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Richard B. Johnston

Researcher at Yale University

Publications -  25
Citations -  3118

Richard B. Johnston is an academic researcher from Yale University. The author has contributed to research in topics: Glutathione & Respiratory burst. The author has an hindex of 19, co-authored 25 publications receiving 3012 citations. Previous affiliations of Richard B. Johnston include University of Colorado Denver.

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Chronic granulomatous disease. Report on a national registry of 368 patients.

TL;DR: A registry of United States residents with chronic granulomatous disease (CGD) was established in 1993 in order to estimate the minimum incidence of this uncommon primary immunodeficiency disease and characterize its epidemiologic and clinical features.
Journal Article

Mechanisms of host defense against Candida species. I. Phagocytosis by monocytes and monocyte-derived macrophages.

TL;DR: Uptake mediated by the macrophage mannose receptor could play a role in clearance of Candida under opsonin-poor conditions.
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Targeted lung expression of interleukin-11 enhances murine tolerance of 100% oxygen and diminishes hyperoxia-induced DNA fragmentation.

TL;DR: It is demonstrated that IL-11 markedly diminishes hyperoxic lung injury and this protection is associated with small changes in lung antioxidants, diminished hyperoxia-induced IL-1 and TNF production, and markedly suppressed hyperoxIA-induced DNA fragmentation.
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S-thiolation of glyceraldehyde-3-phosphate dehydrogenase induced by the phagocytosis-associated respiratory burst in blood monocytes.

TL;DR: Results indicate that during the respiratory burst in monocytes, low molecular weight thiols can bind to specific cytosolic proteins, including GAPDH, including glutathione and cysteine, which serves to modulate cellular metabolic events during phagocytosis.
Journal ArticleDOI

Targeted Lung Expression of Interleukin-11 Enhances Murine Tolerance of 100% Oxygen and Diminishes Hyperoxia-Induced DNA Fragmentation

TL;DR: It is demonstrated that IL-11 markedly diminishes hyperoxic lung injury and this protection is associated with small changes in lung antioxidants, diminished hyperoxia-induced IL-1 and TNF production, and markedly suppressed hyperoxiainduced DNA fragmentation.