1,720,970 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
Development of therapy for circumvention of EGFR-TKI resistance due to BIM polymorphism in EGFR mutant lung cancer
Get PDFBIM遺伝子多型に起因するEGFR-TKI耐性を克服する治療としてHDAC阻害薬の有効性について検証した。BIM多型を有するEGFR変異肺癌細胞株PC-3はゲフィチニブによるアポトーシス誘導に抵抗性を示した。PC-3にボリノスタットを添加すると活性型BIM蛋白の発現が上昇し、ゲフィチニブとの併用によってアポトーシスが誘導された。マウスモデルにおいて、ゲフィチニブ単剤ではPC-3皮下腫瘍は縮小しなかったが、ボリノスタット併用によってアポトーシスが誘導され著明な腫瘍縮小効果を示した。以上より、HDAC阻害薬併用治療がBIM遺伝子多型に起因するEGFR-TKI耐性克服に有効であることが示唆された。We investigated whether vorinostat, a histone deacetylase (HDAC) inhibitor, could circumvent EGFR-TKI resistance in the EGFR mutant lung cancer cell lines, which harbor the BIM polymorphism. We found that PC-3 cells with BIM polymorphism were much less sensitive to gefitinib-induced apoptosis than the EGFR mutant cell lines, which do not harbor this polymorphism. Vorinostat dose-dependently increased the expression of BIM with a pro-apoptotic BH3 domain and, together with gefitinib, induced apoptosis in cells with BIM polymorphism in vitro. In xenograft models, gefitinib did not induce regression of PC-3 subcutaneous tumors, whereas the combination of vorinostat and gefitinib induced marked regression of tumors, accompanied by tumor-cell apoptosis. These results indicate that the combination of HDAC inhibitor and EGFR-TKI may circumvent the resistance due to the BIM polymorphism in EGFR mutant lung cancer.研究課題/領域番号:25860640, 研究期間(年度):2013-04-01 - 2015-03-31出典：研究課題「EGFR変異肺癌のBIM遺伝子多型に起因するEGFR-TKI耐性克服治療の開発」課題番号25860640
（KAKEN：科学研究費助成事業データベース（国立情報学研究所））
（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-25860640/25860640seika/)を加工して作成research repor
Development of novel targeted therapy for lung cancer with activating Ras mutation
Get PDFEGFRチロシンキナーゼ阻害薬(EGFR-TKI)に自然耐性を示すK-ras活性化変異を有する肺がんに対しては、未だ有効な分子標的薬はない。我々はβ-phenylthyl isothiocynate (PEITC)による活性酸素産生を介したK-ras 変異肺がん細胞に対する抗腫瘍効果について検討を行った。PEITCを添加するとK-ras変異肺がん細胞の生存率は低下し、アポトーシスが誘導された。マウス皮下移植モデルにおいては、PEITC投与によって著明な腫瘍縮小効果を認め、毒性はほとんど認めなかった。また、ヒト正常肺線維芽細胞やK-ras野生型の肺がん細胞はPEITCに対する感受性が低かった。以上の結果から、PEITCはK-ras変異肺がん細胞に選択的な殺細胞効果を有することが示唆された。There are still no effective targeted therapies for patients with K-ras activating mutations which is a cause of intrinsic resistance to EGFR-TKI. Here, we assessed therapeutic effect of β-phenylthyl isothiocynate (PEITC) on lung cancer cellswith K-ras activating mutations through production of reactive oxygen species (ROS).Treatment with PEITC reduced cell viability and induced apoptosis in K-ras mutant lung cancer cells. In a xenograft model, PEITC dramatically reduced tumor growth with less toxicity. Moreover, normal human fibloblasts and K-ras wild lung cancer cells weresignificantly less sensitive to PEITC. Our findings suggest that PEITC can selectively kill lung cancer cells with K-ras activating mutations.研究課題/領域番号:23790903, 研究期間(年度):2011-2012出典：研究課題「Rasシグナル活性化変異を有する原発性肺癌を標的とした新規治療法の開発」課題番号23790903
（KAKEN：科学研究費助成事業データベース（国立情報学研究所））
（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-23790903/23790903seika/)を加工して作成research repor
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
アポトーシス抵抗性に起因する変異型選択的EGFR-TKI耐性克服治療の開発
Get PDFEGFR変異肺癌において、BIM遺伝子多型を有するとEGFR-TKIによるアポトーシスに抵抗性を示す。本研究では、変異型選択的EGFR-TKIであるOsimertinibの耐性にBIM遺伝子多型が影響するか検討し、HDAC阻害薬であるVorinostatの併用効果について解析を行った。BIM遺伝子多型を有するEGFR変異肺癌細胞はOsimertinibによるアポトーシス誘導に抵抗性を示し、Vorinostat併用によりアポトーシスが誘導されることが明らかになった。さらに、このVorinostatの効果にはHDAC3阻害活性が重要であり、HDAC3選択的阻害薬の開発が有望であることが示唆された。The BIM deletion polymorphism is associated with apoptosis resistance to EGFR-TKIs, such as gefitinib, in NSCLC harboring EGFR mutations. Here, we investigated whether the BIM deletion polymorphism contributes to resistance against osimertinib, a mutant selective EGFR-TKI.
EGFR-mutated NSCLC cell lines with the BIM deletion polymorphism exhibited apoptosis resistance to osimertinib and this resistance was overcome by combined use with vorinostat in vitro and in vivo. Experiments with homozygous BIM deletion-positive EGFR-mutated NSCLC cells revealed that vorinostat increased the expression of active BIM protein and induced apoptosis in osimertinib-treated cells. These effects were mediated predominantly by HDAC3 inhibition. These findings indicate the importance of developing HDAC3-selective inhibitors, and their combined use with osimertinib, for treating EGFR-mutated lung cancers carrying the BIM deletion polymorphism.研究課題/領域番号:17K09649, 研究期間(年度):2017-04-01 – 2021-03-31出典：「アポトーシス抵抗性に起因する変異型選択的EGFR-TKI耐性克服治療の開発」研究成果報告書 課題番号17K09649
（KAKEN：科学研究費助成事業データベース（国立情報学研究所））
（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K09649/17K09649seika/）を加工して作成research repor
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
- …
