Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Bacterial DNA (bDNA) can activate an innate-immune stimulatory "danger" response via toll-like receptor 9 (TLR9). Mitochondrial DNA (mtDNA) is unique among endogenous molecules in that mitochondria evolved from prokaryotic ancestors. Thus, mtDNA retains molecular motifs similar to bDNA. ⋯ In summary, mtDNA is released into the circulation by shock. Mitochondrial DNA activates PMN p38 MAPK, probably via TLR9, inducing an inflammatory phenotype. Mitochondrial DNA may act as a danger-associated molecular pattern or alarmin after shock, contributing to the initiation of systemic inflammatory response syndrome.
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Blood transfusion remains an essential treatment of acute anemia. Current storage processes allow the efficient administration of blood products. Erythrocytes undergo morphological and biochemical changes during storage that may affect outcomes after transfusion. ⋯ Corpuscular changes consistent with red cell storage lesions appeared earlier in murine samples compared with human stored pRBCs. Compared with human pRBCs, murine pRBCs exhibit similar but more accelerated aging processes under standard storage conditions. Characterization of the murine red cell storage lesion will allow the application of stored blood components to future investigations into the treatment of acute anemia in experimental murine models.