Consanguinity and incidence of thalassaemia in Egypt.
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Biomedical subjects
Publications and source records attributed to J A Böök.
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The epidemiological and genetic investigation of schizophrenic psychoses over the period 1900-1978 which has been carried out in a specified North Swedish geographical isolate was supplemented with a study of suicides. For the period 1890-1980, a total of 90 suicides have been ascertained. Of these, 54 had at least one schizophrenic relative at a maximum genetic distance of 1/8, while 11 had schizophrenic relatives further removed. It is likely that at least some of these suicides were manifestations of acute and/or undiagnosed psychoses. Thus the previously reported high general morbid risk of schizophrenia in this population (2.7%) would be a rather conservative estimate. On the other hand, the findings would not appreciably change the morbid risk for first-degree relatives of schizophrenic probands.
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Plasma dopamine beta-hydroxylase (DBH) activity was determined in 115 members of a North Swedish geographical isolate with a high frequency of schizophrenia, of which 30 persons had schizophrenia, and was compared with a Middle Swedish population of 185 apparently healthy persons. There was no significant difference between the schizophrenic group and their healthy relatives or between the North and Middle-Swedish populations. The number of persons with very low plasma DBH activity in the North Swedish population appeared to be less than those in the control population.
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Conflicting reports on the association between platelet MAO activity and schizophrenia prompted a critical review and determinations on identical samples at one laboratory in Sweden and one in the U.S.A. Samples originated from eight schizophrenics and 27 relatives belonging to a large pedigree, thus ensuring biological homogeneity. In the USA laboratory, a significantly lower MAO activity was found in the schizophrenics when benzylamine or beta-phenylethylamine was used as substrate (but not with tryptamine), while a similar result was obtained in the Swedish laboratory when tryptamine was used (but not with benzylamine or beta-phenylethylamine). Comparisons between materials examined in different laboratories do not seem meaningful until differences in methodologies have been clarified. At present there is neither proof nor disproof of MAO being a "genetic marker" for vulnerability to the schizophrenic disorder.
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The article presents a brief review of the genetic aspects of intelligence as measured by IQ tests. The results from family and twin investigations seem to agree in as much as high heritabilities for IQ can be calculated. There are, however, a large number of insecurities and sources of error which invite to criticism. Although, at present, it is justified to assume that genetic factors contribute substantially to variations in IQs, it would be premature to claim that genetic and other causes of variation could be expressed in precise figures. It seems doubtful if this situation could be further improved by continued use of IQs in genetic investigations. It should be more profitable to use other entities, such as well-defined special abilities, which could be designed directly for genetic analyses.
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Four new cases of incontinentia pigmenti are presented, including chromosome studies of one family. An increased number of chromosome breakages was found in the blood of affected as well as unaffected members of this family.
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