著者

林 順 HAYASHI Jun

出版者

名古屋大学大学院人文学研究科図書・論集委員会

雑誌

名古屋大学人文学フォーラム (ISSN:24332321)

巻号頁・発行日

vol.3, pp.113-128, 2020-03-31

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Tunnel tombs were ancient graves excavated into the side of the hill or cliff in the late of the tumulus period (end of the 5th AD. to the end of the 6th AD.) in Japan. They were characterized by their density, and in many cases, they made some groups in certain areas. In addition, by focusing on the group structure and the rank of the burial goods offered in each grave, it will be able to make clear various social relationships of each man who buried in each grave.This contribution aims to clarify the mortuary principle of the tunnel tombs in Shizuoka area. This means how each man was buried while taking account of the relationships in each group who built these tombs, and between groups who built other graves, that is, mounded tombs. To achieve this object, I analyzed following 2 subjects in this paper: 1) the hierarchy system inside of each groups of the tunnel tombs and 2) the relationships between the tunnel tombs and general mounded tombs which were made nearby them, while focusing on the group structure. As a result of these analyses, I could find out the excellence of Totomi area, especially Saka river basin, from the viewpoint of the clearness of the hierarchy inside of the tunnel tombs, and the superiority of them when compared to the mounded tombs. Finally, I assumed that the background of these phenomena links the way of governing system of burial ground (contains both graves) by central policy.

著者

Takibuchi Gaku Imanishi Hirotake Morimoto Mami Ishikawa Kaori Nakada Kazuto Toyama-Sorimachi Noriko Kikkawa Yoshiaki Takenaga Keizo Hayashi Jun-Ichi

出版者

Elsevier Science

雑誌

Mitochondrion (ISSN:15677249)

巻号頁・発行日

vol.13, no.6, pp.881-887, 2013-11

被引用文献数

8 2

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To examine whether polymorphic mtDNA mutations that do not induce significant respiration defects regulate phenotypes of tumor cells, we used mouse transmitochondrial tumor cells (cybrids) with nuclear DNA from C57BL/6 (B6) strain and mtDNA from allogenic C3H strain. The results showed that polymorphic mutations of C3H mtDNA in the cybrids induced hypoxia sensitivity, resulting in a delay of tumor formation on their subcutaneous inoculation into B6 mice. Therefore, the effects of polymorphic mutations in normal mtDNA have to be carefully considered, particularly when we apply the gene therapy to the embryos to replace their pathogenic mtDNA by normal mtDNA.

著者

Katada Shun Mito Takayuki Ogasawara Emi Hayashi Jun-Ichi Nakada Kazuto

出版者

Genetics Society of America

雑誌

G3: Genes, Genomes, Genetics (ISSN:21601836)

巻号頁・発行日

vol.3, no.9, pp.1545-1552, 2013-09

被引用文献数

15

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Studies in patients have suggested that the clinical phenotypes of some mitochondrial diseases might transit from one disease to another (e.g., Pearson syndrome [PS] to Kearns-Sayre syndrome) in single individuals carrying mitochondrial (mt) DNA with a common deletion (∆mtDNA), but there is no direct experimental evidence for this. To determine whether ∆mtDNA has the pathologic potential to induce multiple mitochondrial disease phenotypes, we used trans-mitochondrial mice with a heteroplasmic state of wild-type mtDNA and ∆mtDNA (mito-mice∆). Late-stage embryos carrying ≥50% ∆mtDNA showed abnormal hematopoiesis and iron metabolism in livers that were partly similar to PS (PS-like phenotypes), although they did not express sideroblastic anemia that is a typical symptom of PS. More than half of the neonates with PS-like phenotypes died by 1 month after birth, whereas the rest showed a decrease of ∆mtDNA load in the affected tissues, peripheral blood and liver, and they recovered from PS-like phenotypes. The proportion of ∆mtDNA in various tissues of the surviving mito-mice∆ increased with time, and Kearns-Sayre syndrome−like phenotypes were expressed when the proportion of ∆mtDNA in various tissues reached >70–80%. Our model mouse study clearly showed that a single ∆mtDNA was responsible for at least two distinct disease phenotypes at different ages and suggested that the level and dynamics of ∆mtDNA load in affected tissues would be important for the onset and transition of mitochondrial disease phenotypes in mice.

著者

Mito Takayuki Kikkawa Yoshiaki Shimizu Akinori Hashizume Osamu Katada Shun Imanishi Hirotake Ota Azusa Kato Yukina Nakada Kazuto Hayashi Jun-Ichi

出版者

Public Library of Science

雑誌

PLoS ONE (ISSN:19326203)

巻号頁・発行日

vol.8, no.2, pp.e55789, 2013-02

被引用文献数

26 5

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Mitochondrial DNA (mtDNA) mutator mice are proposed to express premature aging phenotypes including kyphosis and hair loss (alopecia) due to their carrying a nuclear-encoded mtDNA polymerase with a defective proofreading function, which causes accelerated accumulation of random mutations in mtDNA, resulting in expression of respiration defects. On the contrary, transmitochondrial mito-miceΔ carrying mtDNA with a large-scale deletion mutation (ΔmtDNA) also express respiration defects, but not express premature aging phenotypes. Here, we resolved this discrepancy by generating mtDNA mutator mice sharing the same C57BL/6J (B6J) nuclear background with that of mito-miceΔ. Expression patterns of premature aging phenotypes are very close, when we compared between homozygous mtDNA mutator mice carrying a B6J nuclear background and selected mito-miceΔ only carrying predominant amounts of ΔmtDNA, in their expression of significant respiration defects, kyphosis, and a short lifespan, but not the alopecia. Therefore, the apparent discrepancy in the presence and absence of premature aging phenotypes in mtDNA mutator mice and mito-miceΔ, respectively, is partly the result of differences in the nuclear background of mtDNA mutator mice and of the broad range of ΔmtDNA proportions of mito-miceΔ used in previous studies. We also provided direct evidence that mtDNA abnormalities in homozygous mtDNA mutator mice are responsible for respiration defects by demonstrating the co-transfer of mtDNA and respiration defects from mtDNA mutator mice into mtDNA-less (ρ0) mouse cells. Moreover, heterozygous mtDNA mutator mice had a normal lifespan, but frequently developed B-cell lymphoma, suggesting that the mtDNA abnormalities in heterozygous mutator mice are not sufficient to induce a short lifespan and aging phenotypes, but are able to contribute to the B-cell lymphoma development during their prolonged lifespan.