1,721,051 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
Iron excess impact on S1P/S1PR axis in human osteoblast-like MG-63 cells
No full textLes surcharges en fer, qu’elles soient d’origine génétique ou secondaire, favorisent la baisse de densité minérale osseuse et par conséquent l’apparition d’une ostéoporose. Des liens entre surcharge en fer et perte osseuse ont pu être établis in vivo et in vitro, néanmoins les mécanismes mis en jeu, notamment sur la cellule ostéoblastique, restent incomplètement caractérisés. Notre objectif a donc été de préciser les mécanismes cellulaires conduisant à l’altération du phénotype et de l’activité ostéoblastique observée en présence d’un excès de fer. La réalisation préalable d’une étude transcriptomique sur la lignée ostéoblastique humaine MG-63 nous a permis d’identifier plusieurs gènes susceptibles de voir leur niveau d’ARNm régulé par le fer. Il a été fait l’hypothèse que ces différents gènes pouvaient être impliqués dans la survenue des pertes osseuses observées au cours des surcharges en fer. Ainsi l’expression du gène SPNS2, dont la protéine permet l’export de la Sphingosine-1-Phosphate (S1P), a été identifiée comme potentiellement induite par un excès de fer. Les relations entre l’expression du gène SPNS2 et un excès de fer ont ainsi été investiguées et les résultats obtenus ont mis en évidence une augmentation fer-dépendante de l’ARNm du gène SPNS2 dans la lignée MG-63, non retrouvée dans d’autres types cellulaires. Cette caractérisation nous a ainsi conduits à déterminer, dans la lignée MG-63, l’impact fonctionnel d’une exposition au fer sur l’export cellulaire de la S1P. Nous avons donc pour cela mis au point une méthode d’étude basée sur une stratégie « fluxomique » nous permettant d’évaluer l’efflux de la S1P au moyen d’un outil de spectrométrie de masse. Nos résultats objectivent une diminution des capacités de synthèse et d’export de la S1P en présence de fer et ceci malgré la surexpression du gène SPNS2. La diminution concomitante de l’expression du récepteur S1PR1 et du gène COL1A1 codant pour la chaîne α du collagène de type I suggère un impact fonctionnel de la baisse de concentration en S1P extracellulaire sur la cellule MG-63. La mise en évidence, dans un modèle ostéoblastique, d’une altération fer-dépendante de l’axe de signalisation S1P/S1PR ouvre de nouvelles perspectives quant à la compréhension des mécanismes mis en jeu lors des pertes osseuses associées aux surcharges en fer.Osteoporosis may complicate genetic or secondary iron overload as reported in clinical and animal studies. However, the mechanisms leading to disrupted bone homeostasis are still to be fully elucidated. In vitro, iron exposure of both osteoblast and osteoclast cell models induces phenotypic and functional impairment, but the molecular mechanisms of iron excess on bone cell physiology are not well characterized, particularly in osteoblast. Our objective was to study the impact of iron overload on osteoblast biology and characterize the molecular mechanisms involved. Transcriptomic analysis previously performed by our group on MG-63 osteoblast-like cell-line to identify iron-modulated genes revealed that expression of SPNS2 gene, which encodes a transporter for the signaling lipid sphingosine 1-phosphate (S1P), is potentially induced by iron. The purpose of this work was to characterize the SPNS2 iron-related regulation and analyze its potential impact on S1P efflux and the S1P/S1PR signaling pathway in MG-63 cells. Our findings showed that iron exposure induces a dose-dependent increase of SPNS2 mRNA levels in MG-63 osteoblast-like cells that was not observed in hepatocyte and enterocyte cell models. We then performed a fluxomic assay on MG-63 cells to investigate iron potential impact on S1P efflux. Unexpectedly, our data showed that extracellular S1P levels were decreased in presence of iron excess and its associated SPNS2 upregulation. Furthermore, based on the observed iron associated S1PR1 and COL1A1 decrease, the defect in S1P export system seems to have functional consequence on MG-63 cells. These results suggest that iron may affect osteoblast S1P/SPR signaling and potentially alter a wide range of bone processes, thus participating in bone impairment in situations of chronic iron overload. These data open a new door for the understanding of mechanisms involved in iron-induced osteoporosis
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
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
Mechanisms involved in the development of osteoporosis during iron overload
No full textL’ostéoporose représente un problème de santé publique, particulièrement par l’intermédiaire de ses conséquences en termes de morbi-mortalité. La complication principale de cette maladie est la fracture, occasionnant un surrisque de décès et d’institutionnalisation. La surcharge en fer est une cause bien identifiée d’ostéoporose secondaire. L’intérêt pour cette cause secondaire de perte osseuse est renforcé par le fait que l’augmentation de la ferritinémie chez les femmes ménopausées serait associée à un excès de fragilité osseuse. Les mécanismes cellulaires et moléculaires impliqués dans l'ostéoporose liée au fer ne sont pas entièrement compris. Ceux-ci aboutissent à un déséquilibre de l’homéostasie osseuse, avec activation de la résorption et diminution de la formation osseuse. Notre objectif était d'étudier les rôles respectifs du fer lui-même, mais aussi de l’hepcidine, acteur central de la régulation du niveau de fer plasmatique, et des autres métaux interagissant avec le métabolisme du fer dans le développement de l'ostéoporose liée à la surcharge en fer. En s’appuyant sur des modèles murins de surcharge en fer génétique (Hfe-/-, Bmp6-/-) ou secondaire (fer dextran), puis des modèles cellulaires, nos résultats suggèrent que le fer à lui-seul ne peut pas expliquer l’ensemble du phénotype osseux, avec une perte osseuse retrouvée exclusivement dans les modèles de surcharge génétique. La diminution de l’hepcidine dans les modèles génétiques pourrait avoir un rôle dans la perte osseuse, qui semble apparaitre principalement par dépression ostéoblastique. Concernant les autres métaux, étudiés dans les mêmes modèles ainsi que chez l’humain, les observations montrent une différence de la concentration sérique des métaux entre les sexes avec des différences notables entre homme et femme, notamment concernant l’aluminium et le cadmium. L’ensemble de ce travail permet donc de préciser le mécanisme de la perte osseuse dans le cadre des surcharges en fer, avec potentiellement des applications pouvant s’étendre à la population générale, avec identification de groupes à risque.Osteoporosis is a public health problem, particularly through its consequences in terms of morbidity and mortality. The main complication of this disease is fracture, with an increased risk of death and institutionalization. Iron overload is a well identified cause of secondary osteoporosis. Interest in this secondary cause of bone loss is reinforced by the fact that increased ferritin levels in postmenopausal women seems to be associated with excess bone fragility. The cellular and molecular mechanisms involved in iron-related osteoporosis are not fully understood. These lead to an imbalance in bone homeostasis, with activation of resorption and reduction of bone formation. Our aim was to study the respective roles of iron itself, but also of hepcidin, a central player in the regulation of plasma iron levels, and of other metals interacting with iron metabolism in the development of iron overload-related osteoporosis. Mice models of genetic (Hfe-/-, Bmp6-/-) or secondary (iron dextran) iron overload, and cellular models, suggest that iron alone cannot explain the bone phenotype, with bone loss found exclusively in models of genetic overload. The decrease of hepcidin level in the genetic models could have a role in the bone loss, which seems to occur mainly by osteoblastic depression. Concerning the other metals, studied in the same models as well as in humans, the observations show differences in serum concentration of metals between men and women, particularly concerning aluminum and cadmium. Our work allows to specify the mechanism of bone loss in the context of iron overload, with potential applications that could be extended to the general population, with the identification of risk groups
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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