Disease relevance of Erythrocytes, Abnormal

• The abnormal erythrocytes in paroxysmal nocturnal hemoglobinuria, both PNH II (the moderately abnormal cells) and PNH III (the markedly abnormal cells), lack both acetylcholinesterase (AChE) activity and decay-accelerating factor (DAF) activity [1].
• Six women with mild pregnancy-induced hypertension without proteinuria were studied before and after magnesium sulfate therapy had been given, and no differences in the proportion of abnormal erythrocyte forms were found [2].
• Among the Crohn's patients clearance was increased significantly in those with abnormal erythrocyte sedimentation rates (ESR) (greater than 15 mm/h, p less than 0.005) and diminished serum albumin (less than 35 g/L, p less than 0.005), but not in those with an abnormal Crohn's disease activity index (CDAI less than 150) [3].
• Furthermore, the observation of abnormal erythrocyte hemolysis test values despite "normal" total tocopherol plasma concentrations may be explained by high plasma levels of non-alpha, biologically less active isomers [4].
• The increase in PGI2 production after the adhesion of red cells from patients with diabetes or sickle cell anemia to endothelial cells indicates that endothelium may be damaged by abnormal erythrocyte adhesion [5].

High impact information on Erythrocytes, Abnormal

• In addition, the abnormal erythrocytes from patients with PNH had fewer periodate oxidizable constituents than did normal erythrocytes, indicating a relative deficiency of cell-surface sialic acid [6].
• AMr 73,000 protein isolated from the normal erythrocyte membranes of one PNH patient by using anti-DAF IgG was largely absent from the abnormal erythrocytes of this individual, suggesting that PNH cells lack the DAF protein [7].
• Intravascular red blood cell (RBC) destruction is caused by increased sensitivity of the abnormal erythrocyte to complement-mediated lysis, due to the GPI absence of a membrane-bound glycosylphosphatidylinositol (GPI)-linked protein, which functions as an inhibitor of reactive lysis (CD59) [8].
• The casein and histone kinase activities of normal and abnormal erythrocytes declined significantly with increasing age and buoyant density in Stractan density gradients [9].
• Resolution of iron deficiency was defined as the restoration of transferrin saturation, serum ferritin level, anemia, and abnormal erythrocyte indexes to normal or baseline values [10].

Biological context of Erythrocytes, Abnormal

• A family study indicates that abnormal erythrocyte band 3 structure and function and antibrain immunoreactivity may be phenotypes of two independent, genetically determined factors, that are part of the heterogenic defect of chorea-acanthocytosis [11].

Associations of Erythrocytes, Abnormal with chemical compounds

• BACKGROUND: Solute(s) retained during uraemia cause increased exposure of aminophospholipid phosphatidylserine (PS) on the outer surface of erythrocyte membranes, and this phenomenon may be involved in the pathophysiology of uraemia by promoting abnormal erythrocyte interactions [12].
• Abnormal erythrocyte metabolism in hepatic disease: effect of NADP repletion [13].
• Abnormal erythrocyte pyrimidine nucleotides in uremic subjects [14].
• The combination of tubercidin and NBMPR completely blocked adenosine transport into both normal and abnormal erythrocytes infected with either P. falciparum or P. vivax [15].

Gene context of Erythrocytes, Abnormal

• We have constructed a mouse strain deficient in beta-adducin having abnormal erythrocytes [16].
• Abnormal erythrocyte sodium-lithium countertransport (Na-Li CT) activity, traditionally measured at a single sodium concentration of 140 mmol.l-1 (V140), may represent an inherited risk marker for diabetic nephropathy [17].
• The presence of abnormal erythrocyte glutathione-reductase activity in the mother while she excreted normal amounts of riboflavin in her urine indicates a probable disorder of riboflavin metabolism resulting in multiple acyl-CoA dehydrogenase deficiency [18].
• Abnormal erythrocyte anion exchange in Alzheimer disease [19].
• Absence of abnormal erythrocyte superoxide dismutase, copper, or zinc levels in patients with retinitis pigmentosa [20].

References