Instructions for use Title Insufficient production of urinary trypsin inhibitor forneutrophil elastase release after cardiac arrest
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M. Hayakawa | S. Gando | A. Sawamura | M. Sugano | Y. Yanagida | Nobuhiko Kubota | N. Hoshino | Hirokatsu Hoshino | Y. Sugano | Atsushi Yanagida | M. Kubota | A. Hayakawa | N. Kubota | M. Sawamura
[1] L. Toledo-Pereyra,et al. Molecular signaling pathways in ischemia/reperfusion. , 2004, Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation.
[2] E. Martin,et al. Marked activation of complement and leukocytes and an increase in the concentrations of soluble endothelial adhesion molecules during cardiopulmonary resuscitation and early reperfusion after cardiac arrest in humans , 2002, Critical care medicine.
[3] J. Cavaillon,et al. Successful Cardiopulmonary Resuscitation After Cardiac Arrest as a “Sepsis-Like” Syndrome , 2002, Circulation.
[4] Y. Takikawa,et al. Plasma and urine levels of urinary trypsin inhibitor in patients with acute and fulminant hepatitis , 2002, Journal of gastroenterology and hepatology.
[5] W. Mutschler,et al. Early cellular brain damage and systemic inflammatory response after cardiopulmonary resuscitation or isolated severe head trauma: a comparative pilot study on common pathomechanisms. , 2001, Resuscitation.
[6] H. Tsujimoto,et al. Mechanism of the inhibitory effect of protease inhibitor on tumor necrosis factor alpha production of monocytes. , 2001, Shock.
[7] C. Sprung,et al. Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Working group on "sepsis-related problems" of the European Society of Intensive Care Medicine. , 1998, Critical care medicine.
[8] K. Hossmann. REPERFUSION OF THE BRAIN AFTER GLOBAL ISCHEMIA: HEMODYNAMIC DISTURBANCES , 1997, Shock.
[9] S. Gando,et al. Increased neutrophil elastase release in patients with cardiopulmonary arrest: Role of elastase inhibitor , 1995, Intensive Care Medicine.
[10] V. Negovsky,et al. Post-resuscitation disease--a new nosological entity. Its reality and significance. , 1995, Resuscitation.
[11] B. Gressier,et al. Human leucocyte elastase (HLE) preferentially cleaves the heavy chain H2 of inter-alpha-trypsin inhibitor (ITI). , 1993, Biological chemistry Hoppe-Seyler.
[12] T. Tani,et al. Treatment of septic shock with a protease inhibitor in a canine model: A prospective, randomized, controlled trial , 1993, Critical care medicine.
[13] Y. Iwasaki,et al. [Can ulinastatin be an effective inhibitor of human polymorphonuclear granulocyte elastase under severe stressed state?]. , 1993, Nihon Geka Gakkai zasshi.
[14] H. Granger,et al. Anoxia-reoxygenation-induced, neutrophil-mediated endothelial cell injury: role of elastase. , 1990, The American journal of physiology.
[15] S. Weiss. Tissue destruction by neutrophils. , 1989, The New England journal of medicine.
[16] J. Lott,et al. Pathophysiology and diagnostic value of urinary trypsin inhibitors , 2005, Clinical chemistry and laboratory medicine.
[17] R. Lewis,et al. Tumor necrosis factor-alpha is associated with early postresuscitation myocardial dysfunction. , 2004, Critical care medicine.
[18] H. Eltzschig,et al. Vascular ischaemia and reperfusion injury. , 2004, British medical bulletin.
[19] O. Kemmotsu,et al. Out-of-hospital cardiac arrest increases soluble vascular endothelial adhesion molecules and neutrophil elastase associated with endothelial injury , 2000, Intensive Care Medicine.
[20] B Jennett,et al. Assessment of outcome after severe brain damage. , 1975, Lancet.