アメリカ人は和製英語をどのぐらい理解できるか : 英語母語話者の和製英語の知識と意味推測に関する調査

長岡技術科学大学広島大学ジョージア州立大学Nagaoka University of TechnologyHiroshima UniversityGeorgia State University本研究の目的は,(1)英語を使って作られた和製英語の意味を英語母語話者が推測した場合,どのような語の推測が容易で,どのような語の推測が困難かを調査すること,及び,(2)日本語学習経験のある者が未知の和製英語の意味を推測した場合,日本語学習経験が生かされるかどうかを調査することの2点である。日本語学習者36名と非学習者36名に,30語の和製英語を刺激語として与え,各語の知識を問う二者択一問題と,各語の意味を選ぶ四者択一問題を行った。その結果,日本語学習者は和製英語の知識において非学習者と差がないにも関わらず,意味推測において優れていることが示された。また,(1)英語と形が良く似ている和製英語,(2)後項の語が複合語全体の意味的主要部となり,前項の語が後項の語を修飾している和製英語は意味推測が易しく,反対に,(1)英語の語順規則に則っていない和製英語,(2)英語の概念に共通する部分が少ない和製英語,(3)前項の語も後項の語も,それが構成する複合語の主要な意味とならない和製英語は,英語母語話者にとって意味推測が難しい傾向があることが示された。The present study investigated 1) what kinds of Japanized English loanwords American native English speaking participants can understand through inference, and 2) the extent to which previous experience with studying Japanese helps participants to successfully infer the meaning of previously unknown Japanized English loanwords. A total of 72 American native English speakers, consisting of 36 learners and 36 non-learners of Japanese participated in the study. Thirty Japanized English loanwords were used to determine the extent to which participants had been exposed to them (i.e., knowledge scores). Participants were furthermore asked to identify the correct meaning of each item from among four selections (i.e., inference scores). In terms of knowledge scores, no significant difference was shown between the learners and non-learners groups. Nevertheless, the learners group showed higher scores in inferring the meanings of unknown Japanized English loanwords than the non-learners group. In addition, item-by-item analyses in the present study showed the likelihood that the meanings of Japanized English loanwords of two-unit compounds were easier for native English speakers to infer due to 1) similarity to English forms, or 2) structures containing secondary words being semantic heads which were modified by initial words. On the contrary, compound loanwords whose meanings were difficult to infer 1) ignored English word order rules, 2) shared a lesser degree of English meanings, or 3) had neither an initial word nor secondary word as a semantic head

Heme oxygenase-1 contributes to pathology associated with thrombin-induced striatal and cortical injury in organotypic slice culture

The blood coagulation factor thrombin that leaks from ruptured vessels initiates brain tissue damage after intracerebral hemorrhage. We have recently shown that mitogen-activated protein kinases (MAPKs) activated by thrombin exacerbate hemorrhagic brain injury via supporting survival of neuropathic microglia. Here, we investigated whether induction of heme oxygenase (HO)-1 is involved in these events. Zinc protoporphyrin IX (ZnPP IX), a HO-1 inhibitor, attenuated thrombin-induced injury of cortical cells in a concentration-dependent manner (0.3-3 microM) and tended to inhibit shrinkage of the striatal tissue at 0.3 microM. HO-1 expression was induced by thrombin in microglia and astrocytes in both the cortex and the striatum. The increase of HO-1 protein was suppressed by a p38 MAPK inhibitor SB203580, and early activation of p38 MAPK after thrombin treatment was observed in neurons and microglia in the striatum. Notably, concomitant application of a low concentration (0.3 microM) of ZnPP IX with thrombin induced apoptotic cell death in striatal microglia and significantly decreased the number of activated microglia in the striatal region. On the other hand, a carbon monoxide releaser reversed the protective effect of ZnPP IX on thrombin-induced injury of cortical cells. Overall, these results suggest that p38 MAPK-dependent induction of HO-1 supports survival of striatal microglia during thrombin insults. Thrombin-induced cortical injury may be also regulated by the expression of HO-1 and the resultant production of heme degradation products such as carbon monoxide

Haloperidol, spiperone, pimozide and aripiprazole reduce intracellular dopamine content in PC12 cells and rat mesencephalic cultures: Implication of inhibition of vesicular transport.

Accumulating evidence suggests that antipsychotics affect dopamine release from dopaminergic neurons, but the precise mechanisms are not fully understood. Besides, there are few studies on the effects of antipsychotics on intracellular dopamine content. In this study, the effects of 8 antipsychotics on dopamine release and intracellular dopamine content in PC12 cells were investigated. Pretreatment with haloperidol, spiperone, pimozide, aripiprazole and risperidone markedly inhibited high potassium-evoked dopamine release. By contrast, pretreatment with chlorpromazine slightly increased high potassium-evoked dopamine release, while pretreatment with sulpiride and olanzapine had no effect. Haloperidol, spiperone, pimozide, chlorpromazine, aripiprazole and olanzapine evoked dopamine release, while sulpiride and risperidone had no effect. In addition, haloperidol, spiperone, pimozide, aripiprazole and risperidone reduced intracellular dopamine content in a concentration-dependent manner. These results suggest that the reduction in high potassium-evoked dopamine release by pretreatment with antipsychotics results from the reduction in vesicular dopamine content. Treatment with the 8 antipsychotics did not affect the expression of total or phosphorylated tyrosine hydroxylase. Instead, haloperidol, spiperone, pimozide and aripiprazole as well as reserpine transiently increased extracellular levels of dopamine metabolites. In addition, haloperidol, spiperone, pimozide, aripiprazole and risperidone reduced vesicular [3H]dopamine transport. These results suggest that the inhibition of vesicular dopamine transport by haloperidol, spiperone, pimozide and aripiprazole results in a reduction in vesicular dopamine content

Compensatory role of the Nrf2-ARE pathway against paraquat toxicity: Relevance of 26S proteasome activity

Oxidative stress and the ubiquitin-proteasome system play a key role in the pathogenesis of Parkinson disease. Although the herbicide paraquat is an environmental factor that is involved in the etiology of Parkinson disease, the role of 26S proteasome in paraquat toxicity remains to be determined. Using PC12 cells overexpressing a fluorescent protein fused to the proteasome degradation signal, we report here that paraquat yielded an inhibitory effect on 26S proteasome activity without an obvious decline in 20S proteasome activity. Relative low concentrations of proteasome inhibitors caused the accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2), which is targeted to the ubiquitin-proteasome system, and activated the antioxidant response element (ARE)-dependent transcription. Paraquat also upregulated the protein level of Nrf2 without increased expression of Nrf2 mRNA, and activated the Nrf2-ARE pathway. Consequently, paraquat induced expression of Nrf2-dependent ARE-driven genes, such as γ-glutamylcysteine synthetase, catalase, and hemeoxygenase-1. Knockdown of Nrf2 or inhibition of γ-glutamylcysteine synthetase and catalase exacerbated paraquat-induced toxicity, whereas suppression of hemeoxygenase-1 did not. These data indicate that the compensatory activation of the Nrf2-ARE pathway via inhibition of 26S proteasome serves as part of a cellular defense mechanism to protect against paraquat toxicity

Protective effect of aripiprazole against glutamate cytotoxicity in dopaminergic neurons of rat mesencephalic cultures.

Aripiprazole, a dopamine D(2) receptor partial agonist, is used to treat schizophrenia. Although aripiprazole has been reported to protect non-dopaminergic neurons, its effect on dopaminergic neurons has yet to be investigated. In the present study, we examined whether aripiprazole protected dopaminergic neurons against glutamate-induced cytotoxicity in rat mesencephalic cultures. Pretreatment with aripiprazole protected dopaminergic neurons in a concentration-dependent manner. The neuroprotective effect was not attenuated by sulpiride, a dopamine D(2) receptor antagonist, suggesting that the effect is independent of dopamine D(2) receptors. Aripiprazole reduced intracellular dopamine content in a concentration-dependent manner. In addition, its neuroprotective effect was partially inhibited when dopamine was added. These results suggest that aripiprazole protects dopaminergic neurons against glutamate cytotoxicity partly by reducing intracellular dopamine content

Isolation, identification, and biological evaluation of Nrf2-ARE activator from the leaves of green perilla (Perilla frutescens var. crispa f. viridis)

青ジソから老化やメタボリックシンドローム予防に有望な生体内抗酸化力を高める成分を発見. 京都大学プレスリリース. 2012-08-06.The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway is a cellular defense system against oxidative stress. Activation of this pathway increases expression of antioxidant enzymes. Epidemiological studies have demonstrated that the consumption of fruits and vegetables is associated with reduced risk of contracting a variety of human diseases. The aim of this study is to find Nrf2-ARE activators in dietary fruits and vegetables. We first attempted to compare the potency of ARE activation in six fruit and six vegetables extracts. Green perilla (Perilla frutescens var. crispa f. viridis) extract exhibited high ARE activity. We isolated the active fraction from green perilla extract through bioactivity-guided fractionation. Based on nuclear magnetic resonance and mass spectrometric analysis, the active ingredient responsible for the ARE activity was identified as 2', 3'-dihydroxy-4', 6'-dimethoxychalcone (DDC). DDC induced the expression of antioxidant enzymes, such as γ-glutamylcysteine synthetase (γ-GCS), NAD(P)H: quinone oxidoreductase-1 (NQO1), and heme oxygenase-1. DDC inhibited the formation of intracellular reactive oxygen species and the cytotoxicity induced by 6-hydroxydopamine. Inhibition of the p38 mitogen-activated protein kinase pathway abolished ARE activation, the induction of γ-GCS and NQO1, and the cytoprotective effect brought about by DDC. Thus, this study demonstrated that DDC contained in green perilla enhanced cellular resistance to oxidative damage through activation of the Nrf2-ARE pathway

Reconstruction and quantitative evaluation of dopaminergic innervation of striatal neurons in dissociated primary cultures

Repairing the nigrostriatal pathway is expected to become a future treatment strategy for Parkinson disease. Our aim is to establish an in vitro model for the quantitative analysis of the nigrostriatal projections of dopaminergic neurons using primary dissociated neruons. To form the mesencephalic cell region, mesencephalic cells derived from rat embryos were plated within an isolation wall, which was removed after cell adhesion to the coverslip. After incubation for 11 days, the dopaminergic neurites extending to the outside of the mesencephalic cell region were mainly axons. Treatment with glial cell line-derived neurotrophic factor for 11 days significantly promoted the outgrowth of dopaminergic axons from the mesencephalic cell region in a concentration-dependent manner. When striatal cells were plated outside the mesencephalic cell region, dopaminergic neurites were remarkably extended to the striatal cell region. Moreover, immunocytochemistry for tyrosine hydroxylase and synaptophysin revealed that dopaminergic axons formed synapses with striatal neurons. By contrast, spinal cells did not increase dopaminergic neurite outgrowth. These results indicate that the present method is valuable for evaluating nigrostriatal projections in vitro