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2. Congenital anemias in Macau

Author

Fai Wk, Kuam B, and Tamagnini Gp

Subjects
Antenatal clinics, education.field_of_study, medicine.medical_specialty, China, Macau, business.industry, Obstetrics, Hemoglobins, Abnormal, Biochemistry (medical), Clinical Biochemistry, Population, Primary health care, Anemia, Hematology, Fetal Blood, Pregnancy, Cord blood, Medicine, Humans, Mass Screening, Thalassemia, Female, education, business, Genetics (clinical)
Abstract

The implementation of a Primary Health Care system in Macau has created the need to study the prevalence of Congenital Anemias in the population to facilitate the planning of measures needed for their control. Blood samples from 3815 women attending the antenatal clinics were screened for beta-thalassemia using MCH values as the preliminary test, followed by quantitation of Hb A2 and Hb F. Isoelectric-focusing was used to screen 1091 cord blood samples for the presence of Hb Bart's. The prevalence of alpha- and beta-thalassemia carriers was found to be 6.2% and 3.6%, respectively.

Published
1988

3. Hb Hekinan observed in three Chinese from Macau; identification of the GAG----GAT mutation in the alpha 1-globin gene.

Author

Zhao W, Wilson JB, Webber BB, Kutlar A, Tamagnini GP, Kuam B, and Huisman TH

Subjects
Adult, Amino Acid Sequence, Amino Acids analysis, Aspartic Acid genetics, Base Sequence, China ethnology, Codon genetics, Female, Glutamates genetics, Glutamic Acid, Humans, Macau, Molecular Sequence Data, Mutation, Globins genetics, Hemoglobins, Abnormal genetics
Abstract

Hb Hekinan, an alpha chain variant that is characterized by a Glu----Asp mutation at position alpha 27, was observed in three Chinese females attending a prenatal clinic in Macau. The relative quantities of the stable hemoglobin were 13-14% (average 13.3%); its identification was greatly aided by the separation and purification of the peptides by reversed phase high performance liquid chromatography. Dot-blot analysis of amplified DNA with 32P-labeled probes located the mutation in codon 27 of the minor alpha 1-globin gene; the change involved a GAG (coding for glutamic acid) to GAT (coding for aspartic acid) mutation.

Published
1990
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