Enseignement d\u27Eugène Morel (L\u27) [texte]

Texte de l\u27intervention de Lydie Ducolomb, élève conservateur DCB 19

Avant-garde contemporaine de Morel (L\u27) [texte]

Intervention de Marie Galvez, élève conservateur DCB 19

Modelling of standard and specialty fibre-based systems using finite element methods

We report on the investigation of an approach for modelling light transmission through systems consisting of several jointed optical fibres, in which the analytical modelling of the waveguides was replaced by Finite Element Modelling (FEM) simulations. To validate this approach we first performed FEM analysis of standard fibres and used this to evaluate the coupling efficiency between two singlemode fibres under different conditions. The results of these simulations were successfully compared with those obtained using classical analytical approaches, by demonstrating a maximum loss deviation of about 0.4 %. Further, we performed other more complex simulations that we compared again to the analytical models. FEM simulations allow addressing any type of guiding structure, without limitations on the complexity of the geometrical waveguide cross section and involved materials. We propose as example of application the modelling of the light transmitted through a system made of a hollow core photonic crystal fibre spliced between two singlemode standard optical fibres, and qualitatively compare the results of the simulation with experimental results.Comment: Proceedings article, SPIE conference "Fiber Lasers and Glass Photonics: Materials through Applications

The distance to the Pleiades from orbital solution of the double-lined eclipsing binary HD 23642

Combining precise B,V photoelectric photometry and radial velocities, we have been able to derive a firm orbital solution and accurate physical parameters for the newly discovered eclipsing binary HD 23642 in the Pleiades open cluster. The resulting distance to the binary, and therefore to the cluster, is 132 +/- 2 pc. This closely confirms the distance modulus obtained by classical main sequence fitting methods (m-M = 5.60 or 132 pc), moving cluster techniques and the astrometric orbit of Atlas. This is the first time the distance to a member of the Pleiades is derived by orbital solution of a double-lined eclipsing binary, and it is intended to contribute to the ongoing discussion about the discordant Hipparcos distance to the cluster.Comment: accepted in press in A&A as Letter to the Edito

Bad expression influences time to androgen escape in prostate cancer

<b>OBJECTIVE</b>: To assess the role of selected downstream Bcl-2 family members (Bad, Bax, Bcl-2 and Bcl-xL) in the development of androgen-independent prostate cancer (AIPC), as androgen-deprivation therapy is the treatment of choice in advanced prostate cancer, yet patients generally relapse and progress to an AI state within 18–24 months. <b>PATIENTS, MATERIALS AND METHODS</b>: The patient cohort was established by retrospectively selecting patients with prostate cancer who had an initial response to androgen-deprivation therapy, but subsequently relapsed with AIPC. In all, 58 patients with prostate cancer were included with matched androgen-dependent (AD) and AI prostate tumours available for immunohistochemical analysis; two independent observers using a weighted-histoscore method scored the staining. Changes in Bad, Bax, Bcl-2 and Bcl-xL expression during transition to AIPC were evaluated and then correlated to known clinical variables. <b>RESULTS</b>: High Bad expression in AD tumours was associated with an increased time to biochemical relapse (<i>P</i> = 0.007) and a trend towards improved overall survival (<i>P</i> = 0.053). There were also trends towards a decrease in Bad (<i>P</i> = 0.068) and Bax (<i>P</i> = 0.055) expression with progression to AIPC. There were no significant results for Bcl-2 or Bcl-xL. <b>CONCLUSION</b>: There is evidence to suggest that Bad expression levels at diagnosis influence time to biochemical relapse and overall survival, and that levels of pro-apoptotic proteins Bad and Bax fall during AIPC development. Bad might therefore represent a possible positive prognostic marker and potential therapeutic target for AIPC in the future

Expression of the autoimmune Fcgr2b NZW allele fails to be upregulated in germinal center B cells and is associated with increased IgG production

The inhibitory receptor FcγRIIb regulates B-cell functions. Genetic studies have associated Fcgr2b polymorphisms and lupus susceptibility in both humans and murine models, in which B cells express reduced FcγRIIb levels. Furthermore, FcγRIIb absence results in lupus on the appropriate genetic background, and lentiviral-mediated FcγRIIb overexpression prevents disease in the NZM2410 lupus mouse. The NZM2410/NZW allele Fcgr2b is, however, located in-between Sle1a and Sle1b, two potent susceptibility loci, making it difficult to evaluate Fcr2bNZW independent contribution. By using two congenic strains that each carries only Sle1a (B6.Sle1a(15–353)), or Fcr2bNZW in the absence of Sle1a or Sle1b (B6.Sle1(111–148)), we show that the Fcr2bNZW allele does not upregulate its expression on germinal center B cells and plasma cells, as does the C57BL/6 allele on B6.Sle1a(15–353) B cells. Furthermore, in the absence of the flanking Sle1a and Sle1b, Fcr2bNZW does not produce an autoimmune phenotype, but is associated with an increased number of class-switched plasma cells. These results show that while a lower level of FcγRIIb does not by itself induce the development of autoreactive B cells, it has the potential to amplify the contribution of autoreactive B cells induced by other lupus-susceptibility loci by enhancing the production of class-switched plasma cells

Susceptibility genes in the pathogenesis of murine lupus

Systemic lupus erythematosus (SLE) is the paradigm of a multisystem autoimmune disease in which genetic factors strongly influence susceptibility. Through genome scans and congenic dissection, numerous loci associated with lupus susceptibility have been defined and the complexity of the inheritance of this disease has been revealed. In this review, we provide a brief description of animal models of SLE, both spontaneous models and synthetic models, with an emphasis on the B6 congenic model derived from analyses of the NZM2410 strain. A hypothetical model of disease progression that organizes many of the identified SLE susceptibility loci in three distinct biological pathways that interact to mediate disease pathogenesis is also described. We finally discuss our recent fine mapping analysis, which revealed a cluster of loci that actually comprise the Sle1 locus