Cette thèse traite des technologies persuasives et plus particulièrement de leur adaptation, pour en optimiser l’efficacité et la pertinence auprès de l’utilisateur. Les technologies persuasives sont des technologies conçues pour modifier le comportement de leurs utilisateurs, sans utilisation de la coercition ni de la tromperie. L’étude de la persuasion technologique se caractérise par un grand nombre de techniques pour altérer le comportement de l’utilisateur, mais des méthodes pour mettrent en oeuvre ces technologies encoreperfectibles.Elles ont pour fondement la persuasion inter-personnelle, étudiée depuis plus de deux millénaires dans le champ de la rhétorique, de la philosophie, et plus récemment de la psychologie. Cette dernière discipline proposent des théories et modèles pour rendre compte et comprendre les processus à l’oeuvre dans le choix d’un comportement. Ces théories nous montrent en particulier que les situations persuasives sont complexes, variées, avec de nombreux facteurs d’influence. C’est pourquoi nous proposons la notion de technologies persuasives adaptatives, des technologies capables d’adapter leurs stratégies de persuasion à l’utilisateur dans son contexte. Pour mettre en oeuvre ces dispositifs, nous proposons dans un premier un modèle du contexte persuasif, c’est-à-dire de l’ensemble des contraintes qui influencent l’adoption d’un comportement cible par un individu et à un instant donnés. Chacune de ces contraintes est à la fois un critère d’adaptation et un levier d’action dans la quête persuasive de la technologie. Pour chacun de ces leviers, nous avons identifié les techniques de persuasion qui permettent de les actionner. Dans un second temps, nous avons caractérisé l’adaptation de la persuasion sur un espace problème autour de cinq axes : la finalité, la cible, les critères et la dynamique de l’adaptation, ainsi que le rôle joué par l’utilisateur dans ce processus. Enfin, nous avons montré l’intérêt de l’adaptation, et des outils précédemment cités, dans la mise en oeuvre d’un dispositif persuasif dédié à la régulation du temps d’usage du smartphone. / This thesis deals with persuasive technologies, and in particular adaptation of the persuasion in order to optimize efficiency and relevance of those technologies. Persuasive technologies are technologies design to change behaviors without using coercion or deception. Numerous techniques to shape user behavior but few and perfectible methods to design these technologies characterized the research domain of persuasive technologies.The background of persuasive technologies is the traditional interpersonal persuasion, studied for over two thousand years in rethoric, philosophy, and more recently psychology. This last discipline offers many theories and models to understand more precisely the process that determine human behaviors. These theories show in particular that persuasive situations are complex, varied, with many influence factors. That is why we propose the notion of adaptive persuasive technologies : technologies able to adapt their persuasive stategies to the user context. To design these products and services, we propose in the first place a model of the persuasive context, that is all the constraints that influence the practice of a targeted behavior by the user at a given time. Each constraint in the persuasive context is at the same time an adaptation criteria and an action lever for the adaptive persuasive technology. For each lever, we identify the persuasive principle that can be used to move it. In a second time, we propose a problem space that characterized the adaptation of the persuasion, thanks to five axis : the purpose, the target, the criteria and the dynamic of the adaptation, and the user role in the adaptation process. Finally, by making and assessing TILT, a persuasive application dedicated to smartphone usage regulation, we show that the adaptation of the persuasion, with the use of the persuasive contexte model and the problem space, benefits to the persuasive efficiency.

This project presents the homogenization analysis for a static contact problem with slip dependent friction between an elastic body and a rigid foundation. The homogenization for the static eigenvalue problem associated to this model is studied. We prove that the eigenvalues are of order epsilon. We obtain the limit problem for the contact model. The analysis is carried out by using the Gamma-convergence theory.

Learning and memory offer animals the ability to modify their behavior in response to changes in the environment. A main target of neuroscience is to understand mechanisms underlying learning, memory formation and memory maintenance. Honeybees and bumblebees exhibit remarkable learning and memory abilities with a small brain, which makes them popular models for studying the neurobiological basis of learning and memory. However, almost all of previous molecular level research on bees' learning and memory has focused on the olfactory domain. Our understanding of the neurobiological basis underlying bee visual learning and memory is limited. In this thesis, I explore how synaptic organization and gene expression change in the context of visual learning. In Chapter 2, I investigate the effects of color learning and experience on synaptic connectivity and find that color learning result in an increase of the density of synaptic complexes (microglomeruli; MG), while exposure to color information may play a large role in experience-dependent changes in microglomerular density increase. In addition, microglomerular surface area increases as a result of long-term memory formation. In Chapter 3, I investigate the correlations between synaptic organizations and individual performance and the results show that bees with a higher density of microglomeruli in visual association areas of the brain are predisposed to faster learning and better long-term memory during a visual discrimination task. In Chapter 4, I explore the genes involved in visual learning and memory by transcriptome sequencing and I show the unique gene expression patterns at different times after visual learning. In summary, my findings shed light on the relationship between synaptic connections and visual learning and memory in bees at the group and individual level and show new candidate genes involved in visual learning, which provide new avenue for future study.

No description available.

L'olfaction est un sens clé dans l'adaptation du comportement. Pour permettre des actions appropriées le système olfactif doit effectuer des discriminations fines entre stimuli. Les performances de discrimination peuvent être améliorées via l'apprentissage perceptif et une structure cérébrale clé : le bulbe olfactif. Cette structure est cible d'une forme de plasticité particulière qui est la neurogenèse adulte. C'est là que des nouveaux neurones, majoritairement des cellules granulaires, régulent l'activité des cellules relais. Il a été montré que ces neurones sont requis pour un apprentissage perceptif.La question centrale de cette thèse est d'élucider le rôle et la spécificité des nouveaux neurones dans l'apprentissage olfactif complexe et changeant.Nous avons d'abord étudié l'effet d'un apprentissage perceptif complexe sur la neurogenèse adulte. Cette étude à démontré la nécessité et suffisance des nouveaux neurones dans l'apprentissage perceptif simple. Elle a aussi montré que lorsque l'apprentissage devient complexe, un réseau plus large est recruté, requérant les neurones préexistant.L'environnement olfactif est aussi changeant. Dans une seconde étude nous avons investigué comment la mémoire olfactive est altérée par nouvelle mémoire et le rôle de la neurogenèse adulte dans ce processus. Elle a montré le rôle des nouveaux neurones à sous tendre la mémoire olfactive et l'importance du délai entre apprentissages dans la stabilisation mnésique.Finalement, le recours aux neurosciences computationnelles a eu pour but de définir le rôle des nouveaux neurones granulaire au niveau du premier niveau de transformation de l'information et comment le raffinement des représentations sensorielles émerge par décorrelation.Pour conclure, la perception olfactive est changeante en fonction des modifications environnementales et cette plasticité est sous tendu par une plasticité du circuit du bulbe olfactif, due en grande partie à la neurogenèse adulte / Olfaction is a key player in behavioral adaptation. To perform tasks accurately, the olfactory system has to perform fine discrimination between very close stimuli. The discrimination performances can be enhanced through perceptual learning and a key cerebral structure in this is the olfactory bulb. This structure is the target of a specific form of plasticity that is adult neurogenesis. In this structure, adult-born neurons differentiate mostly in granule cells that regulate the activity of the relay cells. It has previously been shown that these neurons are required to perform perceptual learning. The central question of this thesis work is to elucidate both the role and the specificity of adult born neurons during complex or changing olfactory learning.We first studied the effect of complex perceptual learning on adult neurogenesis. This study demonstrated the necessity and sufficiency of adult-born neurons for simple olfactory learning. It also showed that when learning becomes complex, a larger neural network is involved requiring preexisting neurons.The olfactory environment is also changing. In a second study we investigated how the memory of an olfactory information is altered by the acquisition of a new one and what is the role of adult neurogenesis in this process. This second study highlighted the role of adult-born neurons in underlying olfactory memory and the importance of delay between learning for memory stabilization.Lastly, an approach relying on computational neurosciences aimed at outlining a computational framework explaining the role of adult-born granule cells in early olfactory transformations and how sharpened sensory representations emerge from decorrelation.To conclude, olfactory perception is changing according to environmental modifications and this plasticity is underlain by an important plasticity of the olfactory bulb circuitry due in large part to adult neurogenesis

The plasticity of cells in a multicellular organism is progressively lost during differentiation. This loss is reflected in studies involving the ectopic misexpression of fate-specifying or terminal selector transcription factors (TFs). These TFs can efficiently activate target genes in undifferentiated cells, but lose this ability as cells differentiate. While this phenomenon of cell fate restriction is widely observed, the mechanisms orchestrating it are poorly understood. In this thesis, I have used the ubiquitous overexpression of Zn-finger-TF CHE-1 as a tool to understand the mechanisms that restrict cell fate in Caenorhabditis elegans. When CHE-1 is ubiquitously expressed at embryonic stages, it activates target gene expression in many cell types, while in adults it can only act in a few neurons. To uncover factors that inhibit plasticity of all other adult cells, I first performed an RNAi screen against chromatin-associated factors. Using this approach I found that the removal of either the PRC2 complex, which deposits the H3K27me3 mark, or loss of proteins that indirectly regulate domains of H3K27me3, allows CHE-1 and two other terminal selector TFs to activate target genes in the germline. These data show that the correct distribution of H3K27me3 is crucial for the restriction of germ cell fate. I next took a candidate approach to identify genes that regulate fate restriction in other cell types. We hypothesized that terminal selector TFs themselves, in addition to specifying cellular identity by controlling large gene sets, may also act to inhibit plasticity. To test this, I first assayed the activity of CHE-1 in mutants of COE-TF unc-3, the terminal selector for a subset of cholinergic motor neurons (MNs). I found that in contrast to wildtype MNs, unc-3 mutant MNs remain plastic as CHE-1 can induce expression of target genes in these cells even at the adult stage. This phenotype is also observed in four of six additional terminal selector mutants tested. I further found that the removal of met-2, a protein required for H3K9 methylation, or mes-2, a PRC2 component, also makes differentiated cholinergic MNs amenable to the activity of CHE-1. Preliminary evidence suggests that met-2 may act in the same pathway as unc-3. These results raise the exciting possibility that selector TFs play a role in restricting cell fate by organizing the heterochromatin domains in differentiated cells. Overall, in this work I provide functional evidence to show that specific chromatin-modifying enzymes restrict the fate of germ cells and that both fate-specifying TFs and chromatin-modifying enzymes are required for the fate restriction in neurons.

Ductile and brittle failure of solids are closely related to their plastic and fracture behavior, respectively. The two most common energy dissipation mechanisms in solids possess distinct kinematic characteristics, i.e. large strain and discontinuous displacement, both of which pose challenges to reliable, efficient numerical simulation of material failure in engineering structures. This dissertation addresses the reliability and efficiency issues associated with the kinematic characteristics of plasticity and fracture. At first, studies are conducted to understand the relation between two well recognized large strain plasticity models that enjoy widespread popularity in numerical simulation of plastic behavior of solids. These two models, termed the additive hypo-elasto-plasticity and multiplicative hyper-elasto-plasticity models, respectively, are regarded as two distinct strategies for extending the classical infinitesimal deformation plasticity theory into the large strain regime. One of the most recent variants of the additive models, which features the logarithmic stress rate, is shown to give rise to nonphysical energy dissipation during elastic unloading. A simple modification to the logarithmic stress rate is accordingly made to resolve such a physical inconsistency. This results in the additive hypo-elasto-plasticity models based on the kinetic logarithmic stress rate in which energy dissipation-free elastic response is produced whenever plastic flow is absent. It is then proved that for isotropic materials the multiplicative hyper-elasto-plasticity models coincide with the additive ones if a newly discovered objective stress rate is adopted. Such an objective stress rate, termed the modified kinetic logarithmic rate, reduces to the kinetic logarithmic rate in the absence of strain-induced anisotropy which is characterized as kinematic hardening in the present dissertation. In the second part of the dissertation, the computational complexity of finite element analysis of the onset and propagation of interface cracks in layered materials is addressed. The study is conducted in the context of laminated composites in which interface fracture (delamination) is a dominant failure mode. In order to eliminate the complexities of remeshing for constant initiation and propagation of delamination, two hierarchical approaches, the extended finite element method (XFEM) and the s-version of the finite element method (s-method) are studied in terms of their effectiveness in representing displacement discontinuity across delaminated interfaces. With one single layer of 20-node serendipity solid elements resolving delamination-free response of the layered materials, it is proved that the delamination representations based on the s-method and the XFEM result in the same discretization space as the conventional non-hierarchical ply-by-ply approach which employs one layer of solid elements for each ply as well as double nodes on delaminated interfaces. Delamination indicators based on the s-method representation of delamination are then proposed to detect the onset and propagation of delamination. An adaptive methodology is accordingly developed in which the s-method displacement field enrichment for delamination is adaptively added to interface areas with high likelihood of delamination. Numerical examples show that the computational cost of the adaptive s-method is significantly lower than that incurred by the conventional ply-by-ply approach despite the fact that the two approaches produce practically identical results.

Long-term depression (LTD) induced by low frequency stimulation (LFS; 900x1Hz) at medial perforant path (MPP) synapses in the rat dentate gyrus (DG) has been described as both developmentally regulated and N-methyl D-aspartate receptor (NMDAr) independent, yet sufficient evidence suggest that the processes is not entirely independent of NMDAr activity. In the present study, in vitro DG-LTD LFS was induced in hippocampal slices prepared from rats at postnatal day (PND) 14, 21 and 28 to investigate how the sensitivity of DG-LTD~LFS to the NMDAr antagonist amino-5-phosphonovaleric acid (AP5; 50µM) changes throughout the juvenile developmental period (jDP; PNDs 12-29) that occurs immediately after the period of peak neurogenesis. We further examined the acute effects of the partial NMDAr antagonist ethanol (EtOH) on DG-LTD LFS and NMDAr excitatory post synaptic currents (NMDAr-EPSCs) in dentate granule cells (DGCs) using 50 and 100mM concentrations (50mM ~0.2%BAC) of EtOH. The magnitude of LTD induced at all three time points was not statistically different between age groups, but the probability of successfully inducing LTD did decrease with age. We found that AP5 was insufficient to inhibit DG-LTD LFS at PND14, but significantly inhibited DG-LTD LFS at PND21 and PND28. We also found that 50mM EtOH, but not 100mM EtOH, significantly attenuated the mag-nitude of DG-LTD LFS induced at each time point. Acute effects of 50mM EtOH had relatively little effect on NMDAr-EPSCs at PND14, and showed a slight potentiation of the response at PND21. 50mM EtOH at PND28, and 100mM EtOH at all three developmental time points showed inhibition of the NMDAr-EPSC. These findings provide insight on how developmental changes to the DG network and dentate gran-ule cells (DGCs) influences mechanisms and processes involved in the induction and expression of synaptic plasticity in the DG. / Graduate

Les cellules souches embryonnaires (ESCs) sont dérivées d'embryons au stade blastocyste. Elles sont caractérisées par la capacité de se diviser et de maintenir un phénotype indifférencié et en présence de stimuli, de se différencier en cellules spécialisées dérivées des trois feuillets embryonnaires, c'est la pluripotence. Elles sont un outil puissant pour modéliser des maladies génétiques à des fins de découvertes en recherche fondamentale et aussi dans un but d’applications cliniques. Les mESCs sont maintenues pluripotentes in vitro en présence de LIF (Leukemia Inhibitor Factor), une cytokine de la famille des Interleukines 6 (IL6) présentant des effets pléiotropes en fonction du type et de la maturité cellulaire. Le retrait de LIF conduit à la différenciation hétérogène des mESCs dont une partie meurt par apoptose. Lors du retrait de LIF, les cellules entrent séquentiellement dans des phases d'engagement réversible (jusqu'à 36h après retrait du LIF) et irréversible, au cours desquelles la re-stimulation par le LIF induit des effets différents. Afin de mieux caractériser cet effet de LIF, nous avons mis au point un « test de plasticité » in vitro et avons étudié l'impact de paramètres environnementaux qui pourraient moduler cette plasticité dans les mESCs. Nous avons montré que la MMP1 (Matrix Metalloproteinase 1), qui peut remplacer le LIF dans le maintien de la pluripotence, est moins efficace pour le maintien de la plasticité cellulaire des mESCs. Nous avons aussi montré que les mESCs restent pluripotentes et plastiques à 3% d'O2, in vitro, et qu’elles se caractérisent par un nouvel équilibre d'expression des gènes et des protéines en comparaison à 20% d'O2. / Embryonic Stem Cells (ESCs) are derived from embryo at the blastocyst stage. These cells are characterized by their properties of self-renewal and pluripotency: ability to divide and maintain an undifferentiated phenotype and to differentiate into specialized cells of the three primary germ layers in the presence of stimuli. ESCs are a powerful tool to modelize genetic diseases for fundamental research and clinical applications. Mouse Embryonic Stem Cells (mESCs) are maintained pluripotent in vitro in the presence of Leukemia Inhibitory Factor (LIF), an Interleukin 6 (IL6) cytokine family member which displays pleiotropic functions, depending on both maturity and type of cells. LIF withdrawal leads to heterogeneous differentiation of mESCs and part of the differentiated cells die by apoptosis. During the kinetics of LIF withdrawal, we show that cells enter a LIF-dependent reversible (up to 36h of LIF withdrawal) and irreversible phase of differentiation in which LIF-restimulation induces differential effects. To better characterize this period and LIF-dependent processes, we settled up an in vitro « plasticity test » and investigated the impact of environmental parameters that could regulate cell plasticity in mESCs. Our results reveal that the Matrix Metalloproteinase 1 (MMP1), which can replace LIF cytokine for maintenance of mESCs pluripotency, mimics its effects in the plasticity window, but with less efficiency. In addition, we demonstrate that mESCs maintain plasticity and pluripotency potentials in vitro, under 3% O2 (physioxic condition) with a new equilibrium of gene and protein expression levels compared to 20% O2.

Rapid climate change is a significant threat to the long-term persistence of native tree populations. Concern has been expressed that tree populations might fail to adapt due to rate of change, insufficient adaptive variation in tree populations and limits to dispersal. In contrast, others have contended that most tree species have high phenotypic plasticity, maintain high levels of within-population genetic variation and exhibit effective gene dispersal capability, all characteristics which should enable an adaptive response. To assess the potential adaptability of tree populations we need to understand their genetic diversity and phenotypic plasticity to build on the currently limited evidence base and guide decisions about seed sourcing for establishment of new woodlands desired to meet ambitious planting targets. Currently the seed sourcing system divides the island in four regions of similar size although it is not based on any genetic or ecological information. We discuss the suitability of this system with the insight of the data collected from native tree populations growing in experimental trials. In this thesis we study genetic diversity and phenotypic plasticity patterns in over 30 native tree populations across all Great Britain for three broadleaved species: ash (Fraxinus excelsior), rowan (Sorbus aucuparia), and silver birch (Betula pendula). To obtain these data we assessed the variation in multiple traits in several common garden experiments for each species, which were grown in contrasting environments. There is a tendency in provenance experiments to consider height as a proxy for fitness. We demonstrate that tree height is not enough to understand tree fitness and its adaptability capacity. We assessed our tree populations for growth (survival, tree height, DBH), stem form (number of forks), leaf phenology (leaf flushing and senescence) and leaf anatomical traits (leaf area, stomatal density and stomatal size).Great Britain has very distinct and heterogeneous environments likely to have given rise to adaptive differentiation. Knowing the geographical pattern of the genetic differences we can see the direction selective pressures have had on each of the traits studied, and we compare differences in patterns across the traits and species. Comparing populations growing in different environments we assessed the variation in phenotypic plasticity by trait and the direction of these plasticity. We found that tree populations across Great Britain are highly genetically variable and show genetic differences which have a geographical pattern, and that the patterns and size of the differences vary by species. Phenotypic plasticity varies across traits and interactions between genotype and environment make plasticity in some traits more unpredictable than others. We conclude that tree populations of ash, rowan and birch are well adapted to the diverse and oceanic climate of Great Britain, and that levels of genetic diversity and phenotypic plasticity provide a high capacity to respond to environmental change.