When the light passes through optical elements it can cause deformation of wavefront light due to the damage of materials and optical aberrations. The deformation leads to unprecise imaging and deformation of an image. The diploma work mentions wavefront sensing techniques which are important for determination inappropriate errors of optical elements and the specification of their properties. The purpose of the master's thesis is to suggest and investigate wavefront sensing methods after the light passes through the optical element while using the digital micromirror device. The work deals with the topic of wavefront aberrations and geometric optical defects of optical elements. Different kinds of commercial products determined for wavefront sensing are described too.

A research-scale solid-fuel ramjet test article has been developed to study the secondary combustion zone of solid fuel ramjets. Tests were performed at a constant core air mass flowrate of 0.77 kg/s with 0%, 15%, and 30% bypass ratios. The propulsive performance analysis results indicate that the 0% bypass case had the highest regression rate and fuel mass flowrate. The regression rate and fuel mass flowrate of fuel without carbon black was the lowest. The specific impulse with air mass flowrate included was highest for the 0% bypass case reaching 130 s and lowest for the 30% bypass case reaching 110 s. For specific impulse with air mass flowrate excluded, the 30% bypass case achieved 2,800 s while the 0% bypass case achieved 1,800 s. The characteristic velocity was greatest for 0% bypass reaching 1,025 m/s and lowest for 30% bypass reaching 900 m/s. The combustion efficiency was highest for the 15% bypass case with carbon black addition approaching 0.82. 50 kHz and 75 kHz CH* chemiluminescence imaging was performed. Analyzing thin slivers of the images over 40,001 frames with frequency-domain techniques showed that most of the high amplitude content occurred below 1-5kHz with small peaks near 20 kHz and 30 kHz. Dynamic mode decomposition (DMD) was performed on sets of 10,001 spatially-calibrated images and their corresponding uncalibrated, uncropped images. Most of the tests exhibited low-frequency axial pumping, transverse modes, and other mode shapes indicative of the secondary injection. The prominence of transverse and other jet-related modes over axial modes appeared to be related to increasing bypass ratio. High-frequency axial modes also appeared in a case thought to have high core-flow momentum that did not appear at these high frequencies for other cases. The DMD modes for 0% bypass were indiscernible due to high soot content. Most of the modes corresponding to the calibrated images also appeared in the uncalibrated images, however, with different mode amplitude rankings. PIV was performed at 5 kHz for one test at 15% bypass. The instantaneous vector fields for these tests displayed local velocities up to 600 m/s. The mean images showed velocities up to 250 m/s. The two-dimensional turbulent kinetic energies reached 200 m2/s2 in several regions throughout the flowfield. The turbulence intensity exceeded 0.20 near the bottom of the flowfield.

No description available.

No description available.

Current study demonstrated the impact of heat therapy on skeletal muscle function in a model of Duchenne muscular dystrophy (DMD). The aim of this study was to: (1) examine the impact of treatment temperature on the skeletal muscle adaptation in DBA/2J mice; and (2) determine the impact of repeated HT for 3 consecutive weeks on body composition and skeletal muscle function in D2.mdx, a model of DMD. From study 1, we revealed that HT at 39℃ for 3 weeks significantly promoted relative muscle mass of both EDL and soleus muscle in DBA/2J mice. However, from study 2, HT at 39℃ for 3 weeks does not improve muscle function or increase muscle mass in a mouse model of DMD.

No description available.

No description available.

<p> In recent years, deformable micromirror arrays have become the focus of several attempts to create cost efficient adaptive optics systems for vision science. Conversely, the Digital Micromirror Device™ (DMD™) has been overlooked by several applications, including adaptive optics, due to its inherent bistability. As a means of addressing this limitation, this thesis suggests multiple methods to demonstrate the feasibility of analog operation of the DMD™. The first step in this process involves the characterization of the DMD™ by means of an automated, optical measurement system. This system was developed to actively monitor the angular deflection of individual micromirrors in the MEMS array. Two key mechanical properties of the microstructure - the natural frequency and the quality factor - are determined through analysis of the micromirrors' recorded dynamic behaviour. Further, through automation of the characterization setup, an investigation of device uniformity is presented exposing a clear trend in the measured micromirror properties over 160 tested mirrors in the DMD™ array. This linear trend is attributed to the variation in thickness of the torsional hinges as a result of the sputtering deposition process. Using the DMD™ characteristics discovered through experimentation, a computationally inexpensive, one-dimensional model based on the fourth order Runge-Kutta numerical method is constructed to simulate the response of the DMD™ micromirrors to user defined input voltage waveforms. Simulations are initially used to exhibit the validity of the model for existing DMD™ voltage patterns through a comparison with measured micromirror responses, and subsequently used to demonstrate two proposed methods of analog operation. The first method creates a limited form of analog control by varying the amplitude of 16 analog bias voltage lines, whereas the second method provides complete analog operation of the DMD™ using high frequency pulse width modulation of the underlying address circuitry.</p> / Thesis / Master of Applied Science (MASc)

The purpose of this thesis project was to elucidate the immune transcriptomic changes in the diaphragm of mdx mice treated with microdystrophin gene therapy with and without running wheel activity. Mdx mice are a model of Duchenne Muscular Dystrophy (DMD). Similar to DMD, mdx pathophysiology is associated with chronic inflammation due to sarcolemma fragility and cellular membrane leakage. Immune modulation has not yet been described when endurance exercise and AAV-microdystrophin gene therapy have been combined in mdx mice. An increase of physical activity in DMD individuals is a potential outcome of current clinical studies investigating microdystrophin treatment; therefore, understanding the impacts of physical activity on the immune system, particularly for the diaphragm, may be important to minimize risk. Recently, the Grange lab published the endurance and contractile property outcomes of combined microdystrophin gene therapy and running wheel activity in mdx mice.1 Diaphragm RNA-seq transcriptomic data were also collected from this study for gene expression analysis. Using this dataset, I tested the hypothesis that relative to mdxGT (mdx mice treated with gene therapy), transcripts related to the immune response such as immune cell recruitment, activation, and downstream signals that promote fibrosis deposition were unchanged or downregulated in mdxRGT (mdx mice treated with gene therapy and access to running wheel). DEGs (differentially expressed genes) were analyzed with Microsoft Excel, R, and bioinformatic tools such as KEGG and DAVID to explain immune system adaptations in response to combined microdystrophin treatment and running in mdx mice. Two major inflammatory signaling pathways, the IL-6/JAK/STAT and NF-kB signaling pathways translationally relevant to DMD patients were rescued by gene therapy towards WT expression levels. Although running maintained the majority of the rescued transcriptome profile (691 of 724 genes), some immune response-related gene expressions (33 of 724 genes) were modulated including genes related to chemotaxis and cellular migration. These changes suggested potential signaling for angiogenesis and a fast to slow fiber type shift; however, unbiased analysis with bioinformatic tools did not confirm either of these possibilities. The data from this study revealed inflammatory and fibrotic signaling pathways commonly observed in DMD patients and mdx mice were rescued by the AAV microdystrophin gene therapy and were maintained by voluntary wheel running / Master of Science / Duchenne Muscular Dystrophy (DMD) is an X chromosome-linked muscular dystrophy, a genetic disease that affects around 1 in 14,000 boys globally. DMD is lethal and currently there is no cure. Mutations in the DMD gene results in the absence of the protein dystrophin. The dystrophin protein and other proteins associated with it provide structural support to the skeletal muscle membrane. Without it, muscles are more easily damaged during contraction. This damage promotes recruitment of immune cells which initiates the first stage of muscle repair. Under normal circumstances, this inflammatory reaction caused by immune cells restores the skeletal muscles. However, in DMD patients, repeated breakdown and regeneration of skeletal muscles leads to abnormal inflammation which promotes negative outcomes such as increased fibrosis. Fibrosis impairs muscle function, especially the diaphragm . Hamm et al., 2021 from the Grange lab investigated the effects of microdystrophin gene therapy and increased physical activity in mdx mice, a mouse model of DMD, with the idea that some of the negative changes with muscular dystrophy could be improved. The results showed a positive increase of endurance capacity in mdx mice treated with gene therapy alone (mdxGT group) and a greater increase if the mice also used a running wheel (mdxRGT group) compared to untreated mdx mice (mdx group). These findings suggested that gene therapy can increase a DMD patient's ability to become more physically active. However, the effects of running and microdystrophin gene therapy on the damaging inflammatory response in the diaphragm were not reported. To address this question, gene expression data from diaphragm muscles of all treatment groups were collected in the Hamm et al., 2021 study for later analysis. In my study, these diaphragm gene expression data were used to compare inflammatory signals between the various treatment groups. Indicators of skeletal muscle damage, immune cell accumulation and fibrosis deposition were rescued (i.e., returned to healthy mice levels) by microdystrophin gene therapy (mdxGT group). Running did not exert any negative effects on the majority of genes rescued by the microdystrophin therapy (mdxRGT group). These results indicated that voluntary wheel running could maintain the reduced inflammatory signals due to the microdystrophin gene therapy in mdx mice. If the function of the skeletal muscle of dystrophic boys was similarly improved by microdystrophin gene therapy and exercise did not interfere with its positive effects, DMD boys could potentially be physically active similar to normal boys of their age.

La dystrophie musculaire de Duchenne (DMD) touche un garçon sur 3500, contraint à l'usage du fauteuil roulant à l'âge de 10 ans, et entraîne le décès à une vingtaine d'années. Cette maladie demeure incurable, et les pistes thérapeutiques envisagées nécessitent d'être validées en amont, dans les modèles murins, puis au stade pré-clinique, dans les modèles canins.L'un d'eux, le chien GRMD (Golden Retriever Muscular Dystrophy), est le plus largement utilisé, et présente l'intérêt de partager, avec le patient qu'il modélise, de nombreuses similitudes génotypiques et phénotypiques. Les différentes fonctions touchées doivent donc pouvoir faire l'objet de mesures objectives et quantitatives, à l'aide d'outils dédiés. Par ailleurs, une problématique inhérente à l'utilisation de ce modèle est sa grande variabilité sur le plan phénotypique.L'objectif du travail mené ici a été de développer des outils d'évaluation du chien GRMD, afin de mieux connaître et maîtriser cette hétérogénéité clinique.La mesure de force de flexion du tarse a permis de démontrer que la force tétanique maximale pouvait être utilisée comme indice d'évaluation à différents stades de la maladie, sans que le déficit de force musculaire puisse être relié à l'atteinte motrice globale. De plus, la relaxation s'est avérée altérée chez les chiens GRMD, en corrélation avec leur atteinte motrice.La locomotion, évaluée par accélérométrie tri-dimensionnelle, a pu montrer des altérations multiples, mesurées par différentes variables. Certaines variables sont altérées de manière précoce, tandis que d'autres anomalies s'installent durant les premiers mois, traduisant l'aggravation de la fonction locomotrice.La dysfonction respiratoire, évaluée par spirométrie en respiration de Tidal, et cinématique diaphragmatique sur images radioscopiques, a également pu être objectivée par différents indices. Une moindre mobilité diaphragmatique, une rétraction caudale du diaphragme, et un effondrement du débit expiratoire en fin d'expiration, s'installent au cours des premiers mois.Afin de contrôler l'hétérogénéité clinique ainsi mesurée, une recherche de marqueurs prédictifs de l'évolution clinique a été menée. Différents indices histologiques et cliniques ont été évalués sur leur valeur pronostique à un stade précoce. La fréquence des cycles locomoteurs à 2 mois et le défaut de relaxation à 4 mois se sont avérés prédictifs de formes accélérées.Enfin, les différents outils mis en place ont été évalués dans le cadre du suivi d'animaux au cours d'un essai thérapeutique, qui a, de plus, permis de disposer d'une population de référence sous traitement immunosuppresseur. Une amélioration fonctionnelle des animaux traités a pu être démontrée par nombre des indices mesurés.Ces résultats démontrent que les outils développés sont utilisables au cours d'essais pré-cliniques, et permettent, malgré l'hétérogénéité clinique qu'ils mesurent, de démontrer un bénéfice fonctionnel. Plus largement, ces données permettent d'optimiser l'utilisation pré-clinique du modèle GRMD. / Duchenne Muscular Dystrophy (DMD) affects one boy over 3500 at birth. The affected individuals are wheelchair-bound at about 10 years, and death occurs in the early twenties. DMD remains incurable, and therapeutic strategies need to be validated in murine models, and, subsequently, at the preclinical stage, in canine models.Among the existing canine models, the GRMD (Golden Retriever Muscular Dystrophy) dog is the most widely used. The strong genotypic and phenotypic similarities it shares with DMD patients make this model of great interest. The many affected functions must therefore be reliably measured using dedicated tools, providing objective and quantitative evaluation. Moreover, the wide phenotypic heterogeneity peculiar to this model may compromise its use in preclinical studies.The aim of the present work was to develop evaluation tools for the GRMD dog, in order to better know and handle this clinical variability.The measurement of the contraction force generated by tarsal flexion has shown that the maximal tetanic force could be used as an evaluation index, at different stages of the disease. However, no correlation with the global motor impairment could be found. Conversely, the relaxation has shown to be altered in GRMD dogs, and correlated with the motor impairment.The locomotion was evaluated using three-dimensional accelerometry. This method allowed the measurement of several variables, some of which being early impaired, and some others being altered in a more progressive fashion, reflecting the degradation of the locomotor function.The respiratory impairment has been evaluated by diaphragmatic kinematics using radioscopic acquisitions and by Tidal-breathing spirometry. The diaphragm was shown to be less mobile, and to be caudally displaced. The end-expiration flows were decreased. These abnormalities progressed during the first months.In order to better handle the clinical heterogeneity, some markers able to predict the clinical evolution were looked for. The prognostic value of many histological and clinical indexes at an early stage has been evaluated. The stride frequency at the age of 2 months, as well as the relaxation impairment at the age of 4 months succeeded in predicting severe accelerated forms.Finally, the developed tools have been tested in the context of a clinical follow-up during a therapeutic trial. This trial also aimed to provide a reference-group of GRMD dogs treated with immunosuppressive drugs. Several indexes have demonstrated a clinical improvement of the treated animals.These results show that the developed tools are useable during preclinical trials and allow to quantitatively highlight a functional improvement, despite the clinical heterogeneity. More widely, these data will lead to an optimization of the preclinical use of GRMD dogs.