Cette thèse propose une approche de la collaboration homme-machine, inspirée de la théorie de l'Enaction, dans le domaine de l'interprétation de données complexes. L'autonomie des deux partenaires vise à leur permettre de réaliser une interprétation en s'appuyant sur leurs compétences. Pour préserver leur autonomie, la communication du système avec son partenaire est réalisée au moyen d'annotations. Cette approche est appliquée à la conception d'un système multi-agents pour l'interprétation collaborative de signaux physiologiques de patients en réanimation médicale, i.e. des séries temporelles multivariées. Ce système est capable de construire une interprétation des séries temporelles par la construction (1) de modèles d'évènements et de scénarios (ensembles d'évènements reliés par des relations temporelles) et (2) d'annotations à partir de ces modèles. Les modèles qu'il construit évoluent au cours de l'interprétation pour prendre en compte les annotations du partenaire humain.

Si la perception de notre environnement paraît simple et naturelle, les attributs visuels composant les différents objets sont traités dans des espaces temps qui leur sont propres en engageant des voies neuronales distinctes. La question du liage des informations sensorielles en un percept unique est alors posée. Dans le cadre de cette thèse, la question du liage sensoriel a été étudiée au regard des actes moteurs volontaires. En situation d'observation passive, le point de simultanéité subjective (PSS) montre qu'un changement de couleur doit se produire 40 ms avant un changement de position pour donner lieu à une perception synchrone des deux événements. L'exécution d'un mouvement d'atteinte manuelle réduit significativement ce PSS (-3.3 ms) uniquement lorsque le délai et l'écart spatial entre la fin de l'action motrice et les changements environnementaux n'excède pas 250 ms (-0,6 ms) et 2 cm ( 3,8 ms). Cependant, dans le cas où une situation d'apprentissage est induite par la présence de nouvelles contingences sensori-motrices, le liage sensoriel par l'action peut être observé pour des intervalles de temps plus grands (jusqu'à 1000 ms). Ce liage sensoriel par l'action, mis en évidence pour la première fois, serait sous-tendu par les mécanismes prédictifs associés aux modèles internes. Une dernière étude a révélé l'intérêt diagnostique de l'étude des relations perception/action au cours du vieillissement. Des profils de réponse spécifique ont été observés chez des patients de type Alzheimer lors de tâches testant les relations perception/action. Ces études apportent des arguments en faveur d'un rôle important de l'action dans la perception et la cognition. / If the perception of our environment seems easy and natural, the visual attributes of various objects are processed in space-time which are their own by engaging distinct neural pathways. The issue of binding of sensory information into a single percept is then arise. In this thesis, the issus of sensory bending was studied in relation to voluntary motor action. In position of passive observation, the point of subjective simultaneity (PSS) shows that a color change had to occur 40 ms before a change of position to give rise to a perception of two synchronous events. Performing a manual reaching movement reduced significantly the pSS (-3.3 ms) only when the time and space gap between the end of the motor action and environmental change does not exceed 250 ms (-0.6 ms) and 2 cm (3.8 ms). However, if a learning situation is induced by the presence of new sensorimotor contingencies, sensory binding by action can be observed for larger time intervals (up to 1000ms). This sensory binding by action, demonstrated for the first time, would be underpinned by predictive mechanisms associated with internal models. A last study showed the diagnostic interest of the study of relation perception/action during aging. Specific profiles of responses were observed in patients with Alzheimer on task testing the relations perception/action. These studies provide arguments for an important role of action in perception and cognition.

Baculoviruses are lytic insect viruses. Upon internalisation, the viral genome orchestrates a sequential expression process ultimately leading to lysis of the infected cell. Release of progeny capable of infecting other cells during the process completes the infection cycle. Studies of the infection cycle in cell culture are typically conducted by synchronous infection, i.e. near simultaneous infection of all cells, by means of high virus concentrations. The behaviour of the synchronously infected culture, such as the timing of onset of progeny release, is considered representative for the infection progression within individual cells. In reality, however, the synchronously infected culture only reflects the average behaviour of all infected cells. The infection progresses in individual cells display large variability; this is most obvious in the observation that within the same culture some cells undergo cell lysis at two days post infection while others remain viable up to four days post infection. Such variabilities or asynchronies observed in synchronously infected culture is the topic of this thesis. Using a simple phenomenological model, it is demonstrated that cell death and associated intracellular product release is adequately described assuming that the waiting time from infection to cell death follows a Gaussian distribution with a mean of 59 hours post infection (hpi) and a standard deviation of 15hpi. Unlike other deterministic models developed over the last decade (Licari and Bailey 1992; Nielsen 2000), this stochastic model does not make the biologically inconsistent assumption that cells continue to be metabolically active following loss of membrane integrity. While elegant in its simplicity, the model provides no explanation for the underlying stochasticity. Investigations into the cause of this dispersion of cell death highlighted further asynchronies in the specific recombinant protein yield, in viral DNA content, in virus budding rate, and in cell volume increase instead of clarifying the issue. A modelling framework developed by Licari & Bailey (1992) and later Hu & Bentley (2000) incorporates the number of infectious particles each individual cell receives as a possible source of the dispersions in the host cell responses. However, this was found NOT to be the cause of the observed asynchronies under non-substrate limiting conditions. The timing of cell death, cell volume increase, recombinant product yield, viral DNA content, and virus budding rate is identical in Sf9 cell cultures infected at multiplicities of infection of ~5, ~15, and ~45 infectious particles per cell. Cell cycle variation has previously been suggested as a possible cause for observed asynchronies in baculovirus infections (Brown and Faulkner, 1975). The cell cycle phase is indirectly linked to the cell volume, because a G_2-phase cell prior to division is inherently twice the cell volume of a G_1- phase cell after cell division. By the same logic, it is also apparent that a G_2-phase cell possesses twice the number of ribosomes of a G_1-phase cell and thus a doubled protein production capacity. The effect of the cell cycle or cell volume on the baculovirus infection was determined by splitting an exponentially growing Sf9 cell culture into 5 cell size dependent fractions by centrifugal elutriation. The subsequent infection of these fractions showed (1) no dependency of the timing of cell lysis and cell volume increase and (2) approximately twofold increase of a) recombinant protein yield, b) viral DNA concentration, and c) budded virus yield. The recombinant protein yield showed a strong proportionality to the initial cell volume and the total RNA concentration during the late phase of the infection. As argued in chapter 6, these proportionalities suggest that the observed differences in the responses of the cell fractions to the baculovirus infection are more likely caused by the difference in the protein production capacity than by cell cycle specific molecules. This investigation gave also reason to speculate that infected cells cannot progress beyond the G_2/M phase, and cell cycle progression continues undisturbed until ~8hpi when all cellular DNA replication appears to cease. Resuspended, infected Sf9 cells synchronised by centrifugal elutriation showed an identical cell cycle distribution as the non-infected control cultures for the first ~8hpi; G_1 and G_2/M phase cell proportions remained unchanged, whereas S phase cells progress to G_2/M phase. Subsequently, the non-infected control cells resumed normal cycling whereas all infected cells remained at the same cell cycle phase from 8 to 11hpi. The initial cell cycle arrests in G_2/M phase in both infected and non-infected cultures were caused through medium exchange.