Cette thèse porte sur la déformation et les migrations de fluides associées à la Faille Nord Anatolienne en Mer de Marmara (Turquie).Nous étudions tout d'abord l'évolution de la géométrie et du taux de glissement du système de faille, par deux approches indépendantes: - modélisation thermique de l'histoire d'un bassin, - définition d'un marqueur temporel de type Dépôt de Transport en Masse, daté par interprétation stratigraphique. Nous montrons que: -(1) le système de failles actuel, défini comme une faille principale accommodant la majorité de la déformation inter-plaque, n'a pas significativement évolué depuis 330.000 ± 100.000 ans dans la partie Ouest de la mer; -(2) le système de faille s'est progressivement réorganisé depuis 2.5-1.5 Ma.Dans un deuxième temps, nous étudions les processus d'initiation des Transports en Masse. Nous montrons que: -(1) même si les Transports en Masse sont contrôlés par des processus tectoniques (principalement les séismes et l'extension crustale), leur fréquence et leur taille sont conditionnées par les oscillations glacio-eustatiques; -(2) des Dépôts en Masse ont une périodicité corrélée aux transitions marins/lacustres. Cette cyclicité peut être expliquée par la diffusion d'eau saumâtre, dans les argiles marines entraînant leur gonflement et déstabilisant les sédiments. Dans une troisième partie, nous étudions la diversité des contextes des sites d'émissions de fluides en fonds de mer. Nous montrons que l'occurrence des sites d'émission de fluides est en partie liée au flux ascendant de gaz le long de couches perméables des bassins vers leurs bords, et le long des fractures du socle vers les bords des bassins et les anticlinaux. / This study addresses the issue on the deformation and the fluid migration, associated to the North Anatolian Fault within the Sea of Marmara (Turkey).First, we aim to constrain the evolution of the fault network and the slip rate through time, by two independent approaches: - historical thermal modeling of a basin of the Sea of Marmara; - definition of a Mass Transport Deposit as a fault lateral slip marker, and dated by stratigraphic interpretation. We show that: - (1) the present day fault system, formed by a main fault which accommodated the main part of the inter-plate deformation does not significantly evolved since 330.000 ± 100.000 years - (2) a progressive reorganization of the fault network occurred since the last 2.5-1.5 Ma.Secondly, we discuss the triggers of Mass Transport Processes. We show that: - (1) despite submarine mass movements are related to tectonic activity (mainly earthquakes and crustal stretching), their frequency and their size are also modulated by glacio-eustatic changes; -(2) remarkable Mass Transport Deposits display some cyclicity in stratigraphic sequences which are apparently correlated to transitions between salty marine and lacustrine environments. This cyclicity is perhaps explained by marine clay activity (swelling) under low brackish-fresh water conditions, which can trigger sediment destabilization.Third, we investigate the diversity of active fluid seepages contexts. We propose that the widespread occurrence of fluid expulsion sites can be explained by up-dip gas migration by buoyancy along permeable strata toward their edges, and along fractures within the basement toward both the edges of the basins and topographic highs.

O desmame precoce (DP) causa mudanças na mucosa gástrica, como o aumento da proliferação celular e da expressão do Fator de Crescimento Transformante (TGFa). Neste trabalho, avaliamos o papel desse peptídeo e seu receptor EGFR no controle do crescimento gástrico. Ratos com 15 dias de vida foram divididos em: amamentados (controle) e DP, no qual os filhotes foram separados da mãe e alimentados com pasta de ração. O DP aumentou o número de células marcadas para EGFR, acelerou a diferenciação de células mucosas do colo e elevou a expressão de mucina 6. A inibição do EGFR com AG1478 diminuiu a proliferação celular e o número de células mucosas do colo. Entre as proteínas envolvidas na sinalização de EGFR e ciclo celular, detectamos que o DP elevou os níveis de p-ERK1/2 e p-Src e não alterou p-Akt, p21 e p27. Nós sugerimos que o padrão alimentar influencia a proliferação e diferenciação no epitélio gástrico, e que TGFa/EGFR podem regular esses processos durante o desenvolvimento pós-natal, provavelmente por ativação das vias de sinalização de MAPK e Src. / Early weaning (EW) causes changes in the gastric mucosa, including the increase in cell proliferation and Transforming Growth Factor (TGFa). In the present study, we evaluated the role of this peptide and its receptor EGFR in the control of the gastric growth. 15-d-old rats were divided into two groups: suckling (control) and EW, in which the pups were separated from the dam and fed with powdered chow. EW increased the number of EGFR-positive cells, accelerated the differentiation of mucous neck cells and augmented the expression of mucin 6. EGFR inhibition with AG1478 decreased cell proliferation and the number of mucous neck cells. Among the proteins involved on EGFR signaling pathways and cell cycle, we found that EW increased the levels of p-ERK1/2 and p-Src, but did not change p-Akt, p21 and p27. We suggest that the diet pattern influences proliferation and differentiation in the gastric epithelium, and the TGFa/EGFR can regulate these processes throughout the postnatal development, probably by activating MAPK and Src signaling pathways.

O desmame precoce (DP) causa mudanças na mucosa gástrica, como o aumento da proliferação celular e da expressão do Fator de Crescimento Transformante (TGFa). Neste trabalho, avaliamos o papel desse peptídeo e seu receptor EGFR no controle do crescimento gástrico. Ratos com 15 dias de vida foram divididos em: amamentados (controle) e DP, no qual os filhotes foram separados da mãe e alimentados com pasta de ração. O DP aumentou o número de células marcadas para EGFR, acelerou a diferenciação de células mucosas do colo e elevou a expressão de mucina 6. A inibição do EGFR com AG1478 diminuiu a proliferação celular e o número de células mucosas do colo. Entre as proteínas envolvidas na sinalização de EGFR e ciclo celular, detectamos que o DP elevou os níveis de p-ERK1/2 e p-Src e não alterou p-Akt, p21 e p27. Nós sugerimos que o padrão alimentar influencia a proliferação e diferenciação no epitélio gástrico, e que TGFa/EGFR podem regular esses processos durante o desenvolvimento pós-natal, provavelmente por ativação das vias de sinalização de MAPK e Src. / Early weaning (EW) causes changes in the gastric mucosa, including the increase in cell proliferation and Transforming Growth Factor (TGFa). In the present study, we evaluated the role of this peptide and its receptor EGFR in the control of the gastric growth. 15-d-old rats were divided into two groups: suckling (control) and EW, in which the pups were separated from the dam and fed with powdered chow. EW increased the number of EGFR-positive cells, accelerated the differentiation of mucous neck cells and augmented the expression of mucin 6. EGFR inhibition with AG1478 decreased cell proliferation and the number of mucous neck cells. Among the proteins involved on EGFR signaling pathways and cell cycle, we found that EW increased the levels of p-ERK1/2 and p-Src, but did not change p-Akt, p21 and p27. We suggest that the diet pattern influences proliferation and differentiation in the gastric epithelium, and the TGFa/EGFR can regulate these processes throughout the postnatal development, probably by activating MAPK and Src signaling pathways.