37 research outputs found

    Où est notre avenir ?

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    Lâcheté des élites et sacrifice du peuple, c’est le secret de la double face du Japon, douteux et admirable. La dernière catastrophe, révélant la fragilité du système économique et techno-industriel japonais, rend inévitable un changement radical de la société. Mais la résistance est tenace.The author begins with an explanation of the two faces of Japan that were revealed to the surprise of many around world based on the attitude exhibited by the Japanese government on the occasion of its first nuclear experience; namely, the “spontaneous obedience” shown by the country’s ruling elites to American policy.This kind of melancholy that has always arisen from such a structure of submissiveness was felt once again in the response to the recent earthquake disaster and nuclear accident.This huge catastrophe has served to clearly demonstrate the fragility inherent in a Japanese techno-industrial economy that has developed through its heavy dependency on nuclear energy and its gross negligence of natural conditions. The time has come for a transformation in not only the whole Japanese social structure, but also our core values. Despite the trend among the people in the direction of a spontaneous renaissance, the powers that be continue to stubbornly resist.まず、世界を驚かせた日本の二面性を、最初の核の経験に際して日本政府のとった態度から説明(支配層のアメリカへの「自発的隷従」)する。この構造の不幸が大震災・原発事故に関しても反復された。今回の大災厄は、自然条件を無視して原発に依存し発展して­た日本の技術・産業・経済システムの脆弱さを明らかにし、社会構造全般と価値観の転換を迫っているが、民衆の示した自発的な再生の方向にも関わらず、従来勢力からの抵抗は大­い

    シコ オ フム タメ ノ サンサツ

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    Apop-1, a Novel Protein Inducing Cyclophilin D-dependent but Bax/Bak-related Channel-independent Apoptosis

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    In the intrinsic pathway of apoptosis, mitochondria play a crucial role by releasing cytochrome c from the intermembrane space into the cytoplasm. Cytochrome c release through Bax/Bak-dependent channels in mitochondria has been well documented. In contrast, cyclophilin D (CypD), an important component of permeability transition pore-dependent protein release, remains largely undefined, and no apoptogenic proteins that act specifically in a CypD-dependent manner have been reported to date. Here, we describe a novel and evolutionarily conserved protein, apoptogenic protein (Apop). Mouse Apop-1 expression induces apoptotic death by releasing cytochrome c from mitochondria into the cytosolic space followed by activation of caspase-9 and -3. Apop-1-induced apoptosis is not blocked by Bcl-2 or Bcl-xL, inhibitors of Bax/Bak-dependent channels, whereas it is completely blocked by cyclosporin A, an inhibitor of permeability transition pore. Cells lacking CypD were resistant to Apop-induced apoptosis. Moreover, inhibition of Apop expression prevented the cell death induced by apoptosis-inducing substances. Our findings, thus, indicate that the expression of Apop-1 induces apoptosis though CypD-dependent pathway and that Apop-1 plays roles in cell death under physiological conditions

    Trapping of CDC42 C-terminal variants in the Golgi drives pyrin inflammasome hyperactivation

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    CDC42-C末端異常症に於ける炎症病態を解明 --ゴルジ体への異常蓄積がパイリンインフラマソーム形成を過剰促進--. 京都大学プレスリリース. 2022-05-02.Mutations in the C-terminal region of the CDC42 gene cause severe neonatal-onset autoinflammation. Effectiveness of IL-1β–blocking therapy indicates that the pathology involves abnormal inflammasome activation; however, the mechanism underlying autoinflammation remains to be elucidated. Using induced-pluripotent stem cells established from patients carrying CDC42[R186C], we found that patient-derived cells secreted larger amounts of IL-1β in response to pyrin-activating stimuli. Aberrant palmitoylation and localization of CDC42[R186C] protein to the Golgi apparatus promoted pyrin inflammasome assembly downstream of pyrin dephosphorylation. Aberrant subcellular localization was the common pathological feature shared by CDC42 C-terminal variants with inflammatory phenotypes, including CDC42[*192C*24] that also localizes to the Golgi apparatus. Furthermore, the level of pyrin inflammasome overactivation paralleled that of mutant protein accumulation in the Golgi apparatus, but not that of the mutant GTPase activity. These results reveal an unexpected association between CDC42 subcellular localization and pyrin inflammasome activation that could pave the way for elucidating the mechanism of pyrin inflammasome formation

    Georges Bataille et le mythe du bois.  Une réflexion sur l'impossibilité de la mort

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    A partir d'un pseudonyme de G. Bataille, Dianus, et de son référent mythique, le Roi du Bois, dont il éclaire l'origine et les implications dans la réflexion philosophique de Bataille, O. Nishitani fait apparaître un complexe sacrifié-sacrificateur étroitement lié à l'expérience intérieure de Bataille. « L'entre-deux-morts » du Roi du Bois renvoie au secret de la mort humaine

    Georges Bataille et le mythe du bois.  Une réflexion sur l'impossibilité de la mort

    No full text
    A partir d'un pseudonyme de G. Bataille, Dianus, et de son référent mythique, le Roi du Bois, dont il éclaire l'origine et les implications dans la réflexion philosophique de Bataille, O. Nishitani fait apparaître un complexe sacrifié-sacrificateur étroitement lié à l'expérience intérieure de Bataille. « L'entre-deux-morts » du Roi du Bois renvoie au secret de la mort humaine
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