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Bruce N. Cronstein
Researcher at New York University
Publications - 299
Citations - 23902
Bruce N. Cronstein is an academic researcher from New York University. The author has contributed to research in topics: Adenosine & Adenosine receptor. The author has an hindex of 77, co-authored 290 publications receiving 21738 citations. Previous affiliations of Bruce N. Cronstein include University of York & York University.
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Adenosine receptors: therapeutic aspects for inflammatory and immune diseases
TL;DR: This work has generated excitement regarding the potential use of adenosine-receptor-based therapies in the treatment of infection, autoimmunity, ischaemia and degenerative diseases.
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Adenosine 5'-triphosphate and adenosine as endogenous signaling molecules in immunity and inflammation
TL;DR: The overwhelming evidence indicates that ATP and Ado are important endogenous signaling molecules in immunity and inflammation, and it is proposed that their immunological role is both interdependent and multifaceted, meaning that the nature of their effects may shift from immunostimulatory to immunoregulatory or vice versa depending on extracellular concentrations as well as on expression patterns of purinergic receptors and ecto-enzymes.
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Adenosine: an endogenous regulator of innate immunity
TL;DR: Adenosine, a purine nucleoside that is elaborated at injured and inflamed sites, has a central role in the regulation of inflammatory responses and in limiting inflammatory tissue destruction.
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A mechanism for the antiinflammatory effects of corticosteroids: the glucocorticoid receptor regulates leukocyte adhesion to endothelial cells and expression of endothelial-leukocyte adhesion molecule 1 and intercellular adhesion molecule 1.
TL;DR: These studies suggest that antagonism by dexamethasone of endotoxin-induced inflammation is a specific instance of the general biological principle that the glucocorticoid receptor is a hormone-dependent regulator of transcription.
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The antiinflammatory mechanism of methotrexate. Increased adenosine release at inflamed sites diminishes leukocyte accumulation in an in vivo model of inflammation.
TL;DR: Results indicate that methotrexate is a nonsteroidal antiinflammatory agent, the antiphlogistic action of which is due to increased adenosine release at inflamed sites.