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Carl W. White

Researcher at University of Colorado Denver

Publications -  224
Citations -  9946

Carl W. White is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Lung injury & Hyperoxia. The author has an hindex of 54, co-authored 216 publications receiving 9173 citations. Previous affiliations of Carl W. White include University of Birmingham & National Jewish Health.

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Journal ArticleDOI

Superoxide radical and iron modulate aconitase activity in mammalian cells.

TL;DR: A dynamic and cyclical O-mediated inactivation and iron-dependent reactivation of the mammalian [4Fe-4S] aconitases under normal and stress conditions are demonstrated and provide further evidence for the membrane compartmentalization of O.
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Aconitase is a sensitive and critical target of oxygen poisoning in cultured mammalian cells and in rat lungs

TL;DR: It is proposed that early inactivation of aconitase and inhibition of the energy-producing and biosynthetic reactions of the citric acid cycle contribute to the sequelae of lung damage and edema seen during exposure to hyperoxia.
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Activation of NF-κB by Antineoplastic Agents: ROLE OF PROTEIN KINASE C

TL;DR: It is unlikely that activation of NF-kappaB caused by antineoplastic agents or by paclitaxel is mediated via cytokine up-regulation, as two other groups of anticancer drugs including vinca alkaloids and anthracyclines, neither of which induce TNF or interleukin-1 gene expression, were examined.
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Hypoxia increases production of interleukin-1 and tumor necrosis factor by human mononuclear cells.

TL;DR: It is concluded that hypoxia increases IL-1 and TNF production and speculate that this mechanism aggravates a variety of pathologic conditions involving endotoxin such as adult respiratory distress syndrome (ARDS), multiple organ failure, and septic shock.
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Endotoxin pretreatment increases endogenous myocardial catalase activity and decreases ischemia-reperfusion injury of isolated rat hearts

TL;DR: The results suggest that endotoxin pretreatment decreases cardiac ischemia-reperfusion injury and that increases in endogenous myocardial catalase activity contribute to protection.