VictorJuiz/thesis huggingface dataset:
A terrain of struggle: reading race in social work education

For the past decade, Canadian Schools of Social Work have been required to address issues of racism. This ten-year period has been a time of policy and curriculum revamping, yet, the role of the profession itself in sustaining racial hierarchies remains undisturbed. Instead debates have proliferated over the proper language with which to characterize the problem. In these debates, racial difference is most typically described as a "problem" of diversity and oppression. This research analyzes the development of educational policy and how educators understand the process of infusing anti-racist content into the curriculum. Through a Foucauldian discourse analysis of textual data, as well as semi-structured interviews with social work educators, I trace the various linguistic and technical strategies used within the profession to erase race from the educational agenda. I contend that imperial legacies of diversity management continue to suffuse the profession. Recent efforts to conceptualize race must be understood in light of the profession's historical mission to rescue and manage the degenerate. The contemporary social worker appears very much like her imperial counterpart, the bourgeois social investigator. Anti-racist pedagogies, pedagogies built around the idea of self-reflexivity and the examination of white privilege, confront enormous obstacles in a profession that defines its mandate as the practical and benevolent treatment of society's marginalized and "unfortunate" individuals and groups. Pedagogy about race and racism within social work education is structured to fit within the accepted parameters of how practice is defined. Yet the day to day practices on which the profession rests, and which sustain the profession, reproduce whiteness. Thus "doing" race following this same formula functions to reproduce whiteness and race as one more skill at which to be competent. As long as social work practice is synonymous with diversity management and the development of competencies, we remain unable to reconcile being a "good" social worker with anti-racist practice.

Keywords: Social work education
Social service
Race awareness
Race relations
Free radical determinants of endogenous and amphetamine-enhanced neurodegenerative disease: prostaglandin H synthase-catalyzed free radical formation, reactive oxygen species-mediated oxidative DNA damage and glucose-6-phosphate dehydrogenase-catalyzed neuroprotection

The amphetamine analogs 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy"), 3,4-methylenedioxyamphetamine (MDA) and methamphetamine (METH) are bioactivated by prostaglandin H synthase (PHS) to free radical intermediates that initiate the formation of reactive oxygen species (ROS), which oxidatively damage cellular macromolecules. Using electron paramagnetic resonance spectrometry, the mechanism of free radical formation for MDMA, MDA and METH were evaluated in an in vitro system with purified PHS-1, and the free radical spin trapping agent, alpha-phenyl-N-t-butylnitrone. MDMA, MDA and METH all demonstrated PHS-catalyzed, time- and concentration-dependent formation of a carbon-centered- and/or nitrogen-centered free radical intermediate. Moreover, these amphetamines were stereoselective in causing oxidative DNA damage, which was blocked by the PHS inhibitor, eicosatetraynoic acid. Similarly in vivo, these amphetamines were stereoselective in mediating oxidative DNA damage, dopaminergic neurodegeneration, and permanent motor coordination deficits. These in vivo effects were inhibited by a single pretreatment with the PHS inhibitor aspirin (with MDA), or reduced in a gene dose-dependent manner in PHS-1 knockout mice (with MDMA). In addition to the neurodegenerative effects in adult brain, administration of a single dose of METH to pregnant mice in mid- (organogenesis) or late gestation caused increased DNA damage in fetal brain and permanent neurodevelopmental deficits, evidenced by postnatal impairment of motor coordination. These results implicate PHS-catalyzed free radical formation and ROS-mediated oxidative damage in xenobiotic- and endobiotic-initiated neurodegeneration, and indicate a neuroprotective role for GOD, thus providing a novel hypothesis potentially relevant to the mechanisms and risk factors for neurodegeneration associated with amphetamines, as well as with aging. PHS also bioactivated various endogenous neurotransmitters and precursors in vitro leading to DNA oxidation. Moreover, aged -/- PHS-1-deficient knockout mice had significantly decreased oxidative DNA damage in various brain regions compared to wild-type PHS-1 normal controls, with PHS-1 heterozygotes exhibiting intermediary risk. Thus, oxidative DNA damage initiated in a PHS-dependent fashion by endogenous substrates may contribute to the neurodegeneration associated with aging. The neurodegenerative potential of endogenous ROS was confirmed in mutant mice with a deficiency in the antioxidative enzyme glucose-6-phosphate dehydrogenase (G6PD), as evidenced by increased oxidative DNA damage and neurodegenerative changes in -/- G6PD-deficient mice.
Speaking activities in a secondary core French classroom: who speaks, for how long, and when?

This case study examines the types of speaking activities used in a typical grade 9 core French classroom. The class was observed ten times during a 16-week fall semester. I collected observation data using field notes, and a modified version of the COLT observation scheme. The teacher and students completed feedback forms and a questionnaire towards the end of the observation period. The teacher and nine students were also interviewed. Findings indicate that most students liked the variety of targeted speaking activities used by the teacher. Moreover, there were no major discrepancies between the teacher's beliefs as to students' perceptions of the speaking activities and students' actual perceptions. The implications of this research study may help to guide core French teachers' planning and collaborative work with colleagues.
The role of Rho GTPases in insulin-induced actin remodelling and GLUT4 mobilization in L6 muscle cells

In muscle and fat tissues, insulin stimulates the translocation of glucose transporters (GLUT4) from intracellular compartments to the surface for subsequent glucose uptake. In 3T3-L1 adipocytes, GLUT4 mobilization requires actin remodelling, conventional PI3K rarr;IRS rarr;Akt signalling and a PI3K-independent, CAP-Cbl cascade. While the PI3K pathway and GTPase-mediated actin remodelling are also required for insulin signalling in L6 muscle, the role of the CAP-Cbl cascade in this cell type is undetermined. Reduced insulin-dependent GLUT4 translocation and glucose uptake are hallmarks of insulin resistance. Here, we emulated insulin resistance in muscle cells, using elevated glucose/insulin or exogenous oxidants or lipids; all of which impaired insulin-induced Rac activation and actin remodelling more profoundly than P13K rarr;IRS1 rarr;Akt signalling, suggesting that actin remodelling is targeted before signalling to GLUT4 vesicle traffic. Here, we characterized the CAP-Cbl pathway, including the small GTPase TC10 in L6 muscle cells. We found that Cbl and TC10 were expressed in L6-GLUT4 myc myoblasts and myotubes while CAP expression and insulin-stimulated phosphorylation of Cbl occurred in differentiated myotubes. Insulin also induced TC10 activation in myoblasts (that lack CAP expression and Cbl activation), but dominant negative TC10 did not alter insulin-induced actin remodelling and GLUT4 translocation in these cells. In summary, the CAP-Cbl pathway is active in muscle cells but, TC10 is not required for GLUT4 mobilisation or actin remodelling. Instead, insulin activates Rac in a PI3K-dependent and PAK1-independent manner, to regulate GLUT4 traffic and actin remodelling. These effects are thought to occur through WAVE2 and are susceptible to insulin resistance in L6 muscle cells. Insulin-stimulated actin remodelling in L6 muscle cells manifests as lamellipodia. In migrating cells, lamellipodia arise through PI3K signalling to Rac and its effectors PAK and WAVE, that regulate actin severing and branching, respectively. Here we show that insulin activates Rac, in a PI3K-dependent manner, and inhibition of Rac1 function or expression prevented insulin-induced actin remodelling and GLUT4 translocation in L6 muscle cells. Although insulin induced PAK phosphorylation via PI3K, interfering with PAK expression or activation did not significantly alter insulin-induced actin remodelling or GLUT4 translocation. However, WAVE2 interfering mutants caused a marked reduction in insulin-induced actin remodelling in L6 myoblasts.
The life and career of the caliph Al-Mu`taṣim (218--227AH/833--842 AD): A problem in historiography

This thesis is a historiographical, not a historical, account of the Caliph al-Mu`tasim and his reign. This perspective requires different approaches in appraising his record. Al-Mu`tasim was, in many ways, the son of his father. Hence it might be expected that he would take his father as his model in ruling the caliphate. The changes that took place in the balance of power, however, were the result of the change of the head of state. Both medieval and modern sources discuss the life and the career of the Caliph al-Mu`tasim differently from other caliphs and reigns. His life and career have been viewed through two factors. The first, to his misfortune, is that he succeeded al-Ma`mun, one of the most intellectual caliphs until then. Hence al-Mu`tasim is judged in the sources in comparison with al-Ma`mun. Though in many situations al-Ma`mun may not be named, the thrust of the judgment, whether positive or negative, derives from the implicit comparison with al-Ma`mun. The second is al-Mu`tasim's role in changing the balance of power in the caliphate in favour of the Turks. This is viewed as different from the changes made by his predecessors, e.g. al-Ma`mun's changes in favour of the Persians. This has led to a greater misunderstanding in claiming that al-Ma`mun had nominated al-Mu`tasim as his successor. This view is discussed and its improbability is demonstrated. Had al-Mu`tasim succeeded his father Harun al-Rashid, he and his reign might have been viewed differently. It is noteworthy that the same actions taken by Harun al-Rashid and al-Mu`tasim are judged differently. For example, when Harun al-Rashid established the city of al-Qatul, it is seen as motivated by the desire for a place with a more salubrious climate. When al-Mu`tasim decided to establish Samarra`, it is seen as wanting a new capital and quarters for his Turks, in spite of the fact that among the first questions he asked in deciding on the location of Samarra` was, "Where did al-Rashid used to stroll when he got fed up with staying in Baghdad?"
Design, analysis, testing and implementation of the CanX-1 structural, thermal and attitude control systems

Recent advances made toward miniaturizing electronics and mechanical components have pushed the satellite market toward developing smaller, low cost satellites. In response to this, the Canadian Advanced Nanospace eXperiment (CanX) was initiated at the University of Toronto Institute for Aerospace Studies Space Flight Laboratory, in September 2001. CanX-1, the first satellite designed under this program, has mission objectives of verifying the functionality of several novel electronic technologies in orbital space. This thesis focuses on the design, analysis, testing and implementation of the CanX-1 structural, thermal, and attitude control systems. This includes developing subsystem requirements, completing the design from preliminary to “ready for flight” stages, and performing qualification tests. Analyses and testing verify that the structural and thermal subsystems are sufficient given both launch and on-orbit environments. Simulations predict that the implemented attitude control system can sufficiently detumble CanX-1. CanX-1 was launched through EUROCOT Launch Services on June 30, 2003.

Keywords: Nanosatellites
Nanosatellites, Control systems
Nanosatellites, Attitude control systems
Low-power delta-sigma A/D design for broadband applications

As a consequence of the scaling of CMOS technology, digital signal processing has become ubiquitous, and digital circuits will continue to benefit from the projected advances in technology. It is not clear however that analog blocks will benefit from further technology scaling. In particularly, A/D converters based on delta sigma (ΔΣ) modulation are directly subject to the difficulties imposed by the continued scaling of CMOS submicron technology. A second-order low-pass discrete-time delta-sigma modulator using a fully digital feedforward path, which requires an extra quantizer and a digital adder, with an over-sampling ratio of 24 is designed in a 0.18μ m 1P6M CMOS process with availability of MIM caps and deep N-well, suitable for operation from a 1.8V supply voltage. The digital feedforward path reduces the integrators output swing and relaxes the requirements on analog circuits. Implementation nonidealities have been considered carefully in order to define the circuit requirements for a power-efficient CMOS implementation. Extracted simulations of the chip including the pads show a peak SQNR of 77 dB with a sampling frequency of 96MHz. The total analog and digital power consumptions is 7.2mW from 1.8V supply. The chip is going to be tested during the next few months.
Catalytic dehydrocoupling of group 13 - group 15 adducts: synthetic and mechanistic studies

The dehydrocoupling of primary and secondary amine-borane adducts to afford either monomeric or dimeric aminoboranes and borazines was developed using transition metal complexes as precatalysts. Mechanistic investigations performed on the dehydrocoupling of Me 2 NH*BH 3 suggested the operation of a heterogeneous process involving Rh colloids in which the first step may be an intermolecular dehydrocoupling reaction to give the linear Me 2 NH-BH 2 -NMe 2 -BH 3, followed by a subsequent intramolecular reaction to afford the observed cyclic [Me 2 N-BH 2] 2 . The heterogeneity of the process was evidenced by (i) the presence of a sigmoidal kinetic curve, (ii) the observation of Rh colloids by TEM, (iii) the poisoning of the active catalyst by treatment with mercury or PPh 3, (iv) a reduction in activity upon filtration and (v) the isolation of Rh metal as an active catalyst. A tandem catalytic dehydrocoupling-hydrogenation reaction was developed which involved the reaction of an amine-borane adduct and an unsaturated substrate using a common precatalyst. This reaction allows a stoichiometric quantity of hydrogen to be delivered for the hydrogenation reaction and operates at room temperature. Linear hybrid aminoborane-phosphinoborane chains were synthesized and were found to possess both inter- and intra-molecular proton-hydride bonding of moderate strengths. Remarkably, comparative mechanistic studies performed on the dehydrocoupling of the analogous phosphine-borane system Ph 2 PH*BH 3 suggested the operation of a homogeneous process. This fundamental difference in reactivity between amine-borane and phosphine-borane adducts is thought to arise from (i) differences in the reducing strength of the adducts, (ii) differences in the extent of dissociation of the adducts and (iii) the presence of phosphine ligation/poisoning of the active catalyst. Platinum hydride complexes with primary and secondary phosphine-borane ligands, such as trans -[PtH(PhPR*BH 3)(PEt 3) 2] and cis -[PtH(PhPR*BH 3)(depe)] (where R = Ph, H), were synthesized. However, further reactivity studies of these complexes did not indicate any coupling chemistry to form new P-B bonds at the metal center. The iridium hydride complex [Cp*IrH(PPhH*BH 3)(PMe 3)] was also synthesized, but again displayed no further reactivity when reacted with phosphine-borane adducts. Dehydrocoupling routes for the formation of platinum-phosphorus bonds from the reaction of platinum hydrides with primary and secondary phosphines and phosphine-borane adducts has been demonstrated.
Development of adhesive bonds with reduced strength as ultrasonic NDE benchmarks

A method for producing adhesive-bonded aluminum joints with predictable strength loss was developed and evaluated. The method uses an open-face specimen geometry and a humid high-temperature environment to promote adhesive degradation. The rate of degradation was greatly increased over previous accelerated degradation schemes through the use of MgSO4 as contaminant. The contaminant was applied in a purpose-built aerosol contaminating duct. Specimens were prepared and fractured using a DCB loading jig. Two studies which examined the effects of various exposure and contamination parameters were conducted. It was shown that contaminant surface concentration is a strong determinant of residual adhesive strength. Exposure to the aggressive environment was shown to have little effect beyond an initial threshold. Standard ultrasonic imaging techniques were incapable of differentiating between exposed and unexposed specimens. FESEM and EDX analysis of the fracture surfaces showed residual aluminum, suggesting an intra-oxide locus of failure consistent with other accelerated degradation methods.
Depositional successions on glaciated continental margins: the Cenozoic of Antarctica and the Neoproterozoic of Rodinia

Part II of this thesis focuses on the sedimentological and stratigraphic evidence for glaciation in the Neoproterozoic. Integrating this analysis with a recent understanding of the tectonic setting of Neoproterozoic sedimentary basins provides a basis for an alternative 'zipper-rift' hypothesis for Neoproterozoic glaciations. The 'zipper-rift' model emphasizes a strong linkage between the first-order reorganisation of the Earth's surface created by rifting of Rodinia, the climatic effects of uplifted rift flanks and the resulting sedimentary record deposited in newly formed rift basins. Neoproterozoic glaciation was regional in extent, strongly controlled by tectonics and diachronous in its timing as Rodinia progressively broke apart over some 150 million years. This thesis is presented in two parts. The first half deals with the Cenozoic glacial record of Antarctica and the second half focuses on the Neoproterozoic glacial record of Rodinia. The glacially-influenced Cenozoic continental margin of Antarctica shows a large-scale subsurface seismic stratigraphy consisting of flat-lying 'topsets' recording episodic aggradation of the continental shelf, that rest on seaward-dipping, wedge-shaped 'foresets' formed by the progradation of the continental slope. Strata from topsets record aggradation by till deposition alternating with glacial-marine sedimentation. Strata from foresets record debris flows and turbidity currents on an active slope close to a source of poorly-sorted glacial debris such as an ice sheet margin reaching the shelf break. The original intention at the commencement of the thesis was to use depositional models derived from Antarctica as 'modern' analogues for Neoproterozoic successions. Critical evaluation of Neoproterozoic successions shows that many are not glacial in origin. Many Neoproterozoic 'glacial' successions have been identified as glacial on the basis of the presence of diamictite facies. Diamictite facies are commonly present within thick turbidite successions and are the product of active rifting and the shedding of poorly sorted debris into rapidly subsiding marine rift basins. The sedimentary record from the continental shelf of Prydz Bay, East Antarctica was examined by Ocean Drilling Program Leg 188. This record constrains the onset of glaciation in Antarctica to the late Eocene (c. 39 Ma) and records an important interval in the history of Antarctica, capturing for the first time the transition from a warmer preglacial climate, through early-glacial, and culminating in continental-scale glaciation of Antarctica.
The regulation of digital transmissions in Canada through copyright law

This thesis examines the manner in which international copyright norms and the Canadian Copyright Act deal with digital transmissions. Canada's adherence to international copyright norms is examined in respect of the right of reproduction and communication. It sets out an example of the application of Canadian copyright law to a digital transmission. The thesis concludes by pointing out conceptual problems and inconsistencies in the Copyright Act and in domestic copyright jurisprudence. In respect of the right of reproduction it highlights potential problems in fixation in subsistence and reproduction, the technological neutrality of the Copyright Act, and the relation between copyright, tangible property rights and distribution. In respect of the right of communication it highlights potential problems in the making available right, the regulation of the right of communication in Canada compared to other countries, internal consistency of the Copyright Act and the complexity of regulation in the Copyright Act.

Keywords: Copyright, Computer programs
Copyright, Canada
Verocytotoxin-producing Escherichia coli blocks interferon-gamma-activation of signal transducer and activator of transcription-1

Escherichia coli serotype O157:H7 is the leading cause of Verocytotoxin-producing E. coli (VTEC) infections and outbreaks of hemorrhagic colitis in North America. In addition, multiple non-O157:H7 VTEC (such as serotype O113:H21) are also implicated in human disease. Clinical manifestations of VTEC infection include abdominal cramps, self-limiting diarrhea, hemorrhagic colitis, and the hemolytic-uremic syndrome. VTEC pathogenesis is attributed to multiple virulence factors, including Verocytotoxins, bacterial adhesion, effector proteins, and evasion of the host immune system. Interferon (IFN)-γ is a pro-inflammatory cytokine produced by CD4+ T cells, which are recruited to sites of bacterial infection. Signalling of this cytokine through Jaks-1 and -2 and subsequent STAT-1 tyrosine phosphorylation is required for transcriptional activation of immune function genes, which combat infection. In vitro tissue culture techniques have shown that VTEC O157:H7 and O113:H21, but not enteropathogenic E. coli serotype O127:H6 or non-pathogenic E. coli strain HB101, disrupt the IFNγ-Jak1,2-STAT-1 signalling cascade, as assayed using tyrosine phosphorylation of STAT-1 as a read-out. The inhibitory factor of STAT-1 tyrosine phosphorylation is bacterial in nature, the expression of which is enhanced following bacterial growth in the presence of epithelial cells. This factor is present in conditioned medium, in which it is heat, proteinase K, and trypsin insensitive. In addition, regulatory molecules of the IFNγ-Jak1,2-STAT-1, which include PTPs, SOCS and PIAS, also are not involved in pathogen subversion of this signalling cascade. The probiotic, Lactobacillus helveticus strain R0052 protects cultured epithelial cells from VTEC-induced disruption of STAT-1 activation, thereby representing a potential for use of probiotics in the management of VTEC infections. In summary, suppression of cytokine-induced transcription factors following VTEC challenge represents an immune evasion strategy of this bacterial enteropathogen. Therefore, identification and characterization of the bacterial factor involved will help to elucidate the pathobiology of VTEC infection.

Keywords: Microbiology
Pathology
Immunology
Empirical density fluctuations for zero range models

In this thesis we compute the density fluctuation limit for the k-colour version of the zero range interacting particle dynamics when the system is started out of equilibrium measure. We extend the method of Chang and Yau to the k-colour model setting. A key estimate in the proof of this result is the logarithmic Sobolev inequality. We prove the inequality in the more general setting of a class of inhomogeneous zero range particle systems. We also show how the k-colour density fluctuation result may be used to establish a central limit theorem for the tagged particle at the level of finite dimensional distributions. This is the central limit theorem associated to the propagation of chaos result for the zero range interacting particle system.