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MeSH Review

Erythrocytes, Abnormal

 
 
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Disease relevance of Erythrocytes, Abnormal

 

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

 

Associations of Erythrocytes, Abnormal with chemical compounds

 

Gene context of Erythrocytes, Abnormal

References

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  8. Correction of the PNH defect by GPI-anchored protein transfer. Sloand, E.M., Maciejewski, J.P., Dunn, D., Moss, J., Brewer, B., Kirby, M., Young, N.S. Blood (1998) [Pubmed]
  9. Protein kinases and membrane protein phosphorylation in normal and abnormal human erythrocytes: variation related to mean cell age. Fairbanks, G., Palek, J., Dino, J.E., Liu, P.A. Blood (1983) [Pubmed]
  10. Intravenous iron dextran therapy in patients with iron deficiency and normal renal function who failed to respond to or did not tolerate oral iron supplementation. Barton, J.C., Barton, E.H., Bertoli, L.F., Gothard, C.H., Sherrer, J.S. Am. J. Med. (2000) [Pubmed]
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  15. Laboratory and field comparisons of adenosine influx in Plasmodium falciparum and Plasmodium vivax infected erythrocytes with genetic abnormalities from patients in Myanmar. Myint-Oo, n.u.l.l., O'Sullivan, W.J., Gero, A.M. Southeast Asian J. Trop. Med. Public Health (1997) [Pubmed]
  16. The erythrocyte skeletons of beta-adducin deficient mice have altered levels of tropomyosin, tropomodulin and EcapZ. Porro, F., Costessi, L., Marro, M.L., Baralle, F.E., Muro, A.F. FEBS Lett. (2004) [Pubmed]
  17. Thiol group modulation of sodium-lithium countertransport kinetics in diabetic nephropathy. Jones, S.C., Thomas, T.H., Marshall, S.M. Diabetologia (1997) [Pubmed]
  18. Multiple acyl-CoA dehydrogenase deficiency occurring in pregnancy and caused by a defect in riboflavin metabolism in the mother. Study of a kindred with seven deaths in infancy: Value of riboflavin therapy in preventing this syndrome. Harpey, J.P., Charpentier, C., Goodman, S.I., Darbois, Y., Lefèbvre, G., Sebbah, J. J. Pediatr. (1983) [Pubmed]
  19. Abnormal erythrocyte anion exchange in Alzheimer disease. Greco, F.A., Satlin, A., Solomon, A.K. Arch. Pathol. Lab. Med. (2000) [Pubmed]
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