@entity1779 Contributes to XXXX After Intraventricular Hemorrhage via Aggravating @entity68 Accumulation.

@entity1 @entity1545 @entity5532 @entity1276 @entity548 @entity16 @entity2554 @entity51 @entity1410 @entity35 @entity1779 @entity68
BACKGROUND AND PURPOSE: The @entity548 ( @entity548 ) secondary to @entity1779 ( @entity1779 ) was reported to be relevant to a higher incidence of @entity1276 , which would result in poorer outcomes for @entity1 with @entity1779 . However, the mechanisms responsible for this relationship remain poorly characterized. Thus, this study was designed to further explore the development and progression of @entity1276 after secondary @entity548 . METHODS: Autologous blood injection model was induced to mimic @entity1779 with ventricular extension ( @entity1779 / @entity548 ) or primary @entity548 in @entity35 . Magnetic resonance imaging, Morris water maze, brain water content, Evans blue extravasation, immunohistochemistry staining, Western blot, @entity68 determination, and electron microscopy were used in these @entity35 . Then, @entity5532 treatment was used to clarify the involvement of @entity68 in the development of @entity1276 . RESULTS: Despite the injection of equivalent blood volumes, @entity1779 / @entity548 resulted in more significant @entity2554 , @entity16 , and @entity68 overload, as well as more severe early @entity1545 and @entity51 compared with @entity548 alone. Systemic @entity5532 treatment more effectively reduced ventricular enlargement in @entity1779 / @entity548 compared with primary @entity548 . CONCLUSIONS: Our results show that @entity1779 / @entity548 caused more significant chronic @entity1276 and @entity68 accumulation than primary @entity548 alone. Intracerebral @entity1410 plays a vital role in persistent @entity68 overload and aggravated @entity1276 after @entity1779 / @entity548 .
