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<p>With the advances in MEMS technology, the studies of the properties of magnetic crystals have reached the microscopic level. Critical information such as the magnetization and susceptibility of a magnetic sample can be obtained using a microtorque magnetometer, such as ones incorporating piezoresistive or capacitive detection that have been fabricated and tested by earlier research groups. This type of magnetic information is useful in the study of superconductivity, for example. The microtorque magnetometer designed and fabricated in this thesis has the potential of being used in this field of study.</p> <p>This thesis describes the design, fabrication and testing of a capacitive microtorque magnetometer. By using ANSYS, a computer modelling program, an ideal model of the rotating microtorque magnetometer was devised. Fabrication involved testing a variety of procedures before establishing the successful and efficient method of building the microtorque magnetometer. A fifth order resonant mode was successfully detected during the testing stage. A method of studying the desired resonant mode has been devised and explained in the later chapters of this thesis.</p> / Master of Applied Science (MASc)

<p>Increased muscle stiffness helps prevent excessive movement that can lead to ligament and soft-tissue damage. There is empirical evidence suggesting that muscles are important in preventing injuries caused by excessive translational movements. Very little is known, however, on how our muscles provide translational stiffness. This thesis uses complementary theoretical (Chapters 2 and 3) and experimental (Chapter 4) techniques to address how muscles provide translational joint stiffness.</p> <p>In Chapters 2 and 3, we used an elastic energy approach to successfully derive equations that quantify muscular contributions to joint stiffness. From the equations, we were able to determine how the geometric orientation and mechanical properties of an individual muscle allows it to provide translational stiffness. In Chapter 4, using the techniques developed in the previous chapters, we test the notion that the nervous system is responsive to translational loading.</p> <p>From these works, several important discoveries were found. We are the first to find that muscles with large squared projections (alignment) over a degree-of-freedom are well suited to provide translational stiffness. Further, by explicitly describing the interactions between the translational and rotational stiffnesses we found that ignoring these interactions resulted in an overestimation of principal stiffnesses. This has large implication for stability analyses, where such overestimations could suggest that an unsafe task is actually safe. Experimentally, we found that the nervous system is responsive to translational loading. This was accomplished through increased activity of muscle well suited to provide translational stiffness.</p> <p>Collectively, the works presented provide much needed knowledge on the role muscle play in stabilizing and protecting our joints. This thesis provides a strong foundation for continued joint stiffness, stability, and impedance research.</p> / Doctor of Science (PhD)

Women are more likely to sustain knee injuries (e.g., ACL tears) than their male counterparts. The mechanisms responsible for this disparity are unclear. However fluctuating hormones during the menstrual cycle may be an influencing factor since more ACL injuries have been observed preceding ovulation when estrogen levels increase. Previous research shows females to have increased muscle strength and altered neuromuscular activation prior to ovulation. These findings have not been replicated in females using oral contraceptives (OC). To date, no study has examined all of these factors simultaneously. The purpose of this study was to determine the effect of sex, hormones, and contraceptive use on neuromuscular function at 3 points during a menstrual cycle. A prospective cohort design with independent variables of group [male (n=10), female no-OC (n=10), female OC (n=10)], and testing session (1,2,3) was used to assess knee function (i.e., tibial translation, isometric strength, vertical leg stiffness, and neuromuscular activation) on physically active college-aged participants. Three testing sessions were scheduled throughout a typical menstrual cycle. Tibial translation was measured at the start of each testing session to assess ACL laxity, for handgrip, knee extensors and knee flexors strength. Area EMG activity of the rectus femoris (representing quadriceps) and biceps femoris (representing hamstrings) was recorded over 3 46cm drop jumps, and vertical leg stiffness was calculated based on measurements obtained by a force plate. A 3 (group) x 3 (testing session) MANOVA (p ≤ 0.05) was used to assess knee function, as defined by tibial translation, strength, EMG activation and vertical leg stiffness. A significant difference was found with respect to strength, as males overall displayed greater strength than both female groups. No other significant differences were found. Although this study attempted to explain the effect of estrogen on strength and neuromuscular function with an improved design, no conclusive evidence was found to further explain this relationship. Future studies should use more sensitive and objective measures to explore this dynamic on a greater sample size over multiple menstrual cycle phases. / Kinesiology

The overall goal of this research is to elucidate the effects of stiffness on the activation of pulmonary endothelial cells by inflammatory cytokines. The hypothesis tested is that increasing matrix stiffness in the (patho) physiological range will exacerbate the response of cultured endothelial cells to inflammatory stimuli. To test this hypothesis, we are culturing control and TNF-a stimulated rat lung microvascular endothelial cells (RLMVECs) on hydrogels with tunable stiffnesses of 5, 20, and 45 kPa (measured using compression testing), modeling the stiffness of healthy, intermediate and fibrotic lung tissue respectively. The cellular readout was assessed through RT-qPCR, microscopy, and monocyte adhesion for basal expression and upregulation of vascular cell adhesion molecule-1 (VCAM-1) in quiescent and TNF-a stimulated cultured endothelial cell. This model of microvascular pulmonary inflammation, mimicking a normal, intermediate, and fibrotic lung, is aimed at establishing a correlation between substrate stiffness and inflammation. This research demonstrates the significant increase of basal VCAM-1 gene expression as well as monocyte adhesion as substrate stiffness increases. When using inhibition, it was also found that VCAM-1 is partially activated through the Rho/ROCK, YAP/TAZ, and NF-kB pathway. Our results contribute to a mechanistic understanding of disease pathologies such as idiopathic pulmonary fibrosis, in which treatment is just about limited to a full lung transplant and facilitate testing of new drug therapies. / Bioengineering