21 research outputs found

    Perspectives and future approaches on research of false memory

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    The research field of false memory has been developed based on laboratory experiments, in which tasks including the DRM paradigm and misinformation task are mainly used. However, it has been pointed out that no relationship was found among false memories measured by these tasks, the experimental methods have not been well standardized, and thus there may be difference between each false memory measured by each task. In this paper, we review current research on false memory in following perspectives. First, we summarize methods of experiments on false memory. Secondly, we introduce the DRM paradigm and theories on mechanism false memory would occur. Thirdly, we review relationship between the DRM paradigm and other experimental tasks by which false memories may be measured. Fourthly, we discuss problems of the DRM paradigm and other tasks from the point of view that there may be individual differences among false memories.虚偽記憶の研究分野は,実験室実験に基づいて発展しており,実験課題としてDRMパラダイムや誤情報課題が主に用いられている。しかし,これらの課題間で測定される虚偽記憶には関連が認められないこと,測定方法が統一されていないこと,および測定対象となる虚偽記憶の性質が異なることが指摘されている。そこで本稿は,虚偽記憶研究の現状について,以下の4つの観点から概説することを目的とする。第一に,虚偽記憶の測定方法について概観する。第二に,DRMパラダイムの実験方法とその理論について紹介する。第三に,DRMパラダイムとその他の虚偽記憶課題との関連について概説する。第四に,個人差との関連から虚偽記憶課題の問題点について論じる

    Moral dilemma: Full code or futile code?

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    Protective Effects of Hydrolyzed Nucleoproteins from Salmon Milt against Ethanol-Induced Liver Injury in Rats

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    Dietary nucleotides play a role in maintaining the immune responses of both animals and humans. Oral administration of nucleic acids from salmon milt have physiological functions in the cellular metabolism, proliferation, differentiation, and apoptosis of human small intestinal epithelial cells. In this study, we examined the effects of DNA-rich nucleic acids prepared from salmon milt (DNSM) on the development of liver fibrosis in an in vivo ethanol-carbon tetrachloride cirrhosis model. Plasma aspartate transaminase and alanine transaminase were significantly less active in the DNSM-treated group than in the ethanol plus carbon tetrachloride (CCl4)-treated group. Collagen accumulation in the liver and hepatic necrosis were observed histologically in ethanol plus CCl4-treated rats; however, DNSM-treatment fully protected rats against ethanol plus CCl4-induced liver fibrosis and necrosis. Furthermore, we examined whether DNSM had a preventive effect against alcohol-induced liver injury by regulating the cytochrome p450 2E1 (CYP2E1)-mediated oxidative stress pathway in an in vivo model. In this model, CYP2E1 activity in ethanol plus CCl4-treated rats increased significantly, but DNSM-treatment suppressed the enzyme’s activity and reduced intracellular thiobarbituric acid reactive substances (TBARS) levels. Furthermore, the hepatocytes treated with 100 mM ethanol induced an increase in cell death and were not restored to the control levels when treated with DNSM, suggesting that digestive products of DNSM are effective for the prevention of alcohol-induced liver injury. Deoxyadenosine suppressed the ethanol-induced increase in cell death and increased the activity of alcohol dehydrogenase. These results suggest that DNSM treatment represents a novel tool for the prevention of alcohol-induced liver injury
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