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PubMed1990

Behavior of genetic markers in recipients after bone marrow transplantation and problems in forensic medicine.

The authors report studies on four pairs of donors and recipients in bone marrow transplantation (BMT). A broad range of gene markers at 41 gene loci, including 11 red blood cell markers, 5 human lymphocyte antigen (HLA) types, 12 serum protein markers, 5 red cell enzyme markers, and 8 salivary markers were evaluated before and after BMT over 2 months. As a result, 9 out of 41 gene loci of genetic markers in recipients were transformed into the donor type. BMT between family members may lead to transformation of gene markers, but within a pattern compatible with family inheritance patterns, and no genetic paradox will be found in later surveys of familial genetic relationships. However, in a personal identification system in forensic medicine using genetic markers as an index, the appearance of a phenotype incompatible with a blood relationship is possible after BMT with a non-blood-relative donor. This result is similar to the inheritance pattern observed after artificial insemination by a donor's semen (AID), a more complete out-of-family cross.

Blood Group Antigens↗
PubMed1995

A twin-sibling study of observed parent-adolescent interactions.

Numerous behavioral genetic studies call attention to the strong and pervasive genetic influence on developmental characteristics. However, this research has been criticized for its use of poor environmental measures and a failure to examine the complex processes that are a hallmark of research in child development. This study addresses this criticism by examining the genetic and environmental components of parent-child interactions. Mother, father, and 2 adolescent siblings (10-18 years) from each of 675 families were observed interacting in 10-min dyadic problem-solving sessions. 6 groups of siblings that differed in genetic relatedness were examined (MZ and DZ twins, full siblings in nondivorced families; full, half, and unrelated siblings in stepfamilies). Results suggest a greater genetic component to adolescent behavior than to parent behavior. Both adolescent and parent behavior showed strong effects of nonshared environment, even after error of measurement was removed.

Adolescent↗
PubMed1997

[Relationship between learning behavior and genetic factor on immobility shown during forced swimming test].

The relationship between learning and genetic factor on immobility in mice during a forced swimming test (FST) has been studied. The duration of immobility during the FST did not change significantly after the administration of either scopolamine (2.5 mg/kg, ip) or cyclohexamine (150 mg/kg, ip), although both drugs produced impairment in the learning task. This suggests that the increase in immobility observed during the second trial of the FST may not be related to learning which could occur during the first trial. Concerning the strain difference, first, the duration of immobility in C3H mice was shorter than that in ICR, ddY, C57BL and BALB mice. Second, after receiving shock stress in a box, ICR, ddY and C57BL mice, but not C3H mice showed a marked decrease in locomotor activity when placed in the box again without shock. Also during the FST, both C57BL and ddY mice, but not C3H mice showed prolongation of immobility and reduction in swimming after shock stress. The changes in locomotor activity, and immobility and swimming during the FST caused by shock stress in ddY mice recovered to normal levels after treatment with imipramine. From these results, it is suggested that the immobility shown during the FST, which may be independent of learning and dependent on some genetic factor, is a suitable model of depression in animals.

Animals↗
PubMed1998

Response of monocyte iron regulatory protein activity to inflammation: abnormal behavior in genetic hemochromatosis.

In genetic hemochromatosis (GH), iron overload affects mainly parenchymal cells, whereas little iron is found in reticuloendothelial (RE) cells. We previously found that RE cells from GH patients had an inappropriately high activity of iron regulatory protein (IRP), the key regulator of intracellular iron homeostasis. Elevated IRP should reflect a reduction of the iron pool, possibly because of a failure to retain iron. A defect in iron handling by RE cells that results in a lack of feedback regulation of intestinal absorption might be the basic abnormality in GH. To further investigate the capacity of iron retention in RE cells of GH patients, we used inflammation as a model system as it is characterized by a block of iron release from macrophages. We analyzed the iron status of RE cells by assaying IRP activity and ferritin content after 4, 8, and 24 hours of incubation with lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). RNA-bandshift assays showed that in monocytes and macrophages from 16 control subjects, IRP activity was transiently elevated 4 hours after treatment with LPS and IFN-gamma but remarkably downregulated thereafter. Treatment with NO donors produced the same effects whereas an inducible Nitric Oxide Synthase (iNOS) inhibitor prevented them, which suggests that the NO pathway was involved. Decreased IRP activity was also found in monocytes from eight patients with inflammation. Interestingly, no late decrease of IRP activity was detected in cytokine-treated RE cells from 12 GH patients. Ferritin content was increased 24 hours after treatment in monocytes from normal subjects but not in monocytes from GH patients. The lack of downregulation of IRP activity under inflammatory conditions seems to confirm that the control of iron release from RE cells is defective in GH.

Adult↗
PubMed1991

Classify and control: genetic information in the schools.

Recent advances in molecular and behavioral genetics are providing theoretical models to explain complex behavior--learning disabilities and behavioral problems--in simple biological terms. There are intrinsic difficulties in interpreting genetic information. Yet genetic explanations are particularly appealing in school systems pressed by demands for efficiency and accountability. Thus, genetic explanations are affecting the way children are categorized in the schools. This Article reviews genetic advances bearing on educational issues and their implementation through biological tests. It suggests the social consequences and legal implications of the growing prevalence of genetic assumptions.

Child↗
PubMed2004

Using the Mplus computer program to estimate models for continuous and categorical data from twins.

Historically, the focus of behavior genetic research was to obtain estimates of the sources of familial resemblance for a single phenotype. Current research strategies have moved beyond heritability estimates to the search for physiological and behavioral mechanisms by which genetic risk is translated into individual differences in behavior and disease liability. Such research questions often require multivariate designs and complex analytic models, including the analysis of continuous and categorical dependent variables within the same model. Recent advances in computer software for categorical data analysis have increased the tools available for researchers in behavior genetics. This paper describes how to use the Mplus software program (Muthén and Muthén, 1998, 2002) for the analysis of data obtained from twins. Example analyses include two- and five-group twin models for univariate and bivariate continuous and categorical variables. Data on alcoholism and age at first drink drawn from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders are used to illustrate how Mplus can be used to analyze multiple-category variables, recode and transform variables, select subgroups for analysis, handle subjects with incomplete data, include constraints to ensure non-negative loadings, include model covariates, model sex differences, and test alternative hypotheses about mediation of genetic risk by measured variables.

Adolescent↗
PubMed2000

Extracting meaning from comorbidity: genetic analyses that make sense.

As behavioral genetic strategies have become part of the arsenal of research in developmental psychopathology, a wide variety of genetic analyses are being applied to child psychiatric data. Multivariate genetic techniques have been used to explore comorbidity among traits or disorders and the main analysis undertaken has been to examine whether comorbidity is due to shared genetic and/or environmental factors. However, this model ignores other possible causes of comorbidity, which are reviewed. In particular, genetic analyses of comorbidity have only infrequently considered the model of phenotypic causality (one disorder directly influencing another), which provides an important alternative with potentially different implications for intervention strategies. Data from a recently published article by Wamboldt, Schmitz, and Mrazek (1998) are used to illustrate the potential difficulties of distinguishing between models of shared genetic/environmental risk and phenotypic causality. Given that the sample sizes required to distinguish between these models are often large, and frequently greater than those of the datasets available, it is argued that researchers should select the models that they test based on other lines of evidence that these models are plausible. Where convincing evidence does not exist, researchers should explore alternative models and determine their power to discriminate between these models.

Causality↗
PubMed2004

Studying interactions, reactions, and perceptions: can genetic disorders serve as behavioral proxies?

Different genetic disorders predispose individuals to display specific, etiology-related profiles, personalities, and maladaptive behaviors. Using groups with genetic etiologies as stand-ins or proxies for a specific behavior or set of behaviors, one can then examine how others in the child's environment react and whether such reactions are limited to a particular disorder or occur generally to all individuals showing that behavior. Just as twins, adopted, and institutionalized children have all been used as natural experiments to tell us about typical development, so too can groups with specific genetic syndromes help us to understand the nature and mechanisms of the reactions and behaviors of others.

Child↗
PubMed1998

Genetic and shared environmental influences on adolescent BMI: interactions with race and sex.

The present study uses a behavioral genetic design to investigate the genetic and environmental influences on variation in adolescent body mass index (BMI) and to determine whether the relative influences of genetic and environmental factors on variation in BMI are similar across racial groups and sexes. Data for the present study come from the National Longitudinal Study on Adolescent Health (Add Health), a large, nationally representative study of adolescent health and health-related behaviors. The Add Health sample contains a subset of sibling pairs that differs in levels of genetic relatedness, making it well suited for behavioral genetics analyses. The present study examines whether genetic and environmental influences on adolescent BMI are the same for males and females and for Black and White adolescents. Results indicate that genetic factors contribute substantially to individual differences in adolescent BMI, explaining between 45 and 85% of the variance in BMI. Furthermore, based on an analysis of opposite-sex sibling pairs, the genes that influence variation in adolescent BMI are similar for males and females. However, the relative importance of genetic and environmental influences on variation in BMI differs for males and females and for Blacks and Whites. Although parameter estimates could be constrained to be equal for Black and White males, they could not be constrained to be equal for Black and White females. Moreover, the best-fitting model for Black females was an ADE model, for White females it was an ACE model, and for males it was an AE model. Thus, shared environmental influences are significant for White female adolescents, but not for Black females or males. Likewise, nonadditive genetic influences are indicated for Black females, but not for White females or males. Implications of these results are discussed.

Adolescent↗