A numerical model of a solid oxide fuel cell electrode is presented. Using an already established algorithm for dropping spheres as a base, alterations are made to the algorithm to increase the realism of the model. Two changes are analyzed in detail: the ability to drop pore former particles, and the use of pre-agglomerated solid particles. These changes are characterized by their impact on mean pore size, tortuosity, and effective diffusivity. As pore former volume fraction is increased, so too are mean pore size and tortuosity. A higher mean pore size has a beneficial effect on effective diffusivity due to Knudsen effects, while a higher tortuosity has a detrimental effect on effective diffusivity. The impact of mean pore size and tortuosity on diffusivity generally balances and if the impact of porosity is ignored, pore former volume fraction does not greatly affect effective diffusivity. As pore former particle size is increased, mean pore size and tortuosity also increase. Similarly to before, the effects of mean pore size and tortuosity balance. However, effective diffusivity is shown to decrease slightly with an increasing pore former particle size, suggesting a change in tortuosity has greater impact on diffusivity than a change in mean pore size. For a domain constructed with pre-agglomerated particles, the tortuosity and mean pore size were both noticeably larger than when no pre-agglomerated particles are used. Effective diffusivity was only slightly higher for a domain constructed with pre-agglomerated particles than with no pre-agglomerated particles. It is also shown that the relationship of effective diffusivity with porosity for a domain constructed with pre-agglomerated particles does not fit the correlation proposed by Berson et al. [1] for low porosity structures. A secondary goal of this work is to examine pore size measurement techniques, and present a novel technique that allows the determination of a local pore size, and therefore, a local Knudsen number. Results from the local pore size technique do not match those of the random walk method and so although the novel technique may prove to be a good starting point, it is deemed not yet suitable for use. / Thesis (Master, Mechanical and Materials Engineering) -- Queen's University, 2011-06-13 15:30:00.25

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Background: Anthracyclines, in particular Doxorubicin (DOX), are highly effective chemotherapeutic agents in the breast cancer setting, which are limited by their cardiotoxic side effects. Recently, the introduction of Trastuzumab (TRZ), a novel monoclonal antibody against the HER2 receptor, in the breast cancer setting compounds the issue of DOX mediated cardiac dysfunction. Amongst the potential mechanisms for the deleterious effects of this drug-induced cardiomyopathy, the relationship between nitric oxide synthase 3 (NOS3) and oxidative stress has gained recent attention. Objective: To determine the role of NOS3 in a clinically relevant female murine model of DOX+TRZ induced heart failure. Methods: A total of 120 C57Bl/6 female mice [60 wild type (WT) and 60 NOS3 knockout (NOS3-/-)] were treated with either 0.9% saline, DOX (20 mg/kg), TRZ (10 mg/kg), or DOX+TRZ. Serial echocardiography was performed daily for a total of 10 days, after which the mice were euthanized for histological and biochemical analyses. Results: As compared to WT, NOS3-/- mice demonstrated increased cardiotoxicity following treatment with DOX. This effect was potentiated with DOX+TRZ combination therapy. In WT female mice receiving DOX+TRZ, left ventricular ejection fraction (LVEF) decreased from 75±3% at baseline to 46±2% at day 10 (p<0.05). In the NOS3-/- group, LVEF decreased from 72±3% at baseline to 35±2% at day 10 (p<0.05). LVEF was significantly lower in NOS3-/- mice than WT at day 10 in those receiving DOX+TRZ (p<0.05). As compared to WT, NOS3-/- mice also demonstrated increased mortality following treatment with DOX+TRZ, corroborating the echocardiographic findings. Histological analysis using light and electron microscopy demonstrated increased loss of cell integrity including myofibrillar degradation, cytoplasmic vacuolization, and enlargement of the smooth endoplasmic reticulum in both the WT and NOS3-/- mice treated with DOX+TRZ. There was no significant difference, however, in the degree of cardiac remodeling between the WT and NOS3-/- groups. There was an increasing trend in the degree of cardiac apoptosis in both WT and NOS3-/- mice treated with DOX+TRZ therapy. Conclusion: Congenital absence of NOS3 potentiates the cardiotoxic effects of DOX+TRZ in an acute female murine model of chemotherapy-induced cardiomyopathy.

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