The endothelium in sepsis: source of and a target for inflammation.
about
Targeted inhibition of STATs and IRFs as a potential treatment strategy in cardiovascular diseaseClinical utility of biomarkers of endothelial activation in sepsis--a systematic reviewPlasma thrombin activatable fibrinolysis inhibitor and tissue factor pathway inhibitor changes following sepsisDrotrecogin alfa (activated) in the treatment of severe sepsis patients with multiple-organ dysfunction: data from the PROWESS trial.New and emerging therapies for sepsis.Chronic hyperbaric exposure activates proinflammatory mediators in humans.Reaping of nitric oxide by sickle cell disease.Glutathione peroxidase-1 modulates lipopolysaccharide-induced adhesion molecule expression in endothelial cells by altering CD14 expression.The tyrosine kinase Pyk2 mediates lipopolysaccharide-induced IL-8 expression in human endothelial cells.Hypoxia-inducible factor 2alpha regulates macrophage function in mouse models of acute and tumor inflammationTherapeutic interventions in sepsis: current and anticipated pharmacological agentsThe interface between monitoring and physiology at the bedside.Long term outcomes following hospital admission for sepsis using relative survival analysis: a prospective cohort study of 1,092 patients with 5 year follow up.Fluid resuscitation in acute pancreatitis.Maternal infection and white matter toxicity.FLICE-like inhibitory protein (FLIP) protects against apoptosis and suppresses NF-kappaB activation induced by bacterial lipopolysaccharideInflammation and coagulation: implications for the septic patient.The immunopathogenesis of meningococcal disease.Enhanced expression of cell-specific surface antigens on endothelial microparticles in sepsis-induced disseminated intravascular coagulation.Sepsis-induced coagulation in the baboon lung is associated with decreased tissue factor pathway inhibitor.Characterization and differentiation of equine experimental local and early systemic inflammation by expression responses of inflammation-related genes in peripheral blood leukocytesVascular injury triggers Krüppel-like factor 6 mobilization and cooperation with specificity protein 1 to promote endothelial activation through upregulation of the activin receptor-like kinase 1 gene.Pharmacological utility of melatonin in the treatment of septic shock: experimental and clinical evidence.Decreased ADAMTS 13 Activity is Associated With Disease Severity and Outcome in Pediatric Severe Sepsis.Biomarkers of endothelial cell activation in early sepsisEndothelial bioreactor system ameliorates multiple organ dysfunction in septic rats.LPS-induced MCP-1 expression in human microvascular endothelial cells is mediated by the tyrosine kinase, Pyk2 via the p38 MAPK/NF-kappaB-dependent pathway.Cilostazol protects endothelial cells against lipopolysaccharide-induced apoptosis through ERK1/2- and P38 MAPK-dependent pathways.Using proteomics in perinatal and neonatal sepsis: hopes and challenges for the future.Drotrecogin alfa (activated; Xigris): an effective and cost-efficient treatment for severe sepsis.Analysis of NF-kappaB signaling pathways by proteomic approaches.Lovastatin for adult patients with dengue: protocol for a randomised controlled trial.The role of proteomics in understanding biological mechanisms of sepsis.Microvascular platforms for the study of platelet-vessel wall interactions.Engineered Microvessels for the Study of Human DiseaseMonocytes, peripheral blood mononuclear cells, and THP-1 cells exhibit different cytokine expression patterns following stimulation with lipopolysaccharideMechanisms of leukocyte distribution during sepsis: an experimental study on the interdependence of cell activation, shear stress and endothelial injury.Adsorptive modulation of inflammatory mediators dampens endothelial cell activation.STAT1-mediated signal integration between IFNγ and LPS leads to increased EC and SMC activation and monocyte adhesion.Hyaluronidase decreases neutrophils infiltration to the inflammatory site.
P2860
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P2860
The endothelium in sepsis: source of and a target for inflammation.
description
2001 nî lūn-bûn
@nan
2001 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
The endothelium in sepsis: source of and a target for inflammation.
@ast
The endothelium in sepsis: source of and a target for inflammation.
@en
The endothelium in sepsis: source of and a target for inflammation.
@nl
type
label
The endothelium in sepsis: source of and a target for inflammation.
@ast
The endothelium in sepsis: source of and a target for inflammation.
@en
The endothelium in sepsis: source of and a target for inflammation.
@nl
prefLabel
The endothelium in sepsis: source of and a target for inflammation.
@ast
The endothelium in sepsis: source of and a target for inflammation.
@en
The endothelium in sepsis: source of and a target for inflammation.
@nl
P1476
The endothelium in sepsis: source of and a target for inflammation.
@en
P2093
P356
10.1097/00003246-200107001-00011
P407
P433
P577
2001-07-01T00:00:00Z