Indexing Behaviours Indicative of Ecological Citizenship in Canada

The concept of ecological citizenship, a transformative ideology of citizenship whereby citizens are connected through their moral environmental obligations, has been mainly theoretical in nature within contemporary literature. In addition, the literature on pro-environmental behaviours presupposes that individuals face barriers both externally and internally, preventing their participation in these activities. A lack of nationally representative data exists that quantifies the impacts on pro-environmental behaviour participation. This thesis aims to address these three components by applying the theoretical foundation of ecological citizenship to a dataset covering the environmental household behaviours of a sample of Canadian households (N = 22,363) representative of the majority of the Canadian population. The creation of an index of behaviours that could be theoretically associated with ecological citizenship is the primary goal of this thesis. The analysis then examines the index alongside variables that situate both the geographic, socio-economic, and demographic characteristics of these households. Using a combination of multivariate linear and logistic regressions, the impact of these variables will be analyzed to identify the strength and direction of these variables, taking into consideration the effect of all variables at once. Findings suggest that certain variables have a greater impact on the number of behaviours a household can participate in. From these findings, a discussion of how best to address these impacts is explored within the context of our foundation on ecological citizenship and how best to bring this theoretical concept into an applied sphere of thinking

Intrinsic, Pro-Apoptotic Effects of IGFBP-3 on Breast Cancer Cells are Reversible: Involvement of PKA, Rho, and Ceramide

We established previously that IGFBP-3 could exert positive or negative effects on cell function depending upon the extracellular matrix composition and by interacting with integrin signaling. To elicit its pro-apoptotic effects IGFBP-3 bound to caveolin-1 and the beta 1 integrin receptor and increased their association culminating in MAPK activation. Disruption of these complexes or blocking the beta 1 integrin receptor reversed these intrinsic actions of IGFBP-3. In this study we have examined the signaling pathway between integrin receptor binding and MAPK activation that mediates the intrinsic, pro-apoptotic actions of IGFBP-3. We found on inhibiting protein kinase A (PKA), Rho associated kinase (ROCK), and ceramide, the accentuating effects of IGFBP-3 on apoptotic triggers were reversed, such that IGFBP-3 then conferred cell survival. We established that IGFBP-3 activated Rho, the upstream regulator of ROCK and that beta1 integrin and PKA were upstream of Rho activation, whereas the involvement of ceramide was downstream. The beta 1 integrin, PKA, Rho, and ceramide were all upstream of MAPK activation. These data highlight key components involved in the pro-apoptotic effects of IGFBP-3 and that inhibiting them leads to a reversal in the action of IGFBP-3

Glucose Concentration in Cell Culture Medium Influences the BRCA1-Mediated Regulation of the Lipogenic Action of IGF-I in Breast Cancer Cells

Hyperglycaemia is a common metabolic alteration associated with breast cancer risk and progression. We have previously reported that BRCA1 restrains metabolic activity and proliferative response to IGF-I anabolic actions in breast cancer cells cultured in high glucose. Here, we evaluated the impact of normal physiological glucose on these tumour suppressive roles of BRCA1. Human breast cancer cells cultured in normal physiological and high glucose were treated with IGF-I (0–500 ng/mL). Cellular responses were evaluated using immunoblotting, co-immunoprecipitation, and cell viability assay. As we previously reported, IGF-I induced ACCA dephosphorylation by reducing the association between BRCA1 and phosphorylated ACCA in high glucose, and upregulated FASN abundance downstream of ACCA. However, these effects were not observed in normal glucose. Normal physiological glucose conditions completely blocked IGF-I-induced ACCA dephosphorylation and FASN upregulation. Co-immunoprecipitation studies showed that normal physiological glucose blocked ACCA dephosphorylation by increasing the association between BRCA1 and phosphorylated ACCA. Compared to high glucose, the proliferative response of breast cancer cells to IGF-I was reduced in normal glucose, whereas no difference was observed in normal mammary epithelial cells. Considering these results collectively, we conclude that normal physiological glucose promotes the novel function of BRCA1 as a metabolic restraint of IGF-I actions. These data suggest that maintaining normal glucose levels may improve BRCA1 function in breast cancer and slow down cancer progression

Operation Notes Illustrated With Digital Images

We would like to report on our experience of illustrating our operation notes with pre-, per- and post-operative digital images