A nosocomial outbreak of respiratory syncytial virus infections involved 8 of 17 infants in an Intensive Care Nursery and one additional infant in the adjoining Newborn Nursery. Immunofluorescent staining of nasopharyngeal specimens was positive in six of seven virologically confirmed cases (86%). One additional case with negative viral cultures was also identified by this technique. Viral isolation in tissue cultures required an average of 4.9 days, whereas results of immunofluorescent studies were available in two to four hours. Rapid identification of infected infants by immunofluorescence permitted prompt institution of infection control measures.
B (range + 20 60%) alveolar markers increased significantly in early (n = 4, p < .05) but decreased significantly in late (Ϫ12-50%) (n = 4, p < .05) stages of ILD. In contrast, the expression of ␣SMA increased significantly (n = 4, p < .05) in both the early (+15%) and the late (+60%) stages of ILD, with a much more pronounced increase in the late vs early stage of ILD. Conclusions: Our data clearly suggest an association of SP-C deficiency with disruption of epithelial-mesenchymal interactions and provide a plausible mechanism for the pathogenesis of ILD in SP-C deficiency. However, to determine the specificity of SP-C deficiency for the disruption of PTHrP-driven epithelial-mesenchymal interactions, studies targeting specific molecular intermediates of this epithelial-mesenchymal paracrine loop are in progress.
162WNT5a INHIBITS THE CANONICAL PATHWAY.
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