Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion. - Wikidata - wikimedia - TriplyDB

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

http://www.wikidata.org/entity/Q37051852

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Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium The erythrocyte as instigator of inflammation. Generation of amidated C3 by erythrocyte adenosine deaminase C-reactive protein and complement are important mediators of tissue damage in acute myocardial infarction.Therapeutic potential of complement inhibitors in myocardial ischaemia.Bone marrow MyD88 signaling modulates neutrophil function and ischemic myocardial injury Complement and its implications in cardiac ischemia/reperfusion: strategies to inhibit complement.Complement in ischemia reperfusion injury.Pathways to acute humoral rejection CD59a deficiency exacerbates ischemia-reperfusion injury in mice.Complement component 3 is necessary to preserve myocardium and myocardial function in chronic myocardial infarction.C-reactive protein and cardiovascular disease: new insights from an old molecule.Complement activation promotes muscle inflammation during modified muscle use.Cardiomyopathy is linked to complement activation.Mediators of ischemia-reperfusion injury of rat lung Phagocytic activation of human neutrophils by the detergent component of fluosol.Regulation of complement membrane attack complex formation in myocardial infarction.The effect of C1 inhibitor on myocardial ischemia and reperfusion injury.alpha(4)-integrin mediates neutrophil-induced free radical injury to cardiac myocytes.Innate immune adaptor MyD88 mediates neutrophil recruitment and myocardial injury after ischemia-reperfusion in mice.Complement localization and mediation of ischemic injury in baboon myocardium.Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart The immune system and cardiac repair.Anticomplement therapy.Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice.Ischemia/reperfusion injury: The role of immune cells Toll-like receptors as potential therapeutic targets in cardiac dysfunction.The complement system in ischemia-reperfusion injuries Post-myocardial infarct inflammation and the potential role of cell therapy.Pathophysiology of Myocardial Infarction.Ischemia/Reperfusion.Receptor-directed inhibition of chemotactic factor-induced neutrophil hyperactivity by pyrazolon derivatives. Definition of a chemotactic peptide antagonist Humanized cobra venom factor decreases myocardial ischemia-reperfusion injury.C-reactive protein activates complement in infarcted human myocardium.C-reactive protein as a pro-inflammatory mediator in cardiovascular disease by its ability to activate complement: additional proof and hypothetical mechanisms.Mechanisms of cell death in acute myocardial infarction: pathophysiological implications for treatment Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression.Ischemia-mediated aggregation of the actin cytoskeleton is one of the major initial events resulting in ischemia-reperfusion injury.Leucocyte expression of complement C5a receptors exacerbates infarct size after myocardial reperfusion injury.The effect of C-reactive protein deposition on myocardium with ischaemia-reperfusion injury in rats.IL-17A Produced by Innate Lymphoid Cells Is Essential for Intestinal Ischemia-Reperfusion Injury.

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Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

http://www.wikidata.org/entity/Q37051852

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on March 1978

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

@en

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

@nl

type

label

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

@en

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

@nl

prefLabel

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

@en

Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

@nl

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Journal of Clinical Investigation

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Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion.

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P2093

Carpenter CB

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Chiariello M

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Fishbein MC

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Hale SL

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Knostman JD

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Maroko PR

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Radvany P

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P2860

Intravenous nitroglycerin in acute myocardial infarction

Reversal by phenylephrine of the beneficial effects of intravenous nitroglycerin in patients with acute myocardial infarction

Formation and functional significance of a molecular complex derived from the second and the fourth component of human complement

The reliability of molecular weight determinations by dodecyl sulfate-polyacrylamide gel electrophoresis

Regional distribution of diffusible tracers and carbonized microspheres in the left ventricle of isolated dog hearts.

Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction

Reduction of experimental myocardial infarct size by corticosteroid administration.

Quantitative study of infarcted myocardium in cardiogenic shock

Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis

Coronary artery reperfusion. II. Reduction of myocardial infarct size at 1 week after the coronary occlusion.

P304

661-670

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scholarly article

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10.1172/JCI108978

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3

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61

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1978-03-01T00:00:00Z

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22501454

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641147

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372579

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