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Biomedical subjects

R M Bannerman

Publications and source records attributed to R M Bannerman.

At least 55 records · Page 3Linked to original sources

Mild beta-thalassemia in black subjects.

In two American black families with beta-thalassemia, globin chain synthesis was investigated in vitro. The resultant alpha/beta and alpha/non-alpha labelling ratios were expressed in terms of both specific activity and total counts. In one family, two brothers with clinical presentations compatible with thalassemia intermedia had apparently each inherited two different beta-thalassemia alleles. Thus, they are compound heterozygotes. Their alpha/beta (or alpha/non-alpha) ratios were in the same range as those found in Caucasian subjects with severe Cooley's anemia. In addition, alpha/beta ratios in heterozygotes in this study were the same as those found in Caucasian heterozygotes. A difference in degree of chain imbalance measured by our present method cannot explain the relative lack of severe clinical manifestations of beta-thalassemia in blacks. Further family studies are indicated to discover other genetic or environmental factors modifying the effects of beta-thalassemia.

Adolescent↗

Familial gynecomastia.

A patient with pubertal gynecomastia had a younger brother and two maternal uncles with the same condition. Investigation of one of the two uncles, who are both now infertile, revealed the characteristic features of the del Castillo syndrome. It is suggested that the propositus also has del Castillo syndrome which is probably a peri or postpubertal type of primary testicular deficiency in the early stages of which spermatogenic function is still present.

Adolescent↗

Hereditary defect of intestinal iron transport in mice with sex-linked anemia.

Iron transport by everted duodenal sacs in vitro was studied in mice with sex-linked anemia (gene symbol sla) (an inherited iron deficiency anemia), in normal mice, and in normal mice on iron-deficient and iron supplemented diets. Although the over-all mucosal uptake of iron was the same in sla and normal sacs, transport of iron to the inside of the sac was much decreased in sla. The iron transport defect in sla was emphasized by the fact that genotypically normal mice on an iron-deficient diet demonstrated greatly increased iron transport. Electrophoretic analysis of protein extracted from sla and normal sacs showed only one iron-binding fraction. The sla and normal fractions had the same mobility and corresponded in position to the major band of horse ferritin. It thus appears that the iron deficiency of sla is due to a genetically determined defect in mucosal iron transport and that this defect is not associated with any demonstrable abnormality of a major iron-binding protein.

Anemia, Hypochromic↗