Pulmonary acute edema analysis of morbid-mortality in the ICU 英文参考文献.docVIP

Available online /supplements/9/S1 Critical Care Volume 9 Suppl 2, 2005 Third International Symposium on Intensive Care and Emergency Medicine for Latin America S?o Paulo, Brazil, 22–25 June 2005 Published online: 9 June 2005 These abstracts are online at /supplements/9/S2 ? 2005 BioMed Central Ltd Basic science Figure 1 Figure 2 Figure 3 P1 Decreased activation of NF-κB and expression of related genes in IRAK-1SNP 532 neutrophils from volunteers exposed to 500 400 300 200 100 0 P = 0.05 endotoxin and in unstimulated neutrophils from septic patients J Arcaroli, E Silva, Q He, D Svetkauskaite, C Coldren, J Maloney, JS Park, E Abraham Division of Pulmonary and Critical Care Medicine, University of Colorado, Denver, Colorado, USA Crit Care 2005, 9(Suppl 2):P1 (DOI 10.1186/cc3545) Mutant 532 Wildtype IRAK-1 Introduction Neutrophils have been involved in sepsis-induced organ damage. Neutrophils could be directly activated by TLR binding ligands including LPS. IRAK-1 is one of many intracellular proteins that are activated upon stimulation of TL receptors. This triggers a series of events that results in the migration of NF-κB into the nucleus and the activation NF-κB-dependent genes. Objectives To identify a single nucleotide polymorphism at position 532 (coding SNP) in volunteers and patients with sepsis. To determine whether IRAK-1SNP532 results in a decrease in neutrophil NF-κB activation in volunteers and patients with sepsis. To evaluate neutrophil gene expression patterns in IRAK-1SNP532 5.0 2.5 0.0 and wildtype patients with sepsis. Methods Thirty severe sepsis patients and 34 healthy volunteers were enrolled in this study. Peripheral blood was obtained and neutrophils were isolated by plasma–percoll gradients after dextran sedimentation of erythrocytes. Neutrophils from volunteers were resuspended in RPMI and cultured with or without 100 ng/ml LPS for 60 min. The electrophoretic mobility