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Janet S. Kerr

Researcher at DuPont

Publications -  36
Citations -  1398

Janet S. Kerr is an academic researcher from DuPont. The author has contributed to research in topics: Phospholipase A2 & Extracellular. The author has an hindex of 14, co-authored 36 publications receiving 1348 citations. Previous affiliations of Janet S. Kerr include Harvard University.

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Journal Article

Involvement of endothelial PECAM-1/CD31 in angiogenesis.

TL;DR: Findings provide evidence that PECAM-1 is involved in angiogenesis and suggest that the interactions of endothelial cell-cell adhesion molecules are important in the formation of new vessels.
Journal Article

Anti-inflammatory and safety profile of DuP 697, a novel orally effective prostaglandin synthesis inhibitor.

TL;DR: DuP 697 (5-bromo-2[4-fluorophenyl]-3-[4-methylsulfonylphenyl]-thiophene) is a potent inhibitor of paw swelling in nonestablished and established adjuvant arthritis in rats (ED50 = 0.03 and 0.18 mg/kg/day, respectively).
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2'-substituted chalcone derivatives as inhibitors of interleukin-1 biosynthesis

TL;DR: A series of 2'-substituted chalcone derivatives has been found to show potent inhibition of the production of IL-1 beta from human peripheral blood monocytes stimulated with lipopolysaccharide, suggesting a degree of selectivity which would not be expected for simple, nonspecific alkylating agents.
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Effects of recombinant interleukin-1 beta on phospholipase A2 activity, phospholipase A2 mRNA levels, and eicosanoid formation in rabbit chondrocytes

TL;DR: The effects of recombinant interleukin-1 beta (rIL-1beta) on phospholipase A2 activity (PLA2), PLA2 messenger RNA levels, and eicosanoid production in rabbit chondrocytes are investigated.
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Early Murine Lyme Carditis Has a Macrophage Predominance and Is Independent of Major Histocompatibility Complex Class Ii-Cd4+ T Cell Interactions

TL;DR: It is demonstrated that early murine Lyme carditis requires neither class II antigen expression nor presentation of antigen to CD4+ T lymphocytes and suggested a direct response of macrophages to cardiac tissue invasion by B. burgdorferi.