1,720,953 research outputs found
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
Rupture nucléaire dans les cellules tumorales : la protéine adénovirale E4orf4 comme outil moléculaire pour identifier les mécanismes
No full textTitre de l'écran-titre (visionné le 8 août 2023)Les cellules tumorales malignes accumulent des altérations génétiques qui favorisent une plasticité nucléaire accrue et l'invasion tumorale. La réorganisation des réseaux d'actomyosine cause une augmentation des forces mécaniques qui sont transmises à l'enveloppe nucléaire par des connexions physiques. Ces connexions physiques permettent aux cellules d'ajuster la réponse nucléaire aux stress du microenvironnement tumoral, incluant les carences d'espace et de nutriments, et d'induire une réponse cellulaire adaptative pour échapper à ces contraintes. En outre, ces forces mécaniques causent souvent des ruptures de l'enveloppe nucléaire dans les cellules tumorales. Ces ruptures nucléaires pourraient favoriser les déformations nucléaires requises durant la migration cellulaire à travers les espaces serrés de la matrice extracellulaire. Remarquablement, les cellules tumorales survivent à des ruptures répétées de l'enveloppe nucléaire grâce à des mécanismes de réparation efficaces. Cependant, les ruptures nucléaires répétées causent une accumulation de dommages à l'ADN et pourraient contribuer à l'acquisition d'un phénotype tumoral invasif. Ainsi, élucider les mécanismes moléculaires régulant les processus de rupture et réparation de l'enveloppe nucléaire pourrait identifier des cibles thérapeutiques pertinentes pour contrecarrer l'invasion tumorale. La protéine adénovirale E4orf4 induit une activité toxique sélective chez les cellules tumorales. Cependant, les bases moléculaires de l'action sélective d'E4orf4 demeurent méconnues. Il a été démontré qu'E4orf4 réorganise le réseau d'actomyosine à proximité du noyau et provoque des déformations nucléaires dramatiques. Nous avons émis l'hypothèse que la protéine adénovirale E4orf4 exerce une activité toxique sélective dans les cellules tumorigéniques en perturbant la forme et la dynamique nucléaire, notamment via sa capacité à déréguler l'organisation du cytosquelette d'actine. L'objectif général de ces travaux de thèse est d'étudier la contribution des changements de forme et de dynamique nucléaire dans l'activité toxique d'E4orf4 et les mécanismes impliqués. La prémisse est que les cibles cellulaires d'E4orf4 réguleraient le remodelage de l'enveloppe nucléaire par les forces mécaniques et la plasticité nucléaire. Afin d'adresser cette hypothèse, les effets d'E4orf4 sur le réseau périnucléaire d'actine et sur l'organisation de l'enveloppe nucléaire, de même que les effecteurs cellulaires impliqués, ont été étudiés dans une variété de lignées cellulaires tumorigéniques et non-tumorigéniques. Les travaux présentés au Chapitre 1 indiquent qu'E4orf4 perturbe l'organisation de l'enveloppe nucléaire dans les cellules tumorigéniques seulement, d'une manière qui dépend du recrutement de fibres contractiles à l'enveloppe nucléaire. Ce processus requiert son association avec la protéine de polarité Par3 et la transmission des forces mécaniques à l'enveloppe nucléaire par le complexe LINC. Remarquablement, cette activité toxique sélective d'E4orf4 est associée à des ruptures répétées de l'enveloppe nucléaire provoquant une perte de l'intégrité nucléaire chez une proportion significative de cellules. De plus, les travaux présentés au Chapitre 2 identifient le régulateur épigénétique Ash2L comme substrat de la tyrosine kinase oncogénique Src dont la signalisation est perturbée par E4orf4 qui modifie la réponse nucléaire au stress mécanique. Des analyses moléculaires, biochimiques et fonctionnelles ont révélé que la phosphorylation d'Ash2L par Src est dérégulée par E4orf4 et qu'elle augmente la résistance du noyau aux ruptures de l'enveloppe nucléaire induites soit par E4orf4 ou par un affaiblissement de la lamina nucléaire. De plus, Ash2L régule également les ruptures nucléaires causées par les contraintes physiques appliquées lors de la migration cellulaire sous confinement. Ensemble, ces travaux ont permis d'identifier deux nouvelles cibles cellulaires d'E4orf4, Par3 et Ash2L, qui régulent son action toxique sélective, laquelle est caractérisée par l'induction de ruptures nucléaires répétées. En outre, nos travaux suggèrent que les cibles d'E4orf4 sont des régulateurs authentiques des ruptures nucléaires par le stress mécanique. Ces travaux établissent E4orf4 comme un nouveau paradigme pour étudier les mécanismes qui contrôlent les évènements de rupture et réparation de l'enveloppe nucléaire et la plasticité nucléaire qui ont un effet sur les propriétés métastatiques des cellules tumorales.Malignant tumor cells accumulate genetic alterations that increase nuclear plasticity and tumor invasion. Reorganization of actomyosin networks increases cellular contractility and mechanical forces that are transmit to the nuclear envelope through physical connections. These physical connections enable the cells to adjust their nuclear response to microenvironmental stress, including space and nutrient deficiencies, and to induce an adaptive cellular response to escape these stresses. In addition, these mechanical forces often cause ruptures of the nuclear envelope in tumor cells. Notably, nuclear ruptures are thought to facilitate the nuclear deformations required during cell migration through the tight spaces of the extracellular matrix. Remarkably, tumor cells can survive repeated nuclear ruptures using efficient nuclear envelope repair mechanisms. However, repeated nuclear ruptures cause DNA damage accumulation and could contribute to a more invasive tumor cell phenotype. Thus, understanding the biology of nuclear envelope rupture and repair processes is therapeutically relevant. The adenoviral protein E4orf4 exerts tumor cell selective killing. However, the molecular basis for the selective action of E4orf4 remains poorly understood. E4orf4 has been shown to reorganize the actomyosin network near the nucleus and to cause dramatic nuclear deformations. We hypothesized that E4orf4 exerts a selective toxicity by disrupting the nucleus' shape and dynamics, notably through its capacity to deregulate the actin cytoskeleton organization. The general objective of this thesis work is to study the contribution of the modifications of the nucleus' shape and dynamics in the cytotoxic activity of E4orf4, and identify the mechanisms involved. The premise is that the cellular targets of E4orf4 would regulate the remodeling of the nuclear envelope by mechanical forces and nuclear plasticity. In order to address this hypothesis, we analyzed the effects of E4orf4 on the perinuclear actin network and on the organization of the nuclear envelope in a variety of tumorigenic and non-tumorigenic cell lines and identified the cellular effectors involved. The work presented in Chapter 1 indicates that E4orf4 disrupts the organization of the nuclear envelope in tumorigenic cells only, in a manner that depends on the recruitment of contractile actin fibers at the nuclear envelope surface. This process requires its association with the polarity protein Par3 and the transmission of mechanical forces to the nuclear envelope by the LINC complex. Remarkably, this selective toxic activity of E4orf4 is associated with repetitive ruptures of the nuclear envelope causing a loss of nuclear integrity in a significant proportion of the cells. In addition, the work presented in Chapter 2 identifies the epigenetic regulator Ash2L as a novel substrate of the oncogenic tyrosine kinase Src, that is targeted by E4orf4 and that modifies the nuclear response to mechanical stress. Molecular, biochemical and functional analyzes revealed that Src-mediated Ash2L Tyr phosphorylation is deregulated by E4orf4 and increases the nuclear mechanical resistance to the mechanical stress induced by E4orf4 or lamin A/C deficiency. In addition, Ash2L also regulates nuclear ruptures caused by physical constraints during confined cell migration. Together, this work has identified two novel cellular targets of E4orf4, Par3 and Ash2L, regulating its tumor cell-selective action that is characterized by the induction of repetitive nuclear ruptures. Importantly, these studies suggest that E4orf4's targets are bona fide regulators of nuclear ruptures induced by mechanical stress in tumorigenic cells. This thesis work establishes E4orf4 as a new paradigm for studying the mechanisms controlling nuclear envelope rupture and repair events and nuclear plasticity, which are relevant for the metastatic properties of tumor cells
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
Author Under Sail The Imagination of Jack London, 1893-1902
No full textIn Author Under Sail, Jay Williams offers the first complete literary biography of Jack London as a professional writer engaged in the labor of writing. It examines the authorial imagination in London's work, the use of imagination in both his fiction and nonfiction, and the ways he defined imagination in the creative process in his business dealings with his publishers, editors, and agents. In this first volume of a two-volume biography, Williams traverses the years 1893 to 1902, from London's "Story of a Typhoon" to The People of the Abyss. The Jack London who emerges in the pages of Author Under Sail is a writer whose partnership with publishers, most notably his productive alliance with George Brett of Macmillan, was one of the most formative in American literary history. London pioneered many author models during the heyday of realism and naturalism, blurring the boundaries of these popular genres by focusing on absorption and theatricality and the representation of the seen and unseen. London created an impassioned, sincere, and extremely personal realism unlike that of other American writers of the time. Author Under Sail is a literary tour de force that reveals the full range of London as writer, creative citizen, and entrepreneur at the same time it sheds light on the maverick side of machine-age literature.Intro -- Title Page -- Copyright Page -- Dedication -- Contents -- Acknowledgments -- Introduction -- 1. Spirit Truth -- 2. From Absorption to Theatricality and Back Again -- 3. "I Will Build a New Present" -- 4. Sons as Authors -- 5. Fathers as Publishers -- 6. The Daughter as Author -- 7. Lovers as Authors -- 8. At Sea with the Family -- 9. Yellow News, Yellow Stories -- 10. The Return Home -- Notes -- Bibliography -- Index -- About Jay WilliamsIn Author Under Sail, Jay Williams offers the first complete literary biography of Jack London as a professional writer engaged in the labor of writing. It examines the authorial imagination in London's work, the use of imagination in both his fiction and nonfiction, and the ways he defined imagination in the creative process in his business dealings with his publishers, editors, and agents. In this first volume of a two-volume biography, Williams traverses the years 1893 to 1902, from London's "Story of a Typhoon" to The People of the Abyss. The Jack London who emerges in the pages of Author Under Sail is a writer whose partnership with publishers, most notably his productive alliance with George Brett of Macmillan, was one of the most formative in American literary history. London pioneered many author models during the heyday of realism and naturalism, blurring the boundaries of these popular genres by focusing on absorption and theatricality and the representation of the seen and unseen. London created an impassioned, sincere, and extremely personal realism unlike that of other American writers of the time. Author Under Sail is a literary tour de force that reveals the full range of London as writer, creative citizen, and entrepreneur at the same time it sheds light on the maverick side of machine-age literature.Description based on publisher supplied metadata and other sources.Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, YYYY. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries
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