M
Michael C. Seeds
Researcher at Wake Forest University
Publications - 54
Citations - 4264
Michael C. Seeds is an academic researcher from Wake Forest University. The author has contributed to research in topics: Phospholipase A2 & Arachidonic acid. The author has an hindex of 25, co-authored 51 publications receiving 3959 citations. Previous affiliations of Michael C. Seeds include Brigham and Women's Hospital & Johns Hopkins University.
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Journal Article
Flow cytometric studies of oxidative product formation by neutrophils: a graded response to membrane stimulation.
David A. Bass,J W Parce,Lawrence R. DeChatelet,Pamela Szejda,Michael C. Seeds,Michael J. Thomas +5 more
TL;DR: The data indicate that the DCFH oxidation assay is quantitatively related to the oxidative metabolic burst of PMNL, and they strongly suggest that the reaction is mediated by H2O2 generated by the PMNL.
Journal Article
Subpopulations of neutrophils with increased oxidative product formation in blood of patients with infection.
TL;DR: The marked increase in oxidative metabolic capability of the primed PMNL may be a significant component of the host response to acute infection and contribute to the damage to host tissues such as pulmonary vascular endothelium during bacteremia.
Journal ArticleDOI
Effect of Dietary Fatty Acids on Inflammatory Gene Expression in Healthy Humans
Kelly L. Weaver,Priscilla Ivester,Michael C. Seeds,L. Douglas Case,Jonathan P. Arm,Floyd H. Chilton +5 more
TL;DR: Data reveal that PUFA may exert their clinical effects via their capacity to regulate the expression of signal transduction genes and genes for proinflammatory cytokines, and may impact inflammatory gene expression.
Journal ArticleDOI
Endogenous signals released from necrotic cells augment inflammatory responses to bacterial endotoxin.
Rabab El Mezayen,Mohamed El Gazzar,Michael C. Seeds,Charles E. McCall,Stephen C. Dreskin,Mark R. Nicolls +5 more
TL;DR: It is demonstrated that HMGB1 and HSP70 released from necrotic cells function as endogenous danger signals to augment the proinflammatory responses in monocytes/macrophage and that TREM-1 relays such signals to the cytokine expression cascade.
Journal ArticleDOI
Phospholipase A2 and arachidonate increase in bronchoalveolar lavage fluid after inhaled antigen challenge in asthmatics.
TL;DR: In this paper, the authors examined the release of secretory PLA2 and arachidonic acid into the airways after antigen challenge in 16 subjects with allergic asthma and found no difference between normal and asthmatic subjects in either BAL fluid (BALF) sPLA2 activity or AA concentration at baseline.