<p> The Potterdoal volcanogenic massive sulphide deposit is hosted by a tholeiitic/komatiitic succession located in northern Munro Township, Ontario. An integrated surface and drill core study of this property was undertaken to document the three dimensional structure and stratigraphy of the deposit. Petrography focused on mineralogical changes associated with the hydrothermal alteration within specific units. Several geochemical methods were used to determine the effects of hydrothemal alteration (as quantified by elemental mobility) as well as source magma affinities and tectonic setting. Based on this information, a model for ore genesis was developed. </p> <p> The Potterdoal deposit is hosted by volcanic rock of an iron tholeiite affinity, emplaced within an ocean floor rifting environment. The chemistry of the tholeiites shows similarities to that of large deposits like Kidd Creek, but lacks the felsic component of bimodal volcanism. It is suggested that felsic volcanics are absent because the local crust did not achieve sufficient thickness to allow partial melting of lower crustal material. </p> <p> The deposit consists of a stockwork zone overlain by an extensive massive sulphide lens which lies along a scarp structure defmed in the paleosurface. Stockwork mineralization is narrowly confined to conduits within a fault breccia in the footwall Ore Flow. gabbro, and widens into an overlying tectonic breccia. Sulphide paragenesis appears to be controlled by the thermal solubilities ofthe sulphide minerals, and consists of pyrite, sphalerite, pyrrhotite and chalcopyrite in both stockworks and the massive sulphide lens. The lens occurs at the top of the tectonic breccia near the paleo-seawater interface, and formed by direct replacement of the tectonic breccia. The lens locally exhibits ore grade base metal values (i.e. combined Cu and Zn content of at least 3% ), and shows an upward and outward gradation from chalcopyrite to sphalerite-dominated ore. These features suggest that exhalation of the hydrothermal system was focused into local vent sites. </p> <p> Mass change associated with the hydrothermal alteration envelopes surrounding Ore Flow fault breccia conduits involve loss of Si, Ca, Na and Sr, and gain of Fe, Mg, K, Cu and Zn. These changes are attributed to fluid-rock reactions which are consistent with hydrothermal alteration associated with other VMS deposits, The genetic model suggested for the Potterdoal deposit involves a hydrothermal system driven by heat from the intrusion ofthe Munro-Warden Sill at a high stratigraphic level. The relatively small size of the deposit is probably due to the rapid cooling of the sill, which shortened the life-span of the hydrothermal system. The primary source of metals was the upper portion of the Munro-Warden Sill, as indicated by the high degree of pervasive hydrothermal alteration of this part of the gabbro. </p> <p> Drill core information has also revealed the importance of the Buster Fault in the construction of the currently exposed Potterdoal stratigraphy. Thrusting subparallel to bedding along the Buster Fault during the Kenoran compressional event(~2.6 Ga) was responsible for the local repetition of tholeiitic flows, and has effectively removed the deep footwall rocks originally associated with the Potterdoal mineralization. </p> / Thesis / Master of Science (MSc)

In serial manufacturing processes, localized energy sources (e.g. plasma cutters, arc welders or water jets) induce material geometry transformations that yield a desired product. Simple parameter control of these energy sources does not necessarily ensure an optimal or successful part because of disturbances in the manufacturing process (material and temperature variations, etc). Currently, control in manufacturing is based on statistical process control where large databases for the manufacturing of a fixed process are available and have been compiled over several manufacturing runs. In the absence of a statistical database, and with the increased need for improved monitoring and throughput, there is need for active process control in manufacturing. In this work, Gas Metal Arc Braze-Welding (GMABW) will serve as a test-bed for the implementation of model predictive control (MPC) for a serial manufacturing process. This dissertation investigates the integration of real time modeling of the temperature field with control algorithms to control the evolving temperature field in the ix braze-welded base metal. Fundamental problems involving MPC that are addressed are modeling techniques to calculate temperature fields with reduced computational requirements and control algorithms that utilize the thermal models directly to inform the controller. The dissertation first outlines and compares analytical and computational thermal models and comparison with experimental data are obtained. A thermal model based on a metamodeling approach is used as the plant model for a classical control system and control parameters are found. Various techniques for dealing with signal noise encountered during experimentation are investigated. A proportional controller is implemented in the experimental setup that applies feedback control of the braze –welding process using thermal signals. A novel approach to MPC is explored by using a metamodel as the plant model for the braze-welding process and having the temperature trajectory dictated by the metamodel in the steady state region of the weld. Lastly, future work and extensions of this research are outlined. / text

Cerca de 20 % dos casos familiares de esclerose lateral amiotrófica (ELAf) são causados por mutações na enzima Cu,Zn-superóxido dismutase (SOD1). Inicialmente se supôs que as enzimas mutantes teriam a atividade SOD comprometida, entretanto isto não foi comprovado. Atualmente, considera-se que as enzimas mutantes adquiram propriedades tóxicas. Quais seriam estas propriedades e como levariam à degeneração do neurônio motor são questões ainda não respondidas. Neste trabalho, comparamos neuroblastomas humanos transfectados com SOD1 G93A associada à ELAf (SH-SY5YG93A), e SOD1 selvagem (SH-SY5YWT) com células parentais (SH-SY5Y) em relação ao crescimento, viabilidade, produção basal de oxidantes, atividades SOD e peroxidásica e modificações estruturais da SOD. As células transfectadas apresentaram aumento na taxa de crescimento e na produção basal de oxidantes. As células SH-SY5YWT e SH-SY5YG93A mantiveram a expressão de SOD1 e atividade consistente com o aumento esperado de duas vezes, em estágios iniciais de cultura. A atividade peroxidásica do homogenato da célula SH-SY5YG93A foi maior. Após quatro semanas, a linhagem SH-SY5YG93A manteve a expressão de SOD1, mas as atividades dismutásica e peroxidásica diminuíram. A expressão de SOD1 aumentou a proporção de formas alteradas de SOD1, como enzima reduzida, multímeros formados por ponte dissulfeto e formas insolúveis em detergente, particularmente na linhagem SH-SY5YG93A. Entre estas formas insolúveis, identificamos um dímero covalente de SOD. Estas formas alteradas provavelmente são responsáveis pela ativação do proteassomo e estresse do retículo endoplasmático, verificados nas células transfectadas. Concluindo, a superexpressão da SOD1 foi suficiente para elevar as formas imaturas e oligomerizadas de SOD1 e a oxidação basal, e a mutação G93A ressaltou estes processos. / Some familial ALS (fALS) are caused by mutations in the Cu,Zn-superoxide dismutase enzyme (SOD1). It was thought that the mutated enzymes would have impaired SOD activity, but this has not been corroborated so far. Presently, it is more accepted that the mutated enzymes acquire a new toxic function. What this new toxic function is and how it relates to the degeneration of motor neurons remains debatable. Here, we compared human neuroblastoma cells transfected with fALS mutant G93A (SH-SY5YG93A) or wild-type SOD1 (SH-SY5YWT) with parent cells (SH-SY5Y) in regard to growth, viability, basal oxidant production, SOD and peroxidase activities, and SOD forms. Transfected cells presented increased growth rate and basal oxidant production. SH-SY5YWT and SH-SY5YG93A cells in early culture stage showed SOD expression and activity consistent with the expected two-fold increase; SH-SY5YWT homogenates showed increased peroxidase activity. After four weeks, SH-SY5YG93A maintained SOD1 expression levels but peroxidase and dismutase activities were lower. SOD1 expression increased the levels of altered SOD1 forms such as the reduced enzyme, disulfide multimers and detergent-insoluble forms, particularly in SH-SY5YG93A cells. Among the insoluble forms a covalent SOD dimer was identified. These altered SOD forms are probably responsible for proteasome activation and endoplasmatic reticulum stress response verified in transfected cells. In conclusion, SOD1 over-expression was sufficient to increase intracellular immature and oligomerized SOD1 forms and basal oxidation and the G93A mutation enhanced these processes.

Cerca de 20 % dos casos familiares de esclerose lateral amiotrófica (ELAf) são causados por mutações na enzima Cu,Zn-superóxido dismutase (SOD1). Inicialmente se supôs que as enzimas mutantes teriam a atividade SOD comprometida, entretanto isto não foi comprovado. Atualmente, considera-se que as enzimas mutantes adquiram propriedades tóxicas. Quais seriam estas propriedades e como levariam à degeneração do neurônio motor são questões ainda não respondidas. Neste trabalho, comparamos neuroblastomas humanos transfectados com SOD1 G93A associada à ELAf (SH-SY5YG93A), e SOD1 selvagem (SH-SY5YWT) com células parentais (SH-SY5Y) em relação ao crescimento, viabilidade, produção basal de oxidantes, atividades SOD e peroxidásica e modificações estruturais da SOD. As células transfectadas apresentaram aumento na taxa de crescimento e na produção basal de oxidantes. As células SH-SY5YWT e SH-SY5YG93A mantiveram a expressão de SOD1 e atividade consistente com o aumento esperado de duas vezes, em estágios iniciais de cultura. A atividade peroxidásica do homogenato da célula SH-SY5YG93A foi maior. Após quatro semanas, a linhagem SH-SY5YG93A manteve a expressão de SOD1, mas as atividades dismutásica e peroxidásica diminuíram. A expressão de SOD1 aumentou a proporção de formas alteradas de SOD1, como enzima reduzida, multímeros formados por ponte dissulfeto e formas insolúveis em detergente, particularmente na linhagem SH-SY5YG93A. Entre estas formas insolúveis, identificamos um dímero covalente de SOD. Estas formas alteradas provavelmente são responsáveis pela ativação do proteassomo e estresse do retículo endoplasmático, verificados nas células transfectadas. Concluindo, a superexpressão da SOD1 foi suficiente para elevar as formas imaturas e oligomerizadas de SOD1 e a oxidação basal, e a mutação G93A ressaltou estes processos. / Some familial ALS (fALS) are caused by mutations in the Cu,Zn-superoxide dismutase enzyme (SOD1). It was thought that the mutated enzymes would have impaired SOD activity, but this has not been corroborated so far. Presently, it is more accepted that the mutated enzymes acquire a new toxic function. What this new toxic function is and how it relates to the degeneration of motor neurons remains debatable. Here, we compared human neuroblastoma cells transfected with fALS mutant G93A (SH-SY5YG93A) or wild-type SOD1 (SH-SY5YWT) with parent cells (SH-SY5Y) in regard to growth, viability, basal oxidant production, SOD and peroxidase activities, and SOD forms. Transfected cells presented increased growth rate and basal oxidant production. SH-SY5YWT and SH-SY5YG93A cells in early culture stage showed SOD expression and activity consistent with the expected two-fold increase; SH-SY5YWT homogenates showed increased peroxidase activity. After four weeks, SH-SY5YG93A maintained SOD1 expression levels but peroxidase and dismutase activities were lower. SOD1 expression increased the levels of altered SOD1 forms such as the reduced enzyme, disulfide multimers and detergent-insoluble forms, particularly in SH-SY5YG93A cells. Among the insoluble forms a covalent SOD dimer was identified. These altered SOD forms are probably responsible for proteasome activation and endoplasmatic reticulum stress response verified in transfected cells. In conclusion, SOD1 over-expression was sufficient to increase intracellular immature and oligomerized SOD1 forms and basal oxidation and the G93A mutation enhanced these processes.

El plan de investigación se centra en el estudio y diseño de catalizadores híbridos para el proceso de síntesis directa de dimetil éter (DME) a partir de gas de síntesis, también conocido en la literatura como "Syngas-To-DME o STD process" [1]. Para llevar a cabo el proceso de síntesis directa de DME se emplean catalizadores híbridos constituidos por mezclas físicas del componente de síntesis de metanol (catalizador basado en Cu) y el componente ácido que lleva a cabo la deshidratación de metanol para dar lugar al DME (zeolita) [1]. De manera general, las labores en las que se centra el plan de investigación persiguen lograr un mayor entendimiento de las propiedades del catalizador híbrido que determinan su comportamiento en el proceso de síntesis directa de DME (STD), prestando especial atención al componente zeolítico con el cual están asociadas la mayoría de controversias en la literatura científica. / García Trenco, A. (2013). Desarrollo de catalizadores híbridos CuZnOAl2O3/zeolita para el proceso de síntesis directa de DME [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/34781