No description available.

Parkinson’s disease can be caused by A53T or A30P mutations in the α-synuclein (SNCA) gene, or by multiplication of the gene locus. Patients often experience depression and anxiety. We investigated affect, serotonin content and bioenergetic homeostasis of mice expressing human wild-type (WT), A53T, A30P or A53T+A30P (DM) SNCA transgenes. A30P-Tg mice displayed altered affect, increased serotonin turnover and reduced ATP and complex I+III activity. To determine whether murine α-synuclein (Snca) might mask effects SNCA transgenes we re-examined effects of SNCA transgenes in Snca-/- mice. SNCA transgenes rescued anxiety, serotonin levels and ATP content in Snca-/- mice. Only A53T SNCA abrogated behavioural despair associated with decreased norepinephrine in Snca-/- brains. The A53T residue is the natural sequence of murine Snca, and appears to be important for synuclein function in mice. The Snca-/- mouse provides a means to study the effects of SNCA mutants, and the physiologic roles of Snca in vivo.

Two experiments examined the influence of affective vocal qualities on attitude change according to the degree of congruency between vocal qualities and the message content (i.e., the extent to which the vocal qualities matched the intent of the message content). In Experiment 1, the design was a 2 (attitude formation: affective base vs. cognitive base) x 4 (persuasive message: fully matched vs. partially matched vs. fully mismatched vs. written passage) between participants factorial. In the initial phase, an attitude was created towards a novel object. This goal was accomplished by directing each participant to read either an emotionally evocative passage or an informational passage designed to produce favorable attitudes towards a fictitious animal called a lemphur (Crites, Fabrigar, & Petty, 1994). In the persuasion phase of Experiment 1, participants were exposed to a negative affective message designed to elicit fear. The results indicated the degree of attitude change produced by the fully matched vocal quality (i.e., a fearful voice) was no different relative to the written passage. However, both the partially matched (i.e., a bored voice) and fully mismatched vocal qualities (i.e., a content voice) generated significantly more attitude change than both the written passage as well as fear. In Experiment 2, the attitude formation phase was similar to that of Experiment 1. However, in the persuasion phase of Experiment 2, the focus was on messages that were cognitive in their content. Specifically, participants were exposed to a negative cognitive message designed to convey negative characteristics of the target. The data revealed the degree of attitude change generated by the fully mismatched vocal quality (i.e., an excited voice) was significantly greater than the written passage as well as both the partially matched (i.e., a fearful voice), and fully matched (i.e., an emotionless voice) vocal qualities. No further differences between vocal qualities were found. / Thesis (Master, Psychology) -- Queen's University, 2012-08-14 11:05:05.886

No description available.

Parkinson’s disease can be caused by A53T or A30P mutations in the α-synuclein (SNCA) gene, or by multiplication of the gene locus. Patients often experience depression and anxiety. We investigated affect, serotonin content and bioenergetic homeostasis of mice expressing human wild-type (WT), A53T, A30P or A53T+A30P (DM) SNCA transgenes. A30P-Tg mice displayed altered affect, increased serotonin turnover and reduced ATP and complex I+III activity. To determine whether murine α-synuclein (Snca) might mask effects SNCA transgenes we re-examined effects of SNCA transgenes in Snca-/- mice. SNCA transgenes rescued anxiety, serotonin levels and ATP content in Snca-/- mice. Only A53T SNCA abrogated behavioural despair associated with decreased norepinephrine in Snca-/- brains. The A53T residue is the natural sequence of murine Snca, and appears to be important for synuclein function in mice. The Snca-/- mouse provides a means to study the effects of SNCA mutants, and the physiologic roles of Snca in vivo.

The present thesis was designed to test the proposition that human health can be understood as embedded in a mind/body system. In this light, the primary goal of the thesis was to test several key principles of systems theory as it applies to the natural workings of a psychosomatic system. These primary principles are (i) variables composing a system are interrelated; (ii) dynamic fluctuation of those variables occurs on a continual basis; and (iii) mutual influence of system components occurs through internal feedback. Using an ecological self-report methodology, data on affective states and physical symptomology was collected intensively over a 20 day period among healthy adults as they went about their day-to-day lives. Analysis of the data found evidence for all three systems principles. Specifically, unpleasant affect and physical symptomology were related both concurrently and in a temporal or predictive fashion. These two variables fluctuated in a dynamically stable pattern over a daily and particularly, over a weekly cycle, and the variations in each variable over time were co-related. Finally, a negative feedback process was found to occur, such that heightened levels of unpleasant affect predicted elevated symptomology, while higher levels of symptoms led to lower levels of unpleasant affect. Further, declines in unpleasant affect led to declines in symptomology, thus serving to bring both body and mind back into a healthier balance. The results of the research are discussed as they pertain to each systems principle, a commentary on the testing of systems theory is offered, and implications of the research are discussed in terms of health care practice, work performance, and our understanding of human health.

Typescript. / Thesis (Ph. D.)--University of Hawaii at Manoa, 1978. / Bibliography: leaves 116-125. / Microfiche. / x, 125 leaves ill

Thesis (Ph.D.)--York University, 2005. Graduate Programme in Philosophy. / Typescript. Includes bibliographical references (leaves 197-218). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:NR11620

Thesis(M.S.)--Auburn University, 2006. / Abstract. Vita. Includes bibliographic references.

Thesis (Ph.D.)--The Chinese University of Hong Kong, 2007. / Includes bibliographical references.