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. 2017 Oct 19;6(10):e006680. doi: 10.1161/JAHA.117.006680

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© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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PHD3 overexpression improves IH‐induced cardiac dysfunction. A, Representative echocardiographic images of 2D echocardiograms, M‐mode echocardiograms, pulsed‐wave Doppler echocardiograms, and tissue Doppler echocardiograms in all groups. B, Quantitative analysis of echocardiographic measurements parameters. b1, Interventricular septum dimension (IVSD). b2, Left ventricular end‐diastolic dimension (LVIDd). b3, Left ventricular end‐systolic dimension (LVIDs). b4, Left ventricle posterior wall dimension (LVPWd). b5, Left ventricular ejection fraction (LVEF). b6, Fractional shortening (FS). b7, Early to late mitral flow (E/A). b8, Early to late ratio of diastolic mitral annulus velocities (E′/A′). Data are mean±SD; n=10 per group. *P<0.05 vs IH+LvNC; **P<0.01 vs IH+LvNC. 2D indicates 2‐dimensional; IH, intermittent hypoxia; LvPHD3, lentivirus carrying PHD3 cDNA; PHD3, prolyl 4‐hydroxylase domain protein 3; shPHD3, short‐hairpin PHD3.