De la négritude à la migritude : une analyse sociologique de la littérature de l'Afrique francophone

La transformation de l'imaginaire dans les sociétés d'Afrique francophone noire est indéniable. Le mouvement de la négritude, qui prônait une Afrique unifiée dans les années 50-60, a laissé place à une grande déception suite aux Indépendances. Les dictatures qui ont suivi, la fin du communisme et les guerres ont fini par mettre fin au rêve d'une Afrique unifiée et par pousser une bonne partie de la jeunesse africaine à l'extérieur du continent. De plus, l'impact de la colonisation sur l'imaginaire africain est toujours prégnant, mais ses modalités se sont transformées avec la migration massive des jeunes Africains dans les pays occidentaux. Les écrivains des années 2000, qu'on appelle, ici, écrivains de la migritude, sont partis dans ces pays pour ne plus revenir sur leur terre natale, contrairement aux écrivains de la négritude. Ils ne se sentent plus en phase avec leur patrie, et du coup l'image de l'Afrique se transforme. L'enjeu identitaire est déterminant, autant que le parcours historique de ces jeunes écrivains. Le monde dans lequel ils évoluent est coloré par les migrations massives et le choc de l'incompréhension avec les sociétés d'accueil. Les questions de l'immigration et de l'acculturation sont-elles suffisantes pour transformer l'image identitaire d'un individu? Où subsiste-t-il des substrats dans l'imaginaire de ces écrivains? Ont-ils des liens avec leurs prédécesseurs, les écrivains de la négritude? Ont-ils le rêve d'une Afrique qui émerge, ou sont-ils seulement partis pour devenir autre et autrement? Les écrivains de la migritude sont-ils le symbole de la transformation radicale de l'image de l'Afrique? Pour répondre à ces questions, nous allons d'abord rechercher dans les écrits des romanciers de la migritude ce qu'ils ont en commun. Pour obtenir ces données, nous ferons une lecture des œuvres choisies à partir de la théorie du chronotope de Bakhtine. L'idée étant de trouver une écriture type à travers l'utilisation de l'espace-temps et des différents procédés narratifs. Si les écrivains de la migritude usent des mêmes types de chronotopes, c'est qu'ils partagent un même imaginaire et s'inscrivent de façon particulière dans l'histoire littéraire du continent africain et exercent une influence sur leurs pairs. Ce type d'analyse va permette de mettre en relief la transformation de l'imaginaire qui a cours en Afrique francophone noire et d'y voir les modulations sociétales au plan de l'identité et du devenir imaginé des sociétés africaines. Bien sûr, l'interprétation reste partielle, mais permet de mettre en relief les différences de regards que portent les Africains par rapport à d'autres migrants. Par ailleurs, les écrivains migrants, nombreux à vivre les mêmes questionnements face à l'identité et face à la réalité de la migration à l'époque postcoloniale, vont nous servir de barème afin de voir la particularité africaine. Les enjeux du temps et de l'espace sont incontournables pour comprendre la posture des écrivains en situation de déterritorialisation, puisque la rencontre avec l'autre ne se fait plus à partir des mêmes bases qu'à l'époque coloniale. Il y a dorénavant un regard posé de part et d'autre. Ce n'est plus le seul point de vue occidental qui peut être porté sur les mondes étrangers. L'écrivain migrant va lui aussi poser son regard et former sa critique de façon à être l'objecteur de conscience de la société d'accueil. Cette recherche vise à mettre en lumière la transformation de l'imaginaire et ses modalités en Afrique francophone noire de l'époque coloniale à aujourd'hui, mais aussi, l'influence de cette transformation sur les autres sociétés, puisque la transformation se fait par le biais de migration massive. Il y a donc une interinfluence entre les sociétés. La question du vivre ensemble est alors incontournable et devient le sujet privilégié des écrivains; sujet qui est fondamental dans un monde en restructuration. \ud ______________________________________________________________________________ \ud MOTS-CLÉS DE L’AUTEUR : Imaginaire, Afrique, Négritude, Migritude, Identité, Altérité, Migration, Sociologie, Littératur

Preparation, characterization, and safety evaluation of poly(lactide-co-glycolide) nanoparticles for protein delivery into macrophages.

International audienceFollowing infection, HIV establishes reservoirs within tissues that are inaccessible to optimal levels of antiviral drugs or within cells where HIV lies latent, thus escaping the action of anti-HIV drugs. Macrophages are a persistent reservoir for HIV and may contribute to the rebound viremia observed after antiretroviral treatment is stopped. In this study, we further investigate the potential of poly(lactic-co-glycolic) acid (PLGA)-based nanocarriers as a new strategy to enhance penetration of therapeutic molecules into macrophages. We have prepared stable PLGA nanoparticles (NPs) and evaluated their capacity to transport an active molecule into the human monocyte/macrophage cell line THP-1 using bovine serum albumin (BSA) as a proof-of-concept compound. Intracellular localization of fluorescent BSA molecules encapsulated into PLGA NPs was monitored in live cells using confocal microscopy, and cellular uptake was quantified by flow cytometry. In vitro and in vivo toxicological studies were performed to further determine the safety profile of PLGA NPs including inflammatory effects. The size of the PLGA NPs carrying BSA (PLGA-BSA) in culture medium containing 10% serum was ~126 nm in diameter, and they were negatively charged at their surface (zeta potential =-5.6 mV). Our confocal microscopy studies and flow cytometry data showed that these PLGA-BSA NPs are rapidly and efficiently taken up by THP-1 monocyte-derived macrophages (MDMs) at low doses. We found that PLGA-BSA NPs increased cellular uptake and internalization of the protein in vitro. PLGA NPs were not cytotoxic for THP-1 MDM cells, did not modulate neutrophil apoptosis in vitro, and did not show inflammatory effect in vivo in the murine air pouch model of acute inflammation. In contrast to BSA alone, BSA encapsulated into PLGA NPs increased leukocyte infiltration in vivo, suggesting the in vivo enhanced delivery and protection of the protein by the polymer nanocarrier. We demonstrated that PLGA-based nanopolymer carriers are good candidates to efficiently and safely enhance the transport of active molecules into human MDMs. In addition, we further investigated their inflammatory profile and showed that PLGA NPs have low inflammatory effects in vitro and in vivo. Thus, PLGA nanocarriers are promising as a drug delivery strategy in macrophages for prevention and eradication of intracellular pathogens such as HIV and Mycobacterium tuberculosis

The dog and rat olfactory receptor repertoires

BACKGROUND: Dogs and rats have a highly developed capability to detect and identify odorant molecules, even at minute concentrations. Previous analyses have shown that the olfactory receptors (ORs) that specifically bind odorant molecules are encoded by the largest gene family sequenced in mammals so far. RESULTS: We identified five amino acid patterns characteristic of ORs in the recently sequenced boxer dog and brown Norway rat genomes. Using these patterns, we retrieved 1,094 dog genes and 1,493 rat genes from these shotgun sequences. The retrieved sequences constitute the olfactory receptor repertoires of these two animals. Subsets of 20.3% (for the dog) and 19.5% (for the rat) of these genes were annotated as pseudogenes as they had one or several mutations interrupting their open reading frames. We performed phylogenetic studies and organized these two repertoires into classes, families and subfamilies. CONCLUSION: We have established a complete or almost complete list of OR genes in the dog and the rat and have compared the sequences of these genes within and between the two species. Our results provide insight into the evolutionary development of these genes and the local amplifications that have led to the specific amplification of many subfamilies. We have also compared the human and rat ORs with the human and mouse OR repertoires

Lysosomal and network alterations in human mucopolysaccharidosis type VII iPSC-derived neural cells

Mucopolysaccharidosis type VII (MPS VII) is a lysosomal storage disease caused by deficient β-glucuronidase (β-gluc) activity. Significantly reduced β-gluc activity leads to accumulation of glycosaminoglycans (GAGs) in many tissues, including the brain. Numerous combinations of mutations in GUSB (the gene that codes for β-gluc) cause a range of neurological features that make disease prognosis and treatment challenging. Currently, there is little understanding of the molecular basis for MPS VII brain anomalies. To identify a neuronal phenotype that could be used to complement genetic analyses, we generated two iPSC clones derived from skin fibroblasts of an MPS VII patient. We found that MPS VII neurons exhibited reduced β-gluc activity and showed previously established disease-associated phenotypes, including GAGs accumulation, expanded endocytic compartments, accumulation of lipofuscin granules, more autophagosomes, and altered lysosome function. Addition of recombinant β-gluc to MPS VII neurons, which mimics enzyme replacement therapy, restored disease-associated phenotypes to levels similar to the healthy control. MPS VII neural cells cultured as 3D neurospheroids showed upregulated GFAP gene expression, which was associated with astrocyte reactivity, and downregulation of GABAergic neuron markers. Spontaneous calcium imaging analysis of MPS VII neurospheroids showed reduced neuronal activity and altered network connectivity in patient-derived neurospheroids compared to a healthy control. These results demonstrate the interplay between reduced β-gluc activity, GAG accumulation and alterations in neuronal activity, and provide a human experimental model for elucidating the bases of MPS VII-associated cognitive defects

An integrative multi‐scale approach to regional agriculture to support the assessment and benefit of pest‐regulation services delivered by biodiversity

Ecology is first of all a scientific discipline, with its body of theories and methods, and a constant renewal of its main specific fields and principles. In that regard, Ecology is not different from the other scientific disciplines and produces an increasing number of outstanding publications on both fundamental and applied grounds. Ecology can produce highly theoretical works, which is essential, but Ecology can be -and even moremust be an applied science. Currently, practical applications of Ecology for the benefits of our societies have become more numerous and increasingly urgent. ‘Interactions’, sensu lato, are at the very heart of Ecology which makes it by definition THE science of Biodiversity. Beyond the knowledge of how Life has appeared and developed, Ecology can provide the basis for the preservation of Biodiversity and ensure its management is relevant and efficient into the future. By being more integrative and global, Ecology could establish itself as the cornerstone of sustainable development. In this beginning of the 21st century, the influence of Ecology will inevitably grow and play a key role for Planet Earth and human well-being. Sfécologie2016, an International Conference on ecological sciences would not have taken place without 2 years of hard work from the staff of my Institute (IMBE). That is thus with a real pleasure that we welcome you today in Marseille. (Thierry TATONI IMBE Director

Randomized Controlled Ferret Study to Assess the Direct Impact of 2008–09 Trivalent Inactivated Influenza Vaccine on A(H1N1)pdm09 Disease Risk

During spring-summer 2009, several observational studies from Canada showed increased risk of medically-attended, laboratory-confirmed A(H1N1)pdm09 illness among prior recipients of 2008–09 trivalent inactivated influenza vaccine (TIV). Explanatory hypotheses included direct and indirect vaccine effects. In a randomized placebo-controlled ferret study, we tested whether prior receipt of 2008–09 TIV may have directly influenced A(H1N1)pdm09 illness. Thirty-two ferrets (16/group) received 0.5 mL intra-muscular injections of the Canadian-manufactured, commercially-available, non-adjuvanted, split 2008–09 Fluviral or PBS placebo on days 0 and 28. On day 49 all animals were challenged (Ch0) with A(H1N1)pdm09. Four ferrets per group were randomly selected for sacrifice at day 5 post-challenge (Ch+5) and the rest followed until Ch+14. Sera were tested for antibody to vaccine antigens and A(H1N1)pdm09 by hemagglutination inhibition (HI), microneutralization (MN), nucleoprotein-based ELISA and HA1-based microarray assays. Clinical characteristics and nasal virus titers were recorded pre-challenge then post-challenge until sacrifice when lung virus titers, cytokines and inflammatory scores were determined. Baseline characteristics were similar between the two groups of influenza-naïve animals. Antibody rise to vaccine antigens was evident by ELISA and HA1-based microarray but not by HI or MN assays; virus challenge raised antibody to A(H1N1)pdm09 by all assays in both groups. Beginning at Ch+2, vaccinated animals experienced greater loss of appetite and weight than placebo animals, reaching the greatest between-group difference in weight loss relative to baseline at Ch+5 (7.4% vs. 5.2%; p = 0.01). At Ch+5 vaccinated animals had higher lung virus titers (log-mean 4.96 vs. 4.23pfu/mL, respectively; p = 0.01), lung inflammatory scores (5.8 vs. 2.1, respectively; p = 0.051) and cytokine levels (p>0.05). At Ch+14, both groups had recovered. Findings in influenza-naïve, systematically-infected ferrets may not replicate the human experience. While they cannot be considered conclusive to explain human observations, these ferret findings are consistent with direct, adverse effect of prior 2008–09 TIV receipt on A(H1N1)pdm09 illness. As such, they warrant further in-depth investigation and search for possible mechanistic explanations

Randomized controlled ferret study to assess the direct impact of 2008-09 trivalent inactivated influenza vaccine on A(H1N1)pdm09 disease risk

During spring-summer 2009, several observational studies from Canada showed increased risk of medically-attended, laboratory-confirmed A(H1N1)pdm09 illness among prior recipients of 2008-09 trivalent inactivated influenza vaccine (TIV). Explanatory hypotheses included direct and indirect vaccine effects. In a randomized placebo-controlled ferret study, we tested whether prior receipt of 2008-09 TIV may have directly influenced A(H1N1)pdm09 illness. Thirty-two ferrets (16/group) received 0.5 mL intra-muscular injections of the Canadian-manufactured, commercially-available, non-adjuvanted, split 2008-09 Fluviral or PBS placebo on days 0 and 28. On day 49 all animals were challenged (Ch0) with A(H1N1)pdm09. Four ferrets per group were randomly selected for sacrifice at day 5 post-challenge (Ch+5) and the rest followed until Ch+14. Sera were tested for antibody to vaccine antigens and A(H1N1)pdm09 by hemagglutination inhibition (HI), microneutralization (MN), nucleoprotein-based ELISA and HA1-based microarray assays. Clinical characteristics and nasal virus titers were recorded pre-challenge then post-challenge until sacrifice when lung virus titers, cytokines and inflammatory scores were determined. Baseline characteristics were similar between the two groups of influenza-naïve animals. Antibody rise to vaccine antigens was evident by ELISA and HA1-based microarray but not by HI or MN assays; virus challenge raised antibody to A(H1N1)pdm09 by all assays in both groups. Beginning at Ch+2, vaccinated animals experienced greater loss of appetite and weight than placebo animals, reaching the greatest between-group difference in weight loss relative to baseline at Ch+5 (7.4% vs. 5.2%; p = 0.01). At Ch+ 5 vaccinated animals had higher lung virus titers (log-mean 4.96 vs. 4.23pfu/mL, respectively; p = 0.01), lung inflammatory scores (5.8 vs. 2.1, respectively; p = 0.051) and cytokine levels (p.0.05). At Ch+14, both groups had recovered. Findings in influenza-naïve, systematically-infected ferrets may not replicate the human experience. While they cannot be considered conclusive to explain human observations, these ferret findings are consistent with direct, adverse effect of prior 2008-09 TIV receipt on A(H1N1)pdm09 illness. As such, they warrant further in-depth investigation and search for possible mechanistic explanations

A Concerted Action of Engrailed and Gooseberry-Neuro in Neuroblast 6-4 Is Triggering the Formation of Embryonic Posterior Commissure Bundles

One challenging question in neurogenesis concerns the identification of cues that trigger axonal growth and pathfinding to form stereotypic neuronal networks during the construction of a nervous system. Here, we show that in Drosophila, Engrailed (EN) and Gooseberry-Neuro (GsbN) act together as cofactors to build the posterior commissures (PCs), which shapes the ventral nerve cord. Indeed, we show that these two proteins are acting together in axon growth and midline crossing, and that this concerted action occurs at early development, in neuroblasts. More precisely, we identified that their expressions in NB 6-4 are necessary and sufficient to trigger the formation of the PCs, demonstrating that segmentation genes such as EN and GsbN play a crucial role in the determination of NB 6-4 in a way that will later influence growth and guidance of all the axons that form the PCs. We also demonstrate a more specific function of GsbN in differentiated neurons, leading to fasciculations between axons, which might be required to obtain PC mature axon bundles

NAFLD (facteurs de sévérité et fibrose portale dans la NASH)

But : La NAFLD (non alcoholic fatty liver disease) est une hépatopathie fréquente chez les patients obèses et peut aboutir à la cirrhose avec ses complications notamment le carcinome hépatocellulaire (CHC). Le but de notre travail était d'identifier les marqueurs de stéato-hépatite et de fibrose définissant les patients à risque de développer des lésions histologiques sévères. Méthode : 108 patients français ayant une NAFLD prouvée par une ponction biopsie hépatique sans autre hépatopathie associée ont été sélectionnés. Les données cliniques, biologiques, échographiques recueillies chez ces sujets ont été comparées selon les lésions histologiques. Résultats : 51,9% avaient une stéatose simple, 18,5% une stéato-fibrose ,13,9% une NASH , 10,2% une stéato-hépatite avec fibrose portale et 5,6% une cirrhose avec 1 seul CHC. 71% avaient un BMI>25, 51% une hyperlipidémie, le syndrome métabolique et le diabète étant peu représentés (18,5% et 17,6%). Les facteurs significativement associés (p25, 51% a hyperlipidemia, whereas the metabolic syndrome and diabetes mellitus were less represented (18.5% and 17.6%). The significant risk factors for steato-hepatitis (p<0.05) were the male gender, diabetes mellitus, hyperlipidemia and severity of fatty liver. The significant risk factors for fibrosis (p<0.05) were diabetes mellitus, severity of fatty liver, presence of ballooning degeneration and Mallory bodies. Portal fibrosis was present in 42% of NASH and isolated steato-fibrosis had been reported. Conclusions: Diabetes mellitus and severity of fatty liver are risk factors for advanced forms of NAFLD. Portal fibrosis may be a lesion of NASH fibrosis and steato-fibrosis a lesion of NAFLDPARIS12-CRETEIL BU Médecine (940282101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF