Cette recherche s'inscrit dans la problématique de l'étude de prises de décisions didactiques. Notre principal intérêt est d'étudier la façon dont les professeurs prennent les décisions didactiques afin de faire avancer les élèves vers l'apprentissage d'une connaissance visée, et les éléments qui influencent ces décisions. Ceci nous a amené dans un premier temps à modéliser les connaissances des élèves concernant un objet mathématique donné, la symétrie orthogonale. <br />En nous appuyant sur la formalisation proposée par le modèle cK¢ (Balacheff, 1995) au sein de la Théorie des Situations Didactiques, nous avons fait le choix d'entrer dans la modélisation des conceptions d'élèves sur la notion de symétrie orthogonale, à partir de l'identification de la structure de contrôle des conceptions. En partant de l'hypothèse que les contrôles rendent compte des critères qui renvoient au choix, à la décision, à l'adéquation et à la validité d'une action, nous avons réalisé une étude théorique de la notion de symétrie orthogonale du point de vue mathématique et didactique afin d'identifier a priori les contrôles susceptibles d'être mobilisés par les élèves dans la résolution de problèmes de construction et de reconnaissance de figures symétriques. Ceci nous a permis de construire un dispositif expérimental pour étudier la prise de décisions didactiques. <br />Pour réaliser cette étude, nous nous sommes appuyés sur le modèle des niveaux de l'activité des professeurs (Margolinas, 2002). Nous avons ainsi pu identifier quelques éléments sur lesquels les professeurs fondent leurs décisions didactiques.

This Master's thesis presents a novel approach for detecting and predicting attack vectors based on genetic programming. The proposed method utilizes a genetic algorithm to evolve a set of rules that predict attack vectors over the system based on caught indicators of compromise. The generated rules are then used to identify potential attack vectors and predict how it started and how it will develop in future. The research aims to improve the accuracy and efficiency of existing methods for attack detection and prediction. The proposed approach is evaluated using real-world attack data and compared against several state-of-the-art techniques. Results indicate that the proposed method outperforms existing approaches in terms of detection accuracy and prediction capability. This research has important implications for the field of cybersecurity and can assist organizations in developing more effective and proactive defense strategies against cyberattacks. Background. Cybersecurity is an increasingly critical issue in today's digital age. Cyberattacks are becoming more sophisticated, making it challenging for traditional defense mechanisms to detect and prevent them. Therefore, it is crucial to develop new and innovative methods for identifying and predicting potential attack vectors. In this context, this Master's thesis presents a novel approach to detecting and predicting attack vectors based on genetic programming. The proposed method aims to improve the accuracy and efficiency of existing approaches to cyberattack detection and prediction. Objectives.This Master’s thesis aims to reach the following objectives: 1. To identify the limitations of existing approaches to cyberattack detection and prevention and propose a novel method based on genetic programming. 2. To develop a genetic programming-based algorithm to evolve a model for attack-vectors prediction. 3. To evaluate the effectiveness of the proposed approach using real-world attack data Methods. The methods used in this Master's thesis combine literature review, data collection, algorithm development, experimentation, data analysis, and recommendations to improving approach to detecting and predicting attack vectors using genetic programming. The research aims to contribute to the field of cybersecurity by advancing our understanding of cyberattack detection and prevention. Results. The proposed method has the potential to enhance the accuracy and efficiency of cyberattack detection and prediction, which can help organizations prevent or mitigate the impact of cyberattacks. Future improvements can include more complex MITRE ATT&amp;CK datasets, including Mobile and ICS matrices. Conclusions. The genetic programming-based algorithm developed in this thesis was shown to be effective in detecting and predicting attack vectors using real-world attack data. The proposed approach has the potential to improve organizations' cybersecurity posture by providing a proactive defense strategy against cyberattacks.

No description available.

Made available in DSpace on 2016-06-02T19:22:57Z (GMT). No. of bitstreams: 1 4611.pdf: 1042877 bytes, checksum: b9b33a5c88aa13696432ae2d728a0a21 (MD5) Previous issue date: 2012-05-22 / Financiadora de Estudos e Projetos / Previous animal s research has shown that many protocols with aimed to mimic human exercise has been used. The endurance protocols are studied very often however, some difficulties are encountered to produce resistance exercise protocols. Some animal models of resistance training have been used, as jumping exercise. Among these, stands out the rat model performed on ladder with healthy and unhealthy animals. However, the energy system and acute physiological responses associated with this protocol have not been determined. Thus, the aim of the present study was to evaluate the acute metabolic characteristics and the acute effects on indirect biomarkers of muscular microtrauma of acute resistance exercise performed on ladder. Fifty males Wistar rats were randomly divided into two groups: Exercise (E) and Control (C). The animals of E group climbed a vertical ladder with weights attached to their tails. The session was performed once with 4 9 climbs. The lactate concentration increased at the beginning of training and there was a tendency to stabilize the blood lactate during the exercise session. Serum corticosterone found in E group was significantly higher (59%; p<0.05) when compared to C group. There was no difference between free fatty acids (24% p=0.109), in the liver (8%; p=0.575) and in the gastrocnemius fatty acids content (17%; p=0.219). The glycogen in liver (42%; p<0.05) and soleus (56%; p<0.05) were different between groups. Lactate Dehydrogenase (LDH) and Creatine Kinase (CK) activities were significantly higher (LDH 32%; CK 27%; p<0.05) in the E than in the C group. The results suggest that this protocol is a high intensity exercise able to induce an increase in the lactate concentration at the beginning of exercise. Moreover, there were increases in indirect markers of muscle microtrauma in rats after a single exhaustive session. However, the lactate concentration was low, suggesting that the aerobic metabolism is an important factor during the intervals between the series of climbing. / Atualmente, pesquisas com animais usam muitos protocolos de exercícios, com o objetivo de mimetizar as condições de exercícios realizados por humanos. Os protocolos de endurance (aeróbios) são estudados com grande frequência, no entanto algumas dificuldades são encontradas no sentido de produzir um protocolo de exercício resistido para animais. Alguns protocolos foram criados, utilizando principalmente modelos onde os animais realizam saltos. Um protocolo que tem se destacado é o de escalada e tem sido largamente utilizado em animais saudáveis e não saudáveis. Entretanto, as respostas fisiológicas agudas desse protocolo não foram determinadas até o momento. Portanto, o objetivo do presente estudo foi avaliar as características metabólicas agudas do exercício resistido realizado em escada, e examinar os efeitos agudos em marcadores indiretos de lesão muscular. Foram utilizados 50 ratos Wistar divididos randomicamente em dois grupos: Controle (C) e Exercício Resistido (ER). Os animais do grupo ER escalaram uma escada vertical de 1,1 m com pesos fixados em suas caudas. Foi realizada somente uma sessão com 4-9 escaladas. Os níveis de lactato foram maiores nas primeiras escaladas em relação ao repouso, e se mantiveram constantes até o final do exercício. As concentrações de corticosterona encontradas no grupo ER foram maiores (59%; p<0,05) quando comparadas ao grupo C. Não houve diferença significativa no conteúdo de ácidos graxos do plasma (24% p=0,109), do fígado (8%; p=0,575) e do músculo gastrocnêmio (17%; p=0,219). O conteúdo de glicogênio hepático (42%; p<0,05) e muscular (sóleo) (56%; p<0,05) foi diferente entre os grupos. Os níveis de Lactato Desidrogenase (LDH) e Creatina Kinase (CK) foram maiores (LDH 32%; CK 27%; p<0,05) no grupo ER quando comparados ao grupo C. Os resultados sugerem que esse protocolo de exercício resistido é um exercício de alta intensidade, visto que a concentração de lactato aumentou no início do exercício e houve um maior nível de microlesão muscular após o exercício. No entanto, a concentração do lactato foi baixa, sugerindo que o metabolismo aeróbio contribui de forma importante durante os intervalos entre as séries de escalada.

Les travaux réalisés durant la thèse s'inscrivent dans une problématique scientifique liée à l'étude des transferts radiatifs. Plus particulièrement, l'application de cette étude est la télédétection infrarouge d'un écoulement diphasique réactif et turbulent à haute température. Cette étude a pour objectif la modélisation et la simulation du rayonnement infrarouge émis par cet écoulement et re¸cu par un détecteur. Pour développer un outil de simulation numérique de la signature infrarouge d'un jet de gaz et de particules à haute température, les espèces majoritaires qui sont responsables de l'émission du rayonnement ont été identifiées lors d'expérimentations. Les campagnes expérimentales ont permis la construction de bases de données concernant les gaz (CO2-CO-H2O) et les particules (oxydes métalliques) présents dans le jet. Connaissant la nature des gaz et des particules, le calcul de leurs propriétés radiatives doit être réalisé. Cette étape est nécessaire puisque ces propriétés caractérisent l'émission de rayonnement par le jet et elles doivent être connues pour résoudre l'équation de transfert radiatif. Pour les gaz, un code de calcul raie par raie de spectres synthétiques a été développé. De plus, pour diminuer le temps de calcul d'une signature infrarouge, il est préférable d'utiliser des modèles spectraux de bandes étroites. Le modèle de télédétection infrarouge est un modèle spectral utilisant des k(coefficient d'absorption)-distributions sous l'hypothèse des k-corrélés avec l'approximation d'un gaz unique pour le mélange associée à l'hypothèse des gaz fictifs. Les paramètres de ce modèle (CKFG-SMG), ont été tabulés et validés dans l'étude. En ce qui concerne les propriétés radiatives des nuages de particules sphériques, le modèle de Mie est utilisé car il est valable pour les gammes de fractions volumiques rencontrées. Pour tester l'influence de la diffusion, une étude de sensibilité à la diffusion a été réalisée. En effet, nous avons quantifié l'erreur commise sur le flux émis par différentes couches si les processus de diffusion du rayonnement sont négligés. Cette étude a montré que l'influence de la diffusion peut être négligée dans le cadre de notre étude. La modélisation de la signature infrarouge du jet diphasique réactif issu de la combustion du matériau pyrotechnique, nécessite la connaissance des températures et des concentrations en gaz et particules, en tous les points du jet. Ce jet diphasique réactif a été simulé à l'aide du logiciel Fluent. De plus, une interface graphique a été développée qui recrée la scène optronique en se servant des profils aérothermochimiques du jet diphasique et des données concernant la position du détecteur. De cette fa¸con, un outil de simulation numérique de la signature infrarouge du jet (SIRJET) a été développé qui inclue un modèle de transfert radiatif (lancer de rayon) ainsi que les paramètres tabulés (gaz et particules) du modèle spectral de télédétection infrarouge (CK, CKFG, CK-SMG, CKFG-SMG). Enfin, une confrontation est présentée entre une mesure et le résultat d'une simulation de la signature infrarouge d'un jet diphasique à haute température.

O primeiro artigo desse estudo apresenta a ocorrência de um surto de intoxicação por monensina em búfalos de um rebanho misto com bovinos, os quais não foram afetados. Tal fato sugeriu a possibilidade de que búfalos fossem menos tolerantes à monensina que bovinos. Embora com número reduzido de animais experimentais, dados preliminares foram compatíveis com essa hipótese. O segundo artigo desse trabalho descreve detalhadamente achados clínicopatológicos da intoxicação por monensina em búfalos, confirma a maior susceptibilidade dos búfalos (em comparação com bovinos) à monensina e determina a mínima dose tóxica de monensina para búfalos. Sinais clínicos e lesões característicos de intoxicação por monensina foram induzidos em búfalos dosados (1 dia) com 15, 10, 7,5 e 5 mg/kg de monensina. Apenas os búfalos dosados com 2,5 (1 dia) e 1 mg/kg (7 dias) de monensina não morreram. Os sinais clínicos iniciaram aproximadamente 6 h após dosagem com monensina e incluíram apatia, anorexia, diarréia, sialorréia, fraqueza muscular, taquicardia, dificuldade locomotora, dispnéia, distensão da jugular, decúbito e morte. As dosagens de creatinina quinase (CK) dos búfalos aumentaram acentuadamente após dosagem com monensina. As alterações macroscópicas foram ascite, hidrotórax, hidropericárdio, cardiomegalia, hepatomegalia e áreas pálidas focais no miocárdio e nos músculos esqueléticos. Degeneração e necrose de miofibras foram os principais achados histopatológicos. Os búfalos intoxicados naturalmente no surto desenvolveram predominantemente lesões nos músculos esqueléticos e os búfalos experimentais tiveram lesões cardíacas mais pronunciadas. Por outro lado, nenhuma evidência de doença, nem mesmo alteração nos níveis de CK, foram observados nos bovinos dosados com as mesmas dosagens de monensina, confirmando observações preliminares que esses animais são mais resistentes à monensina que os búfalos. / The first article of this study reports the occurrence of an outbreak of monensin toxicosis in water buffaloes from a feedlot in which buffaloes and cattle were kept together but only the former were affected. This suggested that buffaloes were less tolerant to monensin than cattle. Although tested with small number of experimental animals, preliminary data were consistent with this hypothesis. The second manuscript describes the clinicopathological findings in monensin toxicosis in water buffaloes, confirms that buffaloes are more susceptible to monensin than cattle, and presents the minimal toxic dosage of monensin to buffaloes. Typical clinical signs and lesions of monensin intoxication were induced in water buffaloes dosed with single doses of 15, 10, 7.5, and 5 mg/kg of monensin. Only buffaloes dosed with 2.5 mg/kg (1 d) and 1 mg/kg (7 d) survived. Clinical signs initiated approximately 6 h postdosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the main histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. Buffaloes in field cases predominantly developed lesions in skeletal muscles, and those from the trial had cardiac lesions as the most pronounced changes. In addition, this report presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as monitoring tools in the management of buffalo herds supplemented with monensin.

O primeiro artigo desse estudo apresenta a ocorrência de um surto de intoxicação por monensina em búfalos de um rebanho misto com bovinos, os quais não foram afetados. Tal fato sugeriu a possibilidade de que búfalos fossem menos tolerantes à monensina que bovinos. Embora com número reduzido de animais experimentais, dados preliminares foram compatíveis com essa hipótese. O segundo artigo desse trabalho descreve detalhadamente achados clínicopatológicos da intoxicação por monensina em búfalos, confirma a maior susceptibilidade dos búfalos (em comparação com bovinos) à monensina e determina a mínima dose tóxica de monensina para búfalos. Sinais clínicos e lesões característicos de intoxicação por monensina foram induzidos em búfalos dosados (1 dia) com 15, 10, 7,5 e 5 mg/kg de monensina. Apenas os búfalos dosados com 2,5 (1 dia) e 1 mg/kg (7 dias) de monensina não morreram. Os sinais clínicos iniciaram aproximadamente 6 h após dosagem com monensina e incluíram apatia, anorexia, diarréia, sialorréia, fraqueza muscular, taquicardia, dificuldade locomotora, dispnéia, distensão da jugular, decúbito e morte. As dosagens de creatinina quinase (CK) dos búfalos aumentaram acentuadamente após dosagem com monensina. As alterações macroscópicas foram ascite, hidrotórax, hidropericárdio, cardiomegalia, hepatomegalia e áreas pálidas focais no miocárdio e nos músculos esqueléticos. Degeneração e necrose de miofibras foram os principais achados histopatológicos. Os búfalos intoxicados naturalmente no surto desenvolveram predominantemente lesões nos músculos esqueléticos e os búfalos experimentais tiveram lesões cardíacas mais pronunciadas. Por outro lado, nenhuma evidência de doença, nem mesmo alteração nos níveis de CK, foram observados nos bovinos dosados com as mesmas dosagens de monensina, confirmando observações preliminares que esses animais são mais resistentes à monensina que os búfalos. / The first article of this study reports the occurrence of an outbreak of monensin toxicosis in water buffaloes from a feedlot in which buffaloes and cattle were kept together but only the former were affected. This suggested that buffaloes were less tolerant to monensin than cattle. Although tested with small number of experimental animals, preliminary data were consistent with this hypothesis. The second manuscript describes the clinicopathological findings in monensin toxicosis in water buffaloes, confirms that buffaloes are more susceptible to monensin than cattle, and presents the minimal toxic dosage of monensin to buffaloes. Typical clinical signs and lesions of monensin intoxication were induced in water buffaloes dosed with single doses of 15, 10, 7.5, and 5 mg/kg of monensin. Only buffaloes dosed with 2.5 mg/kg (1 d) and 1 mg/kg (7 d) survived. Clinical signs initiated approximately 6 h postdosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the main histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. Buffaloes in field cases predominantly developed lesions in skeletal muscles, and those from the trial had cardiac lesions as the most pronounced changes. In addition, this report presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as monitoring tools in the management of buffalo herds supplemented with monensin.

O primeiro artigo desse estudo apresenta a ocorrência de um surto de intoxicação por monensina em búfalos de um rebanho misto com bovinos, os quais não foram afetados. Tal fato sugeriu a possibilidade de que búfalos fossem menos tolerantes à monensina que bovinos. Embora com número reduzido de animais experimentais, dados preliminares foram compatíveis com essa hipótese. O segundo artigo desse trabalho descreve detalhadamente achados clínicopatológicos da intoxicação por monensina em búfalos, confirma a maior susceptibilidade dos búfalos (em comparação com bovinos) à monensina e determina a mínima dose tóxica de monensina para búfalos. Sinais clínicos e lesões característicos de intoxicação por monensina foram induzidos em búfalos dosados (1 dia) com 15, 10, 7,5 e 5 mg/kg de monensina. Apenas os búfalos dosados com 2,5 (1 dia) e 1 mg/kg (7 dias) de monensina não morreram. Os sinais clínicos iniciaram aproximadamente 6 h após dosagem com monensina e incluíram apatia, anorexia, diarréia, sialorréia, fraqueza muscular, taquicardia, dificuldade locomotora, dispnéia, distensão da jugular, decúbito e morte. As dosagens de creatinina quinase (CK) dos búfalos aumentaram acentuadamente após dosagem com monensina. As alterações macroscópicas foram ascite, hidrotórax, hidropericárdio, cardiomegalia, hepatomegalia e áreas pálidas focais no miocárdio e nos músculos esqueléticos. Degeneração e necrose de miofibras foram os principais achados histopatológicos. Os búfalos intoxicados naturalmente no surto desenvolveram predominantemente lesões nos músculos esqueléticos e os búfalos experimentais tiveram lesões cardíacas mais pronunciadas. Por outro lado, nenhuma evidência de doença, nem mesmo alteração nos níveis de CK, foram observados nos bovinos dosados com as mesmas dosagens de monensina, confirmando observações preliminares que esses animais são mais resistentes à monensina que os búfalos. / The first article of this study reports the occurrence of an outbreak of monensin toxicosis in water buffaloes from a feedlot in which buffaloes and cattle were kept together but only the former were affected. This suggested that buffaloes were less tolerant to monensin than cattle. Although tested with small number of experimental animals, preliminary data were consistent with this hypothesis. The second manuscript describes the clinicopathological findings in monensin toxicosis in water buffaloes, confirms that buffaloes are more susceptible to monensin than cattle, and presents the minimal toxic dosage of monensin to buffaloes. Typical clinical signs and lesions of monensin intoxication were induced in water buffaloes dosed with single doses of 15, 10, 7.5, and 5 mg/kg of monensin. Only buffaloes dosed with 2.5 mg/kg (1 d) and 1 mg/kg (7 d) survived. Clinical signs initiated approximately 6 h postdosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the main histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. Buffaloes in field cases predominantly developed lesions in skeletal muscles, and those from the trial had cardiac lesions as the most pronounced changes. In addition, this report presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as monitoring tools in the management of buffalo herds supplemented with monensin.

La morphine constitue l'un des analgésiques les plus utilisés en milieu hospitalier pour soulager les douleurs aiguës et chroniques. Elle exerce ses effets analgésiques en se liant aux récepteurs opioïdes μ (MOR) présents au niveau central et périphérique et possède des effets secondaires, incluant la tolérance, qui limitent son usage à long terme. La première partie de mes travaux avait pour objectif d'étudier le phénomène de tolérance à la morphine et d'en déterminer les mécanismes sous-jacents. A l'heure actuelle, ce phénomène est décrit comme résultant d'une désensibilisation des MOR conduisant à leur endocytose. Nos résultats montrent qu'en cas de tolérance, le catabolisme de la morphine est exacerbé au niveau du système nerveux central. Mes travaux ont également porté sur la caractérisation de la Créatine Kinase (CK) comme étant une protéine liant la morphine à très haute affinité. Nos résultats montrent que la CK possède 2 sites de liaison pour la morphine avec des affinités similaires. En étudiant l'effet potentiel de la CK sur l'analgésie induite par la morphine in vivo, nous avons mis en évidence, que les peptides correspondant aux 2 sites de liaison à la morphine étaient par eux-mêmes analgésiques et que cette analgésie semblait dépendre des récepteurs opioïdes. / Morphine is one of the most used analgesics in hospitals to relieve acute and chronic pain. Morphine exerts its analgesic effects by binding central and peripheral μ opioid receptors (MORs) and has many side effects that limit its long-term use including tolerance. The first part of my thesis was aimed to study the phenomenon of morphine tolerance and to determine the underlying mechanisms. Previously, this phenomenon was explained as resulting !rom MORs desensitization by endocytosis. However, our results show that in case of tolerance, the catabolism of morphine is exacerbated in the central nervous system in particular in astocytes. The second part of my work has focused on the characterization of the Creatine Kinase (CK) as a novel protein that binds morphine with a high affinity. Our results showed that CK has two binding sites with a similar affinity for morphine. Surprisingly, by studying the potential effect of CK on morphine-induced analgesia in vivo, we noticed that the two peptides corresponding to morphine binding sites are analgesics and such analgesia seems to be mediated by opioid receptors.

No description available.