84 research outputs found

    Le paradoxe des émigrants indésirables pendant la monarchie de Juillet, ou les origines de lŽémigration assistée vers lŽAlgérie

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    DĂšs le dĂ©but de la conquĂȘte française, l’AlgĂ©rie a Ă©tĂ© perçue comme une possible colonie de peuplement. Toutefois, l’accomplissement de ce projet d’une « Nouvelle France » sur la rive sud de la MĂ©diterranĂ©e a rencontrĂ© de nombreux obstacles : les rĂ©ticences des Français Ă  Ă©migrer, la violence de la conquĂȘte militaire, mais aussi la difficultĂ© Ă  s’approprier les terres algĂ©riennes et « l’inaptitude » des premiers colons. La politique coloniale de la monarchie de Juillet visait Ă  contourner ces difficultĂ©s en encourageant l’émigration de « bons sujets », rĂ©pondant Ă  des critĂšres moraux, professionnels et physiques. Cet article, en analysant la politique d’émigration assistĂ©e, revient sur la dĂ©finition du « bon colon », sur les tentatives de recrutement de provinciaux pour l’AlgĂ©rie, mais aussi sur les conflits que cette Ă©migration a fait surgir entre Paris, Alger et les autoritĂ©s locales. Il met aussi en Ă©vidence les caractĂ©ristiques sociales des quelque vingt mille individus bĂ©nĂ©ficiaires d’un « passage gratuit » dans les deux premiĂšres dĂ©cennies de la conquĂȘte.From the beginning of the French conquest, Algeria was never seriously envisioned as anything other than a settler colony. France’s colonial history and Frenchmen’s reluctance to emigrate, as well as the violence of the military conquest, the difficulty of expropriating Algerian property, and the “inaptitude” of the first colonists, however, hindered the realization of this vision of a “new France” across the Mediterranean. The settlement policy developed under the July Monarchy sought to overcome these obstacles primarily by promoting the emigration of “bons sujets” who met particular moral, professional and physical criteria. By tracing the elaboration of this assisted emigration policy, I explore the definition of the “good colonist”, the mechanisms put in place to recruit emigrants in provincial France, the conflicts that arose between Paris, Algiers, and departmental and local authorities over Algerian emigration, and the identity of some twenty thousand individuals who were accorded free passages to Algeria in the first two decades of French colonization.Von Beginn der französischen Eroberung an wurde Algerien als mögliche Siedlungskolonie angesehen. Zahlreiche Hindernisse standen allerdings bei der Umsetzung des Projektes « Neues Frankreich » auf dem SĂŒdufer des Mittelmeers im Weg : das Zögern der Franzosen bei der Auswanderung, die Gewalt der militĂ€rischen Eroberung, aber auch die Schwierigkeit bei der Aneignung des algerischen Landes und die « Untauglichkeit » der ersten Siedler. Die Kolonialpolitik der Julimonarchie versuchte den Schwierigkeiten zu begegnen, indem « gute Untertanen », die moralischen, beruflichen und physischen Kriterien genĂŒgten, bei der Auswanderung unterstĂŒtzt wurden. Dieser Artikel analysiert die Politik der UnterstĂŒtzung der Auswanderer und geht dabei auf die Definition des „guten Kolonisten », wie auf die Versuche der Rekrutierung der französischen Provinzbevölkerung fĂŒr Algerien ein, aber auch auf die Konflikte, die diese Auswanderung zwischen Paris, Alger und den lokalen AutoritĂ€ten hervorrief. Der Artikel hebt außerdem die sozialen Eigenschaften der etwa 20.000 Personen hervor, die wĂ€hrend der ersten beiden Jahrzehnte der Eroberung von der GratisĂŒberfahrt nach Algerien profitierten

    An examination of shared leadership configurations and their effectiveness in teams

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    A key challenge in the shared leadership literature has been a limited understanding of how multiple leadership activities are shared across team members and roles. We address this issue by conceptualizing and operationalizing shared leadership using both its content (i.e., what leadership roles are shared) and distribution (i.e., how leadership is shared across members and roles). In an exploratory study comprised of 129 work teams, we use latent profile analysis (LPA) to identify multiple shared leadership configurations that vary in the extent of sharing. Our second study of 103 MBA teams supports these findings and further (a) considers what shared leadership configurations have the greatest influence on team effectiveness, (b) examines the mediating role of teamwork processes, and (c) investigates the moderating role of temporal dispersion. We advance current research by demonstrating that shared leadership typically manifests in collective (i.e., members share all leadership roles) and distributed configurations (i.e., members hold one leadership role while other members hold other leadership roles), which has implications for team processes and effectiveness. Specifically, we show that collective configurations have higher team effectiveness (compared to distributed configurations) owing to improved teamwork processes and observe that these effects are more pronounced when temporal dispersion is high

    Patient-specific iPSCs carrying an SFTPC mutation reveal the intrinsic alveolar epithelial dysfunction at the inception of interstitial lung disease

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    Alveolar epithelial type 2 cell (AEC2) dysfunction is implicated in the pathogenesis of adult and pediatric interstitial lung disease (ILD), including idiopathic pulmonary fibrosis (IPF); however, identification of disease-initiating mechanisms has been impeded by inability to access primary AEC2s early on. Here, we present a human in vitro model permitting investigation of epithelial-intrinsic events culminating in AEC2 dysfunction, using patient-specific induced pluripotent stem cells (iPSCs) carrying an AEC2-exclusive disease-associated variant (SFTP

    CemOrange2 fusions facilitate multifluorophore subcellular imaging in C. elegans

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    Due to its ease of genetic manipulation and transparency, Caenorhabditis elegans (C. elegans) has become a preferred model system to study gene function by microscopy. The use of Aequorea victoria green fluorescent protein (GFP) fused to proteins or targeting sequences of interest, further expanded upon the utility of C. elegans by labeling subcellular structures, which enables following their disposition during development or in the presence of genetic mutations. Fluorescent proteins with excitation and emission spectra different from that of GFP accelerated the use of multifluorophore imaging in real time. We have expanded the repertoire of fluorescent proteins for use in C. elegans by developing a codon-optimized version of Orange2 (CemOrange2). Proteins or targeting motifs fused to CemOrange2 were distinguishable from the more common fluorophores used in the nematode; such as GFP, YFP, and mKate2. We generated a panel of CemOrange2 fusion constructs, and confirmed they were targeted to their correct subcellular addresses by colocalization with independent markers. To demonstrate the potential usefulness of this new panel of fluorescent protein markers, we showed that CemOrange2 fusion proteins could be used to: 1) monitor biological pathways, 2) multiplex with other fluorescent proteins to determine colocalization and 3) gain phenotypic knowledge of a human ABCA3 orthologue, ABT-4, trafficking variant in the C. elegans model organism

    Discovery of a novel CHD7 CHARGE syndrome variant by integrated omics analyses

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    Chromodomain helicase DNA-binding protein 7 (CHD7) pathogenic variants are identified in more than 90% of infants and children with CHARGE (Coloboma of the iris, retina, and/or optic disk; congenital Heart defects, choanal Atresia, Retardation of growth and development, Genital hypoplasia, and characteristic outer and inner Ear anomalies and deafness) syndrome. Approximately, 10% of cases have no known genetic cause identified. We report a male child with clinical features of CHARGE syndrome and nondiagnostic genetic testing that included chromosomal microarray, CHD7 sequencing and deletion/duplication analysis, SEMA3E sequencing, and trio exome and whole-genome sequencing (WGS). We used a comprehensive clinical assessment, genome-wide methylation analysis (GMA), reanalysis of WGS data, and CHD7 RNA studies to discover a novel variant that causes CHD7 haploinsufficiency. The 7-year-old Hispanic male proband has typical phenotypic features of CHARGE syndrome. GMA revealed a CHD7-associated epigenetic signature. Reanalysis of the WGS data with focused bioinformatic analysis of CHD7 detected a novel, de novo 15 base pair deletion in Intron 4 of CHD7 (c.2239-20_2239-6delGTCTTGGGTTTTTGT [NM_017780.3]). Using proband RNA, we confirmed that this novel deletion causes CHD7 haploinsufficiency by disrupting the canonical 3â€Č splice site and introducing a premature stop codon. Integrated genomic, epigenomic, and transcriptome analyses discovered a novel CHD7 variant that causes CHARGE syndrome

    Project Report No. 59, Site Index Equations for Loblolly and Slash Pine Plantations in East Texas, Update: Fall 1997

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    Each published set of equations was developed from analyses of East Texas Pine Plantation Research Project (ETPPRP) data collected from the array of ETPPRP permanent research plots located throughout East Texas

    Altered Germination and Subcellular Localization Patterns for PUB44/SAUL1 in Response to Stress and Phytohormone Treatments

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    BACKGROUND: In plants, the ubiquitin-proteasome system is emerging as a significant regulatory system throughout the plant lifecycle. The ubiquitination of a target protein requires the sequential actions of the E1, E2 and E3 enzymes, with the latter E3 enzyme conferring target selection in this process. There are a large number of predicted E3 enzymes in plant genomes, and very little is known about the functions of many of these predicted genes. Here we report here an analysis of two closely-related members of the Arabidopsis Plant U-box (PUB) family of E3 ubiquitin ligases, PUB43 and PUB44. PRINCIPAL FINDINGS: Homozygous pub44/pub44 mutant seedlings were found displayed a seedling lethal phenotype and this corresponded with widespread cell death lesions throughout the cotyledons and roots. Interestingly, heterozygous PUB44/pub44 seedlings were wild-type in appearance yet displayed intermediate levels of cell death lesions in comparison to pub44/pub44 seedlings. In contrast, homozygous pub43/pub43 mutants were viable and did not show any signs of cell death despite the PUB43 gene being more highly expressed than PUB44. The PUB44 mutants are not classical lesion mimic mutants as they did not have increased resistance to plant pathogens. We also observed increased germination rates in mutant seeds for both PUB44 and PUB43 under inhibitory concentrations of abscisic acid. Finally, the subcellular localization of PUB44 was investigated with transient expression assays in BY-2 cells. Under varying conditions, PUB44 was observed to be localized to the cytoplasm, plasma membrane, or nucleus. CONCLUSIONS: Based on mutant plant analyses, the Arabidopsis PUB43 and PUB44 genes are proposed to function during seed germination and early seedling growth. Given PUB44's ability to shuttle from the nucleus to the plasma membrane, PUB44 may be active in different subcellular compartments as part of these biological functions

    The CYCLIN-A CYCA1;2/TAM Is Required for the Meiosis I to Meiosis II Transition and Cooperates with OSD1 for the Prophase to First Meiotic Division Transition

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    Meiosis halves the chromosome number because its two divisions follow a single round of DNA replication. This process involves two cell transitions, the transition from prophase to the first meiotic division (meiosis I) and the unique meiosis I to meiosis II transition. We show here that the A-type cyclin CYCA1;2/TAM plays a major role in both transitions in Arabidopsis. A series of tam mutants failed to enter meiosis II and thus produced diploid spores and functional diploid gametes. These diploid gametes had a recombined genotype produced through the single meiosis I division. In addition, by combining the tam-2 mutation with AtSpo11-1 and Atrec8, we obtained plants producing diploid gametes through a mitotic-like division that were genetically identical to their parents. Thus tam alleles displayed phenotypes very similar to that of the previously described osd1 mutant. Combining tam and osd1 mutations leads to a failure in the prophase to meiosis I transition during male meiosis and to the production of tetraploid spores and gametes. This suggests that TAM and OSD1 are involved in the control of both meiotic transitions

    Restoring Specific Lactobacilli Levels Decreases Inflammation and Muscle Atrophy Markers in an Acute Leukemia Mouse Model

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    The gut microbiota has recently been proposed as a novel component in the regulation of host homeostasis and immunity. We have assessed for the first time the role of the gut microbiota in a mouse model of leukemia (transplantation of BaF3 cells containing ectopic expression of Bcr-Abl), characterized at the final stage by a loss of fat mass, muscle atrophy, anorexia and inflammation. The gut microbial 16S rDNA analysis, using PCR-Denaturating Gradient Gel Electrophoresis and quantitative PCR, reveals a dysbiosis and a selective modulation of Lactobacillus spp. (decrease of L. reuteri and L. johnsonii/gasseri in favor of L. murinus/animalis) in the BaF3 mice compared to the controls. The restoration of Lactobacillus species by oral supplementation with L. reuteri 100-23 and L. gasseri 311476 reduced the expression of atrophy markers (Atrogin-1, MuRF1, LC3, Cathepsin L) in the gastrocnemius and in the tibialis, a phenomenon correlated with a decrease of inflammatory cytokines (interleukin-6, monocyte chemoattractant protein-1, interleukin-4, granulocyte colony-stimulating factor, quantified by multiplex immuno-assay). These positive effects are strain- and/or species-specific since L. acidophilus NCFM supplementation does not impact on muscle atrophy markers and systemic inflammation. Altogether, these results suggest that the gut microbiota could constitute a novel therapeutic target in the management of leukemia-associated inflammation and related disorders in the muscle
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