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K K Kidd

Publications and source records attributed to K K Kidd.

At least 199 records · Page 11Linked to original sources
PubMed1987

Early onset (under age 30 years) and panic disorder as markers for etiologic homogeneity in major depression.

Early onset of major depression (age, less than 30 years) in probands confers high risk to relatives, whereas late-onset depression (age, greater than 40 years) involves no elevation of risk over population rates. Analyses of data from families of probands with early onset from the Yale Family Study (47 three generation and 17 two generation) favored a major gene effect over polygenic inheritance. However, no genetic model was supported unambiguously. The increase in prevalence of depression over the past several decades complicates the genetic interpretation of results. Restriction of analyses to older (age, greater than 18 years) age cohorts appeared to simplify the pattern of transmission, but a consequent reduction of sample size provided only limited power for tests of competing genetic hypotheses. In a subgroup of 28 families in which the proband had both depression and panic disorder, a major gene mode of inheritance was not supported.

Adolescent↗
PubMed1987

Searching for major genes for psychiatric disorders.

Many of the major psychiatric disorders show sufficient familial clustering to raise the suspicion that genetic factors are important in determining who is and who is not affected. There is reasonable evidence from many sources to support a major genetic component to these common disorders. However, no simple mode of inheritance can be convincingly demonstrated. A genetic linkage study seems to be the most promising approach towards identifying aetiological factors in these disorders. The neurochemical complexity of the relevant parts of the brain and the absence of any biochemical abnormalities that appear to be aetiologically relevant also give strong impetus for a molecular genetic approach that uses genetic linkage. 'Large-scale' genetic linkage studies using restriction fragment length polymorphisms are under way for manic depressive illness (among other disorders) and are providing evidence against the involvement of some candidate genes. Some strongly positive evidence has also begun to emerge.

Bipolar Disorder↗
PubMed1987

Exclusion of autosomal dominant dystonia gene from large regions of chromosomes 11p, 13q, and 21q by multi-point linkage analysis.

Multi-point linkage analyses of autosomal dominant form of torsion dystonia with linkage groups on chromosomes 11p, 13q, 21q are reported. Analyses are based on family data from a single, large, non-Jewish pedigree. Large portions of chromosomes 11p and 13q, and virtually the entire long arm of chromosome 21 are excluded from linkage with dystonia. Practical aspects of designing multi-point analyses are discussed.

Chromosome Mapping↗
PubMed1987

Research design considerations for linkage studies of affective disorders using recombinant DNA markers.

A genetic linkage study is one approach to resolving the etiology of a major psychiatric disorder either by testing involvement of a specific candidate gene or by demonstrating the existence of some unidentified gene in a specific place on the genome. Because of the complexities of psychiatric disorders, a successful linkage study must be built upon accurate and reliable diagnosis, families with multiple affected members, highly informative genetic markers, and powerful multipoint linkage methods. Over the last decade, great advances have been made in all these areas. Linkage studies are not only appropriate for affective and other major psychiatric disorders but are already beginning to yield promising results.

DNA, Recombinant↗
PubMed1987

Linkage analysis of multiple endocrine neoplasia type 2A (MEN-2A) and three DNA markers on chromosome 20: evidence against synteny.

Members of four families in which multiple endocrine neoplasia type 2A (MEN-2A) is segregating were genotyped for three chromosome #20 DNA markers. Close linkage is excluded for the genetic locus of MEN-2A (MEN2A) with each marker locus tested. Using multipoint analysis, the MEN2A locus was excluded from a region 32.5 cM in length encompassing D20S5 and D20S6, two loci that previously had been mapped to the chromosome 20p12.2 region containing the putative deletion associated with MEN-2. In total, we excluded approximately 90.5 cM of chromosome #20 as a possible location of the MEN2A locus. The data from this study do not support increased recombination on the short arms of chromosome #20 and were insufficient to support heterogeneity of MEN-2A as possible explanations for failure to detect linkage between MEN2A and D20S5 or D20S6.

Chromosome Banding↗
PubMed1987

Localization and linkage of three polymorphic DNA sequences on human chromosome 20.

The D20S6 locus has been sublocalized by in situ hybridization using the pD3H12 probe to human chromosome band 20p12 and the D20S4 locus using the pMS1-27 probe to 20q13.2. A rare new restriction fragment length polymorphism detected in MspI-digested DNA by the pMSI-27 probe is reported. Linkage studies in nine families have shown that the D20S6 locus is linked to D20S5 (formerly mapped to 20p12 by in situ hybridization) with a maximum likelihood estimate of 0.07 for the recombination frequency (lod score = 9.07) and a confidence interval of 0.02 to 0.14. Estimated recombination frequencies were similar in males and females. Using both two- and multipoint analyses, linkage of D20S4 with the D20S5 and D20S6 loci was excluded and the suggested order for the three loci on chromosome 20 is D20S5-D20S6-centromere-D20S4. D20S5 and D20S6 are very useful markers for linkage studies because of their close proximity and reasonably good polymorphic information content values.

Chromosome Banding↗
PubMed1987

Family-genetic studies and identification of valid diagnostic categories in adult and child psychiatry.

Family-genetic studies of child and adult psychiatric disorders have become increasingly fashionable over the past decade. The development of structured diagnostic interview schedules, the emergence of uniform diagnostic criteria such as DSM-III, and the use of refined design and analytic techniques from the field of chronic disease epidemiology have made substantial contributions to the methodology of such studies. Advances in molecular genetics, particularly our emerging capacity to perform chromosomal linkage studies throughout the human genome, have renewed hope that the constitutional underpinnings of some psychiatric disorders can be identified and that the pathophysiology of these disorders can be elucidated. Family-genetic techniques in child and adult psychiatry are discussed with a particular focus on their potential value in validating diagnostic categories spanning developmental epochs.

Family↗
PubMed1987

An efficient strategy for gene mapping using multipoint linkage analysis: exclusion of the multiple endocrine neoplasia 2A (MEN2A) locus from chromosome 13.

Members of four families in which multiple endocrine neoplasia type 2A (MEN-2A) is segregating were typed for seven DNA markers and one red cell enzyme marker on chromosome 13. Close linkage was excluded between the MEN2A locus and each marker locus tested. By means of multipoint analysis and the genetic map of chromosome 13 developed by Leppert et al., MEN2A was excluded from any position between the most proximal marker locus (D13S6) and the most distal marker locus (D13S3) and from within 12 cMorgans outside these two loci, respectively. However, the support of exclusion within an interval was diminished under the assumption of a substantially larger genetic map in females. The strategy of multipoint analysis, which excluded between 1.5 and 2.0 times more chromosome 13 than did two-point analysis, demonstrates the utility of linkage maps in mapping disease genes.

Chromosome Mapping↗
PubMed1987

Study of 47 DNA markers in five populations from four continents.

Forty seven DNA markers from 30 genes or chromosomal regions were investigated in five populations (Biaka and Mbuti Pygmies, Melanesians, Chinese and Caucasoids). Both the variation between populations (measured by FST) and between markers is highly significant. The average heterozygosity for all markers is .284 and the average FST is .145. There was no significant difference in the FST values, or in the average heterozygosity between known genes and random segments. The FST distance between all populations considered in pairs, and averaged over all loci favours a primary split between Eurasia and Africa, but this conclusion is neither statistically significant nor uncomplicated. Condensing the 47 markers into 30 "genes" where 10 were treated as haplotypes, it was found that the haplotypes always give higher FST's than the separate markers, although similar conclusions can be drawn.

Africa↗
PubMed1987

Mapping the Wilson disease locus to a cluster of linked polymorphic markers on chromosome 13.

Linkage of both several chromosome 13 DNA markers and the locus for the red cell enzyme esterase D (ESD) to Wilson disease (WD), an autosomal recessive disorder affecting copper metabolism, was investigated in five Middle-Eastern kindreds. The single-copy probe 7D2, identifying the polymorphic region D13S10, was demonstrated to lie 7.5 centiMorgans (cM) from the locus, since a maximum lod score of 4.66 at a recombination frequency of .07 (7.5 cM) was found between the locus for WD (WND) and D13S10. Multipoint linkage analysis between several chromosome 13 markers and WND enables us to propose that the order of markers closely linked to WND is as follows: centromere-D13S10-ESD-WND.

Chromosome Mapping↗