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Jill B. Lewis

Researcher at Georgia Regents University

Publications -  82
Citations -  3098

Jill B. Lewis is an academic researcher from Georgia Regents University. The author has contributed to research in topics: Cytokine secretion & Oxidative stress. The author has an hindex of 32, co-authored 82 publications receiving 2953 citations. Previous affiliations of Jill B. Lewis include Western University of Health Sciences.

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Green Tea Polyphenol Causes Differential Oxidative Environments in Tumor versus Normal Epithelial Cells

TL;DR: It is concluded that pathways activated by GTPPs or EGCG in normal epithelial versus tumor cells create different oxidative environments, favoring either normal cell survival or tumor cell destruction, which may lead to applications of naturally occurring polyphenols to enhance the effectiveness of chemo/radiation therapy to promote cancer cell death while protecting normal cells.
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Green Tea Polyphenols Induce Differentiation and Proliferation in Epidermal Keratinocytes

TL;DR: The results suggest that tea polyphenols may be used for treatment of wounds or certain skin conditions characterized by altered cellular activities or metabolism.
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In vitro cytotoxicity of resin-containing restorative materials after aging in artificial saliva.

TL;DR: It is concluded that all of these commercially available resin-based dental materials continue to release sufficient components to cause lethal effects or alter cellular function in vitro even after 2 weeks of aging in artificial saliva.
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Roles of catalase and hydrogen peroxide in green tea polyphenol-induced chemopreventive effects.

TL;DR: It was found that normal human keratinocytes with high catalase activity are least susceptible to H2O2, whereas H2 O2 caused significant cytotoxicity in oral carcinoma cell lines, however, the EGCG-induced differential effects could not be duplicated by H 2O2alone.
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Estrogenicity of bisphenol A and bisphenol A dimethacrylate in vitro

TL;DR: Flow cytometric methods demonstrated that these mitogenic effects occurred within 24 h of exposure to estrogen, BPA, or BPA-DM, and the increase in DNA synthesis was analogous to that seen with estrogen stimulation.