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Sridevi Devaraj

Researcher at Baylor College of Medicine

Publications -  390
Citations -  23771

Sridevi Devaraj is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Metabolic syndrome & Proinflammatory cytokine. The author has an hindex of 85, co-authored 365 publications receiving 21831 citations. Previous affiliations of Sridevi Devaraj include University of Madras & Boston Children's Hospital.

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Journal ArticleDOI

Regulation of Inflammatory Phenotype in Macrophages by a Diabetes-Induced Long Noncoding RNA

TL;DR: The diabetic macrophage transcriptome is defined and novel functional roles for lncRNAs in macrophages that could lead to lncRNA-based therapies for inflammatory diabetes complications are defined.
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α-Tocopherol Decreases Interleukin-1β Release From Activated Human Monocytes by Inhibition of 5-Lipoxygenase

TL;DR: In activated human monocytes, AT exerts a novel biological effect of inhibiting the release of the proinflammatory cytokine, IL-1β, via inhibition of the 5-lipoxygenase pathway.
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Oxidative stress, inflammation, and diabetic vasculopathies: the role of alpha tocopherol therapy.

TL;DR: Alpha tocopherol therapy, especially at high doses, clearly shows a benefit with regards to LDL oxidation, isoprostanes and a decrease in inflammatory markers such as C-reactive protein, pro-inflammatory cytokines and PAI-1 levels, and it appears that, in diabetes, alpha tocop herol therapy could emerge as an additional therapeutic modality.
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C-Reactive Protein Decreases Tissue Plasminogen Activator Activity in Human Aortic Endothelial Cells Evidence that C-Reactive Protein Is a Procoagulant

TL;DR: This study provides additional novel data that CRP is a procoagulant and has implications for atherothrombosis, and in volunteers that have high CRP levels, euglobulin clot lysis time was significantly increased compared with those that have low CRP Levels, providing further evidence that highCRP levels are associated with a pro coagulants state.
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α-Tocopherol decreases CD36 expression in human monocyte-derived macrophages

TL;DR: AT decreases both CD36 and SR-A expression and cholesteryl ester accumulation in human macrophages, providing additional scientific support for the antiathero- genic properties of AT.