Yoga exercise versus traditional exercise in the control of non-insulin diabetes mellitus - Poster presentation

The sample population was selected from 3 municipals of Havana City. The population size was selected using the programme EP16 with the option statcalc. From a population size of 17,068 diabetics, a sample size of 100 diabetics was calculated as the minimum population size required to obtain a confidence level of 95 percent. Patients were divided into two groups (yoga and traditional group) and were matched according to the following criteria: Age +/- 5 years, Sex, Type of treatment, Evolution of NIDDM, BMI. The two groups of 63 diabetics were matched according to the criteria described above and were then grouped as "yoga exercise group" and "traditional exercise group". Biochemical analysis was done at the start of the investigation, and included: HDL - C Tryglyceride, LDL - C, Total cholesterol, Glycated haemoglobin, Insulinic receptors, Microalbuminuria, Blood glucose, quantification of T3, T4 Insulin, GH, and TSH, Oxidative stress enzymes serum, creatinine. The Second Stage: Both groups had similar diet and practised their respective physical exercise at the same duration and frequency for periods of 3 and 6 months. The biomedical analysis was done at these intervals. The biochemical analysis at the start showed: In most cases there were alterations in lipid metabolism, renal function as seen as hyperlipidaemia and hypercortisolaemia and a reduction in the union and internalization of insulin in the receptors of lymphocytes. There was a correlation between GH and T4. These findings show that it is necessary to deepen the investigation of these patients as there exists a difference in the laboratory results and the clinical manifestations of endocrine metabolc diseases.(AU)

Microchromatographic quantitation of hemoglobin A levels in phenotypes of sickle cell-beta thalassemia

The inheritance of the sickle cell gene in combination with a gene for á+ thalassemia results in a spectrum of sickle cell-á+ thalassemia syndromes with varying levels of hemoglobin A (HbA). Some severe sickle cell-á+ thalassemia syndrome have small amounts of HbA, which may be difficult to quantitate in the presence of fetal hemoglobin. A microcolumn chromatographic method, using 0.5 M Tris-acetic acid developers with varying pH values from 9.0 to 6.0 appears to adequately quantitate small amounts of HbA. This method is relatively simple and cheaper than high-performance liquid chromatography, a major consideration in developing countries.(AU)

Haemoglobin reference values in the Jamaican population - abstract

In a study of the iron nutritional status of the Jamaican population, the reference range for haemoglobin (Hb) was determined. Mean Hb levels in all age groups were markedly lower than internationally accepted values (Table). The cut-off points used to define anaemia were also determined and they were also markedly lower than the international values. Use of the local cut-off points resulted in a lower prevalence of anaemia than if international values were used and in the identification of one third of individuals with iron deficiency (determined by iron stores measurement) as being anaemic. Local reference ranges for haemoglobin should be developed, wherever possible, as this study clearly shows that the internationally accepted ranges are not universally applicable (AU)

The development of haematological changes in homozygous sickle cell disease: a cohort study from birth to 6 years

A cohort study of sickle cell disease from birth has allowed observations on the disease without the symptomatic selection inherent in previous series. The development of haematological indices from birth to 6 years in male and female infants with homozygous sickle cell (SS) disease is presented and compared with values in age and sex matched controls with a normal haemoglobin (AA) genotype previously presented elsewhere. In SS disease total haemoglobin levels fell rapidly from birth to a plateau at 3-6 months before falling again to 15 months after which no age related change occured. Mean cell haemoglobin concentration fell from birth to lowest values at 15-18 months before increasing to reach the level present at birth by the age of 5 years. Red cell counts fell rapidly after birth to a plateau at 2 months, increased slightly to 2 months and then fell steadily throughout the remaining period of study. The mean cell voloume and mean cell haemoglobin also fell rapidly after birth reaching the lowest values by 6 months and then increased progressively. Female patients showed significantly higher haemoglobin levels from 15 months to 4« years. Compared to AA controls, SS patients manifested significantly lower levels of haemoglobin from 2 weeks, and red cell counts from 1 month, and significantly higher levels of MCHA from 4 months to 3 years, MCV from 8 months to 5 years, and serum iron levels from 1 to 4 years. Children with SS disease were partially protected from iron deficiency in early childhood, perhaps by increased intestinal absorption of iron, and the associated increase in intracellular haemoglobin concentration might be disadvantageous during this high risk period (Summary)

The development of haemoglobin A2 in normal negro infants and in sickle cell disease

The development of haemoglobin A2 levels from birth to 3 years has been compared in normal, á-thalassaemia trait, sickle cell (SS) disease, and S-á-thalassaemia genotypes. Hb A2 levels were almost identical in normals and in children with SS disease at 1, 2 and 3 years. The most rapid increases in Hb A2 levels occurred before 6 months but levels were still rising at the end of the third year. Sickle cell-á+ thalassaemia could be differentiated from SS disease by the higher Hb A2 levels between 6 months and 1 year. Insufficient data were available on S-᧠thalassaemia but since Hb A2 levels in this condition are generally higher than those in S-á+ thalassaemia, differentiation from SS disease may also be possible from the age of 6 months (AU)

Gamma chain variants in Jamaica newborns

15,661 cord bloods from Jamaican infants were examined for abnormal hemoglobins using alkaline cellulose acetate electrophoresis for the initial screening, supplemented by acid agar gel electrophoresis for samples exhibiting abnormal hemoglobin bands. Of the 16 electrophoretic variants which were detected, six were fully characterized and found to be: four Hb F Port Royal (alpha2 Ggamma2 125 Glu replaced by Ala) and two Hb F Victoria Jubilee (alpha2Agamma2 80 Asp replaced by Tyr). The Hb F Port Royal samples each constituted about one eighth of the total Hb F as did seven additional samples presumed to be Hb F Port Royal. The infants with this variant exhibited no special hematological characteristics or other consistent associations. Both Hb F Victoria Jubilee samples ocurred in somewhat lower proportions of the total Hb F compared with Hb F Port Royal and exhibited an apparent increase of free alpha chains in the whole hemolysate. The data available on detectable gamma chain variants suggest that a specific point mutation may occur in either a HbGgamma or a HbAgamma locus. (AU)

Hemoglobin O Arab in four negro families and its interaction with Hemoglobin S and Hemoglobin C

Hemoglobin O Arab was found in 25 members of four apparently unrelated negro families in the West Indies of Jamaica. In each family the propositus had Hb SO disease. Two cases had been mistakenly diagnosed as Hb SC disease. Two persons heterozygous for both Hb C and Hb O Arab were found in these families, and Hb O Arab áthalassemia in one other relative. The clinical course and symptomatology of Hb SO disease is incomparable to that in Hb SD (O2á2121 Glu-> GluNH2) disease and more severe than Hb S2C2 disease. In vitro mixtures of Hb O Arab and Hb S change from a liquid to a gel phase at total hemoglobin concentrations weaker than those required to gel pure Hb S, whereas mixtures of Hb S with Hb A or Hb C require a stronger total hemoglobin concentration before gelling will occur. Oxygen dissociation studies on red cells containing Hb SO show a lowered oxygen affinity comparable to that found in homozygous sickle-cell anemia and outside the range for subjects with sickle-cell Hb C disease.(AU)

Hereditary persistence of foetal haemoglobin: A family study suggesting allelism of the F gene to the S and C haemoglobin genes

A large family is described in which the inheritance of a gene responsible for high levels of foetal haemoglobin (the F gene) and its interaction with the gene for haemoglobin-S is followed through three generations. Four cases of SF combination are reported. An example of the the CF combination is described. Evidence is produced that the F gene is situated at the same locus as the S and C genes and the gene for classical thalassaemia, and that it is therefore an allele of them. As an altenative explanation it is suggested that the high levels of foetal haemoglobin may not result from direct gene action but may be due to a failure of inheritance of normal haemoglobin following a deletion at the A-S-C locus (or a mutation lethal for beta-chain production), with a consequent revival of the dormant mechanism of foetal haemoglobin synthesis. Sickle-cell anaemia and the SF combination are phenotypically indistinguishable, and the difficulties in explaining the very marked clinical difference between them are discussed (Summary)

An unusual type of hemoglobinopathy resembling sickle cell-thalassemia disease in a Jamaican family

Three generations of a Jamaican family of African extraction are desribed, in several members of which an abnormal gene is carried. This gene produces high levels of fetal hemoglobin unassociated with the usual stigmata of thalassemia. It is found in all three generations of the family associated with hemoglobin A only and is also found in at least two members of the family interacting with hemoglobin S. In the latter combination little or no disability results. The mode of inheritance of this abnormal gene is discussed, and reasons are put forward for a possible protective effect of high fetal hemogobin levels due to inhibition of sickling. The findings in the cord blood of the youngest child, including an unusually high percentage of sickling, are discussed, together with follow-up studies to the age of 25 weeks.(AU)