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Étude de la compartimentalisation de la dystrophine dans le muscle squelettique et ses cellules souches résidentes
No full textDuchenne muscular dystrophy (DMD) is an X-linked recessive disorder caused by the loss of full-length dystrophin at the sarcolemma, resulting in myofiber fragility, degeneration, and impaired regeneration. Beyond this classical view, dysfunction of muscle stem cells (mSCs) has been proposed to contribute to disease progression, with studies suggesting that polarized dystrophin within mSCs regulates asymmetric division and self-renewal. My study aimed to elucidate the dynamic processes governing the establishment of dystrophin compartmentalization within muscle satellite cells. In this study, we reassessed the presence and distribution of dystrophin in mSCs using a mouse model expressing a dystrophin-EGFP fusion and tdTomato protein specifically in mSCs. Despite high Dmd transcription, no dystrophin protein was detected in mSCs at any activation state, as confirmed by in vivo imaging, histology, FACS, and capillary electrophoresis.Dystrophin accumulation observed near mSCs originated from the sarcolemma, rather than from the mSCs themselves, and showed no consistent polarity. These findings challenge the prevailing hypothesis that dystrophin plays a direct role in establishing muscle stem cell polarity, and question the requirement for mSC-intrinsic dystrophin expression as a prerequisite for effective muscle regeneration. While our results do not question the importance of polarized division in mSC biology or the existence of stem cell dysfunction in DMD, they argue against dystrophin as a regulator of these processes. Alternative mechanisms may underlie mSC impairment. This work refines our understanding of DMD pathophysiology and suggests that therapeutic restoration of dystrophin in mSCs may not be necessary for effective muscle regeneration.La dystrophie musculaire de Duchenne (DMD) est une pathologie récessive liée à l'X, causée par l'absence de dystrophine à la membrane des myofibres, entraînant leur fragilité, leur dégénérescence et une régénération musculaire altérée. Au-delà de cette vision classique, le dysfonctionnement des cellules souches musculaires (mSCs) a été suggéré comme un facteur contribuant à la progression de la maladie, certaines études proposant que la polarisation de la dystrophine au sein des mSCs régule leur division asymétrique et leur auto-renouvellement. Mon étude visait à élucider les processus dynamiques régissant l'établissement de la compartimentalisation de la dystrophine au sein des cellules satellites musculaires. Dans ce but, nous avons utilisé un modèle murin exprimant une protéine de fusion dystrophine-EGFP et le tdTomato spécifiquement dans les mSCs. Malgré une transcription élevée du gène Dmd, aucune protéine dystrophine n'a été détectée dans les mSCs, quel que soit leur état d'activation, comme l'ont confirmé l'imagerie in vivo, l'histologie, le FACS et l'électrophorèse capillaire. L'accumulation de dystrophine observée à proximité des mSCs provenait du sarcolemme, et non des mSCs elles-mêmes, sans présenter de polarité cohérente. Ces résultats remettent en question l'hypothèse selon laquelle la dystrophine jouerait un rôle direct dans l'établissement de la polarité des cellules souches musculaires, ainsi que la nécessité d'une expression intrinsèque de la dystrophine par ces cellules pour assurer une régénération musculaire efficace. Bien que nos résultats ne remettent pas en cause l'importance des divisions polarisées dans la biologie des mSCs ni l'existence d'un dysfonctionnement des cellules souches dans la DMD, ils réfutent l'idée selon laquelle la dystrophine jouerait un rôle dans ces processus. D'autres mécanismes pourraient sous-tendre le dysfonctionnement des mSCs. Cette étude affine notre compréhension de la physiopathologie de la DMD et suggère que la restauration thérapeutique de la dystrophine dans les mSCs n'est pas nécessaire pour une régénération musculaire efficace
Étude de la compartimentalisation de la dystrophine dans le muscle squelettique et ses cellules souches résidentes
No full textDuchenne muscular dystrophy (DMD) is an X-linked recessive disorder caused by the loss of full-length dystrophin at the sarcolemma, resulting in myofiber fragility, degeneration, and impaired regeneration. Beyond this classical view, dysfunction of muscle stem cells (mSCs) has been proposed to contribute to disease progression, with studies suggesting that polarized dystrophin within mSCs regulates asymmetric division and self-renewal. My study aimed to elucidate the dynamic processes governing the establishment of dystrophin compartmentalization within muscle satellite cells. In this study, we reassessed the presence and distribution of dystrophin in mSCs using a mouse model expressing a dystrophin-EGFP fusion and tdTomato protein specifically in mSCs. Despite high Dmd transcription, no dystrophin protein was detected in mSCs at any activation state, as confirmed by in vivo imaging, histology, FACS, and capillary electrophoresis.Dystrophin accumulation observed near mSCs originated from the sarcolemma, rather than from the mSCs themselves, and showed no consistent polarity. These findings challenge the prevailing hypothesis that dystrophin plays a direct role in establishing muscle stem cell polarity, and question the requirement for mSC-intrinsic dystrophin expression as a prerequisite for effective muscle regeneration. While our results do not question the importance of polarized division in mSC biology or the existence of stem cell dysfunction in DMD, they argue against dystrophin as a regulator of these processes. Alternative mechanisms may underlie mSC impairment. This work refines our understanding of DMD pathophysiology and suggests that therapeutic restoration of dystrophin in mSCs may not be necessary for effective muscle regeneration.La dystrophie musculaire de Duchenne (DMD) est une pathologie récessive liée à l'X, causée par l'absence de dystrophine à la membrane des myofibres, entraînant leur fragilité, leur dégénérescence et une régénération musculaire altérée. Au-delà de cette vision classique, le dysfonctionnement des cellules souches musculaires (mSCs) a été suggéré comme un facteur contribuant à la progression de la maladie, certaines études proposant que la polarisation de la dystrophine au sein des mSCs régule leur division asymétrique et leur auto-renouvellement. Mon étude visait à élucider les processus dynamiques régissant l'établissement de la compartimentalisation de la dystrophine au sein des cellules satellites musculaires. Dans ce but, nous avons utilisé un modèle murin exprimant une protéine de fusion dystrophine-EGFP et le tdTomato spécifiquement dans les mSCs. Malgré une transcription élevée du gène Dmd, aucune protéine dystrophine n'a été détectée dans les mSCs, quel que soit leur état d'activation, comme l'ont confirmé l'imagerie in vivo, l'histologie, le FACS et l'électrophorèse capillaire. L'accumulation de dystrophine observée à proximité des mSCs provenait du sarcolemme, et non des mSCs elles-mêmes, sans présenter de polarité cohérente. Ces résultats remettent en question l'hypothèse selon laquelle la dystrophine jouerait un rôle direct dans l'établissement de la polarité des cellules souches musculaires, ainsi que la nécessité d'une expression intrinsèque de la dystrophine par ces cellules pour assurer une régénération musculaire efficace. Bien que nos résultats ne remettent pas en cause l'importance des divisions polarisées dans la biologie des mSCs ni l'existence d'un dysfonctionnement des cellules souches dans la DMD, ils réfutent l'idée selon laquelle la dystrophine jouerait un rôle dans ces processus. D'autres mécanismes pourraient sous-tendre le dysfonctionnement des mSCs. Cette étude affine notre compréhension de la physiopathologie de la DMD et suggère que la restauration thérapeutique de la dystrophine dans les mSCs n'est pas nécessaire pour une régénération musculaire efficace
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Get PDF“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
koamabayili/VECTRON-author-checklist: VECTRON author checklist
No full textWe have done our best to complete the author checklist relating to the use of animals in the hut study. Note that the objective for the hut study was to evaluate the IRS treatment applications for residual efficacy against Anopheles mosquitoes, including the local An. coluzzii mosquito population. Cows were only used to attract mosquitoes into the huts and no tests were carried out directly on the cows. The author checklist is intended for use with studies where experiments are carried out on animals, which is why we have had such difficulty in completing this for the hut study, as many of the questions do not relate to how the cows were used
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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