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dc.contributor.authorV. Thonglairuamen_US
dc.contributor.authorP. Winichagoonen_US
dc.contributor.authorS. Fucharoenen_US
dc.contributor.authorP. Wasien_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2018-06-14T09:13:00Z-
dc.date.available2018-06-14T09:13:00Z-
dc.date.issued1989-01-01en_US
dc.identifier.citationHemoglobin. Vol.13, No.2 (1989), 117-124en_US
dc.identifier.issn03630269en_US
dc.identifier.other2-s2.0-0024549950en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0024549950&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/15726-
dc.description.abstractAE-Bart's disease is a thalassemia intermedia resulting from the interaction between αthalassemia and heterozygous Hb E. In this study we analyzed the αglobin genes of 25 patients designated as AE-Bart's disease by starch gel electrophoresis. Twenty-one cases had Hb Constant Spring in addition to Hbs E + A + Bart's, and the remaining four cases had only Hbs E + A + Bart's. DNA mapping revealed the αglobin genotype of αthalassemia-1/αthalas-semia-2 in four patients who had Hbs E + A + Bart's, whereas the α genotype of the remainder is αthalassemia-1/nondeletion αthalassemia. The nondeletion αthalassemia is Hb Constant Spring as indicated by starch gel electrophoresis. Hematologic data and hemoglobin analysis showed that Constant Spring-AE-Bart's disease is a more severe clinical syndrome than AE-Bart's disease. © 1989 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0024549950&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectMedicineen_US
dc.titleThe molecular basis of AE-bart's diseaseen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.3109/03630268908998061en_US
Appears in Collections:Scopus 1969-1990

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