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K K Kidd

Publications and source records attributed to K K Kidd.

At least 235 records · Page 13Linked to original sources
PubMed1985

Linkage analysis of a DNA marker localized to 20p12 and multiple endocrine neoplasia type 2A.

A DNA segment D20S5 isolated from a chromosome 19/20 flow-sorted library was shown to identify two restriction fragment length polymorphisms (RFLPs) with MspI and PvuII. The probe was localized by hybridization in situ to 20p12, the putative site of an interstitial deletion in some MEN 2A and 2B patients. Linkage of the D20S5 and MEN 2A loci was excluded at theta less than or equal to .13 using two large MEN 2A kindreds. These data suggest that the MEN 2A locus may not lie within 20p12 as previously suggested.

Chromosome Mapping↗
PubMed1984

Psychiatric disorders in the relatives of probands with affective disorders. The Yale University--National Institute of Mental Health Collaborative Study.

A family study of psychiatric disorders in 2,003 first-degree relatives of 335 probands found increased rates of bipolar I disorder and major depression (MD) in the relatives of probands with bipolar disorder and increased rates of MD in the relatives of probands with MD. There was a similarity in rates of affective disorders in the relatives of ambulatory and of hospitalized depressed probands (suggesting that ambulatory depressed patients may be as suitable as hospitalized ones for biological studies) and a comparability of rates of illness in relatives between centers for most disorders when comparable diagnostic criteria and procedures were used.

Adult↗
PubMed1984

Subtypes of depression. Family study perspective.

To address the validity of subtype distinctions within a large family study of major depression, probands (N = 133) were classified into several non-mutually exclusive subcategories, including endogenous (n = 89), melancholic (n = 61), autonomous (n = 50), and delusional (n = 21). Age-corrected lifetime rates of depression and subtypes among first-degree relatives were then compared by the proband's depression subtype. Rates of major depression were highest for the relatives of probands with the autonomous and delusional subtypes, and while lower for the relatives of endogenous and melancholic probands, these rates were still higher than for the relatives of the remaining depressed probands or the relatives of normal controls. The depressed relatives of depressed probands with the endogenous, melancholic, autonomous, or delusional subtypes were more likely to have one of these subtypes than the depressed relatives of either the remaining depressed probands or the normal controls.

Adult↗
PubMed1984

Onset of major depression in early adulthood. Increased familial loading and specificity.

In a family study of 133 probands with major depression and 82 normal control subjects, and 1,518 of their first-degree relatives, we found a substantial inverse relationship between the age of onset of major depression in the probands and the risk of major depression in their relatives. The relatives of probands whose onset of major depression occurred when they were younger than 20 years of age had the highest risk of major depression, compared with the relatives of probands who had later ages of onset or with the relatives of normal subjects. Probands with an age of onset of 40 years or more had familial loading that was only slightly higher than the families of normal control subjects. Our statistical methods enabled us to examine the relationship of the ages of onset in the probands and their relatives while accounting for possible confounding factors. More studies will be needed to sort out secular changes in the rates of the occurrence of major depression among young persons (cohort effect) from the high familial loading of major depression that has its onset in childhood and adolescence, and to determine whether the specificity of transmission of early-onset depression is the result of a single homogeneous disorder.

Adolescent↗
PubMed1984

Utilizing automated methods to improve estimates of recurrence risk with linked genetic markers.

Information on linked markers can greatly improve estimates of recurrence risk for genetic disorders. However, when linkage is incomplete, utilizing the information in genetic counseling requires complex, repetitive calculations to estimate correct risks whenever the parental linkage phase is not precisely known. This paper demonstrates with examples how the computer program LIPED can be used for any pedigree to estimate risk precisely within bounds determined only by confidence limits on the recombination fraction.

Adult↗
PubMed1984

Genetic Analysis Workshop II: further consideration of segregation and linkage analyses in Problem 3.

We analyzed disease-marker associations in Problem 3 for the Genetic Analysis Workshop II, using PAP for segregation analysis and LIPED for linkage analysis. In this report we present aspects of our analyses that are not reported in the summary [MacCluer et al, 1984]. Certain features that we added to the running of LIPED to facilitate the analysis are discussed. Furthermore, we tested for Mendelian transmission in the hypothetical trait locus and we calculated modified relative risks for marker-trait genotypes. Some of the problems involved in analyzing complex associations among loci are discussed.

Alleles↗
PubMed1984

Segregation analyses of stuttering.

Although stuttering is known to be a familial disorder, no clear evidence regarding precise mode of transmission has arisen from previous research. In this report segregation analysis is applied to data on 386 stuttering probands and their first-degree relatives in an effort to discriminate among possible genetic models for the transmission of stuttering. Two different segregation analysis programs, PAP and POINTER, gave comparable results with respect to both hypothesis testing and parameter estimation. Specifically, the transmission of stuttering observed in these families cannot be adequately explained by a Mendelian major locus. The hypothesis of no polygenic component in the transmission of stuttering can, however, be rejected. Existence in these data of potential heterogeneity and possible violations of assumptions concerning ascertainment are considered in interpreting the results.

Adolescent↗
PubMed1984

The detection of major loci by segregation and linkage analysis: a simulation study.

Simulated multigenerational pedigrees were analyzed using the program GENPED and POINTER to examine the 1) limits of segregation analysis for detecting single locus, two-allele transmission of a dichotomous trait and 2) accuracy of the parameter estimates. Ten data sets of 30 pedigrees each (approximately 25 persons per pedigree) were simulated. The genotypic penetrance values were varied but the population prevalence of the trait was kept constant at 2%. For some data sets a linked marker locus was also simulated. Previous results had shown that a single major locus could be easily detected when the heterozygote penetrance (f1) was high or midway between the two homozygote penetrances. In this study, we found a single major locus could not be consistently detected by either method of segregation analysis when f1 was "low" to "intermediate." Accuracy of the parameter estimates depended on assumptions about the population prevalence. In those cases where the major locus could not be detected by segregation analysis, linkage to a marker locus could be detected as long as the marker was closely linked and there were not phenocopies in the population. Owing to the limited number of simulations in this study, we cannot generalize these findings. However, they provide a basis for further testing of methods of segregation analysis when factors such as the parameter values, family structure, and ascertainment scheme are varied.

Biometry↗
PubMed1984

Outcomes on lithium treatment as a tool for genetic studies in affective disorders.

From a genetic point of view, the application of mathematical models to affective disorders has not yet been useful, since they do not indicate a specific mode of transmission. To use these models correctly, we need to identify homogeneous genetic subgroups among those sharing the common phenotypic feature of affective illness. Our useful criterion for this is outcome on long-term lithium therapy, since experimental data suggest the existence of a close relationship between the genetic mechanisms that underly the affective disorders and those that underly outcome on lithium. We have studied 145 subjects with primary affective disorders, 92 of whom did not relapse during lithium treatment and 53 of whom did, together with 864 of their first-degree relatives. The data for both groups fit both single major locus and multifactorial polygenic models for genetic analysis, including a sex effect and therefore neither mode of transmission can be excluded.

Age Factors↗
PubMed1984

Some environmental factors and hypotheses for stuttering in families with several stutterers.

Individuals in families with several stutterers (five or more) and individuals in families with no stutterers were the basis of a broad study designed to elucidate both genetic and nongenetic factors relevant to stuttering. In order to examine both nongenetic hypotheses regarding the etiology of stuttering as well as environmental factors possibly predisposing to stuttering, data were collected using two structured case-history interviews and four self-report inventories. We were unable to identify prenatal, developmental, or medical factors that distinguish stutterers from their nonstuttering family members. Further, we found no evidence of (a) anxiety levels differing among stutterers, their nonstuttering family members, and nonstuttering controls; (b) familial attitudes toward speech differing between nonstuttering family members and those of nonstuttering controls; or (c) ratings of parental behavior or children's traits which distinguished stutterers from nonstuttering family members.

Environment↗
PubMed1984

Identification of a recent recombination event within the human beta-globin gene cluster.

In a detailed study of inheritance of DNA sequence polymorphism in a large reference pedigree, an individual was identified with an apparent genetic recombination event within the human beta-globin gene cluster. Analysis of the haplotypes of relevant individuals within this pedigree suggested that the meiotic crossing-over event is likely to have occurred within a 19.8-kilobase-pair region of the beta-globin gene cluster. Analysis of other DNA markers closely linked to the beta-globin gene cluster--segment 12 of chromosome 11 (D11S12) and loci for insulin, the cellular oncogene c-Ha-ras, and preproparathyroid hormone--confirmed that a crossover event must have occurred within the region of chromosome 11 between D11S12 and the beta-globin gene cluster. It is suggested that the event observed has occurred within a DNA region compatible with recombinational "hot spots" suggested by population studies.

Alleles↗