This paper argues in favour of principle-based securities regulation for Canada. The author examines the current state of Canadian securities regulation and why change is needed. The author then examines the characteristics of principle-based regulation and contrasts it against rule-based regulation while exposing the advantages and disadvantages of both regulatory models. In proposing a principle-based model for Canadian securities regulation, the author looks to the use of this type of regulation in the capital markets of certain Canadian provinces, the United States and the United Kingdom and then examines certain attributes of Canadian capital markets that have to be considered in the application of principle-based securities regulation to Canada. In supporting principle-based regulation as the modern form of securities regulation, the author discusses lessons learned from the global financial crisis and how those lessons can be applied in the promotion of principle-based securities regulation for Canada.

What explains the creation and strengthening of international securities market standards through the International Organization of Securities Commissions (IOSCO)? This thesis addresses this question by analyzing the creation and strengthening of four of IOSCO’s international securities market standards between 1991 and 2010 relating to the following issues: the governance of cross-border financial crime, the objectives and principles of domestic securities market regulation, the regulation of credit rating agencies, and the regulation of hedge funds. This thesis argues that the creation and strengthening of these standards is derived from the role and influence of three different political actors: the transgovernmental network of securities market regulators, domestic legislatures, and states. The role and influence of these different political actors differs across issue areas and across time. To account for the differentiated sources of international securities market standards, this thesis proposes a Principal-Agent (PA) analytical framework. Domestic legislatures (the principal) delegate to securities regulators (the agent) the authority to oversee and regulate domestic securities markets by granting regulators specific forms of statutory authority. Exercising discretion within this act of delegation, domestic securities regulators act together in a transgovernmental network to create and strengthen international securities market standards. They are prompted to act by threats to the integrity and stability of developed financial centers from under-regulated or ineffectively regulated foreign financial centers, as well as by new policy preferences of domestic legislatures seeking to regulate previously unregulated financial market actors. Domestic legislatures also use multiple agents to ensure that agents act consistent with their policy preferences: their concerns about the costs of under-regulated foreign jurisdictions can generate direct pressure from states on international financial regulatory institutions to strengthen the implementation of international financial standards. This thesis makes an empirical contribution to existing literature by analyzing previously understudied international securities market standards. This thesis also makes a theoretical contribution to both IPE literature and PA theory within International Organization (IO) literature. For IPE literature, this thesis establishes a theoretical framework that accounts for the differentiated role and influence of the transgovernmental network of securities market regulators, domestic legislatures, and states in the creation and strengthening of international securities market standards. For PA theory within IO literature, this thesis highlights the role of the principled professional interests of the transgovernmental network of securities market regulators in creating and strengthening international securities market standards.

We previously described BT2, a BTB/POZ domain containing protein, as an activator of telomerase in Arabidopsis thaliana. In the current study, I present evidence of its interesting roles in mediating multiple hormone, stress and metabolic responses in plants. Steady-state expression of BT2 mRNA was regulated diurnally and was under the control of circadian clock, with a maximum expression in the dark. BT2 mRNA was responsive to nutrient status and to multiple biotic and abiotic stress signals. Using bt2 loss-of-function and BT2 over-expressing lines, I show that BT2 suppresses sugar and ABA-mediated responses during germination. BT2 is also essential for transcriptional gene activation mediated by CaMV 35S enhancers in Arabidopsis. Loss of BT2 in several well-characterized 35S enhancer activation-tagged lines such as yucca1d, pap1d, jaw1d etc., resulted in suppression of the activation phenotypes. The suppression of the phenotypes was due to decreased transcription of the activation-tagged genes. I further demonstrate that BT2 genetically interacts with CULLIN3. I propose that BT2 and CULLIN3 are components of a ubiquitin ligase complex. Together with associated proteins BET9 and BET10, the BT2 complex is required for CaMV 35S enhancer-mediated activation of gene expression and may regulate expression of target genes involved in multiple responses to fluctuating biotic and abiotic conditions. I also found that BT2 protein levels are tightly regulated in plants. BT2 protein was primarily localized in the nucleus and was developmentally regulated. BT2 turn-over was regulated in part by the 26S-proteosome, and rare codons present in its open reading frame affected BT2 protein accumulation. In addition to BT2, its orthologs, BT1, BT3, BT4 and BT5, also responded to light, clock and nutrients, with some differences. Moreover, BT1, BT3 and BT4 were also required for 35S enhancer-mediated activation of gene expression. I propose that BT family proteins assemble into multi-protein complexes to mediate multiple responses to changing environmental and nutritional conditions.

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What explains the creation and strengthening of international securities market standards through the International Organization of Securities Commissions (IOSCO)? This thesis addresses this question by analyzing the creation and strengthening of four of IOSCO’s international securities market standards between 1991 and 2010 relating to the following issues: the governance of cross-border financial crime, the objectives and principles of domestic securities market regulation, the regulation of credit rating agencies, and the regulation of hedge funds. This thesis argues that the creation and strengthening of these standards is derived from the role and influence of three different political actors: the transgovernmental network of securities market regulators, domestic legislatures, and states. The role and influence of these different political actors differs across issue areas and across time. To account for the differentiated sources of international securities market standards, this thesis proposes a Principal-Agent (PA) analytical framework. Domestic legislatures (the principal) delegate to securities regulators (the agent) the authority to oversee and regulate domestic securities markets by granting regulators specific forms of statutory authority. Exercising discretion within this act of delegation, domestic securities regulators act together in a transgovernmental network to create and strengthen international securities market standards. They are prompted to act by threats to the integrity and stability of developed financial centers from under-regulated or ineffectively regulated foreign financial centers, as well as by new policy preferences of domestic legislatures seeking to regulate previously unregulated financial market actors. Domestic legislatures also use multiple agents to ensure that agents act consistent with their policy preferences: their concerns about the costs of under-regulated foreign jurisdictions can generate direct pressure from states on international financial regulatory institutions to strengthen the implementation of international financial standards. This thesis makes an empirical contribution to existing literature by analyzing previously understudied international securities market standards. This thesis also makes a theoretical contribution to both IPE literature and PA theory within International Organization (IO) literature. For IPE literature, this thesis establishes a theoretical framework that accounts for the differentiated role and influence of the transgovernmental network of securities market regulators, domestic legislatures, and states in the creation and strengthening of international securities market standards. For PA theory within IO literature, this thesis highlights the role of the principled professional interests of the transgovernmental network of securities market regulators in creating and strengthening international securities market standards.

Children's difficulties with regulating or controlling emotion are associated with externalizing problems (Eisenberg et al., 2001). Emotion regulation develops through interactions with caregivers during childhood, where children are socialized about the management and expression of emotions (Kopp, 1989). The parent-child relationship is thus one factor associated with children's externalizing problems and, to date, research on children’s externalizing problems has focused on relationships with parental emotion socialization and parent-child emotions (Granic & Lamey, 2002; Lengua, 2006). However, parent-child co-regulation— the bidirectional process whereby individuals mutually regulate emotions with others (Fogel, 1993)— is also likely a proximal factor in children's externalizing problems. Over time, dyadic patterns emerge and are reinforced through co-regulation, and children develop regulated or dysregulated emotional patterns with their parents (Granic & Lamey, 2002). Co-regulation is also likely related to differences in externalizing symptomatologies, as dyads with children with co-occurring externalizing and internalizing problems (MIXED) show more mutual hostility over the course of a conflict than dyads with purely externalizing children (EXT; Granic & Lamey, 2002). The current study examined co-regulation in 255 parent-child dyads, of which 80 had EXT children (73% male), 111 had MIXED children (87% male), and 64 had typically-developing children (63% male). Children were between the ages of 8 and 12 (M = 9.56). Behaviours during positive and conflict discussions were coded with a new observational tool, the Co-Regulation of Emotion (CORE) coding system. CORE's validity was supported with associations with independent raters’ impressions of the interactions. Generally, co-regulation was higher during the conflict as compared to the positive discussions, as expected. Contrary to hypotheses, dyads with EXT and MIXED children did not show more non-supportive co-regulation than dyads with typically-developing children, and dyads with typically-developing children did not show more supportive co-regulation. Similarly, group differences on the association between interaction partners' supportive and non-supportive co-regulation and negative affect were not significant. Overall, MIXED dyads did not show more non-supportive co-regulation than EXT dyads, as had been expected. The findings did not support the hypothesis that emotion co-regulation differentiates dyads with externalizing children from dyads with typically-developing children in middle childhood. / Thesis (Master, Psychology) -- Queen's University, 2012-08-07 11:41:10.329

Organizations in many domains such as healthcare, finances, telecommunications, educa-tion, and software development, must comply with an ever-increasing number of regula-tions, including laws and policies. In order to measure compliance to regulation, several recent approaches propose modelling regulations using goals and indicators. However, creating goal models for regulations is time consuming and prone to errors, especially as this is usually done manually. This thesis tackles this issue by automating some of the steps for creating goal models, and by offering better ways to create graphical views of goal models than what is currently available nowadays in goal modelling tools. The notation used in this thesis is the Goal-oriented Requirement Language (GRL), which is part of the User Requirements Notation standard and is supported by the jUCMNav tool. The concepts of regulations and their indicators are captured using a tab-ular presentation in Comma-Separated Value (CSV) files. An import mechanism is added to jUCMNav to automatically create regulation goal models from such files. The imported GRL model can then by visualized using novel features that enable the addition of multiple views/diagrams in an efficient and usable way.

The enzyme carbonic anhydrase (CA) contributes to multiple physiological processes by catalysing the reversible hydration of carbon dioxide. However, regulation of CA activity in response to homeostatic challenges remains poorly understood. The objectives of this thesis were to investigate whether CA is transcriptionally regulated by cortisol in fish and whether post-translational modification (PTM) of CA occurs in fish. The results of an in vivo reporter assay used to investigate potential transcriptional regulation of zebrafish, Danio rerio, cytoplasmic CA (CAc) were inconsistent, and it remains unclear whether zebrafish CAc is regulated transcriptionally by cortisol. Phosphorylation of rainbow trout, Oncorhynchus mykiss, CAc was predicted from in silico analysis of the putative amino acid sequence and confirmed by Western analysis of phosphoprotein levels following in vitro incubation of CA, purified from trout gill, under conditions designed to potentiate endogenous kinases. Again using in vitro incubations designed to potentiate endogenous kinases and phosphatases, changes to the phosphorylation state of CAc were found to modulate its enzymatic properties. These findings suggest that CA activity may be regulated by signalling pathways that activate cellular protein kinases, and future work should focus on identifying these pathways.

Psychological conditions, including stress, compromise immune defenses. Although this concept is not novel, the molecular mechanism behind it remains unclear. Neuropeptide Y (NPY), regulates anxiety and is a part of the stress response. The NPY system also modulates immune functions such as cytokine release, cell migration, and innate immune cell activity. Postganglionic sympathetic nerves innervating lymphoid organs release NPY, which together with other peptides activate five receptors (Y1, Y2, Y4, Y5, and y6). Additionally, immune cells themselves release NPY following activation. Previous studies have shown that Y1 mediates NPY-immune effects and data presented here shows expression of Y1 on a wide range of immune cells. Results presented in this thesis, using Y1-deficient mice (Y1-/-), have uncovered a novel role for Y1 on immune cells. NPY acts endogenously to inhibit T cell activation whereas Y1-/- T cells are hyper-responsive to activation and trigger severe colitis after transfer into lymphopenic mice. Thus, signalling through the Y1 receptor on T cells inhibits T cell activation and controls the magnitude of T cell responses. Paradoxically, in Y1-/- mice, T cell differentiation to Th1 T cells appears to be defective as these mice were resistant to T helper type 1 (Th1) cell???mediated inflammatory responses and showed reduced levels of the Th1 cell???promoting cytokine interleukin 12 and reduced interferon ?? production. This defect was due to functionally impaired antigen presenting cells (APCs). Y1-deficient APCs are defective in their ability to produce Th1-promoting cytokines and present antigens to T cells and consequently, Y1-/- mice had reduced numbers of effector T cells. Key reciprocal bone marrow chimera experiments indicated that this effect is intrinsic to immune cells and not driven by other Y1-expressing cell types. These results demonstrate a fundamental bimodal role for the Y1 receptor in the immune system, serving as a strong negative regulator on T cells as well as a key activator of APC function. The findings presented in this thesis uncover a sophisticated molecular mechanism regulating immune cell functions and thus adds to a growing number of signalling pathways shared by the immune and nervous system.

Psychological conditions, including stress, compromise immune defenses. Although this concept is not novel, the molecular mechanism behind it remains unclear. Neuropeptide Y (NPY), regulates anxiety and is a part of the stress response. The NPY system also modulates immune functions such as cytokine release, cell migration, and innate immune cell activity. Postganglionic sympathetic nerves innervating lymphoid organs release NPY, which together with other peptides activate five receptors (Y1, Y2, Y4, Y5, and y6). Additionally, immune cells themselves release NPY following activation. Previous studies have shown that Y1 mediates NPY-immune effects and data presented here shows expression of Y1 on a wide range of immune cells. Results presented in this thesis, using Y1-deficient mice (Y1-/-), have uncovered a novel role for Y1 on immune cells. NPY acts endogenously to inhibit T cell activation whereas Y1-/- T cells are hyper-responsive to activation and trigger severe colitis after transfer into lymphopenic mice. Thus, signalling through the Y1 receptor on T cells inhibits T cell activation and controls the magnitude of T cell responses. Paradoxically, in Y1-/- mice, T cell differentiation to Th1 T cells appears to be defective as these mice were resistant to T helper type 1 (Th1) cell???mediated inflammatory responses and showed reduced levels of the Th1 cell???promoting cytokine interleukin 12 and reduced interferon ?? production. This defect was due to functionally impaired antigen presenting cells (APCs). Y1-deficient APCs are defective in their ability to produce Th1-promoting cytokines and present antigens to T cells and consequently, Y1-/- mice had reduced numbers of effector T cells. Key reciprocal bone marrow chimera experiments indicated that this effect is intrinsic to immune cells and not driven by other Y1-expressing cell types. These results demonstrate a fundamental bimodal role for the Y1 receptor in the immune system, serving as a strong negative regulator on T cells as well as a key activator of APC function. The findings presented in this thesis uncover a sophisticated molecular mechanism regulating immune cell functions and thus adds to a growing number of signalling pathways shared by the immune and nervous system.