1,720,986 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe 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
Full text link“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
Full text linkWe 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
Unravelling of a senescence associated with a secretory phenotype triggered by the mechanical defects of the endothelial cell upon the loss of CCM2 in a model of cerebral cavernoma.
No full textLes lésions CCM (Cerebral Cavernous Malformations) sont formées d’un empilement de vaisseaux capillaires tortueux, dilatés et hémorragiques situés dans le cerveau. Ces capillaires cérébraux sont dépourvus de cellules murales et sont formés d’une monocouche de cellules endothéliales (CE) peu jointives. La mutation perte de fonction de l’un des 3 gènes ccm (ccm1, ccm2 et ccm3) est suffisante pour induire la formation de lésions CCM chez l’Homme.Dans les différents modèles mutants ccm, les CE présentent une homéostasie tensionnelle défectueuse caractérisée par un défaut de coordination entre les forces d’adhésions cellule-matrice et cellule-cellule. Ceci se traduit par la formation de fibres contractiles d’actomyosine ancrées sur de nombreuses adhérences focales à intégrine B1 et par la perte des jonctions intercellulaires dépendantes de VE-cadhérine. L’association des protéines CCM1-3 forme une plateforme moléculaire qui contrôle, en aval de RhoA, l’activité des kinases ROCK1 et ROCK2 sur l’organisation du cytosquelette d’acto-myosine. Le complexe CCM recrute ROCK2 aux jonctions dépendantes de VE-cadhérine pour promouvoir un réseau d’actine cortical stabilisateur de ces jonctions intercellulaires alors que dans le même temps, il inhibe l’activité de ROCK1 pour réduire la formation de fibres de stress ventrales et ainsi limiter l’adhésion de la CE à la matrice extracellulaire. Il est connu que le microenvironnement de la lésion est remodelé notamment par des cellules immunitaires qui s’infiltrent pour déclencher une réponse inflammatoire chronique et favoriser l’expansion de la lésion. Il est également connu que les CE mutantes sécrètent des métalloprotéases et des cytokines, qu’elles surproduisent des ROS et qu’elles subissent une transition endothélio-mésenchymateuse (endoMT). Enfin, les lésions CCM sont des mosaïques de CE mutantes et sauvages qui sont recrutées au cours du temps dans la lésion. Néanmoins, le lien qui existe entre tous ces phénomènes favorables à la progression de la lésion CCM est encore mal compris et reste à élucider.Les travaux que j’ai effectués au cours de cette thèse m’ont permis de proposer un modèle qui unifie l’ensemble de ces comportements cellulaires. En effet, j’ai mis en lumière le vieillissement prématuré des cellules endothéliales déplétées en CCM2. J’ai montré que cette sénescence est associée à un comportement sécrétoire SASP (Senescence Associated with a Secretory Phenotype) qui confère à la CE la capacité de remodeler activement son environnement notamment en le dégradant de manière localisée, de l’envahir et d’attirer par chimio-attraction des CE sauvages et des cellules immunitaires. Le second apport majeur de mon travail a été de montré que cette SASP est due aux dérèglements dans la mécanique de la CE. En effet, j’ai montré que l’augmentation de la contractilité intracellulaire, associée à un défaut de coordination entre les activités de ROCK1 et ROCK2, est responsable de cette SASP. L’inhibition de la myosine II ou la déplétion préférentielle de ROCK1 ou de ROCK2, restaure l’expression de la moitié des gènes dérégulés par la perte de CCM2, bloque l’apparition des marqueurs de sénescence ainsi que les capacités invasives et chimio-attractantes des CE déplétées pour CCM2. Ces résultats ouvrent la voie vers l’identification de nouvelles cibles thérapeutiques pour bloquer les mécanismes à l’origine de l’apparition et de l’expansion des lésions CCM.CCM (Cerebral Cavernous Malformations) lesions are formed by stacks of tortuous, dilated and hemorrhagic capillaries located in the brain. These brain capillaries are devoid of mural cells and are formed of a monolayer of weakly joined endothelial cells (EC). The loss of function mutation in one of the 3 ccm genes (ccm1, ccm2 and ccm3) is sufficient to induce the formation of CCM lesions in humans.In the different ccm mutant models, the ECs present defective tensional homeostasis characterized by a lack of coordination between the cell-matrix and cell-cell forces. This results in the formation of contractile actomyosin fibers anchored on numerous focal adhesions containing B1 integrin and in the loss of VE-cadherin-dependent intercellular junctions. The association of CCM1-3 proteins forms a molecular scaffold that controls downstream of RhoA the activity of ROCK1 and ROCK2 on the organization of the acto-myosin cytoskeleton. The CCM complex recruits ROCK2 at the VE-cadherin dependent junctions to promote a network of cortical actin stabilizing these intercellular junctions while at the same time, it inhibits the activity of ROCK1 to reduce the formation of ventral stress fibers and thus limit the adhesion of the EC to the extracellular matrix. It is known that the microenvironment in the lesion is reshaped in particular by immune cells that infiltrate it to trigger a chronic inflammatory response and promote the expansion of the lesion. It is also known that mutant ECs secrete metalloproteases and cytokines, that they overproduce ROS and that they undergo an endothelio-mesenchymal transition (endoMT). Finally, CCM lesions are mosaics of mutant and wild-type ECs recruited into the lesion over time. However, whether a link exists between all these phenomena conducive to the progression of the CCM lesion is not known and remains to be elucidated.My work during this PhD allowed me to propose a model that unifies all these cellular behaviors. Indeed, I have highlighted a premature aging of endothelial cells depleted in CCM2. I have shown that this senescence is associated with a secretory behavior SASP (Senescence Associated with a Secretory Phenotype) which gives the EC the ability to actively reshape its environment, in particular by degrading it locally, to invade it and attract by chemo-attraction wild EC and immune cells. The second major contribution of my work has been to show that this SASP is due to the dysregulation of the mechanics of the EC. Indeed, I have shown that the increase in intracellular contractility, associated with the loss of balance between the activities of ROCK1 and ROCK2, is responsible for this SASP. Inhibiting myosin II or depleting ROCK1 or ROCK2 restores the expression of half of the genes dysregulated by the loss of CCM2, blocks the appearance of senescence markers as well as the invasive and chemo-attractive capacities of CCM2-depleted ECs. These results open the way to the identification of new therapeutic targets responsible for the appearance and expansion of CCM lesions
Dispelling the Myths Behind First-author Citation Counts
Full text linkWe 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
Régulation par le complexe CCM du dialogue entre intégrines et cadhérines pour le maintien de la stabilité vasculaire.
No full textLes interactions cellule-cellule et cellule-matrice extracellulaire (MEC) sont cruciales pour entretenir la cohésion tissulaire. Ces deux types d'adhésions sont fonctionnellement interconnectés par un dialogue permanent qui met en jeu des voies de signalisation convergentes régulant notamment l'architecture et la contractilité du cytosquelette d'acto-myosine sous-jacent. Ce dialogue permet d'établir un équilibre de forces intracellulaires en réponse à la tension appliquée par le milieu extérieur. L'endothélium des vaisseaux sanguins est un tissu soumis à des conditions mécaniques particulières. En plus des compressions intercellulaires subies par tout épithélium, les cellules endothéliales (CEs) doivent également subir et résister aux forces hémodynamiques du flux sanguin et à la rigidité de la lame basale – deux signaux mécaniques agissant de part et d'autre de l'endothélium. Les Cerebral Cavernous Maformations (CCM) ou encore angiomes caverneux sont des lésions vasculaires hémorragiques d'origine génétique qui se développent au niveau des capillaires du système nerveux central et qui se caractérisent par des défauts dans l'environnement proche des CEs. La perte des jonctions intercellulaires et du recouvrement par les cellules murales, l'organisation aberrante de la membrane basale aussi que la stagnation du flux sanguin sont les caractéristiques des CCM. C'est pourquoi nous avons choisi cette pathologie comme modèle intéressant de mécanotransduction mettant en jeu le dialogue entre les intégrines et les cadhérines. En effet, les trois gènes indifféremment mutés dans cette pathologie codent pour des protéines, CCM1-3, qui s'associent en un complexe ternaire et qui sont reconnues comme des acteurs importants de la régulation des jonctions adhérentes. Des études moléculaires et protéomiques montrant que le complexe CCM interagit avec la protéine ICAP-1, un régulateur négatif de l'intégrine β1, nous ont conduit à formuler l'hypothèse selon laquelle ce complexe jouerait un rôle pivot dans la signalisation croisée entre ces intégrines et cadhérines. Les études effectuées pendant ma thèse ont démontré que les protéines CCM régulent l'homéostasie tensionnelle médiée par les structures d'adhérence intercellulaires et à la MEC par leur action inhibitrice sur l'intégrine β1 et en controlant une balance d'activité entre les deux isoformes de ROCK, ROCK1 et ROCK2. Nous avons montré que, suite à la perte des protéines CCMs, la suractivation de l'intégrine β1 augmente la sensibilité des CEs aux signaux mécaniques comme la rigidité de la MEC ou les forces hémodynamiques du flux sanguin. Il en résulte une suractivation de la contractilité cellulaire dépendante de ROCK1 déclenchant une boucle de rétrocontrôle mécanique conduisant à l'amplification des tensions intra- et extracellulaire et brisant ainsi l'homéostasie tensionnelle pour favoriser le phénotype malin.Cell-cell or cell-matrix interactions have crucial roles in the maintenance of the physical cohesion of any tissue. In addition, growing body of evidence indicates that these two adhesion systems do not act independently, but rather are functionally interconnected by a permanent crosstalk. This dialog usually operates via common molecules that trigger convergent signaling as well as by actomyosin network which, by providing physical link, contributes to establishment of intracellular force counterbalancing tension applied by extracellular surrounding. Blood vessels endothelium is a particular tissue in term of mechanical conditions. Apart from intracellular compression, endothelial lining needs to resist hemodynamic forces as well as rigidity of the basal membrane - two mechanical inputs acting from opposite sides of the endothelial layer. Cerebral Cavernous Malformation (CCM) is a sporadically acquired or inherited disease of venous capillaries within neuro-vascular unit characterized by defects in all aspects of local microenvironment. Loss of intra-endothelial junctions and mural cell coverage, aberrant organization of basal lamina as well as stagnant blood flow are features of CCM lesions. Thereby, CCM became for us an interesting model to study mechanotrasduction process and in this context, the cross-talk between integrin and cadherin mediated adhesion structures. Indeed, CCM proteins are well recognized players involved in a control of VE-cadherin mediated intracellular junctions. In addition, CCM1 was found to interact with ICAP-1, a negative regulator of β1 integrin, raising the possibility that this complex most likely acts as molecular node regulating β1 integrin/ VE-cadherin convergent signaling pathways.Studies performed during this thesis have demonstrated that CCM complex coordinates cadherin- and integrin-mediated tensional homeostasis by repressing β1 integrin activation and maintaining a balance of activity between the two isoforms of RhoA-associated kinases ROCK1 and ROCK2. We have found that β1 integrin sustained over-activation upon CCM proteins loss contributes to increased ECs sensitivity to mechanical cues, such as ECM physical reorganization or hemodynamic force that in turn activates ROCK1-dependent contractility. This establishes a positive feedback mechanical loop that breaks tensional homeostasis and switches on the malignant phenotype
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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