Death of the image/the image of death: Temporality, torture and transience in Sunohara Yuuri and Akita Masami’s Harakiri Cycle

Sunohara Yuuri and Akita Masami's series of six seppuku films (1990) are solely constituted by images of fictionalized death, revolving around the prolonged selftorture of a lone figure committing harakiri. I contend that the protagonist's autoimmolation mirrors a formal death, each frame `killing' the moment it represents. My analysis aims to explore how the solipsistic nature of selfhood is appositely symbolized by the isolation of the on-screen figures and the insistence with which the six films repeat the same scenario of protracted agony across the cycle. The centralization of suffering, I argue, parallels the distance between viewer and image with the isolating nature of embodied existence. Thus, this article seeks to probe the relationship between form and content, asking what the image of death reveals about the death of the image

Characterization of a Novel Interaction between Bcl-2 Members Diva and Harakiri

Interactions within proteins of the Bcl-2 family are key in the regulation of apoptosis. The death-inducing members control apoptotic mechanisms partly by antagonizing the prosurvival proteins through heterodimer formation. Structural and biophysical studies on these complexes are providing important clues to understand their function. To help improve our knowledge on protein-protein interactions within the Bcl-2 family we have studied the binding between two of its members: mouse Diva and human Harakiri. Diva has been shown to perform both prosurvival and killing activity. In contrast, Harakiri induces cell death by interacting with antiapoptotic Bcl-2 members. Here we show using ELISA and NMR that Diva and Harakiri can interact in vitro. Combining the NMR data with the previously reported three-dimensional structure of Diva we find that Harakiri binds to a specific region in Diva. This interacting surface is equivalent to the known binding area of prosurvival Bcl-2 members from the reported structures of the complexes, suggesting that Diva could function at the structural level similarly to the antiapoptotic proteins of the Bcl-2 family. We illustrate this result by building a structural model of the heterodimer using molecular docking and the NMR data as restraints. Moreover, combining circular dichroism and NMR we also show that Harakiri is largely unstructured with residual (13%) α-helical conformation. This result agrees with intrinsic disorder previously observed in other Bcl-2 members. In addition, Harakiri constructs of different length were studied to identify the region critical for the interaction. Differential affinity for Diva of these constructs suggests that the amino acid sequence flanking the interacting region could play an important role in binding

In utero exposure to cigarette smoke dysregulates human fetal ovarian developmental signalling

STUDY QUESTION How does maternal cigarette smoking disturb development of the human fetal ovary?<p></p> SUMMARY ANSWER Maternal smoking increases fetal estrogen titres and dysregulates several developmental processes in the fetal ovary.<p></p> WHAT IS KNOWN ALREADY Exposure to maternal cigarette smoking during gestation reduces human fetal ovarian cell numbers, germ cell proliferation and subsequent adult fecundity.<p></p> STUDY DESIGN, SIZE, DURATION The effects of maternal cigarette smoking on the second trimester human fetal ovary, fetal endocrine signalling and fetal chemical burden were studied. A total of 105 fetuses were studied, 56 from mothers who smoked during pregnancy and 49 from those who did not.<p></p> PARTICIPANTS/MATERIALS, SETTING METHODS Ovary, liver and plasma samples were collected from electively terminated, normally progressing, second trimester human fetuses. Circulating fetal hormones, levels of 73 fetal ovarian transcripts, protein localization, density of oocytes/primordial follicles and levels of 16 polycyclic aromatic hydrocarbons (PAHs) in the fetal liver were determined.<p></p> MAIN RESULTS AND THE ROLE OF CHANCE Circulating fetal estrogen levels were very high and were increased by maternal smoking (ANOVA, P = 0.055–0.004 versus control). Smoke exposure also dysregulated (two-way ANOVA, smoking versus gestation weeks interaction, P = 0.046–0.023) four fetal ovarian genes (cytochrome P450 scc [CYP11A1], NOBOX oogenesis homeobox [NOBOX], activator of apoptosis harakiri [HRK], nuclear receptor subfamily 2, group E, member 1 [NR2E1]), shifted the ovarian Inhibin βA/inhibin α ratio (NHBA/INHA) transcript ratio in favour of activin (ANOVA, P = 0.049 versus control) and reduced the proportion of dominant-negative estrogen receptor 2 (ERβ: ESR2) isoforms in half the exposed fetuses. PAHs, ligands for the aryl hydrocarbon receptor (AHR), were increased nearly 6-fold by maternal smoking (ANOVA, P = 0.011 versus control). A fifth transcript, COUP transcription factor 1 (nuclear receptor subfamily 2, group F, member 1: NR2F1, which contains multiple AHR-binding sites), was both significantly increased (ANOVA, P = 0.026 versus control) and dysregulated by (two-way ANOVA, smoking versus gestation weeks interaction, P = 0.021) maternal smoking. NR2F1 is associated with repression of FSHR expression and smoke-exposed ovaries failed to show the normal increase in FSHR expression during the second trimester. There was a significantly higher number of DEAD (Asp-Glu-Ala-Asp) box polypeptide 4 (DDX4) VASA-positive (ANOVA, P = 0.016 versus control), but not POU domain, class 1, transcription factor 1 (POU5F1) OCT3/4-positive, oocytes in smoke-exposed fetuses and this matched with a significantly higher number of primordial follicles (ANOVA, P = 0.024 versus control).<p></p> LIMITATIONS, REASONS FOR CAUTION The effects of maternal smoking on establishment of the maximum fetal primordial follicle pool cannot be reliably studied in our population since the process is not completed until 28 weeks of gestation and normal fetuses older than 21 weeks of gestation are not available for study. Our data suggest that some fetal ovaries are affected by smoke exposure while others are not, indicating that additional studies, with larger numbers, may show more significant effects.<p></p> WIDER IMPLICATIONS OF THE FINDINGS Fetal exposure to chemicals in cigarette smoke is known to lead to reduced fecundity in women. Our study suggests, for the first time, that this occurs via mechanisms involving activation of AHR, disruption of inhibin/activin and estrogen signalling, increased exposure to estrogen and dysregulation of multiple molecular pathways in the exposed human fetal ovary. Our data also suggest that alterations in the ESR2 positive and dominant negative isoforms may be associated with reduced sensitivity of some fetuses to increased estrogens and maternal smoking

Implicating Buddhism in Madame Butterfly’s Tragedy: Japonisme and Japan-Bashing in Fritz Lang’s Harakiri (1919)

This chapter extensively examines Fritz Lang’s Harakiri (1919), an adaptation of the Madame Butterfly story made by Lang during his first year as a director. It studies the production and reception histories of the film, which was believed to be lost until a print was discovered in the Netherlands. In comparing the restored version of Harakiri with earlier versions of the story, the chapter observes that Lang’s film distinguishes itself by dramatizing the double hara-kiri of O-Take-San and her father and by transforming the Buddhist bonze (monk), who makes only a brief appearance in Puccini’s opera, into Butterfly’s principal antagonist. By portraying the bonze as evil, the film shifts the responsibility for Butterfly’s tragedy to Buddhism and, by extension, to Japanese culture itself. The chapter considers both historical and contemporary reasons for the harsh portrayal of Buddhism in the film, while recognizing that the negative projection of Japan stands in tension with the film’s own Japonisme, a product of Lang’s passion for East Asian art. Furthermore, a spectacular scene described in a contemporary review but missing from the restored version of the film alludes to the fact that Harakiri did not provide a vehicle for Lang’s preferred visual style

PENYIMPANGAN NILAI BUSHIDO OLEH TOKOH CHIJIWA MOTOME PADA FILM DEATH OF A SAMURAI (HARAKIRI)

PENYIMPANGAN NILAI BUSHIDO OLEH CHIJIWA MOTOME PADA FILM DEATH OF A SAMURAI (HARAKIRI) Niken Pratiwi, NPM: C12.2010.00298, 40 halaman isi, 1 daftar pustaka, 9 halaman lampiran. Semarang: Program Studi Sastra Jepang, Universitas Dian Nuswantoro. Skripsi ini membahas tentang penyimpangan nilai bushido yang dilakukan oleh Chijiwa Motome. Tujuan penelitian ini adalah untuk mengetahui bentuk penyimpangan nilai bushido yang dilakukan Chijiwa Motome. Penelitian ini menggunakan sumber data film Death Of A Samurai (Harakiri). Bentuk penyimpangan nilai Bushido yang dilakukan Chijiwa Motome dalam film Death Of A Samurai (Harakiri) menunjukkan Chijiwa Motome melakukan tiga penyimpangan yaitu Meiyo, Yuu dan Makoto. Berdasarkan hasil penelitian yang penulis lakukan disimpulkan bahwa demi tuntutan ekonomi, Chijiwa Motome berani melakukan penyimpangan nilai bushido dan melakukan seppuku atau harakiri

Harakiri

Em dic Clàudia Codina i tinc 20 anys. Vaig començar a escriure a l’escola, quasi per obligació, i em vaig adonar que m’agradava. Des de llavors m’he presentat en nombrosos certàmens literaris i escriure s’ha convertit en una afició. Malauradament, per falta de temps no escric habitual ni regularment, tan sols en comptades ocasions

Intrinsic Order and Disorder in the Bcl-2 Member Harakiri: Insights into Its Proapoptotic Activity

Harakiri is a BH3-only member of the Bcl-2 family that localizes in membranes and induces cell death by binding to prosurvival Bcl-xL and Bcl-2. The cytosolic domain of Harakiri is largely disorder with residual α-helical conformation according to previous structural studies. As these helical structures could play an important role in Harakiri's function, we have used NMR and circular dichroism to fully characterize them at the residue-atomic level. In addition, we report structural studies on a peptide fragment spanning Harakiri's C-terminal hydrophobic sequence, which potentially operates as a transmembrane domain. We initially checked by enzyme immunoassays and NMR that peptides encompassing different lengths of the cytosolic domain are functional as they bind Bcl-xL and Bcl-2. The structural data in water indicate that the α-helical conformation is restricted to a 25-residue segment comprising the BH3 domain. However, structure calculation was precluded because of insufficient NMR restraints. To bypass this problem we used alcohol-water mixture to increase structure population and confirmed by NMR that the conformation in both milieus is equivalent. The resulting three-dimensional structure closely resembles that of peptides encompassing the BH3 domain of BH3-only members in complex with their prosurvival partners, suggesting that preformed structural elements in the disordered protein are central to binding. In contrast, the transmembrane domain forms in micelles a monomeric α-helix with a population close to 100%. Its three-dimensional structure here reported reveals features that explain its function as membrane anchor. Altogether these results are used to propose a tentative structural model of how Harakiri works

Intrinsic Order and Disorder in the Bcl-2 Member Harakiri: Insights into Its Proapoptotic Activity

Harakiri is a BH3-only member of the Bcl-2 family that localizes in membranes and induces cell death by binding to prosurvival Bcl-xL and Bcl-2. The cytosolic domain of Harakiri is largely disorder with residual α-helical conformation according to previous structural studies. As these helical structures could play an important role in Harakiri's function, we have used NMR and circular dichroism to fully characterize them at the residue-atomic level. In addition, we report structural studies on a peptide fragment spanning Harakiri's C-terminal hydrophobic sequence, which potentially operates as a transmembrane domain. We initially checked by enzyme immunoassays and NMR that peptides encompassing different lengths of the cytosolic domain are functional as they bind Bcl-xL and Bcl-2. The structural data in water indicate that the α-helical conformation is restricted to a 25-residue segment comprising the BH3 domain. However, structure calculation was precluded because of insufficient NMR restraints. To bypass this problem we used alcohol-water mixture to increase structure population and confirmed by NMR that the conformation in both milieus is equivalent. The resulting three-dimensional structure closely resembles that of peptides encompassing the BH3 domain of BH3-only members in complex with their prosurvival partners, suggesting that preformed structural elements in the disordered protein are central to binding. In contrast, the transmembrane domain forms in micelles a monomeric α-helix with a population close to 100%. Its three-dimensional structure here reported reveals features that explain its function as membrane anchor. Altogether these results are used to propose a tentative structural model of how Harakiri works