“…Decreased PCor lecithin-to-sphingomyelin ratios in amniotic fluid or lung secretions are used clinically to predict the risk of RDS in preterm infants (27,28). At E18.5, fractional content of PC and saturated PC were significantly decreased, whereas that of phosphatidylethanolamine (PE), sphingomyelin (SM), and phosphatidylserine (PS) was increased in the lungs of Foxa2 ⌬/⌬ mice ( Table 1).…”
Toward the end of gestation in mammals, the fetal lung undergoes a process of differentiation that is required for transition to air breathing at birth. Respiratory epithelial cells synthesize the surfactant proteins and lipids that together form the pulmonary surfactant complex necessary for lung function. Failure of this process causes respiratory distress syndrome, a leading cause of perinatal death and morbidity in newborn infants. Here we demonstrate that expression of the forkhead gene Foxa2 in respiratory epithelial cells of the peripheral lung controls pulmonary maturation at birth. Newborn mice lacking Foxa2 expression in the lung develop severe pulmonary disease on the first day of life, with all of the morphological, molecular, and biochemical features of respiratory distress syndrome in preterm infants, including atelectasis, hyaline membranes, and the lack of pulmonary surfactant lipids and proteins. RNA microarray analysis at embryonic day 18.5 demonstrated that Foxa2-regulated expression of a group of genes mediating surfactant protein and lipid synthesis, host defense, and antioxidant production. Foxa2 regulates a complex pulmonary program of epithelial cell maturation required for transition to air breathing at birth.forkhead ͉ transcription factor ͉ pulmonary epithelium ͉ surfactant
“…Decreased PCor lecithin-to-sphingomyelin ratios in amniotic fluid or lung secretions are used clinically to predict the risk of RDS in preterm infants (27,28). At E18.5, fractional content of PC and saturated PC were significantly decreased, whereas that of phosphatidylethanolamine (PE), sphingomyelin (SM), and phosphatidylserine (PS) was increased in the lungs of Foxa2 ⌬/⌬ mice ( Table 1).…”
Toward the end of gestation in mammals, the fetal lung undergoes a process of differentiation that is required for transition to air breathing at birth. Respiratory epithelial cells synthesize the surfactant proteins and lipids that together form the pulmonary surfactant complex necessary for lung function. Failure of this process causes respiratory distress syndrome, a leading cause of perinatal death and morbidity in newborn infants. Here we demonstrate that expression of the forkhead gene Foxa2 in respiratory epithelial cells of the peripheral lung controls pulmonary maturation at birth. Newborn mice lacking Foxa2 expression in the lung develop severe pulmonary disease on the first day of life, with all of the morphological, molecular, and biochemical features of respiratory distress syndrome in preterm infants, including atelectasis, hyaline membranes, and the lack of pulmonary surfactant lipids and proteins. RNA microarray analysis at embryonic day 18.5 demonstrated that Foxa2-regulated expression of a group of genes mediating surfactant protein and lipid synthesis, host defense, and antioxidant production. Foxa2 regulates a complex pulmonary program of epithelial cell maturation required for transition to air breathing at birth.forkhead ͉ transcription factor ͉ pulmonary epithelium ͉ surfactant
“…Several samples or duplicates can be handled at once. More results are required to compare the predictive value of this test with that of the L/S ratio test of Gluck et al (1971), the shake test of Clements et al (1972), and the lecithin assay of Bhagwanani et al (1973).…”
“…Gestationswoche nachgewiesenen Abnahme der Ober flächenspannung um 100%. Diese wiederum ist unter Berücksichtigung anderer Untersuchungen [2,7] die Folge einer zunehmenden Konzentra tion von Surfactant in den peripheren Lufträumen, der bei gleichbleiben dem Transpulmonaldruck eine rasch zunehmende Entfaltbarkeit von morphologisch bereits ausdifferenzierten Lufträumen ermöglicht. Be trachtet man die deutliche Zunahme der TK, der C8tat und der Gewebs elastizität bei relativ geringen Änderungen der übrigen Parameter während der ersten 3 Lebenswochen, so muss angenommen werden, dass in diesem Zeitraum eine funktionelle Reifung des Lungengewebes, besonders der elastischen Elemente, als Antwort auf die Beanspruchung durch die At mung im Vordergrund steht.…”
Section: Die Normale Lungenentwicklungunclassified
On 31 pairs of lungs from still borns and newborns of differing stages of maturation and age (23rd week of gestation up to the 24th week after birth) statical measurements including liquid fillings were performed. On account of the histomechanical tests as well as morphological and clinical data, the group could be divided into normal lungs and lungs with decreased surfactant activity. Between the 35th week of gestation and the 5th week after birth a marked increase in pulmonary maturation with unproportional changes of the histomechanical values could be demonstrated. In lungs with decreased surfactant activity the influence of life span upon the mechanical properties of pulmonary tissue could be shown. The high surface tension decreases, presumably on account of surfactant synthesis, while the values of tissue elasticity decrease as a result of overstretching.
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