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Impact of Malaria on Genetic Polymorphism and Genetic Diseases in Africans and African Americans
Pages 99-112

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From page 99...
... Louis H Miller is chief, Laboratory of Malaria Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
From page 100...
... The ovalocytic erythrocyte is partially resistant to invasion by malaria parasites. Homozygosity for this mutation is lOO
From page 101...
... (iv) Despite the slow evolution of the human genome compared to that of the parasite, the host innate resistance mechanisms can afford improved survival.
From page 102...
... The exact definition of how potassium affects parasite growth is complicated by the fact that the parasite grows at a normal rate in erythrocytes treated with ouabain, which increases intraerythrocytic sodium and decreases intraerythrocytic potassium (14, 15~. It is possible that the shift in sodium/potassium may reduce parasite growth through a third factor such as hemoglobin S or that other ouabain-insensitive transporters may affect parasite growth.
From page 103...
... If altered iron metabolism is proven to confer resistance to malaria, it would be an impetus to explore iron-related pathways in malaria therapy. In addition, this African disease may cause increased liver disease in African Americans.
From page 104...
... The peptide presented by HLA-class I molecules usually consists of eight or nine amino acids, depending on the class I molecule. The peptides eluted from the groove were sequenced, and from this information the invariant anchor amino acid, praline, at position 2 of the nonapeptides, was identified.
From page 105...
... One of the genes encoding Rh has recently been cloned, and it is predicted to cross the membrane 13 times (39~. Although the function of Rh remains a mystery, it is possible that it may be involved in membrane transport or membrane integrity and may affect survival of the intraerythrocytic parasite.
From page 106...
... The question of whether this lower neutrophil count is causally related to Duffy negativity remains to be determined. The involvement of Duffy antigens in chemokine metabolism also raises the question of whether Duffy negativity in West Africa provides a survival advantage in terms of the ability to control P
From page 107...
... inhibited erythrocyte binding to COS cells expressing the binding domain of EBA-175. Second, glycophorin A or the N-terminal 64 amino acids of glycophorin A blocked binding of EBA-175 to erythrocytes; shorter N-terminal peptides that contain most O-linked oligosaccharide and the one N-linked oligosaccharide did not block attachment.
From page 108...
... Dantu results from a recombination between the glycophorin A gene and the glycophorin B gene, which leads to a mutant that has part of the extracellular domain of glycophorin B and the transmembrane and cytoplasmic domains of glycophorin A Dantu also has a normal copy of glycophorin A and lacks glycophorin B
From page 109...
... Victor Gordeuk (George Washington University) for sharing unpublished data on iron metabolism, Dr.
From page 110...
... 1101 LOUIS H MILLER West, G., Ndambier, S., Emmanual, J., Nkanza, N., Chapanduka, Z., Randall, M., Boone, P., Romano, P., Martell, R
From page 111...
... (In press) in Molecular Basis of Major Human Blood Group Antigens, eds.


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