In this thesis, I explore my artistic practice, which confronts the institutionalized cultural norms that control women's identity and sexuality in rural Kenya. Utilizing self-portraiture, my work serves as a mirror, reflecting on my own identity and experiences growing up in Kenya. In some of the artworks, I subvert these restrictions, reclaiming my place both physically and metaphorically. My studio practice encompasses drawing, painting, installation, and fiber arts. Inspired by my culture, my work questions the balance between cultural tradition and personal identity. I use various materials, including charcoal, fabric, oil paints, pastels, and bleach. Through my art, I invite viewers into a broader conversation on the liberation and autonomous expression of women, compelling them to question and ultimately redefine the boundaries imposed upon them by their cultural spheres.

No description available.

Mycket av vår kognitiva förmåga beror på lagringen och bearbetande av meningen olika objekt, ord eller handlingar innefattar. Denna mening kallas för semantik där semantik inom arbetsminne har till största del ignorerats och istället tillskrivits långtids semantiskt minne. Med användning Baddley och Hitch model av arbetsminne är målet av denna studie att tillskriva semantisk bearbetning till en komponent inom modellen, undersöka skillnader mellan typer av semantiskt material till episodiskt material och hur dessa är påverkade av seriella positionseffekter. Relaterad semantik, orelaterad semantik och episodiskt material var inkluderade i studien och var representerade av ord-par. 42 deltagare, med användningen av en bekvämlighetsurvalsmetod, blev slumpmässigt tilldelade ett av tre experimentella förhållanden designade för att förändra mängden material som de kan memorera. Det första experimentella förhållandet fastställde att med direkt återkallelse hade semantiskt material högre grad av återkallelse än episodiskt material. Det andra experimentella förhållandet visade att effekten av artikulatoriskt undertryckande (articulatory suppression) inte signifikant sänker mängden som memorerat. Det tredje förhållandet demonstrerade att fördröjd återkallelse signifikant förminskade mängden orelaterad semantik. Dessa resultat visade att semantiskt material återkallas till högre grad men relaterad semantik och orelaterad semantik lagras av olika system då orelaterad semantik är påverkad av förfall (decay) eller störning (interference). Resultaten visade betydelsen av att använda simpelt och precist språk för att ge ett mer effektivt sätt att memorera och lära sig. / Much of our cognitive abilities rely on maintaining and processing the meaning of different objects, words or actions. This meaning is known as semantics however, the use of semantics in working memory have been mostly ignored and instead attributed to long-term semantic memory. Using Baddeley and Hitch’s model of working memory this study aims to attribute semantic maintenance to a component within the model, examine differences between types of semantic material to episodic material and how these were affected by serial position effects. Related semantics, unrelated semantics and episodic material were included in the study which were all represented by word-pairs. 42 participants, using a convenience sampling method, were randomly assigned to one of three experimental conditions designed to alter the amount of material memorized. The first experimental condition, by using immediate recall, demonstrated that semantic materials had a significantly superior recall rate than episodic materials. The second experimental condition showed that the effect articulatory suppression didn’t significantly reduce the amount memorized. The third condition demonstrated that delayed recall significantly reduced the amount of unrelated semantics. These findings showed that semantic materials had superior recall but related and unrelated semantic material were found to be maintained by different systems as unrelated material was subject to decay or interference. The results showed the importance using simple and precise language to provide a more effective way to memorize and learn.

D’après les théories inférentielles de la perception, notre cerveau tire parti des régularités statistiques présentes dans l’environnement pour générer des prédictions qui façonnent nos contenus perceptifs. Le travail réalisé pendant cette thèse inclut 3 études principales, dans le but de caractériser les déterminants neuronaux des fausses perceptions et la nature des prédictions neuronales.Les erreurs perceptives pourraient résulter d’une tentative de notre système visuel d’expliquer des entrées sensorielles imprécises par une hypothèse erronée. Dans une 1ère étude en Imagerie par Résonance Magnétique fonctionnelle (IRMf), nous montrons que les fausses détections sont associées à un état imprécis et biaisé des circuits sensoriels avant la perception.La répétition d’une image génère une activité neurale diminuée (‘Repetition Suppression’) et des temps de réponse plus courts (‘amorçage’). Ces phénomènes pourraient résulter de mécanismes prédictifs, sous une prédiction implicite de répétition. Dans une 2nde étude IRMf, nous montrons que cette prédiction ne peut pas être modulée par l’expérience, ce qui suggère une implémentation locale. Dans une série d’études comportementales, nous montrons que l’amorçage est modulé par les prédictions, suggérant un mécanisme prédictif. Notre 2nde étude IRMf montre aussi qu’une région de moyen niveau sensible aux visages code des prédictions liées à l’identité, ce qui nous informe sur la nature des prédictions visuelles.Nos résultats montrent que notre perception est façonnée par l’interaction de nos entrées sensorielles avec l’état des circuits neuronaux avant stimulation, qu’il s’agisse de l’activité spontanée ou des stimuli précédents. / According to theoretical frameworks casting perception as inference, our brain can learn the statistical regularities present in the sensory world, and use this prior information to generate predictions, which in turn shape our perceptual contents. The work conducted in this PhD includes three main studies aimed at characterizing the neural determinants of misperceptions, as well as the nature of neural predictions. Perceptual errors may arise from an attempt of our visual system to 'explain' impreciseinputs with an erroneous hypothesis. In a first functional Magnetic Resonance Imaging (fMRI) study, we show that during a detection task, hallucinations are associated with animprecise and biased state of sensory circuits preceding sensation. Stimulus repetition is associated with decreased neural responses, known as Repetition Suppression, and shorter response times, known as priming. These phenomena may reflectpredictive mechanisms under an implicit prior over repetition. In a second fMRI study, we show that this putative prior cannot be changed by experience, suggesting a local, possibly hard-wired neural implementation. In a series of behavioral experiments, we show thatpriming is modulated by predictions, supporting a predictive account of this phenomenon. Our second fMRI study also shows that a mid-level face-sensitive region codes for exemplarspecific predictions, which sheds light on the nature of the predictions encoded along thevisual hierarchy. Altogether, our results speak to the dependence of perception on prior brain states. Both spontaneous activity in sensory circuits and previous stimulation interact with sensory inputsto shape our perceptual contents.

Les ruminations mentales sont majoritairement exprimées sous forme verbale et il a été proposé de les considérer, par conséquent, comme une forme dysfonctionnelle de parole intérieure (i.e., production mentale de parole). D’autre part, les recherches sur la psychophysiologie de la parole intérieure ont révélé que les processus neuronaux impliqués dans la parole à voix haute et dans la parole intérieure sont similaires. Ces observations sont cohérentes avec l’idée que certaines formes de parole intérieure pourraient être considérées comme une forme de simulation de la parole à voix haute, de la même manière que certaines actions imaginées peuvent être considérées comme le résultat d’une simulation de l’action correspondante (par exemple, marcher et s’imaginer en train de marcher). En d’autres termes, l’hypothèse de la simulation motrice suggère que le système moteur de la parole devrait également être impliqué lors de la production de parole intérieure. L’hypothèse corollaire peut être formulée, selon laquelle la production de parole intérieure (et de ruminations) devrait être perturbée par une perturbation du système moteur de la parole. Nous avons mené une série de cinq études visant à sonder le rôle du système moteur de la parole dans les ruminations. Dans l’ensemble, nos résultats soulignent que, bien que la rumination verbale puisse être considérée comme une forme de parole intérieure, elle ne semble pas recruter spécifiquement le système moteur de la parole. Plus précisément, nous soutenons que la rumination peut être considérée comme une forme de parole intérieure particulièrement condensée, qui s’exprimerait sous la forme d’une représentation phonologique, et dont les traits articulatoires ne seraient pas complètements spécifiés. Nous faisons le lien entre ces résultats et l’hypothèse théorique du cadre “habitude-but” de la rumination dépressive et nous discutons de leurs implications pour les théories de la production de parole intérieure. / Rumination is known to be a predominantly verbal process and has been proposed to be considered as such as a dysfunctional form of inner speech (i.e., the silent production of words in one’s mind). On the other hand, research on the psychophysiology of inner speech revealed that the neural processes involved in overt and covert speech tend to be very similar. This is coherent with the idea that some forms of inner speech could be considered as a kind of simulation of overt speech, in the same way as imagined actions can be considered as the result of a simulation of the corresponding overt action (e.g., walking and imagined walking). In other words, the motor simulation hypothesis suggests that the speech motor system should be involved as well during inner speech production. The corollary hypothesis might be drawn, according to which the production of inner speech (and rumination) should be disrupted by a disruption of the speech motor system. We conducted a series of five studies aiming to probe the role of the speech motor system in rumination. Overall, our results highlight that although verbal rumination may be considered as a form of inner speech, it might not specifically involve the speech motor system. More precisely, we argue that rumination might be considered as a particularly strongly condensed form of inner speech that does not systematically involve fully specified articulatory features. We discuss these findings in relation to the habit-goal framework of depressive rumination and we discuss the implications of these findings for theories of inner speech production.

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal.

Paracoccidioides brasiliensis, um fungo termodimórfico, é o agente causador da paracoccidioidomicose (PCM), a micose sistêmica prevalente da América Latina. A patogenicidade aparenta estar intimamente relacionada com a transição dimórfica da forma de micélio para a de levedura, que é induzida pela mudança da temperatura do ambiente pela temperatura do hospedeiro mamífero. Há poucas informações disponíveis sobre genes de P. brasiliensis que são necessários durante a fase patogênica. Nós, então, realizamos as técnicas de SSH (“Suppression Subtraction Hybridization") e de “Macroarray" com o objetivo de identificar genes que sejam preferencialmente expressos na fase leveduriforme do isolado Pb18. Genes identificados em ambos os procedimentos estão mais expressos na fase leveduriforme e estão envolvidos em metabolismo básico, transdução de sinal, crescimento e morfogênese e metabolismo do enxofre. Para testar se as mudanças observadas na expressão gênica refletem as diferenças entre as condições de crescimento usadas para obter as duas formas morfológicas preferivelmente às diferenças intrínsecas dos tipos celulares, nós realizamos experimentos com RT-PCR em tempo real utilizando preparações de RNA derivadas de ambas as fases, micélio e levedura, crescidas a 26°C e 37°C nos meios de cultura completos (YPD e Sabouraud) e meio mínimo. Vinte genes, incluindo AGS1 ( -1,3-glucan synthase) e TSA1 (thiol-specific antioxidant), foram mostrados como mais expressos na levedura patogênica em relação ao micélio. Embora a expressão de RNA mensageiro foi bastante diferente em relação aos meios completos e meio mínimo, mostramos uma tendência geral para que esses genes serem mais expressos nas células leveduriformes patogênicas de P.x brasiliensis. Além disso, mostramos a complementação dos genes METR e SCONC de P. brasiliensis e uma cepa com estes genes deletados de Aspergillus nidulans, sugerindo uma possível homologia entre eles. Mostramos também a análise de genes da via do metabolismo do enxofre foram mais expressos na levedura patogênica de P. brasiliensis em relação ao micélio saprofítico. / Paracoccidioides brasiliensis, a thermodimorphic fungus, is the causative agent of paracoccidioidomycosis (PCM), a prevalent systemic mycosis in Latin America. Pathogenicity appears to be intimately related to the dimorphic transition from the hyphal to the yeast form, which is induced by a shift from environmental temperature to the temperature of the mammalian host. Little information is available on the P. brasiliensis genes necessary during the pathogenic phase. We have therefore undertaken Suppression Subtraction Hybridization (SSH) and macroarray analyses with the aim of identifying genes that are preferentially expressed in the yeast phase. Genes identified by both procedures as being more highly expressed in the yeast phase are involved in basic metabolism, signal transduction, growth and morphogenesis, and sulfur metabolism. In order to test whether the observed changes in gene expression reflect the differences between the growth conditions used to obtain the two morphological forms rather than differences intrinsic to the cell types, we performed real-time RT-PCR experiments using RNA derived from both yeast cells and mycelia that had been cultured at 37 and 26°C in either complete medium (YPD or Sabouraud) or minimal medium. Twenty genes, including AGS1 ( 1,3-glucan synthase) and TSA1 (thiol-specific antioxidant), were shown to be more highly expressed in the yeast cells than in the hyphae. Although their levels of expression could be different in rich and minimal media, there was a general tendency for these genes to be more highly expressed in the yeast cells. Moreover, complementation of P. brasiliensis METR and SCONC genes in strains of Aspergillus nidulans with these genes deleted suggested a possible homology between them. We show the analyses of genes involved in the xii sulphur metabolism pathway and these genes were more expressed in the pathogenic yeast than saprophytic mycelia of P. brasiliensis.

Neste trabalho é desenvolvido um sistema de controle ativo para supressão de flutter de uma asa utilizando-se sensores de pressão em pontos estratégicos de sua superfície. O flutter é um fenômeno aeroelástico que caracteriza um acoplamento instável entre estrutura flexível e escoamento aerodinâmico não estacionário. Quando a modificação da estrutura ou da aerodinâmica da asa não é viável, o uso de sistemas de controle passa a ser uma boa opção. Para o desenvolvimento do sistema de controle proposto, é primeiramente desenvolvido um modelo numérico de asa flexível. Com esse modelo numérico e a pressão na superfície da asa medida em certos pontos e realimentada ao sistema controlador, são determinadas correções no ângulo de uma superfície de controle no bordo de fuga. A tentativa de se utilizar um sistema de controle bem simples, com o uso de um único sensor de pressão, mostra a viabilidade de se implementar um sistema deste tipo em aeronaves reais. Esse sistema pode tornar-se uma alternativa aos desenvolvidos até então com o uso de acelerômetros, além de ser útil em sistemas onde se procura prever o estol e observar o comportamento da distribuição de pressão sobre a asa em vôo. / In this work, a wing flutter suppression active control system using pressure sensors in strategic points is developed. Flutter is an aeroelastic phenomenon characterized by an unstable coupling of a flexible structure and a non-stationary aerodynamic flow. When changes of the wing structure or of the aerodynamics are not viable, the use of automatic control systems becomes a good option. For the developing of the suggested control system, a numeric model of a finite flexible wing is firstly done. With this model and the pressure over the wing surface read in certain points and fedback to the control system, changes of the control surface angle on the trailing edge are determined. The attempt to use a simple control system, with a unique pressure sensor shows the viability of implanting this kind of system in real aircrafts. This system may become an alternative to those developed until now, using accelerometers. Yet, it could be useful, in systems where it is necessary to predict stall and observe the pressure load behavior over the wing in flight.

Le contrôle cognitif de l’action est un processus permettant de supprimer un comportement inapproprié au profit d’une action dirigée par l’intention. Il est particulièrement important en situation de conflit où l’expression de comportements alternatifs entre en compétition. Ce processus est largement soutenu par des réseaux cortico-sous-corticaux frontaux dont le bon fonctionnement est impacté par la maladie de Parkinson. Nous nous sommes intéressés au rôle de ces différentes structures cérébrales dans le contrôle cognitif de l’action en s’appuyant sur l’impact de la maladie de Parkinson et de ses traitements. Plus précisément, nous avons discuté des aspects dynamiques de sélection et de suppression des réponses impulsives tel que proposé par le modèle d’activation-suppression dans le cas de réponses oculaires. Nous avons donc adapté une tâche expérimentale de conflit classique, la Simon task, utilisant les mouvements oculaires, et validé son utilisation de notre dans le cadre de ce modèle. Les travaux suivant ont porté sur l’impact de divers facteurs sur ce processus. Nous avons montré que le vieillissement normal exacerbe la sélection impulsive des actions qui pourrait être compensée par la mise en place d’une inhibition sélective plus efficace. Ces résultats sont en accord avec de récentes théories proposant le recrutement plus important des structures préfrontales afin de pallier aux déficits cognitifs entrainés par le vieillissement. Nos résultats ont également indiqué que la maladie de Parkinson entraine une augmentation très importante de la sélection impulsive des actions ce que nous attribuons au dysfonctionnement des boucles cortico-sous-corticales causé par la maladie. Finalement, nous nous sommes intéressés à l’impact de la stimulation cérébrale profonde du noyau subthalamique. Nos résultats préliminaires n’ont pas montré d’effet de ce traitement sur les capacités de contrôle cognitif de l’action. Nous discutons l’ensemble de nos résultats à la lumière des travaux majeurs portant sur les structures cérébrales impliquées dans le contrôle cognitif de l’action et proposons plusieurs perspectives de recherches pouvant avoir un impact fondamental ou clinique. / Cognitive action control is a process that allows suppressing an inappropriate behavior to the benefit of an intentionally-guided action. It is particularly important in situations of conflict when alternative behaviors compete for their expression. This process relies mostly on cortical-subcortical networks which functioning is impaired by Parkinson’s disease. We were interested in the role of these different brain structures in cognitive action control by focusing on the impact of Parkinson’s diseases and its treatments. More precisely, we addressed the dynamic aspects of impulsive action selection and suppression as proposed by the recent activation-suppression model regarding oculomotor responses. We thus adapted a classical experimental conflict task, the Simon task, using eye movements, and validated its use within the context of the activation-suppression model. Our further work focused on the impact of several factors on cognitive action control. We showed that normal aging enhances impulsive action selection that could be compensated for by the set-up of a more efficient selective inhibition. These results are in accordance with recent theories proposing that age-related cognitive deficits are compensated for by an increased recruitment of prefrontal structures. Our results also revealed that Parkinson’s disease results in a strong increase in impulsive action selection which we attribute to the impairment of the cortical-basal ganglia loops. Finally, we were interested by the impact of deep brain stimulation of the subthalamic nucleus. Our preliminary results revealed no effect of this treatment on cognitive action control. We discuss all of our results according to previous researches on the brain structures involved in cognitive action control and we propose several perspective that can have a fundamental or clinical impact.

La protéine p53 est surtout étudiée pour sa capacité à empêcher la prolifération de cellules dont le génome est endommagé. Toutefois, en analysant les souris p53Δ31/Δ31 qui expriment une protéine p53 hyperactive, notre laboratoire a découvert un rôle inattendu de p53 dans la régulation du métabolisme des télomères. Ces souris modélisent la dyskératose congénitale (DC), un syndrome d’insuffisance médullaire héréditaire (SIMH) causé par un dysfonctionnement télomérique. Mon projet de thèse a combiné les analyses de modèles murins et de lignées cellulaires humaines afin d’approfondir l'étude de cette nouvelle fonction de p53 et de mieux comprendre le rôle de la voie p53 dans le développement des SIMH.En poursuivant notre analyse du modèle murin p53Δ31, nous avons montré que les cellules p53Δ31/Δ31 présentent une diminution d’expression de 12 gènes mutés dans l’anémie de Fanconi (AF), un autre SIMH étroitement lié à la DC. De plus, ces cellules montrent une capacité réduite à réparer les ponts inter-brins de l’ADN, une caractéristique typique de l’AF. Notre étude suggère que l’activation soutenue de p53 pourrait ainsi contribuer aux similitudes cliniques entre ces deux syndromes. Par ailleurs, nous avons identifié par quel mécanisme p53 régule négativement le métabolisme des télomères et la voie Fanconi de réparation de l’ADN. Ce mécanisme de régulation indirect, via p21 et E2F4, est très conservé entre la souris et l’Homme. De fait, les cellules p53Δ31/Δ31 constituent un outil puissant pour identifier de nouvelles cibles de p53 réprimées par ce mécanisme. Ainsi, elles nous ont permis de montrer que deux gènes essentiels pour la structure des centromères sont réprimés par p53.L’activation de p53 est clairement impliquée dans les étapes ultimes d’une insuffisance médullaire, mais le rôle d’une suractivation de p53 dans l’initiation d’un SIMH chez l'Homme reste, à ce jour, controversé. En effet, une mutation inactivatrice de la ribonucléase PARN a été trouvée chez des patients atteints de DC. Il a été proposé que cette protéine déstabilise l’ARNm de p53 tout en favorisant la maturation de l’ARN de la télomérase, si bien que les conséquences d’une inactivation de PARN restent mal comprises. Au cours de ma thèse, j'ai également étudié de nouveaux modèles murins et établi des modèles cellulaires humains pour déterminer l’implication d’une activation de p53 dans l’initiation d’un SIMH chez l’homme. Les résultats en cours, particulièrement prometteurs, devraient notamment déterminer l’impact d’une déficience en Parn sur la voie de régulation de p53.En conclusion, nous avons montré qu’une activation soutenue de p53 conduit à des phénotypes principalement associés aux SIMH. Par ailleurs, nous avons montré que p53 réprime de nombreux gènes impliqués dans la maintenance du génome, ce qui peut sembler surprenant au regard du concept de « gardien du génome » communément attribué à p53, et nous a amené à rediscuter ce concept. Ainsi, les résultats obtenus pendant ma thèse devraient permettre de mieux comprendre les mécanismes impliqués dans l’insuffisance médullaire, la suppression tumorale et le vieillissement. / The p53 protein is mostly studied for its capacity to prevent the proliferation of cells with damaged genome. However, while studying p53Δ31/Δ31 mice that express a hyperactive p53 protein, our laboratory uncovered an unexpected role of p53 in the regulation of telomere metabolism. These mice model dyskeratosis congenita (DC), an inherited bone marrow failure syndrome (IBMFS) caused by defects in telomere maintenance. My PhD project combined analyses of mouse models and human cell lines to extend the study of this new function for p53 and to understand the role of the p53 pathway in the development of IBMFS.By extending our analysis of the p53Δ31 mouse model, we revealed that the p53Δ31/Δ31 cells exhibit decreased expression levels for 12 genes mutated in Fanconi anemia (FA), another IBMFS closely related to DC. Furthermore, these cells display a reduced capacity to repair DNA inter-strand crosslinks, a typical feature of FA cells. Our study suggests that a sustained activation of p53 might actually contribute to the clinical overlap between both syndromes. Importantly, we identified the mechanism used by p53 to downregulate telomere metabolism and the FA DNA repair pathway. This regulatory mechanism is indirect, via p21 and E2F4, and largely conserved between mice and humans. In fact, the p53Δ31/Δ31 cells constitute a powerful tool to find p53 target genes downregulated through this regulatory pathway. Accordingly, they were useful to show that two genes essential for centromere structure are also downregulated by p53.p53 activation is clearly involved in the final stages of bone marrow failure, but to-date, the role of p53 hyperactivation in the initiation of IBMFS remains controversial. Indeed, an inactivating mutation of the PARN gene, encoding a ribonuclease, was found in patients with DC. This protein was proposed to destabilize the p53 mRNA while promoting the maturation of the telomerase RNA, so that the consequences of PARN inactivation remain poorly understood. During my thesis, I also studied new mouse models and established human cellular models to determine the contribution of p53 activation in initiating IBMFS in humans. The current results, which are particularly promising, should notably determine the impact of Parn deficiency on the p53 regulatory pathway.In conclusion, we demonstrated that a sustained activation of p53 leads to phenotypes mainly associated with IBMFS. In addition, we showed that p53 suppresses many genes involved in genome maintenance, which may seem surprising in view of the concept of "guardian of the genome" commonly attributed to p53, leading us to revisit this concept. Hence, the results obtained during my thesis should help to better understand the mechanisms involved in bone marrow failure, tumor suppression and aging.