Es werden effiziente Algorithmen vorgestellt, die auf algebraischen Methoden beruhen um die Unerfüllbarkeit aussagenlogischer 4-SAT Formeln zu zertifizieren. Die Algorithmen werden implementiert und auf praktische Weise hinsichtlich der Laufzeit mit Backtracking-Algorithmen verglichen.

Ramanujan introduced his now celebrated mock theta functions in 1920, grouping them into families parameterized by an integer called the order. In 2010 Bringmann and Ono discovered generalizations of Ramanujan's mock theta functions for any order relatively prime to 6; this result was later strengthened by Garvan in 2016. It was also shown that by adding suitable nonholomorphic completion terms to the mock theta functions the family of mock theta functions corresponding to a given order constitute a complex vector space which is closed under the action of the modular group. We strengthen the Bringmann, Ono, and Garvan result by constructing a vector-valued modular form of weight 1/2 transforming according the Weil representation for orders greater than 3 by introducing an algorithm which simultaneously numerically constructs the form and proves its transformation laws. We also explicitly construct the 7th order form and prove analytically that it has the proper modular transformations. It is conjectured the same method will apply for other orders.

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Vision identifies objects rapidly and efficiently. In contrast, object recognition by touch is much slower. Furthermore, haptics usually serially accumulates information from different parts of objects, whereas vision typically processes object information in parallel. Is haptic object identification slower simply due to sequential information acquisition and the resulting memory load or due to more fundamental processing differences between the senses? To compare the time course of visual and haptic object recognition, we slowed visual processing using a novel, restricted viewing technique. In an electroencephalographic (EEG) experiment, participants discriminated familiar, nameable from unfamiliar, unnamable objects both visually and haptically. Analyses focused on the evoked and total fronto-central theta-band (5–7 Hz; a marker of working memory) and the occipital upper alpha-band (10–12 Hz; a marker of perceptual processing) locked to the onset of classification. Decreases in total upper alpha-band activity for haptic identification of objects indicate a likely processing role of multisensory extrastriate areas. Long-latency modulations of alpha-band activity differentiated between familiar and unfamiliar objects in haptics but not in vision. In contrast, theta-band activity showed a general increase over time for the slowed-down visual recognition task only. We conclude that haptic object recognition relies on common representations with vision but also that there are fundamental differences between the senses that do not merely arise from differences in their speed of processing.

京都大学 / 新制・課程博士 / 博士(理学) / 甲第23679号 / 理博第4769号 / 新制||理||1683(附属図書館) / 京都大学大学院理学研究科数学・数理解析専攻 / (主査)教授 池田 保, 教授 雪江 明彦, 准教授 市野 篤史 / 学位規則第4条第1項該当 / Doctor of Science / Kyoto University / DFAM

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Clostridium perfringens is the most common cause of gas gangrene (clostridial myonecrosis), a disease that begins when ischemic tissues become contaminated with C. perfringens. C. perfringens quickly multiplies in ischemic tissues and spreads to healthy areas, leading to high levels of morbidity and mortality. As a species, the bacterium can synthesize thirteen different toxins. The alpha toxin (PLC) and perfringolysin O (PFO) are thought to be important virulence factors in gangrene. We wished to understand how C. perfringens is capable of avoiding killing by the host immune system, and determine if PLC and PFO play a role in this avoidance. We found C. perfringens was not killed by J774-33 cells or mouse peritoneal macrophages under aerobic or anaerobic conditions. Using electron microscopy, we showed that C. perfringens could escape the phagosome of J774-33 and mouse peritoneal macrophages. We believe the ability of C. perfringens to survive in the presence of macrophages is due to its ability to escape the phagosome. Using a variety of inhibitors of specific receptors, we identified those used by J774-33 cells to phagocytose C. perfringens. The scavenger receptor, mannose receptor(s), and complement receptor (CR3) were involved in the phagocytosis of C. perfringens. To determine if PFO or PLC were involved in the ability of C. perfringens to survive in the presence of macrophages, we constructed C. perfringens strains lacking these toxins. The ability of C. perfringens to survive in the presence of J774-33 cells is dependent on PFO, while survival in mouse peritoneal macrophages is dependent on PFO and PLC. The ability of C. perfringens to escape the phagosome of J774-33 cells and mouse peritoneal macrophages is mediated by either PFO or PLC. Using a mouse model, we found that PFO and PLC were necessary for C. perfringens to survive in vivo using infectious doses 1000 times lower than those required to initiate a gangrene infection. We propose that PFO and PLC play a critical role in the survival of C. perfringens during the early stages of gangrene infections, when phagocytic cells are present and bacterial numbers are low. / Ph. D.

Les mécanismes cellulaires et moléculaires qui sous-tendent la mémoire et l’apprentissage chez les mammifères sont incomplètement compris. Le rythme thêta de l’hippocampe constitue l’état « en ligne » de cette structure qui est cruciale pour la mémoire déclarative. Dans la région CA1 de l’hippocampe, les interneurones inhibiteurs LM/RAD démontrent des oscillations de potentiel membranaire (OPM) intrinsèques qui pourraient se révéler importantes pour la génération du rythme thêta. Des travaux préliminaires ont suggéré que le courant K+ I(A) pourrait être impliqué dans la génération de ces oscillations. Néanmoins, peu de choses sont connues au sujet de l’identité des sous-unités protéiques principales et auxiliaires qui soutiennent le courant I(A) ainsi que l’ampleur de la contribution fonctionnelle de ce courant K+ dans les interneurones. Ainsi, cette thèse de doctorat démontre que le courant I(A) soutient la génération des OPM dans les interneurones LM/RAD et que des protéines Kv4.3 forment des canaux qui contribuent à ce courant. De plus, elle approfondit les connaissances sur les mécanismes qui régissent les interactions entre les sous-unités principales de canaux Kv4.3 et les protéines accessoires KChIP1. Finalement, elle révèle que la protéine KChIP1 module le courant I(A)-Kv4.3 natif et la fréquence de décharge des potentiels d’action dans les interneurones. Nos travaux contribuent à l’avancement des connaissances dans le domaine de la modulation de l’excitabilité des interneurones inhibiteurs de l’hippocampe et permettent ainsi de mieux saisir les mécanismes qui soutiennent la fonction de l’hippocampe et possiblement la mémoire chez les mammifères. / Cellular and molecular mechanisms underlying learning and memory in mammals are incompletely understood. The theta rhythm in the hippocampus constitutes the « on-line » state of this structure which is crucial for declarative memory. In the CA1 hippocampal area, LM/RAD inhibitory interneurons exhibit intrinsic membrane potential oscillations (MPOs) that could be important for the generation of theta rhythm. Preliminary work suggested that K+ current I(A) could be involved in the generation of these oscillations. Nevertheless, little is known about the identity of the principal and auxiliary protein subunits underlying I(A) current and the extent of the functional contribution of this K+ current in hippocampal interneurons. Thus, this Ph.D. thesis shows that I(A) current underlies MPO generation in LM/RAD interneurons and that Kv4.3 proteins form channels that contribute to this current. Also, it deepens the knowledge on the mechanism controlling the interactions between Kv4.3 channel-forming principal subunits and KChIP1 auxiliary proteins. Finally, it reveals that KChIP1 modulates native I(A)-Kv4.3 current and the action potential discharge frequency in interneurons. Our work takes part in advancing the knowledge on the field of modulation of excitability in hippocampal inhibitory interneurons and allows a better understanding of the mechanisms underlying the function of the hippocampus and possibly memory in mammals.

La douleur sociale est une forme de douleur non physique dérivant de la perception de l'exclusion sociale. L'importance de la compréhension de ses modulations comportementales et neuronales est fondamentale, car ses conséquences sur le long terme peuvent être très néfastes. Dans ce travail de thèse, j'ai exploré ces aspects à travers une étude comportementale à l‟aide d‟enregistrements par SCR (Skin Conductance Recording), et trois études en iEEG (électro-encéphalographie intracrânienne) chez des patients épileptiques. La première étude comportementale a exploré la direction dans laquelle l'exclusion sociale est influencée par une récompense et ses réactions sur le long terme. Ainsi, la récompense monétaire altère l'équilibre social et augmente l‟activité électrodermale. La personne ayant été exclue met alors en oeuvre des mécanismes de vengeance en défavorisant la personne qui l‟a exclue précédemment. Les études en iEEG ont été une fenêtre unique d'exploration du cerveau lors de différentes types de modulation de l'exclusion. Dans la première étude en iEEG, nous avons observé que la douleur sociale produit une activation des oscillations thêta (3-7 Hz), lors de d'exclusion, dans l'insula, l'ACC, le cortex préfrontal et le gyrus fusiforme. La deuxième étude iEEG s'est intéressée aux modulations produites par la douleur sociale dans BA 19 et BA 17 présentant des P1 d'amplitude majeure lors de l'observation des photos du joueur qui exclut. La troisième étude en iEEG a exploré la réponse neuronale de l'influence d'une variable monétaire lors de l'exclusion. Nos résultats démontrent que l'insula postérieure présente une activation thêta indépendante du fait que l'exclusion soit positive (exclusion et gain d'argent) ou encore négative (exclusion et perte d'argent), à la différence de l'insula antérieure, active seulement lors d'une exclusion négative / Pain is a form of social non-physical pain arising from the perception of social exclusion. The importance of understanding its behavioral and neuronal modulations has a critical value, since its long lasting consequences can be extremely harmful. In this thesis I firstly explored these issues through a behavioral SCR study (Skin Conductance Recording), and successively through three iEEG studies in patients with epilepsy (intracranial EEG). The SCR study explored the direction in which social exclusion is influenced by a reward and its long lasting reactions. Money affects social equilibrium and increases the SCR pics. The excluded individual implements revenge attitudes toward the person who excluded in a previuous interaction. The iEEG studies were a unique window for exploring the brain during different types of social pain modulations. In the first iEEG study, we found that social pain produced activation of theta oscillations (3-7 Hz) during exclusion in the insula, in the ACC, in the prefrontal cortex and in the fusiform face area. The second iEEG study wanted to explore deeply the primitive modulations produced by social pain in visual area. We found in BA 19 and BA 17 greater P1 peak amplitude during excluder pictures presentation. The third iEEG study investigated the neuronal modulations produced by a monetary reward during social pain. These results demonstrated that the posterior insula has a theta activation independent of whether the exclusion is positive (excluded but gaining money) or more negative (excluded but losing money), whereas the anterior insula, has a theta activation only during a negative exclusion