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Fetal Lung (fetal + lung)
Terms modified by Fetal Lung Selected AbstractsInfection and preterm birth: Evidence of a common causal relationship with bronchopulmonary dysplasia and cerebral palsyJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2000R Vigneswaran Abstract: Subclinical genital tract infection has been clearly established as a significant cause of spontaneous preterm birth, particularly in early gestations. Bacterial vaginosis organisms rank highly among the pathogens involved in preterm labour and there is considerable beneficial evidence from the use of prophylactic antibiotics for women at high risk of preterm birth. The pathogenesis involves activation of macrophages and the generation of pro-inflammatory cytokines. Bronchopulmonary dysplasia is seen in the most immature of survivors and appears to be secondary to interruption of normal development and maturation of the lungs. The link between chorioamnionitis and lung injury in utero and subsequent development of bronchopulmonary dysplasia has now been substantiated. Exposure to pro-inflammatory cytokines is implicated in the impairment of the fetal lung. A significant body of evidence supports the association between chorioamnionitis, periventricular leukomalacia and cerebral palsy. Biological mechanisms that explain the association between chorioamnionitis and fetal brain injury involve pro-inflammatory cytokines. Similarity in the pattern of expression of cytokines suggests a common pathway for the initiation of preterm labour and also injury to the lung and the central nervous system of the fetus. [source] Sex differences in response to steroids in preterm sheep lungs are not explained by glucocorticoid receptor number or binding affinity,PEDIATRIC PULMONOLOGY, Issue 1 2001Jana Kovar BScHons Abstract We recently reported that prenatal glucocorticoid therapy is less effective at promoting an improvement in lung function in male than in female sheep. This observation, and the higher incidence of respiratory distress syndrome in human males, suggests that the male fetal lung may be less responsive to glucocorticoids than is the female fetal lung. Since glucocorticoids are known to exert their effects via specific cytoplasmic glucocorticoid receptors (GR), we hypothesized that there may be sexual dimorphism in either the number or binding affinity of lung GR. To test the hypothesis, binding of dexamethasone (a synthetic glucocorticoid, 0.5,40 nM) by cytosolic fractions of male (n,=,16) and female (n,=,16) fetal sheep lung was measured at 125 days gestation (term,=,148 days). Scatchard analysis of dexamethasone binding showed that the total number of GR (Bmax) did not significantly differ between male (346,±,42 fmol/mg protein) and female (277,±,23 fmol/mg protein) fetuses. The measured binding affinity (Kd) in male fetal lungs (6.85,±,0.43 nM) was not significantly different from that in females (8.46,±,1.02 nM). In conclusion, this study suggests that sex differences in fetal sheep lung responses to glucocorticoid therapy are not due to differences in the number or binding affinity of lung GR. Pediatr Pulmonol. 2001; 32:8,13. © 2001 Wiley-Liss, Inc. [source] Assessment of fetal lung development by quantitative ultrasonic tissue characterization: a methodical studyPRENATAL DIAGNOSIS, Issue 9 2004Ismail Tekesin Abstract Objectives This study was performed to evaluate the quantitative ultrasonic tissue characterization of the normal fetal lung development by using acoustic raw data captured after preprocessing. Methods One hundred and sixty-two patients with completed gestational ages between 22 and 37 weeks were enrolled in this study. Longitudinal and transverse sections of the fetal thorax and upper abdomen were imaged. A region of interest of constant size was defined and the tissue-specific gray scale was determined by using an interactive software. Results A total of 162 patients met the inclusion criteria. The echogenicity of the fetal lung showed a particular changing pattern during pregnancy: the mean gray value of the fetal lung (MGV) is almost the same as the MGV of the fetal liver at 22 and 23 weeks, decreases between 22 and 31 weeks and increases between 31 and 37 weeks. The MGV of the fetal liver decreases significantly from 24 weeks to 31 weeks and increases significantly again toward 37 weeks. We stated that the MGV of the lung is smaller than the MGV of the liver during 31 weeks of gestation and the relation reverses in late gestation. At term, the MGV of the liver is greater than the MGV of the lung. The lung-to-liver ratio is <1 between 24 and 29 weeks and >1 between 30 and 35 weeks. Conclusion The echogenicity of the fetal lung showed a particular changing pattern during pregnancy, which corresponds to morphologic changes of the fetal lung development. Copyright © 2004 John Wiley & Sons, Ltd. [source] The long-term effects of perinatal glucocorticoid exposure on the host defence system of the respiratory tractTHE JOURNAL OF PATHOLOGY, Issue 1 2006E Theogaraj Abstract Glucocorticoids are used to mature the fetal lung at times of threatened premature delivery. These drugs modify leukocyte profiles when administered in adulthood, but their effects on the mature host defence system following administration during the perinatal period are incompletely understood. In this study, the long-term effects of perinatal dexamethasone exposure on rodent host defence cells in the pulmonary airspaces, the perivascular compartment of the lung, and the blood were investigated. Rats were treated prenatally (gestational days 16,19) or neonatally (postnatal days 1,7) by inclusion of dexamethasone in the mothers' drinking water (1 µg/ml). The pups were then allowed to develop to adulthood (P60-80), at which time respiratory tissues were collected for light and electron microscopy and bronchoalveolar lavage (BAL), and blood for cell count and fluorescent activated cell-sorting (FACS) analysis. Prenatal treatment had no effect on any parameter examined. Following neonatal dexamethasone exposure, light microscopy of the lung tissue revealed a significant reduction in the number of cells in the perivascular space in both the central and the peripheral regions of the adult lung, but no differences in the number of cells in the airspaces. Neonatal dexamethasone exposure was also characterized by a significant reduction in the total number of white cells in the peripheral blood in adulthood and in particular, the number of lymphocytes relative to neutrophils was significantly reduced at maturity in these animals. The results show that neonatal, but not prenatal, dexamethasone exposure significantly alters the distribution of host defence cells in the blood and lung at maturity compared with control animals. The early neonatal period is characterized by the stress hyporesponsive period in the rat, when endogenous glucocorticoid levels are very low. Therefore, exogenous glucocorticoids administered during this time are likely to have marked ,programming' effects on glucocorticoid-sensitive tissues. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Sex differences in response to steroids in preterm sheep lungs are not explained by glucocorticoid receptor number or binding affinity,PEDIATRIC PULMONOLOGY, Issue 1 2001Jana Kovar BScHons Abstract We recently reported that prenatal glucocorticoid therapy is less effective at promoting an improvement in lung function in male than in female sheep. This observation, and the higher incidence of respiratory distress syndrome in human males, suggests that the male fetal lung may be less responsive to glucocorticoids than is the female fetal lung. Since glucocorticoids are known to exert their effects via specific cytoplasmic glucocorticoid receptors (GR), we hypothesized that there may be sexual dimorphism in either the number or binding affinity of lung GR. To test the hypothesis, binding of dexamethasone (a synthetic glucocorticoid, 0.5,40 nM) by cytosolic fractions of male (n,=,16) and female (n,=,16) fetal sheep lung was measured at 125 days gestation (term,=,148 days). Scatchard analysis of dexamethasone binding showed that the total number of GR (Bmax) did not significantly differ between male (346,±,42 fmol/mg protein) and female (277,±,23 fmol/mg protein) fetuses. The measured binding affinity (Kd) in male fetal lungs (6.85,±,0.43 nM) was not significantly different from that in females (8.46,±,1.02 nM). In conclusion, this study suggests that sex differences in fetal sheep lung responses to glucocorticoid therapy are not due to differences in the number or binding affinity of lung GR. Pediatr Pulmonol. 2001; 32:8,13. © 2001 Wiley-Liss, Inc. [source] Transfer of maternally administered fusogenic liposome-DNA complexes into monkey fetuses in a pregnancy modelTHE JOURNAL OF GENE MEDICINE, Issue 5 2002Makoto Hirano Abstract Background Materno-fetal transfer of intravenously administered liposome-plasmid DNA complexes has been demonstrated only in mice. Studies on its materno-fetal transfer in the pregnant monkey model is needed because of critical differences in placental structure between primates including humans and rodents. Methods The reporter plasmid pEGFP-C1 was formulated in cationic lipid containing polybrene and vesicular stomatitis virus G protein. The fusogenic liposome-plasmid DNA complexes were intradermally injected into pregnant common marmosets (N=2), a New World monkey, near term. DNA extracted from fetal tissues was subjected to PCR for detection of the egfp gene. Confocal microscopy and immunostaining were performed to determine the sites of transgene expression in the fetal organs. Results The egfp gene was detected in fetal blood and major organs (heart, liver, lung). The encoded protein was mainly produced in the endothelial cells of blood vessels in the fetal lungs. Conclusions This is the first report on materno-fetal transfer of intradermally administered fusogenic liposome-plasmid DNA complexes and fetal expression of a transgene in primates. Copyright © 2002 John Wiley & Sons, Ltd. [source] Regulation of bone morphogenetic protein signalling in human pulmonary vascular development,THE JOURNAL OF PATHOLOGY, Issue 1 2008M Southwood Abstract The bone morphogenetic protein (BMP) type II receptor (BMPR-II) is predominantly expressed on the vascular endothelium in the adult lung. Although mutations in BMPR-II are known to underlie many cases of familial pulmonary arterial hypertension (FPAH), little is known regarding the expression of BMPs and their signalling pathways during normal lung development or the impact of BMPR-II mutations on endothelial cell function. We determined the cellular localization and expression levels of BMP4, BMP receptors, and activation of downstream signalling via phospho-Smad1 in a developmental series of human embryonic and fetal lungs by immunohistochemistry. The expression of BMP4 and BMP receptors was temporally and spatially regulated during lung development. BMPR-II expression correlated with phosphorylation of tissue Smad1 and was highest during the late pseudoglandular and early canalicular stage of lung development, when vasculogenesis is intense. Phospho-Smad1 expression was associated with markers of proliferation in endothelial cells. In vitro studies confirmed that BMPs 2 and 4 induced phosphorylation of Smad1/5 and pulmonary artery endothelial cell (PAEC) migration and proliferation. Adenoviral transfection of PAECs with mutant kinase-deficient BMPR-II, or siRNA knockdown of BMPR-II, inhibited Smad signalling and the proliferative response to BMP4. Our findings support a critical role for BMPs in lung vasculogenesis. Dysfunctional BMP signalling in PAECs during development may lead to abnormal pulmonary vascular development and contribute to the pathogenesis of FPAH. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Mobile phone base station-emitted radiation does not induce phosphorylation of Hsp27BIOELECTROMAGNETICS, Issue 2 2007H. Hirose Abstract An in vitro study focusing on the effects of low-level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system was conducted to test the hypothesis that modulated RF fields act to induce phosphorylation and overexpression of heat shock protein hsp27. First, we evaluated the responses of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole-body SAR for general public exposure defined as a basic restriction in the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and Wideband Code Division Multiple Access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced activation or gene expression of hsp27 and other heat shock proteins (hsps). Human glioblastoma A172 cells were exposed to W-CDMA radiation at SARs of 80 and 800 mW/kg for 2,48 h, and CW radiation at 80 mW/kg for 24 h. Human IMR-90 fibroblasts from fetal lungs were exposed to W-CDMA at 80 and 800 mW/kg for 2 or 28 h, and CW at 80 mW/kg for 28 h. Under the RF field exposure conditions described above, no significant differences in the expression levels of phosphorylated hsp27 at serine 82 (hsp27[pS82]) were observed between the test groups exposed to W-CDMA or CW signal and the sham-exposed negative controls, as evaluated immediately after the exposure periods by bead-based multiplex assays. Moreover, no noticeable differences in the gene expression of hsps were observed between the test groups and the negative controls by DNA Chip analysis. Our results confirm that exposure to low-level RF field up to 800 mW/kg does not induce phosphorylation of hsp27 or expression of hsp gene family. Bioelectromagnetics © 2006 Wiley-Liss, Inc. [source] | |||||||||||||