Journal ArticleDOI
The pathophysiology of severe falciparum malaria
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TLDR
Rodney Phillips and David Warrell as discussed by the authors reviewed aspects of that work and attempt to unravel the mysteries of the pathophysiology of severe malaria in man, and found that an understanding of these mechanisms forms an important basis for the clinical management of affected patients.About:
This article is published in Parasitology Today.The article was published on 1986-10-01. It has received 56 citations till now. The article focuses on the topics: Malaria.read more
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TNF concentration in fatal cerebral, non-fatal cerebral, and uncomplicated Plasmodium falciparum malaria.
Dominic P. Kwiatkowski,Adrian V. S. Hill,I. Sambou,P. Twumasi,J. Castracane,K. R. Manogue,Anthony Cerami,David Brewster,Brian Greenwood +8 more
TL;DR: It is concluded that increased TNF production is a normal host response to P falciparum infection, but that excessive levels of production may predispose to cerebral malaria and a fatal outcome.
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Tumor Necrosis Factor and Disease Severity in Children with Falciparum Malaria
Georges E. Grau,Terrie E. Taylor,Malcolm E. Molyneux,Jack J. Wirima,Pierre Vassalli,Marcel Hommel,Paul-Henri Lambert +6 more
TL;DR: The level of tumor necrosis factor is frequently increased in patients with severe falciparum malaria, particularly in those with cerebral malaria or hypoglycemia, and whether it is important in the pathogenesis of the signs and symptoms of the disease requires further study.
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Malaria during pregnancy: A priority area of malaria research and control
TL;DR: Although the special features of malaria during pregnancy have been recognized for nearly a century, it is only recently that it is being considered as a priority for malaria research and control.
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Tumor-Necrosis Factor and other Cytokines in Cerebral Malaria: Experimental and Clinical Data
TL;DR: Evidence is presented here that tumor necrosis factor/cachectin (TNF), is of crucial importance in the pathogenesis of cerebral malaria and metabolic parameters of CM and its main lesion in both mouse and human, correspond to the known properties of TNF.
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The pathophysiology of falciparum malaria.
Ian A. Clark,William B. Cowden +1 more
TL;DR: It is plausible that this will be demonstrable in severe falciparum malaria, and it is argued that it can best be understood in terms of excessive stimulation of normally useful pathways mediated by inflammatory cytokines, the prototype being tumor necrosis factor (TNF).
References
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A physiological approach to hepatic drug clearance
TL;DR: The proposed classification of drug metabolism based on the hepatic extraction ratio allows prediction and interpretation of the effects of individual variations in drug‐metabolizing activity, route of administration, pharmacokinetic interactions, and disease states on hepatic drug elimination.
Journal Article
Human cerebral malaria. A quantitative ultrastructural analysis of parasitized erythrocyte sequestration.
TL;DR: It is concluded that there is no evidence for an inflammatory or immune pathogenesis for human cerebral malaria and that the clinical effects probably relate to anoxia and the metabolic activities of the parasites.
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The release and fate of vaso‐active hormones in the circulation
TL;DR: Some of Gaddum's first publications were on the development of specific and sensitive methods for biological assay, and he maintained a deep interest in this subject for the rest of his life.
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The Significance of Iron in Infection
TL;DR: Iron-binding proteins transferrin and lactoferrin appear to be essential for the bactericidal function of polymorphonuclear leukocytes against Pseudomonas aeruginosa and Liberation of heme compounds can enhance clinical infections.
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Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.
TL;DR: These studies suggest that intravascular activation of the complement system leads to neutrophil aggregation and activation, intrapulmonary capillary sequestration of neutrophils, and vascular injury, which may be related to production of toxic oxygen metabolites by complement-activated neutrophILS.