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Neutrophils induce sequential focal changes in endothelial adherens junction components: role of elastase.Endothelial E- and P-selectin expression in iNOS- deficient mice exposed to polymicrobial sepsis.Neutrophil-endothelial cell interactions during the development of tolerance to ischaemia/reperfusion in isolated cells.Interaction between reactive oxygen metabolites and nitric oxide in oxidant tolerance.Human severe sepsis cytokine mixture increases β2-integrin-dependent polymorphonuclear leukocyte adhesion to cerebral microvascular endothelial cells in vitro.Inflammatory response in microvascular endothelium in sepsis: role of oxidants.Mechanisms and consequences of acquired brain injury during development.Translational research in pediatrics II: blood collection, processing, shipping, and storage.Anoxia/reoxygenation-induced tolerance with respect to polymorphonuclear leukocyte adhesion to cultured endothelial cells. A nuclear factor-kappaB-mediated phenomenon.Early mobilization in the critical care unit: A review of adult and pediatric literature.Elevated Leukocyte Azurophilic Enzymes in Human Diabetic Ketoacidosis Plasma Degrade Cerebrovascular Endothelial Junctional Proteins.Pretreatment of human cerebrovascular endothelial cells with CO-releasing molecule-3 interferes with JNK/AP-1 signaling and suppresses LPS-induced proadhesive phenotype.Lung-derived mediators induce cytokine production in downstream organs via an NF-κB-dependent mechanism.Tumor necrosis factor-alpha-induced cytokine-induced neutrophil chemoattractant-1 (CINC-1) production by rat gastric epithelial cells: role of reactive oxygen species and nuclear factor-kappaB.Simulated diabetic ketoacidosis therapy in vitro elicits brain cell swelling via sodium-hydrogen exchange and anion transport.Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice.PAF-induced elastase-dependent neutrophil transendothelial migration is associated with the mobilization of elastase to the neutrophil surface and localization to the migrating front.Albumin leak across human pulmonary microvascular vs. umbilical vein endothelial cells under septic conditions.Inducible NO synthase (iNOS) in human neutrophils but not pulmonary microvascular endothelial cells (PMVEC) mediates septic protein leak in vitro.Anti-alpha4beta1 integrin antibody induces receptor internalization and does not impair the function of circulating neutrophilic leukocytes.Mediators released from LPS-challenged lungs induce inflammatory responses in liver vascular endothelial cells and neutrophilic leukocytes.Carbon monoxide-releasing molecules protect against ischemia-reperfusion injury during kidney transplantation.Cardiac myocytes activated by septic plasma promote neutrophil transendothelial migration: role of platelet-activating factor and the chemokines LIX and KC.Diabetic ketoacidosis elicits systemic inflammation associated with cerebrovascular endothelial cell dysfunction.Hindlimb ischemia/reperfusion-induced remote injury to the small intestine: role of inducible nitric-oxide synthase-derived nitric oxide.Human neutrophil-pulmonary microvascular endothelial cell interactions in vitro: differential effects of nitric oxide vs. peroxynitrite.Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice.Endotoxin-induced adhesion of human red blood cells to vascular endothelium does not depend on the presence of leukocytes but is modified by different flow pattern.Nitric oxide synthase activities in white blood cells of septic patients.Carbon monoxide-releasing molecule, CORM-3, modulates alveolar macrophage M1/M2 phenotype in vitro.Traumatic injury elicits JNK-mediated human astrocyte retraction in vitro.Systemic Administration of Carbon Monoxide-Releasing Molecule-3 Protects the Skeletal Muscle in Porcine Model of Compartment Syndrome.[Molecular mechanism of inhibition of early pulmonary injury and inflammatory response by exogenous carbon monoxide: experiment with mice].Carbon monoxide-releasing molecule 3 inhibits myeloperoxidase (MPO) and protects against MPO-induced vascular endothelial cell activation/dysfunction.Carbon Monoxide-Releasing Molecule-401 Suppresses Polymorphonuclear Leukocyte Migratory Potential by Modulating F-Actin Dynamics.Systemic application of carbon monoxide-releasing molecule 3 protects skeletal muscle from ischemia-reperfusion injury.Carbon monoxide releasing molecules inhibit cell death resulting from renal transplantation related stress.Carbon monoxide releasing molecule-3 improves myocardial function in mice with sepsis by inhibiting NLRP3 inflammasome activation in cardiac fibroblasts.Compartment syndrome causes systemic inflammation in a rat.Contribution of inflammation to cellular injury in compartment syndrome in an experimental rodent model.
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