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The purpose of this study was to understand how social anxiety arises in a foreign language learning environment and how it is affected, and to gain a better understanding of the actual situation of learners with social anxiety. A semi-structured interview was conducted with a female socially anxious learner for 7 hours on 7 occasions, and the interview data were analyzed using a grounded theory approach. The analysis was divided into four steps, generating five hypothetical findings and their models. The results showed that social anxiety does not develop abruptly in a foreign language learning environment, but rather appears gradually through conditioning and that foreign language anxiety may increase at the same time. In addition, these anxieties cause not only a loss of self-confidence but also self- and existence-denial that persists even after leaving the conditioning. However, learners with social anxiety tendencies can be helped to move in a more positive direction with support from others. Since this can be associated with other psychiatric disorders, it remains an issue to consider and generalize the results in such fields., 本研究は，外国語学習環境において社交不安がどのように生まれ，どのような影響があるのかを知り，社交不安を抱える学習者の実態を少しでも把握することを目的としておこなわれた．社交不安傾向を抱える女性1名に，合計7回，7時間の半構造化面接をおこない，その中から得られたインタビューデータを，グラウンデッド・セオリー・アプローチを用いて分析をおこなった．分析のステップは4つに分かれ，4つの仮説的知見とそのモデルを生成した．その結果，外国語学習環境下で，社交不安は急に発現するのではなく条件付けにより徐々に現れ，同時に外国語不安も増大する可能性があることが分かった．また，それらの不安によって，自信をなくすだけでなく，条件付けから離れても続く自己否定・存在否定までも引き起こされる．だが，社交不安傾向を抱える学習者は他者からのサポート次第で，よりよい方向に進めることが明らかになった．これは他の精神疾患とも関連付けられるため，そのような分野との関連を考慮し，一般化していくことが課題として残された．

Alcohol-induced liver injury is linked to oxidative stress and increased production of reactive oxygen species (ROS). Oxidative stress is an early event in the process of apoptosis. However, it is not completely understood how ethanol-induced oxidative stress induces apoptosis. In contrast, nicotinamide adenine dinucleotide phosphate oxidase (NOX) is known to generate ROS in hepatocytes. The purpose of the present study was to determine whether or not ethanol-induced ROS generation stimulates the death receptor or mitochondrial pathways of apoptosis in alcohol dehydrogenase containing human liver adenocarcinoma (SK-HEP-1) cells. Treatment with ethanol increased the generation of ROS and expression of NOX4 mRNA, and also induced mitochondrial dysfunction in SK-HEP-1 cells. Moreover, ethanol induced the activation of caspase-8 and -3 in hepatocytes. These activities were suppressed by pretreatment with N-acetyl-cysteine, an antioxidant, or apocynin, an inhibitor of NOX activity. These results suggested that ethanol induces an increase in NOX-derived ROS generation upstream of caspase-8 activation and in the mitochondria in SK-HEP-1 cells. In conclusion, this study demonstrated that ethanol increases the generation of ROS and subsequently induces apoptosis using a mechanism involving mitochondrial dysfunction and caspase activation in SK-HEP-1 cells.

Nonalcoholic steatohepatitis (NASH) is regarded as a hepatic manifestation of the metabolic syndrome which can progress to hepatic cirrhosis and hepatocellular carcinoma. It is thought that matrix metalloproteinases (MMPs) play an important role in hepatic fibrosis and we previously reported a correlation between oxidative stress and MMP-9 expression. However, the expression of MMPs and tissue inhibitors of metalloproteinases (TIMPs) in the progression of NASH is unclear. In this study we used spontaneously hypertensive and hyperlipidemic rats (SHHR) fed a high-fat diet and 30% sucrose solution (HFDS) as a model for NASH, in order to clarify the relationships between oxidative stress, liver weight (LW), MMPs and TIMPs at various time-points in the progression of NASH. Male SHHR and Sprague-Dawley (SD) rats were divided into four groups: SHHR-normal diet (ND), SHHR-HFDS, SD-ND and SD-HFDS. Hepatic fibrosis was clearly increased at 13 months in SHHR-HFDS, resembpling NASH. LW and oxidative stress markers in plasma were increased in SHHR-HFDS compared to the other groups. Oxidative stress was correlated with LW in all rats. Expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 mRNA, measured by real-time polymerase chain reaction, was increased in the liver of SHHR-HFDS at 13 months. This study suggests that oxidative stress, MMPs and TIMPs may play an important role in the progression of NASH.