Abstract-Endothelial progenitor cells (EPCs) contribute to endothelial regeneration. Angiotensin II (Ang II) through Ang II type 1 receptor (AT 1 -R) activation plays an important role in vascular damage. The effect of Ang II on EPCs and the involved molecular mechanisms are incompletely understood. Stimulation with Ang II decreased the number of cultured human early outgrowth EPCs, which express both AT 1 -R and Ang II type 2 receptor, mediated through AT 1 -R activation and induction of oxidative stress. Ang II redox-dependently induced EPC apoptosis through increased apoptosis signal-regulating kinase 1, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase phosphorylation; decreased Bcl-2 and increased Bax expression; and activation of caspase 3 but had no effect on the low cell proliferation. In addition, Ang II impaired colony-forming and migratory capacities of early outgrowth EPCs. Ang II infusion diminished numbers and functional capacities of EPCs in wild-type (WT) but not AT 1 a-R knockout mice (AT 1 a Ϫ/Ϫ). Reendothelialization after focal carotid endothelial injury was decreased during Ang II infusion. Salvage of reendothelialization by intravenous application of spleen-derived progenitor cells into Ang II-treated WT mice was pronounced with AT 1 a Ϫ/Ϫ cells compared with WT cells, and transfusion of Ang II-pretreated WT cells into WT mice without Ang II infusion was associated with less reendothelialization. Transplantation of AT 1 a Ϫ/Ϫ bone marrow reduced atherosclerosis development in cholesterol-fed apolipoprotein E-deficient mice compared with transplantation of apolipoprotein E-deficient or WT bone marrow. Randomized treatment of patients with stable coronary artery disease with the AT 1 -R blocker telmisartan significantly increased the number of circulating CD34/KDR-positive EPCs. Ang II through AT 1 -R activation, oxidative stress, and redox-sensitive apoptosis signal-regulating kinase 1-dependent proapoptotic pathways impairs EPCs in vitro and in vivo, resulting in diminished vascular regeneration. (Hypertension. 2011;58:394-403.) • Online Data Supplement

This is the first time the patient population of a center experienced with esophageal cancer surgery was assessed for the occurrence of general and esophageal cancer surgery-specific perioperative complications. Our results indicated that these complications did not affect long-term survival of EAC and SCC patients. Our data support the hypothesis that neoadjuvant treatment might not affect the incidence of perioperative complications or long-term survival after treatment of these tumor subtypes.

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All subjects improved in skill significantly throughout the week regardless of the timing of the training intervention. Simulation training can be offered outside of regular working hours with acceptable effectiveness.