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Biomedical subjects

O Ransome-Kuti

Publications and source records attributed to O Ransome-Kuti.

At least 19 recordsLinked to original sources
PubMed1990

A new breed of doctors.

Medical education in Nigeria is by and large still geared to international recognition. It is high time to discard this hangover from the colonial past. While maintaining international standards of excellence, Nigeria's medical schools need to turn out doctors equipped to solve Nigeria's health problems, not those of other countries.

Education, Medical↗
PubMed1985

Intra-uterine growth, birthweights and maturity of the African newborn.

The prevalence of low birthweight in many African countries is higher than in developed countries. This is largely because of the greater number of babies who are light for gestational age. In general, mean birthweights of African babies at various gestational ages are lower than those of developed countries. This is due mainly to environmental factors, but an increased prevalence of twinning is one genetic factor. When babies of mothers in optimum health were studied, birthweights for gestational age were similar to Caucasian babies.

Adult↗
PubMed1981

Exchange transfusion using G-6-PG deficient or Hgb-AS blood in icteric neonates.

The sickle cell trait (Hgb-AS) and G-6-PD deficiency are two genetic defects which increase the hemolytic susceptibility of erythrocytes. As these two traits are common in Nigeria, blood transfusions with such defective cells are frequently given. In this study, the immediate and long-term effects of using either normal blood or blood with either or these defects for exchange transfusions in 115 neonates have been examined. Infants transfused with G-6-PD deficient blood were compared with those transfused with G-6-PD normal blood. Similarly, neonates transfused with Hgb-AS blood were compared with those who received Hgb-AA blood. There was no statistically significant difference in post-exchange serum bilirubin levels (followed for one week), hemoglobin, hematocrit, and reticulocyte counts (followed for three months). It was concluded that under normal circumstances, the use of G-6-PD deficient blood or Hgb-AS blood does not increase the risk of exchange transfusion in infants with hyperbilirubinemia.

Anemia, Sickle Cell↗
PubMed1980

The risk of jaundice in glucose-6-phosphate dehydrogenase deficient babies exposed to menthol.

A major cause of neonatal morbidity and mortality in Lagos, Nigeria, is severe neonatal jaundice seen in G-6-PD deficient babies. The observation that the jaundice is more severe in outpatient than in inpatient babies suggests that its cause is exogenous. "Mentholated" powder which is commonly used in many clinics and at home to dress umbilical cords was suspected to be the offending agent. A controlled study of the effects of one of these powders was carried out on 60 consecutive G-6-PD deficient babies. In 30 of them the umbilical cords were dressed daily with the powder while the remaining half who were untreated served as controls. The treated babies developed statistically more significant jaundice than the controls. Inability of neonates to conjugate menthol in this power is probably responsible for the jaundice developed by these G-6-PD deficient babies. It is concluded that the use of menthol and/or camphor-containing commerical products on neonates be discontinued, especially in communities where the incidence of G-6-PD deficiency is high as the use of such products may be contributiing to the severity of neonatal jaundice.

Bilirubin↗
PubMed1975

A genetic study of lactose digestion in Nigerian families.

The ability to digest orally administered lactose was determined in individuals representing a number of Nigerian ethnic groups. The data are mainly presented as family pedigrees. In those families where both parents were unable to digest lactose, all of the progeny were lactose nondigestors. If one parent, usually of Northern garopena origin or of the Fulani tribe, could digest lactose, then the progeny contained some or all individuals who were capable of digesting the disaccharide. There was no difference in the results when either the mother or the father was the lactose digestor. Ten families were studied where one parent was of Europena or Yoruba-European origin (lactose digestor) while the other was proper Yoruba 0lactose nondigestor). From these matings, there were 18 lactose digestors and 11 lactose nondigestors. We have concluded that the ability to digest lactose is transmitted as an autosomal dominant and represents the mutated gene or a polymorphism.

Adult↗