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. 2014 Aug 21;3(4):e001015. doi: 10.1161/JAHA.114.001015

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© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 4. — EETs limit accumulation of oligomeric amylin at cardiac myocyte sarcolemma. A, The ratio of total EETs to DHETs in plasma from APAU‐treated and untreated HIP rats at the end of the 13 weeks study period. B, Top panel shows representative (of 4 experiments) Western blot with an antiamylin antibody on ventricular myocyte lysates from treated (HIP‐T) vs (HIP‐UT) untreated HIP rats. Bottom panel displays the intensity analysis of the molecular weight bands corresponding to amylin trimers (≈12 kDa), tetramers (≈16 kDa), 16‐mers (≈64 kDa), and 20‐mers (≈80 kDa) in the top panel. C, Total oligomerized amylin in myocyte lysates from rats in HIP‐T and HIP‐UT groups obtained by integrating all molecular weight bands in (B). *P<0.05. APAU indicates (1‐(1‐acetypiperidin‐4‐yl)‐3‐adamantanylurea; DHETs, dihydroxyeicosatrienoic acids; EETs, epoxyeicosatrienoic acids; HIP, human amylin in the pancreas.