1,720,955 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
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
Étude longitudinale d’un modèle murin de dystonie progressive causée par un gain de fonction du récepteur bêta de l’acide rétinoïque
No full textRécemment, notre laboratoire a décrit plusieurs patients atteints d’une forme sévère et progressive de dystonie présentant des mutations de novo dans le gène du récepteur bêta de l’acide rétinoïque (RARB). RARB est un facteur de transcription activé lors de sa liaison à l’acide rétinoïque (AR), un élément essentiel au bon développement du cerveau. Des études de transfection indiquent que ces mutations augmentent l’activité transcriptionnelle de RARB, suggérant qu’elles confèrent un gain de fonction (GDF) à la protéine. La dystonie est typiquement expliquée par un dysfonctionnement du striatum, la structure où RARB est principalement exprimé. Chez la souris, la perte de fonction de Rarb entraîne une réduction des neurones striatonigraux et des anomalies motrices, suggérant une perturbation du développement des circuits striataux. Nous avons ainsi émis l’hypothèse selon laquelle la dystonie des patients porteurs de mutations de GDF serait causée par un accroissement de la signalisation de RARB, pouvant perturber l’homéostasie des mêmes circuits que ceux affectés par une diminution de la signalisation de Rarb. En utilisant la technologie CRISPR-Cas9, nous avons généré des souris portant la mutation p.R394C, homologue de la p.R387C retrouvée chez plusieurs patients. Ces souris RarbR394C/+ présentent des anomalies locomotrices rappelant celles d’autres modèles murins de dystonie, ainsi qu’une diminution des neurones striatopallidaux. Ceci suggère que les mutations de GDF de RARB induisent la dystonie en perturbant l’équilibre dans la signalisation dopaminergique striatale. Finalement, cette étude pourrait contribuer à comprendre les troubles neurodégénératifs moteurs, comme les maladies de Huntington et de Parkinson, dans lesquels la signalisation de l’AR semble être compromise.We previously described several patients with a severe and progressive form of early-onset dystonia who carried de novo mutations in the retinoic acid receptor beta gene (RARB). RARB is a transcription factor that is activated upon binding to retinoic acid (RA), whose signaling is required for proper development of the brain. Transfection studies indicate that these de novo mutations increase RARB transcriptional activity, suggesting that they confer a gain-of-function (GOF) propriety to the protein. Dystonia is typically explained by some dysfunction of the striatum, a region where RARB is predominantly expressed. Interestingly, loss of Rarb function in mice leads to a reduction of striatonigral neurons and motor abnormalities, suggesting a disruption in early development of striatal circuits. We hypothesized that the motor impairment of patients with RARB GOF mutations is caused by increased RARB signaling in the striatum, possibly disrupting homeostatic control of the same pathways as those affected by decreased Rarb signaling. Using CRISPR-Cas9 technology, we generated mice carrying the mutation p.R394C, which is homologous to the GOF mutation p.R387C found in several patients. These RarbR394C/+ mice show locomotor impairments reminiscent of that of other mouse models of dystonia, along with a decreased striatopallidal neuronal population. Our data suggest that GOF mutations in RARB induce dystonia by disrupting striatal dopaminergic signaling necessary for functional equilibrium. This work might also shed light on common neurodegenerative disorders of the basal ganglia including Huntington’s and Parkinson’s disease, in which RA and RARB signaling appear to be compromised
Étude du rôle des protéines d’adhésion synaptiques Neuroligine-1 et Neuroligine-2 dans la régulation du sommeil chez la souris femelle
Full text linkLe sommeil est un comportement universel et nécessaire, mais dont notre compréhension est encore incomplète. Les neuroligines (NLGNs) sont des protéines d’adhésion cellulaire qui se retrouvent spécifiquement aux synapses et qui sont impliquées, entre autres, dans la plasticité synaptique. De plus, NLGN1 et NLGN2 ont été reliées à la régulation de la neurotransmission excitatrice et inhibitrice, respectivement, et des mutations retrouvées dans les gènes NLGN1 et NLGN2 sont associées à des conditions pathologiques pour lesquelles des troubles du sommeil sont fréquemment rapportés, comme les troubles du spectre de l’autisme, la dépression, la schizophrénie et la maladie d’Alzheimer. Dans la littérature, il est connu que l’absence de NLGN1 ou NLGN2 induit des altérations dans la régulation de l’éveil et du sommeil chez la souris mâle. Cependant, les impacts de l’absence de l’une ou l’autre de ces protéines d’adhésion synaptique sur la régulation de l’éveil et du sommeil demeurent inconnus chez la souris femelle. Sachant que les portraits cliniques des pathologies susmentionnées et que les symptômes associés au sommeil qui sont rapportés diffèrent en fonction du sexe biologique, le but de cette thèse était donc de caractériser le phénotype entourant la régulation du sommeil et de l’éveil chez les souris femelles dont NLGN1 ou NLGN2 est absente. Dans les deux études présentées dans cette thèse, les souris ont été implantées d’électrodes électrocorticographiques (ECoG) et leurs signaux ont été enregistrés en conditions sans perturbation, de même que pendant et suite à une privation de sommeil. Les signaux enregistrés ont permis, entre autres, l’analyse de l’architecture, de l’activité spectrale et de l’activité multifractale lors de l’éveil, du sommeil à ondes lentes et du sommeil paradoxal. Dans le premier manuscrit présenté, uniquement des femelles ont été utilisées, alors le phénotype de sommeil des femelles Nlgn1-/- est comparé à celui des femelles Nlgn1+/+, puis des parallèles sont tirés entre ces observations et celles rapportées dans des articles précédents chez des mâles portant la même mutation. Comparativement aux femelles Nlgn1+/+, les femelles Nlgn1-/- passent plus de temps en sommeil paradoxal en conditions normales, présentent plus de fragmentation des trois stades de vigilance suite à la privation de sommeil, possèdent des altérations de l’activité ECoG dans les trois stades et leur activité multifractale montrent moins d’antipersistance pendant le sommeil à ondes lentes. Dans le second manuscrit inclus dans cette thèse, des femelles et des mâles ont été utilisés, permettant ainsi de comparer directement les souris Nlgn2-/- entre les sexes. Comparativement aux souris Nlgn2+/+, les souris Nlgn2-/- des deux sexes passent plus de temps éveillées et moins de temps endormies, en conditions normales et suite à la privation de sommeil, les mâles Nlgn2-/- passant significativement moins de temps en sommeil paradoxal pendant les périodes de lumière et d’obscurité, alors que cette diminution n’est présente qu’en période d’obscurité chez les femelles Nlgn2-/-. De plus, de l’instabilité dans l’architecture des trois stades de vigilance est présente chez les animaux Nlgn2-/- et semble plus prononcée chez les mâles que les femelles Nlgn2-/- en conditions normales. Aussi, l’absence de NLGN2 modifie l’activité ECoG des souris dans les trois stades, les femelles Nlgn2-/- étant affectées sur une gamme de fréquences un peu plus étendue en sommeil paradoxal que les mâles Nlgn2-/-. Finalement, les souris femelles et les mâles Nlgn2-/- ont moins d’antipersistance dans l’activité multifractale pendant les trois stades, mais seulement les femelles Nlgn2-/- présentent moins de multifractalité lors du sommeil paradoxal. En conclusion, les résultats décrits et discutés dans cette thèse contribueront à la compréhension des mécanismes régulant l’éveil et le sommeil chez les femmes et les hommes, et seront utiles pour le développement de traitements personnalisés en fonction du sexe en médecine du sommeil, notamment pour certaines pathologies neuro-développementales commes les troubles du spectre de l’autisme.Sleep is a universal and necessary behavior, but our understanding of it is still incomplete. Neuroligins (NLGNs) are cell adhesion proteins found specifically at synapses and are involved, amongst other things, in synaptic plasticity. In addition, NLGN1 and NLGN2 have been linked to the regulation of excitatory and inhibitory neurotransmission, respectively, and mutations found in the NLGN1 and NLGN2 genes are associated with pathological conditions for which sleep disorders are frequently reported, such as autism spectrum disorders, depression, schizophrenia, and Alzheimer’s disease. It is known that the absence of NLGN1 or NLGN2 induces alterations in the regulation of wakefulness and sleep in male mice. However, the impacts of the absence of either of these synaptic adhesion proteins on the regulation of wakefulness and sleep remain unknown in female mice. Given that the clinical profiles of the aforementioned pathologies and the associated sleep symptoms that are reported differ depending on biological sex, the aim of this thesis was to characterize the phenotype related to sleep and wakefulness regulation in female mice lacking NLGN1 or NLGN2. In the two studies presented in this thesis, mice were implanted with electrocorticographic (ECoG) electrodes and their signals were recorded under undisturbed conditions, as well as during and following sleep deprivation. The recorded signals enabled, amongst others, the analysis of architecture, spectral activity, and multifractal activity during wakefulness, slow-wave sleep, and paradoxical sleep. In the first manuscript presented, only females were used, so the sleep phenotype of Nlgn1-/- females was compared to that of Nlgn1+/+ females, and parallels were drawn between these observations and those reported in previous articles using males carrying the same mutation. In comparison to Nlgn1+/+ females, Nlgn1-/- females spend more time in paradoxical sleep under normal conditions, display more fragmentation of the three vigilance states following sleep deprivation, have alterations in ECoG activity in all three states, and their multifractal activity shows less antipersistence during slow-wave sleep. In the second manuscript included in this thesis, both females and males were used, allowing for a direct comparison of Nlgn2-/- mice between sexes. Compared to Nlgn2+/+ mice, Nlgn2-/- mice of both sexes spend more time awake and less time sleeping, under normal conditions and following sleep deprivation, with Nlgn2-/- males spending significantly less time in paradoxical sleep during both the light and dark periods, whereas this reduction is only present during the dark period in Nlgn2-/- females. In addition, instability in the architecture of the three vigilance states is present in Nlgn2-/- mice and appears to be more pronounced in Nlgn2-/- males than females, under normal conditions. Furthermore, the absence of NLGN2 alters the ECoG activity of mice in all three states, with Nlgn2-/- females being affected over a slightly wider range of frequencies during paradoxical sleep than Nlgn2-/- males. Finally, Nlgn2-/- females and males have less antipersistence in multifractal activity during all three states, but only Nlgn2-/- females show less multifractality during paradoxical sleep. In conclusion, the results described and discussed in this thesis will contribute to the understanding of the mechanisms regulating wakefulness and sleep in women and men, and will be useful for the development of sex-personalized treatments in sleep medicine, particularly for certain neurodevelopmental disorders such as autism spectrum disorders
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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