1,720,974 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
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
Oncogenic ALK signaling in neuroblastoma
No full textOver the last decade Anaplastic Lymphoma Kinase (ALK), a receptor tyrosine kinase (RTK) has been identified as a translocation partner in diverse cancer types. In tumors, where the full-length ALK RTK itself is mutated, such as neuroblastoma, the picture is less clear regarding ALKs role as an oncogenic driver. Neuroblastoma is a heterogeneous disease of the sympathetic nervous system, accounting for 10-15% of all childhood cancer deaths. A number of small tyrosine kinase inhibitors (TKIs) have been developed to inhibit ALK activity. The data acquired thus far suggests that ALK TKI mono-treatment may not be as effective solution for ALK positive neuroblastoma patients. Therefore, there is a need for combination therapy using drugs towards different targets or signaling pathways to combat the disease. The overall aim of this thesis is to identify targets in signaling pathways that can be inhibited by specific drugs, as a potential poly-therapy treatment strategy in ALK positive neuroblastoma patients.
Using an MS-based phosphor-proteomics approach, we identified STAT3 as a potential downstream target of oncogenic ALK signaling (Paper I). ALK activation of STAT3 results in increased phosphorylation of STAT3 in PC12 cells expressing a gain-of-function ALK mutation. Pharmacologic inhibition of STAT3 using FLLL32 and STATTIC resulted in decreased phosphorylation levels of STAT3 and MYCN protein and mRNA levels. This study identified STAT3 as a target of ALK signaling and showed that inhibition of STAT3 using FLLL32 and STATTIC decreases proliferation of neuroblastoma cell lines and regulates the transcription of MYCN.
In a subsequent paper, we identified ERK5 as a potential ‘druggable’ target for ALK positive neuroblastoma patients (Paper II). Inhibition of ERK5 activity, reduced proliferation of ALK positive neuroblastoma cells as well as MYCN mRNA levels. Combination of ALK and ERK5 inhibitors abrogated tumor growth and cell proliferation synergistically. Overall, this study showed that ALK activates ERK5 via the PI3K pathway and regulates MYCN transcriptionally, suggesting that targeting both ALK and ERK5 might be beneficial for ALK positive neuroblastoma patients.
In paper III, we addressed whether MEK inhibition alone or in combination with ALK inhibitor(s) has therapeutic value in a large panel of neuroblastoma cell lines. MEK inhibition alone in ALK positive neuroblastoma cells or xenografts did not abrogate cell or tumor growth. We showed that pharmacological inhibition of MEK-ERK pathway in ALK-positive neuroblastoma cells results in increased levels of activation/phosphorylation of AKT and ERK5. This feedback response is regulated by the mTOR complex 2 protein SIN1. Our results contraindicate the use of MEK inhibitors as effective therapeutic strategy in ALK-positive neuroblastoma.
Together, this study highlights the importance of full length ALK receptor signaling in neuroblastoma. Further, it shows that combination of ALK inhibitor with PI3K/Akt/mTOR/ERK5 pathway inhibitors might be a potential therapeutic treatment strategy for ALK positive neuroblastoma patients
Oncogenic ALK signaling in neuroblastoma
No full textOver the last decade Anaplastic Lymphoma Kinase (ALK), a receptor tyrosine kinase (RTK) has been identified as a translocation partner in diverse cancer types. In tumors, where the full-length ALK RTK itself is mutated, such as neuroblastoma, the picture is less clear regarding ALKs role as an oncogenic driver. Neuroblastoma is a heterogeneous disease of the sympathetic nervous system, accounting for 10-15% of all childhood cancer deaths. A number of small tyrosine kinase inhibitors (TKIs) have been developed to inhibit ALK activity. The data acquired thus far suggests that ALK TKI mono-treatment may not be as effective solution for ALK positive neuroblastoma patients. Therefore, there is a need for combination therapy using drugs towards different targets or signaling pathways to combat the disease. The overall aim of this thesis is to identify targets in signaling pathways that can be inhibited by specific drugs, as a potential poly-therapy treatment strategy in ALK positive neuroblastoma patients. Using an MS-based phosphor-proteomics approach, we identified STAT3 as a potential downstream target of oncogenic ALK signaling (Paper I). ALK activation of STAT3 results in increased phosphorylation of STAT3 in PC12 cells expressing a gain-of-function ALK mutation. Pharmacologic inhibition of STAT3 using FLLL32 and STATTIC resulted in decreased phosphorylation levels of STAT3 and MYCN protein and mRNA levels. This study identified STAT3 as a target of ALK signaling and showed that inhibition of STAT3 using FLLL32 and STATTIC decreases proliferation of neuroblastoma cell lines and regulates the transcription of MYCN. In a subsequent paper, we identified ERK5 as a potential ‘druggable’ target for ALK positive neuroblastoma patients (Paper II). Inhibition of ERK5 activity, reduced proliferation of ALK positive neuroblastoma cells as well as MYCN mRNA levels. Combination of ALK and ERK5 inhibitors abrogated tumor growth and cell proliferation synergistically. Overall, this study showed that ALK activates ERK5 via the PI3K pathway and regulates MYCN transcriptionally, suggesting that targeting both ALK and ERK5 might be beneficial for ALK positive neuroblastoma patients. In paper III, we addressed whether MEK inhibition alone or in combination with ALK inhibitor(s) has therapeutic value in a large panel of neuroblastoma cell lines. MEK inhibition alone in ALK positive neuroblastoma cells or xenografts did not abrogate cell or tumor growth. We showed that pharmacological inhibition of MEK-ERK pathway in ALK-positive neuroblastoma cells results in increased levels of activation/phosphorylation of AKT and ERK5. This feedback response is regulated by the mTOR complex 2 protein SIN1. Our results contraindicate the use of MEK inhibitors as effective therapeutic strategy in ALK-positive neuroblastoma. Together, this study highlights the importance of full length ALK receptor signaling in neuroblastoma. Further, it shows that combination of ALK inhibitor with PI3K/Akt/mTOR/ERK5 pathway inhibitors might be a potential therapeutic treatment strategy for ALK positive neuroblastoma patients
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
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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