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Carol A. Colton

Researcher at Duke University

Publications -  132
Citations -  10771

Carol A. Colton is an academic researcher from Duke University. The author has contributed to research in topics: Microglia & Apolipoprotein E. The author has an hindex of 52, co-authored 129 publications receiving 9820 citations. Previous affiliations of Carol A. Colton include University of Nevada, Reno & Georgetown University.

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The chemical biology of nitric oxide: implications in cellular signaling.

TL;DR: Signal transduction and the chemical biology of NO in terms of the direct and indirect reactions are discussed, with general results that promote cell survival and proliferation, whereas higher levels favor cell cycle arrest, apoptosis, and senescence.
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Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain

TL;DR: The immune response in the brain has been widely investigated and while many studies have focused on the proinflammatory cytotoxic response, the brain’s innate immune system demonstrates significant heterogeneity.
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Production of superoxide anions by a CNS macrophage, the microglia

TL;DR: The specific ability of microglia to secrete the superoxide radical ion in response to a complement activated agent, opsonized zymosan, and to phorbol myristate acetate is demonstrated.
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Nitric oxide and redox mechanisms in the immune response

TL;DR: The chemistry of NO and ROS in the context of antipathogen activity and immune regulation is discussed and similarities and differences between murine and human production of these intermediates are discussed.
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Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD

TL;DR: The findings confirmed that treatment of microglia with anti-inflammatory cytokines such as IL-4 and IL-13 induces a gene profile typical of alternative activation similar to that previously observed in peripheral macrophages and suggest that innate immune cells in AD may exhibit a hybrid activation state that includes characteristics of classical and alternative activation.