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Alexander H. Kortsaris

Researcher at Aristotle University of Thessaloniki

Publications -  19
Citations -  961

Alexander H. Kortsaris is an academic researcher from Aristotle University of Thessaloniki. The author has contributed to research in topics: Cytotoxicity & Apoptosis. The author has an hindex of 16, co-authored 19 publications receiving 930 citations.

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Optimization of the sulforhodamine B colorimetric assay

TL;DR: It is concluded that aspiration of the growth medium prior to fixing comprises a safe and reliable practice which improves CV, linearity and the signal-to-noise ratio of the SRB assay.
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Copper(II) Schiff base coordination compounds of dien with heterocyclic aldehydes and 2-amino-5-methyl-thiazole: synthesis, characterization, antiproliferative and antibacterial studies. Crystal structure of CudienOOCl2.

TL;DR: The study of the biological activity of the compounds synthesized against a panel of different normal and cancer cell lines and bacteria showed that the adducts of the type [ Cu(dienXXY(2))(2a-5mt)] exhibit increased activity both in cancer cells and in bacteria, compared to the starting material of type [Cu(diensXXY (2))].
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In vitro evaluation of the cytotoxicity of calcium hydroxide-based root canal sealers

TL;DR: The cytotoxicity of three calcium hydroxide-containing root canal sealers was tested by using L929 and BHK 21/C13 cells and Apexit proved to be the least toxic material.
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Antiproliferative effect of mineral trioxide aggregate, zinc oxide-eugenol cement, and glass-ionomer cement against three fibroblastic cell lines.

TL;DR: The degree of antiproliferative effect in ascending order was mineral trioxide aggregate, glass-ionomer cement, and zinc oxide-eugenol cement in all cell lines tested.
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Antiproliferative activity of mixed-ligand dien-Cu(II) complexes with thiazole, thiazoline and imidazole derivatives.

TL;DR: All [(dien)Cu(B)NO(3) NO(3)) complexes had an activity against colon cancer cells (HT-29), inducing G2/M cell cycle arrest, an effect that for most of the complexes could be attributed to p34cdc2 inhibition by tyrosine-phosphorylation and/or to induction of (cyclin-dependent kinase inhibitor) p21(WAF1).