Read e-book online Anemia PDF

By D. Silverberg

ISBN-10: 9535101382

ISBN-13: 9789535101383

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Membrane phospholipid asymmetry in human thalassemia. Blood 91, 3044-3051. , & Wieder, T. (2002). Enhanced erythrocyte apoptosis in sickle cell anemia, thalassemia, and glucose-6-phosphate dehydrogenase deficiency. Cell Physiol Biochem 12, 365-372. , & Wieder, T. (2004). Involvemnt of ceramide in hyperosmotic shock-induced death of erythrocytes. Cell Death Differ 11, 231-243. , & Lang, F. (2005). Mechanisms of suicidal erythrocyte death. Cell Physiol Biochem 15, 195-202. M. (2005). PGE(2) in the regulation of programmed erythrocyte death.

It has been shown that mild oxidants, such as potassium ferricyanade, diamide, and hydrogen peroxide stimulate red blood cell glycolysis in proportion to the elevation of band 3 tyrosine phophorylation. Band 3 24 Anemia sequences surrounding tyrosine residues have been associated with intracellular binding of several cytosolic proteins, including hemoglobin and the glycolytic enzymes aldolase, phosphofructokinase, and glyceraldehyde-3-phosphate dehydrogenase. In vitro, the tyrosine phosphorylation of band 3 prevented the binding of these glycolytic enzymes.

In summary, phosphatidylserine translocation, now generally accepted as a hallmark of cells in apoptosis, results from the inhibition of aminophospholipid translocase activity and activation of scramblase. Surface exposure of phosphatidylserine on apoptotic cells presents a recognition and engulfment signal for removal by phagocytosis competent cells even before the development of morphological changes usually associated with death (Schlegel & Williamson, 2001). 4 Erythrocyte morphology The volume of red cells decreases with cell aging and substantial amount of hemoglobin is lost from circulating erythrocytes during total lifespan.

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Anemia by D. Silverberg


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