1,720,981 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
The 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
“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
We 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
Optogenetic control of membrane potential and calcium homeostasis in skeletal muscle cells : impact on myogenic processes
Le calcium est un second messager qui participe à de nombreux processus cellulaires tels que la prolifération, la migration, la différenciation, l’apoptose et la transmission de messagers neuronaux. Dans le modèle musculaire squelettique, le calcium est un acteur important dans le processus du couplage excitation-contraction. Il est également impliqué dans la myogenèse et dans les processus de réparation. Une dérégulation du calcium dans les cellules musculaires participe à leur dégénérescence comme il a été observé dans la dystrophie musculaire de Duchenne (DMD). L’objectif de cette thèse a été par des approches innovantes d’optogénétique, d’explorer et de moduler des mécanismes fondamentaux dépendants du calcium tels que la migration, la fusion, la différenciation et la contraction dans différents modèles musculaires. 1- Dans un premier temps, l’effet de la stimulation de l’halorhodopsine (eNpHR) sur le contrôle du potentiel de membrane et sur le processus de migration de myoblastes C2C12 a été étudié. La transfection de eNpHR3.0 dans des myoblastes C2C12 a permis de générer des courants sortants diminuant le potentiel de membrane vers des valeurs stabilisées tout le long de la stimulation. Cette polarisation membranaire induit des élévations transitoires de calcium cytosolique, dépendant du canal TRPV2 localisé à la membrane plasmique. Après avoir démontré l’implication de TRPV2 dans les processus migratoires des myoblastes, les entrées de calcium induites par la stimulation lumineuse ont permis d’augmenter la migration TRPV2-dépendante des myoblastes C2C12. 2- Dans un second temps, l’impact de la stimulation par le canal rhodopsine 2 (ChR2) a été évalué pour le contrôle de l’activité calcique et sur les processus de différenciation dans des cultures primaires de myotubes murins. Après avoir caractérisé la signature calcique des cultures primaires de myotubes en différenciation avec la protéine fluorescente sensible au calcium GCaMP, un protocole de simulation optique a été développé pour reproduire la signature calcique spontanée de myotubes différenciés. En premier lieu, le contrôle de l’activité calcique par la stimulation optique de ChR2 a été confirmé au niveau d’une cellule unique ainsi qu’à l’échelle d’une culture entière. Par la suite, l’application d’un protocole de stimulation optique en culture pendant la différenciation a permis de moduler les processus de différenciation tels que la fusion et la contraction des myotubes primaires. 3- La signature calcique de cellules dystrophiques représentatives de la DMD a été explorée dans deux modèles cellulaires différents composés de cultures primaires isolées de souris mdx et de cellules musculaires humaines dérivés d’hiPSCs provenant de patients DMD. Des dérégulations de la signature calcique ont été observées dans ces deux modèles dystrophiques. Une exploration fonctionnelle a été réalisée sur les cellules musculaires dérivées d’hiPSCs au travers de stimulations électriques, pharmacologiques et optiques démontrant leur capacité à développer un phénotype musculaire et confirmant leur intérêt potentiel pour la modélisation de maladies telles que la DMD.Ces travaux ouvrent des perspectives sur l’utilisation de l’optogénétique pour évaluer la fonctionnalité des cellules et pour moduler certains processus cellulaires pour de futures applications thérapeutiques.Calcium is a second messenger which participates in many cellular processes such as proliferation, migration, differentiation, apoptosis and transmission of neuronal messengers. In skeletal muscle, calcium is an important player in the process of excitation-contraction coupling. It is also involved in myogenesis and in repair processes. Deregulation of calcium in muscle cells contributes to their degeneration as observed in Duchenne Muscular Dystrophy (DMD). The objective of this thesis was to explore and modulate basic calcium-dependent mechanisms such as migration, fusion, differentiation and contraction in different muscle models through innovative optogenetic approaches. 1- First, the effect of halorhodopsin (eNpHR) stimulation on the control of membrane potential and on the migration process of C2C12 myoblasts was studied. Transfection of eNpHR3.0 into C2C12 myoblasts generated outward currents decreasing the membrane potential to stable values throughout stimulation. This membrane polarization induces cytosolic calcium transients, dependent on the TRPV2 channel located at the plasma membrane. After demonstrating the involvement of TRPV2 in the migratory process of myoblasts, the light-induced calcium constitutive entries allowed to increase the TRPV2-dependent migration of C2C12 myoblasts. 2- Secondly, the impact of channelrhodopsin 2 (ChR2) stimulation was evaluated for the control of calcium activity and on the differentiation processes in primary cultures of murine myotubes. We characterized the calcium signature of myotube primary cultures with the fluorescent calcium sensitive protein GCaMP. An optical simulation protocol was then developed to reproduce the spontaneous calcium signature of differentiated myotubes. To reach this goal, we first confirmed the control of calcium activity by optical stimulation of ChR2 at the single cell level as well as at the level of a whole culture. Finally, the application of an optical stimulation protocol in culture during differentiation allowed to modulate differentiation processes such as fusion and contraction of primary myotubes. 3- The calcium signature of dystrophic cells representative of DMD was explored in two different cell models: primary cultures isolated from mdx mice and human muscle cells derived from DMD hiPSCs. Changes in calcium signature was observed in these two dystrophic models. A functional exploration was performed on muscle cells derived from hiPSCs through electrical, pharmacological and optical stimulation demonstrating their ability to develop a muscle phenotype and confirming their potential interest in modeling diseases such as DMD.This work opens perspectives on the use of optogenetics to evaluate cell functionality and to modulate some cellular processes for future therapeutic applications
Dispelling the Myths Behind First-author Citation Counts
We 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
Effects of axial stretch on murine deficient-dystrophin cardiomyocytes : calcium deregulation and TRPs channels
La dystrophie musculaire de Duchenne (DMD) est la conséquence de la perte de la dystrophine, protéine sous membranaire indispensable au maintien mécanique et fonctionnel du sarcolemme. Cette déficience augmenterait les influx cationiques par des microruptures de la membrane ou par la dérégulation de canaux tels que les canaux activés par l'étirement (SACs: Stretch-activated channel). Dans ce travail, les effets d'une stimulation mécanique ont été explorés sur des cardiomyocytes dans le contexte pathologique de la cardiomyopathie dilatée associée à la DMD. L'utilisation de fibres de carbone a permis de réaliser un étirement axial similaire aux conditions physiologiques de remplissage ventriculaire. Dans ces conditions, l'exploration de la topographie membranaire par la microscopie de conductance ionique à balayage n'a montré aucune évolution de la surface ni de lésion du sarcolemmel dans les conditions d'étirement. L'étude s'est donc focalisée sur l'activité de candidats moléculaires des SACs et plus particulièrement ceux appartenant à la famille des TRPs (Transient Receptor Potential) dans le dérèglement de l'homéostasie calcique induite par l'étirement. Les influx cationiques évalués par la technique d'extinction de fluorescence et l'étude de la concentration intracellulaire de Ca2+ ([Ca2+]i) grâce à la sonde Fluo8 montrent une implication des canaux TRPV2 et TRPCs. Les premiers semblent responsables d'une entrée cationique et d'une augmentation de [Ca2+]i importante dans les cardiomyocytes mdx. Les seconds, bien que responsables d'un influx, ne participeraient pas à l'augmentation de [Ca2+]i. Ces résultats révèlent que les canaux TRPV2 pourraient jouer un rôle important dans la dérégulation calcique observée dans les cardiomyocytes déficients en dystrophine.Duchenne muscular dystrophy (DMD) is the consequence of the loss of dystrophin, a subsarcolemmal protein essential for mechanical and functional maintenances of the sarcolemma. This deficiency could increase cationic influxes by membrane microruptures or by dysregulation of channels such as stretch-activated channels (SACs). In this work, the effects of a mechanical stretch were explored on cardiomyocytes in the pathological context of dilated cardiomyopathy associated with DMD. Using carbon fibers, an homogenous axial stretch was performed to mimic physiological conditions of ventricular filling. In these conditions, exploration of membrane topography using the scanning ion conductance microscopy did not show any surface evolution or sarcolemma disruption in stretch condition. The study was thus focused on activity and identification of molecular candidates for SACs, especially the TRPs (Transient Receptor Potential) channels in the stretch-induced. Ca2+ homeostasis dysregulation. Cationic influxes assessed by Mn2+-quenching and assessment of the intracellular Ca2+ concentration ([Ca2+]i) using fluo-8 fluorescence demonstrated an involvement of TRPV2 and TRPCs channels. The first ones seem to be responsible for cationic entry and [Ca2+]i increase in mdx cardiomyocytes. The latter, though responsible for an influx, do not contribute to [Ca2+]i increase. These findings reveal that TRPV2 channels could play an important role in calcium dysregulation observed in dystrophin-deficient cardiomyocytes
koamabayili/VECTRON-author-checklist: VECTRON author checklist
We 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.
Author-wise bibliometric analysis based on entropy.</p
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