191 research outputs found

    Projet Ecotic. Rapport final. Technologies numériques et crise environnementale : peut-on croire aux TIC vertes ?

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    La prise de conscience d’une crise environnementale majeure ainsi que la numĂ©risation croissante denos modes de vie constituent deux Ă©lĂ©ments saillants des transformations actuelles de notre sociĂ©tĂ©.Notre Ă©tude a pour objectif de mieux comprendre la nature du lien entre ces deux facettes de notresociĂ©tĂ© et questionne les enjeux Ă©cologiques des technologies numĂ©riques de l’information et de lacommunication (TNIC).Le terme de « Green IT » ou « TIC vertes » commence Ă  se diffuser, afin d’affirmer le potentielĂ©cologique de ces technologies ou, au contraire, d’en souligner le caractĂšre usurpateur. La productionet l’usage des TIC participent-ils Ă  rendre notre sociĂ©tĂ© plus Ă©cologique ou bien gĂ©nĂšrent-il despollutions et des « effets rebonds » qui pourraient bien faire plus qu’annuler les bĂ©nĂ©ficesescomptĂ©s ? Notre Ă©tude vise Ă  dresser un tableau de la rĂ©alitĂ© des TIC vertes et pose la question :peut-on croire aux « TIC vertes » ?Pour rĂ©pondre Ă  cette interrogation, notre Ă©tude s’appuie sur une approche interdisciplinaire relevant Ă la fois des sciences sociales (philosophie, sociologie, sciences politiques, gestion, marketing) et dessciences de l’ingĂ©nieur. La mĂ©thode de recherche mobilise conjointement une large revue de lalittĂ©rature acadĂ©mique et professionnelle, des entretiens avec des acteurs clĂ©s ainsi que destechniques de focus group auprĂšs d’utilisateurs des TNIC.Dans la premiĂšre partie de l’étude, un bilan des connaissances sur le domaine est rĂ©alisĂ©. Suite Ă  unpanorama des grands enjeux, un Ă©tat des lieux est apportĂ© sur la question environnementale en lienavec le dĂ©veloppement des technologies numĂ©riques. Les chiffres clĂ©s sont prĂ©sentĂ©s, montrantl’urgence de la question. Les mĂ©thodes d’analyse actuelles permettant d’évaluer le caractĂšreenvironnemental des technologies numĂ©riques sont Ă©tudiĂ©es d’un point de vue critique : centrĂ©es surles effets directs « de premier ordre » et sur le cycle de vie des technologies, ces mĂ©thodes d’analysene soulĂšvent gĂ©nĂ©ralement pas ou peu les questions sociales et sociĂ©tales qui s’imposent.La seconde partie de notre Ă©tude, plus empirique, vise Ă  approfondir les reprĂ©sentations et lesengagements des acteurs socioĂ©conomiques vis-Ă -vis des technologies numĂ©riques vertes. Cesinvestigations se penchent aussi bien sur les points de vue des producteurs, des distributeurs, despouvoirs publics que ceux du mouvement associatif ou des consommateurs. Nous abordons aussi lesĂ©lĂ©ments quantitatifs qui sont mis en avant. Comment leurs rapports entre Ă©cologie et technologiesnumĂ©riques diffĂšrent, se complĂštent ou s’opposent-t-ils ? C’est lĂ  que rĂ©side toute la difficultĂ© decomprĂ©hension de la notion de technologie numĂ©rique « verte ».La conclusion de l’étude apporte plusieurs rĂ©ponses en soulignant les diffĂ©rentes prioritĂ©s qui existentet le jeu de report de responsabilitĂ©s qui s’opĂšre entre acteurs. Ces rĂ©sultats nous amĂšnent Ă  Ă©largirle dĂ©bat autour de la notion de consommation verte (consommer sa juste part de nature) etd’acception de la notion de modernitĂ©. OĂč la modernitĂ© ne se rĂ©duit pas Ă  un tout numĂ©rique. (rĂ©sumĂ© exĂ©cutif

    Quasi-linear Masking to Protect Kyber against both SCA and FIA

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    The recent technological advances in Post-Quantum Cryptography (PQC) rise the questions of robust implementations of new asymmetric cryptographic primitives in today’s technology. This is the case for the lattice-based CRYSTALS-Kyber algorithm which has been selected as the first NIST standard for Public Key Encryption (PKE) and Key Encapsulation Mechanisms (KEM). We have notably to make sure the Kyber implementation is resilient against physical attacks like Side-Channel Analysis (SCA) and Fault Injection Attacks (FIA). To reach this goal, we propose to use the masking countermeasure, more precisely the generic Direct Sum Masking method (DSM). By taking inspiration of a previous paper on AES, we extend the method to finite fields of characteristic prime other than 2 and even-length codes. In particular, we investigated its application to Keccak, which is the hash-based function used in Kyber. We also provided the first masked implementation of Kyber providing both SCA and FIA resilience while not requiring any conversion between different masking methods

    Carbon Nanotubes by a CVD Method. Part I: Synthesis and Characterization of the (Mg, Fe)O Catalysts

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    The controlled synthesis of carbon nanotubes by chemical vapor deposition requires tailored and wellcharacterized catalyst materials. We attempted to synthesize Mg1-xFexO oxide solid solutions by the combustion route, with the aim of performing a detailed investigation of the influence of the synthesis conditions (nitrate/urea ratio and the iron content) on the valency and distribution of the iron ions and phases. Notably, characterization of the catalyst materials is performed using 57Fe Mošssbauer spectroscopy, X-ray diffraction, and electron microscopy. Several iron species are detected including Fe2+ ions substituting for Mg2+ in the MgO lattice, Fe3+ ions dispersed in the octahedral sites of MgO, different clusters of Fe3+ ions, and MgFe2O4-like nanoparticles. The dispersion of these species and the microstructure of the oxides are discussed. Powders markedly different from one another that may serve as model systems for further study are identified. The formation of carbon nanotubes upon reduction in a H2/CH4 gas atmosphere of the selected powders is reported in a companion paper

    Association of breast cancer risk in BRCA1 and BRCA2 mutation carriers with genetic variants showing differential allelic expression:Identification of a modifier of breast cancer risk at locus 11q22.3

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    Cis-acting regulatory SNPs resulting in differential allelic expression (DAE) may, in part, explain the underlying phenotypic variation associated with many complex diseases. To investigate whether common variants associated with DAE were involved in breast cancer susceptibility among BRCA1 and BRCA2 mutation carriers, a list of 175 genes was developed based of their involvement in cancer-related pathways.Using data from a genome-wide map of SNPs associated with allelic expression, we assessed the association of similar to 320 SNPs located in the vicinity of these genes with breast and ovarian cancer risks in 15,252 BRCA1 and 8211 BRCA2 mutation carriers ascertained from 54 studies participating in the Consortium of Investigators of Modifiers of BRCA1/2.We identified a region on 11q22.3 that is significantly associated with breast cancer risk in BRCA1 mutation carriers (most significant SNP rs228595 p = 7 x 10(-6)). This association was absent in BRCA2 carriers (p = 0.57). The 11q22.3 region notably encompasses genes such as ACAT1, NPAT, and ATM. Expression quantitative trait loci associations were observed in both normal breast and tumors across this region, namely for ACAT1, ATM, and other genes. In silico analysis revealed some overlap between top risk-associated SNPs and relevant biological features in mammary cell data, which suggests potential functional significance.We identified 11q22.3 as a new modifier locus in BRCA1 carriers. Replication in larger studies using estrogen receptor (ER)-negative or triple-negative (i.e., ER-, progesterone receptor-, and HER2-negative) cases could therefore be helpful to confirm the association of this locus with breast cancer risk.</p

    Assessing associations between the AURKAHMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers

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    While interplay between BRCA1 and AURKA-RHAMM-TPX2-TUBG1 regulates mammary epithelial polarization, common genetic variation in HMMR (gene product RHAMM) may be associated with risk of breast cancer in BRCA1 mutation carriers. Following on these observations, we further assessed the link between the AURKA-HMMR-TPX2-TUBG1 functional module and risk of breast cancer in BRCA1 or BRCA2 mutation carriers. Forty-one single nucleotide polymorphisms (SNPs) were genotyped in 15,252 BRCA1 and 8,211 BRCA2 mutation carriers and subsequently analyzed using a retrospective likelihood appr

    Control of Oxo-Group Functionalization and Reduction of the Uranyl Ion

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    yesUranyl complexes of a large, compartmental N8-macrocycle adopt a rigid, “Pacman” geometry that stabilizes the UV oxidation state and promotes chemistry at a single uranyl oxo-group. We present here new and straightforward routes to singly reduced and oxo-silylated uranyl Pacman complexes and propose mechanisms that account for the product formation, and the byproduct distributions that are formed using alternative reagents. Uranyl(VI) Pacman complexes in which one oxo-group is functionalized by a single metal cation are activated toward single-electron reduction. As such, the addition of a second equivalent of a Lewis acidic metal complex such as MgN″2 (N″ = N(SiMe3)2) forms a uranyl(V) complex in which both oxo-groups are Mg functionalized as a result of Mg−N bond homolysis. In contrast, reactions with the less Lewis acidic complex [Zn(N″)Cl] favor the formation of weaker U−O−Zn dative interactions, leading to reductive silylation of the uranyl oxo-group in preference to metalation. Spectroscopic, crystallographic, and computational analysis of these reactions and of oxo-metalated products isolated by other routes have allowed us to propose mechanisms that account for pathways to metalation or silylation of the exo-oxogroup

    Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

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    A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3â€Č-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk

    Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk

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    BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat

    The FANCM:p.Arg658* truncating variant is associated with risk of triple-negative breast cancer

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    Abstract: Breast cancer is a common disease partially caused by genetic risk factors. Germline pathogenic variants in DNA repair genes BRCA1, BRCA2, PALB2, ATM, and CHEK2 are associated with breast cancer risk. FANCM, which encodes for a DNA translocase, has been proposed as a breast cancer predisposition gene, with greater effects for the ER-negative and triple-negative breast cancer (TNBC) subtypes. We tested the three recurrent protein-truncating variants FANCM:p.Arg658*, p.Gln1701*, and p.Arg1931* for association with breast cancer risk in 67,112 cases, 53,766 controls, and 26,662 carriers of pathogenic variants of BRCA1 or BRCA2. These three variants were also studied functionally by measuring survival and chromosome fragility in FANCM−/− patient-derived immortalized fibroblasts treated with diepoxybutane or olaparib. We observed that FANCM:p.Arg658* was associated with increased risk of ER-negative disease and TNBC (OR = 2.44, P = 0.034 and OR = 3.79; P = 0.009, respectively). In a country-restricted analysis, we confirmed the associations detected for FANCM:p.Arg658* and found that also FANCM:p.Arg1931* was associated with ER-negative breast cancer risk (OR = 1.96; P = 0.006). The functional results indicated that all three variants were deleterious affecting cell survival and chromosome stability with FANCM:p.Arg658* causing more severe phenotypes. In conclusion, we confirmed that the two rare FANCM deleterious variants p.Arg658* and p.Arg1931* are risk factors for ER-negative and TNBC subtypes. Overall our data suggest that the effect of truncating variants on breast cancer risk may depend on their position in the gene. Cell sensitivity to olaparib exposure, identifies a possible therapeutic option to treat FANCM-associated tumors
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