VictorJuiz/thesis huggingface dataset:
The Social Organization of the Lives of 'Semi-skilled' International Migrant Workers in Alberta: Political Rationalities, Administrative Logic and Actual Behaviours
Keywords: temporary foreign workers
skill codification
institutional ethnography
Canada
social organization

This institutional ethnography is an inquiry into the particular migrant category of International Migrant Workers (IMW) in Canada (otherwise known as Temporary Foreign Workers). It looks at how the daily lives of IMWs who have been deemed as ‘semi-skilled’ by the National Occupational Classification (NOC) system are organized by their immigration and job status in Canada. These IMWs are working primarily in the food service, hotel or retail industries in front-line and often precarious employment in Southern and Western Alberta. The data was collected through a literature review, interviews, observations, and textual analysis. The participants that informed this inquiry are IMWs, service providers in the immigrant sector, representatives from the Alberta Government, and an immigrant recruiter/consultant. This study uses an ‘ideological circle’ (Yan, 2003), which maps out the process through which governmental ideology is filtered down to all levels of society via a set of ideas, knowledge, procedures and methods about people and processes. It provides a vehicle to identify the specific social relations that organize people in different sites. It becomes apparent through this mapping that along with the political rationalities of neoliberal criteria and the logic of globalization, and market civilization and citizenship, certain administrative logic and technologies of government such as situating IMWs as economic units in the Canadian nation-state, processes of skill codification, and devolution of immigration policies and programs, become the foundations for the ways that IMWs live their lives in Canada. In particular, we can see how and why they ‘work’ for permanent residency, how and why they become vulnerable to precarious employment in their workplace and in other ways, and how and why they become isolated through family separation. The thesis ends with a look into how social workers and social service organizations are managing ‘professional’ relationships with migrant populations whose lives are organized in the above ways, and questions whether it’s possible at all to move beyond supporting ‘bare life’ (Agamben, 1998).
Chronic Hepatitis C among Immigrants Living in Canada: Natural History, Disease Burden, and Cost-effectiveness of Screening
Keywords: hepatitis C
immigrant
cost
disease burden
Markov model
obesity
diabetes
cost-effectiveness
screening

Aims: To investigate the natural history of CHC, estimate the disease burden of CHC, and assess the cost-effectiveness of screening for CHC among immigrants living in Canada. Methods: A retrospective cohort study compared the prognosis of CHC between immigrant patients and native-born patients who had advanced fibrosis. A cross-sectional study assessed the association between obesity and hepatitis C viremia. The disease burden of CHC among immigrants was estimated through Markov cohort model. The cost-effectiveness of screening for CHC was assessed among immigrants. Results: The retrospective cohort study including 318 patients demonstrated that immigrant patients had significantly higher risk of hepatocellular carcinoma than Canadian-born patients (p=0.005). The hazard ratio associated with ‘immigrant’ for hepatocellular carcinoma in multivariate Cox proportional-hazards analyses reduced to the least and non-significant (p=0.318) after adjusting age and type 2 diabetes. The prevalence of obesity in 1118 individuals tested positive for hepatitis C antibody was 28.8%. Multiple regression analyses and propensity score methods suggested a significant association between obesity and hepatitis C viremia. The disease burden study estimated that immigrants with CHC had much shorter average life years (26.9 years vs. 39.1 years) and quality adjusted life years (20.6 years vs. 32.4 years) than the age matched immigrants without CHC. The cost-effectiveness study indicated that screening for CHC among immigrants from 183 countries (72.1% of immigrant population in Canada) had an incremental cost-effectiveness ratio less than $50,000 per quality adjusted life year gained. Conclusion: Immigrant patients with CHC could have a higher risk of HCC than native-born patients. The significant association between obesity and hepatitis C viremia could explain the observed high prevalence of type 2 diabetes in patients with CHC. CHC reduces the average life expectancy of immigrants with CHC more than 10 years. Screening for CHC is cost-effective among over 70% of immigrants living in Canada.
Poetics of Denial: Expressions of National Identity and Imagined Exile in English-Canadian and Romanian Dramas
Keywords: Post-colonialism, post-communism, imagined exile, national identity, Romanian drama, English Canadian drama, Ceausescu, Macdonald, borders, exilic drama, multiculturalism.

After the change of their country’s political and international statuses, post-colonial and respectively post-communist individuals and collectives develop feelings of alienation and estrangement that do not involve physical dislocation. Eventually, they start imagining their national community as a collective of individuals who share this state. Paraphrasing Benedict Anderson’s definition of the nation as an “imagined community,” this study identifies this process as “imagined exile,” an act that temporarily compensates for the absence of a metanarrative of the nation during the post-colonial and post-communist transitions. This dissertation analyzes and compares ten English Canadian and Romanian plays, written between 1976 and 2004, and argues that they function as expressions and agents of post-colonial and respectively post-communist imagined exile, helping their readers and audiences overcome the identity crisis and regain the feeling of belonging to a national community. Chapter 1 explores the development of major theoretical concepts, such as nation, national identity, national identity crisis, post-colonialism, and post-communism. Chapter 2 and Chapter 3 analyze dramatic rewritings of historical events, in “1837: The Farmers’ Revolt” by the theatre Passe Muraille with Rick Salutin as dramaturge, and “A Cold” by Marin Sorescu, and of past political leaders, in “Sir John, Eh!” by Jim Garrard and “A Day from the Life of Nicolae Ceausescu” by Denis Dinulescu. Chapter 4 examines the expression of the individual and collective identity crises in “Sled” by Judith Thompson and “The Future Is Rubbish” by Vlad Zografi. Chapter 5 explores the treatment of physical and cultural borders and borderlands in Kelly Rebar’s “Bordertown Café”, Guillermo Verdecchia’s “Fronteras Americanas”, Petre Barbu’s “God Bless America”, and Saviana Stanescu’s “Waxing West”. The concluding chapter briefly discusses the concept of imagined exile in relation to other investigations of post-colonial and post-communist dramas and reviews some of the latest perspectives of national identity, reassessing this study from a diachronic perspective.
To Which of Thine Selves be True? Changes in Viscerosomatic Neural Activity with Mindfulness Meditation Training Reflect Improved Present-moment Self-awareness
Keywords: Cognitive Neuroscience
Mindfulness
Meditation
fMRI
Insula
Self-Reference

Mindfulness training cultivates momentary awareness, a form of attention directed to non-evaluative, immediate sensation. This form of attention stands in contrast to a more temporally extended awareness, which allows for the evaluative organization of experience into a personal narrative. The neural mechanisms underlying such awareness, and their role in regulating emotions, are poorly understood. Thus, in three functional magnetic resonance imaging (fMRI) experiments, I explored the thesis that momentary and extended awareness represent dissociable modes of self-reference, with momentary self-reference reducing ruminative elaboration of events by biasing attention towards interoceptive signals from the body. I compared individuals who were randomly-assigned to either an 8-week Mindfulness-Based Stress Reduction (MBSR) training course against a waitlisted group (Controls). Three distinct studies examined the impact of Mindfulness on: 1) the contrast between explicitly directed momentary and extended self referential processing; 2) reactions to an induced sadness challenge; and 3) the contrast between interoceptive (breath-monitoring) and exteroceptive (visual) attention. In all three studies MBSR led to a shift in neural activity away from cortical midline structures, such as the medial prefrontal and posterior cingulate cortices, to predominantly right-lateralized viscerosomatic structures, and specifically the insular cortex. Cortical midline activity is thought to support habitual patterns of evaluation, and stands as the neural correlate of a narrated, extended self, while right-lateralized insula activity is thought to represent the recurrent integration of present moment context, the neural correlate of the momentary self. These data revealed that MBSR may enhance the distinction between momentary and extended self-reference, reducing cortical midline responses and recruiting a novel, right-lateralized viscerosomatic network. Additionally, MBSR graduates demonstrated reduced emotional reactivity to a film-based sadness mood induction, reducing cortical midline activity and inhibition of the right insula. Moreover, the MBSR group demonstrated enhanced right middle insula recruitment during the monitoring of sensory experience associated with breath monitoring, a core mindfulness practice. The data from this final study also suggest that MBSR promoted an integration of posterior insular sensory representations with anterior insular subjective representations of present moment status. Preserved viscerosomatic activity in the face of emotional challenge may be a predictor of enhanced well-being following mindfulness training.
Trafficking of Fc&gamma;RIIA and Fc&gamma;RIIB2 upon Endocytosis of Immune Complexes
Keywords: Immunology
host-pathogen interaction
autoimmunity
receptor trafficking
endocytosis
Fc receptors

Fcγ receptors (FcγR) which recognize the Fc fraction of IgG play key roles in the modulation of a range of cellular responses as part of the host defense against foreign microbes and antigens. An important function of FcγR is to mediate internalization of soluble IgG-containing immune complexes via endocytosis. The mechanisms of internalization and intracellular transport of FcγR after internalization are less clear. In this thesis, I investigated the trafficking behaviours of human FcγRIIA and FcγRIIB2 upon clustering with immune complexes. In Chapter 3, I demonstrate FcγRIIA, when engaged with multivalent heat aggregated IgG (agIgG), is delivered along with its ligand to lysosomal compartments for degradation, whereas FcγRIIB2 becomes dissociated from the ligand and routed separately into a recycling pathway. FcγRIIA sorting to lysosomes requires receptor multimerization, but does not require either Src family kinase (SFK) activity or receptor ubiquitylation. Upon co-engagement, these two receptors are sorted independently to distinct final fates after dissociating from their co-clustering ligand. In Chapter 4, I show that while the ubiquitin-conjugating system is required for FcγRIIA-mediated endocytosis, it is not required for FcγRIIB2 endocytosis. FcγRIIB2 internalizes immune complexes at a faster rate than FcγRIIA and accelerates the endocytosis of FcγRIIA upon receptor co-engagement. Taken together, these results reveal fundamental differences in the trafficking behaviour of FcγRIIA and FcγRIIB2 both during the initial induction of endocytosis as well as during subsequent intracellular sorting.
DNA Damage-dependent Regulation and Function of akt-1 in Caenorhabditis elegans
Keywords: Apoptosis
Radiation

The roundworm Caenorhabditis elegans possesses a single, conserved phosphatidylinositol 3-kinase (PI3K) signaling pathway that regulates somatic developmental decisions and lifespan through the Insulin-like receptor tyrosine kinase (RTK) DAF-2, the class I PI3K AGE-1 and the 3-phosphoinositide-dependent protein kinase 1 (PDK1) homologue PDK-1. This pathway ultimately controls the action of Akt homologues on the forkhead transcription factor DAF-16. The C. elegans Akt orthologue akt-1 also negatively regulates the DNA damage-dependent apoptosis of worm germ cells by indirectly interfering with activation of the key transcription factor CEP-1, the sole homologue of p53 in the worm. Because upstream regulation by RTK/PI3K signaling is known to couple with downstream Akt kinase activity, I hypothesized that the worm daf-2/age-1/pdk-1 pathway would function upstream of akt-1/Akt in response to DNA damage. Surprisingly, this was not the case: daf-2/InsR and pdk-1/PDK1 do not function upstream of akt-1/Akt and instead promote DNA damage-induced germ cell apoptosis independently of CEP-1/p53 by regulating the B cell lymphoma (Bcl2) homologue CED-9 and the Apoptotic protease-activating factor 1 (Apaf1)-like adapter protein CED-4, respectively. Furthermore, PDK-1/PDK1 promotes germ cell apoptosis by a mechanism that does not include changes in the subcellular localization or absolute levels of CED-4/Apaf1, but does require the presence of CEP-1/p53. Therefore, daf-2/RTK, pdk-1/PDK1, and cep-1/p53 co-operate from independent pathways to drive germ cell death. The separation of worm Akt function from canonical RTK/PI3K regulation is consistent with the ability of AKT-1 to function without major changes in phosphorylation at threonine 350, a site homologous to Thr308 in mammals. Since this modification is an essential step in the activation of Akt proteins by PDK1, it is likely that damage-dependent germline activity of AKT-1 is controlled by a novel mechanism that does not involve phosphorylation by PDK-1 on key regulatory sites. These data argue that C. elegans re-arranges single homologous components of a signalling pathway to respond to different stimuli in vivo. Finally, I present data identifying the C. elegans ataxia and telangectasia and Rad3-related (ATR) kinase homologue ATL-1 as a potential target of AKT-1. Collectively, my work has uncovered a novel DNA damage-dependent pathway that allows AKT-1 to control CEP-1/p53-dependent apoptosis.
Selectively Transparent and Conducting Photonic Crystals and their Potential to Enhance the Performance of Thin-film Silicon-based Photovoltaics and Other Optoelectronic Devices
Keywords: photonic crystals
thin-film light trapping
photovoltaics
solar energy

The byproducts of human engineered energy production are increasing atmospheric CO2 concentrations well above their natural levels and accompanied continual decline in the natural reserves of fossil fuels, necessitates the development of green energy alternatives. Solar energy is attractive because it is abundant, can be produced in remote locations and consumed on site. Specifically, thin-film silicon-based photovoltaic (PV) solar cells have numerous inherent advantages including their availability, non-toxicity, and they are relatively inexpensive. However, their low-cost and electrical performance depends on reducing their thickness to as great an extent as possible. This is problematic because their thickness is much less than their absorption length. Consequently, enhanced light trapping schemes must be incorporated into these devices. Herein, a transparent and conducting photonic crystal (PC) intermediate reflector (IR), integrated into the rear side of the cell and serving the dual function as a back-reflector and a spectral splitter, is identified as a promising method of boosting the performance of thin-film silicon-based PV. To this end a novel class of PCs, namely selectively transparent and conducting photonic crystals (STCPC), is invented. These STCPCs are a significant advance over existing 1D PCs because they combine intense wavelength selective broadband reflectance with the transmissive and conductive properties of sputtered ITO. For example, STCPCs are made to exhibit Bragg-reflectance peaks in the visible spectrum of 95% reflectivity and have a full width at half maximum that is greater than 200nm. At the same time, the average transmittance of these STCPCs is greater than 80% over the visible spectrum that is outside their stop-gap. Using wave-optics analysis, it is shown that STCPC intermediate reflectors increase the current generated in micromorph cells by 18%. In comparison, the more conventional IR comprised of a single homogeneous transparent conducting oxide film increases the current generated in the same cell by just 8%. Moreover, the benefit of using STCPC IRs in building integrated photovoltaics is also presented.
Therapeutic Implications of the 4-1BB Costimulatory Pathway on CD8 T Cells during Chronic HIV Infection
Keywords: HIV
CD8 T cell dysfunction
Costimulation
TRAF1
4-1BB
therapy
chronic infection

A hallmark of chronic human immunodeficiency virus (HIV) infection is the impairment of CD8 T cell survival and effector functions, which likely contributes to HIV pathogenesis. A number of factors could be attributed to this impairment, including the declining number of CD4 T cells, progressive destruction of secondary lymphoid tissues and an increasingly inhibitory environment. As highly active antiretroviral therapy shows limited efficacy in improving CD8 T cell functions, this thesis explores the therapeutic application of costimulatory molecules in directly stimulating non-functional HIV-specific CD8 T cells and ultimately their relevance to the control of chronic HIV infection. Costimulatory molecules are adjuvants for functional activation of T cells that act in concert with the antigen-specific signal. The Tumor Necrosis Factor (TNF) family member, 4-1BBL, emerges as the most effective costimulatory molecule in the antigen-specific expansion of human memory CD8 T cells as compared to the related TNF family members CD70 and LIGHT. As well, 4-1BBL improves the cytolytic function of T lymphocytes on a per cell basis. Furthermore, 4-1BBL is identified as a key component in the therapeutic rescue of CD8 T cell function and its effect is at least partially dependent on its signaling adaptor TNF receptor associated factor 1 (TRAF1), both in vitro and in vivo. This thesis also identifies the loss of TRAF1 as a new mechanism of immune dysregulation of HIV-specific CD8 T cells during the chronic phase of HIV infection and offers a means to correct it. The loss of TRAF1 has functional relevance in HIV suppression and HIV-specific CD8 T cell responses. Finally, a combination therapy involving agonistic anti-4-1BB antibody is shown to be successful in a proof of concept treatment of chronic lymphocytic chroriomeningitis virus (LCMV) infection in mice, resulting in sustained reduction in viral load. A new model of HIV-specific CD8 T cell dysfunction is constructed based on these findings.
Elucidating the Role of Fli-1 in Normal Development and Malignant Transformation
Keywords: erythroleukemia
Fli-1

Previous studies of genes associated with retroviral-induced neoplasia have provided the foundation for much of our current knowledge of both tumor suppressor and oncogenes, and have contributed to our understanding of both gene function and malignant transformation. The study of Friend virus-induced erythroleukemia, a well-studied example of multistage malignancy, has led to the identification of several oncogenes, including the Ets transcription factor, fli-1. Fli-1 plays a vital role in hematopoiesis, and vasculogenesis through the transcriptional regulation of its target genes, some of which are critical for the control of cellular proliferation, differentiation, and survival. The aberrant regulation of Fli-1 is associated with a number of cancers and human diseases, including erythroleukemia, Ewing’s sarcoma, lupus, and Jacobsen or Paris Trousseau syndrome. The essential goal set out to be achieved by the research presented herein is to establish a better understanding of both the oncogenic and developmental roles of Fli-1 by investigating the molecular basis by which its deregulated expression leads to fundamental aberration in the fine balance between proliferation and differentiation.
Somatostatin Receptor Type 2 (SSTR2) Antagonism and Hypoglycemia in Diabetes
Keywords: hypoglycemia
diabetes
counterregulation
somatostatin receptor type 2

Hypoglycemia is one of the most serious acute complications in intensively treated diabetes. Recurrent hypoglycemia predisposes individuals to subsequent hypoglycemia, and diminished counterregulatory hormone responses increase this threat. Elevated pancreatic and/or circulating somatostatin has been reported in diabetic humans and animals, and we postulated that excessive somatostatin contributes to the attenuation of counterregulatory hormone release during hypoglycemia in diabetes. It is known that somatostatin suppresses stimulated secretion of glucagon, epinephrine, and corticosterone. We hypothesized that selective somatostatin receptor type 2 (SSTR2) antagonism would: (Study 1) improve hormone counterregulation to hypoglycemia, and (Study 2) ameliorate hypoglycemia in recurrently hypoglycemic rats. Using both high (10 U/kg) and low (5 U/kg) dose insulin to induce hypoglycemia, we demonstrate that inhibiting the action of somatostatin on SSTR2 normalizes the severely attenuated glucagon and corticosterone responses to acute hypoglycemia in diabetic rats. These improvements were specific to diabetes since SSTR2 antagonism did not increase these hormones in non-diabetic rats in response to hypoglycemia. In the absence of hypoglycemia, SSTR2 antagonist neither markedly alters glycemia nor causes sustained elevations in counterregulatory hormones in diabetic animals. Diabetic rats exhibit up to 65% and 75% more pancreatic and plasma somatostatin than non-diabetic rats following hypoglycemia, respectively. Despite improvements of glucagon and corticosterone, expression of gluconeogenic enzymes PEPCK1 and G6Pase was unaltered. SSTR2 antagonism reduced the glucose requirement during a hypoglycemic clamp induced with a lower dose of insulin. In recurrently hypoglycemic diabetic rats, we demonstrate that SSTR2 antagonist treatment reduces the depth and duration of hypoglycemia and promotes the recovery to euglycemia, without affecting the glycemia-lowering effect of insulin. This amelioration of hypoglycemia by SSTR2 antagonism may be attributable in part to the observed modest improvements of glucagon, epinephrine, and corticosterone counterregulation following recurrent hypoglycemia. These results implicate an important role for increased pancreatic, and possibly circulating, somatostatin in defective hypoglycemic counterregulation in diabetes.