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Japanese Eliot in Pre-war Years: Perspectives and Issues
Akira Nakai 한국T.S.엘리엇학회 2011 T.S. 엘리엇 연구 Vol.21 No.2
T. S. Eliot began to make his appearance on the Japanese scene in the latter half of the 1920s. Along with the establishment of the English Literary Society of Japan in 1929, the study of Eliot began to flourish in the 1930s. This brief account examines his reception in the context of social and political situation of the day. Different perspectives and issues Eliot raised will be demonstrated by memoirs and writings of those who visited to teach, as well as those who read Eliot at home. To succeed Peter Quennell, William Empson came to Tokyo in 1931. When he had hardly settled, the “Manchurian Incident” broke out in September. Japan established the puppet state of Manchukuo in March in 1932, and chose her isolation in the international community in March in 1934, declaring to walk out of the League of Nations. Ironically the period saw the first flowering of Eliot study. Foreign books were coming in abundance uninterrupted. But after the outbeak of Shino-Japanese war in 1937, under the strict controls on foreign currency, the importation of periodicals and books began to dwindle, and virtually stopped by the end of 1939. In the meantime, however, Eliot began to attract general readership. When John Morris came in 1938, the war in China was to be expanded into the Pacific War in 1941. He took the last repatriation ship specially arranged for Europe. In his Traveller from Tokyo (1943), reporting that there was “a great interest in all forms of modern poetry, particularly for that of T. S. Eliot”, Morris predicted: “a Japanese T. S. Eliot will undoubtedly arise before many more years have passed”. The War ended in 1945. Eventually, the legacy from the pre-war years prepared the surge for Eliot studies, which, after premonitory rumbles in the early part of the 1950s, culminated in the next decade.
Performance-Based Seismic Design for High-Rise Buildings in Japan
Nakai, Masayoshi,Koshika, Norihide,Kawano, Kenichi,Hirakawa, Kiyoaki,Wada, Akira Council on Tall Building and Urban Habitat Korea 2012 International journal of high-rise buildings Vol.1 No.3
This paper introduces the outlines of review and approval processes, general criteria and usual practices taken in Japan for the seismic design of high-rise buildings. The structural calculations are based on time-history analyses followed by performance evaluations. This paper also introduces structural design of two high-rise buildings: one is a 100 m high reinforced concrete residential building, and the other is a 300 m high steel building for mixed use.
Tetsuo Sonomura,Nobuyuki Kawai,Kazushi Kishi,Akira Ikoma,Hiroki Sanda,Kouhei Nakata,Hiroki Minamiguchi,Motoki Nakai,Seiki Hosokawa,Hideyuki Tamai,Morio Sato 대한영상의학회 2014 Korean Journal of Radiology Vol.15 No.2
We present a case of a patient with rapid deterioration of esophageal varices caused by portal hypertension accompanied by a large arterioportal shunt that developed after radiofrequency ablation of hepatocellular carcinoma. We used n-butyl cyanoacrylate (NBCA) as an embolic material to achieve pinpoint embolization of the shunt, because the microcatheter tip was 2 cm away from the shunt site. Under hepatic arterial flow control using a balloon catheter, the arterioportal shunt was successfully embolized with NBCA, which caused an improvement in the esophageal varices.
A novel HSF1-mediated death pathway that is suppressed by heat shock proteins
Hayashida, Naoki,Inouye, Sachiye,Fujimoto, Mitsuaki,Tanaka, Yasunori,Izu, Hanae,Takaki, Eiichi,Ichikawa, Hitoshi,Rho, Jaerang,Nakai, Akira Wiley (John WileySons) 2006 The EMBO journal Vol.25 No.20
<P>Heat shock response is an adoptive response to proteotoxic stress, and a major heat shock transcription factor 1 (HSF1) has been believed to protect cells from cell death by inducing heat shock proteins (Hsps) that assist protein folding and prevent protein denaturation. However, it is revealed recently that HSF1 also promotes cell death of male germ cells. Here, we found a proapoptotic Tdag51 (T-cell death associated gene 51) gene as a direct target gene of HSF1. Heat shock and other stresses induced different levels of Hsps and Tdag51, which depend on cell types. Hsps bound directly to the N-terminal pleckstrin-homology like (PHL) domain of Tdag51, and suppressed death activity of the C-terminal proline/glutamine/histidine-rich domain. Tdag51, but not major Hsps, were induced in male germ cells exposed to high temperatures. Analysis of Tdag51-null testes showed that Tdag51 played substantial roles in promoting heat shock-induced cell death in vivo. These data suggest that cell fate on proteotoxic condition is determined at least by balance between Hsp and Tdag51 levels, which are differently regulated by HSF1.</P>