Texte remanié de: Doct.-diss.--Philos.--Edmonton--University of Alberta, 1980. / Bibliogr. p. 386-415.

The current work contains experimental and theoretical work about the formation of martensite from the austenitic state of the steel Hardox 450. Simulation of rolling and subsequent quenching of martensitic steel plates requires a model that can account for previous deformation, current stresses and the temperature history, therefore dilatometry experiments were performed, with and without deformation. Two austenitization schedules were used and in the standard dilatometry the cooling rates varied between 5-100 °C/s, in order to find the minimum cooling rate that gives a fully martensitic microstructure. Cooling rates larger than 40°C/s gave a fully martensitic microstructure. The cooling rate of 100 °C/s was used in the deformation dilatometry tests where the uniaxial deformation varied from 5-50 %. The theoretical work involved modelling of the martensite formation and the thermal/transformation strains they cause in the steel. Characterizations were done using light optical microscopy, hardness tests and electron backscatter diffraction technique. The parent austenite grains of the martensitic structure were reconstructed using the orientation relationship between the parent austenite and the martensite. Kurdjumov-Sachs orientation relationships have previously been proven to work well for low-carbon steels and was therefore selected. The standard implementation of the Koistinen-Marburger equation for martensite formation and a more convenient approach were compared. The latter approach does not require the storage of initial austenite fraction at start of martensite formation. The comparison shows that the latter model works equally well for the martensite formation. The results showed that the use of martensite start and finish temperatures calibrated versus experiments for Hardox 450 works better when computing thermal expansion than use of general relations based on the chemistry of the steel. The results from deformation dilatometry showed that deformation by compressive uniaxial stresses impedes the martensite transformation. The simplified incremental model works well for deformation with 5 % and 10 %. However, the waviness in the experimental curve for deformation 50 % does not fit the model due vi to large barrelling effect and the large relative expansion for the material that the sample holders are made of. Crystallographic reconstruction of parent austenite grains were performed on a hot-rolled as-received reference sample and dilatometry samples cooled with 60 °C/s and 100 °C/s. The misorientation results showed that the samples match with the Kurdjumov-Sachs orientation relationship in both hot rolled product and dilatometry samples. When misorientation between adjacent pixels are between 15° and 48°, then the boundary between them was considered as a parent austenite grain. The austenitic grain boundaries of the sample cooled at 100 °C/s is in general identical with the hot rolled sample when considering high angle boundaries (15°-48°). The results from the hardness tests showed that the rolled product exhibits higher hardness as compared to samples cooled by 100 °C/s and 60 °C/s. This can be attributed to the formation of transition-iron-carbides in the hot rolled product due to longer exposure of coiling temperature.

The current work contains experimental and theoretical work about the formation of martensite from the austenitic state of the steel Hardox 450. Simulation of rolling and subsequent quenching of martensitic steel plates requires a model that can account for previous deformation, current stresses and the temperature history, therefore dilatometry experiments were performed, with and without deformation. Two austenitization schedules were used and in the standard dilatometry the cooling rates varied between 5-100 °C/s, in order to find the minimum cooling rate that gives a fully martensitic microstructure. Cooling rates larger than 40°C/s gave a fully martensitic microstructure. The cooling rate of 100 °C/s was used in the deformation dilatometry tests where the uniaxial deformation varied from 5-50 %. The theoretical work involved modelling of the martensite formation and the thermal/transformation strains they cause in the steel. Characterizations were done using light optical microscopy, hardness tests and electron backscatter diffraction technique. The parent austenite grains of the martensitic structure were reconstructed using the orientation relationship between the parent austenite and the martensite. Kurdjumov-Sachs orientation relationships have previously been proven to work well for low-carbon steels and was therefore selected. The standard implementation of the Koistinen-Marburger equation for martensite formation and a more convenient approach were compared. The latter approach does not require the storage of initial austenite fraction at start of martensite formation. The comparison shows that the latter model works equally well for the martensite formation. The results showed that the use of martensite start and finish temperatures calibrated versus experiments for Hardox 450 works better when computing thermal expansion than use of general relations based on the chemistry of the steel. The results from deformation dilatometry showed that deformation by compressive uniaxial stresses impedes the martensite transformation. The simplified incremental model works well for deformation with 5 % and 10 %. However, the waviness in the experimental curve for deformation 50 % does not fit the model due vi to large barrelling effect and the large relative expansion for the material that the sample holders are made of. Crystallographic reconstruction of parent austenite grains were performed on a hot-rolled as-received reference sample and dilatometry samples cooled with 60 °C/s and 100 °C/s. The misorientation results showed that the samples match with the Kurdjumov-Sachs orientation relationship in both hot rolled product and dilatometry samples. When misorientation between adjacent pixels are between 15° and 48°, then the boundary between them was considered as a parent austenite grain. The austenitic grain boundaries of the sample cooled at 100 °C/s is in general identical with the hot rolled sample when considering high angle boundaries (15°-48°). The results from the hardness tests showed that the rolled product exhibits higher hardness as compared to samples cooled by 100 °C/s and 60 °C/s. This can be attributed to the formation of transition-iron-carbides in the hot rolled product due to longer exposure of coiling temperature.

Lysosomal storage disorders are a group of rare neurodegenerative diseases that are collectively common, sharing many aspects with other neurodegenerative disorders, including substrate build-up and neuroinflammation. The GM2 Gangliosidoses, Tay-Sachs disease and Sandhoff disease, are pathologically overlapping lysosomal storage disorders, with high prevalence within specific ethnicities. Their effects are neurologically devastating and often fatal at young ages. Current treatments only slow or stall an inevitable decline in health. Novel treatment targets are needed for these disorders, and others with similar pathologies. In these works we demonstrate the negative effect the inflammatory cytokine tumour necrosis factor-alpha has on survival of a model of Sandhoff disease. We demonstrate its role in the upregulation of astrogliosis, and apoptosis, and we present evidence that this effect on astrogliosis occurs through an upregulation of the JAK-2/STAT3 pathway. Though fruitful, a singular focus on inflammation/gliosis in these diseases has left a vacuum in the research into neuron specific molecular processes. We observe the development of inflammation, astrogliosis and neuronal processes in our model, and demonstrate a bi-phasic disease progression, in which early onset microgliosis precedes terminal astrogliosis, apoptosis, and a decline in excitatory glutamate receptors, suggesting neuron-specific malfunction. Furthermore, we show that knockout of the synaptic protein neuronal pentraxin 1 retards neurodegeneration and extends the lifespan of Sandhoff disease mice, independent of inflammation or astrogliosis. Through electrophysiology, we provide evidence of dysregulation of glutamate receptors in Sandhoff disease, and show that knockout of neuronal pentraxin 1 provides rescue from this dysregulation. This work expands on research into gliosis in GM2 gangliosidoses, presents the finding of a novel protein isoform, and presents a new focus on non-glial disease mechanisms and treatments for these and other neurodegenerative disorders. / Thesis / Doctor of Philosophy (PhD) / Lysosomal storage disorders are a group of neurological diseases that are debilitating, and often fatal at a young age. Two diseases of this group- Tay-Sachs disease and Sandhoff disease – are similar in their causes and symptoms. Current treatments for these diseases only slow or stall an inevitable decline in health. New targets for treatment are required, and we provide data suggesting several proteins that may fit this criterion. We also provide evidence of the discovery of a new form of one of these proteins, which is found in high levels in the disease, indicating it may be important in these and other neurodegenerative diseases. Finally, we provide findings indicating that a certain cell type, which is largely ignored in current research for these diseases, may be important in the disease progress. These findings increase our knowledge of Tay-Sachs disease and Sandhoff disease, and open new avenues for medicinal intervention.

No description available.

No description available.

<p>GM2 gangliosidoses encompass a group of chronic neurodegenerative disorders characterized by metabolic defects in ganglioside catabolism and marked intralysosomal accumulation of GM2 in central nervous system (CNS)-resident neurons. Included in this group are Tay-Sachs and Sandhoff disease. Human cases of Tay-Sachs and Sandhoff disease present with devastating neurological deterioration; however, murine models display drastically divergent phenotypes. Tay-Sachs mice avoid pathology via a sialidase-mediated bypass of β-hexosaminidase A (HEXA) deficiency, though the precise mechanism of avoidance is not fully elucidated. The following work aimed to: i) determine if the murine sialidase-mediated bypass could be potentiated in human cells, and ii) help clarify the mechanism of disease avoidance in Tay-Sachs animals.</p> <p>Adenoviral overexpression of truncated CCAAT displacement protein (CDP^831-1505) in human Tay-Sachs neuroglia augmented neuraminidase 1/lysosomal sialidase (NEU1) protein levels, which reduced intralysosomal GM2 accumulations. Chromatin immunoprecipitation revealed binding of CDP^831-1505 to the human <em>NEU1</em> promoter in Tay-Sachs neuroglia. These results provide mechanistic and functional evidence supporting therapeutic exploitation of <em>NEU1</em> for Tay-Sachs disease.</p> <p>Comparison of immunological responses of bone marrow-derived macrophages (BMDMs) to pathogen associated molecular patterns (PAMPs) or GM2 demonstrated that Sandhoff macrophages secrete increased TNF and reduced IL-10 following lipopolysaccharide stimulation. GM2 treatment failed to stimulate an immune response. Such behaviour occurred in the absence of clearly observable intralysosomal ganglioside accumulations. Altered LAMP2 protein size, potentially due to aberrant glycosylation, is hypothesized to disrupt autophagosomal/lysosomal fusion. Subsequent autophagosomal accumulation could result in inherent macrophage hypersensitivity and immunologic irritability. Downstream interleukin-10 (IL-10)/signal transducer and activator of transcription 3 (Stat3) axis, mitogen activated protein kinase (MAPK), and glycogen synthase kinase 3-beta (GSK3β) signaling pathways were affected in Sandhoff BMDMs. These data indicate inherent differences in immunological responses of BMDMs from Sandhoff mice, presumably related to their β-hexosaminidase B (HEXB) deficiency.</p> <p>Data presented here provides evidence to suggest a paradigm shift in the neurodegenerative model of Tay-Sachs and Sandhoff Diseases towards one that places immune cells as an initiating factor for widespread neuroinflammation.</p> / Master of Science (MSc)

2007年是中華電信企業民營化的第二年，如同以往地在業務面及財務面締造了佳績。然而，在2007年9月時，中華電信與香港高盛簽下一紙長達10年期的外匯避險合約，使得中華電信在隔年第一季公佈高達新台幣40億元的未實現匯兌損失，引起市場一片譁然與投資人的輿論，認為此合約讓收入多以新台幣計價的中華電信陷入了不必要的衍生性商品陷阱之中。本個案讓閱讀者以當時中華電信財務長謝劍平的角度，帶領閱讀者解構、分析這個極具爭議的的結構型商品。過程中牽涉到避險決策、契約評價、代理問題、公司治理、外匯預測、市場效率性等議題。2008年10月契約觸及匯價32.7終止，中華電信最終獲利新台幣3010萬元出場，新台幣10多億的帳面損失也全數回沖。個案閱讀者能從中學習到重要的思考過程，並做出權衡之下對股東利益最好的決策，我們發現這個外匯避險契約本身並無絕對好壞，因為這是一個風險控管與節省成本的抵換關係，端看決策者的出發點、需求及風險偏好決定。 / 2007 was the second year after the privatization of Chunghwa Telecom, the financial performance was strong as usual. However, on September of the same year, Chunghwa Telecom had signed a 10-year currency hedging contract with Goldman Sachs, which leads to NTD 4 billion unrealized book losses in the first season of 2008. Investor and the public were shocked about it, because it was not compatible with the company’s corporate image, and the book losses was too huge. Many public opinion criticized that it was a big mistake for Chunghwa Telecom, which let them fall into the trap of financial derivatives. This case put students back to the scenario of September 2007, played the role as Chunghwa Telecom’s CFO, CP Shieh. The case will guide them understand how to decompose and analyze a tailor made structure product provided by investment bank. In the analyzing process, readers will involve many interesting issues, like hedging decision, contract valuation, agency problem, corporate governance, forex forecasting and market efficiency. October 2008, the contract knocked out by reaching NTDUSD quote 32.7. Chunghwa Telecom end up gained NTD 30.1 million from the contract and over NTD 1 billion unrealized book losses were also reversed. Case readers can acquire important intuition during the analyzing process and make decision based on the shareholder’s best interest. There is no absolute answer to dictate whether this hedging contract was good or not, because it was a tradeoff between risk control and cost saving. It depends on the decision maker’s point of view, demand and risk preference.

I denna uppsats genomför jag en närläsning av Lauren Weisbergers roman The Devil Wears Prada. Syftet är att undersöka kulturella paradigm och koder; hur de upprätthålls eller bryts genom betydelsebildande handlingar samt hur de manifesteras i huvudkaraktärens kläder. Min utgångspunkt är att det i moderna berättelser finns moraliserande och fostrande budskap till kvinnor där den kvinnliga identiteten genomgående kopplas samman med det yttre, såsom kropp och kläder. Dessa förhållanden analyseras och synliggörs med hjälp av semiologiska verktyg och performativitetsteorin. Jag finner att huvudkaraktärens utveckling på jobbet och dess konsekvenser i privatlivet följs av en yttre förvandling, där kläderna fungerar symboliskt för rådande paradigm och huvudkaraktärens position till det feminina. Huvudkaraktärens utveckling slutar i en ”gyllene medelväg” där hon representerar ”den gyllene medelkvinnan”. Romanen skildrar fostrande både inom paradigmens ramar och mot skapandet av det egna subjektet, och rymmer därför inläsning av flera olika budskap.

Magister Artium - MA (English) / After the 1976 student uprising, South Africa entered a period of increased violent state repression. The struggle against apartheid also became increasingly globalised, as can be seen in the UN resolution and the rise of various international anti-apartheid organisations. My thesis looks at the various ways in which art was used as a response to the crisis of late apartheid in the 1980s, focusing on a landmark international exhibition, the Art Contre Apartheid exhibition which opened in Paris on 1983. It examines the context and history of the Art Contre Apartheid collection, and follows its path to its current location at the Mayibuye Archive at the University of the Western Cape, where it mostly languishes in packing crates. My research locates its analysis of the works in broader debates around art and politics during the struggle years in South Africa, but also to highlights the continuities and contrasts between international responses to apartheid, and local struggle art produced in the period surrounding the launch of the exhibition. Some of most compelling works of art in the collection depict the human form, and register acts of torture. The analysis focuses specifically on depictions of a fragmentation and dismemberment of the human body. Drawing on Elaine Scarry's argument about the limitations of language as an adequate response to trauma, my research develops an analysis of these works that demonstrates how the body becomes a privileged site in which violent political contestations are made visible. The thesis also deals extensively with the 'absence of form', which highlights the various instances in the ACA collection where abstract art was used as a signifier of pain, and thus the unspeakable effects of apartheid.