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La réalisation d'un ordinateur quantique est un défi scientifique et technique de taille du 21e siècle et plusieurs approches sont poursuivies afin d'atteindre ce but. Cette thèse s'intéresse principalement à l'une d'entre elles: le calcul quantique basé sur les modes de Majorana. Cette approche s'inscrit dans le cadre de l'informatique quantique topologique et vise à tirer profit des propriétés exotiques des phases topologiques de la matière afin d'effectuer du calcul quantique intrinsèquement robuste aux erreurs. À défaut de connaître des supraconducteurs topologiques facilement accessibles dans la nature, des modes de Majorana peuvent être obtenus en faisant l'ingénierie d'un dispositif mésoscopique alliant matériaux semiconducteurs et supraconducteurs. En choisissant les bons ingrédients, il est alors possible de créer des modes de Majorana aux extrémités de nanofils hybrides formant un circuit supraconducteur topologique. Séparés en deux volets, les travaux de recherche présentés dans cette thèse s'attaquent à différents problèmes reliés à l'ingénierie et à la caractérisation de modes de Majorana dans un système mésoscopique. Un premier volet de cette thèse vise à faciliter l'ingénierie de systèmes physiques permettant l'émergence de modes de Majorana robustes. Pour ce faire, on développe une nouvelle méthode numérique efficace basée sur les fonctions de Green récursives et inspirée par l'algorithme d'ingénierie d'impulsions par montée de gradients utilisé dans le domaine du contrôle optimal. Ce nouvel algorithme vise l'optimisation du profil spatial de paramètres et tire profit de résultats d'abord obtenus dans le contexte de l'optimisation de la dynamique de systèmes quantiques dissipatifs. La méthode développée est appliquée à l'optimisation de réseaux de microaimants permettant l'ingénierie de modes de Majorana dans des semiconducteurs à faible couplage spin-orbite comme le silicium. Le second volet de cette thèse étudie les signatures micro-ondes de joncti

Au cours des dernières années, le développement de l’amplificateur paramétrique Josephson a permis de grandement accroître la fidélité de la mesure des qubits supraconducteurs. De plus, ce nouvel outil a ouvert un éventail de possibilités expérimentales telles la mesure de sauts quantiques et la compression de la lumière. Par contre, de récents résultats expérimentaux [Murch et al. Nature 499, 62 (2013), Zhong et al. NJP 15, 125013 (2013)] démontrent que, malgré les bonnes propriétés de cet amplificateur à faible bruit, des imperfections limitent ses performances. Dans le cadre de ce mémoire, une modélisation de l’amplificateur paramétrique Josephson (JPA) au-delà des approximations standards est présentée afin de mieux comprendre et caractériser ces imperfections. Pour la première fois, le JPA à pompe de courant monochromatique, le JPA à pompe de courant bichromatique et le JPA à pompe de flux sont comparés dans un même formalisme. Ceci permet une analyse des avantages et inconvénients de chacun au-delà de ce qui se trouve dans la littérature. En particulier, l’analyse démontre que ces différentes pompes mènent à des corrections d’ordres supérieurs différentes. À l’aide d’outils numériques et analytiques, on caractérise le champ en sortie de l’amplificateur. On démontre alors que le niveau de compression de ce champ est limité par les corrections d’ordres supérieurs généralement négligées dans la modélisation du JPA. Ce résultat numérique est comparé aux résultats expérimentaux obtenus par nos collaborateurs du laboratoire de nanoélectronique quantique de l’Université de Berkeley. Finalement, les cumulants de troisième et quatrième ordres sont calculés et démontrent que le caractère non gaussien du champ en sortie d’un amplificateur paramétrique Josephson augmente avec le gain et la non-linéarité.

Thesis (Ph. D. in Molecular and Systems Bacterial Pathogenesis)--Massachusetts Institute of Technology, Biological Engineering Division, 2005., This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections., Includes bibliographical references., Helicobacter hepaticus infection of A/JCr mice is a model of liver cancer resulting from chronic active inflammation. We monitored hepatic global gene expression profiles and correlated them to histological liver lesions in H. hepaticus infected and control male A/JCr mice at 3 months, 6 months, and 1 year of age. We used an Affymetrix-based oligonucleotide microarray platform on the premise that a specific genetic expression signature at isolated time points would be indicative of disease status. Model based expression index comparisons generated by dChip yielded consistent profiles of differential gene expression for H. hepaticus infected male mice with progressive liver disease versus uninfected control mice within each age group. Linear discriminant analysis and principal component analysis allowed segregation of mice based on combined age and lesion status, or age alone. Up-regulated genes present throughout the 12 month study involved inflammation, tissue repair, and host immune function. Upregulation of putative tumor and proliferation markers correlated with advancing hepatocellular dysplasia. Transcriptionally down-regulated genes in mice with liver lesions included those related to peroxisome proliferator, cholesterol, and steroid metabolism pathways. Transcriptional profiling of hepatic genes documented gene expression signatures in the livers of H. hepaticus infected male A/JCr mice with chronic progressive hepatitis and preneoplastic liver lesions, complemented the histopathological diagnosis, and suggested molecular targets for the monitoring and intervention of disease progression prior to the onset of hepatocellular neoplasia. Our laboratory, in collaboration with Professors Suerbaum and Schauer, recently identified a, (cont.) 70kb genomic island in Helicobacter hepaticus strain ATCC 51488 as a putative pathogenicity island (HhPAI) (Suerbaum et al, PNAS, 2003). This region within H. hepaticus contains genes HH0233-HH0302, a differential GC content, several long tandem repeats but no flanking repeats, and three components of a type IV secretion system (T4SS). A/JCr mice were experimentally infected with three naturally occurring strains of H. hepaticus including the type strain H. hepaticus ATCC 51488 strain (Hh 3B1) isolated from A/JCr mice, MIT 96-1809 (Hh NET) isolated from mice shipped from the Netherlands, and MIT-96-284 (HhG) isolated from mice acquired from Germany.4 HhNET (missing most of the HhPAI) infected male A/JCR mice exhibited a significantly lower prevalence (p<.05) of hepatic lesions at 6 months post infection than Hh 3B1 with an intact HhPAI. Hh G also has a large segment of the genomic island deleted, but not as many genes are deleted as compared to Hh NET. Hh G also demonstrated a lower prevalence of hepatic lesions. This variable pathological effect was evident in male mice only. The severity of chronic active inflammation in the liver of the H. hepaticus infected A/JCr mice depended on H. hepaticus liver colonization levels. The in vivo results support the presence of the HhPAI as a legitimate virulence determinant and predictor of severity of liver lesions in H. hepaticus infected A/JCr male mice. To further determine the differences in virulence of the H. hepaticus strains Hh 3B1, Hh NET, Hh G and an isogenic mutant H. ..., by Samuel R. Boutin., Ph.D.in Molecular and Systems Bacterial Pathogenesis

Thesis (Ph. D. in Molecular and Systems Bacterial Pathogenesis)--Massachusetts Institute of Technology, Biological Engineering Division, 2005., This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections., Includes bibliographical references., Helicobacter hepaticus infection of A/JCr mice is a model of liver cancer resulting from chronic active inflammation. We monitored hepatic global gene expression profiles and correlated them to histological liver lesions in H. hepaticus infected and control male A/JCr mice at 3 months, 6 months, and 1 year of age. We used an Affymetrix-based oligonucleotide microarray platform on the premise that a specific genetic expression signature at isolated time points would be indicative of disease status. Model based expression index comparisons generated by dChip yielded consistent profiles of differential gene expression for H. hepaticus infected male mice with progressive liver disease versus uninfected control mice within each age group. Linear discriminant analysis and principal component analysis allowed segregation of mice based on combined age and lesion status, or age alone. Up-regulated genes present throughout the 12 month study involved inflammation, tissue repair, and host immune function. Upregulation of putative tumor and proliferation markers correlated with advancing hepatocellular dysplasia. Transcriptionally down-regulated genes in mice with liver lesions included those related to peroxisome proliferator, cholesterol, and steroid metabolism pathways. Transcriptional profiling of hepatic genes documented gene expression signatures in the livers of H. hepaticus infected male A/JCr mice with chronic progressive hepatitis and preneoplastic liver lesions, complemented the histopathological diagnosis, and suggested molecular targets for the monitoring and intervention of disease progression prior to the onset of hepatocellular neoplasia. Our laboratory, in collaboration with Professors Suerbaum and Schauer, recently identified a, (cont.) 70kb genomic island in Helicobacter hepaticus strain ATCC 51488 as a putative pathogenicity island (HhPAI) (Suerbaum et al, PNAS, 2003). This region within H. hepaticus contains genes HH0233-HH0302, a differential GC content, several long tandem repeats but no flanking repeats, and three components of a type IV secretion system (T4SS). A/JCr mice were experimentally infected with three naturally occurring strains of H. hepaticus including the type strain H. hepaticus ATCC 51488 strain (Hh 3B1) isolated from A/JCr mice, MIT 96-1809 (Hh NET) isolated from mice shipped from the Netherlands, and MIT-96-284 (HhG) isolated from mice acquired from Germany.4 HhNET (missing most of the HhPAI) infected male A/JCR mice exhibited a significantly lower prevalence (p<.05) of hepatic lesions at 6 months post infection than Hh 3B1 with an intact HhPAI. Hh G also has a large segment of the genomic island deleted, but not as many genes are deleted as compared to Hh NET. Hh G also demonstrated a lower prevalence of hepatic lesions. This variable pathological effect was evident in male mice only. The severity of chronic active inflammation in the liver of the H. hepaticus infected A/JCr mice depended on H. hepaticus liver colonization levels. The in vivo results support the presence of the HhPAI as a legitimate virulence determinant and predictor of severity of liver lesions in H. hepaticus infected A/JCr male mice. To further determine the differences in virulence of the H. hepaticus strains Hh 3B1, Hh NET, Hh G and an isogenic mutant H. ..., by Samuel R. Boutin., Ph.D.in Molecular and Systems Bacterial Pathogenesis