1,721,000 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
The regulatory role of Malat1 on the alternative splicing factor SRSF1 during CD4+ T cell differentiation
No full textThe proper activation and subsequent differentiation of naive CD4+ T cells into effector T helper and regulatory T cells is vital for directing an appropriate adaptive immune response to specific infections. Recent evidence has identified long non-coding RNAs as novel regulators of CD4+ T cell activation and differentiation. Work by the Lagos group and others has identified the long non-coding RNA Metastasis associated lung adenocarcinoma transcript 1 (Malat1) as a critical regulator of Th cell function and immune response to chronic infection in mice. However, the mechanism behind this regulation by Malat1 is not yet fully understood. This project aimed to investigate the RNA binding protein and splicing factor SRSF1, a known Malat1 binding partner and prominent regulator of gene expression and alternative splicing in the immune system, as a mediator for Malat1 regulation of Th cell function. Through analysis of individual-nucleotide resolution UV crosslinking and immunoprecipitation (iCLIP), we have shown that SRSF1 displays alternative RNA binding behaviour in Th2 cells upon Malat1 loss. This alternative binding is directed towards RNA transcripts involved in T cell activation and differentiation, including Il2ra and Runx3. Following this, we found that Runx3 abundance is reduced and isoform usage is altered upon Malat1 loss in Th2 cells. To complement studies within Malat1-/- CD4+ T cells we attempted to develop Srsf1-/- CD4+ T cell models. Attempts to develop Srsf1-/- EL4 cell lines using CRISPRCas9- editing caused just a transient knockdown of SRSF1 expression, suggesting SRSF1 is essential for viability in this mouse T cell lymphoma cell line. Initial studies for establishing CRISPR-Cas9 RNP transfection into in vitro primary CD4+ T cell activation assays were unsuccessful at producing an SRSF1 knockout but have laid a foundation for further optimisation. Overall, our results identified Malat1 regulation of SRSF1 mediated RNA interaction during the Th2 cell differentiation, which serves as a promising mechanism for further investigation to better characterise Malat1 regulation of Th cell phenotype and cytokine expression
The regulatory role of Malat1 on the alternative splicing factor SRSF1 during CD4+ T cell differentiation
Get PDFThe proper activation and subsequent differentiation of naive CD4+ T cells into effector T helper and regulatory T cells is vital for directing an appropriate adaptive immune response to specific infections. Recent evidence has identified long non-coding RNAs as novel regulators of CD4+ T cell activation and differentiation. Work by the Lagos group and others has identified the long non-coding RNA Metastasis associated lung adenocarcinoma transcript 1 (Malat1) as a critical regulator of Th cell function and immune response to chronic infection in mice. However, the mechanism behind this regulation by Malat1 is not yet fully understood. This project aimed to investigate the RNA binding protein and splicing factor SRSF1, a known Malat1 binding partner and prominent regulator of gene expression and alternative splicing in the immune system, as a mediator for Malat1 regulation of Th cell function. Through analysis of individual-nucleotide resolution UV crosslinking and immunoprecipitation (iCLIP), we have shown that SRSF1 displays alternative RNA binding behaviour in Th2 cells upon Malat1 loss. This alternative binding is directed towards RNA transcripts involved in T cell activation and differentiation, including Il2ra and Runx3. Following this, we found that Runx3 abundance is reduced and isoform usage is altered upon Malat1 loss in Th2 cells. To complement studies within Malat1-/- CD4+ T cells we attempted to develop Srsf1-/- CD4+ T cell models. Attempts to develop Srsf1-/- EL4 cell lines using CRISPRCas9- editing caused just a transient knockdown of SRSF1 expression, suggesting SRSF1 is essential for viability in this mouse T cell lymphoma cell line. Initial studies for establishing CRISPR-Cas9 RNP transfection into in vitro primary CD4+ T cell activation assays were unsuccessful at producing an SRSF1 knockout but have laid a foundation for further optimisation. Overall, our results identified Malat1 regulation of SRSF1 mediated RNA interaction during the Th2 cell differentiation, which serves as a promising mechanism for further investigation to better characterise Malat1 regulation of Th cell phenotype and cytokine expression
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
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
Malat1 is a Sex-Specific Determinant of Th Cell Differentiation
Get PDFUnderstanding cell intrinsic mediators of sexual dimorphism in lymphocytes is critical to addressing differences in incidence and severity of immunopathologies between females and males. Here, we demonstrate that the nuclear speckle-associated lincRNA Malat1, one of the most highly abundant transcripts in mammalian cells, exerts a sex-specific function in Th2 differentiation by controlling early differentiation and endpoint cytokine expression in female cells. Malat1 deficiency impairs in vitro Th2 differentiation only in female mice, characterised by transcriptome-wide suppression of differentiation associated gene expression and cytokine expression, with particularly strong effects on IL10. Using an in vivo model of lung inflammation, we validated the sex-specific effects of Malat1 loss, demonstrating altered Th2 differentiation in both the lung and spleen for only female mice. Mechanistically, naïve T helper cells from Malat1-/- female mice demonstrate impaired early differentiation in the gene expression programme, along with upregulation of an interferon stimulated gene module associated with naïve CD4+ T cells. This is followed by suppression of the IL2 receptor, which in turn inhibits IL2 mediated differentiation. Male Th2 differentiation was less sensitive to effects of Malat1 loss due to stronger early activation, higher constitutive interferon responsive gene expression, and lower sensitivity to exogenous levels of IL2. Malat1 deficiency during early Th2 differentiation suppressed differentiation-associated changes in nuclear architecture in a sex-specific manner, with effects on nuclear speckle biogenesis, Xi complex localisation, and H3K27me3 deposition. Overall, this suggests that, despite neither being X/Y linked nor sex hormone responsive, Malat1 is a critical sex-specific regulator of Th cell differentiation, with profound implications in our understanding of how non-coding RNA drives immune sexual dimorphism
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