88 research outputs found
Création artistique et relation esthétique : objets, cadres catégoriels et fonctions
Jean-Marie Schaeffer, directeur d’étudesYolaine Escande, Nathalie Heinich, directrices de recherche au CNRSDenis Vidal, directeur de recherche à l’IRD La formation des préférences esthétiques et artistiques. II Durant cette année conclusive du séminaire consacré à l’étude de la relation esthétique, nous avons analysé la composante « publique » de l’appréciation esthétique, ce qu’on appelle traditionnellement le « jugement de goût ». Dans notre étude nous avons pris cette expression en son ext..
Création artistique et relation esthétique : objets, cadres catégoriels et fonctions
Jean-Marie Schaeffer, directeur d’étudesGabriel Ruget, professeur à l’ENS-CachanYolaine Escande, directrice de recherche au CNRSDenis Vidal, directeur de recherche à l’IRD Le fait esthétique III : l’esthétique littéraire Dans la continuité des années précédentes, le séminaire a exploré le pôle esthétique de la problématique des arts. Après avoir abordé les modalités de la relation esthétique dans le champ de la vision, des images et des sons (2005-2007), on s’est penché sur les caractéristiqu..
Création artistique et relation esthétique : objets, cadres catégoriels et fonctions
Jean-Marie Schaeffer, directeur d’étudesGabriel Ruget, professeur à l’ENS-CachanYolaine Escande, directrice de recherche au CNRSDenis Vidal, directeur de recherche à l’IRD Le fait esthétique III : l’esthétique littéraire Dans la continuité des années précédentes, le séminaire a exploré le pôle esthétique de la problématique des arts. Après avoir abordé les modalités de la relation esthétique dans le champ de la vision, des images et des sons (2005-2007), on s’est penché sur les caractéristiqu..
Transcriptional profiling of ion channel genes in Brugada syndrome and other right ventricular arrhythmogenic diseases
Approximation of integral operators using product-convolution expansions
International audienceWe consider a class of linear integral operators with impulse responses varying regularly in time or space. These operators appear in a large number of applications ranging from signal/image processing to biology. Evaluating their action on functions is a computationally intensive problem necessary for many practical problems. We analyze a technique called product-convolution expansion: the operator is locally approximated by a convolution, allowing to design fast numerical algorithms based on the fast Fourier transform. We design various types of expansions, provide their explicit rates of approximation and their complexity depending on the time varying impulse response smoothness. This analysis suggests novel wavelet based implementations of the method with numerous assets such as optimal approximation rates, low complexity and storage requirements as well as adaptivity to the kernels regularity. The proposed methods are an alternative to more standard procedures such as panel clustering, cross approximations, wavelet expansions or hierarchical matrices
Routine molecular profiling of cancer: results of a one-year nationwide program of the French Cooperative Thoracic Intergroup (IFCT) for advanced non-small cell lung cancer (NSCLC) patients.
International audienceBackground: The molecular profiling of patients with advanced non-small-cell lung cancer (NSCLC) for known oncogenic drivers is recommended during routine care. Nationally, however, the feasibility and effects on outcomes of this policy are unknown. We aimed to assess the characteristics, molecular profiles, and clinical outcomes of patients who were screened during a 1-year period by a nationwide programme funded by the French National Cancer Institute. Methods This study included patients with advanced NSCLC, who were routinely screened for EGFR mutations, ALK rearrangements, as well as HER2 (ERBB2), KRAS, BRAF, and PIK3CA mutations by 28 certified regional genetics centres in France. Patients were assessed consecutively during a 1-year period from April, 2012, to April, 2013. We measured the frequency of molecular alterations in the six routinely screened genes, the turnaround time in obtaining molecular results, and patients' clinical outcomes. This study is registered with ClinicalTrials.gov, number NCT01700582. Findings 18 679 molecular analyses of 17 664 patients with NSCLC were done (of patients with known data, median age was 64·5 years [range 18–98], 65% were men, 81% were smokers or former smokers, and 76% had adenocarcinoma). The median interval between the initiation of analysis and provision of the written report was 11 days (IQR 7–16). A genetic alteration was recorded in about 50% of the analyses; EGFR mutations were reported in 1947 (11%) of 17 706 analyses for which data were available, HER2 mutations in 98 (1%) of 11 723, KRAS mutations in 4894 (29%) of 17 001, BRAF mutations in 262 (2%) of 13 906, and PIK3CA mutations in 252 (2%) of 10 678; ALK rearrangements were reported in 388 (5%) of 8134 analyses. The median duration of follow-up at the time of analysis was 24·9 months (95% CI 24·8–25·0). The presence of a genetic alteration affected first-line treatment for 4176 (51%) of 8147 patients and was associated with a significant improvement in the proportion of patients achieving an overall response in first-line treatment (37% [95% CI 34·7–38·2] for presence of a genetic alteration vs 33% [29·5–35·6] for absence of a genetic alteration; p=0·03) and in second-line treatment (17% [15·0–18·8] vs 9% [6·7–11·9]; p<0·0001). Presence of a genetic alteration was also associated with improved first-line progression-free survival (10·0 months [95% CI 9·2–10·7] vs 7·1 months [6·1–7·9]; p<0·0001) and overall survival (16·5 months [15·0–18·3] vs 11·8 months [10·1–13·5]; p<0·0001) compared with absence of a genetic alteration. Interpretation Routine nationwide molecular profiling of patients with advanced NSCLC is feasible. The frequency of genetic alterations, acceptable turnaround times in obtaining analysis results, and the clinical advantage provided by detection of a genetic alteration suggest that this policy provides a clinical benefit
Variable Nav1.5 Protein Expression from the Wild-Type Allele Correlates with the Penetrance of Cardiac Conduction Disease in the Scn5a+/− Mouse Model
BACKGROUND: Loss-of-function mutations in SCN5A, the gene encoding Na(v)1.5 Na+ channel, are associated with inherited cardiac conduction defects and Brugada syndrome, which both exhibit variable phenotypic penetrance of conduction defects. We investigated the mechanisms of this heterogeneity in a mouse model with heterozygous targeted disruption of Scn5a (Scn5a(+/-) mice) and compared our results to those obtained in patients with loss-of-function mutations in SCN5A. METHODOLOGY/PRINCIPAL FINDINGS: Based on ECG, 10-week-old Scn5a(+/-) mice were divided into 2 subgroups, one displaying severe ventricular conduction defects (QRS interval>18 ms) and one a mild phenotype (QRS53 weeks), ajmaline effect was larger in the severely affected subgroup. These data matched the clinical observations on patients with SCN5A loss-of-function mutations with either severe or mild conduction defects. Ventricular tachycardia developed in 5/10 old severely affected Scn5a(+/-) mice but not in mildly affected ones. Correspondingly, symptomatic SCN5A-mutated Brugada patients had more severe conduction defects than asymptomatic patients. Old severely affected Scn5a(+/-) mice but not mildly affected ones showed extensive cardiac fibrosis. Mildly affected Scn5a(+/-) mice had similar Na(v)1.5 mRNA but higher Na(v)1.5 protein expression, and moderately larger I(Na) current than severely affected Scn5a(+/-) mice. As a consequence, action potential upstroke velocity was more decreased in severely affected Scn5a(+/-) mice than in mildly affected ones. CONCLUSIONS: Scn5a(+/-) mice show similar phenotypic heterogeneity as SCN5A-mutated patients. In Scn5a(+/-) mice, phenotype severity correlates with wild-type Na(v)1.5 protein expression
PROPRIETES BIOELECTRIQUES DE L'EPITHELIUM RESPIRATOIRE (ROLE DE CFTR)
NANTES-BU Médecine pharmacie (441092101) / SudocPARIS-BIUM (751062103) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF
- …