エイゾウ サクヒン オ リヨウ シタ ニホンゴ キョウイク ノ タイケイカ ニ ムケテ : カイガイ ニオケル リヨウ ジッタイ ト キョウシ ノ イシキ カラ

本稿は、映画、TV ドラマ、アニメといった映像作品を日本語教育に有効利用できることを目標に、これまでの先行研究で明らかになった使用上の問題点などを整理した上で、ベトナム・香港・ヨーロッパで実施した調査を客観主義と構成主義の観点から分析して、示唆を得るものである。分析の結果、映像作品の授業利用は客観主義的アプローチのものが大半で、教師は映像作品が学習の動機づけとしてだけでなく、言語形式や文化を学習するリソースとしての有効性を認識しながら利用していることが分かった。また、特に香港では、構成主義的アプローチに基づく実践も芽生えており、実践数は限られているものの、対話を促す学習リソースとして有効利用できる可能性がうかがえた。利用上の問題点としては、特に、映像利用を行う際の授業目標が明確ではないという問題が浮かび上がった。この結果から、映像作品を利用した授業目標の体系化と具体的な授業デザインを提案する必要性が示唆された。この結果を基に、今後は、ヨーロッパ共通言語参照枠（CEFR）のような、映像作品の有効利用のための参照枠組みの構築を目指したい

タイジン キョウシ ト ニホンジン キョウシ ノ ヨリヨイ キョウドウ ヲ ジツゲン スル タメ ニ ヒツヨウナ ヨウソ コウコウ ニ オケル ジレイ ヨリ

In Thailand, the number of learners who study Japanese as a foreign language at schools has been increasing, and many of them are high school students. Most of the Japanese language teachers there are Thai teachers who are non-native Japanese speaker teachers (NNJSTs). Recently native Japanese speaker teachers (NJSTs) very often participate to teach Japanese with Thai teachers at high schools. However, the reports and studies on how Thai and Japanese teachers work collaboratively to teach Japanese at high schools are limited in publication. This paper examines essential elements for better collaborations between Thai and Japanese teachers in Japanese language teaching at high schools in Thailand. This study presents an analysis of the interview data obtained from these teachers in Thailand, utilizing the SCAT (Steps for Coding and Theorization) method. It is important for both Thai and Japanese teachers to maintain communication to share information and understand with each other, and have positive attitudes for collaborative teaching between NNJSTs and NJSTs. They need to have more experience in collaborative teaching of Japanese and to be flexible in their collaboration styles.研究論文Article

Minna no Nihongo Shokyu Yasashii Sakubun = Mengarang Bahasa Jepang Mudah

xiv+123 hlm.;26 c

Differential effects of diet- and genetically-induced brain insulin resistance on amyloid pathology in a mouse model of Alzheimer’s disease

Abstract Background Based on epidemiological and experimental studies, type 2 diabetes mellitus (T2DM), especially insulin resistance that comprises the core mechanism of T2DM, has been recognized as a significant risk factor for Alzheimer’s disease (AD). Studies in humans and diabetic AD model mice have indicated a correlation between insulin resistance and increased amyloid deposition in the brain. Paradoxically, mice with targeted disruption of genes involved in the insulin signaling pathway showed protective effects against the AD-related pathology. These conflicting observations raise an issue as to the relationship between dysregulation of insulin signaling and AD pathophysiology. Methods To study the causal relations and molecular mechanisms underlying insulin resistance-induced exacerbation of amyloid pathology, we investigated the chronological changes in the development of insulin resistance and amyloid pathology in two independent insulin-resistant AD mouse models, i.e., long-term high-fat diet (HFD) feeding and genetic disruption of Irs2, in combination with dietary interventions. In addition to biochemical and histopathological analyses, we examined the in vivo dynamics of brain amyloid-β (Aβ) and insulin by microdialysis technique. Results HFD-fed diabetic AD model mice displayed a reduced brain response to peripheral insulin stimulation and a decreased brain to plasma ratio of insulin during the hyperinsulinemic clamp. Diet-induced defective insulin action in the brain was accompanied by a decreased clearance of the extracellular Aβ in vivo and an exacerbation of brain amyloid pathology. These noxious effects of the HFD both on insulin sensitivity and on Aβ deposition in brains were reversibly attenuated by dietary interventions. Importantly, HFD feeding accelerated Aβ deposition also in the brains of IRS-2-deficient AD mice. Conclusions Our results suggested a causal and reversible association of brain Aβ metabolism and amyloid pathology by diet-dependent, but not genetically-induced, insulin-resistance. These observations raise the possibility that the causal factors of insulin resistance, e.g., metabolic stress or inflammation induced by HFD feeding, but not impaired insulin signaling per se, might be directly involved in the acceleration of amyloid pathology in the brain