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Biomedical subjects

M Baron

Publications and source records attributed to M Baron.

At least 235 records · Page 13Linked to original sources
PubMed1981

Platelet monoamine oxidase values and genetic heterogeneity in schizophrenia research.

Platelet monoamine oxidase (MAO) activity is significantly reduced in chronic schizophrenics with family history of schizophrenia. The degree of reduction is related to the extent of genetic load. Schizophrenics with no affected relatives do not differ from control subjects. These findings are consistent with the hypothesis of genetic heterogeneity in schizophrenia. Discrepancies among previously reported data sets can thus be explained by overrepresentation of nongenetic phenocopies with normal MAO levels. The implications for biologic and genetic research in schizophrenia are discussed.

Blood Platelets↗
PubMed1981

Multiple-threshold transmission of affective disorders.

Data on bipolar and unipolar affective disorders were gathered on first-degree relatives of 255 patients with both illness types. As consistent with a model of continuous liability, bipolar probands were found to have more bipolar relatives and more relatives with any affective disorder than unipolar probands. Multiple-threshold models of inheritance were applied to the data using clinical polarity as a threshold determinant. The hypothesis of multifactorial inheritance was ruled out. Autosomal single-major-locus inheritance provided an acceptable fit to the data. It is proposed that separate genetic mechanisms for bipolar and unipolar disorders need not be present. The two illness types are represented in the model at different thresholds on a single continuum of genetic-environmental liability in which bipolar illness is claimed to be more deviant genetically than unipolar illness.

Bipolar Disorder↗
PubMed1981

X-linkage in bipolar affective illness. Perspectives on genetic heterogeneity, pedigree analysis and the X-chromosome map.

The search for genetic markers is a powerful strategy in psychiatric genetics. The present article examines four areas relevant to discrepancies among X-linkage studies in bipolar affective disorder. These are questions of ascertainment, analytic methods, the X-chromosome map and genetic heterogeneity. The following conclusions are reached: (a) Positive linkage findings cannot be attributed to ascertainment bias or association between affective illness and colorblindness. (b) The possibility that falsely positive linkage results were obtained by using inappropriate analytic methods is ruled out. (c) Reported linkages of bipolar illness to colorblind and G6PD loci are compatible with known map distances between X-chromosome loci. Linkage to the Xg antigen remains uncertain. (d) The discrepancy among the various data sets on affective illness and colorblindness is best explained by significant linkage heterogeneity among pedigrees informative for the two traits.

Bipolar Disorder↗
PubMed1981

Assortative mating in affective disorders.

Assortative mating was determined in 170 spouses of patients with major affective illness (bipolar and unipolar). An increase in affective disorders was found in both wives of affected men and husbands of affected women. The data suggest that assortative mating is present in the familial transmission of affective disorder.

Adult↗
PubMed1981

The schedule for Schizotypal Personalities (SSP): a diagnostic interview for schizotypal features.

The validity and reproducibility of psychiatric diagnosis are crucial to psychiatric research. To establish confidence in assigning schizotypal features, three paradigms estimating the reliability of a new instrument, the Schedule for Schizotypal personalities (SSP), were tested. The first paradigm considered joint, but independent evaluations made by two raters simultaneously. The second paradigm assessed evaluations on different occasions, with a mean interim time of 5.9 months (test-retest procedure). Both reliability paradigms demonstrated high levels of agreement for all of the scaled items. Ninety percent of the intraclass correlation coefficients were 0.80 or better for the joint evaluations, and 70% were 0.80 or better for the test-retest evaluation. The third paradigm measured the reliability of DSM-III Schizotypal Personality Disorder. The kappa value for measuring diagnostic agreement was 0.88. The authors recommend the use of the SSP as an interview schedule and discuss the implications of their findings for genetic and biological research of schizophrenia spectrum disorders.

Borderline Personality Disorder↗
PubMed1981

Genetic models of sex effect in unipolar affective illness.

Family study data on unipolar affective illness are analyzed by multiple threshold models of inheritance that incorporate sex effect. In these models males and females share a common genetic-environmental liability, but the less prevalent sex, i.e., males, has a higher genetic threshold for the disorder. Neither single major locus (SML) nor multifactorial-polygenic (MFP) transmission can account for the sex differences in the morbid risk for unipolar disorder. The implications for genetic research in affective disorders are discussed.

Chromosome Mapping↗
PubMed1981

Age-of-onset and genetic transmission in affective disorders.

Age-of-onset data were gathered on first-degree relatives of 252 probands with bipolar and unipolar affective disorders. Early onset probands (younger than 40 at onset) had more early onset relatives and a greater risk for affective disorder among their relatives than late onset probands (40 or older). This indicates that age-of-onset is a familial factor correlated with the liability to affective illness. Multiple threshold models of inheritance were applied to the data using age-of-onset as a liability-threshold determinant. The hypothesis of autosomal single-major locus was ruled out. Multifactorial-polygenic inheritance provided a better fit to the data. The data suggest that early and late onset affective disorders can be placed at different thresholds on a genetic environmental continuum and that the early onset form is more deviant genetically than the late onset type. The implications for genetic research in affective disorder are discussed.

Affective Disorders, Psychotic↗
PubMed1981

Genetic heterogeneity in affective disorders. Implications for psychobiological research.

The extent of genetic heterogeneity in major affective illness was estimated via three paradigms of single-major-locus inheritance. In the first paradigm bipolar and unipolar disorders were represented at different liability thresholds on a genetic-environmental continuum. The second paradigm incorporated sex-related thresholds into the model, thereby testing the hypothesis that affective illness is a transmitted trait whose phenotypic expression is a function of the individual's sex. The third paradigm included both clinical polarity and sex effect as threshold phenomena. All three paradigms predicted considerable genetic heterogeneity in affective disorders. Bipolar homozygotes were far more common than unipolar homozygotes, although the majority of ill individuals in the first two paradigms were heterozygotes. According to the third paradigm bipolar males had the highest proportion of homozygotes amongst the affected population. Significant increases in homozygosity occurred using the dual mating sampling method. Depending on the model paradigm and parameters these increases were 140-25,000% over the random sample method. The implications for biologic and genetic research in affective disorders were discussed.

Affective Disorders, Psychotic↗
PubMed1981

Morbidity risks in subtypes of unipolar depressive illness: differences between early and late onset forms.

Despite the high prevalence of unipolar depression in the general population, few genetic studies are available on subtypes of unipolar illness. We evaluated morbid risks for depression, alcoholism and/or sociopathy in the relatives of early onset (before age 40) and late onset (after age 40) unipolar patients in a sample of 106 probands consecutively admitted to the New York State Psychiatric Institute. unipolar patients with an early onset disease have a greater familial morbidity for depression, alcoholism and sociopathy than unipolar patients with a late onset disease. There is an excess of unipolar depression in female relatives of early onset unipolars when compared to late onset probands, regardless of the proband's sex. Alcoholism and sociopathy are also more prevalent in the relatives of early onset unipolars versus late onset probands. Our morbidity risk data show familial genetic differences between early and late onset forms of unipolar illness and partially confirm Winokur's concept of two subtypes of unipolar depression.

Adult↗
PubMed1981

Genetic analysis of Tourette syndrome suggesting major gene effect.

Data on Gilles de la Tourette syndrome are analyzed by multiple threshold models in inheritance that incorporate sex effect. The polygenic-multifactorial model is rejected. Single major locus inheritance can account for the data, although many of the occurrences of Tourette are due to nongenetic phenocopies. In both models, males and females share a common genetic environmental liability, but the less prevalent sex, that is, females, has a higher genetic loading for the disorder. The predicted population prevalences in the single major locus model are 2.3% for males and 0.8% for females. The implications for genetic and biological research in Tourette syndrome are discussed.

Female↗
PubMed1981

Lymphocyte subpopulations and reactivity to mitogens in patients with scleroderma.

T lymphocyte subpopulations were studied in 40 patients with scleroderma (PSS), 26 of whom were studied simultaneously for lymphoproliferative responses to phytohaemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM). PSS patients exhibited a reduction relative to 42 age- and sex-matched controls in the absolute number and percentage of early E rosettes, late E rosettes and E rosettes formed with aminoethylisothiouronium bromide (AET) treated sheep red blood cells. There was no difference between patients and controls in the proportions of B lymphocytes. PSS patients exhibited normal lymphocyte transformation responses to PHA and ConA and an augmented response to PWM. The mitogen responses did not correlate with the absolute number or percentage of lymphocytes or T and B lymphocyte subpopulations. No correlation was observed between any immunological variable studied and the extent of skin or organ involvement, disease duration or therapy.

Adult↗
PubMed1980

Platelet monoamine oxidase activity: relation to genetic load of schizophrenia.

Platelet monoamine oxidase (MAO) activity is significantly lower in chronic schizophrenic patients with a family history of schizophrenia compared to schizophrenics with no affected relatives and normal controls. These results are consistent with the concept of genetic and biologic heterogeneity in schizophrenia and suggest that the lack of uniformity across previous MAO studies of schizophrenia may be explained in part by the presence of biochemically normal phenocopies.

Blood Platelets↗
PubMed1980

Human platelet monoamine oxidase and the menstrual cycle.

Endocrine factors are known to affect platelet monoamine oxidase (MAO) activity. To assess the role of sex steroid hormones in regulating MAO, blood samples for platelet MAO assay were obtained twice weekly from 12 women. Peak MAO activity occurred during the ovulatory interval and a nadir occurred in the postovulatory phase, 5 to 6 days later. A 17% mean effect of menstrual variation from peak to nadir was noted. The implications for MAO studies in psychiatric research are discussed.

Adolescent↗
PubMed1980

Low platelet monoamine oxidase activity: a possible biochemical correlate of borderline schizophrenia.

Platelet monoamine oxidase (MAO) activity, psychiatric disorders, and family history of psychopathology were studied in 115 nonhospitalized, previously undiagnosed college student volunteers. Subjects were classified into two extreme groups: those with platelet MAO activity two standard deviations below the mean ("low-MAO" probands) and those with platelet MAO activity two standard deviations above the mean ("high"-MAO probands). Low-MAO probands were found to have a significant increase in the incidence of borderline schizophrenia and other psychiatric disorders compared to high-MAO probands. First-degree relatives of low-MAO probands were more often affected with psychiatric disorders and borderline schizophrenia than relatives of high-MAO probands. The data suggest that reduced platelet MAO activity is associated with psychiatric vulnerability and that the spectrum of schizophrenia may be more closely related to this vulnerability than other psychiatric disorders.

Adult↗