The potential role of fibronectin and other cytokines as mediators and markers of BPD may thus allow for earlier detection and identification of those infants with RDS who are at greatest risk to develop BPD, as well as aiding in the development and selection of therapeutic interventions that can more effectively treat and possibly prevent the deleterious consequences of bronchopulmonary dysplasia.
The potential role of fibronectin and other cytokines as mediators and markers of BPD may thus allow for earlier detection and identification of those infants with RDS who are at greatest risk to develop BPD, as well as aiding in the development and selection of therapeutic interventions that can more effectively treat and possibly prevent the deleterious consequences of bronchopulmonary dysplasia.
The potential role of fibronectin and other cytokines as mediators and markers of BPD may thus allow for earlier detection and identification of those infants with RDS who are at greatest risk to develop BPD, as well as aiding in the development and selection of therapeutic interventions that can more effectively treat and possibly prevent the deleterious consequences of bronchopulmonary dysplasia.
It is suggested that the high levels of PCB-BP at the postconceptional age of less than 38 weeks observed in infants with BPD may reflect inflammatory injury and regeneration of airway epithelium, associated with proliferation of Clara cells.
Taken together these data indicate that the premature baboon is capable of mounting an antioxidant response and that increased MnSOD protein expression in BPD and BPD-infected premature baboons is regulated, at least in part, at a posttranscriptional level.
The association between epsilon4 and early onset bipolar disorder (BPD) with psychotic symptoms suggests that APO E gene is a risk factor for a subgroup of BPD, or influences the phenotypic expression (i.e. psychotic symptoms or age at onset) of manic depressive illness.
We conclude that the CRH gene is not linked to BPD; if genes involved in the regulation of stress response are indeed linked to BPD, the search should be directed towards those that regulate CRH secretion or its effects on target tissues.
In order to identify which pulmonary cells synthesize FN and to test the hypothesis that FN is more abundant in lungs with BPD, we examined the distribution of pulmonary FN by in situ hybridization (for mRNA) and immunohistochemistry (for protein) in neonatal autopsy lung specimens, comparing lungs with BPD to those without.
Immunohistochemical staining of human neonatal lung tissue demonstrated increased TRAF1 in lungs of infants dying of pneumonia or BPD in comparison with those dying of congenital malformation.
A significant decrease in leptin mRNA level was observed in comparison with pretreatment in BPD patients (59+/-34 vs 143+/-85 arbitrary units, P<0.01).
These data suggest that overexpression of TGF-beta 1 during the critical period of postnatal rat lung alveolarization gives rise to pathological, biochemical, and morphological changes consistent with those seen in human bronchopulmonary dysplasia, thus inferring a pathogenic role for TGF-beta in this disorder.