83 research outputs found

    Onomastique et histoire sociale, XIXe-XXe siĂšcles

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    Guy Tassin Le sĂ©minaire prend en compte divers aspects de l’onomastique mais se fonde surtout sur l’étude des noms de personne. L’anthroponymie est un matĂ©riau frĂ©quent pour les linguistes et les historiens de la littĂ©rature mais semble moins familiĂšre aux historiens. MĂȘme les anthropologues, dans le relativisme ambiant, n’exploitent guĂšre la fonction de marqueur assignĂ©e au nom par Claude LĂ©vi-Strauss. Cependant le nom reste au cƓur de prĂ©occupations fort voyantes, dans la mesure oĂč la trans..

    Christophe Pons, Le Spectre et le Voyant. Les Ă©changes entre morts et vivants en Islande

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    Cet ouvrage a Ă©tĂ© Ă©laborĂ© Ă  partir d’une thĂšse soutenue Ă  Aix-en-Provence en 1999. Constatant la prĂ©sence des morts dans la vie quotidienne d’Isafjör∂ur, ville du nord-ouest de l’Islande qui avait dĂ©jĂ  Ă©tĂ© le terrain de son mĂ©moire de maĂźtrise, Christophe Pons a voulu dĂ©passer la rĂ©action, sceptique ou ironique, lĂ©guĂ©e par le rationalisme, et comprendre comment cette croyance aux relations entre morts et vivants s’intĂšgre Ă  la culture islandaise, culture qu’il dĂ©finit, Ă  la maniĂšre de Gregory..

    Onomastique et histoire sociale, XIXe-XXe siĂšcles

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    Guy Tassin Le sĂ©minaire prend en compte divers aspects de l’onomastique mais se fonde surtout sur l’étude des noms de personne. L’anthroponymie est un matĂ©riau frĂ©quent pour les linguistes et les historiens de la littĂ©rature mais semble moins familiĂšre aux historiens. MĂȘme les anthropologues, dans le relativisme ambiant, n’exploitent guĂšre la fonction de marqueur assignĂ©e au nom par Claude LĂ©vi-Strauss. Cependant le nom reste au cƓur de prĂ©occupations fort voyantes, dans la mesure oĂč la trans..

    Cahiers ethnologiques. Histoire et Culture, 1998, 20, n. s. : Samigiel cealkagat. Paroles sùmes

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    La lutte des SĂąmes (ou Lapons) pour la reconnaissance de leur identitĂ© et de leurs intĂ©rĂȘts Ă©conomiques ne trouve que peu d’écho en France. D’oĂč l’utilitĂ© de cette livraison de l’UniversitĂ© de Bordeaux qui prĂ©sente en outre le prĂ©cieux avantage de rassembler des tĂ©moignages directs de SĂąmes responsables et informĂ©s. Il n’en est pas moins dommage que la plupart des textes datent des annĂ©es 90 et 91, ce qui prive le lecteur des dĂ©veloppements rĂ©cents d’une situation politique et sociale qui Ă©vo..

    Negative diffraction pattern dynamics in nonlinear cavities with left-handed materials

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    We study a ring cavity filled with a slab of a right-handed material and a slab of a left-handed material. Both layers are assumed to be nonlinear Kerr media. First, we derive a model for the propagation of light in a left-handed material. By constructing a mean-field model, we show that the sign of diffraction can be made either positive or negative in this resonator, depending on the thicknesses of the layers. Subsequently, we demonstrate that the dynamical behavior of the modulation instability is strongly affected by the sign of the diffraction coefficient. Finally, we study the dissipative structures in this resonator and reveal the predominance of a two-dimensional up-switching process over the formation of spatially periodic structures, leading to the truncation of the homogeneous hysteresis cycle.Comment: 8 pages, 5 figure

    Biogenic amines and their metabolites are differentially affected in the Mecp2-deficient mouse brain

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    International audienceBACKGROUND: Rett syndrome (RTT, MIM #312750) is a severe neurological disorder caused by mutations in the X-linked methyl-CpG binding protein 2 (MECP2) gene. Female patients are affected with an incidence of 1/15000 live births and develop normally from birth to 6-18 months of age before the onset of deficits in autonomic, cognitive, motor functions (stereotypic hand movements, impaired locomotion) and autistic features. Studies on Mecp2 mouse models, and specifically null mice, revealed morphological and functional alterations of neurons. Several functions that are regulated by bioaminergic nuclei or peripheral ganglia are impaired in the absence of Mecp2. RESULTS: Using high performance liquid chromatography, combined with electrochemical detection (HPLC/EC) we found that Mecp2(-/y) mice exhibit an alteration of DA metabolism in the ponto-bulbar region at 5 weeks followed by a more global alteration of monoamines when the disease progresses (8 weeks). Hypothalamic measurements suggest biphasic disturbances of norepinephrine and serotonin at pathology onset (5 weeks) that were found stabilized later on (8 weeks). Interestingly, the postnatal nigrostriatal dopaminergic deficit identified previously does not parallel the reduction of the other neurotransmitters investigated. Finally, dosage in cortical samples do not suggest modification in the monoaminergic content respectively at 5 and 8 weeks of age. CONCLUSIONS: We have identified that the level of catecholamines and serotonin is differentially affected in Mecp2(-/y) brain areas in a time-dependent fashion

    Analysis of Xq27-28 linkage in the international consortium for prostate cancer genetics (ICPCG) families.

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    BACKGROUND: Genetic variants are likely to contribute to a portion of prostate cancer risk. Full elucidation of the genetic etiology of prostate cancer is difficult because of incomplete penetrance and genetic and phenotypic heterogeneity. Current evidence suggests that genetic linkage to prostate cancer has been found on several chromosomes including the X; however, identification of causative genes has been elusive. METHODS: Parametric and non-parametric linkage analyses were performed using 26 microsatellite markers in each of 11 groups of multiple-case prostate cancer families from the International Consortium for Prostate Cancer Genetics (ICPCG). Meta-analyses of the resultant family-specific linkage statistics across the entire 1,323 families and in several predefined subsets were then performed. RESULTS: Meta-analyses of linkage statistics resulted in a maximum parametric heterogeneity lod score (HLOD) of 1.28, and an allele-sharing lod score (LOD) of 2.0 in favor of linkage to Xq27-q28 at 138 cM. In subset analyses, families with average age at onset less than 65 years exhibited a maximum HLOD of 1.8 (at 138 cM) versus a maximum regional HLOD of only 0.32 in families with average age at onset of 65 years or older. Surprisingly, the subset of families with only 2-3 affected men and some evidence of male-to-male transmission of prostate cancer gave the strongest evidence of linkage to the region (HLOD = 3.24, 134 cM). For this subset, the HLOD was slightly increased (HLOD = 3.47 at 134 cM) when families used in the original published report of linkage to Xq27-28 were excluded. CONCLUSIONS: Although there was not strong support for linkage to the Xq27-28 region in the complete set of families, the subset of families with earlier age at onset exhibited more evidence of linkage than families with later onset of disease. A subset of families with 2-3 affected individuals and with some evidence of male to male disease transmission showed stronger linkage signals. Our results suggest that the genetic basis for prostate cancer in our families is much more complex than a single susceptibility locus on the X chromosome, and that future explorations of the Xq27-28 region should focus on the subset of families identified here with the strongest evidence of linkage to this region.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

    Chromosomes 4 and 8 implicated in a genome wide SNP linkage scan of 762 prostate cancer families collected by the ICPCG

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    BACKGROUND In spite of intensive efforts, understanding of the genetic aspects of familial prostate cancer (PC) remains largely incomplete. In a previous microsatellite‐based linkage scan of 1,233 PC families, we identified suggestive evidence for linkage (i.e., LOD ≄ 1.86) at 5q12, 15q11, 17q21, 22q12, and two loci on 8p, with additional regions implicated in subsets of families defined by age at diagnosis, disease aggressiveness, or number of affected members. METHODS In an attempt to replicate these findings and increase linkage resolution, we used the Illumina 6000 SNP linkage panel to perform a genome‐wide linkage scan of an independent set of 762 multiplex PC families, collected by 11 International Consortium for Prostate Cancer Genetics (ICPCG) groups. RESULTS Of the regions identified previously, modest evidence of replication was observed only on the short arm of chromosome 8, where HLOD scores of 1.63 and 3.60 were observed in the complete set of families and families with young average age at diagnosis, respectively. The most significant linkage signals found in the complete set of families were observed across a broad, 37 cM interval on 4q13–25, with LOD scores ranging from 2.02 to 2.62, increasing to 4.50 in families with older average age at diagnosis. In families with multiple cases presenting with more aggressive disease, LOD scores over 3.0 were observed at 8q24 in the vicinity of previously identified common PC risk variants, as well as MYC , an important gene in PC biology. CONCLUSIONS These results will be useful in prioritizing future susceptibility gene discovery efforts in this common cancer. Prostate 72:410–426, 2012. © 2011 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90245/1/21443_ftp.pd

    Germline variation at 8q24 and prostate cancer risk in men of European ancestry

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    An Author Correction to this article was published on 17 January 2019.Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10 −15 ), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification. © 2018, The Author(s).Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10 −15 ), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification. © 2018, The Author(s).Peer reviewe
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