1,720,971 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
Identification of VEGFR3 and SOX18 as genes mutated in lymphedema and alopecia-lymphedema
No full textLe lymphœdème est un œdème chronique dû à une déficience du système lymphatique. La maladie s’aggrave avec le temps et provoque chez les patients des souffrances psychologiques, de l’inconfort, des problèmes de mobilité et des risques accrus d’infection. Selon l’origine de la maladie, on classe les lymphœdèmes en lymphœdèmes primaires, causés par un défaut intrinsèque des voies lymphatiques, et en lymphœdèmes secondaires, résultant de l’obstruction ou de l’altération de ces voies, suite à une parasitose, un accident ou un acte chirurgical dans le traitement d’un cancer. Certaines formes de lymphœdèmes primaires sont familiales, comme le lymphœdème précoce ou maladie de Milroy, le lymphœdème tardif ou maladie de Meige, ou encore certaines formes syndromiques. L’existence de ces formes héréditaires permet d’utiliser les outils de la génétique moléculaire humaine pour tenter d’identifier les gènes responsables. Avant le début de ma thèse, des études de liaison avaient permis l’identification d’un locus pour le lymphœdème précoce héréditaire dans la bande q35 du chromosome 5. L’examen des gènes présents dans l’intervalle révèle la présence d’un excellent candidat, codant le « vascular endothelial growth factor receptor 3 » (VEGFR3). Dans l’embryon de souris, l’expression de ce récepteur tyrosine kinase est observée d’abord dans l’ensemble du système vasculaire, mais, vers le milieu de la gestation, elle devient limitée aux vaisseaux lymphatiques. En outre, la surexpression dans la peau du ligand activateur de ce récepteur, le « vascular endothelial growth factor C » (Vegfc), induit l’hypertrophie des vaisseaux lymphatiques chez la souris. Le gènes VEGFR2 avait déjà été criblé par les auteurs de l’étude de liaison, sans qu’une preuve définitive de son implication ne soit apportée. Nous avons donc entrepris l’étude d’une famille présentant la maladie pour tenter de clarifier cette situation. La famille présentait une liaison avec la région chromosomique 5q35, confirmant ce locus, et le criblage du gène VEGFR3 a été entrepris. Ceci a permis la détection d’un changement nucléotidique causant la substitution d’une acide aminé situé dans la boucle catalytique du domaine kinase du récepteur (H1035R). Le résidu muté, une histidine, est conservé dans tous les récepteurs tyrosine kinases. Nous avons émis l’hypothèse que cette mutation interfère avec l’activité kinase de la protéine et pour tester cette idée, avons entrepris une collaboration avec le laboratoire du professeur Kari Alitalo, en Finlande. L’expression de la protéine mutée dans un système du culture cellulaire a démontré, comme attendu, la perte de son activité de trans-phosphorylation, ce qui prouve que la mutation est responsable des l lymphœdèmes dans la famille étudiée. Ensuite, nous avons cherché à identifier le gène responsable d’un syndrome rare associant alopécie, lymphœdème et télangiectasies. Une recherche dans les bases de données de phénotypes murins avec des mots-clés relatifs aux lymphœdèmes a permis de dresser une liste de modèles possibles de cette maladie. Nous avons ensuite cherché parmi ces modèles ceux qui présentaient des anomalies associées similaires à celles trouvées dans le syndrome humain. Ceci a permis d’identifier le gène SOX18, encodant un facteur de transcription, comme un candidat prometteur pour le syndrome d’alopécie- lymphœdème-télangiectasie, parce que la souris ragged, présentant une mutation du gène orthologue Sox18, possède un pelage clairsemé, de même qu’une accumulation de chyle dans le péritoine, symptomatique d’une anomalie des vaisseaux lymphatiques. Le séquençage du gène SOX18 dans deux familles consanguines présentant le syndrome a révélé, chez les membres affectés, des mutations faux-sens à l’état homozygote. Ces deux mutations sont localisées dans le domaine de liaison à l’ADN du facteur de transcription et affectent des résidus conservés. E plus de ces mutations récessives, nous avons identifié une mutation non-sens de novo causant une amputation de la protéine dans son domaine transactivateur, chez un enfant affecté et chez son frère, décédé in utero avec un hydrops fetalis. Des mutations dans SOX18 sont donc responsables de formes dominantes et récessives du syndrome d’alopécie- lymphœdème-télangiectasie, et, peut-être, de certains cas d’hydrops fetalis. En conclusion, nous avons identifié au cours de cette thèse deux gènes dont les mutations causent des lymphœdèmes. Le premier, VEGFR3, est associé au lymphœdème congénital héréditaire ou maladie de Milroy, et le second, SOX18, avec le syndrome d’alopécie- lymphœdème-télangiectasieLymphedema is a chronic swelling of tissues due to inadequate interstitial fluid drainage by the lymphatic system. The disease aggravates with time and leads to psychosocial discomfort, disability and increased risk of infection. Depending on the origin of the disease, lymphedema is classified as either primary lymphedema, caused by an intrinsic defect of the lymphatic system, or secondary lymphedema, where the lymphatic pathways are obstructed, damaged or even removed, because of parasitic disease, trauma or anti-cancer therapy. Some forms of primary lymphedema are familial, including early-onset lymphedema or Milroy's disease, puberty-onset lymphedema or Meige's disease, and syndromic forms where lymphedema is observed in association with other abnormalities. The existence of these hereditary forms allows the techniques of molecular genetics to be used for the identification of the causative genes. Before the beginning of my thesis, a locus for early-onset lymphedema had been mapped to chromosome 5q35 using linkage analyses. Examination of the genes in the linked interval revealed the presence of a promising candidate gene, encoding the vascular endothelial growth factor receptor 3 (VEGFR3). Previous studies had shown that, in the murine embryo, the expression of this receptor tyrosine kinase (RTK) is initially observed in the whole vascular system, but from about mid-gestation it becomes restricted to the lymphatic system. Moreover, when the activating ligand of this receptor, the vascular endothelial growth factor C, is over-expressed in the skin of a transgenic mouse, hyperplasic lymphatic vessels are observed. VEGFR3 was screened by the authors of the linkage analysis, but no indisputable proof of its involvement in the disease was obtained. To clarify the implication of VEGFR3 in early-onset hereditary lymphedema, we undertook the study of one family with this disorder. The family was linked to 5q35, confirming the locus, and the portion of the gene corresponding to the intracellular part of the VEGFR3 receptor was screened for mutations. The gene presented a nucleotide change resulting in an amino acid substitution, H1035R, affecting a histidine residue localized in the catalytic loop of the kinase domain and conserved in all members of the RTK family. We hypothesized that this mutation would interfere with the kinase activity of the protein, and, to test this, initiated a collaboration with the laboratory of professor Kari Alitalo, in Finland. Indeed, expression of the mutated protein in a cell culture system demonstrated a loss of kinase activity, implying that VEGFR3 mutation is the cause of primary lymphedema in this family. Subsequently, we sought to identify the gene responsible for a rare syndrome associating alopecia, lymphedema and telangiectasia. As the patient material was too limited to undertake positional cloning, we first looked for functional candidate genes on the basis of murine models. A search with various terms related to lymphedema in mutant mice databases retrieved a list of candidate models for lymphatic system disorders. This list was further examined for the occurrence of associated abnormalities similar to those found in the human syndrome. In this manner, we identified the SOX18 gene, encoding a transcription factor, as a promising candidate for the alopecia-lymphedema-telangiectasia syndrome, because the ragged mouse, mutated in the orthologous gene Sox18, presents a sparse pelage, as well as chylous ascites, an accumulation of chyle in the peritoneum, symptomatic of a lymphatic system dysfunction. Sequencing of the SOX18 gene in two consanguineous families revealed, in affected members, homozygous missense mutations in the DNA-binding domain of the transcription factor affecting conserved residues. In addition, we found a de novo nonsense mutation causing premature truncation of the protein in its transactivation domain, in the DNA of a young affected boy and of his brother, deceased in utero from hydrops fetalis. Thus, SOX18 mutations are responsible for both a recessive and a dominant form of alopecia-lymphedema-telangiectasia, and maybe also for some cases of hydrops fetalis, a fatal generalized edema of the fetus. In conclusion, we identified, during the course of this thesis, two genes mutated in hereditary lymphedema. The first one, VEGFR3, is associated with early-onset lymphedema; the second, SOX18, with the alopecia-lymphedema-telangiectasia syndrome.Thèse de doctorat en sciences biomédicales (SBIM 3) -- UCL, 200
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
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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