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. 2015 Feb 17;12:4. doi: 10.1186/2045-8118-12-4

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© Engelhardt et al.; licensee BioMed Central. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Hypoxic/ischemic exposure differentially modulates metabolic activity of EC and perivascular cells. Viability of primary ECs, ACs and PCs was measured by MTT conversion after exposure to NX, HX and AX in presence (solid bars) and absence (hatched bars) of glucose for 24 h (A) and 48 h (B). Data was normalized to normoxic baseline (NX + Glc). N = 3-5. **P < 0.01, ***P < 0.001; 1-way ANOVA compared to normoxia + glucose. ^§§ P < 0.01, ^§§§ P < 0.001; 1-way ANOVA compared to normoxia-glucose. ^# P < 0.05, ^## P < 0.01, ^### P < 0.001; 2-way ANOVA comparing + to - glucose. EC: primary endothelial cell, AC: astrocyte, PC: pericyte, NX: normoxia, HX: hypoxia, AX: near anoxia, +Glc: with glucose, -Glc: without glucose.