The Open Data Smart City: A Case Study of Smart City Progress through Open Data Initiatives

Smart cities, cities that are supported by an extensive digital infrastructure of sensors, databases and intelligent applications, have become a major area of academic, governmental and public interest. Simultaneously, there has been a growing interest in open data, the unrestricted use of organizational data for public viewing and use. Drawing on Science and Technology Studies (STS), Urban Studies and Political Economy, this thesis examines how digital processes, open data and the physical world can be combined in smart city development, through the qualitative interview-based case study of a Southern Ontario Municipality, Anytown. The thesis asks what are the challenges associated with smart city development and open data proliferation, is open data complimentary to smart urban development; and how is expertise constructed in these fields? The thesis concludes that smart city development in Anytown is a complex process, involving a variety of visions, programs and components. Although smart city and open data initiatives exist in Anytown, and some are even overlapping and complementary, smart city development is in its infancy. However, expert informants remained optimistic, faithful to a technologically sublime vision of what a smart city would bring. The thesis also questions the notion of expertise within the context of smart city and open data projects, concluding that assertions of expertise need to be treated with caution and scepticism when considering how knowledge is received, generated, interpreted and circulates, within organizations.

ENVIRONMENTAL INFLUENCES AND EPIGENETIC MECHANISMS IN RISK FOR DEPRESSION

Genetic and environmental factors interact to influence vulnerability for internalizing psychopathology, including Major Depressive Disorder (MDD). The mechanisms that account for how environmental stress can alter biological systems are not yet well understood yet are critical to develop more accurate models of vulnerability and targeted interventions. Epigenetic influences, and more specifically, DNA methylation, may provide a mechanism by which stress could program gene expression, thereby altering key systems implicated in depression, such as frontal-limbic circuitry and its critical role in emotion regulation. This thesis investigated the role of environmental factors from infancy and throughout the lifespan affecting the serotonergic (5-HT) system in the vulnerability to and treatment of depression and anxiety and potential underlying DNA methylation processes. First, we investigated the contributions of additive genetic vs. environmental factors on an early trait phenotype for depression (negative emotionality) in infants and their stability over time in the first 2 years of life. We provided evidence of the substantial contributions of both genetic and shared environmental factors to this trait, as well as genetically- and environmentally- mediated stability and innovation. Second, we studied how childhood environmental stress is associated with peripheral DNA methylation of the serotonin transporter gene, SLC6A4, as well as long-term trajectories of internalizing behaviours. There was a relationship between childhood psychosocial adversity and SLC6A4 methylation in males, as well as between SLC6A4 methylation and internalizing trajectory in both sexes. Third, we investigated changes in emotion processing and epigenetic modification of the SLC6A4 gene in depressed adolescents before and after Mindfulness-Based Cognitive Therapy (MBCT). The alterations from pre- to post-treatment in connectivity between the ACC and other network regions and SLC6A4 methylation suggested that MBCT may work to optimize the connectivity of brain networks involved in cognitive control of emotion as well as also normalize the relationship between SLC6A4 methylation and activation patterns in frontal-limbic circuitry. Our results from these three studies strengthen the theory that environmental influences are critical in establishing early vulnerability factors for MDD, driving epigenetic processes, and altering brain processes as an individual undergoes treatment, or experiences relapse.