexposed females; results of this experiment were negative. In general, enflurane treatments did not adversely affect reproductive indices. Effects on fetal development were minimal, being somewhat greater than those reported in previous experiments with methoxyflurane but less than those seen with halothane. The smallest exposure at which effects were seen was approximately 100 times greater than the level of human occupational exposure in unscavenged operating rooms.

Abnormalities, Drug-Induced↗
PubMed1990

Immunohistochemical demonstration of cytochrome P-450 monooxygenase in regenerating tracheal epithelium: a recapitulation of fetal development.

The cytochrome P-450 monooxygenase enzymes, NADPH-reductase and form 2, were demonstrated immunohistochemically in hamster tracheal epithelium that was regenerating after mechanical injury. Bromodeoxyuridine (BrdU), a thymidine analogue, was used to map the location and extent of the wound sites between 8 and 144 h post-injury. In the control and non-wounded areas of the epithelium, the secretory cells were labelled for the monooxygenase enzymes. Label was heaviest in the apical cytoplasm of these columnar cells. At 8 h, secretory cells at the wound margins migrated to cover the wound sites, becoming progressively flattened. Reaction product for monooxygenase enzymes was strong in these flat cells but immunolabelling for BrdU was very low. At 24 h many cells at the wound sites were labelled for BrdU (indicative of a high rate of cell division). Some cells were labelled for monooxygenase but many were not stained at this time. At 48 and 72 h post-injury, none of the cells within the wound sites (regenerating epithelium) were stained. Immunochemical labelling for the monooxygenase enzymes was restored to the nascent secretory cells as they differentiated in the wound sites, beginning at 96 h post-injury. Labelling was stronger at 120 and 144 h post-injury, comparable to that in the control epithelium. The observations suggest that the monooxygenase enzymes were retained by the secretory cells in the wound sites before they divided but were lost from their progeny. Then, the temporal sequence of monooxygenase expression was similar to the pattern of differentiation of nascent secretory cells during fetal development of the tracheal epithelium.

Animals↗
PubMed2002

Chromosome translocations and covert leukemic clones are generated during normal fetal development.

Studies on monozygotic twins with concordant leukemia and retrospective scrutiny of neonatal blood spots of patients with leukemia indicate that chromosomal translocations characteristic of pediatric leukemia often arise prenatally, probably as initiating events. The modest concordance rate for leukemia in identical twins ( approximately 5%), protracted latency, and transgenic modeling all suggest that additional postnatal exposure and/or genetic events are required for clinically overt leukemia development. This notion leads to the prediction that chromosome translocations, functional fusion genes, and preleukemic clones should be present in the blood of healthy newborns at a rate that is significantly greater than the cumulative risk of the corresponding leukemia. Using parallel reverse transcriptase-PCR and real-time PCR (Taqman) screening, we find that the common leukemia fusion genes, TEL-AML1 or AML1-ETO, are present in cord bloods at a frequency that is 100-fold greater than the risk of the corresponding leukemia. Single-cell analysis by cell enrichment and immunophenotype/fluorescence in situ hybridization multicolor staining confirmed the presence of translocations in restricted cell types corresponding to the B lymphoid or myeloid lineage of the leukemias that normally harbor these fusion genes. The frequency of positive cells (10(-4) to 10(-3)) indicates substantial clonal expansion of a progenitor population. These data have significant implications for the pathogenesis, natural history, and etiology of childhood leukemia.

Base Sequence↗
PubMed2003

Vitamin A depletion is associated with low phosphoenolpyruvate carboxykinase mRNA levels during late fetal development and at birth in mice.

Expression of the phosphoenolpyruvate carboxykinase (PEPCK) gene is repressed during fetal liver development and activated at birth. It has been shown that the PEPCK gene is a retinoid-responsive gene, but whether it is regulated by vitamin A in the fetus has not been established. In this study, we found that PEPCK mRNA can be detected in the murine fetal liver as early as gestational d 17. In addition, expression and cAMP induction of the PEPCK gene during late gestation and at birth require vitamin A sufficiency in the fetus and neonate. The PEPCK promoter contains several regulatory elements that bind a diverse array of transcription factors and nuclear coregulators, although it is largely unknown which of these factors are expressed early in liver development. Expression of some of these nuclear factors in livers of fetal mice was investigated by immunohistochemistry (IHC). Fetuses were from dams that were fed from the beginning of gestation diets that were adequate or devoid of vitamin A. Hepatocyte nuclear factor 4alpha (HNF4alpha) was expressed at the earliest stage of liver development on d 11, whereas retinoid X receptor alpha (RXRalpha) and nuclear coactivator CREB-binding protein (CBP) were expressed from d 16 onward. Although expressions of RXRalpha and CBP in livers of vitamin A-sufficient and vitamin A-depleted fetal mice did not differ, the level of HNF4alpha was consistently lower in the latter. Our findings strongly suggest that vitamin A is required during liver development for staged expression of the PEPCK gene and that HNF4alpha may be involved in mediating vitamin A regulation of the PEPCK gene at these critical periods.

Animals↗
PubMed2006

Preimplantation and fetal development of mouse embryos cultured in a protein-free, chemically defined medium.

Mouse two-cell embryos of block (ICR) or nonblock (F1 of C57BL x DBA) strains were cultured in modified Chatot, Ziomek, and Bavister medium, supplemented with bovine serum albumin or polyvinyl alcohol, a synthetic macromolecule. The supplementation did not influence morula compaction and blastocyst formation, mean cell numbers of total blastomeres, inner cell mass (ICM) cells and trophectodermal (TE) cells in blastocysts, rates of pregnancy and delivery, mean litter size, number of implantation spots in pregnant females, and the expression of several genes related to pluripotency, organogenesis, and implantation.

Animals↗
PubMed1986

Maternal-fetal ABO/Rh antigenic relationships and human fetal development.

Six hundred ninety-nine primigravid mothers and their neonates were grouped into three distinct classes on the basis of maternal-fetal antigenic relationships for the ABO and Rh blood groups. Maternal-fetal units were classified as maternal dominant if the mother possessed more antigens than the neonate, equivalent if both possessed the same number of antigens, and fetal dominant if the neonate possessed more antigens than the mother. After confounding variables were controlled, a significant increase in adjusted mean birth weight was observed from maternal-fetal equivalence to fetal dominance and there was a significant increase in adjusted crown-heel length from maternal dominance to fetal dominance. No trends were observed for adjusted head circumference. However, when the sample was stratified on the basis of sex of the neonate, a highly significant increase in adjusted mean head circumference was observed for female infants from maternal dominance through fetal dominance. These observations suggest maternal-fetal ABO/Rh relationships are associated with differential fetal growth trends.

ABO Blood-Group System↗