1,720,992 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
Management of oxidative stress, involvement of two news targets : CFTR and activation pathway of eIF5A
No full textLe stress oxydatif définit un phénomène cellulaire particulier caractérisé par un niveau élevé de molécules hautement réactives, essentiellement lié à l’utilisation de l’oxygène par les systèmes biologiques via la respiration. La dérégulation de l’état oxydatif de la cellule est à l’origine soit de processus d’adaptations efficaces (adaptation à l’altitude) soit de pathologies (AVC, infarctus). Ce travail de thèse s’est porté sur l’étude de deux nouvelles cibles pouvant induire une résistance/tolérance à la variation du stress oxydatif : la première est la protéine canal CFTR («Cystic Fibrosis Transmembrane conductance Regulator») et la seconde la voie d’activation d’eIF5A («eukaryotic Initiation translation Factor 5A»). Nous avons pu mettre en évidence que la protéine CFTR grâce à sa perméabilité au glutathion (l’antioxydant majoritaire cellulaire) est un modulateur de l’état oxydatif de la cellule, que ce soit lors de l’exposition à des agents cytotoxiques (cisplatine) ou lors de l’adaptation à des conditions hypoxiques chroniques. La deuxième cible identifiée est le facteur eIF5A qui est la seule protéine activée par la fixation d’un résidu hypusine. L’inhibition de cette modification post-traductionnelle protège les cellules d’une production d’espèces réactives induite par l’anoxie. Cette résistance à l’anoxie est accompagnée d’un profond remodelage métabolique et mitochondrial. Sur des modèles animaux d’ischémie (rein et cerveau), l’inhibition de l’activation d’eIF5A conduit à une protection des organes face à un manque d’oxygène. Ces études fondamentales ont des applications cliniques potentielles dans des pathologies humaines (infarctus, AVC, transplantation).Oxidative stress represents a particular cellular condition, characterized by an intracellular increase in thereactive species level. These species are highly reactive towards biomolecules and result of oxygenconsumption by biological systems essentially through respiration. Deregulation of the cellular oxidativestate can initiate adaptive processes (as elevation adaptation) or several human pathologies (stroke,infarct). This thesis work has been devoted to the study of two news potential targets allowing atolerance/resistance towards disequilibrium of oxidative stress; the first one is CFTR, a channel protein(«Cystic Fibrosis Transmembrane conductance Regulator»), and the second one is the activation pathwayof the translation factor eIF5A («eukaryotic Initiation translation Factor 5A»). Based on the peculiaractivity of CFTR, consisting in the transport of glutathione, the major antioxidant of the cell, weevidenced the role of CFTR in the management of cellular oxidative state during cytotoxic drugexposure (cisplatin) or during adaptation to chronical hypoxia. The second target, eIF5A is the only oneprotein described as post-translationally modified by fixation of a hypusine residue. We demonstratedthat inhibition of eiF5A activation protect cells from reactive oxygen species generated during anoxia. Atcellular level, this protection is accompanied with deep metabolic and mitochondrial changes. Usinganimal models, we showed that inhibition of this eiF5A activation allows a tolerance against ischemicaccident in different organs (kidney and brain). These fundamentals results can have extensiveapplication in human clinical use (infarct, stroke, graft)
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
Pyrophosphate homeostasis during calcifying diseases
No full textCertaines maladies chroniques, notamment hépatiques ou rénales, sont associées à une forte prévalence de calcification artérielle dont les déterminants ne sont pas connus. Aux stades les plus évolués de ces maladies, caractérisées par une fibrose d’organe et une insuffisance fonctionnelle, la transplantation hépatique ou rénale est proposée.Le pyrophosphate est un puissant inhibiteur physiologique circulant de la calcification. En pathologie, un déficit en pyrophosphate est associé aux calcifications artérielles au cours de maladies génétiques secondaires à l’inactivation des gènes codants pour ABCC6 (adénosine triphosphate ATP-binding cassette, sous-famille C, membre 6) ou ENPP-1 (ectonucléotide pyrophosphatase/phosphodiestérase 1). Ces deux protéines sont principalement exprimées dans le foie et elles synthétisent le pyrophosphate qui est éliminé intact par voie urinaire et par hydrolyse grâce aux phosphatases alcalines. L’influence de la transplantation d’organe sur l’homéostasie du pyrophosphate est inconnue.Les objectifs de la thèse sont d’étudier les déterminants de la concentration plasmatique en pyrophosphate et des calcifications artérielles avant et après transplantation hépatique ou rénale.Dans une première partie, une nouvelle méthode de dosage standardisée du pyrophosphate dans le plasma a été mise au point pour différents fluides biologiques (milieux de culture, plasma, urine, salive, liquide articulaire). Une demande de brevet européen a été déposée.Dans une deuxième partie, des patients hémodialysés et transplantés rénaux ont été comparés entre eux et à des témoins. Les patients hémodialysés et les patients transplantés ont un déficit en pyrophosphate par rapport aux témoins. L ‘élimination urinaire de pyrophosphate est inchangée. L’activité plasmatique d’ENPP1 est identique entre les groupes mais l’activité plasmatique des phosphatases alcalines est négativement corrélée à la concentration plasmatique de pyrophosphate. Le déficit en pyrophosphate persiste chez les patients transplantés rénaux malgré une activité plasmatique des phosphatases alcalines normale à distance de la transplantation.Dans une troisième partie, des patients présentant une fibrose hépatique et une insuffisance hépatocellulaire, d’étiologies variables, ont été comparés entre eux avant et 3 mois après transplantation hépatique. La concentration plasmatique de pyrophosphate est basse avant transplantation, d’autant plus que les scores cliniques de fibrose ou d’insuffisance hépatocellulaire sont élevés. L ‘élimination urinaire de pyrophosphate est inchangée. L’activité plasmatique des phosphatases alcalines est augmentée. L’expression hépatique des ARNms d’ABCC6 et d’ENPP1 est significativement abaissée par rapport à celle de témoins non cirrhotiques. Les scores radiologiques de calcifications artérielles coronaires ou aortiques sont positivement corrélés à la sévérité de la fibrose ou de l’insuffisance hépatocellulaire.En conclusion, l’élévation de l’activité plasmatique des phosphatases alcalines avant transplantation hépatique ou rénale participe au déficit en pyrophosphate en augmentant son hydrolyse. La correction complète du déficit en pyrophosphate par la transplantation hépatique indique que le foie est la principale source de pyrophosphate. Le caractère incomplet de la correction du déficit en pyrophosphate par la transplantation rénale est évocateur d’un dialogue foie-rein. Les calcifications artérielles ne sont pas directement corrélées au pyrophosphate, suggérant l’intervention de d’autres agents qu’ils restent à caractériser.Some chronic diseases, notably liver or kidney diseases, are associated with a high prevalence of arterial calcification, the determinants of which are not known. In the most advanced stages of these diseases, characterized by organ fibrosis and then organ failure, liver or kidney transplantation is suggested.Pyrophosphate is a potent circulating physiological inhibitor of calcification. In pathology, pyrophosphate deficiency is associated with arterial calcifications during genetic diseases due to mutations in the genes coding for ABCC6 (adenosine triphosphate ATP-binding cassette, subfamily C, member 6) or ENPP-1 (ectonucleotide pyrophosphatase/phosphodiesterase 1). Both proteins are mainly expressed in the liver and are involved in pyrophosphate synthesis while it is eliminated by urinary and alkaline phosphatase hydrolysis. The influence of organ transplantation on pyrophosphate homeostasis is unknown.The objectives of this thesis are to study the determinants of plasma pyrophosphate concentration and arterial calcifications before and after liver or kidney transplantation.In the first part, a new standardized method for determining the concentration of inorganic pyrophosphate in different biological fluids (culture media, plasma, urine, saliva, joint fluid) was developed. A European patent application has been filed.In the second part, haemodialysis and kidney transplant patients were compared to each other and to controls. Both haemodialysis and transplant patients have a pyrophosphate deficit compared to controls. Urinary pyrophosphate excretion is unchanged. Plasma ENPP1 activity is identical between groups but plasma alkaline phosphatase activity is negatively correlated with plasma pyrophosphate concentration. Pyrophosphate deficiency persists in renal transplant patients despite normal plasma alkaline phosphatase activity two years after transplantation.In the third part, patients with hepatic fibrosis and hepatocellular insufficiency, of varying etiologies, were compared before and 3 months after liver transplantation. Plasma pyrophosphate concentration is low before transplantation, and negatively correlated with the clinical scores of fibrosis or hepatocellular insufficiencies are high. While urinary pyrophosphate elimination remains unchanged, plasma alkaline phosphatase activity is increased. Hepatic expression of ABCC6 and ENPP1 mRNA is significantly decreased in patients with chronic liver pathologies compared to non-cirrhotic controls. Radiological scores of coronary or aortic arterial calcifications are positively correlated with the severity of fibrosis or hepatocellular insufficiency.In conclusion, the elevation of plasma alkaline phosphatase activity before liver or kidney transplantation contributes to pyrophosphate deficiency by increasing its hydrolysis. The complete correction of pyrophosphate deficiency by liver transplantation indicates that the liver is the main source of pyrophosphate. Incomplete correction of pyrophosphate deficiency by renal transplantation suggests a liver-kidney dialogue. Arterial calcifications are not directly correlated with pyrophosphate, suggesting the involvement of other agents that are yet to be determined
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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