The AVuPUR project (Assessing the Vulnerabiliy of Peri-Urbans Rivers): experimental set up, modelling strategy and first results

International audienceLe projet AVuPUR a pour objectif de progresser sur la compréhension et la modélisation des flux d'eau dans les bassins versants péri-urbains. Il s'agit plus particulièrement de fournir des outils permettant de quantifier l'impact d'objets anthropiques tels que zones urbaines, routes, fossés sur les régimes hydrologiques des cours d'eau dans ces bassins. Cet article présente la stratégie expérimentale et de collecte de données mise en ½uvre dans le projet et les pistes proposées pour l'amélioration des outils de modélisation existants et le développement d'outils novateurs. Enfin, nous présentons comment ces outils seront utilisés pour simuler et quantifier l'impact des modifications d'occupation des sols et/ou du climat sur les régimes hydrologiques des bassins étudiés. / The aim of the AVuPUR project is to enhance our understanding and modelling capacity of water fluxes within suburban watersheds. In particular, the objective is to deliver tools allowing to quantify the impact of anthropogenic elements such as urban areas, roads, ditches on the hydrological regime of suburban rivers. This paper presents the observation and data collection strategy set up by the project, and the directions for improving existing modelling tools or proposing innovative ones. Finally, we present how these tools will be used to simulate and quantify the impact of land use and climate changes on the hydrological regimes of the studied catchments

Genome-wide association analyses identify new Brugada syndrome risk loci and highlight a new mechanism of sodium channel regulation in disease susceptibility

Brugada syndrome (BrS) is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel NaV1.5, susceptibility genes remain largely unknown. Here we performed a genome-wide association meta-analysis comprising 2,820 unrelated cases with BrS and 10,001 controls, and identified 21 association signals at 12 loci (10 new). Single nucleotide polymorphism (SNP)-heritability estimates indicate a strong polygenic influence. Polygenic risk score analyses based on the 21 susceptibility variants demonstrate varying cumulative contribution of common risk alleles among different patient subgroups, as well as genetic associations with cardiac electrical traits and disorders in the general population. The predominance of cardiac transcription factor loci indicates that transcriptional regulation is a key feature of BrS pathogenesis. Furthermore, functional studies conducted on MAPRE2, encoding the microtubule plus-end binding protein EB2, point to microtubule-related trafficking effects on NaV1.5 expression as a new underlying molecular mechanism. Taken together, these findings broaden our understanding of the genetic architecture of BrS and provide new insights into its molecular underpinnings

Integration of DNA Copy Number Alterations and Transcriptional Expression Analysis in Human Gastric Cancer

Background: Genomic instability with frequent DNA copy number alterations is one of the key hallmarks of carcinogenesis. The chromosomal regions with frequent DNA copy number gain and loss in human gastric cancer are still poorly defined. It remains unknown how the DNA copy number variations contributes to the changes of gene expression profiles, especially on the global level. Principal Findings: We analyzed DNA copy number alterations in 64 human gastric cancer samples and 8 gastric cancer cell lines using bacterial artificial chromosome (BAC) arrays based comparative genomic hybridization (aCGH). Statistical analysis was applied to correlate previously published gene expression data obtained from cDNA microarrays with corresponding DNA copy number variation data to identify candidate oncogenes and tumor suppressor genes. We found that gastric cancer samples showed recurrent DNA copy number variations, including gains at 5p, 8q, 20p, 20q, and losses at 4q, 9p, 18q, 21q. The most frequent regions of amplification were 20q12 (7/72), 20q12-20q13.1 (12/72), 20q13.1-20q13.2 (11/72) and 20q13.2-20q13.3 (6/72). The most frequent deleted region was 9p21 (8/72). Correlating gene expression array data with aCGH identified 321 candidate oncogenes, which were overexpressed and showed frequent DNA copy number gains; and 12 candidate tumor suppressor genes which were down-regulated and showed frequent DNA copy number losses in human gastric cancers. Three networks of significantly expressed genes in gastric cancer samples were identified by ingenuity pathway analysis. Conclusions: This study provides insight into DNA copy number variations and their contribution to altered gene expression profiles during human gastric cancer development. It provides novel candidate driver oncogenes or tumor suppressor genes for human gastric cancer, useful pathway maps for the future understanding of the molecular pathogenesis of this malignancy, and the construction of new therapeutic targets. © 2012 Fan et al.published_or_final_versio

Genome-wide association analyses identify new Brugada syndrome risk loci and highlight a new mechanism of sodium channel regulation in disease susceptibility

Brugada syndrome (BrS) is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel NaV1.5, susceptibility genes remain largely unknown. Here we performed a genome-wide association meta-analysis comprising 2,820 unrelated cases with BrS and 10,001 controls, and identified 21 association signals at 12 loci (10 new). Single nucleotide polymorphism (SNP)-heritability estimates indicate a strong polygenic influence. Polygenic risk score analyses based on the 21 susceptibility variants demonstrate varying cumulative contribution of common risk alleles among different patient subgroups, as well as genetic associations with cardiac electrical traits and disorders in the general population. The predominance of cardiac transcription factor loci indicates that transcriptional regulation is a key feature of BrS pathogenesis. Furthermore, functional studies conducted on MAPRE2, encoding the microtubule plus-end binding protein EB2, point to microtubule-related trafficking effects on NaV1.5 expression as a new underlying molecular mechanism. Taken together, these findings broaden our understanding of the genetic architecture of BrS and provide new insights into its molecular underpinnings

Genome-wide association analyses identify new Brugada syndrome risk loci and highlight a new mechanism of sodium channel regulation in disease susceptibility.

Brugada syndrome (BrS) is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel Na1.5, susceptibility genes remain largely unknown. Here we performed a genome-wide association meta-analysis comprising 2,820 unrelated cases with BrS and 10,001 controls, and identified 21 association signals at 12 loci (10 new). Single nucleotide polymorphism (SNP)-heritability estimates indicate a strong polygenic influence. Polygenic risk score analyses based on the 21 susceptibility variants demonstrate varying cumulative contribution of common risk alleles among different patient subgroups, as well as genetic associations with cardiac electrical traits and disorders in the general population. The predominance of cardiac transcription factor loci indicates that transcriptional regulation is a key feature of BrS pathogenesis. Furthermore, functional studies conducted on MAPRE2, encoding the microtubule plus-end binding protein EB2, point to microtubule-related trafficking effects on Na1.5 expression as a new underlying molecular mechanism. Taken together, these findings broaden our understanding of the genetic architecture of BrS and provide new insights into its molecular underpinnings

Recueil de données du bassin versant de l'Yzeron. Année 2008

[Notes_IRSTEA]Accompagné d'un CDRom [Departement_IRSTEA]Eaux [TR1_IRSTEA]ARCEAUCe document présente les données suivies en continu sur le bassin hydrographique de l'Yzeron, site atelier géré par l'unité de recherche Hydrologie-hydraulique du Cemagref de Lyon. Quelques données de mesures ponctuelles ou à caractère discontinu complète ce document. Au document papier est joint un CD-ROM, rassemblant sous forme de fichiers les différentes données recueillies

Modélisation dans la ville d'Oullins. Projet rives / Hy2ville. Année 2008

[Departement_IRSTEA]Eaux [TR1_IRSTEA]ARCEAURecueil des données hydrométéorologiques collectées sur la ville d'Oullins

Mesures hydrosédimentaires sur le bassin versant de l'Arc. Année 2009

[Departement_IRSTEA]Eaux [TR1_IRSTEA]ARCEAUCe rapport présente les sites de mesure sur le bassin versant de l'Arc et son affluent l'Arvan. Une description technique des outils de mesure y est faite ainsi que la présentation des données collectées et le recensement des incidents d'exploitation

Expertise de la station hydrométrique de la Nartuby à Trans

[Departement_IRSTEA]Eaux [TR1_IRSTEA]ARCEAU [Relecteur_IRSTEA]Camenen, B. ; Dramais, G. ; Paquier, A.Suite à la crue violente du 15 juin 2010 ayant détruit la station hydrométrique de la Nartuby à Trans-en-Provence, une expertise hydrométrique a été sollicitée par le SPC MedEst et la DREAL PACA, dans le cadre de la convention SCHAPI/Cemagref. La relation hauteur-débit à la station actuelle est analysée et modélisée. Le site du pont de pierre en aval est proposé pour constituer une station-fille permettant de mieux mesurer les fortes crues, à l'aide par exemple d'un radar combiné hauteur-vitesse. Des recommandations sont données en vue d'une étude hydraulique du site