S
Samuel S. Edwin
Researcher at Wayne State University
Publications - 91
Citations - 5820
Samuel S. Edwin is an academic researcher from Wayne State University. The author has contributed to research in topics: Amnion & Amniotic fluid. The author has an hindex of 41, co-authored 91 publications receiving 5585 citations. Previous affiliations of Samuel S. Edwin include United States Department of Health and Human Services & Seoul National University.
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A fetal systemic inflammatory response is followed by the spontaneous onset of preterm parturition
Roberto Romero,Ricardo Gomez,Fabio Ghezzi,Bo Hyun Yoon,Moshe Mazor,Samuel S. Edwin,Stanley M. Berry +6 more
TL;DR: In this article, the authors proposed that preterm labor in the setting of infection results from the actions of proinflammatory cytokines secreted as part of the fetal and/or maternal host response to microbial invasion.
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Evidence supporting a role for blockade of the vascular endothelial growth factor system in the pathophysiology of preeclampsia: Young Investigator Award
Tinnakorn Chaiworapongsa,Roberto Romero,Jimmy Espinoza,Emmanuel Bujold,Yeon Mee Kim,Luís F. Gonçalves,Ricardo Gomez,Samuel S. Edwin +7 more
TL;DR: Observations suggest the participation of VEGF and its soluble receptor in the pathophysiology of preeclampsia is suggested, and the elevation of sVEGFR-1 concentration is correlated with the severity of the disease.
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Pathogenesis of preterm labor and preterm premature rupture of membranes associated with intraamniotic infection
TL;DR: Evidence is provided that infection is an important factor in the pathogenesis of these conditions, preterm parturition should be considered as a syndrome with multiple causes.
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Interleukin-6 stimulates prostaglandin production by human amnion and decidual cells
TL;DR: The concentrations of interleukin-6 required for this stimulatory action are within the range measured in amniotic fluid of women with intrauterine infections and preterm labor, and may contribute to the mechanism of pre term labor under these conditions.
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A role for matrix metalloproteinase-9 in spontaneous rupture of the fetal membranes.
Neil Athayde,Samuel S. Edwin,Roberto Romero,Ricardo Gomez,Eli Maymon,Percy Pacora,Ramkumar Menon +6 more
TL;DR: A role for matrix metalloproteinase-9 in the mechanisms responsible for membrane rupture in term and preterm gestations is supported, and spontaneous rupture of membranes at term is associated with a significant increase in the amniotic fluid concentrations of matrix meetallop Proteinase 9.