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Elias Castanas

Researcher at University of Crete

Publications -  211
Citations -  10660

Elias Castanas is an academic researcher from University of Crete. The author has contributed to research in topics: Receptor & Cancer. The author has an hindex of 45, co-authored 206 publications receiving 9367 citations. Previous affiliations of Elias Castanas include Pierre-and-Marie-Curie University & National and Kapodistrian University of Athens.

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A new automated method for the determination of the Total Antioxidant Capacity (TAC) of human plasma, based on the crocin bleaching assay

TL;DR: An automated assay to calculate the antioxidant capacity of plasma after a subtraction of all interference deriving from endogenous and/or exogenous metabolites is presented, which can be used as a useful indicator of the antioxidant value of foods and beverages in the daily diet.
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Estrogen anti-inflammatory activity on human monocytes is mediated through cross-talk between estrogen receptor ERα36 and GPR30/GPER1

TL;DR: The expression of estrogen receptors is assessed and it is reported that the only estrogen receptors expressed are estrogen receptor‐α 36‐kDa splice variant and G‐protein coupled receptor 30/G‐protein estrogen receptor 1, in a sex‐independent manner.
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Membrane androgen receptor activation induces apoptotic regression of human prostate cancer cells in vitro and in vivo.

TL;DR: Evidence is provided that activation of mAR by nonpermeable, BSA-coupled testosterone results in inhibition of L NCaP cell growth and induction in LNCaP cells of both apoptosis and the proapoptotic Fas protein, suggesting that activators of m AR may represent a new class of antitumoral agents of prostate cancer.
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Decreased Total and Corrected Antioxidant Capacity in Patients with Inflammatory Bowel Disease

TL;DR: TAC and cTAC are significantly reduced in IBD patients compared with controls irrespective of disease activity, suggesting decreased antioxidant defenses may be a primary phenomenon severely compromising the mucosa and therefore increase susceptibility to oxidative tissue damage.