1,721,239 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
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
The regulation of oxidative stress in the development of drug resistance in the treatment of breast cancer
No full textBreast cancer is the most common type of female cancer. Reactive oxygen species (ROS) plays an important role in regulating signaling pathways that control cell survival and cell proliferation. Oxidative stress refers to the imbalance between ROS generation and ROS elimination. A number of chemotherapeutic drugs, such as taxanes, platinum compounds and anthracyclines trigger cell death via induction of oxidative stress. Development of drug resistance in cancer is associated with the adaptive response to oxidative stress. NRF2 is the main regulator of cytoprotective response to oxidative stress. Increased activity of NRF2 enhances cell growth and increases chemoresistance, providing growth advantage for malignant cells.
My study aims to identify molecular mechanisms that are involved in the development of drug resistance via modulation of oxidative stress in breast cancer. The novel molecular mechanisms through which NRF2 activity would be enhanced to confer drug resistance in breast cancer cells are explained.
FOXM1 is a well-known oncogene which contributes to all hallmarks of cancer. In Chapter 3, we hypothesized that FOXM1 and NRF2 are involved together in contributing to chemoresistance via modulation of oxidative stress. We showed that chemoresistant breast cancer cells express higher levels of FOXM1 and NRF2. These resistant cells have higher resistance to oxidative stress-mediated cell death and to ROS induction by tBHP. In drug sensitive MCF-7, we found that FOXM1 regulates NRF2 and NRF2 target genes expression. Transcriptional activation on antioxidant response element (ARE) was mediated by FOXM1 in response to epirubicin. ChIP-qPCR result further supported that FOXM1 transcriptionally controlledNRF2 expression. However, the identified FOXM1/NRF2 axis was deregulated in chemoresistant cells. Nevertheless, the use of NRF2 inhibitor could enhance the efficacy of epirubicin treatment to treat breast cancer. Our findings showed that FOXM1 regulates the transcription of NRF2 which mediates response to epirubicin and eventual epirubicin resistance in breast cancer cells.
Our group have identified BQ323636.1 (BQ), as a novel splice variant of NCOR2 which could predict tamoxifen resistance in the treatment of breast cancer. In Chapter 4, we hypothesized that BQ could modulate oxidative stress in breast cancer. Overexpressing BQ in breast cancer cell lines could promote cell proliferation and protect cells from oxidative stress. In addition, we showed overexpression of BQ could reduce the levels of ROS. By RT-qPCR assay, several downstream NRF2 targets were found to be up-regulated in BQ overexpressing cells, suggesting that NRF2 transcriptional activity could be modulated by BQ. Luciferase reporter assay showed that NCOR2 could repress the transcriptional activity via antioxidant response element (ARE), which is the primary binding site of NRF2 in the promoter region. Furthermore, BQ could reverse the repressive effect of NCOR2 on ARE. These results suggest that BQ might modulate NRF2 activity via NCOR2. Immunoprecipitation assay indicated NCOR2 interacted with NRF2 and BQ overexpression could inhibit this interaction. Taken together, our findings suggested BQ regulates NRF2 signaling pathway via interfering with NCOR2 activity. Our findings reveal a novel role for BQ as a modulator of NRF2 and oxidative stress in breast cancer.published_or_final_versionPathologyDoctoralDoctor of Philosoph
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
Regulation of estrogen receptor alpha expression by translation or degradation and the relevance to tamoxifen resistance in breastcancer
No full textBreast cancer is one of the most prevalent cancers affecting women worldwide. In the breast, estrogen receptor alpha (ERα), upon binding with ligands, activates gene transcription and promotes cell growth and proliferation. Tamoxifen, a selective antagonist of ERα in breast, has been proved to be effective therapeutically. In spite of this, resistance remains a prominent issue and underlying mechanisms are not yet fully understood. Aberrant regulation of ER expression at genetic and transcriptional levels has been implicated as the mechanisms accounting for tamoxifen resistance. However, regulation of ERα expression at translational level including protein synthesis and degradation has not yet been characterized and its relevance to tamoxifen resistance has not been described.
At level of protein synthesis, eukaryotic translation initiation factor 4E (eIF4E) selectively enhances the translation of 4E-sensitive mRNAs which contain long and complex 5’-untraslated regions (5’-UTR). eIF4E is often over-expressed in cancers. In silico analysis revealed that ERα contained a highly structured 5’-UTR similar to reported eIF4E-sensitive mRNAs, suggesting that ERα mRNA might be eIF4Esensitive. We showed by polysome fractionation and subsequent Q-PCR quantification that the ERα mRNAs were more actively translated in the cell line expressing higher levels of eIF4E. Consistently, transient transfection of eIF4E into an ERα-positive cell line resulted in enhanced protein expression of ERα. Moreover, subcelluar fractionation showed that eIF4E was bound with ERα mRNAs in the nucleus thus participating in transportation of mRNAs from the nucleus into the cytoplasm. Therefore, eIF4E could positively modulate protein synthesis of ERα by enhancing mRNA export in the nucleus as well as translation in the cytoplasm. Their positive correlation was validated in vivo using 106 Chinese breast cancer samples (Chi-square test, p=0.004). It was also found that elevated expression of eIF4E could mediate resistance to tamoxifen treatment and enhance cell survival. This could be due to enhanced expression of ERα or activation of PI3K/Akt pathway upon eIF4E over-expression.
At the level of degradation, ERα is conjugated to poly-ubiquitin chains catalyzed by multiple enzymes and degraded by 26S polysomes. Carboxyl-terminus of Hsc70- interacting protein (CHIP) is an E3 enzyme specific for ERα degradation through interaction with ERα’s ligand-binding domain (LBD). Various splicing variants of ERα have been reported and implicated in tamoxifen resistance by interfering with functions of ERα wild type. Variants ERαΔ4, ERαΔ5, ERαΔ6/7 and ERαΔ7 with different degrees of truncation in their LBDs and differential expression were detected or reported in human breast cancers. Their interactions with CHIP may be different, resulting in variations in degradation. We found that the degradation of ERαΔ6/7 through ubiquitin-proteasome pathway was impaired whilst the degradation of other variants were less affected. This finding suggests that the binding site of CHIP to ERαmight be located within the peptide sequences encoded by exon6. Furthermore, as ERαΔ6/7 plays a dominant negative role in regulating functions of ERα wild type, aborted degradation of this variant may result in accumulation of this variant in the cell, inhibiting and inactivating ERα, making the cells refractile to tamoxifen treatment.published_or_final_versionPathologyMasterMaster of Philosoph
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