@entity16 in the evolution of XXXX in the @entity3474 .

@entity1 @entity82 @entity66 @entity8855 @entity649 @entity26 @entity16 @entity3474 @entity4 @entity651 @entity2107 @entity6599 @entity11283
Pulmonary immaturity, @entity26 exposure that elicits cellular damage by free radicals, and @entity11283 induced by mechanical ventilation are implicated in the pathogenesis of @entity2107 . In the adult counterpart of adult @entity649 , @entity16 characterizes a histopathological sequence of lung findings that can occur during the disease course. Although adult @entity649 has many etiologies, elevated @entity26 exposure is known to be a contributor to the ensuing @entity651 . In @entity2107 , @entity26 exposure is thought to be a primary agent of injury. The evolution of the histopathological findings in the premature @entity3474 model of @entity8855 / @entity2107 was investigated in this study and compared to that in @entity26 -treated adult @entity6599 with adult @entity649 . Findings from lung specimens of 121 prematurely delivered @entity6599 at 0, 0.5, 1, 2, 3-6, 7-11+ days after delivery document that the premature lung has a delayed and more blunted exudative response when compared to that of @entity1 and @entity3474 adults. Saccular @entity4 , not hyaline membranes, is the dominant histopathological finding in the exudative phase of @entity16 and occurs later (7-11 days) in @entity1 lungs when compared to comparably treated adult lungs in which maximal exudative changes are seen at 3-6 days. The reparative response in the premature @entity3474 is characterized by saccular wall thickening and @entity82 , with less intramural organization of exudate in saccular/alveolar spaces when compared to adults. The airway changes in the premature are more severe than those seen in @entity66 . These findings indicate that @entity16 does occur in the immature lung albeit with differing characteristics when contrasted to comparably injured adults.(ABSTRACT TRUNCATED AT 250 WORDS)
