9 research outputs found

    La conservation et la gestion des biomatériaux au sein du CCE d’Alsace

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    National audienceCentre for Conservation and Study (in French CCE) of Alsace, supported by Archéologie Alsace, departments of Bas-Rhin and Haut-Rhin and DRAC Grand Est, was inaugurated in 2016 in Sélestat with the aim of improving the conservation and management of archaeological material throughout Alsace. Biomaterials are particularly well represented at the CCE, notably because the main Alsatian museums, due to a lack of space and suitable premises, are sometimes unable to accommodate them when large lots are involved (fauna in particular). They are therefore kept at the CCE in specific depots in order to guarantee optimal conservation and management, according to their nature. Regular exchanges with specialists aim to gradually enrich the inventories with study data. Thanks to the CCE’s study rooms, which also include reference collections, these remains are regularly studied and easily accessible. Protocols and procedures to be followed in the event of sampling for destructive analyses have recently been drawn up in order to better manage the numerous requests.Le Centre de Conservation et d’Étude (CCE) d’Alsace, porté par Archéologie Alsace, les départements du Bas-Rhin et du Haut-Rhin et la DRAC Grand Est, a été inauguré, en 2016, à Sélestat en vue d’améliorer la conservation et la gestion du mobilier archéologique à l’échelle de l’Alsace. Les biomatériaux sont particulièrement bien représentés au CCE, notamment parce que les principaux musées alsaciens, par manque de place et de locaux adaptés, ne peuvent parfois pas les accueillir lorsqu’il s’agit de lots importants (faune notamment). Ils sont dès lors conservés au CCE dans des dépôts spécifiques afin de garantir une conservation et une gestion optimale, en fonction de leur nature. Des échanges réguliers avec les spécialistes ont pour objectif d’enrichir progressivement les inventaires avec les données d’étude. Grâce aux salles d’étude du CCE, comprenant également des collections de référence, ces restes sont régulièrement étudiés et facilement accessibles. Des protocoles et procédures à respecter en cas de prélèvement pour analyses destructrices ont été récemment élaborés afin de cadrer au mieux les nombreuses sollicitations

    Association between Parkinson's disease and the HLA-DRB1 locus.: Parkinson's Disease and HLADRB1

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    International audienceTwo genome-wide association studies (GWASs) recently highlighted the HLA-DRA and HLA-DRB5 genes as associated with Parkinson disease (PD). However, because HLA-DRA displays a low level of polymorphisms and HLA-DRB5 is only present in approximately 20% of the population, these findings are difficult to interpret. Our aims were: (1) to replicate and investigate in greater detail the association between PD and the HLA-DR region; (2) to identify PD-associated HLA alleles; and (3) to perform a meta-analysis of our top finding. As part of 2 French population-based case-control studies of PD including highly ethnically homogeneous participants, we investigated the association between PD and 51 Single-nucleotide polymorphisms (SNPs) in the HLA-DR region. HLA-DRB1 alleles were imputed using the HLA(*) IMP software. HLA typing was performed in a subsample of the participants. We performed a meta-analysis of our top finding based on 4 GWAS data sets. Among 499 cases and 1123 controls, after correction for multiple testing, we found an association with rs660895 (OR/minor allele, 0.70; 95% CI, 0.57-0.87) within the HLA-DRB1 gene, which encodes the most polymorphic HLA-DR chain (DRβ). A meta-analysis (7996 cases, 36455 controls) confirmed this association (OR, 0.86; 95% CI, 0.82-0.91; P < .0001). SNP-based imputation of HLA alleles showed an inverse association between PD and the HLA-DRB1(*) 04 allele. We replicated an association between PD and the HLA-DR region and provided further insight into the loci and alleles involved. The highly polymorphic HLA-DRB1 locus contains rs660895, which represents a more legitimate candidate than previous ones. Our finding is in agreement with the hypothesis of an immune component in PD pathophysiology. © 2012 Movement Disorder Society

    Lack of replication of the GRIN2A-by-coffee interaction in Parkinson disease.

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    International audienceOverview The etiology of Parkinson disease (PD) involves both genetic susceptibility and environmental exposures. In particular, coffee consumption is inversely associated with PD but the mechanisms underlying this intriguing association are unknown. According to a recent genome-wide gene–environment interaction study, the inverse coffee–PD association was two times stronger among carriers of the T allele of SNP rs4998386 in gene GRIN2A than in homozygotes for the C allele. We attempted to replicate this result in a similarly sized pooled analysis of 2,289 cases and 2,809 controls from four independent studies (Denmark, France, Seattle-United States (US), and Rochester-US) with detailed caffeinated coffee consumption data and rs4998386 genotypes. Using a variety of definitions of coffee drinking and statistical modeling techniques , we failed to replicate this interaction. Notably, whereas in the original study there was an association between rs4998386 and coffee consumption among controls, but not among cases, none of the datasets analyzed here indicated an association between rs4998386 and coffee consumption among controls. Based on large, well-characterized datasets independent from the original study, our results are not in favor of an interaction between caffeinated coffee consumption and rs4998386 for PD risk and suggest that the original finding may have been driven by an association of coffee consumption with rs4998386 in controls. The next years will likely see an increasing number of papers examining gene–environment interactions at the genome-wide level, which poses important methodological challenges. Our findings underline the need for a careful assessment of the findings of such studies

    Association of coffee drinking with the CT-TT genotype of rs4998386 in the <i>GRIN2A</i> gene among controls.

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    <p>Odds ratios (OR) and 95% confidence intervals (CI) were computed using logistic regression and adjusted for sex, age in quartiles, ever cigarette smoking, and dataset. ORs compare the odds of carrying the rs4998386-CT or TT genotypes (outcome) in coffee drinkers (exposure) to the odds of carrying the rs4998386-CT/TT genotypes in never coffee drinkers among controls (France, Denmark, Seattle-US, N = 2494; Rochester, N = 315; pooled analysis, N = 2809).</p><p>Association of coffee drinking with the CT-TT genotype of rs4998386 in the <i>GRIN2A</i> gene among controls.</p

    Association of coffee drinking with the CT-TT genotype of rs4998386 in the <i>GRIN2A</i> gene among Parkinson disease cases.

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    <p>Odds ratios (OR) and 95% confidence intervals (CI) were computed using logistic regression and adjusted for sex, age in quartiles, ever cigarette smoking, and dataset. ORs compare the odds of carrying the rs4998386-CT or TT genotypes (outcome) in coffee drinkers (exposure) to the odds of carrying the rs4998386-CT/TT genotypes in never coffee drinkers among cases (France, Denmark, Seattle-US, N = 1974; Rochester, N = 315; pooled analysis, N = 2289).</p><p>Association of coffee drinking with the CT-TT genotype of rs4998386 in the <i>GRIN2A</i> gene among Parkinson disease cases.</p

    Independent and joint effects of coffee drinking and <i>GRIN2A</i>-rs4998386 for Parkinson disease.

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    a<p>Odds ratios (OR) and 95% confidence intervals (CI) computed using unconditional logistic regression and adjusted for sex, age in quartiles, ever cigarette smoking, and dataset (1974 cases, 2494 controls).</p>b<p>Odds ratios (OR) and 95% confidence intervals (CI) computed using conditional logistic regression and adjusted for sex, age in quartiles, and ever cigarette smoking (315 cases, 315 controls).</p>c<p>Odds ratios (OR) and 95% confidence intervals (CI) computed by pooling individual data from the matched and unmatched case-control analyses and adjusted for sex, age in quartiles, ever cigarette smoking, and dataset (2289 cases, 2809 controls).</p>d<p>Global test of interaction: p-values were computed using a likelihood ratio test that compared the likelihood of models with and without interaction terms.</p><p>Independent and joint effects of coffee drinking and <i>GRIN2A</i>-rs4998386 for Parkinson disease.</p
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