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. 2019 Nov 7;40(1):189–205. doi: 10.1161/ATVBAHA.119.313336

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© 2019 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 1. — Mouse model of aortic dissection (AD). The mouse AD model was created by continuous infusion of β-aminopropionitrile (BAPN) and Ang II (angiotensin II) for 14 d. A, Representative macroscopic and histological images from hematoxylin-eosin (HE) and Elastica van Gieson (EVG) staining taken before (normal) and after BAPN+Ang II (B+A) treatment. Scale bar=500 μm. B, The incidence of AD for the indicated doses of B+A (1000 ng/kg per min). C, The incidence of AD by 150 mg/kg per d BAPN and 1000 ng/kg per min Ang II. The numbers of mice in each group are shown in parentheses. D, Volcano plots comparing the control (Cont; without any challenge) and B+A AD models, and human aortas with a normal tricuspid aortic valve (TAV) and congenitally abnormal bicuspid aortic valve (BAV). The blue-shaded area and the red-shaded area indicate the genes with significant (P<0.05) suppression (fold change, <0.5) and induction (fold change, >2), respectively.