1,721,018 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
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
Impact of endothelial and leukocyte senescence in circulatory shock states
No full textParmi les conséquences à long terme du sepsis (également appelé "syndrome post-sepsis"), l'augmentation du risque de développer des complications cardiovasculaires inexpliquées et/ou un épisode infectieux récurrent sont des préoccupations émergentes. Ces complications expliquent en grande partie la morbi-mortalité chez les survivants d’un choc septique. Récemment, la sénescence, définie comme l’arrêt irréversible du cycle cellulaire, a été identifiée comme un mécanisme de dysfonction cellulaire qui perdure dans le temps. Habituellement liée à l’âge lorsqu’il s’agit de sénescence réplicative, elle peut aussi être « induite » de manière « prématurée » par un stress majeur. Ainsi,une sénescence prématurée induite par le choc septique au niveau du système cardio-vasculaire et immunitaire pourrait en partie contribuer à la physiopathologie et aux conséquences à long terme du syndrome post-sepsis. Ce travail de thèse a pour objectif d’appréhender les relations potentielles entre le sepsis et la sénescence prématurée induite (ou sénescence accélérée). En particulier, les mécanismes cellulaires clés contribuant aux infections récurrentes et aux événements cardiovasculaires chez des patients convalescents déjà lourdement affectés par un choc septique. Les principaux résultats de nos travaux sont que le sepsis induit un dysfonctionnement artériel avec une acquisition in situ, dépendante du temps, d'un phénotype d'inflammation et de sénescence dans les artères de conduction et de résistance, ce qui indique un effet systémique persistant pouvant expliquer en partie la physiopathologie des conséquences cardio-vasculaires à long terme.Among the long-term consequences of sepsis (also called "post-sepsis syndrome"), the increased risk of developing unexplained cardiovascular complications and/or a recurrent infectious episode are emerging concerns. These complications account for much of the morbidity and mortality in survivors of septic shock. Recently, senescence, defined as irreversible cell cycle arrest, has been identified as a mechanism of cell dysfunction that persists over time. Usually linked to age when it is replicative senescence, it can also be "induced" in a "premature" way by a major stress. Thus, premature senescence induced by septic shock at the level of the cardiovascular and immune system could partly contribute to the pathophysiology and long-term consequences of the post-sepsis syndrome.The aim of our work is to understand the potential relationship between sepsis and induced premature senescence (or accelerated senescence). In particular, the key cellular mechanisms contributing to recurrent infections and cardiovascular events in convalescent patients already heavily affected by sepsis. The main finding of our work is that sepsis induced arterial dysfunction with a time dependent in situ acquisition of inflammation and senescence phenotype in both conductance and resistance arteries, therefore pointing at a systemic long-lasting effect that may partly explain the pathophysiology of long-term cardiovascular consequences
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
Évaluation de la sénescence endothéliale et leucocytaire dans le choc septique
No full textAmong the long-term consequences of sepsis (also called "post-sepsis syndrome"), the increased risk of developing unexplained cardiovascular complications and/or a recurrent infectious episode are emerging concerns. These complications account for much of the morbidity and mortality in survivors of septic shock. Recently, senescence, defined as irreversible cell cycle arrest, has been identified as a mechanism of cell dysfunction that persists over time. Usually linked to age when it is replicative senescence, it can also be "induced" in a "premature" way by a major stress. Thus, premature senescence induced by septic shock at the level of the cardiovascular and immune system could partly contribute to the pathophysiology and long-term consequences of the post-sepsis syndrome.The aim of our work is to understand the potential relationship between sepsis and induced premature senescence (or accelerated senescence). In particular, the key cellular mechanisms contributing to recurrent infections and cardiovascular events in convalescent patients already heavily affected by sepsis. The main finding of our work is that sepsis induced arterial dysfunction with a time dependent in situ acquisition of inflammation and senescence phenotype in both conductance and resistance arteries, therefore pointing at a systemic long-lasting effect that may partly explain the pathophysiology of long-term cardiovascular consequences.Parmi les conséquences à long terme du sepsis (également appelé "syndrome post-sepsis"), l'augmentation du risque de développer des complications cardiovasculaires inexpliquées et/ou un épisode infectieux récurrent sont des préoccupations émergentes. Ces complications expliquent en grande partie la morbi-mortalité chez les survivants d’un choc septique. Récemment, la sénescence, définie comme l’arrêt irréversible du cycle cellulaire, a été identifiée comme un mécanisme de dysfonction cellulaire qui perdure dans le temps. Habituellement liée à l’âge lorsqu’il s’agit de sénescence réplicative, elle peut aussi être « induite » de manière « prématurée » par un stress majeur. Ainsi,une sénescence prématurée induite par le choc septique au niveau du système cardio-vasculaire et immunitaire pourrait en partie contribuer à la physiopathologie et aux conséquences à long terme du syndrome post-sepsis. Ce travail de thèse a pour objectif d’appréhender les relations potentielles entre le sepsis et la sénescence prématurée induite (ou sénescence accélérée). En particulier, les mécanismes cellulaires clés contribuant aux infections récurrentes et aux événements cardiovasculaires chez des patients convalescents déjà lourdement affectés par un choc septique. Les principaux résultats de nos travaux sont que le sepsis induit un dysfonctionnement artériel avec une acquisition in situ, dépendante du temps, d'un phénotype d'inflammation et de sénescence dans les artères de conduction et de résistance, ce qui indique un effet systémique persistant pouvant expliquer en partie la physiopathologie des conséquences cardio-vasculaires à long terme
Évaluation de la sénescence endothéliale et leucocytaire dans le choc septique
No full textAmong the long-term consequences of sepsis (also called "post-sepsis syndrome"), the increased risk of developing unexplained cardiovascular complications and/or a recurrent infectious episode are emerging concerns. These complications account for much of the morbidity and mortality in survivors of septic shock. Recently, senescence, defined as irreversible cell cycle arrest, has been identified as a mechanism of cell dysfunction that persists over time. Usually linked to age when it is replicative senescence, it can also be "induced" in a "premature" way by a major stress. Thus, premature senescence induced by septic shock at the level of the cardiovascular and immune system could partly contribute to the pathophysiology and long-term consequences of the post-sepsis syndrome.The aim of our work is to understand the potential relationship between sepsis and induced premature senescence (or accelerated senescence). In particular, the key cellular mechanisms contributing to recurrent infections and cardiovascular events in convalescent patients already heavily affected by sepsis. The main finding of our work is that sepsis induced arterial dysfunction with a time dependent in situ acquisition of inflammation and senescence phenotype in both conductance and resistance arteries, therefore pointing at a systemic long-lasting effect that may partly explain the pathophysiology of long-term cardiovascular consequences.Parmi les conséquences à long terme du sepsis (également appelé "syndrome post-sepsis"), l'augmentation du risque de développer des complications cardiovasculaires inexpliquées et/ou un épisode infectieux récurrent sont des préoccupations émergentes. Ces complications expliquent en grande partie la morbi-mortalité chez les survivants d’un choc septique. Récemment, la sénescence, définie comme l’arrêt irréversible du cycle cellulaire, a été identifiée comme un mécanisme de dysfonction cellulaire qui perdure dans le temps. Habituellement liée à l’âge lorsqu’il s’agit de sénescence réplicative, elle peut aussi être « induite » de manière « prématurée » par un stress majeur. Ainsi,une sénescence prématurée induite par le choc septique au niveau du système cardio-vasculaire et immunitaire pourrait en partie contribuer à la physiopathologie et aux conséquences à long terme du syndrome post-sepsis. Ce travail de thèse a pour objectif d’appréhender les relations potentielles entre le sepsis et la sénescence prématurée induite (ou sénescence accélérée). En particulier, les mécanismes cellulaires clés contribuant aux infections récurrentes et aux événements cardiovasculaires chez des patients convalescents déjà lourdement affectés par un choc septique. Les principaux résultats de nos travaux sont que le sepsis induit un dysfonctionnement artériel avec une acquisition in situ, dépendante du temps, d'un phénotype d'inflammation et de sénescence dans les artères de conduction et de résistance, ce qui indique un effet systémique persistant pouvant expliquer en partie la physiopathologie des conséquences cardio-vasculaires à long terme
- …
