The primary objective of the present thesis was to investigate factors that influence the creation of false memories using the Deese-Roediger-McDermott (DRM) paradigm. The experimental research addressed the effect of age, list length, and list content on the magnitude of the DRM illusion with a view to testing assumptions derived from activation-monitoring theory and Fuzzy Trace Theory. In the first experiment, I wanted to determine whether the DRM paradigm is appropriate for use with New Zealand English-speaking adults. In addition, Experiment 1 was designed to assess the effect of prior recall on recognition performance. To answer these questions, I assigned half of the participants to a recall-plus-recognition condition and the remaining participants to a recognition-only condition. Rates of false recall and recognition were comparable to those reported in the literature, which suggested that the task is suitable for use with New Zealand adults. Furthermore, prior recall enhanced correct recognition but it did not affect false recognition. In Experiment 2, I examined how manipulations of list-length affected children and adults' susceptibility to the DRM illusion. Ten-year-olds and adults studied eight lists of either 7 or 14 words. In the 14-word condition, adults falsely recalled more critical targets than children; however, in the 7-word condition, there was no age difference in false recall. In addition, adults falsely recognised a greater proportion of critical targets than children, however, this effect was not dependent on the length of the study list. In Experiments 3A and 3B, I examined whether presenting highly familiar study materials would enhance children's susceptibility to false memories. Ten-year-old children and adults studied four standard DRM lists, four new lists that centred on 'child-friendly' concepts, such as birthday and school (CF lists), and four lists derived from child word-association norms. In both experiments, there was no age difference in rates of false recall. In addition, presenting material that was deemed more developmentally appropriate did not enhance children's susceptibility to false memories relative to adults. In Experiment 4, I introduced a post-recall phase to examine why the DRM illusion is less likely to occur when short lists are presented and when the materials are child-friendly. During the post-recall phase, participants were asked to report any other words that they had thought of during the presentation or recall of the study lists. Thinking about the target word, but remembering that it had not been presented, could not account for decreased levels of false recall in the short-list condition. Similarly, with the CF lists, it appeared that the list items were less likely to activate the critical target for both children and adults. In the final three experiments, I explored the assumptions outlined in activation-monitoring theory and fuzzy-trace theory to determine which model provided the best account of the findings obtained to date. To explore the activation-monitoring account, children and adults completed word association tasks. To explore fuzzy-trace theory, children and adults were given a gist extraction task where they had to identify the critical targets associated with each list. Collectively, the results of the present thesis fit more comfortably within an activation-monitoring framework than they do within the fuzzy-trace framework. Although the precise mechanisms underlying the DRM illusion have yet to be elucidated, the present findings suggest that gist extraction, activation processes, and source monitoring each play a substantial role in mediating false memory levels.

Background Polycystic ovary syndrome (PCOS) is a common endocrine condition in women associated with obesity, reproductive and metabolic abnormalities. It improves with weight loss, however currently no specific dietary recommendations exist and there may be abnormalities in appetite regulation in PCOS that contribute to difficulty in weight management. Aims To assess the effect of 1) short and long-term weight loss and weight maintenance strategies on weight loss, reproductive and metabolic parameters in overweight women with PCOS and to 2) assess the relative effect of weight loss on cardiovascular risk factors and 3) postprandial appetite, appetite hormones (ghrelin, CCK, PYY) and food intake in overweight women with and without PCOS. Results Overweight women with PCOS followed an 8-week weight loss (2 meal replacements/day, 4904.4±127 kJ, n=32) followed by a 6 month carbohydrate (<120 g/day) or fat restricted (<50 g/day) weight maintenance regime (n=23). Reductions in weight (5.6±2.4 kg) and improvements in body composition, insulin, reproductive hormones and menstrual cyclicity occurred and were sustained equivalently for both diet groups. We then assessed the effect of weight loss (4.2±0.7 kg over 8 weeks as described above) in overweight women with (n=15) and without (n=17) PCOS on cardiovascular risk factors. All subjects had similar improvements in body composition, triglycerides, reproductive hormones and fasting and post-prandial insulin. C-reactive protein decreased with weight loss for non-PCOS women (-1.2±0.5 mg/L, P=0.025) but not for PCOS women. We finally assessed appetite regulation in PCOS. Women with (n=20) and without (n=12) PCOS followed a standard protein (55% carbohydrate, 15% protein) or high protein diet (40% carbohydrate, 30% protein) for 16 weeks (~6000 kJ/day). Non-PCOS subjects were more satiated (P=0.001) and less hungry (P=0.007) after the test meals and had a 70% higher fasting baseline ghrelin (P=0.011), a greater increase in fasting ghrelin (57.5 versus 34.0%, P=0.033), a greater post-prandial ghrelin decrease at week 16 (113.5±46.3 versus 49.3±12.2 pg/mL, P=0.05) and a greater maximal decrease in post-prandial ghrelin (-144.1±58.4 versus -28.9±14.2 pg/mL, P=0.02) following weight loss than subjects with PCOS. Lastly, women with (n=14) and without (n=14) PCOS undertook an 8-week weight loss regime (4.2±0.7 kg as described above). At week 0 and 8, women with PCOS again displayed lower ghrelin levels (P=0.01 and P=0.097 respectively) and a lesser post-prandial ghrelin decrease (P=0.048 and P=0.069 respectively) but similar post-prandial appetite, buffet consumption and fasting or post-prandial peptide YY and cholecystokinin compared to women without PCOS. Conclusion Meal replacements and moderate macronutrient restriction are effective strategies for the dietary management of PCOS. Equivalent weight losses improved cardiovascular risk factors similarly for overweight women with and without PCOS with the exception of CRP which did not decrease with weight loss for overweight women with PCOS. PCOS status is associated with altered fasting and post-prandial ghrelin levels but is not consistently associated with other impairments in post-prandial gut peptides or food intake. Further investigation is required to assess if appetite regulation is impaired in PCOS and the optimal strategies and amount of weight loss for improvement of reproductive and metabolic parameters in PCOS. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1282329 / Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2007

Bibliography: leaves 204-215. / xviii, 215, [14] leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This study investigates the food consumption of overweight women over three menstrual cycles within a randomised double blind placebo controlled design. The aims of the study were: 1) to determine whether women identified as exhibiting PMS symptoms including increased appetite, have a preference for carbohydrate; 2) to determine if low brain levels of serotonin are involved in contributing to increased carbohydrate intake, and whether increasing the availablility of serotonin by using dexfenfluramine reduces total food intake or solely selectively reduces carbohydrate intake in women with PMS; 3) to determine whether there is a link between changes in food consumption, and the severuty of PMS symptoms. / Thesis (Ph.D.)--University of Adelaide, Dept. of General Practice, 2003

Thesis (M. Sc.)--University of Hong Kong, 2007. / Title proper from title frame. Also available in printed format.

Thèse (M.Sc.)--Université Laval, 200. / Bibliogr.: f. 68-75. Publié aussi en version électronique.

No description available.

The association between cardiovascular reactivity and the metabolic syndrome, as well as individual metabolic syndrome criterion variables, was investigated in adolescents. Cardiovascular reactivity has been examined as a risk marker or factor in the pathogenesis of hypertension or cardiovascular disease, but few studies have looked at its relationship with the metabolic syndrome. Blood pressure (BP) and heart rate (HR) cardiovascular reactivity to three tasks, evaluated speaking, mirror star tracing, and cold pressor, were assessed in 148 adolescents. Using the American Heart Association (AHA) adult definitional criteria, individuals were classified into metabolic syndrome groups (presence vs. absence of metabolic syndrome), and 16% of individuals met criteria for the metabolic syndrome. In logistic regression analyses, the occurrence of the metabolic syndrome was negatively associated with HR reactivity to the cold pressor (OR = 0.920, 95% CI = 0.873, 0.969), and positively associated with diastolic blood pressure (DBP) reactivity to the star tracing task (OR = 1.089, 95% CI = 1.008, 1.177). Results of multiple regression analyses that included individual metabolic syndrome risk variables indicated that cold pressor reactivity explained 7% of the variance in casual BP, while star tracing reactivity accounted for 7% of the variance waist circumference and 6% of the variance triglycerides (ps < .05). The findings indicate that cardiovascular reactivity to physical or behavioral challenge is associated with the metabolic syndrome in a sample of adolescents. Cardiovascular reactivity may be an important clinical tool for identifying individuals at risk of the metabolic syndrome and cardiovascular disease.

No description available.

Williams-Beuren Syndrome (WBS) is an autosomal dominant neurodevelopmental disorder caused by hemizygous deletion of a 1.5 Mb region on chromosome 7q11.23. Symptoms are numerous and include behavioural and cognitive components. One of the deleted genes, GTF2IRD1, a putative transcription factor, has been implicated in the neurological features of WBS by studying patients with atypical deletions of 7q11.23. Gtf2ird1-targeted mice have features consistent with the WBS phenotype, namely reduced innate fear and increased sociability. To identify neural targets of GTF2IRD1, microarray analyses were performed comparing gene expression in whole brains of Gtf2ird1-/- and wildtype (WT) mice at embryonic day 15.5 and at birth. Overall, the changes in gene expression in the mutant mice were not striking, with most falling in the range of 0.3 to 2 fold. qRT-PCR was used to verify the expression levels of candidate genes and examination of verified genes revealed that most were located on chromosome 5, within 50 Mb of Gtf2ird1. Expression of these candidate genes in Gtf2ird1-/- mice was found to be the same as in WT 129S1/SvImJ mice, indicating the differences were the result of flanking chromosomal material from the, 129-derived, R1 ES cells from which the Gtf2ird1-/- mice were generated, and that expression differences were unrelated to Gtf2ird1 dosage. Further analysis found that while many genes showed decreased expression using primers targeting the 3’ UTR, expression of upstream exons was not affected. Transcripts using alternative polyadenylation sites were identified using 3’ RACE, and qRT-PCR showed that expression of different 3’ UTR isoforms can occur in a strain specific manner. Expression analysis of previously identified GTF2IRD1 targets also failed to demonstrate an in vivo effect. In summary, I was unable to find any in vivo neuronal targets of this putative transcription factor, despite its robust expression in the developing rodent brain.

<p>Background: There is limited information available about the prevalence of Metabolic Syndrome (MetS), its trend over time and its predisposing risk factors according to different definitions in Canadian adults. No studies have compared the ability of the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP III) and the International Diabetes Federation (IDF) definitions to predict Cardiovascular Disease (CVD) mortality among Canadian adults.</p> <p>Objectives: a) To examine the age and sex specific prevalence of the Metabolic Syndrome in Canadian adults by using the ATP III and the IDF definitions. b) To examine the risk factors for Metabolic Syndrome in Canadian adults by using the ATP III and the IDF definitions. c) To examine the association between Metabolic Syndrome and cardiovascular disease mortality in Canadian adults by using the ATP III and the IDF definitions.</p> <p>Methods: The Canadian Heart Health Survey was a cross-sectional probability sample survey conducted in all 10 Canadian provinces between 1986 and 1992.The first two studies in this thesis were based on individuals for whom full anthropometric measurements were obtained and for whom data on all components of MetS were available (provinces of Alberta, Manitoba, Ontario, Quebec and Saskatchewan). Statistics Canada linked the CHHS data set to Canadian Mortality Database. The third study was based on three provinces (Alberta, Manitoba, and Saskatchewan) for whom full anthropometric measurements, mortality data, and data on all components of MetS were available. MetS was defined according to ATP III and IDF definitions. A weighted analysis using SPSS PASW Complex Samples (version18) was used to conduct stepwise logistic regression analysis to identify risk factors significantly associated with MetS (p < 0.05). Cox-regression analyses using the STATA (version11) was conducted to predict CVD mortality.</p> <p>Results: According to ATP III, 17.9% and 15.3% of men and women have MetS, while according to IDF, 23.8% and 17.3% of men and women have MetS, respectively. Kappa agreement between the definitions is 72 % for men and 80% for women (pâ¤0.05). Older age and low level of physical activity are significant risk factors for the MetS regardless of gender and definition. Higher level of education and alcohol consumption are additional significant protective factors for women, whereas retirement and being unemployed are additional significant risk factors for men. The hazards of death due to CVD events in women with the syndrome according to the ATP III and the IDF definitions are 3.96(1.30-12.09) and 2.56 (1.32-4.97), respectively. The comparable numbers for men are 2.21(1.16-4.02) and 2.50(1.50-4.17). Conclusion: In Canadian adults the prevalence of MetS is higher when the IDF definition is applied but the metabolic derangement of individuals identified is less severe. Demographic, socio economic factors, and lifestyle habits are significantly associated with MetS among the Canadian adults. The ATP III definition predicts CVD mortality better in women, while the IDF definition predicts CVD mortality better in men.</p>