Effects of @entity221 on @entity75 in the immature @entity35 : its influence on XXXX protease.

@entity1545 @entity63 @entity75 @entity26 @entity24182 @entity519 @entity19744 @entity35 @entity4124 @entity221 @entity528 @entity130
OBJECTIVE: Recent clinical studies suggested that intrapartum maternal fever is a strong independent risk factor for neonatal @entity75 . With use of a well-studied @entity35 model of neonatal @entity63 , this study investigated the hypothesis that intraischemic @entity221 accelerates and worsens @entity1545 in immature animals and examined whether apoptotic cell death machinery is involved in the underlying mechanisms. STUDY DESIGN: Seven-day-old @entity35 underwent a combination of left common carotid artery ligation and exposure to 8% @entity26 for 15 minutes (n = 32 @entity35 ). During the 15-minute @entity519 insult, body temperature was elevated to 40 degrees C in 16 animals ( @entity519 ), and was maintained at 37 degrees C in 16 animals (normothermic @entity519 insult group). Then both groups were placed in the same chamber in a water bath at 37 degrees C for 24 hours and finally returned to the mothers. @entity24182 activity was assessed 36 hours after the @entity63 . One week later, @entity19744 immunostaining was used to examine @entity528 . RESULTS: Intraischemic @entity221 was shown to activate the @entity4124 activity 36 hours after @entity519 - @entity63 while @entity4124 was activated insignificantly in the normothermic @entity519 insult group at that time. The @entity519 also showed a reduced @entity19744 -positive area 7 days after @entity519 - @entity63 compared with that in the normothermia group. CONCLUSION: @entity221 during @entity519 - @entity63 makes the immature brain inordinately susceptible to @entity63 and causes @entity1545 , even if @entity63 is so mild that it causes no or @entity130 by itself. This effect may be mediated by the escalation of the apoptotic cell death pathway in the immature animal.
