1,721,022 research outputs found

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    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

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    “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

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    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

    Dispelling the Myths Behind First-author Citation Counts

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    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

    Author Index

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    koamabayili/VECTRON-author-checklist: VECTRON author checklist

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    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

    Etude de l'impact de la phosphatase SHP-1 dans la réponse au TGF-ß des cellules de néoplasies myéloprolifératives

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    Les néoplasies myéloprolifératives BCR::ABL1 négatives (NMP) se caractérisent par une prolifération incontrôlée des cellules sanguines liée à l'acquisition de mutations dans les gènes JAK2, CALR ou MPL. La mutation JAK2V617F est la mutation la plus fréquente. Le TGFß, dont la sécrétion dans la moelle osseuse est augmentée dans les NMP, est connu pour réguler négativement la prolifération des cellules souches hématopoïétiques (CSH). Nous avons émis l'hypothèse que les CSH mutées JAK2V617F sont résistantes à l'effet antiprolifératif du TGFß expliquant l'invasion pathologique des cellules souches dans la myélofibrose. En utilisant des approches multiomiques nous avons identifié une sous-expression de la phosphatase SHP-1 dans les cellules mutées JAK2V617F. Comme il a été montré que SHP-1 est nécessaire à la quiescence des CSH régulée par le TGFß, nous avons émis l'hypothèse d'une relation entre la sous-expression de SHP-1 et la résistance des cellules mutées JAK2V617F à l'effet antiprolifératif du TGFß. L'expression de SHP-1 est réduite dans les cellules UT-7 transduites avec JAK2V617F en comparaison avec les cellules transduites avec JAK2 sauvage (WT). L'expression de la protéine SHP-1 est aussi diminuée dans les cellules de la moelle osseuse de souris JAK2V617F « Knock in » par rapport aux souris sauvages. Nous avons également confirmé la sous-expression de SHP-1 dans des cellules CD34+ de patients NMP mutés JAK2V617F en comparaison avec des sujets sains. Pour étudier le mécanisme régulant l'expression de SHP-1, nous avons montré qu'un traitement des cellules UT-7 par l'EPO réduit significativement l'expression de SHP-1. Cet effet est abrogé en présence de ruxolitinib, un inhibiteur de JAK2, suggérant que l'expression de SHP-1 est régulée négativement par la signalisation de JAK2. Bien que l'expression des récepteurs TGFß et de SMAD2/3 soit similaire dans les deux types de cellules, la phosphorylation de SMAD2/3 en réponse au TGFß est réduite dans les cellules UT-7 JAK2V617F par rapport aux cellules JAK2 WT. La prolifération des cellules UT-7 JAK2V617F n'est pas réduite par le TGFß, au contraire des UT-7 JAK2 WT. Pour restaurer des niveaux plus élevés de la protéine dans la lignée HEL mutée JAK2V617F, nous avons transduit l'ADNc codant pour SHP-1 et étudié la prolifération en présence de TGFß. Celle-ci est significativement réduite par rapport aux cellules transduites avec le vecteur vide confirmant la dépendance à SHP-1 dans la réponse au TGFß des cellules mutées JAK2V617F. Dans un test compétitif les cellules UT-7 JAK2V617F transduites par un vecteur fluorescent m-cherry ont été mélangées avec des UT-7 JAK2 WT et cultivées avec du TGFß. Dans ces expériences nous avons observé une sélection positive des cellules JAK2V617F confirmant notre hypothèse de départ. La transduction dans les cellules HEL du cDNA sauvage ou du cDNA muté pour invalider l'activité enzymatique de SHP-1 a permis, par des tests de compétition, de montrer que l'effet de SHP-1 nécessite son activité enzymatique. Dans le but de proposer de nouvelles approches thérapeutiques aux malades atteints de NMP nous avons testé l'effet de molécules agonistes de SHP-1 afin de renforcer l'activité phosphatase dans les cellules mutées JAK2V617F. Le SC1 augmente l'activité de SHP-1 et s'oppose à la sélection des cellules mutées JAK2V617F en présence de TGFß in vitro. Cependant nous n'avons pas réussi à confirmer in vivo son efficacité dans un modèle murin de greffe compétitive de cellules JAK2 sauvages et mutées.En conclusion, nous avons mis en évidence dans les cellules de patients NMP une sous-expression de SHP-1 qui est dépendante de JAK2 et qui est liée à la résistance des cellules JAK2V617F à l'effet antiprolifératif du TGFß, expliquant ainsi la sélection clonale des cellules mutées dans les NMP. Enfin nous proposons une nouvelle approche thérapeutique par augmentation de l'activité de la phosphatase SHP-1 qu'il est nécessaire de tester de manière plus approfondie.BCR::ABL1 negative myeloproliferative neoplasms (MPN) are characterized by an increased production of blood cells due to the acquisition of mutations in the JAK2, CALR or MPL genes. JAK2V617F is the most frequent mutation. TGFß, whose secretion is increased in the bone marrow of MPN, is known to negatively regulate hematopoietic stem cell (HSC) proliferation. We hypothesized that JAK2V617F mutated HSCs are resistant to the antiproliferative effect of TGFß explaining the pathological stem cell invasion in myelofibrosis. Using multiomics approaches, we identified a down regulation of SHP-1 phosphatase expression in JAK2V617F mutated cells. As SHP-1 has been shown to be required for the regulation of HSC quiescence by TGFß, we hypothesized a relationship between SHP-1 down regulation and the resistance of JAK2V617F mutated cells to the antiproliferative effect of TGFß. SHP-1 expression is reduced in UT-7 cells transduced with JAK2V617F compared with cells transduced with wild-type (WT) JAK2. SHP-1 protein expression is also decreased in bone marrow cells from JAK2V617F "knock in" mice compared to wild type mice. We also confirmed the down regulation of SHP-1 in CD34+ cells from JAK2V617F mutated MPN patients compared with healthy donors. To investigate the mechanism regulating SHP-1 expression, we showed that treatment of UT-7 cells with EPO significantly reduces SHP-1 expression. This effect was abrogated in the presence of ruxolitinib, a JAK2 inhibitor, suggesting that SHP-1 expression is negatively regulated by JAK2 signaling. Although TGFß receptors and SMAD2/3 expressions are similar in both cell types,TGFß-induced phosphorylation of SMAD2/3 is reduced in UT-7 JAK2V617F cells compared with JAK2 WT cells. Similarly, proliferation of UT-7 JAK2V617F cells is not decreased by TGFß, in contrast to UT-7 JAK2 WT. To restore higher levels of SHP-1 protein in the JAK2V617F mutated HEL cell line, we transduced the cDNA encoding SHP-1 and studied the proliferation in presence of TGFß. Proliferation was significantly reduced compared with cells transduced with the empty vector, confirming SHP-1 dependence in the TGFß response of JAK2V617F mutated cells. In a competitive assay UT-7 JAK2V617F cells transduced with a fluorescent m-cherry vector were mixed with UT-7 JAK2 WT cells and cultured with TGFß. In these experiments we observed a positive selection of JAK2V617F cells confirming our initial hypothesis. Transduction into HEL cells of wild-type cDNA or cDNA mutated to invalidate SHP-1 enzymatic activity showed in a competitive assay, that the effect of SHP-1 requires its enzymatic activity. Aiming to propose new therapeutic approaches to MPN patients, we tested the effect of SHP-1 agonist molecules to enhance phosphatase activity in JAK2V617F mutated cells. SC1 increases SHP-1 activity and inhibits the selection of JAK2V617F mutated cells in the presence of TGFß in vitro. However, we failed to confirm its efficiency in vivo, using a mouse model with competitive transplantation of JAK2 wild-type and mutated cells. In conclusion, we demonstrated a JAK2 dependent down regulation of SHP-1 in MPN patient cells. This down regulation is related to the resistance of JAK2V617F cells to the antiproliferative effect of TGFß, thus explaining the clonal selection of mutated cells in MPN. Finally, we propose a new therapeutic approach by increasing SHP-1 phosphatase activity, which needs to be further investigated

    Author Under Sail The Imagination of Jack London, 1893-1902

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    In 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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