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Biomedical subjects

K K Kidd

Publications and source records attributed to K K Kidd.

At least 289 records · Page 16Linked to original sources
PubMed1976

Genetic analyses of pyloric stenosis suggesting a specific maternal effect.

Data on pyloric stenosis are analysed by multiple threshold methods that incorporate the sex effect. The polygenic model of inheritance is rejected; the single major locus model can only account for 37% of the cases having a genetic aetiology, requiring an environmental effect to account for the remainder of the cases. A maternal-fetal interaction for gastrin production and sensitivity is postulated to explain all the existing data. The empirical risk figures given are considered to be the most accurate basis for genetic counselling until additional studies provide a sound biological basis for a quantitative genetic model.

Female↗
PubMed1976

Estimating the genetic contribution to schizophrenia.

The authors discuss the limitations of the concept of heritability in schizophrenia and, using reported incidence figures, assess two alternatives--the multifactorial and single major locus (SML) models. Both models predict genetic heterogeneity in schizophrenia. For some parameter values, the SML model indicates that homozygotes are rare but at very high risk. According to the multifactorial model, 9.1% of the schizophrenic population has a genetic risk of 99% or more. The authors conclude that neither model adequately accounts for the data but that predictions from both can be used to design sampling procedures which will increase the probability of selecting for study individuals whose illness is highly genetically determined.

Diseases in Twins↗
PubMed1973

Shockley.

Explore the source record for details and available documents.

Black People↗
PubMedDate not supplied

Drug response as a predictor of transmission of non-bipolar major depression within families.

The purpose of this study was to demonstrate the approach of using the degree of familial aggregation to validate a subtype of affective illness. In order to determine whether clinical response to pharmacological therapy in the proband treated for non-bipolar major depression constitutes a distinct subtype of depression, rates of affective illness were examined among relatives of probands who were categorized according to the speed and magnitude of their response to somatic treatment in controlled clinical trials. First-degree relatives of probands who experienced rapid improvement during the first week and poor response on termination of treatment, were found to have the highest rates of major depression. These results require replication.

Antidepressive Agents↗
PubMedDate not supplied

Bipolar affective disorders linked to DNA markers on chromosome 11.

An analysis of the segregation of restriction fragment length polymorphisms in an Old Order Amish pedigree has made it possible to localize a dominant gene conferring a strong predisposition to manic depressive disease to the tip of the short arm of chromosome 11.

Adolescent↗