Activation of the host response in human Plasmodium falciparum malaria: relation of parasitemia to tumor necrosis factor/cachectin, thrombin-antithrombin III, and protein C levels
Article Abstract:
Malaria is an infectious disease caused by the parasite Plasmodium. Infection with Plasmodium falciparum is associated with an increase in the number of platelets (cells involved in blood clotting) and changes in blood flow that promote coagulation. These effects may be due to tumor necrosis factor/cachectin (TNF alpha), which is a cytokine, or growth-regulating factor. TNF-alpha was shown to reduce levels of protein C (PC), which prevents blood coagulation, and increase levels of a protein that enhances blood coagulation. The relation between the severity of P. falciparum malaria, parasitemia (the presence of parasites in the blood) and hemostatic (blood flow-related) changes was assessed in 47 patients with P. falciparum malaria. The levels of certain factors that control blood coagulation were measured, including the anticoagulant PC and several factors that enhance coagulation: coagulation factor IX, TNF-alpha, and thrombin-antithrombin III(TAT). Before treatment with antimalarial agents, the blood levels of TNF-alpha and TAT were increased, whereas the levels of PC and its inhibitor, referred to as PCI-1, were decreased. These trends were correlated with the severity of malaria and number of parasites in the blood. However, coagulation factor IX was not changed. When endothelial cells, which line the surface of some tissues, were exposed to the blood of a patient with severe malaria under laboratory conditions, the coagulation activity and genetic material that codes for coagulant factors in the endothelial cells increased. These findings show that P. falciparum infection results in the development of conditions that enhance blood coagulation. The changes in blood flow may be a reaction to P. falciparum infection, because hemostatic changes are correlated with the number of parasites in the blood and can be restored to normal conditions by antimalarial therapy. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Workshop V - what is a risk factor and what is not: theoretical and practical implications
Article Abstract:
An important question in assessing what factors in a person's life predispose him or her to diseases such as coronary artery disease (CAD) is what constitutes a true risk factor for the disease, and what are simply correlated variables. (CAD is the development of fatty atherosclerotic plaques on the inner lining of the coronary arteries, which reduces the blood supply to the heart.) For example, hypertension (high blood pressure) is commonly assumed to be a risk factor for the development of CAD, but treatment with antihypertensive agents (that successfully reduce blood pressure) has not been effective in preventing the onset of CAD, suggesting that hypertension might be more accurately described as a risk marker than a risk factor. On the other hand, blood lipids, such as cholesterol, may in fact represent true risk factors, because lowering blood cholesterol does, in fact, reduce the risk of disease development. Another issue that needs to be addressed more fully than it has been is whether it is really necessary to understand the subcellular mechanisms involved in the development of a disease if the symptoms can be treated satisfactorily. In the current climate of limited resources for medical expenditures, a complete understanding of the molecular mechanisms of disease development may be an unnecessary luxury if the disease can be prevented or treated with less complete understanding. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Alpha2-adrenoreceptors and endothelium-derived relaxing factor
Article Abstract:
Blood vessels are dynamic structures which can contract or relax under a variety of physical and chemical influences. Some of these influences are modulated by the endothelial cells which line the inside of the vessel. In experiments with femoral veins removed from dogs, it can be shown that norepinephrine causes the smooth muscle of the vein to contract. If the endothelial cells which line the smooth muscle tube of the vein are removed, an equivalent amount of norepinephrine causes greater contraction. The endothelial cells possess alpha-2-adrenoreceptors, just as do the smooth muscle cells. But while the stimulation of the adrenoreceptors on the muscle cells causes them to contract, the stimulation of the adrenoreceptors on the endothelial cells causes them to release a substance defined by its effect, endothelial-derived relaxing factor. This relaxing factor counteracts some of the contraction-inducing effect of the norepinephrine on the smooth muscle cells. Without this modulating effect, as in the veins stripped of endothelia, the norepinephrine-induced contraction is greater. At sufficiently high concentrations of norepinephrine, however, the same contraction is achieved in the veins regardless of the presence of the endothelial cells. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1989
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- Abstracts: Replication of the human immunodeficiency virus 1 and impaired differentiation of T cells after in vitro infection of bone marrow immature T cells
- Abstracts: Differential expression of the two human arginase genes in hyperargininemia. Enzymatic, pathologic, and molecular analysis
- Abstracts: An exploratory analysis of the occupational correlates of large pigmented nevi at Lawrence Livermore National Laboratory
- Abstracts: Prospective study of the standard meal provocative test in Zollinger-Ellison syndrome. Cost-effectiveness of prospective and continuous parenteral antibiotic control: experience at the Palo Alto Veterans Affairs Medical Center from 1987 to 1989
- Abstracts: Melena, anemia, renal insufficiency, and respiratory failure in a 47-year-old woman. Weight loss, anemia, elevated paraprotein levels, and renal failure in a 61-year-old man (Clinicopathologic Conference)