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K K Kidd

Publications and source records attributed to K K Kidd.

At least 217 records · Page 12Linked to original sources
PubMed1986

Understanding the clinical heterogeneity of major depression using family data.

For major depression, putative subgroups have been defined by age at onset, clinical severity, symptom patterns, or the presence of other disorders (comorbidity), yet the high degree of overlap in clinical presentation makes it difficult to determine which combination of criteria for defining subgroups best predicts familial aggregation. In dealing with this overlap, we found that only early age at onset, or major depression with an anxiety disorder or secondary alcoholism, were independently related to increased risk of major depression in relatives. Once the effects of these proband factors had been taken into account, endogenous, delusional, melancholic, or autonomous symptom patterns, recurrent depression, history of hospitalization, and suicidal ideation or attempts in probands were not associated with increased risk of major depression in relatives.

Adolescent↗
PubMed1986

Family-genetic studies of psychiatric disorders. Developing technologies.

During the past decade new concepts and technologies have improved the conduct of family-genetic studies in psychiatry. We compiled and critically evaluated these advances, including study design, pedigree collection, diagnostic procedures in adults and children, and epidemiologic and genetic approaches to data analysis. These approaches have improved the collection of accurate information on the nature and patterns of psychiatric illness in families. The data generated from well-designed and well-conducted family studies are useful for the identification of homogeneous subgroups of psychiatric disorders, for understanding the spectrum of psychiatric disorders, for examining the associations between psychiatric disorders, and for studying the continuity between adult and childhood manifestations of psychiatric disorders. Findings from these studies also may enhance our capacity to identify the mode of transmission of the psychiatric disorders and to select potentially informative families for future genetic linkage studies using the new recombinant DNA techniques. The adaptation of these methods to routine clinical practice and new directions in the application of family-genetic studies employing more refined assessments and analytic methods are also discussed.

Data Collection↗
PubMed1986

Gilles de la Tourette's syndrome and attention deficit disorder with hyperactivity. Evidence against a genetic relationship.

Results of a family study of Gilles de la Tourette's syndrome (TS) suggest that TS and attention deficit disorder (ADD) with hyperactivity are genetically separate disorders transmitted independently in families at risk. Although the rate of TS among the relatives of the two proband groups was virtually the same (10.3% vs 11.1%), the rate of ADD among the relatives of probands with TS and ADD with hyperactivity was approximately eight times higher than the rate of ADD among the relatives of the probands with TS only. In those families where the proband had both TS and ADD, the two traits segregated independently. Therefore, there is no evidence to suggest that the two disorders are genetically related.

Adolescent↗
PubMed1986

Genetics of a wild population of rhesus monkeys (Macaca mulatta): II. The Dunga Gali population in species-wide perspective.

Genetic variability in a population of wild rhesus monkeys near the village of Dunga Gali, Northwest Frontier Province, Pakistan (Melnick et al., Am. J. Phys. Anthropol. 63:341-360, 1984) was compared to similar variation in other wild-caught rhesus monkeys. Regional samples of rhesus from different parts of Asia all displayed similar amounts of variation (i.e., P and Hi) and were consistently more variable than the Dunga Gali local population. Despite these differences in the level of genetic variation, genetic diversity is fairly evenly distributed across the species range. Thus only 3-9% of the total gene diversity of Macaca mulatta can be attributed to differences among major regions. The differences that do exist tend toward a weak geographic cline with clustering of populations into an eastern and a western group. Both selection and drift/migration models explain this general genetic homogeneity. More genetic (protein and DNA) and zoogeographic data are necessary to choose between these models.

Alleles↗
PubMed1986

Progress toward resolving the possible linkage of multiple endocrine neoplasia type 2A to haptoglobin and group-specific loci: use of restriction fragment length polymorphisms extends exclusion region.

In an earlier paper, positive but nonsignificant lod scores were found in pair-wise linkage tests between multiple endocrine neoplasia type 2A (MEN-2A) and both the haptoglobin (HP) locus on chromosome 16 and group-specific component (GC) locus on chromosome 4. Recently discovered restriction fragment length polymorphisms for HP and for metallothionein 2 processed pseudogene 1 (MT2P1) near GC have made it possible to carry out a more powerful set of linkage tests with MEN-2A. This paper reports the results of such linkage analyses employing both pair-wise and multipoint tests. Close linkage of HP on chromosome 16 and MEN-2A is excluded. Linkage of MEN-2A on chromosome 4 with GC is excluded on the MT2P1 side of GC in a 7-centimorgan interval around MT2P1.

Blood Protein Electrophoresis↗
PubMed1986

Recurrence risks in an oligogenic threshold model: the effect of alterations in allele frequency.

The polygenic threshold model assumes that the distribution of the underlying liability is approximately normal. This paper examines the impact of deviations from normality in the underlying liability distribution when the number of loci affecting liability is finite, but large (e.g. 5-10). Skewness and kurtosis of the liability distribution are produced by varying the frequency of pathogenic alleles while population risk of illness is held constant by parallel changes in the threshold of manifestation. For a given population risk of illness, the recurrence risk in relatives varies widely as a function of the shape of the liability distribution. These results raise questions about the accuracy of the polygenic threshold approximation for the calculation of recurrence risks for human 'polygenic' disorders.

Alleles↗
PubMed1986

Linkage analyses of multiple endocrine neoplasia, type 2 (MEN-2) with 23 classical genetic polymorphisms.

Linkage analyses were performed in a single large family with multiple endocrine neoplasia, type 2 (MEN-2) between 23 classical genetic polymorphisms and MEN-2. We exclude close linkage of the locus for MEN-2 with ABO, ACP1, BF, ESD, Fy, GALT, GLO1, Jk, MNSs, P, PGM1, Rh and TF, as well as absolute linkage with GPT. These results raise to about 6% the proportion of the genome that has been excluded in this one family. Somewhat positive lod scores were obtained for GC (0.92 at theta = 0), GPT (0.73 at theta = 0.1) and HP (1.49 at theta = 0.05); although not statistically significant, these findings suggest regions of the genome that warrant additional study.

Alleles↗
PubMed1986

Linkage analyses of multiple endocrine neoplasia, type 2A (MEN-2A) with 20 DNA polymorphisms: 5% of the genome excluded.

Pairwise linkage analyses are reported between the locus for multiple endocrine neoplasia type 2A (MEN-2A) and 20 restriction fragment length polymorphisms (RFLPs) in a single large kindred which was previously screened for linkage with this form of cancer using 23 blood group and serum protein polymorphisms. No significant, positive lod scores have been obtained so far. These 20 RFLPs have excluded the MEN2 locus from about as much of the genome as did the 23 classical markers previously reported. This is a clear demonstration of the value of RFLPs for linkage studies since these 20 RFLPs were not selected for being the most polymorphic of those available. Over 10% of the human genome has been excluded from linkage with the MEN2 locus in this particular family.

Chromosome Mapping↗
PubMed1986

Gilles de la Tourette's syndrome: tics and central nervous system stimulants in twins and nontwins.

Thirty-four of 170 surveyed individuals with Tourette's syndrome (TS) were treated with CNS stimulants before age 18. In 24% of treated individuals, persistent exacerbation of tics was closely associated with treatment. In 3%, tic response was transient, and in 24%, tics were not obviously associated with treatment. Six pairs of monozygotic twins were discordant for stimulant treatment, and all untreated co-twins also developed TS. The number of individuals in whom stimulants permanently exacerbate tics may be small, but the risk appears to be real. Genetic vulnerability and duration and timing of treatment may mediate response.

Antipsychotic Agents↗
PubMed1986

Familial Tourette's syndrome: report of a large pedigree and potential for linkage analysis.

We studied a large Mennonite kindred affected by chronic motor tics (CMTs) and vocal tics in a probable autosomal dominant pattern. We administered a standardized questionnaire to 69 family members and reviewed our videotapes of 47. Using DSM III criteria and independent ratings, we diagnosed 10 subjects as having definite Tourette's syndrome (TS), 3 with definite CMTs, 15 with probable TS, and 1 with probable CMT. The clinical features of this family are presented. This is the largest known kindred with TS. Permanent lymphoblastoid cell lines have been established from 67 family members for genetic linkage analysis.

Adolescent↗
PubMed1986

DNA polymorphisms for the nerve growth factor receptor gene exclude its role in familial dysautonomia.

Alleles for the single human nerve growth factor receptor gene (NGFR) on chromosome 17q can be distinguished by two polymorphic restriction sites for XmnI and one for HincII. The combined information content for haplotypes is quite high, making the NGFR locus an excellent genetic marker. Two of these polymorphisms were used to follow the inheritance of NGFR alleles in families with two or more members affected with familial dysautonomia. This rare disease is inherited in an autosomal recessive mode in the Ashkenazic Jewish population. Affected individuals show a severe depletion of NGF-dependent nerve populations from birth. Linkage analysis excluded a role for NGFR in this disease with odds of greater than 10(6):1 against the dysautonomia gene being within 1 centiMorgan of the mutation. In a previous study the gene for the beta subunit of NGF (NGFB) was also excluded in this disease. A possible role for other genes involved in NGF action or those coding for other developmentally determining neuronal factors is indicated.

Alleles↗
PubMed1985

A twin study of Tourette syndrome.

In 43 pairs of same-sex twins, in which at least one co-twin had Tourette syndrome (TS), 30 pairs were probably monozygotic (MZ) and 13 were probably dizygotic (DZ). Concordances for TS were 53% and 8% for MZ and DZ pairs, respectively. When diagnostic criteria were broadened to include any tics in co-twins, concordance rates were 77% and 23% for MZ and DZ pairs, respectively. These concordances are consistent with genetic etiology. However, the fact that only 53% of MZ twins were fully concordant indicates nongenetic factors affect expression of TS. Presence of tics in discordant co-twins and timing of onset in partially concordant co-twins support an association between TS and tics in families with TS present. The data are inconclusive on whether some MZ twins with discordant co-twins are etiologically different from those who are concordant.

Adolescent↗
PubMed1985

Multiple threshold models for the affective disorders: the Yale-NIMH collaborative family study.

From the Yale-NIMH collaborative family study, the 1482 first degree relatives of 90 bipolar 1, and 163 major depression probands were examined to test the hypothesis that bipolar 1 and major depression are due to a single underlying genetic liability. We attempted to fit multifactorial-polygenic and single-major-locus multiple threshold models for sex and severity to the relatives in the major depression and bipolar 1 families. With relatives classified as affected only if they met criteria for major depression or bipolar 1, there was at best only marginal support for these models. Differences between these and previously reported results were examined in relation to differences in underlying assumptions. Additional analyses of these and other data from families of NIMH bipolar 2 and schizoaffective probands suggest that different methods of age adjustment, the relative placement of bipolar 2 and schizoaffective disorders in a hypothesized liability continuum and the inclusion or exclusion of sex thresholds were not primarily responsible for differences in the fit of genetic threshold models. Factors which do appear to be important are variability in rates between samples, the possibility of genetic heterogeneity, and the presence of a large secular increase in affective illness over the past three generations; the secular trend cannot be accommodated in the models of genetic transmission examined.

Adult↗