Thesis (M.A)--University of North Carolina Wilmington, 2009. / Title from PDF title page (January 11, 2010) Includes bibliographical references (p. 122-135)

Thesis (Ph.D.)--University of Tennessee Health Science Center, 2009. / Title from title page screen (viewed on September 18, 2009). Research advisor: Robert W. Williams, Ph.D. Document formatted into pages (ix,128 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 106-127).

Behavioral difficulties in the early school years pose a risk to psychosocial functioning. The failure model suggests that peer rejection explains longitudinal associations between aggression and internalizing symptoms. The model postulates that aggression leads to increases in peer rejection, which, in turn, contributes to internalizing symptoms. This study tests pathways posited by the failure model, examining direct and indirect longitudinal effects. Direct effects models examined associations between reactive aggression and internalizing problems, reactive aggression and peer rejection, and peer rejection and internalizing symptoms. A mediation model examined the indirect effect of reactive aggression to internalizing symptoms, via peer rejection. Because distinct components of the failure model are presumed to share genetic influences, removing potential genetic contributions is important when examining the environmental influences over developmental pathways posited by the model. To this end, longitudinal tests were conducted with traditional (non-genetically controlled) and MZ twin difference (genetically controlled) designs. The latter disentangled nonshared environment effects from those for genetic factors from environmental factors. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2020. / FAU Electronic Theses and Dissertations Collection

<p dir="ltr">This dissertation sought to contribute a pair of genetically informed studies strategically designed to make potentially causal inferences about potential co-developing processes of internalizing symptoms, body mass index (BMI) and relative pubertal timing during adolescence. Paper 1 used the Early Growth and Development Study (EGDS; N=561), a prospective adopted-at-birth design which primarily accounts for passive gene environment correlation by virtue of youth having been adopted at birth and placed in non-relative adoptive families. Paper 2 used the discordant sibling design from a subsample of siblings from the Adolescent Brain Cognitive Development (ABCD) Study (N=3792), which by design accounts for all confounding of the effects of a risk factor with all shared familial influences that siblings share and all environmental differences that exist between families. The hypothesized associations were further examined in subsamples of twins and MZ twins to make increasingly strict, potentially causal inferences. Across the two studies, I hypothesized that higher internalizing symptoms and higher BMI would positively co-develop at the within person and within family level, respectively for each paper. I hypothesized that there would be unidirectional within person effects of relatively earlier pubertal development on higher internalizing symptoms, across both studies. Finally, I hypothesized that there would be positive co-development of higher BMI and earlier relative pubertal timing early on in both studies, but that only higher BMI would continue to unidirectionally predict earlier relative pubertal timing across the two studies’ ends. In paper 1, specific hypotheses were completely unsupported. In Paper 2, hypotheses were partially supported for two of out three pairs of phenotypes. Specifically, there was evidence of one within family cross-lagged effect between higher discordance in internalizing symptoms at age 10 and higher discordance in BMI at age 11. There was also evidence of one within family cross-lagged effect between higher discordance in relative pubertal timing at age 12 and higher discordance in internalizing symptoms at 13. Findings from both papers indicated that the association between BMI and relative pubertal timing is likely largely confounded by common stable between person, stable discordance, and stable family average factors. Implications and limitations are discussed.</p>

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"Local genetic adaptation and homing behavior in anadromous fish favors the formation of local populations across their geographic range of distribution. Spawning- and natal-site fidelity repeated over generations restricts gene flow and allows genetic differences to accumulate resulting in reproductive isolation. This leads to progressive genetic differentiation and population structuring among different river populations. Alewife, Alosa pseudoharengus, are anadromous fish which are estimated to have high rates of reproductive fidelity and hence might show population structuring among different breeding streams. Alewife are fish of economic importance since they have both commercial and recreational value. Alewife populations have been declining over the past decades and conservation measures to restore the populations have been implemented. Since maintaining genetic integrity of natural populations is one of the main concerns, identification of population structure can assist in designing appropriate restocking programs. In this study, I used microsatellite markers developed for shad to study population structuring in alewife. Samples were collected from two sites in Connecticut and one in Lake Michigan and genetic differentiation among these populations was estimated using five microsatellite loci. My studies indicate that microsatellite loci developed for shad can be used for alewife. Results from this preliminary study indicated subtle but significant genetic differentiation among populations. This suggests that care should be taken when restocking alewife from different sites in order to maintain genetic diversity among these populations."

abstract: This study examined whether early adversity at 30-months moderated the heritability of common and individual components of EF at 8 years. It was hypothesized that early adversity would not moderate the common EF factor, but instead moderate individual EF components. The sample included 208 twin pairs from the Arizona Twin Project. Early Adversity, assessed at 30 months of age, included Parenting Daily Hassles, low perceived MOS social support, punitive punishment (Parental Responses to Child Misbehavior), home chaos (Confusion, Hubbub, and Order Scale), CES-D maternal depression, and low maternal emotional availability. EF at 8 years included the Eriksen Flanker Task, Continuous Performance Task, Digit Span Forward and Backward, and parent-reported Attentional Focusing and Inhibitory Control (Temperament in Middle Childhood Questionnaire). For both early adversity and EF, the first principal components were extracted as composites. A confirmatory factor analysis was also conducted to index common EF. Genetic analyses were tested on the common EF composites as well as each individual task using umx. Univariate models revealed genetic influences on all individual measures and common EF, with broad sense heritability from .22 (Digit Span Backwards) to .61 (parent-reported inhibitory control). Shared environmental influences were found for the Flanker Task (.13) and parent-reported inhibitory control (.24), and E was moderate to high (.40-.73) for all measures except parent-report inhibitory control (.15) and attentional focusing (.31). Moderation of heritability was not observed in for Digit Span Forward, Digit Span Backward, and Attentional Focusing. However, the nonshared environment was moderated for Common EF, and the Flanker Task, and additive genes and the nonshared environment were moderated for the Continuous Performance Task and Inhibitory Control. Generally, total variance decreased as early adversity increased, suggesting that homes with low levels of adversity may allow children to interact with more proximal processes that can promote EF development. / Dissertation/Thesis / Masters Thesis Psychology 2018

Although the rates of delinquent behavior have been decreasing since the 1990s, adolescent delinquent behavior continues to take a great toll on society as well as on perpetrators themselves. In this way, it is essential to understand the process of delinquency development. The current dissertation is comprised of three studies that analyzed the predictors and the development of delinquency using genetically-informed designs. The sample used for all studies comes from the Add Health dataset, a nationally-representative data on adolescents followed across 14 years. The first study modeled the longitudinal development of delinquency in three adolescent cohorts: early, middle, and late adolescence. The results showed significant heritability effects on delinquency, with varying estimates across cohorts. The longitudinal stability of delinquency was mostly driven by heritability, while changes were affected by nonshared environmental influences. The second study tested the GxE interaction between two dopaminergic polymorphisms (DRD4 7-repeat allele and DRD2 A1 allele) and parenting, operationalized by child abuse on the one negative extreme and maternal closeness on the other, in longitudinally predicting delinquent behaviors. Main effects of maternal closeness and childhood abuse on later delinquency were found. On the other hand, no significant interaction of DRD2 or DRD4 polymorphisms with either maternal closeness or childhood abuse were observed. The third study used a twin design to test whether neighborhood disadvantage has a genetic component and whether this might be explained by an individual’s IQ and self-control. The results showed substantial heritability of the neighborhoods the individuals moved into as adults. This was partly explained by IQ, as adolescents’ IQ predicted neighborhood disadvantage 14 years later.

Scholars in diverse disciplines are currently engaged in debates concerning the causes and consequences of human social interaction in areas including personality development, interpersonal characteristics, social attachments and support, family life, religious involvement, civic engagement, socioeconomic attainment, and health and wellbeing, among others. Unfortunately, researchers in these areas are compartmentalized into two, largely isolated, camps: (1) social scientists who base their research on the assumption that social outcomes are primarily, if not exclusively, the products of social-environmental influences; and (2) biologists, geneticists, psychiatrists, and some psychologists, all of whom assume that genetic factors are important as well. The purpose of this dissertation, therefore, is to begin integrating sociological and biomedical research on social life. To facilitate this task, four specific research questions are addressed: Do genetic and environmental factors both influence social life, and if so, what is the relative contribution of each? Why and how do genetic factors influence social life, and what are the pathways by which they operate? Are genetic and environmental influences on social life correlated (i.e., non-additive), and do genetic factors bias social scientific studies that do not take them into consideration? Do genetic and environmental factors interact to produce social outcomes? To answer these questions, twin sibling data from the National Survey of Midlife Development in the United States (MIDUS) is analyzed. In response to the first question, results reveal that both genetic and environmental factors are indeed important predictors of individual-level variation on several different aspects of social life, including religious involvement, civic engagement, personality and interpersonal characteristics, family relations, socioeconomic status, community attachment, neighborhood quality, and psychological distress. Further, genetic effects on several of these outcomes (e.g., civic engagement, psychological distress) are mediated by personality, interpersonal characteristics, and social relationships, which provides insight into the second and third research questions. With respect to the final question, the findings presented here suggest that genetic and environmental influences on at least one social outcome--health and well-being--function in both a correlated and interactive manner. Overall, the theoretical and empirical research provided in this dissertation highlights a growing need for research that integrates sociological and biological approaches to the study of social life. / text

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2007. / Härtill 5 uppsatser.