24,404 research outputs found
Colinette : polka pour le piano / par J. Bertin
No full textTitre uniforme : Bertin, J. (18..-19.. ; compositeur). Compositeur. [Colinette. Piano]Piano, Musique de -- +* 1900......- 1999......+:20e siècle:Polkas (piano) -- +* 1900......- 1999......+:20e siècle
Les Beaujeu de Franche-Comté dans le duché de Bourgogne, l'Auxerrois, le Tonnerrois, la Champagne, etc. / par le Dr J. Bertin,...
No full textAvec mode text
Voyage au pays des défauts / par M. Bertin,...
No full textCollection : Petite bibliothèque blancheAppartient à l’ensemble documentaire : UnivJeun0Contient une table des matièresAvec mode text
Voyage au pays des défauts / par M. Bertin,...
No full textCollection : Petite bibliothèque blancheAppartient à l’ensemble documentaire : UnivJeun0Contient une table des matièresAvec mode text
Retracing reconstruction. An assessment method for urban metamorphoses following extreme events
No full textNumerous research projects have faced the problem of the interpretation of post-disaster reconstructions. Several contributions have approached the problem in terms of identifying urban-setting reconstruction models, some attempting a systemization on a historiographic basis. To date, however, there has been no comprehensive work aimed at developing a quantitative method for evaluating and comparing reconstruction experiences. This article proposes a reproducible method for the systematic classification of post-disaster reconstructions, based on critical redrawing and data analysis. In the paper, the method is applied to 30 cases of reconstruction after the Second World War
Measurement of the ratio of prompt χ c to J / ψ production in pp collisions at √s = 7 TeV
Get PDFThe prompt production of charmonium χ c and J / ψ states is studied in proton-proton collisions at a centre-of-mass energy of √s = 7 TeV at the Large Hadron Collider. The χ c and J / ψ mesons are identified through their decays χ c → J / ψ γ and J / ψ → μ + μ - using 36 pb - 1 of data collected by the LHCb detector in 2010. The ratio of the prompt production cross-sections for χ c and J / ψ, σ (χ c → J / ψ γ) / σ (J / ψ), is determined as a function of the J / ψ transverse momentum in the range 2 < p T J / ψ < 15 GeV / c. The results are in excellent agreement with next-to-leading order non-relativistic expectations and show a significant discrepancy compared with the colour singlet model prediction at leading order, especially in the low p T J / ψ region
Evidence for the decay B0→J/ψω and measurement of the relative branching fractions of meson decays to J/ψη and J/ψη′
Get PDFFirst evidence of the B 0 → J / ψ ω decay is found and the B s 0 → J / ψ η and B s 0 → J / ψ η ′ decays are studied using a dataset corresponding to an integrated luminosity of 1.0 fb -1 collected by the LHCb experiment in proton-proton collisions at a centre-of-mass energy of sqrt(s) = 7 TeV. The branching fractions of these decays are measured relative to that of the B 0 → J / ψ ρ 0 decay:frac(B (B 0 → J / ψ ω), B (B 0 → J / ψ ρ 0)) = 0.89 ± 0.19 (stat) - 0.13 + 0.07 (syst),frac(B (B s 0 → J / ψ η), B (B 0 → J / ψ ρ 0)) = 14.0 ± 1.2 (stat) - 1.5 + 1.1 (syst) - 1.0 + 1.1 (frac(f d, f s)),frac(B (B s 0 → J / ψ η ′), B (B 0 → J / ψ ρ 0)) = 12.7 ± 1.1 (stat) - 1.3 + 0.5 (syst) - 0.9 + 1.0 (frac(f d, f s)), where the last uncertainty is due to the knowledge of f d / f s, the ratio of b-quark hadronization factors that accounts for the different production rate of B 0 and B s 0 mesons. The ratio of the branching fractions of B s 0 → J / ψ η ′ and B s 0 → J / ψ η decays is measured to befrac(B (B s 0 → J / ψ η ′), B (B s 0 → J / ψ η)) = 0.90 ± 0.09 (stat) - 0.02 + 0.06 (syst)
Trim17, novel E3 ubiquitin-ligase, initiates neuronal apoptosis
No full textAccumulating data indicate that the ubiquitin-proteasome system controls apoptosis by regulating the level and the function of key regulatory proteins. In this study, we identified Trim17, a member of the TRIM/RBCC protein family, as one of the critical E3 ubiquitin ligases involved in the control of neuronal apoptosis upstream of mitochondria. We show that expression of Trim17 is increased both at the mRNA and protein level in several in vitro models of transcription-dependent neuronal apoptosis. Expression of Trim17 is controlled by the PI3K/Akt/GSK3 pathway in cerebellar granule neurons (CGN). Moreover, the Trim17 protein is expressed in vivo, in apoptotic neurons that naturally die during post-natal cerebellar development. Overexpression of active Trim17 in primary CGN was sufficient to induce the intrinsic pathway of apoptosis in survival conditions. This pro-apoptotic effect was abolished in Bax(-/-) neurons and depended on the E3 activity of Trim17 conferred by its RING domain. Furthermore, knock-down of endogenous Trim17 and overexpression of dominant-negative mutants of Trim17 blocked trophic factor withdrawal-induced apoptosis both in CGN and in sympathetic neurons. Collectively, our data are the first to assign a cellular function to Trim17 by showing that its E3 activity is both necessary and sufficient for the initiation of neuronal apoptosis. Cell Death and Differentiation (2010) 17, 1928-1941; doi: 10.1038/cdd.2010.73; published online 18 June 201
La danse du gâteau Cake-Walk : chansonnette créée par Robert Bertin [illustration Georges Dola (1872-1950)]
No full textLa danse du gâteau Cake-Walk : chansonnette créée par Robert Bertin ; chantée par Mmes Esther Lekain, Brésina, Delly-Mô, Gomez, Juniori, Mimi Bonjour, Lily Murcy, Eva Mireth, Mommarts, Marthelette ; chantée par MMrs Strit [Marius Strit], Morin, Darius M., Robert Negrel, Perrier, M. Chicot, Delfort, René Raoult, Vaillant, Grinda, Darbon [Marc Darbon], Denance ; (dédicace) “A l’ami Higonenc, directeur de l’Eldorado de Montpellier” ; illustration Georges Dola ; [document extrait d’un recueil factice relié, chanson n°84 (numéroté au crayon bleu)] ; paroles de A. Mas [Antoine Mas (1872-1936)] ; musique, nouvelle et arrangée par J[ean] Taillefer ; Orgeret éditeur, Lyon Chansons, 72 passage de l’Argue [Lyon], dépôt à Paris [chez] Labbé ; imprimerie Crevel ; [intérieur : “version pour dame” “chansonnette créée par Robert Bertin” “musique, nouvelle et arrangée par J[ean] Taillefer” ; cotage JMO200 ; gravure imprimerie Crevel frères] ; verso catalogue (titres/genres/auteurs/compositeurs - aucun crédit pour les interprètes] ; incipit “A mon déhanchement” [extrait “C’est qu’ maintenant Paris / Adopte la danse des mal blanchis”] ; datation (titre) 1903 par BNF et par cotage (D&L) [1903 pour exemplaire par titres au catalogue verso]
Hundreds of variants clustered in genomic loci and biological pathways affect human height
Get PDFMost common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits(1), but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait(2,3). The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P<0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways
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