Accurate 3D protein structure prediction is one of the most challenging problems facing bioinformaticians today. This thesis develops and examines an evaluation module for ranking predicted super-secondary structures – specifically a-helix pairs – as part of a case-based reasoning system. The proposed module is part of the Triptych project, which aims at the accurate prediction of the three-dimensional structure of proteins from contact maps. Triptych is an advanced case-based reasoning system that utilizes a library of existing protein structures and motifs to help predict the structure of a known polypeptide chain of amino acids that represents a target a-helix pair. The proposed module evaluates possible solutions by integrating multiple strategies, learning methods and sources of knowledge in the form of expert advisors. It uses advisors which integrate knowledge from the fields of biology, biochemistry, classical physics, and statistical data analysis obtained from pre-determined structures. Lastly, the proposed evaluation module would allow for the integration of more sources of knowledge, in the form of expert advisors, as well as serve as a framework for evaluating other structural motifs in future. / Thesis (Master, Computing) -- Queen's University, 2007-09-09 19:42:59.094

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal

Previous research has demonstrated that exposure to family disruption/father absence (due to parental relationship dissolution) is a significant risk factor for early pubertal development in daughters. Moreover, the earlier in life that this exposure occurs, the greater the risk of these outcomes for girls. Two opposing classes of explanation have been proposed for this reliable finding. First, evolutionary-based developmental experience models have proposed that father absence may actually cause early pubertal development in daughters through mechanisms that remain to be elucidated. Second, this association may arise from either a genetic or a family-wide environmental confound. To discriminate between these two competing classes of explanation (i.e., causal vs. noncausal), a retrospective study employing a community sample of full biological sister pairs was conducted in New Zealand. This study examined menarchael age in (a) a primary group comprising age-discrepant biologically disrupted/father absent sister pairs (n = 68), and (b) a matched control group comprising age-discrepant biologically intact/father present sister pairs (n = 93). According to the causation model, if greater exposure to family disruption/father absence causes earlier pubertal development in girls, then in families in which (a) full biological sisters are discrepant in age, and (b) the younger sister has experienced more prolonged father absence than has her older sister, younger sisters should be at greater risk for earlier pubertal development. By contrast, if a genetic or family-wide environmental confound explains this association, full biological sisters should not systematically differ in pubertal timing as a function of birth order, even if they have experienced different amounts of father absence. The unique contribution of the current study to this area of inquiry is its employment of a differential sibling exposure design to test the explanatory value of the two opposing classes of explanation (i.e., causal versus noncausal). This genetically and environmentally controlled sibling design was utilised (a) to test the central hypothesis that the birth order/age discrepancy (older versus younger) between sisters would interact with family type (biologically disrupted vs. biologically intact) to predict the size of sibling differences in menarcheal age, and (b) to test for potential moderating effects of paternal dysfunction. Consistent with evolutionary causal models, the current sibling comparison study revealed that within biologically disrupted/father-absent families, younger sisters (who had more prolonged exposure to father absence) had earlier menarcheal ages than did their older sisters. The current study was therefore not only able to distinguish between the two competing classes of explanations, but its findings plausibly supported a causal rather than a noncausal explanation for the association between father absence and earlier pubertal timing in girls. Moreover, it revealed that this association is more nuanced than previously thought, because the accelerating effect of family disruption/father absence on daughters’ menarcheal timing was moderated by fathers’ functioning in the family. The current study has eight important limitations that can be used to direct future research. These limitations are detailed along with proffered suggestions (where applicable) for addressing them in future studies. Possible mediating mechanisms for the earlier menarcheal timing found in daughters from biologically disrupted/father absent families are also proposed. Finally, the implications of the current study’s findings for both parents and daughters in biologically disrupted/father absent families are discussed.

A phonological disorder is a communication disorder of the speech sound system characterized by an impaired ability to use developmentally expected speech sounds and sound patterns to communicate with others (Bauman-Waengler, 2004). This impairment affects the clarity of a child's speech and how easily a child's speech can be understood. As stated in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American Psychiatric Association, 1994), difficulties with speech sound production may interfere with academic achievement, social communication, or future occupational achievement. Children with phonological impairments are generally viewed as being at risk for reading difficulties (American Speech-Language-Hearing Association, 2001).Clinicians and researchers in speech-language pathology agree that efficient treatment of children who have moderate to severe phonological disorders is critical. Although imitation and structured practice are primary strategies employed by speech- language pathologists for practicing speech production, using communicative tasks to facilitate generalization during phonological intervention has been suggested in the literature.The purpose of this study was to determine if communication-centered phonological intervention would be effective in improving speech production in preschool children with moderate to severe phonological disorders. A single subject multiple probe across subjects research design (Horner andamp; Baer, 1978) was used to assess the effectiveness of communication-centered phonological intervention with three preschool children. The communication-centered phonological intervention in this investigation consisted of the combined application of focused stimulation of key words during joint storybook reading and interactive practice of key words using communicative feedback.All three subjects demonstrated some type of phonological improvement following the communication-centered intervention. Two out of the three subjects demonstrated improvement in the use of the target phonological patterns during theintervention sessions with one of these participants demonstrating generalization of the target phonological pattern to conversational speech. Although the third subject did not demonstrate improvement during the intervention period, follow-up testing revealed some system-wide changes in his phonology that may be attributed to the intervention. Further investigation of communication-centered phonological intervention is warranted.

No description available.

Thesis (M. Phil.)--University of Hong Kong, 2008. / Includes bibliographical references (leaf 99-108) Also available in print.

Thesis (doctoral)--Universität Wien, 2007. / Includes bibliographical references (p. [337]-346).

Thèse (M.A.)--Université Laval, 2008. / Bibliogr.: f. 33-34. Publié aussi en version électronique dans la Collection Mémoires et thèses électroniques.

Thèse (de maîtrise)--Université Laval, 1997. / Bibliogr.: f. [122]-125. Publié aussi en version électronique.