A Neutrophil Elastase Inhibitor, Sivelestat, Reduces Lung Injury Following Endotoxin-Induced Shock in Rats by Inhibiting HMGB1
暂无分享,去创建一个
[1] J. Mccollam,et al. Recognizing and Managing Severe Sepsis: A Common and Deadly Threat , 2007, Southern medical journal.
[2] I. Fukuda,et al. Neutrophil elastase inhibitor, sivelestat, attenuates acute lung injury after cardiopulmonary bypass in the rabbit endotoxemia model. , 2007, The Annals of thoracic surgery.
[3] D. Pisetsky,et al. The role of IFN-alpha and nitric oxide in the release of HMGB1 by RAW 264.7 cells stimulated with polyinosinic-polycytidylic acid or lipopolysaccharide. , 2006, Journal of immunology.
[4] K. Tracey,et al. HMGB1 SIGNALS THROUGH TOLL-LIKE RECEPTOR (TLR) 4 AND TLR2 , 2006, Shock.
[5] A. Norrby-Teglund,et al. The role of high mobility group box-1 protein in severe sepsis , 2006, Current opinion in infectious diseases.
[6] I. A. Schettino,et al. The lung in sepsis: guilty or innocent? , 2006, Endocrine, metabolic & immune disorders drug targets.
[7] E. Lillehoj,et al. Neutrophil elastase induces IL-8 gene transcription and protein release through p38/NF-{kappa}B activation via EGFR transactivation in a lung epithelial cell line. , 2006, American journal of physiology. Lung cellular and molecular physiology.
[8] A. Malik,et al. NF-κB activation as a pathological mechanism of septic shock and inflammation , 2006 .
[9] E. Abraham,et al. High mobility group box 1 protein interacts with multiple Toll-like receptors. , 2006, American journal of physiology. Cell physiology.
[10] L. Traber,et al. Sepsis: emerging role of nitric oxide and selectins. , 2006, Clinics.
[11] A. Malik,et al. NF-kappa B activation as a pathological mechanism of septic shock and inflammation. , 2006, American journal of physiology. Lung cellular and molecular physiology.
[12] M. Antonelli,et al. Year in review in intensive care medicine, 2005. II. Infection and sepsis, ventilator-associated pneumonia, ethics, haematology and haemostasis, ICU organisation and scoring, brain injury , 2006, Intensive Care Medicine.
[13] Y. Abe,et al. Plasma concentrations and importance of high mobility group box protein in the prognosis of organ failure in patients with disseminated intravascular coagulation , 2005, Thrombosis and Haemostasis.
[14] K. Tracey,et al. Persistent elevation of high mobility group box-1 protein (HMGB1) in patients with severe sepsis and septic shock* , 2005, Critical care medicine.
[15] M. Antonelli,et al. Year in review in intensive care medicine, 2004. I. Respiratory failure, infection, and sepsis , 2004, Intensive Care Medicine.
[16] Masaki Tanaka,et al. Contributions of high mobility group box protein in experimental and clinical acute lung injury. , 2004, American journal of respiratory and critical care medicine.
[17] R. Bellomo,et al. Hidden evidence to the West: multicentre, randomised, controlled trials in sepsis and systemic inflammatory response syndrome in Japanese journals , 2004, Intensive Care Medicine.
[18] S. Moochhala,et al. Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome , 2004, The Journal of pathology.
[19] G. Downey,et al. Proteases and lung injury , 2003, Critical care medicine.
[20] D. Herndon,et al. Heparin Nebulization Attenuates Acute Lung Injury in Sepsis Following Smoke Inhalation in Sheep , 2002, Shock.
[21] K. Tracey,et al. HMGB1 as a late mediator of lethal systemic inflammation. , 2001, American journal of respiratory and critical care medicine.
[22] T. Pritts,et al. Activation of NF-kappaB varies in different regions of the gastrointestinal tract during endotoxemia. , 2000, Shock.
[23] K. Tracey,et al. Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein-1 by pituicytes. , 1999, Surgery.
[24] K. Tracey,et al. HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.
[25] S. Akira,et al. Unresponsiveness of MyD88-deficient mice to endotoxin. , 1999, Immunity.
[26] P. Ricciardi-Castagnoli,et al. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. , 1998, Science.
[27] Adcock Im. Transcription factors as activators of gene transcription: AP-1 and NF-kappa B. , 1997 .
[28] I. Adcock. Transcription factors as activators of gene transcription: AP-1 and NF-kappa B. , 1997, Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace.
[29] Vender Rl. Therapeutic potential of neutrophil-elastase inhibition in pulmonary disease. , 1996 .
[30] R. Shenkar,et al. Nuclear factor-kappa B is activated in alveolar macrophages from patients with acute respiratory distress syndrome. , 1996, Critical care medicine.
[31] A. Ishizaka,et al. Effect of a specific neutrophil elastase inhibitor, ONO-5046, on endotoxin-induced acute lung injury. , 1996, American journal of respiratory and critical care medicine.
[32] R. Vender. Therapeutic potential of neutrophil-elastase inhibition in pulmonary disease. , 1996, Journal of investigative medicine : the official publication of the American Federation for Clinical Research.
[33] M. Suzuki,et al. ONO-5046, a novel inhibitor of human neutrophil elastase. , 1991, Biochemical and biophysical research communications.
[34] S. Weiss. Tissue destruction by neutrophils. , 1989, The New England journal of medicine.
[35] S. Crawford. NEUTROPHILS AND ADULT RESPIRATORY DISTRESS SYNDROME , 1984, The Lancet.