53 research outputs found

    イブンカ コミュニケーション ニオケル ダイガクセイ ノ ジコ カイジ ニカンスル ヒカク ケンキュウ : ニッチュウカン ダイガクセイ ノ ヒカク オ チュウシン ニ

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    日中韓3ヵ国の大学生の自文化における自己開示の傾向には開示行動、開示意向、開示方法について多くの共通点がみられるが、開示動機については相違点がみられる。その傾向の日中韓比較においては各々の特徴も見出される。これらの相違や特徴を背景とした異文化コミュニケーションにおける自己開示に際して、戸惑い、誤解、文化差などが経験される。各々の自己開示は、言語的制約を内包しつつ、文化的社会的制約を常に負う。また、文化的な相互依存と文化的な相互対峙が地球規模で急速に進んでいるグローバリゼーションの状況に人間は直面している。それゆえに、文化的社会的制約を負いつつも他者を他者性として自覚し、対話的な自己開示を遂行していく人間としての在り方が絶えず問題になる。自己開示を通して人間の人間性を問題にし続けること、多文化社会に生きる人間としての在り方を絶えず志向することが大学教育において要請される

    Mémento 2 : Résidences 1999-2000

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    This richly illustrated catalogue documents the work of 35 artists who took part in six residencies (including two events - La Cueillette and La Ruche) that took place in 1999 and 2000 at Centre Est-Nord-Est. The centre’s director, F. Michel, describes the nature and purpose of the residencies as well as that of the catalogue : to reflect each participant’s experience. Includes brief comments by the artist on their work and on their stay. Text in French and English. Biographical notes

    Necdin, a p53-Target Gene, Is an Inhibitor of p53-Mediated Growth Arrest

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    In vitro, cellular immortalization and transformation define a model for multistep carcinogenesis and current ongoing challenges include the identification of specific molecular events associated with steps along this oncogenic pathway. Here, using NIH3T3 cells, we identified transcriptionally related events associated with the expression of Polyomavirus Large-T antigen (PyLT), a potent viral oncogene. We propose that a subset of these alterations in gene expression may be related to the early events that contribute to carcinogenesis. The proposed tumor suppressor Necdin, known to be regulated by p53, was within a group of genes that was consistently upregulated in the presence of PyLT. While Necdin is induced following p53 activation with different genotoxic stresses, Necdin induction by PyLT did not involve p53 activation or the Rb-binding site of PyLT. Necdin depletion by shRNA conferred a proliferative advantage to NIH3T3 and PyLT-expressing NIH3T3 (NIHLT) cells. In contrast, our results demonstrate that although overexpression of Necdin induced a growth arrest in NIH3T3 and NIHLT cells, a growing population rapidly emerged from these arrested cells. This population no longer showed significant proliferation defects despite high Necdin expression. Moreover, we established that Necdin is a negative regulator of p53-mediated growth arrest induced by nutlin-3, suggesting that Necdin upregulation could contribute to the bypass of a p53-response in p53 wild type tumors. To support this, we characterized Necdin expression in low malignant potential ovarian cancer (LMP) where p53 mutations rarely occur. Elevated levels of Necdin expression were observed in LMP when compared to aggressive serous ovarian cancers. We propose that in some contexts, the constitutive expression of Necdin could contribute to cancer promotion by delaying appropriate p53 responses and potentially promote genomic instability
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