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Background: Blood product transfusions are necessary for critically ill neonates on extracorporeal membrane oxygenation (ECMO). Transfusions are administered in response to unstudied arbitrary thresholds and may be associated with adverse outcomes. The objective of this study was to identify relationships between blood product components and mortality in neonates receiving ECMO support for respiratory indications.Study Design and Methods: A retrospective review of neonates receiving ECMO for respiratory indications from 2002 to 2019 from a single quaternary-referral neonatal intensive care unit (NICU). Demographic and outcome data and transfusion volume (ml/kg/day) were harvested

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Activation of the T cell receptor (TCR) through antigen binding results in chromatin decondensation required for the clonotypic proliferation observed during a proper immune response. Activation of the TCR results in the cleavage of phospholipase biphosphate (PIP2) into diacylglyercol (DAG) and inositol trisphosphate (IP3) by phospholipase C-γ (PLC-γ). Previous studies have shown that both the DAG and IP3 pathways can decondense chromatin, and that intracellular calcium is required for proper TCR-mediated chromatin decondensation. In this study, we used flow cytometry to analyze histone accessibility of chromatin in T cells and found that PKC activation is also required for proper activation-induced chromatin decondensation. Furthermore, we show that calcium is required for proper PKC-mediated chromatin decondensation. Our studies suggest that the PKC isoform(s) required for decondensation may be calcium-dependent. Finally, we show that activation of PKC and not IP3 is required for T cells to gain competence to respond to cytokine stimulation. Taken together, our data suggest that IP3 and PKC signaling work cooperatively to decondense chromatin and regulate clonotypic expansion of T cells during an immune response.