Perte ou vol d'une carte bancaire : quel régime probatoire ? Réflexion sur la nature juridique du dispositif prévu à l'article L. 132-3 du code monétaire et financier

L\u27article L. 132-3 du code monétaire et financier relève le titulaire d\u27 une carte bancaire des débits opérés en cas de perte ou de vol, au-delà de 150 €, sauf faute lourde de sa part ou opposition tardive. Deux arrêts récents de la Cour de cassation ont jugé que la composition du code confidentiel de la carte n\u27établissait pas, à elle seule, l\u27existence d\u27une faute lourde. La solution a suscité une certaine inquiétude : elle favoriserait la fraude du titulaire à qui il suffirait de déclarer la perte ou le vol de sa carte après avoir opéré achats et retraits. Mais une question majeure demeure en suspens. Que la composition du code par un tiers n\u27implique pas une faute lourde, c\u27est une chose. En résulte-t-il, pour autant, que le titulaire puisse se contenter de déclarer la perte ou le vol, sans avoir à en rapporter la preuve ? La négative s\u27impose à première vue puisque, en vertu d\u27une célèbre clause du « contrat porteur », les opérations réalisées au moyen du code sont présumées émaner du titulaire ; à charge pour ce dernier, donc, de rapporter la preuve contraire. Reste que cette clause ne trouve probablement pas à s\u27appliquer ici. C\u27est, en tout cas, l\u27une des hypothèses à laquelle conduit l\u27analyse de la nature juridique du dispositif prévu à l\u27article L. 132-3

Crystal Structure of the Complex mAb 17.2 and the C-Terminal Region of Trypanosoma cruzi P2β Protein: Implications in Cross-Reactivity

Patients with Chronic Chagas' Heart Disease possess high levels of antibodies against the carboxyl-terminal end of the ribosomal P2ß protein of Trypanosoma cruzi (TcP2ß). These antibodies, as well as the murine monoclonal antibody (mAb) 17.2, recognize the last 13 amino acids of TcP2ß (called the R13 epitope: EEEDDDMGFGLFD) and are able to cross-react with, and stimulate, the ß1 adrenergic receptor (ß1-AR). Indeed, the mAb 17.2 was able to specifically detect human β1-AR, stably transfected into HEK cells, by flow cytometry and to induce repolarisation abnormalities and first degree atrioventricular conduction block after passive transfer to naïve mice. To study the structural basis of this cross-reactivity, we determined the crystal structure of the Fab region of the mAb 17.2 alone at 2.31 Å resolution and in complex with the R13 peptide at 1.89 Å resolution. We identified as key contact residues on R13 peptide Glu3, Asp6 and Phe9 as was previously shown by alanine scanning. Additionally, we generated a model of human β1-AR to elucidate the interaction with anti-R13 antibodies. These data provide an understanding of the molecular basis of cross-reactive antibodies induced by chronic infection with Trypanosoma cruzi

Adsorption of Line Segments on a Square Lattice

We study the deposition of line segments on a two-dimensional square lattice. The estimates for the coverage at jamming obtained by Monte-Carlo simulations and by $7^{th}$-order time-series expansion are successfully compared. The non-trivial limit of adsorption of infinitely long segments is studied, and the lattice coverage is consistently obtained using these two approaches.Comment: 19 pages in Latex+5 postscript files sent upon request ; PTB93_

Specific Humoral Immunity versus Polyclonal B Cell Activation in Trypanosoma cruzi Infection of Susceptible and Resistant Mice

Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 10–12 million people in Latin America. Patent parasitemia develops during acute disease. During this phase, polyclonal B cell activation has been reported to generate high levels of serum antibody with low parasite specificity, and delayed protective humoral immunity, which is necessary to prevent the host from succumbing to infection. In this manuscript, data show that relatively resistant mice have improved parasite-specific humoral immunity and decreased polyclonal B cell activation compared to susceptible mice. Parasite-specific humoral immunity was associated with differential expansion of B cell subsets and T cells in the spleen, as well as with increased Th1 and decreased Th2 cytokine production. These data suggest that host susceptibility/genetic biases impact the development of humoral responses to infection. Th2 cytokines are generally associated with improved antibody responses. In the context of T. cruzi infection of susceptible mice, Th2 cytokines were associated with increased total antibody production concomitant with delayed pathogen-specific humoral immunity. This study highlights the need to consider the effect of host biases when investigating humoral immunity to any pathogen that has reported polyclonal B cell activation during infection