Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surface phenotype of peripheral blood lymphocytes (PBL) from preterm infants was evaluated using monoclonal antibodies which define T cell membrane antigens associated with processes of maturation and activation of these cells. In the majority of preterm infants born during the 25th and 26th week of gestation, PBL included higher percentages of cells bearing an immature/activated surface phenotype characterized by the presence of CD1, CD38, and CD71 surface antigens than in term newborns. In these gestational age groups, PBL included, in particular, very high percentages of lymphocytes (range: 22-60) expressing the p55 chain of interleukin-2 receptor (IL-2R). After the 26th week of gestation, PBL of some preterm neonates included, as well, high percentages of lymphocytes bearing immature/activated phenotype; their median values, however, were not significantly different from those observed in term newborns. Our data suggest that the presence of the p55 chain of IL-2R on the surface of neonatal lymphocytes could be correlated with the immaturity of these cells.
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PMID:Lymphocyte subpopulations in preterm infants: high percentage of cells expressing P55 chain of interleukin-2 receptor. 207 24

It is still uncertain whether cell cultures attain the functional maturity of corresponding in vivo cells. The degree of differentiation of cultured collecting-duct (CD) epithelium cells was therefore examined using immunohistochemical procedures. Three monoclonal antibodies (mabs CD1, CD2, and CD3) were raised against proteins (PCD) isolated from the renal papilla. At Western-blot analysis, each of these antibodies reacted with a specific protein that was distinguishable according to its molecular weight [PCD1, 190 kilodaltons (kDa); PCD2, 210 kDa; PCD3, 50 kDa]. Using immunofluorescence, these proteins were found to be localized exclusively in the renal CD system. Other renal structures, such as the proximal or distal tubular portions, the glomeruli and the interstitial network, were not reactive. The mabs, CD2 and CD3, labeled both the cortical and medullary CD in a uniform way, whereas mab CD1 produced heterogeneous immunolabeling along the length of the cortical, medullary, and papillary CD. As revealed by immunohistochemistry, the mabs revealed differences with respect to the expression of the specific renal proteins in cultured CD cells. In polar-differentiated epithelium cultured for 5 days on a specific renal support, mab CD1 was unreactive, whereas mabs CD2 and CD3 were positive. This demonstrated the biochemical immaturity of this cultured epithelium with respect to CD1 reactivity. In morphologically dedifferentiated CD monolayer cells grown on the bottom of a culture dish, only a weak reaction for mab CD3 was observed. The loss of epithelial polarization in CD monolayer cells obviously coincides with the absence of the renal proteins PCD1 and PCD2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The expression of specific proteins in cultured renal collecting duct cells. 328 51

DNA damage and repair in kidney and liver of mouse fetuses exposed to selected doses of N-nitrosodimethylamine (NDMA) (CAS No. 62.75.9) were studied using the alkaline elution technique. CD1 female mice (15 days pregnant) were treated i.p. with 2 and 10 mg/kg b.w. of NDMA; a slight increase in DNA damage was observed in their fetuses compared to untreated controls. A 2-fold higher extent of DNA damage was induced when mice were treated by intrafetal injections of a rat S9 activating fraction (S9) immediately before exposure to the same dose of NDMA by transplacental means. The DNA-strand breaks disappeared as a function of time in animals treated with NDMA alone. In contrast, a significant persistence of DNA damage was detected in the liver and lung of fetuses which were treated with S9 and NDMA in sequence. These experiments demonstrate the metabolic immaturity of unborn mice as far as the carcinogenic activation of NDMA is concerned and show the high susceptibility of fetal tissues to DNA-damaging agents. The alkaline elution applied in vivo by the transplacental route combined with the intrafetal injection of an exogenous activating microsomal fraction allow to extend our knowledge on the interaction of metabolism-dependent chemicals with fetal tissues.
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PMID:A new method to reveal the genotoxic effects of N-nitrosodimethylamine in pregnant mice. 334 94

The murine Foxf1 gene, encoding a forkhead - or winged helix - transcription factor, is expressed in splanchnic mesenchyme during organogenesis. The concentration of expression to subepithelial mesenchyme suggested that Foxf1 is activated by paracrine signals from endodermal epithelia. Homozygous Foxf1-null mice die before embryonic day 10, owing to defects in extra-embryonic mesoderm, and do not provide any information about the role of Foxf1 in morphogenesis of endodermally derived organs. We show that, on CD1 genetic background, Foxf1 heterozygote perinatal mortality is around 90%. The haploinsufficiency causes a variable phenotype that includes lung immaturity and hypoplasia, fusion of right lung lobes, narrowing of esophagus and trachea, esophageal atresia and tracheo-esophageal fistula. Similar malformations are observed in mutants that are defective in the sonic hedgehog (Shh) signaling pathway, and we show that exogenous Shh activates transcription of Foxf1 in developing lung. Foxf1 mRNA is absent in the lungs, foregut and sclerotomes of Shh(-/-) embryos, but persists in tissues where indian hedgehog (Ihh) is expressed. In lung organ cultures, activation of Foxf1 by Shh is counteracted by bone morphogenetic protein 4 (BMP4). Fibroblast growth factor (FGF) 10 and FGF7 both decrease Foxf1 expression and we speculate that this is mediated by transcriptional activation of epithelial Bmp4 (in the case of FGF10) and by inhibition of Shh expression for FGF7.
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PMID:Haploinsufficiency of the forkhead gene Foxf1, a target for sonic hedgehog signaling, causes lung and foregut malformations. 1149 58