Identification, characterization, and gene expression profiling of endotoxin-induced XXXX .

@entity296 @entity295 @entity326 @entity39 @entity409 @entity842 @entity1850 @entity299 @entity3623 @entity2401
In @entity326 , reversible @entity299 starts within 24 h. @entity296 factors are thought to cause @entity409 , resulting in alterations of intrinsic cardiac function. @entity842 is a @entity296 factor candidate. Here we identify endotoxin-induced @entity2401 (EIM) a previously uncharacterized pathophysiological entity. Features of EIM include differential patterns of @entity3623 ( @entity3623 ) mRNA induction in the left (LV) and right (RV) ventricles during the @entity1850 ( @entity1850 ) and the presence of @entity2401 with focal areas of @entity39 in the RV 24 h after @entity1850 induction. Even though clinical data lead to the presumption of @entity296 in @entity295 , the underlying pathophysiological mechanisms have not been previously elucidated. Gene expression profiling was used to test the hypothesis of differential LV and RV responses in EIM, and revealed novel patterns of qualitative and quantitative expansion of transcription. Those genes are novel targets for drug development in @entity1850 and @entity295 . Our results demonstrate spatial and temporal heterogeneity of myocardial responses in EIM. These findings justify the design of treatments to ameliorate tissue injury in the RV. Because the complexity of the inflammatory response increases substantially as time elapses, we suggest a stepwise and multitarget therapeutic approach for @entity1850 and @entity295 . Our findings can help identify innate immune pathways that could become targets for immunotherapy in the treatment of disease caused by potential bioterrorism agents.
