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Elaine M. Conner

Researcher at Louisiana State University

Publications -  18
Citations -  1637

Elaine M. Conner is an academic researcher from Louisiana State University. The author has contributed to research in topics: Transcription factor & Proinflammatory cytokine. The author has an hindex of 14, co-authored 18 publications receiving 1579 citations. Previous affiliations of Elaine M. Conner include LSU Health Sciences Center Shreveport.

Papers
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Journal ArticleDOI

Inflammation, free radicals, and antioxidants

Elaine M. Conner, +1 more
- 01 Apr 1996 - 
TL;DR: Keeping adequate antioxidant status may provide a useful approach in attenuating the cellular injury and dysfunction observed in some inflammatory disorders.
Journal ArticleDOI

Role of the proteasome and NF-κB in streptococcal cell wall-induced polyarthritis

TL;DR: Oral administration of PS-341 had anti-inflammatory effects in a model of Streptococcal cell wall-induced polyarthritis and liver inflammation in rats and demonstrated that the ubiquitin-proteasome pathway and NF-kappaB play important roles in regulating chronic inflammation and that proteasome inhibition has an anti- inflammation effect.
Journal Article

Proteasome Inhibition Attenuates Nitric Oxide Synthase Expression, VCAM-1 Transcription and the Development of Chronic Colitis

TL;DR: It is concluded that the 26S proteasome complex plays an important role in regulating the PG/PS-induced up-regulation of iNOS and VCAM-1 in vivo and appears to be important in regulating colonic and splenic inflammation.
Book ChapterDOI

Inhibition of nf-kappa b activation in vitro and in vivo : role of 26s proteasome

TL;DR: Data obtained from studies in the laboratories demonstrate that the proteasome plays an important role in the inflammatory cascade by regulating the activation of NF-kappa B.
Journal ArticleDOI

Role of reactive metabolites of oxygen and nitrogen in inflammatory bowel disease: Toxins, mediators, and modulators of gene expression

TL;DR: Data suggest that the sustained overproduction of these reactive species in the chronically inflamed gut may contribute to the pathophysiology of IBD by enhancing the production of toxins, mediators, and modulators of gene expression.