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Charles C. Caldwell

Researcher at University of Cincinnati

Publications -  161
Citations -  6965

Charles C. Caldwell is an academic researcher from University of Cincinnati. The author has contributed to research in topics: Sepsis & Inflammation. The author has an hindex of 41, co-authored 149 publications receiving 6000 citations. Previous affiliations of Charles C. Caldwell include Cincinnati Children's Hospital Medical Center & Medical University of South Carolina.

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Physiological control of immune response and inflammatory tissue damage by hypoxia-inducible factors and adenosine A2A receptors.

TL;DR: A2A receptor-triggered generation of intracellular cAMP inhibits activated immune cells in a delayed negative feedback manner to prevent additional tissue damage, and targeting A2A adenosine receptors may have important clinical applications.
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Differential effects of physiologically relevant hypoxic conditions on T lymphocyte development and effector functions.

TL;DR: The ambient 20% oxygen tension (plus 2-ME) is remarkably well suited for immunologic specificity and cytotoxicity studies, but oxygen dependence should be taken into account during the design and interpretation of results of in vitro T cell development assays and gene expression studies in vivo.
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Oxygenation inhibits the physiological tissue-protecting mechanism and thereby exacerbates acute inflammatory lung injury.

TL;DR: It is shown that this potential complication of clinically widely used oxygenation procedures could be completely prevented by intratracheal injection of a selective A2AR agonist to compensate for the oxygenation-related loss of the lung tissue-protecting endogenous adenosine.
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IL-7 Promotes T Cell Viability, Trafficking, and Functionality and Improves Survival in Sepsis

TL;DR: Rec recombinant human IL-7 efficacy and potential mechanisms of action were tested in a murine peritonitis model and showed that rhIL-7 markedly improved host survival, blocked apoptosis of CD4 and CD8 T cells, restored IFN-γ production, and improved immune effector cell recruitment to the infected site.