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. 2022 Dec 1;43(2):267–285. doi: 10.1161/ATVBAHA.122.317800

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© 2022 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 7. — Absence of staphylocoagulases, but not of nucleases, improves endocarditis outcome. A–D, Proportions of mice that developed inflammation-induced endocarditis (A) or sterile thrombi (B) at day 3, bacteremia levels at end point (n=9, 10, C), and survival rates (n=12, 12, D) of mice infected with the nuclease mutant (Δnuc [nucleases]) compared to wild-type (WT) Staphylococcus aureus USA300. E–H, Proportions of mice that developed inflammation-induced endocarditis (E) or sterile thrombi (F) at day 3, bacteremia levels at endpoint (n=23, 26, G), and survival rates (n=27, 26, H) of mice infected with a mutant doubly deficient in ΔcoaΔvwb (coagulase and von Willebrand factor binding protein) compared to WT S. aureus USA300. Median (interquartile range) are represented in C and G. Fisher Exact (A and B, E and F), Mann-Whitney test (C and G), and log-rank (Mantel-Cox; D and H) tests were conducted to determine significance. CFU indicates colony-forming units.