Architecture des systèmes complexes : modélisation et pilotage par l'incertitude.

National audienceLa conception des systèmes complexes et plus précisément la conception de l'automobile fait face à des évolutions technologiques continues qu'il faut savoir intégrer et adapter. Dans cet article, nous proposons une méthode pour modéliser l'architecture des produits et des organisations et nous présentons brièvement ce que pourrait être un outil, basé sur pilotage par l'incertitude, permettant de faire coévoluer l'organisation et le produit dans le but d'atteindre un niveau de prestation donné

A method to manage the co-evolution of product an organization architectures.

International audienceComplex systems design and especially automotive design is facing continuous technological evolution that needs stronger integration. To tackle this issue, a method for modeling products and organizations architectures is presented. This method will be completed by a "management by uncertainty" tool to help managers anticipate the co-evolutions of project domains and properly structure these domains

Architecture des produits et des organisations : modélisation et pilotage par l'incertitude.

International audienceLa conception des systèmes complexes et plus précisément la conception de l'automobile fait face à des évolutions technologiques continues qu'il faut savoir intégrer et adapter. Dans cet article, nous proposons une méthode pour représenter l'architecture des produits et des organisations et nous présentons brièvement ce que pourrait être un outil, basé sur la gestion de l'incertitude, permettant de faire coévoluer l'organisation et le produit dans le but d'atteindre un niveau de prestation donné

Defining product architectures.

International audienceIdentifying product architectures is recognized as a critical activity during the preliminary design phase since the selected architecture has a great impact on the product quality, on the organization of the following phases of the design project and on the global performance of this project. System architects need methods to pre-determine cohesive modules and integrative elements. In this paper we present a new method to jointly design the functional and physical architectures. Starting from an incidence matrix that represents the couplings between elements of two domains (here, functions and components), it generates a Design Structure Matrix (DSM) for each domain. Each DSM is then rearranged by a clustering algorithm in order to reveal a "satisfactory" architecture. To illustrate our approach, we present an industrial case study in the framework of a new automobile engine development project

Simulating change propagation between product architecture and development organization.

International audienceIn order to limit the effects of technological change on product design, concepts like product architecture and modularity have been introduced, in order to support complex product development. In engineering design, numerous works have studied this central issue but change propagation within product architecture has been hardly addressed. Concerning organizational issues, many researchers in the field of industrial engineering have paid careful attention to new organization design but hardly to an incremental evolution of project organization. Galbraith (1977) highlighted that product architecture and development organization were strongly interrelated. However, little research has studied this relationship, and the need for a coherent model of product and organization co-evolution remains. This paper aims at presenting a matrix-based method that should help design managers to simulate change propagation between product architecture and development organization. This method uses a "management by uncertainty" approach and a mathematical model in order to propagate change. An industrial case study illustrates it in case of component changes

Product, Processes and Organization Architectures Modeling : from strategic expectations to strategic competences.

International audienceComplex systems design and especially automotive design is facing continuous technological evolution that needs stronger integration. In this paper, a method for representing system architecture is presented. This method is based on dependencies and constraints propagation which allows us to focus on the co-evolution of product, organization and processes domains

Guanylate cyclase C limits systemic dissemination of a murine enteric pathogen

BACKGROUND: Guanylate Cyclase C (GC-C) is an apically-oriented transmembrane receptor that is expressed on epithelial cells of the intestine. Activation of GC-C by the endogenous ligands guanylin or uroguanylin elevates intracellular cGMP and is implicated in intestinal ion secretion, cell proliferation, apoptosis, intestinal barrier function, as well as the susceptibility of the intestine to inflammation. Our aim was to determine if GC-C is required for host defense during infection by the murine enteric pathogen Citrobacter rodentium of the family Enterobacteriacea. METHODS: GC-C(+/+) control mice or those having GC-C genetically ablated (GC-C(−/−)) were administered C. rodentium by orogastric gavage and analyzed at multiple time points up to post-infection day 20. Commensal bacteria were characterized in uninfected GC-C(+/+) and GC-C(−/−) mice using 16S rRNA PCR analysis. RESULTS: GC-C(−/−) mice had an increase in C. rodentium bacterial load in stool relative to GC-C(+/+). C. rodentium infection strongly decreased guanylin expression in GC-C(+/+) mice and, to an even greater degree, in GC-C(−/−) animals. Fluorescent tracer studies indicated that mice lacking GC-C, unlike GC-C(+/+) animals, had a substantial loss of intestinal barrier function early in the course of infection. Epithelial cell apoptosis was significantly increased in GC-C(−/−) mice following 10 days of infection and this was associated with increased frequency and numbers of C. rodentium translocation out of the intestine. Infection led to significant liver histopathology in GC-C(−/−) mice as well as lymphocyte infiltration and elevated cytokine and chemokine expression. Relative to naïve GC-C(+/+) mice, the commensal microflora load in uninfected GC-C(−/−) mice was decreased and bacterial composition was imbalanced and included outgrowth of the Enterobacteriacea family. CONCLUSIONS: This work demonstrates the novel finding that GC-C signaling is an essential component of host defense during murine enteric infection by reducing bacterial load and preventing systemic dissemination of attaching/effacing-lesion forming bacterial pathogens such as C. rodentium