VictorJuiz/thesis huggingface dataset:
Accounting Discourse and Textual Practices of Ruling, a Study of Institutional Transformation and Restructuring in Higher Education

This is a study of accounting as a documentary practice of knowledge. It is also a study of organizational change and institutional transformation in postsecondary education. These two themes are combined through an investigation of the use of accounting texts in restructuring in the Ontario college system. The analysis is organized into two main parts. The first part sketches an historical overview of accounting as a text-based form of knowledge that has developed concomitantly with capitalist economic relations. The present-day organization of accounting as a conceptual and textual practice of representation is also examined, with a focus on the kinds of visibility produced in accounting statements and the ways these texts mediate organizational work processes and inter-organizational relations of property and obligation. The second part uses an institutional ethnography approach to investigate the use of accounting as a practice of knowledge in the administration of the Ontario college system in the early 1990s. State policies of privatization and fiscal retrenchment were promoting a competitive market in adult vocational training. Colleges were pulled into this market in pursuit of federal funds and, from the other side, pushed by budget freezes and cuts in provincial funding. College administrators responded to these changes, and tried to participate successfully in market relations, by positioning their colleges to be more "entrepreneurial," "efficient," and "businesslike" in operation and orientation. Accounting played a central role in this restructuring. New practices of managerial accounting produced the observability of organizational work processes in ways that fitted them to the new interpretive frame of "efficiency" and "customer orientation." How they did this is explored through a close focus on one college's introduction of program costing, an accounting exercise that establishes unit costs for each academic program. This examination of the production and use of a new documentary form of knowledge offers a view of restructuring as it occurs through the text-mediated activities of actual people.
Orphan G protein-coupled receptors

G protein-coupled receptors (GPCRs) are integral membrane proteins that mediate signals to the interior of the cell via activation of heterotrimeric G proteins, which subsequently interact with and activate various effector proteins, ultimately resulting in a physiological response. GPCRs are involved in a number of behaviours, and have been implicated in such processes as drug addiction and neuropsychiatric diseases. To further our understanding of the molecular mechanisms involved beyond the known GPCR-endogenous ligand systems we endeavored to discover novel GPCRs, in particular opioid and opioid related receptors, potentially involved in these processes. In order to achieve this we applied two distinct homology cloning strategies to identify the DNA sequences encoding novel GPCRs. Firstly, PCR amplification of human genomic DNA and cDNA using degenerate oligonucleotides derived from the transmembrane domains (TMs) of the opioid and the related somatostatin receptors, and secondly, querying publicly available sequence databases using the amino add sequence of known GPCRs. We have discovered a novel family comprised of two receptors, named 'GPR7' and 'GPR8', and a third receptor, named 'GPR14', that are most closely related to the opioid receptors. Our experiments also led to the cloning and successful ligand assignment of a novel P2 receptor subtype, named P2Y4, that selectively binds uridine nucleotides. We also report the discovery of three P2Y4 related receptors, ' GPR20, GPR34', and 'GPR35'. We also successfully identified an additional novel family comprised of three receptors, 'GPR3, GPR6 ', and 'GPR12', most closely related to the cannabinoid receptors. We also identified a novel GPCR, named GPR26, which is activated by high LPA concentrations (EC50 = 0.5 [mu]M). The other receptors we isolated, ' GPR1, GPR30, GPR32, GPR33' are all related to chemoattractant receptors, and we have identified two related GPCR pseudogenes, <math> <f> <g>4</g></f> </math>GPR32 and <math> <f> <g>4</g></f> </math>GPR33. The endogenous ligands for most of these receptors have not been assigned, hence they are referred to as orphan receptors, and are useful targets for endogenous ligand discovery. Examination of the mRNA tissue expression patterns by Northern blot and 'in situ' hybridization revealed that most are abundantly and discretely expressed in the brain, suggesting a unique role for each of these receptors in the central nervous system (CNS). Fluorescence in situ hybridization (FISH) was performed to assign each gene to a human chromosome. The cloning and identification of these novel GPCRs provide a unique opportunity for ligand discovery, and is the critical first step in the identification of many novel endogenous ligand-receptor systems.
The structural organization of the human skeletal muscle ryanodine receptor gene (RYR1) and its involvement in malignant hyperthermia

The ryanodine receptor ('RYR1') gene encoding the Ca2+ release channel of human skeletal muscle sarcoplasmic reticulum. has been cloned and the exon/intron boundaries have been determined. The gene contains 106 exons, of which two are alternatively spliced. The length of the gene, determined by the alignment of 16 genomic phage clones, a cosmid done and several long PCR products, was found to be approximately 158 kbp. Previously published errors in the cDNA sequence of the 'RYR1' gene were confirmed and corrected. In the 5' region of the 'RYR1' gene, a proposed CCAAT box and several Sp1 binding sites were identified within the proposed promoter sequence. SSCP analysis was used to screen 'RYR1' exons 44 and 45 in malignant hyperthermia (MH) patients. A polymorphism in two unrelated individuals was found to result from the substitution of A for G7300, leading to the substitution of Arg for Gly2434. Subsequent screening of MH probands identified the mutation in 4 of 106 families tested and its absence from about 1000 other chromosomes. The mutation was present in all individuals in 4 families who had a MH reaction. Discordance was found in 2 of the 4 families. The discrepancies between the clinical assessment and the genetic results could best be explained by inaccuracies in the caffeine/halothane contracture test (CHCT), leading to apparent false positive and negative test results. Knowledge of the structure of the 'RYR1' gene has also been utilized in studies. The first study involved the refinement of a diagnostic assay for the analysis of the Arg614 to Cys mutation in the human 'RYR1' gene. The second study involved the identification of a His for Arg2435 mutation in the 'RYR1' gene that was associated with central core disease in a large Canadian family. Genomic information was utilized to design a genomic based restriction endonuclease digestion based diagnostic test to screen patients with CCD. The determination of the 'RYR1' genomic structure now provides the basis for the analysis of 'RYR1' exons in MH or CCD probands from genomic DNA.
Actor Training in Toronto, Theory in Practice

The decision to examine acting theories prevalent amongst performance teachers in Toronto emanated from a perceived lack of research into the subject of acting in English Canadian theatre studies. When the project began, I did not realize that the more general subject of acting theory has received little attention in theatre scholarship as well. In order to study the acting theories of Toronto teachers, it became necessary to define acting and its theory, distinguish it from performance theory, and determine prominent concepts within acting theory which could serve as a framework within which to compare and contrast the ideas and practices of various theorists and practitioners. In Chapter 2, the key concepts of acting theory outlined in Chapter 1 are employed in an examination of the ideas of some prominent acting theorists of the past century. The data engendered by the research leading to this portion of the study served as a foundation for an historical as well as conceptual understanding of modern acting theory. This framework proved invaluable in the preparation and analysis of a survey distributed to Toronto performance teachers (outlined and analyzed in Chapter 3), and in an examination of the acting theories of six Toronto teachers studied in depth through interview and classroom observation (Chapter 4). When the primary materials examined for this study are compared in Chapter 5, several distinct tendencies are revealed concerning acting theories held by performance teachers in Toronto. These are: a view of the function of theatre as experiential, as well as enlightening; the primacy of the actuality of the actor, particularly qualities of instinct and impulse; the predominance of internal approaches to actor training and practice; a devaluation of the primacy of the play text and, thus of the author's intent; a dismissal of the technical areas of theatre as elements of actor study; a growing awareness that actors need training in the business as well as the art of making theatre; and an open minded and eclectic approach to actor training, suggesting a similar attitude towards theory.
Effect of nitrogen on Fe-Mn-based shape memory alloys

Shape memory effect is due to a reversible martensitic transformation. The major drawback in case of Fe-Mn-based shape memory alloys is their inferior shape memory effect compared to Ni-Ti and Cu-based shape memory alloys and their low strength and corrosion resistance compared to steel alloys. It is known that by increasing the alloy strength the shape memory effect can be improved. Nitrogen in solid solution can increase the strength of steels to a greater extent than other major alloying elements. However, its effect on shape memory effect of Fe-Mn-based alloys is ambiguous. In this work first we investigated the effect of nitrogen addition in solid solution on both shape memory effect (SME) and strength of a Fe-Mn-Cr-Ni-Si shape memory alloy (SMA). It was found that interstitial nitrogen suppressed the shape memory effect in these alloys. As an example addition of 0.24 wt % nitrogen in solid solution to the alloy system suppressed the SME by ~80% and increased the strength by 20%. A reduction of martensitic phase formation was found to be the dominant factor in suppression of the SME. This was related, experimentally and theoretically to stacking fault energy of the alloy as well as the driving force and friction force during the transformation. The second approach was doping the alloy with both 0.36 wt% of nitrogen and 0.36 wt% of niobium. Niobium has great affinity for nitrogen and thus NbN dispersed particles can be produced in the alloy following hot rolling. Then particles prevent growth of the alloy and increase the strength of the alloy due to reduced grain size, and precipitation hardening. The improvement of SME in this alloy compared to the interstitial containing alloys was due to the large removal of the nitrogen from solid solution. In case of all the alloys studied in this work, the presence of nitrogen in solid solution improved the corrosion resistance of the alloy. This suggests that nitrogen can replace nickel in the alloy. One of the proposed applications for high strength Fe-Mn-based alloys is as tendon rods in prestressed concrete. The advantage of M alloys in this application is the possibility of producing curved structural prestressed concrete.
Genetic regulation of contingent macrophage- and T-cell-dependent steps in islet inflammation

Insulin dependent diabetes mellitus (IDDM) is a complex disease that is conferred by at least nineteen susceptibility genes ('Idd1-19') in the nonobese, diabetic (NOD) mouse, of which only 'Idd1' has been identified. Although NOD and nonobese, diabetes resistant (NOR) mice are 88% genetically-identical, C57BLKS/J-derived alleles at 'Idd4, 5, 9, 11' and '13' protect NOR animals from destructive islet inflammation. In an effort to define immunotherapeutic targets in high risk individuals, our major focus is to delineate how and when 'Idd ' genes regulate the cellular and molecular effectors of IDDM pathogenesis. Unlike IDDM, which is the convergence of multiple, genetically-regulated pathways, our hypothesis is that the obligate steps that drive early islet inflammation may be more directly related to the action of individual 'Idd' genes. My thesis demonstrates the utility of this approach. I present novel data showing that NOD-derived alleles at 'Idd4, 5, 9, 11' and ' 13' regulate the contingent macrophage and T cell-dependent pathways that drive islet infiltration (insulitis). We found that the T cells first recruited to islets lesions of young NOD mice exerted a profound impact on downstream disease severity. Genetic analysis revealed that the T cell recruitment to islets drove progression of insulitis and was regulated by NOD-derived alleles at 'Idd5' and 'Idd13'. The absence of either of these genetic determinants led to the uncoupling of T cell from APC infiltration of islet lesions, mild insulitis and IDDM resistance. Strikingly, we also found that islet-reactive T cell pathogenesis is macrophage-dependent, as NOD macrophages; induced IDDM in genetically-resistant NOR recipient mice. A comparative analysis of NOD and NOR macrophage function linked dysregulated nitric oxide synthase ('Nos2') gene expression to inheritance of the NOD-derived 'Idd4' locus. A critical role for NOD-derived alleles at both 'Idd4' and 'Idd9'/'11 ' was also observed in the susceptibility to the macrophage- and T cell-dependent steps that mediated a chemically-accelerated model of NOD IDDM. Thus, my research shows that a subset of essential 'Idd' loci control the T cell- and macrophage-dependent pathways that drive IDDM pathogenesis. Our analyses have overcome a fundamental limitation in diabetes research.
Spatial localization of transcription and splicing compartments in interphase nuclei

The interphase nucleus is a topologically ordered, three-dimensional space. If this structural organization represents compartmentalization of function, it would likely be reflected in the spatial coupling of molecular factors involved in related events. The work presented here was designed to define the spatial relationship between transcriptionally competent chromatin domains, including specific gene sequences, and splicing factors, using the techniques of immunocytochemistry, 'in situ' nick translation, chromosome painting and fluorescence 'in situ' hybridization. In naive PC12 cells, both DNAse hypersensitive chromatin (DHC) domains and the SC35 splicing factor colocalize with small nuclear ribonucleoproteins, (snRNPs), as pan-nuclear speckles. During nerve growth factor (NGF)-induced differentiation, however, both snRNPs and DHC migrate to the nuclear periphery, to form a shell apposed to the nuclear envelope. The migration of DHC precedes that of snRNPs, as early as 8 hours post-NGF, resulting in their transient separation. The formation of DHC shells temporally coincides with NGF-induced upregulation of neurofilament light chain mRNA. This indicates that the expression of this sequence may be associated with its spatial transposition to the nuclear periphery. 'In situ' nick translation in human breast tumour cell lines MCF-7, SK-Br-3 and ZR-75-1, cells which exhibit different levels of expression and amplification of the 'ERBB-2' sequence, also reveal a peripheral shell-like distribution of DHC. In all three cell types, the 'ERBB-2' sequence is positioned at the nuclear periphery, within the DHC compartment, suggesting that the nuclear periphery may represent a transcriptionally competent compartment. Interestingly, the remainder of the parent chromosome 17 mass, however, exhibits no association with the nuclear periphery. Taken together with the observation that 'ERBB-2' sequences are located at that surface of the chromosome 17 territory which faces the nuclear envelope, the data indicate that the peripheral placement of 'ERBB-2' sequences is associated with a specific conformation of chromosome 17. The results indicate that the spatial association of expressed gene sequences with DHC and snRNPs at the nuclear periphery may represent a functional coupling of transcription, splicing and nuclear export. Furthermore, the non-random positioning of the 'ERBB-2' sequence within chromosome 17 suggests that the conformation of chromosome territories may represent a fundamental control mechanism in gene expression.
More than brush strokes

Within the context of an experiential course in the expressive arts for personal growth and transformation, adults explore the connection between the creative process and the unfolding of inner knowing. Through engaging in a series of intermodal expressive arts projects, the participants in this study explore creating symbols for the life of feeling, creating ways in which the inner life may be made knowable. To connect through creativity to this inner world of knowing, opens up possibilities for ways of being in the world. The creative process itself involves a form of meditation in action, a mindful awareness of movement and gesture centred in present action; one in which the artist experiences a fusion into a feeling of wholeness, where material and oneself are no longer felt to be separate, nor is feeling and action, thought and sensation. The deepest meaning of these encounters can be found in the fuller understanding of the two ways of knowing: the kind that separates the knower from the known, the seer from the seen and the kind that does not. This knowledge provides implications for both self-knowledge and educational practice.
The process of healing in bulimia as described by women who have experienced this process

The purpose of this study was to describe the process of healing in bulimia from the perspective of women who had experienced this process. Currently there is a paucity of literature examining healing from this perspective. This phenomenological study was guided by the values of feminism and community psychology. Qualitative interviews were conducted with twenty women who had healed from bulimia. The researcher, who has herself healed from bulimia, utilised her personal experience both to facilitate rapport and to suggest areas for in-depth exploration. The women in this study fell along a continuum of healing experiences representing three groupings: (1) complete healing; (2) body disdain (asymptomatic with lingering food and/or weight issues); and (3) addiction model (belief that bulimia is a chronic illness). Although all asymptomatic, it is argued that the latter two groups represent an incomplete state of healing. The study findings suggest that healing is a dualistic process involving: healing related to purging and, healing related to bingeing. For the women in this study, purging stemmed from a profound dissatisfaction with the size and shape of their body. Therefore, healing related to purging required a rejection of the current physical ideal (no more dieting) and an acceptance of their natural body. Coming to accept one's natural shape and size was the most difficult aspect of healing, especially for large women. Bingeing was connected to a range of underlying issues including: low self esteem, unaddressed needs, repressed emotions, isolation, sexuality, control and dysfunctional family dynamics. It is argued that all of these issues can be seen to stem from the socialisation of women in industrialised countries. Complete healing required that the underlying causal issues were identified and addressed. Thus, it was deemed essential that the focus of professional help be on these underlying issues. Finally, this study supports the suggestion in the literature that a false self identity is a central feature of bulimia and connects the development of this false self identity to female socialisation. Implications for this new definition of healing are discussed in relation to quality of life and symptom conversion.
Peel test for the evaluation of environmental effects on fiber-polymer interface

Traditional methods for measuring the adhesion between fiber and polymers, using single fibers, have problems due to the unknown frictional effects, Poisson's shrinkages or expansions, and uncertainties about failure process. Also environmental studies using these techniques are hindered by large environmental exposure time and results are accompanied by a large coefficient of variation. All this made it difficult to quantitatively judge the results obtained from these techniques. The peel test was developed to avoid these problems. In this test, single fibers of carbon, glass and Kevlar were been embedded in the epoxy to depth of about half their diameter in an epoxy resin and then peeled off. The work of fracture GI can be estimated from the peel force by simple formula, so long as the fibers are fully elastic during peel process. This was true with glass, which had GI = 140 Jm -2 and carbon with GI = 60 Jm-2. With Kevlar, inelastic effects obscured the results. This technique gave straightforward, rapid and clear results of environmental effects on fiber-polymer interface. The effect of water on the glass-epoxy interface was readily shown, which reduced the fracture toughness to 90°C after 40h of 25°C immersion. At elevated temperature the process is much faster and needs a shorter time. Carbon however, required high temperature water at the interface to cause significant losses. Sulphuric and acetic acids at 25°C had about the same effect as water at 90°C. Organic fluids such as Kerosene had very little effect. Similar environment effects could also be detected with Kevlar, though further work is required to separate out inelastic contributions.
The health of nations, infectious disease and its effects on state capacity, prosperity, and stability

This thesis investigates the influence of infectious disease upon state capacity, stability and prosperity. It argues that the increasing global proliferation of infectious human pathogens will have a significant negative effect upon the ability of the state to govern itself effectively, and to maximize its economic power. First, this thesis defines the scope of the problem of emerging and re-emerging human pathogens and explores the pathways of disease emergence. Second, it presents a methodology that includes quantifiable measures of State Capacity, and proxy measures for the global burden of disease. Third, it presents the findings of the correlations run on the independent and dependent variables, and concludes that there is in fact a strong and significant negative association between infectious disease prevalence and state capacity. Fourth, this thesis argues that infectious disease will contribute to increasing poverty, and have a significant negative impact on the formation and consolidation of human capital. Given that infectious disease may generate increasing poverty and deprivation of the population, while simultaneously reducing the state's ability to govern effectively, this may lead to increasing levels of intra-state violence and political instability.