Study of the R-(Zr,W)-(O,N) (R = Y, Nd, Sm, Gd, Yb) oxynitride system

International audienceThe replacement of tantalum by the couple Zr/W within the RTa-O-N systems (R = Y, Nd, Sm, Gd, Yb), enables the preparation of novel oxide and oxynitride phases in the R-Zr-W-O-N system. R2Zr2xWxO7+x oxides exhibit the fluorite-type (x < 0.9) and scheelite (x 1) structures. Corresponding oxynitride compositions are of the fluorite-type and show different colors, for example in the case of ytterbium: pale yellow (x = 0.2 or 0.25), green (x = 0.5-0.8) and brown for the tungsten-rich samples (x = 0.9, 1). Photocatalytic activity measurements have been performed to investigate the overall water splitting behavior of these colored phases

Comparisons of day-time and night-time hydroacoustic surveys in temperate lakes

In recent years, due to an increased need for non-intrusive sampling techniques, hydroacoustics has attracted attention in fishery science and management. Efforts to promote standardisation are increasing the accuracy, efficiency, and comparability of this method. The European Water Framework Directive and the Standard Operating Procedures for Fisheries Hydroacoustic Surveys in North American Great Lakes has recommended that surveys be conducted at night. At night, fish usually disperse in the water column, thus allowing for single echo detection and subsequent accurate fish size estimation, while day-time schooling behaviour hampers the estimation of fish size. However, sampling during the day would often be safer and cheaper. This study analyses how fisheries hydroacoustic results differ between day-time and night-time surveys, using data from 14 natural temperate lakes of various size. Data collected during the day and night at two depth layers linked to thermal stratification were compared in terms of acoustic scattering strength, target strength, and biomass estimates. The results showed a significant correlation between day-time and night-time estimates, though biomass in the upper layer was biased for day-time surveys, mainly due to incorrect fish size estimates resulting from rare single echo detections and schooling behaviour. Biomass estimates for the lower depth layer did not significantly differ between the two diel periods. Thus, this study confirms that hydroacoustic sampling in temperate lakes should be performed at night for accurate fish stock biomass estimates

Coral reefs of Réunion Island in 2007 : status report and monitoring network

Réunion Island is 2500 km2 and belongs to the outermost regions of European Union (EU). The population attained 774 600 inhabitants in 2004 with 25 % living in the western part of the island, 80 % in the littoral zone (called "bas"). The gross domestic product (GDP) per capita is less than 50 % of the mean index of the EU. The rate of unemployment was of 33 % in 2004. Coral reef ecosystems extend over 12 km2 along 25 km of the west and south coasts of the island. In addition to the natural infl uence of climatic events (global change) coral reef ecosystems are impacted by direct and indirect infl uences of the increase of human population. Direct impacts are mainly due to human overfrequenting of reef flats and overfishing. Indirect impacts are due to urbanization and to industrial, agricultural and urban pollutions. The competence in marine environment is assumed by an administration (Direction Régionale de l’Environnement). Researches on coral reefs are run by research institutes and NGO. The first coral reef monitoring network was set up in 1998 on the Saint-Gilles/La Saline reef. Since then, it was extended to the three other main reef units (Saint-Leu, Étang-Salé, Saint-Pierre) and the data are gathered since 2001 by ecoguards of the association "Parc Marin de la Réunion", with the partnership of the university (Laboratoire d’Ecologie Marine). Data are stored in a database (COREMO) and analysed by ARVAM (Agence pour la Recherche et la Valorisation Marine). The operation is funded both by the state administration and a local administration (Conseil Régional). Réunion Island is a part of the South-West Indian Ocean node of the Global Coral Reef Monitoring Network (GCRMN). It is regularly involved in the writing of the "Status of coral reefs of the world". At the same time another network involving stakeholders is built using the Reef Chek protocole. At the present time, coral reefs of Réunion Island are deteriorated. If the density of the targeted species of fi" sh has not changed since 1999, the surface of live corals has shown a significant decrease on half of the 14 stations, particularly after two bleaching events in 2003 and 2004. The various negative impacts due to human activities contribute to weaken these ecosystems and to decrease their resilience. Hence, they are less and less able to resist exceptional climatic events (hurricanes, swells) and the bad impacts of global change (bleaching). To face to the stake of long term development, 75 % of the reef units of the island are protected since February 2007 by the status of "Réserve Naturelle Nationale Marine" (35 km2 of marine protected area)La Réunion est une île de 2500 km2 qui fait partie des régions ultrapériphériques de l'Union Européenne. La population était de 774 600 habitants en 2004 avec 25 % localisés dans la partie ouest de l'île et 80 % dans la frange littorale (appelée communément "les bas"). L'index PIB par habitant est de 50 % de celui de l'UE (rapport PIB par habitant local/PIB moyen UE). Le taux de chômage était de 33 % en 2004. Les écosystèmes récifaux couvrent 12 km2 et s'étendent sur un linéaire côtier de 25 km dans l'ouest et le sud de l'île. Les écosystèmes coralliens subissent en plus des influences naturelles des événements climatiques (réchauffement), les impacts anthropiques directs et indirects liés à la croissance démographique. Les impacts directs sont liés majoritairement à la surfréquentation des platiers et à la surexploitation des ressources. Les impacts indirects sont liés à l'urbanisation et aux pollutions d'origine urbaine, industrielle et agricole. La compétence en matière d'environnement marin est assurée par un service de l'État (Direction Régionale de l'Environnement). Les recherches sur les récifs coralliens sont menées par des Instituts de recherche (Université et IRD) et des ONG. Le premier réseau d'observation des récifs coralliens a été mis en place en 1998 sur l'unité récifale de Saint-Gilles/La Saline. Depuis il a été étendu aux trois autres principales unités récifales (Saint-Leu, Étang-Salé, Saint-Pierre) et la récolte des données est assurée depuis 2001 par les écogardes de l'Association Parc Marin de la Réunion, en partenariat avec le laboratoire ECOMAR (Université). Les données sont stockées dans une base de données (COREMO) et sont traitées par l'ARVAM (Agence pour la Recherche et la Valorisation Marine). Le financement de l'opération est assuré conjointement par l'État et le Conseil Régional. La Réunion fait partie du noeud Sud-Ouest Océan Indien du Global Coral ReefMonitoring Network (GCRMN). Elle participe régulièrement à la rédaction du rapport "Status ofcoral reefs ofthe world" sur l'état de santé des récifs dans le monde. En parallèle au réseau scientifique se met en place un réseau selon le protocole ReefCheck. Les récifs de la Réunion se dégradent actuellement. Si la densité des espèces de poissons ciblées par l'échantillonnage n'a pas varié significativement depuis 1999, la couverture corallienne vivante, elle, a diminué sensiblement sur la moitié des 14 stations suivies, notamment après deux phénomènes importants de blanchissement survenus en 2003 et 2004. Les divers impacts négatifs liés aux activités humaines contribuent à fragiliser ces milieux et à diminuer leur capacité de résilience. Ils sont ainsi de moins en moins aptes à résister aux événements climatiques exceptionnels (cyclones, houles) et aux conséquences néfastes du réchauffement climatique (blanchissement corallien). Pour faire face à ces enjeux de développement durable, depuis février 2007, 75 % des unités récifales de l'île ont acquis le statut de Réserve Naturelle Nationale Marine (35 km2 d'espaces marins protégés)

Genetic predisposition to ductal carcinoma in situ of the breast.

BACKGROUND: Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer. It is often associated with invasive ductal carcinoma (IDC), and is considered to be a non-obligate precursor of IDC. It is not clear to what extent these two forms of cancer share low-risk susceptibility loci, or whether there are differences in the strength of association for shared loci. METHODS: To identify genetic polymorphisms that predispose to DCIS, we pooled data from 38 studies comprising 5,067 cases of DCIS, 24,584 cases of IDC and 37,467 controls, all genotyped using the iCOGS chip. RESULTS: Most (67 %) of the 76 known breast cancer predisposition loci showed an association with DCIS in the same direction as previously reported for invasive breast cancer. Case-only analysis showed no evidence for differences between associations for IDC and DCIS after considering multiple testing. Analysis by estrogen receptor (ER) status confirmed that loci associated with ER positive IDC were also associated with ER positive DCIS. Analysis of DCIS by grade suggested that two independent SNPs at 11q13.3 near CCND1 were specific to low/intermediate grade DCIS (rs75915166, rs554219). These associations with grade remained after adjusting for ER status and were also found in IDC. We found no novel DCIS-specific loci at a genome wide significance level of P < 5.0x10(-8). CONCLUSION: In conclusion, this study provides the strongest evidence to date of a shared genetic susceptibility for IDC and DCIS. Studies with larger numbers of DCIS are needed to determine if IDC or DCIS specific loci exist

Genetic predisposition to ductal carcinoma in situ of the breast

Background: Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer. It is often associated with invasive ductal carcinoma (IDC), and is considered to be a non-obligate precursor of IDC. It is not clear to what extent these two forms of cancer share low-risk susceptibility loci, or whether there are differences in the strength of association for shared loci. Methods: To identify genetic polymorphisms that predispose to DCIS, we pooled data from 38 studies comprising 5,067 cases of DCIS, 24,584 cases of IDC and 37,467 controls, all genotyped using the iCOGS chip. Results: Most (67 %) of the 76 known breast cancer predisposition loci showed an association with DCIS in the same direction as previously reported for invasive breast cancer. Case-only analysis showed no evidence for differences between associations for IDC and DCIS after considering multiple testing. Analysis by estrogen receptor (ER) status confirmed that loci associated with ER positive IDC were also associated with ER positive DCIS. Analysis of DCIS by grade suggested that two independent SNPs at 11q13.3 near CCND1 were specific to low/intermediate grade DCIS (rs75915166, rs554219). These associations with grade remained after adjusting for ER status and were also found in IDC. We found no novel DCIS-specific loci at a genome wide significance level of P < 5.0x10-8. Conclusion: In conclusion, this study provides the strongest evidence to date of a shared genetic susceptibility for IDC and DCIS. Studies with larger numbers of DCIS are needed to determine if IDC or DCIS specific loci exist

Fine scale mapping of the 17q22 breast cancer locus using dense SNPs, genotyped within the Collaborative Oncological Gene-Environment Study (COGs)

Genome-wide association studies have found SNPs at 17q22 to be associated with breast cancer risk. To identify potential causal variants related to breast cancer risk, we performed a high resolution fine-mapping analysis that involved genotyping 517 SNPs using a custom Illumina iSelect array (iCOGS) followed by imputation of genotypes for 3,134 SNPs in more than 89,000 participants of European ancestry from the Breast Cancer Association Consortium (BCAC). We identified 28 highly correlated common variants, in a 53 Kb region spanning two introns of the STXBP4 gene, that are strong candidates for driving breast cancer risk (lead SNP rs2787486 (OR = 0.92; CI 0.90–0.94; P = 8.96 × 10−15)) and are correlated with two previously reported risk-associated variants at this locus, SNPs rs6504950 (OR = 0.94, P = 2.04 × 10−09, r2 = 0.73 with lead SNP) and rs1156287 (OR = 0.93, P = 3.41 × 10−11, r2 = 0.83 with lead SNP). Analyses indicate only one causal SNP in the region and several enhancer elements targeting STXBP4 are located within the 53 kb association signal. Expression studies in breast tumor tissues found SNP rs2787486 to be associated with increased STXBP4 expression, suggesting this may be a target gene of this locus

Genetic predisposition to in situ and invasive lobular carcinoma of the breast.

Invasive lobular breast cancer (ILC) accounts for 10-15% of all invasive breast carcinomas. It is generally ER positive (ER+) and often associated with lobular carcinoma in situ (LCIS). Genome-wide association studies have identified more than 70 common polymorphisms that predispose to breast cancer, but these studies included predominantly ductal (IDC) carcinomas. To identify novel common polymorphisms that predispose to ILC and LCIS, we pooled data from 6,023 cases (5,622 ILC, 401 pure LCIS) and 34,271 controls from 36 studies genotyped using the iCOGS chip. Six novel SNPs most strongly associated with ILC/LCIS in the pooled analysis were genotyped in a further 516 lobular cases (482 ILC, 36 LCIS) and 1,467 controls. These analyses identified a lobular-specific SNP at 7q34 (rs11977670, OR (95%CI) for ILC = 1.13 (1.09-1.18), P = 6.0 × 10(-10); P-het for ILC vs IDC ER+ tumors = 1.8 × 10(-4)). Of the 75 known breast cancer polymorphisms that were genotyped, 56 were associated with ILC and 15 with LCIS at P<0.05. Two SNPs showed significantly stronger associations for ILC than LCIS (rs2981579/10q26/FGFR2, P-het = 0.04 and rs889312/5q11/MAP3K1, P-het = 0.03); and two showed stronger associations for LCIS than ILC (rs6678914/1q32/LGR6, P-het = 0.001 and rs1752911/6q14, P-het = 0.04). In addition, seven of the 75 known loci showed significant differences between ER+ tumors with IDC and ILC histology, three of these showing stronger associations for ILC (rs11249433/1p11, rs2981579/10q26/FGFR2 and rs10995190/10q21/ZNF365) and four associated only with IDC (5p12/rs10941679; rs2588809/14q24/RAD51L1, rs6472903/8q21 and rs1550623/2q31/CDCA7). In conclusion, we have identified one novel lobular breast cancer specific predisposition polymorphism at 7q34, and shown for the first time that common breast cancer polymorphisms predispose to LCIS. We have shown that many of the ER+ breast cancer predisposition loci also predispose to ILC, although there is some heterogeneity between ER+ lobular and ER+ IDC tumors. These data provide evidence for overlapping, but distinct etiological pathways within ER+ breast cancer between morphological subtypes

Evidence that the 5p12 Variant rs10941679 Confers Susceptibility to Estrogen Receptor-Positive Breast Cancer through FGF10 and MRPS30 Regulation

Genome-wide association studies (GWASs) have revealed increased breast cancer risk associated with multiple genetic variants at 5p12. Here, we report the fine mapping of this locus using data from 104,660 subjects from 50 case-control studies in the Breast Cancer Association Consortium (BCAC). With data for 3,365 genotyped and imputed SNPs across a 1 Mb region (positions 44,394,495–45,364,167; NCBI build 37), we found evidence for at least three independent signals: the strongest signal, consisting of a single SNP rs10941679, was associated with risk of estrogen receptor-positive (ER+) breast cancer (per-g allele OR ER+ = 1.15; 95% CI 1.13–1.18; p = 8.35 × 10−30). After adjustment for rs10941679, we detected signal 2, consisting of 38 SNPs more strongly associated with ER-negative (ER−) breast cancer (lead SNP rs6864776: per-a allele OR ER− = 1.10; 95% CI 1.05–1.14; p conditional = 1.44 × 10−12), and a single signal 3 SNP (rs200229088: per-t allele OR ER+ = 1.12; 95% CI 1.09–1.15; p conditional = 1.12 × 10−05). Expression quantitative trait locus analysis in normal breast tissues and breast tumors showed that the g (risk) allele of rs10941679 was associated with increased expression of FGF10 and MRPS30. Functional assays demonstrated that SNP rs10941679 maps to an enhancer element that physically interacts with the FGF10 and MRPS30 promoter regions in breast cancer cell lines. FGF10 is an oncogene that binds to FGFR2 and is overexpressed in ∼10% of human breast cancers, whereas MRPS30 plays a key role in apoptosis. These data suggest that the strongest signal of association at 5p12 is mediated through coordinated activation of FGF10 and MRPS30, two candidate genes for breast cancer pathogenesis

Identification of a BRCA2-Specific modifier locus at 6p24 related to breast cancer risk

Common genetic variants contribute to the observed variation in breast cancer risk for BRCA2 mutation carriers; those known to date have all been found through population-based genome-wide association studies (GWAS). To comprehensively identify breast cancer risk modifying loci for BRCA2 mutation carriers, we conducted a deep replication of an ongoing GWAS discovery study. Using the ranked P-values of the breast cancer associations with the imputed genotype of 1.4 M SNPs, 19,029 SNPs were selected and designed for inclusion on a custom Illumina array that included a total of 211,155 SNPs as part of a multi-consortial project. DNA samples from 3,881 breast cancer affected and 4,330 unaffected BRCA2 mutation carriers from 47 studies belonging to the Consortium of Investigators of Modifiers of BRCA1/2 were genotyped and available for analysis. We replicated previously reported breast cancer susceptibility alleles in these BRCA2 mutation carriers and for several regions (including FGFR2, MAP3K1, CDKN2A/B, and PTHLH) identified SNPs that have stronger evidence of association than those previously published. We also identified a novel susceptibility allele at 6p24 that was inversely associated with risk in BRCA2 mutation carriers (rs9348512; per allele HR = 0.85, 95% CI 0.80-0.90, P = 3.9×10−8). This SNP was not associated with breast cancer risk either in the general population or in BRCA1 mutation carriers. The locus lies within a region containing TFAP2A, which encodes a transcriptional activation protein that interacts with several tumor suppressor genes. This report identifies the first breast cancer risk locus specific to a BRCA2 mutation background. This comprehensive update of novel and previously reported breast cancer susceptibility loci contributes to the establishment of a panel of SNPs that modify breast cancer risk in BRCA2 mutation carriers. This panel may have clinical utility for women with BRCA2 mutations weighing options for medical prevention of breast cancer