Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transcapillary escape rate and capillary permeability to albumin were studied in five patients with Plasmodium falciparum malaria and six control subjects by using 125I-HSA. The mean transcapillary escape rate of albumin, calculated from the slope of the plasma disappearance curve of 125I-HSA, was found to be significantly higher in the malaria patients than in the control group. As the plasma volume increased while the plasma albumin concentration decreased in these patients, this resulted in a significantly higher plasma clearance and outflux of albumin from the intravascular to the extravascular compartments. Both the effective capillary pore area per unit path length available for restricted diffusion and the specific permeability coefficient of the capillary to albumin were found to be grossly elevated in the patients' group. These findings indicated that there was an increased leakage of plasma albumin in patients with P. falciparum malaria as a result of increased capillary surface area and an increased capillary permeability to albumin.
 ...
PMID:Transcapillary escape rate and capillary permeability to albumin in patients with Plasmodium falciparum. 305 33

IgG and IgM antibodies were detected on non-parasitized as well as parasitized erythrocytes (E) from mice surviving over 15 days after infection with rodent malaria, Plasmodium berghei, whereas C3 was detected exclusively on parasitized E. Parasitized E, however, were quite resistant to the haemolytic activity of guinea pig complement and effectively inactivated human C3b to iC3b on their surface. Similarly, parasitized E were extremely resistant to homologous complement as assessed by haemolysis and C3 binding even when regulatory proteins (decay-accelerating factor, DAF; complement receptor related gene y, Crry; heat-stable antigen, HSA) were blocked with specific antibodies. DAF and Crry were equally expressed on both normal E and parasitized E from mice within a week post-infection; therefore, molecules that inhibit the haemolysis or C3 binding of parasitized E appear to be independent of DAF and Crry. Unexpectedly, the molecular forms of HSA and DAF in parasitized erythrocyte membranes were found to be different from those of normal erythrocyte membranes: DAF was detected as three bands (85,000, 64,000 and 30,000 MW) by immunoblotting. HSA was detected as more highly glycosylated forms than normal HSA. These alterations of DAF and HSA could be explained by the modification of membrane proteins and polysaccharides induced by parasitization, and we hypothesize that these changes of membranes or membrane proteins are involved in the resistance of parasitized E against homologous complement.
 ...
PMID:The serum resistance of malaria-infected erythrocytes. 920 59