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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
Etude du rôle de l’autophagie et de la réponse UPR dans la résistance des cellules cancéreuses contre l’apoptose induite par le paclitaxel.
Get PDFCancer cell resistance against chemotherapy is still a heavy burden to improve anticancer treatments. Understanding the mechanisms responsible for the resistance against chemotherapy-induced cell death is of interest since the number of patients with cancer increases and relapse is commonly observed. Development of hypoxic regions is known to promote cancer cell adaptation to the stressful tumoral microenvironment and resistance against anti-cancer therapies. The HIF-1 signaling pathway, activated under hypoxia, promotes cancer cell adaptation and resistance against chemotherapy. Other biological processes are also activated under hypoxia and/or after chemotherapy treatment and are known to promote cancer cell survival. Autophagy and UPR (unfolded protein response) are part of these processes. Therefore, during the first part of this work, we sought to evaluate the role of autophagy and hypoxia on the taxol-induced apoptosis in MDA-MB-231 breast cancer cells. Results showed that taxol induced apoptosis after 16 h of incubation, and that hypoxia protected MDA-MB- 231 cells from taxol-induced apoptosis. In parallel, taxol induced autophagy activation already after 2 h of incubation both under normoxia and hypoxia. Autophagy activation during taxol exposure was shown to be a protective mechanism against taxol-induced cell death both under normoxia and hypoxia. However, at longer incubation times, the autophagic process reached a saturation point under normoxia leading to cell death, whereas under hypoxia, autophagy flow still correctly took place allowing the cells to survive. Autophagy induction was initiated via mechanistic target of rapamycin (mTOR) inhibition, which is more important in cells exposed to hypoxia. Taxol also induced c-Jun N-terminal kinase (JNK) activation and phosphorylation of its substrates B-cell CLL/lymphoma 2 (Bcl2) and Bcl2-like 1 (BclXL) under normoxia and hypoxia very early after taxol exposure. Bcl2 and BclXL phosphorylation was decreased more importantly under hypoxia after long incubation times. The role of JNK in autophagy and apoptosis induction was studied using siRNAs. The results showed that JNK activation promoted resistance against taxol-induced apoptosis under normoxia and hypoxia without being involved in induction of autophagy. In conclusion, the resistance against taxol-induced cell death observed under hypoxia can be explained by a more effective autophagic flow activated via the classical mTOR pathway and by a mechanism involving JNK, which could be dependent on Bcl2 and BclXL phosphorylation but independent of JNK-induced autophagy activation. During the second part of this work, the impact of UPR combined to hypoxia on autophagy and apoptosis activation during taxol exposure was investigated in MDA-MB-231 breast cancer cells. Results showed that taxol rapidly induced endoplasmic reticulum (ER) stress and UPR activation and that hypoxia modulated taxol-induced UPR activation. The putative involvement of PERK (protein kinase double-stranded RNA-dependent (PRK)-like ER Kinase), ATF6 (activating transcription factor 6) and IRE1 (inositol-requiring enzyme-1) signaling pathways in autophagy or in apoptosis regulation after taxol exposure was investigated. No link between the activation of these three ER stress sensors and autophagy or apoptosis regulation was evidenced. However, UPR played a role in the induction of VEGF (vascular Endothelial Growth Factor) secretion triggered by taxol exposure specifically in cells incubated under hypoxia. Results also showed that ATF4 (activating transcription factor 4) activation was involved in taxol-induced autophagy completion and in the mechanisms leading to cancer cell adaptation and resistance against taxol-induced cell death. Finally, our results demonstrate that the expression of ATF4, in association with hypoxia-induced genes, could be used as a biomarker of a poor prognosis in human breast cancer patients supporting the conclusion that ATF4 might play a role in adaptation and resistance of breast cancer cells to chemotherapy in hypoxic tumors.La résistance des cellules cancéreuses à la chimiothérapie est un problème crucial pour améliorer les traitements anticancéreux. La compréhension des mécanismes responsables de la résistance à la mort cellulaire induite par la chimiothérapie est toujours d’actualité car le nombre de patients atteints d’un cancer ne cesse d’augmenter et des rechutes sont souvent observées. Le développement de régions hypoxiques au sein des tumeurs est connu pour favoriser l’adaptation des cellules cancéreuses à leur environnement stressant et la résistance aux thérapies anticancéreuses. Les voies de signalisation dépendantes de HIF-1 (hypoxiainducible factor-1), qui sont activées en hypoxie, favorisent l’adaptation des cellules cancéreuses et la résistance à la chimiothérapie. D’autres processus biologiques, activés en hypoxie et/ou suite à un traitement chimiothérapeutique, sont également connus pour favoriser la survie des cellules cancéreuses. L’autophagie et l’UPR font partie de ces processus biologiques. Pour cette raison, durant la première partie de ce travail, nous avons étudié le rôle de l’autophagie et de l’hypoxie dans l’apoptose induite par le taxol dans les cellules MDA-MB- 231 issues d’un cancer du sein triple négatif. Les résultats montrent que le taxol induit l’apoptose après 16 heures d’incubation et que l’hypoxie protège les cellules MDA-MB-231 de l’apoptose induite par le taxol. En parallèle, le taxol induit l’activation de l’autophagie après 2 heures d’incubation en normoxie et en hypoxie. L’activation de l’autophagie dans les cellules incubées avec du taxol est un mécanisme protecteur contre l’apoptose induite par le taxol en normoxie et en hypoxie. Cependant, après des temps d’incubation plus longs, le processus autophagique atteint un seuil de saturation en normoxie, conduisant à la mort cellulaire. En hypoxie, le flux autophagique se déroule correctement même après des temps d’incubation plus longs, ce qui permet aux cellules de survivre. L’autophagie est activée via l’inhibition de mTOR (mechanistic target of rapamycin), qui est plus importante dans les cellules incubées en hypoxie. Le taxol induit également l’activation de la JNK (c-Jun Nterminal kinase) et la phosphorylation de ses substrats Bcl2 (B-cell CLL/lymphoma 2) et BclXL (Bcl2-like 1) en normoxie et en hypoxie, très tôt au cours de l’exposition au taxol. Après des temps d’incubation plus longs, la phosphorylation de Bcl2 et BclXL diminue de manière plus importante dans les cellules incubées en hypoxie. Le rôle de la JNK dans l’activation de l’autophagie et de l’apoptose a été étudié à l’aide de siRNAs. Les résultats montrent que l’activation de la JNK favorise la résistance à l’apoptose induite par le taxol en normoxie et en hypoxie sans être impliquée dans l’activation de l’autophagie. En conclusion, la résistance à la mort cellulaire induite par le taxol observée en hypoxie peut être expliquée par un flux autophagique plus efficace activé par la voie classique mTOR et également pas un mécanisme impliquant la JNK, qui pourrait dépendre de la phosphorylation de Bcl2 et BclXL mais qui ne dépend pas de l’activation de l’autophagie par la JNK. Durant la seconde partie de ce travail, l’impact de l’UPR, combinée à l’hypoxie, sur l’activation de l’autophagie et de l’apoptose, durant une exposition au taxol, fut étudié dans les cellules MDA-MB-231. Les résultats montrent que le taxol induit rapidement un stress au réticulum endoplasmique et l’activation de l’UPR et que l’hypoxie module l’activation de l’UPR induite par le taxol. L’implication des voies de signalisation en aval de PERK (protein kinase double-stranded RNA-dependent (PRK)-like ER Kinase), d’ATF6 (activating transcription factor 6) et d’IRE1 (inositol-requiring enzyme-1) dans la régulation de l’autophagie ou de l’apoptose lors d’une incubation en présence de taxol fut investiguée. Aucun lien entre l’activation de ces trois senseurs du stress au RE et la régulation de l’autophagie ou de l’apoptose ne fut mis en évidence. Cependant, l’UPR régule la sécrétion du VEGF (vascular Endothelial Growth Factor) induite par le taxol uniquement dans les cellules incubées en hypoxie. Les résultats montrent aussi qu’ATF4 (activating transcription factor 4) favorise l’accomplissement de l’autophagie et est impliqué dans les mécanismes qui permettent l’adaptation des cellules cancéreuses et la résistance à l’apoptose induite par le taxol. Enfin, les résultats montrent que l’expression d’ATF4, en association avec l’expression de gènes induits en hypoxie, peut être utilisée comme biomarqueur reflétant un mauvais pronostic pour les patients atteints d’un cancer du sein. Ces résultats renforcent la conclusion qu’ATF4 peut jouer un rôle dans l’adaptation et la résistance des cellules cancéreuses du sein contre la chimiothérapie, en hypoxie.(DOCSC03) -- FUNDP, 201
Etude des effets de l'hypoxie sur l'apoptose induite par le taxol ou l'épirubicine dans des cellules du cancer du sein : rôle du facteur de transcription HIF-1
Get PDFCaractérisation des effets du taxol et de l'épirubicine sur des cellules de cancer du sein: effet de l'hypoxie
No full textDispelling 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
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