Volume 150, Issue 2, Pages 471-473 (August 2016) Normoxic Recovery Reverses Intermittent Hypoxia-Induced Systemic and Vascular Inflammation  Claire Arnaud, PharmD, PhD, Pauline Béguin, PhD, Patrick Lévy, MD, PhD, Jean-Louis Pépin, MD, PhD  CHEST  Volume 150, Issue 2, Pages 471-473 (August 2016) DOI: 10.1016/j.chest.2016.05.031 Copyright © 2016 American College of Chest Physicians Terms and Conditions

Figure 1 A-C, Splenic chemokine mRNA expressions (A), splenocyte proliferative capacities in response to increasing doses of concanavalin A (Con-A) (B), and aortic NF-κB protein expression (C). All these experiments were realized on tissues from mice exposed to either 14 days of intermittent hypoxia (IH) or normoxia (N) and 14 days of IH or N, followed by 7 days of normoxic recovery (n = 5-10 per group; *P < .05 vs N). GADPH = glyceraldehyde 3-phosphate dehydrogenase; MCP-1 = monocyte chemotactic protein-1; MIP-1 = macrophage inflammatory protein-1; p50NFκB = p50 subunit of nuclear factor kappa B; RANTES = regulated on activation, normal T cell expressed and secreted. (Reprinted with permission of the American Thoracic Society from by Arnaud et al.2 Copyright © 2016 American Thoracic Society.) CHEST 2016 150, 471-473DOI: (10.1016/j.chest.2016.05.031) Copyright © 2016 American College of Chest Physicians Terms and Conditions