Französisch-Fehler von Lernenden der französischen Rechtssprache: Fehleranalyse einer universitären Klausuren-Stichprobe

Gegenstand dieser Dissertation sind die allgemeinsprachlichen Fehler von Lernenden der französischen Rechtssprache im Hochschulkontext: Welche allgemeinsprachlichen Sprachschwierigkeiten bringen die Lernenden in den fachsprachlichen Unterricht mit, die im fachsprachlichen Unterrichtscurriculum berücksichtigt werden sollten? Eine Stichprobe von Klausuren wurde mit der Methode der Fehleranalyse untersucht. Zum Forschungshintergrund situiert sich diese Arbeit an der Kreuzung zwischen (Fehler-)Linguistik, Fachsprachenforschung sowie nah an der fachspachlichen Fehlerlinguistik. Die forschungsinterne Relevanz der Arbeit wird u.a. mit Fluck (1992) untermauert, dessen Behauptung immer noch hochaktuell ist: „Es fällt auf, daß lediglich die Wirtschaftssprache der gängigsten Fremdsprachen fehlerlinguistisch bereits einigermaßen erfaßt worden ist; Studien zu den Fehlern in verschiedenen Fächern […] stellen derzeit das vielleicht dringendste Desideratum einer fachsprachlichen Fehlerlinguistik dar.“ (Fluck 1992: 213) Er stellt weiterhin fest, dass es „Defizite bei der Fehleranalyse im fachsprachlichen Unterricht“ gibt (ebd.). Ergebnis dieser Untersuchung sind 7 Fehlerkategorien aus der genutzten Taxonomie, die nach quantitativer deskriptiv-statistischer Auswertung besonders repräsentiert sind und deren qualitative Untersuchung die 10 fachsprachlich merkmalarme Grundregeln ergibt, denen (nicht nur) der francais juridique-Unterricht Beachtung schenken könnte

Développement d'un modèle logiciel de cellule sur processeurs multi-cœurs pour la simulation de morphogenèse de tissus

The main purpose of this thesis is to present tools built in order to numerically study the development of cellular tissues through an individual-based approach that includes biomechanical elements as well as an artificial chemistry. The objective of such proposals is to gain a better understanding of the mechanisms that rule the development of multicellular tissues using numerical simulation as a complement to in vitro and in vivo experiments. This objective is difcult to achieve. However technological means in the field of cellular and molecular biology allow the observation and the gathering of many data. Moreover, the development of multi-core devices allows the simulation of complex systems, such as multi-cellular systems. Multi-cellular systems exhibit mainly two levels of complexity : the first one concerns the potentially large amount of cells they contain, which requires a considerable computing power when this point is addressed through individual-based approach; the second level concerns the diversity of biological cells’ behaviors. This level requires specific algorithms, for example to deal with complex behavior such as mitosis. The conception of 1) models that integrate biological data and 2) dedicated algorithms adapted to heterogenous and multi-core devices make it possible to solve, at least to some extent, these two levels of complexity. In order to numerically study both healthy and pathological tissue developpement, we propose two elements. The first is a biomechanical cell model that includes the behaviors involved in tissue morphogenesis (mitosis, diferentiation, adhesion, migration, cell-cell signaling and apoptosis). The second element is a parallel simulator that relies on a non-specialized software architecture and on dedicated data structures and algorithms used to benefit from the power of multi-core hardware. In this document, we present several case studies that gives some validation elements of both our model and our simulator.L’objectif principal de cette thèse est de proposer des outils permettant l’étude numérique du développement de tissus cellulaires à travers une approche individus-centrée comprenant des aspects biomécaniques et chimiques. De telles propositions doivent permettre de mieux comprendre les mécanismes régissant le développement de tissus multi-cellulaires grâce à la simulation numérique, en complément d’expérimentations in vitro et in vivo. La réalisation de ces objectifs est difficile, mais les avancées dans les domaines de la biologie cellulaire et moléculaire permettent l’observation et la collecte d’un grand nombre de données. En outre, le développement de matériels parallèles permet la simulation de systèmes complexes tels que des systèmes multi-cellulaires. Les systèmes multi-cellulaires exhibent essentiellement deux niveaux de complexité lorsque l’on souhaite les simuler: le premier concerne le nombre potentiellement très important de cellules qu’ils contiennent, nécessitant alors une grande puissance de calcul; le second concerne la multiplicité des comportements des cellules vivantes, tant au niveau individuel que collectif, ce qui requiert des algorithmes bien spécifiques. La conception de modèles, intégrant à la fois des données biologiques pertinentes, des algorithmes adaptés et reposant sur des processeurs puissants permet de résoudre, au moins en partie, ces deux niveaux de complexité, mais doivent reposer sur une architecture logicielle dédiée. Dans l’idée d’étudier, en simulation numérique, le développement de tissus sains et pathologiques, nos travaux apportent deux éléments. Le premier est un modèle biomécanique de cellule virtuelle comportant des processus impliqués dans la morphogenèse de tissus tels que la division, la différentiation, l’adhésion, la migration, la signalisation et l’apoptose. Le second est un simulateur parallèle reposant sur une architecture logicielle généraliste ainsi que sur des structures de données et des algorithmes originaux permettant d’exploiter la puissance de calcul offerte par les matériels multi-cœurs. Nous présentons dans ce mémoire plusieurs cas d’études qui permettent d’apporter des éléments de validation sur la réalisation de notre modèle et de notre simulateur

Progressive Retinal Atrophy in the Border Collie: A new XLPRA

<p>Abstract</p> <p>Background</p> <p>Several forms of progressive retinal atrophy (PRA) segregate in more than 100 breeds of dog with each PRA segregating in one or a few breeds. This breed specificity may be accounted for by founder effects and genetic drift, which have reduced the genetic heterogeneity of each breed, thereby facilitating the identification of causal mutations. We report here a new form of PRA segregating in the Border Collie breed. The clinical signs, including the loss of night vision and a progressive loss of day vision, resulting in complete blindness, occur at the age of three to four years and may be detected earlier through systematic ocular fundus examination and electroretinography (ERG).</p> <p>Results</p> <p>Ophthalmic examinations performed on 487 dogs showed that affected dogs present a classical form of PRA. Of those, 274 have been sampled for DNA extraction and 87 could be connected through a large pedigree. Segregation analysis suggested an X-linked mode of transmission; therefore both XLPRA1 and XLPRA2 mutations were excluded through the genetic tests.</p> <p>Conclusion</p> <p>Having excluded these mutations, we suggest that this PRA segregating in Border Collie is a new XLPRA (XLPRA3) and propose it as a potential model for the homologous human disease, X-Linked Retinitis Pigmentosa.</p

Inactive matrix gla protein plasma levels are associated with peripheral neuropathy in Type 2 diabetes.

AIMS/HYPOTHESIS Diabetic peripheral neuropathy is a frequent and severe complication of diabetes. As Matrix-gla-protein (MGP) is expressed in several components of the nervous system and is involved in some neurological disease, MGP could play a role in peripheral nervous system homeostasis. The aim of this study was to evaluate factors associated with sensitive diabetic neuropathy in Type 2 Diabetes, and, in particular, dephospho-uncarboxylated MGP (dp-ucMGP), the inactive form of MGP. METHODS 198 patients with Type 2 Diabetes were included. Presence of sensitive diabetic neuropathy was defined by a neuropathy disability score (NDS) ≥6. Plasma levels of dp-ucMGP were measured by ELISA. RESULTS In this cohort, the mean age was 64+/-8.4 years old, and 80% of patients were men. Peripheral neuropathy was present in 15.7% of the patients and was significantly associated (r = 0.51, p<0.0001) with dp-ucMGP levels (β = -0.26, p = 0.045) after integrating effects of height (β = -0.38, p = 0.01), insulin treatment (β = 0.42, p = 0.002), retinopathy treated by laser (β = 0.26, p = 0.02), and total cholesterol levels (β = 0.3, p = 0.03) by multivariable analysis. CONCLUSIONS The association between diabetic neuropathy and the inactive form of MGP suggests the existence of new pathophysiological pathways to explore. Further studies are needed to determine if dp-ucMGP may be used as a biomarker of sensitive neuropathy. Since dp-ucMGP is a marker of poor vitamin K status, clinical studies are warranted to explore the potential protective effect of high vitamin K intake on diabetic peripheral neuropathy

Identification of OCA2 as a novel locus for the co-morbidity of asthma-plus-eczema

Background: Numerous genes have been associated with the three most common allergic diseases (asthma, allergic rhinitis or eczema) but these genes explain only a part of the heritability. In the vast majority of genetic studies, complex phenotypes such as co- morbidity of two of these diseases, have not been considered. This may partly explain missing heritability. Objective: To identify genetic variants specifically associated with the co-morbidity of asthma-plus-eczema. Methods: We first conducted a meta-analysis of four GWAS (Genome-Wide Association Study) of the combined asthma-plus-eczema phenotype (total of 8807 European-ancestry subjects of whom 1208 subjects had both asthma and eczema). To assess whether the association with SNP(s) was specific to the co- morbidity, we also conducted a meta-analysis of homogeneity test of association according to disease status (“asthma-plus-eczema” vs. the presence of only one disease “asthma only or eczema only”). We then used a joint test by combining the two test statistics from the co-morbidity-SNP association and the phenotypic heterogeneity of SNP effect meta-analyses. Results: Seven SNPs were detected for specific association to the asthma-plus-eczema co-morbidity, two with significant and five with suggestive evidence using the joint test after correction for multiple testing. The two significant SNPs are located in the OCA2 gene (Oculocutaneous Albinism II), a new locus never detected for significant evidence of association with any allergic disease. This gene is a promising candidate gene, because of its link to skin and lung diseases, and to epithelial barrier and immune mechanisms. Conclusion: Our study underlines the importance of studying sub-phenotypes as co-morbidities to detect new susceptibility genes

Analysis of GWAS-nominated loci for lung cancer and COPD revealed a new asthma locus

Background: Asthma, lung cancer (LC) and chronic obstructive pulmonary disease (COPD) are three respiratory diseases characterized by complex mechanisms underlying and genetic predispositions, with asthma having the highest calculated heritability. Despite efforts deployed in the last decades, only a small part of its heritability has been elucidated. It was hypothesized that shared genetic factors by these three diseases could help identify new asthma loci. Methods: GWAS-nominated LC and COPD loci were selected among studies performed in Caucasian cohorts using the GWAS Catalog. Genetic analyses were carried out for these loci in the Saguenay–Lac-Saint-Jean (SLSJ) asthma familial cohort and then replicated in two independent cohorts (the Canadian Cohort Obstructive Lung Disease [CanCOLD] and the Epidemiological Study of the Genetics and Environment of Asthma [EGEA]). Results: Analyses in the SLSJ cohort identified 2851 and 4702 genetic variants to be replicated in the CanCOLD and EGEA cohorts for LC and COPD loci respectively. Replication and meta-analyses allowed the association of one new locus with asthma, 2p24.3, from COPD studies. None was associated from LC studies reported. Conclusions: The approach used in this study contributed to better understand the heritability of asthma with shared genetic backgrounds of respiratory diseases

Interleukin 9–induced In Vivo Expansion of the B-1 Lymphocyte Population

The activity of interleukin (IL)-9 on B cells was analyzed in vivo using transgenic mice that constitutively express this cytokine. These mice show an increase in both baseline and antigen-specific immunoglobulin concentrations for all isotypes tested. Analysis of B cell populations showed a specific expansion of Mac-1+ B-1 cells in the peritoneal and pleuropericardial cavities, and in the blood of IL-9 transgenic mice. In normal mice, the IL-9 receptor was found to be expressed by CD5+ as well as CD5− B-1 cells, and repeated injections of IL-9 resulted in accumulation of B-1 cells in the peritoneal cavity, as observed in transgenic animals. Unlike other mouse models, such as IL-5 transgenic mice, in which expansion of the B-1 population is associated with high levels of autoantibodies, IL-9 did not stimulate the production of autoantibodies in vivo, and most of the expanded cells were found to belong to the B-1b subset (IgM+Mac-1+CD5−). In addition, we found that these IL-9–expanded B-1b cells do not share the well-documented antibromelain-treated red blood cell specificity of CD5+ B-1a cells. The increase of antigen-specific antibody concentration in immunized mice suggests that these B-1 cells are directly or indirectly involved in antibody responses in IL-9 transgenic mice

Molecular Adaptation to Folivory and the Conservation Implications for Madagascar’s Lemurs

The lemurs of Madagascar include numerous species characterized by folivory across several families. Many extant lemuriform folivores exist in sympatry in Madagascar’s remaining forests. These species avoid feeding competition by adopting different dietary strategies within folivory, reflected in behavioral, morphological, and microbiota diversity across species. These conditions make lemurs an ideal study system for understanding adaptation to leaf-eating. Most folivorous lemurs are also highly endangered. The significance of folivory for conservation outlook is complex. Though generalist folivores may be relatively well equipped to survive habitat disturbance, specialist folivores occupying narrow dietary niches may be less resilient. Characterizing the genetic bases of adaptation to folivory across species and lineages can provide insights into their differential physiology and potential to resist habitat change. We recently reported accelerated genetic change in RNASE1, a gene encoding an enzyme (RNase 1) involved in molecular adaptation in mammalian folivores, including various monkeys and sifakas (genus Propithecus; family Indriidae). Here, we sought to assess whether other lemurs, including phylogenetically and ecologically diverse folivores, might show parallel adaptive change in RNASE1 that could underlie a capacity for efficient folivory. We characterized RNASE1in 21 lemur species representing all five families and members of the three extant folivorous lineages: (1) bamboo lemurs (family Lemuridae), (2) sportive lemurs (family Lepilemuridae), and (3) indriids (family Indriidae). We found pervasive sequence change in RNASE1 across all indriids, a dN/dS value \u3e 3 in this clade, and evidence for shared change in isoelectric point, indicating altered enzymatic function. Sportive and bamboo lemurs, in contrast, showed more modest sequence change. The greater change in indriids may reflect a shared strategy emphasizing complex gut morphology and microbiota to facilitate folivory. This case study illustrates how genetic analysis may reveal differences in functional traits that could influence species’ ecology and, in turn, their resilience to habitat change. Moreover, our results support the body of work demonstrating that not all primate folivores are built the same and reiterate the need to avoid generalizations about dietary guild in considering conservation outlook, particularly in lemurs where such diversity in folivory has probably led to extensive specialization via niche partitioning

Frequency and Risk Indicators of Tooth Decay among Pregnant Women in France: A Cross-Sectional Analysis

INTRODUCTION: Little is known on the prevalence of tooth decay among pregnant women. Better knowledge of tooth decay risk indicators during pregnancy could help to develop follow-up protocols for women at risk, along with better prevention strategies. The aim of this study was to assess the frequency of tooth decay and the number of decayed teeth per woman in a large sample of pregnant women in France, and to study associated risk indicators. METHODS: A secondary cross-sectional analysis of data from a French multicentre case-control study was performed. The sample was composed of 1094 at-term women of six maternity units. A dental examination was carried out within 2 to 4 days post-partum. Socio-demographic and behavioural characteristics were obtained through a standardised interview with the women. Medical characteristics were obtained from the women's medical records. Risk indicators associated with tooth decay were identified using a negative binomial hurdle model. RESULTS: 51.6% of the women had tooth decay. The mean number of decayed teeth among women having at least one was 3.1 (s.d. = 2.8). Having tooth decay was statistically associated with lower age (aOR = 1.58, 95%CI [1.03,2.45]), lower educational level (aOR = 1.53, 95%CI [1.06,2.23]) and dental plaque (aOR = 1.75, 95%CI [1.27,2.41]). The number of decayed teeth was associated with the same risk indicators and with non-French nationality and inadequate prenatal care. DISCUSSION: The frequency of tooth decay and the number of decayed teeth among pregnant women were high. Oral health promotion programmes must continue to inform women and care providers about the importance of dental care before, during and after pregnancy. Future research should also assess the effectiveness of public policies related to oral health in target populations of pregnant women facing challenging social or economic situations