Thesis (Ph. D.)--Ball State University, 2009. / Title from PDF t.p. (viewed on Nov. 12, 2009). Includes bibliographical references (p. 150-173).

Thesis (M.S. in pharmacology and toxicology)--Washington State University, May 2010. / Title from PDF title page (viewed on July 23, 2010). "Graduate Program in Pharmacology and Toxicology." Includes bibliographical references (p. 25-30).

Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 237-258). Also available on the Internet.

Thesis--Catholic University of America. / On spine: Girls with a specific learning disability. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 95-103).

Thesis (Ph. D.)--Catholic University of America.

Title from PDF of title page (University of Missouri--Columbia, viewed on Feb. 15, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Dr. Martha Markward. Vita. Includes bibliographical references.

One of sociology´s to assess the effects of political decision. According to sociologist Anders Persson the society is changing, and in that change social fear appear. In the reaction of social fear some people are being excluded. In that more narrow frame for normality laws are created that makes some parents and their children “the other”. Nine years ago the sociologist Eva Kärfve published a book that was very critical to the newborn psychiatrics diagnosing of children as a way of segregating groups in society. I am sad to say but she was right. According to the theory of Howard Becker I use a social interaction perspective to understand and interpret people´s actions. This perspective means that people through their actions creates phenomena in society. Becker´s book Tricks of the trade gives tools to investigate situations in society. The purpose of this study is to through a case study increase the understanding of a parent´s experiences in a case where municipality moved a pupil against the parents will. The method is case study, where the bulk is an interview with a pupil´s parents. The study shows the steps of human interaction that lead to the moving of a pupil against the parents will. The result indicates that the decision of what a violation of the norm is decides if the new law is to be executed. I present the school´s action from a view of the society and conclude with the questions: If we are using laws instead of giving schools economic resources, is that really what we want? If just one child is taken away from his school for the wrong reasons, is that not a case too much? The sociology is supposed to plead people without a voice cause. Reflect a structure of society and elucidate problems according to different theoretic perspectives. For me personally, the area of problem preceded the method. This study had not been what it is without the case. It takes a great deal of courage to invite a stranger to one´s home and talk about painful experiences. In the end I like to purpose that life is for everybody. / 0709902656

Children become diagnosed with neuropsychiatry diagnostic. The diagnostic of children is critiqued from. The national board of health and welfare because the child psychiatric clinics differ in the reliability of diagnostic. This is a problem both in the same clinic and between clinics. The purpose is to investigate if parents of children with neuropsychiatry diagnostic consider that the diagnostic criteria were met when the child was diagnosed. The method was first a pilot study with surveys and interviews. The study was a telephone survey with parents of diagnosed children. The result indicates that the parents didn’t experience that the diagnostic criteria was met. The discussion suggests that communication between parents, child psychiatry and school needs to improve. / 0761777843

Evidence suggests comorbidity of ADHD and eating disorders (EDs) among females. Capitalizing on the comorbidity of ADHD and EDs and subsequent obesity could lead to improved prevention and treatment of all three conditions. However, additional information regarding the comorbidity is necessary to develop such interventions, as little is known about how or why this co-occurrence exists. A comprehensive model of the underlying mechanisms associated with comorbid ADHD and EDs is needed to improve understanding of the development of the comorbidity. Moreover, while there are gender differences within each disorder, literature is limited regarding to the comorbidity among males, leading to a call for further investigation. Based on the literature, this study investigated three hypotheses of the underlying mechanisms of the ADHD/ED comorbidity, including: 1) ADHD and EDs are the expression of a common genetic or neurobiological dysfunction that manifests itself as binge eating and ADHD, 2) psychosocial factors common to both EDs and ADHD mediate the association between the two conditions, and 3) a third underlying mental health condition mediates the relationship between the two conditions. Underlying factors proposed within these three hypotheses include dopamine, serotonin, and monoamine oxidase A genes, family support, social support, neuroticism, conscientiousness, cognitive control, working memory, major depression, anxiety disorder, alcohol use and substance use disorders, and childhood abuse. In order to simultaneously investigate the three hypotheses, this study utilized secondary data analysis from 6,289 females and 5,248 males as part of the National Longitudinal Study of Adolescent Health. This data was used to test a model constructed via a combination of five theories, specifically, the Biopsychosocial Model, the Life Course Approach, the Risk Regulator Framework, the Research Domain Criteria Matrix, and the Person-Environment Transaction Theory. Findings of this study suggest that cognitive control, family support, and additional comorbid mental health illnesses such as depression, anxiety, and substance abuse disorder all mediate the relationship between ADHD and EDs. However, rather than leading to the comorbidity, ADHD led to other mental health issues which were then subsequently correlated to EDs; suggesting a comorbidity between these additional disorders and EDs with ADHD being a possible predictor of that comorbidity. In regards to genetics, the factors investigated in this study were not found to be directly associated with the comorbidity. Rather, these factors were connected to the psychosocial and psychiatric mediators, suggesting an indirect relationship between genetics and the comorbidity. With regards to males, differences were found between males with the comorbidity, ADHD alone, EDs alone, and neither disorder in regards to education attainment, BMI and obesity, delinquent behavior, and sexual behaviors were all observed. However, very few of the proposed underlying mechanisms among females were significantly associated with the comorbidity among males. Results provide initial support for continued research on the underlying mechanisms of the ADHD/ ED comorbidity. This research has potential implications in many areas including primary and secondary prevention of EDs, improved treatment plans, prevention of psychostimulant medication abuse, and prevention and treatment of obesity. Next steps include the use of advanced statistical techniques in order to explore multiple combinations of underlying factors to the comorbidity and direct interactions between factors, including gene x environment interactions. Additional study replications are also needed with the incorporation of additional genetic components.

<p>Developmental disabilities, including intellectual disability (ID), attention-deficit hyperactivity disorder (ADHD), and autism spectrum disorders (ASD), affect approximately 1 in 6 children in the United States. Attempts to produce treatment for developmental disabilities have been hampered by our current lack of understanding of the molecular mechanisms underlying these disorders. Advancements in genome sequencing and animal modeling technologies have proven to be an invaluable resource in the elucidation of potential disease mechanisms, with recent studies reporting novel mutations of the Ptchd1 and Shank3 genes in patients with developmental disabilities. Though these two genes have been proposed to play important roles in neural development, their function in the normal brain and defective behavioral output are poorly understood. </p><p>In this dissertation, I characterize the circuit and behavioral dysfunction of the genetically-engineered Ptchd1 and Shank3 knockout mice. With respect to Ptchd1, I found that expression is developmentally enriched in the thalamic reticular nucleus (TRN), which is a group of GABAergic neurons serving as the major source of inhibition for thalamo-cortical neurons. Slice and in vivo electrophysiological experiments revealed that deletion of this gene in mice disrupts SK2 currents and burst firing mechanisms in the TRN, a region that has previously been shown to play an important role in sleep, attention, and cognition. Consistent with clinical findings, Ptchd1 knockout mice display behavioral phenotypes indicative of hyperactivity, attention deficits, motor dysfunction, hyperaggression, and cognitive impairment. Interestingly, attention-like deficits and hyperactivity are rescued by SK2 pharmacological enhancement, suggesting a potential molecular target for developing treatment. </p><p>Shank3 knockout mice display ASD-like phenotypes, including social interaction deficits and repetitive behaviors. In addition, biochemical, electrophysiological, and morphological abnormalities were discovered in the medium spiny neurons (MSNs) of these mice. However, the exact neural circuits and cell types responsible for the autistic-like behaviors have not been identified. To address this important question, I developed a new conditional Shank3 knockout mouse. Importantly, the behavioral abnormalities reported in the original Shank3 knockout mice were recapitulated in this novel conditional Shank3 knockout mouse, indicating that this mouse may be useful for future pathway-specific dissections of ASD-like behaviors. Together, these two sets of studies not only provide mouse models for dissecting the function of PTCHD1and SHANK3 in normal and abnormal neural development, but also demonstrate a critical role for PTCHD1 in TRN neurons and SHANK3 in MSN cells and in the case of PTCHD1, identify potential cellular and circuit pathway targets for much-needed pharmacological intervention.</p> / Dissertation