189 research outputs found

    Evocations : pour orchestre

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    Orgánico [Les dieux dans lombre des cavernes]: 3[1.2.3/pic] 3[1.2.Eh] 3[1.2.bcl] 3[1.2.cbn] -- 4 3 3 1 -- tmp + 4 -- 2hp -- strperc: sd, tri, tamtam, cym, bd, tdOrgánico [La ville rose]: 3[1.2.3/pic] 3[1.2.Eh] 3[1.2.bcl] 3[1.2.cbn] -- 4 3 3 1 -- tmp + 3 -- 2hp -- strperc: bd, cym, sus cym, tri, glockDuración: nº. 1 = 15 ; nº. 2 = 13Sumario: Dos partes del Tríptico `Evocaciones`. Poema sinfónico estrenado en la Sociedad Nacional de París el 18 de mayo de 1912.Copia digital. España : Ministerio de Cultura y Deporte. Subdirección General de Coordinación Bibliotecaria, s2021Tít. de la carp.: `Evocations`Partes: Fl 1 + 2, 2 (ms.), 3/Pic, Ob 1 + 2, 2 (ms.), Eh, Cl 1 + 2, 2 (ms.), Bcl, Bn 1 + 2, 2 (ms.), Cbn, Hn 1 + 2, 2 (ms.), 3 + 4, 4 (ms.), Tp 1 + 2, 2 (ms.), 3, Tbn 1 + 2, Tbn mib (ms.), 2 (ms.), 3, Tuba, Tmp, [Tri + Tamtam + Td + Bd + Cym + Sus cym] (2), Tri (ms.), Glock, Hp 1 +2, Vn 1 (8), Vn 2 (7), Va (5), Vc (5), Db (4)Contiene: I. Les dieux dans lombre des cavernes [Los dioses en la sombra de las cavernas] -- II. La ville rose [La ciudad rosa

    Representaciones extraordinarias de bailes del Teatro Nacional de la Ópera de París

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    Castor y Polux; Giselle d'Adolphe Adam; La Grisi d'Henri TomasiDe cada obra s'ha digitalitzat un programa sencer. De la resta s'han digitalitzat les parts que són diferents.Direcció artística Juan Mestres CalvetEmpresa Juan Mestres Calve

    Despedida de la compañía de bailes del Teatro Nacional de la Ópera de París

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    De cada obra s'ha digitalitzat un programa sencer. De la resta s'han digitalitzat les parts que són diferents.Direcció artística Juan Mestres CalvetEl Festín de la Araña d'Albert Roussel; Dafnis y Cloe de Maurice Ravel; Alejandro el Grande de Philippe GaubertEmpresa Juan Mestres Calve

    Temporada coreográfica primavera 1974

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    Bacchus et Arianne : Música d'Albert Roussel, coreografia de Dimitri Parlic ; Golem : Música de Francis Burt, coreografia de Dimitri Parlic ; Don Quijote (paso a dos) : Música de Ludwig Minkus, coreografia de M. Petipa ; Danzas Polovtsianas de el Príncipe Igor : música d'Alexander Borodin, coreografia de Michel Fokine, adaptada per Anica PrelieDe cada obra s'ha digitalitzat un programa sencer. De la resta s'han digitalitzat les parts que són diferents.Empresa: Juan A. PamiasOrquestra del Gran Teatre del Liceu dirigida per Dusan Miladinovi

    The Amyotrophic Lateral Sclerosis M114T PFN1 Mutation Deregulates Alternative Autophagy Pathways and Mitochondrial Homeostasis

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    International audienceMutations in profilin 1 (PFN1) have been identified in rare familial cases of Amyotrophic Lateral Sclerosis (ALS). PFN1 is involved in multiple pathways that could intervene in ALS pathology. However, the specific pathogenic role of PFN1 mutations in ALS is still not fully understood. We hypothesized that PFN1 could play a role in regulating autophagy pathways and that PFN1 mutations could disrupt this function. We used patient cells (lymphoblasts) or tissue (post-mortem) carrying PFN1 mutations (M114T and E117G), and designed experimental models expressing wild-type or mutant PFN1 (cell lines and novel PFN1 mice established by lentiviral transgenesis) to study the effects of PFN1 mutations on autophagic pathway markers. We observed no accumulation of PFN1 in the spinal cord of one E117G mutation carrier. Moreover, in patient lymphoblasts and transfected cell lines, the M114T mutant PFN1 protein was unstable and deregulated the RAB9-mediated alternative autophagy pathway involved in the clearance of damaged mitochondria. In vivo, motor neurons expressing M114T mutant PFN1 showed mitochondrial abnormalities. Our results demonstrate that the M114T PFN1 mutation is more deleterious than the E117G variant in patient cells and experimental models and suggest a role for the RAB9-dependent autophagic pathway in ALS

    Genome-wide association study reveals novel genetic loci:a new polygenic risk score for mitral valve prolapse

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    AIMS: Mitral valve prolapse (MVP) is a common valvular heart disease with a prevalence of >2% in the general adult population. Despite this high incidence, there is a limited understanding of the molecular mechanism of this disease, and no medical therapy is available for this disease. We aimed to elucidate the genetic basis of MVP in order to better understand this complex disorder. METHODS AND RESULTS: We performed a meta-analysis of six genome-wide association studies that included 4884 cases and 434 649 controls. We identified 14 loci associated with MVP in our primary analysis and 2 additional loci associated with a subset of the samples that additionally underwent mitral valve surgery. Integration of epigenetic, transcriptional, and proteomic data identified candidate MVP genes including LMCD1, SPTBN1, LTBP2, TGFB2, NMB, and ALPK3. We created a polygenic risk score (PRS) for MVP and showed an improved MVP risk prediction beyond age, sex, and clinical risk factors. CONCLUSION: We identified 14 genetic loci that are associated with MVP. Multiple analyses identified candidate genes including two transforming growth factor-beta signalling molecules and spectrin beta. We present the first PRS for MVP that could eventually aid risk stratification of patients for MVP screening in a clinical setting. These findings advance our understanding of this common valvular heart disease and may reveal novel therapeutic targets for intervention. KEY QUESTION: Expand our understanding of the genetic basis for mitral valve prolapse (MVP). Uncover relevant pathways and target genes for MVP pathophysiology. Leverage genetic data for MVP risk prediction. KEY FINDING: Sixteen genetic loci were significantly associated with MVP, including 13 novel loci. Interesting target genes at these loci included LTBP2, TGFB2, ALKP3, BAG3, RBM20, and SPTBN1. A risk score including clinical factors and a polygenic risk score, performed best at predicting MVP, with an area under the receiver operating characteristics curve of 0.677. TAKE-HOME MESSAGE: Mitral valve prolapse has a polygenic basis: many genetic variants cumulatively influence pre-disposition for disease. Disease risk may be modulated via changes to transforming growth factor-beta signalling, the cytoskeleton, as well as cardiomyopathy pathways. Polygenic risk scores could enhance the MVP risk prediction

    Temporada coreográfica primavera 1974

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    Programa de la Temporada coreogràfica de la primavera de 1974. El Ballet del Teatre Nacional de Belgrad era dirigit per M. Jovanovic, el director d'orquestra va ser D. Miladinovic i el pianista acompanyant fou M. Zamurovic. Van estrenar "Ana Karenina", amb música de R. Schredin, "Golem", amb música de F. Burt i "Bacchus et Arianne" amb música d'A. Roussel. D. Parlic va ser el coreògraf de totes elles. També es van representar "Simfonia en do" amb música de G. Bizet i coreografia de D. Parlic, "Danses Polovtsianes d'El príncep Ígor" amb música d'A. Borodin i coreografia de M. Fokine adaptada per Anica Prelie, i passos a dos de "Don Quixote" amb música de L. Minkus, "El llac dels cignes" i "El trencanous" amb música de P. I. TxaikovskiEl Ballet del Teatre de l'òpera alemanya del Rhin estava dirigit per E. Walter, que també n'era coreògraf. L'orquestra va ser dirigida per R. Schaub, R. Kubik i A. Quennet i els pianistes W. Riddlespurger i A. Roth-Schutzbach. Van estrenar una nova versió de "Romeo i Julieta" amb música de S. Prokofiev i coreografia d'E. Walter, "Apollon Musagette" amb música d'I. Stravinsky i coreografia de G. Balanchine, "La mort i la donzella" amb música de F. Schubert i coreografia d'E. Walter, i "Jeux", amb música de C. Debussy i coreografia d'E. Walter. També van dansar les reposicions de "Giselle" amb música d'Adolphe Adam amb coreografia de R. Mazalova i E. Walter, "El mandarí meravellós" amb música de Bela Bartók i coreografia d'E. Walter, i "Daphnis et Chloe" amb música de M. Ravel i coreografia d'E. Walte

    Nutrition for the ageing brain: towards evidence for an optimal diet

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    As people age they become increasingly susceptible to chronic and extremely debilitating brain diseases. The precise cause of the neuronal degeneration underlying these disorders, and indeed normal brain ageing remains however elusive. Considering the limits of existing preventive methods, there is a desire to develop effective and safe strategies. Growing preclinical and clinical research in healthy individuals or at the early stage of cognitive decline has demonstrated the beneficial impact of nutrition on cognitive functions. The present review is the most recent in a series produced by the Nutrition and Mental Performance Task Force under the auspice of the International Life Sciences Institute Europe (ILSI Europe). The latest scientific advances specific to how dietary nutrients and non-nutrient may affect cognitive ageing are presented. Furthermore, several key points related to mechanisms contributing to brain ageing, pathological conditions affecting brain function, and brain biomarkers are also discussed. Overall, findings are inconsistent and fragmented and more research is warranted to determine the underlying mechanisms and to establish dose-response relationships for optimal brain maintenance in different population subgroups. Such approaches are likely to provide the necessary evidence to develop research portfolios that will inform about new dietary recommendations on how to prevent cognitive decline

    Phenome-wide association analysis of LDL-cholesterol lowering genetic variants in PCSK9

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    Abstract: Background: We characterised the phenotypic consequence of genetic variation at the PCSK9 locus and compared findings with recent trials of pharmacological inhibitors of PCSK9. Methods: Published and individual participant level data (300,000+ participants) were combined to construct a weighted PCSK9 gene-centric score (GS). Seventeen randomized placebo controlled PCSK9 inhibitor trials were included, providing data on 79,578 participants. Results were scaled to a one mmol/L lower LDL-C concentration. Results: The PCSK9 GS (comprising 4 SNPs) associations with plasma lipid and apolipoprotein levels were consistent in direction with treatment effects. The GS odds ratio (OR) for myocardial infarction (MI) was 0.53 (95% CI 0.42; 0.68), compared to a PCSK9 inhibitor effect of 0.90 (95% CI 0.86; 0.93). For ischemic stroke ORs were 0.84 (95% CI 0.57; 1.22) for the GS, compared to 0.85 (95% CI 0.78; 0.93) in the drug trials. ORs with type 2 diabetes mellitus (T2DM) were 1.29 (95% CI 1.11; 1.50) for the GS, as compared to 1.00 (95% CI 0.96; 1.04) for incident T2DM in PCSK9 inhibitor trials. No genetic associations were observed for cancer, heart failure, atrial fibrillation, chronic obstructive pulmonary disease, or Alzheimer’s disease – outcomes for which large-scale trial data were unavailable. Conclusions: Genetic variation at the PCSK9 locus recapitulates the effects of therapeutic inhibition of PCSK9 on major blood lipid fractions and MI. While indicating an increased risk of T2DM, no other possible safety concerns were shown; although precision was moderate

    New genetic loci link adipose and insulin biology to body fat distribution.

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    Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms
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