Details of a Researcher - Hashiguchi, Akinori

Papers - Hashiguchi, Akinori

Division display 341 - 360 of about 362 ／ All the affair displays >>

津村, 宏, 橋口, 明典, 武市, 光司, 秦, 順一

医療マネジメント学会雑誌 (Japan Society for Health Care Management) 4 ( 3 ) 365 - 370 2003.12

Joint Work, ISSN 1345-6903

病理組織所見の写真300枚を電子画像化し,そのデータをもとに病理学総論実習のパソコン用教材を作成した.作成にあたってはマイクロメディア社のディレクタを用いた.この教材をCD-ROMにして学生に配布し,実習終了後にアンケート調査を行った結果,本教材には次のような利点のあることが明らかになった.何時何処でも利用できることから学習の機会を増やせる.予習・復習に活用することで実習を有意義に行える.実際の顕微鏡像が見られること,及びマーキングなどの補助手段により学習が容易になる

木村病と抗好中球細胞質抗体(ANCA)関連腎炎を合併した再発性多発軟骨炎の1例

楢林敦, 粟津緑, 棗田とも, 井ノ口美香子, 新庄正宜, 高橋孝雄, 西川武二, 佐藤慎二, 平形道人, 亀山香織, 橋口明典

日本小児科学会雑誌 ((公社)日本小児科学会) 107 ( 10 ) 1418 - 1418 2003.10

Joint Work, ISSN 0001-6543

Giant seminoma in a patient with 5a-reductase-2 deficiency

Sasaki Gen, Nakagawa Ken, Hashiguchi Akinori, Hasegawa Tomonobu, Ogata Tsutomu, Murai Masaru

Journal of urology 169 ( 3 ) 1080-1081 2003.03

Research paper (scientific journal), Joint Work

性幹細胞（組織幹細胞）の分離，増殖，分化誘導体

Hashiguchi Akinori, Sakamoto Michiie, Umezawa Akihiro

日本臨牀 61 ( 3 ) 390-395 2003.03

Research paper (scientific journal), Joint Work

【再生医療】再生医療にかかわる基本的事項再生医療に利用可能な細胞とその供給源体性幹細胞(組織幹細胞)の分離,増殖,分化誘導

橋口, 明典, 坂元, 亨宇, 梅澤, 明弘

日本臨床 61 ( 3 ) 390 - 395 2003.03

Joint Work, ISSN 0047-1852

原発性皮膚B細胞リンパ腫の1例

斎藤, 昌孝, 村木, 良一, 石橋, 了知, 橋口, 明典, 梅澤, 明弘 and 向井, 清

臨床皮膚科 57 ( 2 ) 193 - 196 2003.02

ISSN 0021-4973

75歳女.頭部および顔面に生じた原発性皮膚B細胞リンパ腫である.頭部には表面平滑な小結節,顔面には表面に鱗屑を伴う浸潤性紅斑を認めたが,病変は皮膚に限局して皮疹部には病理組織学的に胚中心細胞様細胞やリンパ上皮性病変を認め,免疫グロブリン重鎖遺伝子の再構成が検出された.頭部および顔面皮疹は電子線照射後に消退した.MALTリンパ腫の皮膚での相当病変として,SALTからリンパ腫が発生する可能性が指摘されており,SALT関連B細胞リンパ腫という名称が提唱されている

原発性皮膚B細胞リンパ腫の1例

Saitou Masataka, Muraki Ryouichi, Ishibashi Ryouichi, Hashiguchi Akinori, Umezawa Akihiro, Mukai Kiyoshi

臨床皮膚科 57 ( 2 ) 193-196 2003.02

Research paper (scientific journal), Joint Work

Giant seminoma in a patient with 5 alpha-reductase type 2 deficiency

Sasaki Goro, Nakagawa Ken, Hashiguchi Akinori, Hasegawa Tomonobu, Ogata Tsutomu, Murai Masaru

Journal of urology 169 ( 3 ) 1080-1081 - 1 2003

Research paper (scientific journal), Joint Work, ISSN 0022-5347

体性幹細胞（組織幹細胞）の分裂，増殖，分化誘導

Hashiguchi Akinori, Sakamoto Michiie, Umezawa Akihiro

日本臨床 61 ( 3 ) 390-395 2003

Research paper (scientific journal), Joint Work

Correlation between a specific Wilms tumor suppressor gene (WT1) mutation and the histological findings in Wilms tumor(WT)

Shibata Rie, Hashiguchi Akinori, Sakamoto J, Yamada Taketo, Umezawa Akihiro, Hata Junichi

Journal of medical genetics 39 ( 12 ) 83-83 2002.12

Research paper (scientific journal), Joint Work

CiNii Research

経口糖負荷試験で糖尿病型を示さなかった糖尿病性腎症の一例

Jou Yuusuke, Ichihara Atsuhiro, Eguchi Takashi, Kurihara Isao, Hashiguchi Akinori, Konishi Kounosuke, Hayashi Matsuhiko, Saruta Takao

日本腎臓学会誌 44 ( 7 ) 552-557 2002.10

Research paper (scientific journal), Joint Work

経口糖負荷試験で糖尿病型を示さなかった糖尿病性腎症の1例

城, 祐輔, 市原, 淳弘, 江口, 高, 栗原, 勲, 橋口, 明典, 小西, 孝之助, 林, 松彦, 猿田, 享男

日本腎臓学会誌 44 ( 7 ) 738 - 743 2002.10

Joint Work, ISSN 0385-2385

46歳男.両下腿に浮腫をきたした.以後増悪し,全身に浮腫及び,著明な高血圧と腎機能障害を認めたため入院した.血液検査上,糖尿病を示唆する所見はなかった.高血圧に対しニフェジピン,カンデサルタンシレキセチル,ドキサゾシンにより血圧をコントロールし,浮腫に対してフロセミド,スピロノラクトンを投与した.腎生検後,75g OGTTを施行したが糖尿病型ではなかった.又,糖尿病性変化の精査のため蛍光眼底造影を施行した.両眼底とも網膜動脈狭細化,反射亢進,動静脈交叉部での動脈の途絶があり,網膜動脈硬化所見を呈していた.高血圧性網膜症を合併した両糖尿病網膜症(前増殖型)と診断した.第52病日,血圧130/80台を維持,浮腫も改善したため退院した

Exogenous expression of heat shock protein 90kDa retards the cell cycle and impairs the heat shock response

Zhao Chen, Hashiguchi Akinori, Kondoh Kensuke, Du Wenlin, Hata Jun-ichi, Yamada Taketo

Experimental cell research (ACADEMIC PRESS INC ELSEVIER SCIENCE) 275 ( 2 ) 200-214 - 214 2002.05

Research paper (scientific journal), Joint Work, ISSN 0014-4827

The 90-kDa heat shock protein, HSP90, is an abundant molecular chaperone which functions in cellular homeostasis in prokaryotes and eukaryotes. It is well known that HSP90 plays a critical and indispensable role in regulating cell growth through modulations of various signal transduction pathways, but its roles in cell cycle control are not so well known. We transferred human HSP90 (wild-type or mutated types) expression vectors into NTH-3T3 cells in order to study certain functions of HSP90 in the cell cycle and cell growth under physiological conditions. We found that the exogenous expression of HSP90 (wild-type) induced a decrease in cell growth via retardation of the G1/S transition. The inhibition of cell growth was caused by reduced expressions of cyclin D3 and cyclin A mRNA and protein. On the other hand, no stable transfectants with the three types of mutated HSP90 were obtained. Unexpectedly, exogenous HSP90 expression impaired the heat shock response by inhibiting both heat shock transcription factor 1 (HSF1) activation and transportation of HSF1 into the nucleus. The HSF1 function was disrupted by the direct association between HSF1 and exogenous HSP90, which was present as a monomer. These results reveal important roles of HSP90 in cell cycle control and in the stress response of nontransformed cells. (C) 2002 Elsevier Science (USA).

Access to Document (DOI)

Exogenous expression of heat shock protein 90 retards the cell cycle and impairs the heat shock response

Zhao Chen, Hashiguchi Akinori, Kondoh Kensuke, Du Wenglin, Hata Jun-ich, Yamada Taketo

Experimental cell research 275 ( 2 ) 200-214 2002.05

Research paper (scientific journal), Joint Work

Exogenous　expression of heat shock protein 90kDa retards the cell cycle and impairs the heat shock resonse

Zhao　Chen, Hashiguchi　Akinori, Kondoh　Kensuke, Du　Wenlin, Hata　Jun-ichi, Yamada　Taketo

Experimental Cellular Research 275 ( 2 ) 200-214 2002.03

Research paper (scientific journal), Joint Work

Augmentation of megakaryocytopoiesis by hematopoietotic microenviromnment of human granulocyte colony-stimulating factor transgenic mice

Fujita T, Yamada T, Hashiguchi A, Fukushima S, Kondoh K, Fujimoto J, Hata J,

Experimental Hematology 29 ( 8 ) 1010-1018 2001.08

Research paper (scientific journal), Joint Work

Augmentation of megakaryocytopoiesis within the hematopoietic microenvironment of human granulocyte colony-stimulating factor transgenic mice

T Fujita, T Yamada, A Hashiguchi, S Fukushima, K Kondoh, J Fujimoto, J Hata

EXPERIMENTAL HEMATOLOGY (ELSEVIER SCIENCE INC) 29 ( 8 ) 1010 - 1018 2001.08

Joint Work, ISSN 0301-472X

Objective. Megakaryocytopoiesis was dramatically augmented in human granulocyte colony-stimulating factor transgenic mice (G-Tg) compared to littermates. We examined the characteristics of megakaryocytes and megakaryocyte progenitor cells in these mice.
Materials and Methods. The numbers of colony-forming unit megakaryocytes (CFU-MK) and megakaryocytes in hematopoietic organs were counted. The megakaryocytes of G-Tg were examined ultrastructurally, and bone marrow transplantation studies using congenic G-Tg (Ly5.2) and C57BL/6 (Ly5.1) were performed. The number of day-14 colony-forming unit spleen (CFU-S) that contained megakaryocytes in [Ly5.1 > G-Tg] and [G-Tg > Ly5.1] mice also was counted.
Results. The number of CFU-MK increased markedly in the spleen, bone marrow, and peripheral blood. The number of megakaryocytes in the spleen and bone marrow also were increased in G-Tg mice. Ultrastructural analyses revealed that megakaryocytes in G-Tg mice were immature. Bone marrow transplantation studies of [Ly5.1 > G-Tg] mice resulted in a significantly increased number of megakaryocytes compared to [G-Tg > Ly5.1] mice. The number of day-14 CFU-S that contained megakaryocytes was increased markedly in [Ly5.1 > G-Tg] mice compared to [G-Tg > Ly5.1] mice. In vitro differentiation of megakaryocytes in [Ly5.1 > G-Tg] mice was induced by interleukin-11 and thrombopoietin.
Conclusion. The results showed that the hematopoietic marrow microenvironment of G-Tg is important in augmenting megakaryocytopoiesis. [Ly5.1 > G-Tg] mice are potentially useful as a source of murine megakaryocytes and their progenitors. (C) 2001 International Society for Experimental Hematology. Published by Elsevier Science Inc.

A case of generalized Hailey-Hailey disease with fatal liver injury

Amagai M, Kobayashi M, Wakabayashi K, Hakuno M, Hashiguchi A, Nishikawa T, Hata J

The Keio Journal of Medicine 50 ( 2 ) 109-116 2001.06

Research paper (scientific journal), Joint Work

A case of generalized Hailey-Hailey disease with fatal liver injury

Amagai M, Kobayashi M, Wakabayashi K, hakuno M, Hashiguchi A, Nishikawa T, Hata J

Keio Journal of Medicine 50 ( 2 ) 109-116 2001.06

Research paper (scientific journal), Joint Work

Augmentation of human leukemic cell invasion by activation of a small GTP-binding protein Rho

Fukushima S, Yamada T, Hashiguchi A, Nakata Y, Hata J

Experimental Hematology (ELSEVIER SCIENCE INC) 28 ( 4 ) 391-400 - 400 2000.04

Research paper (scientific journal), Joint Work, ISSN 0301-472X

Objective. The functions of a small GTP-binding protein, Rho, in human leukemic cell invasion was investigated in vivo and in vitro.
Materials and Methods. Human leukemic KM3 and Reh cells (derived from B-cell-type common acute lymphoid leukemias) were inoculated into severe combined immundeficiency (SCID) mice, Alteration of invasion in SCID mice inoculated with KM3 cells that were introduced with the expression vector for Rho Val14 (Rho V14), an activated mutant form of Rho, was observed.
Results. SCID mice inoculated with KM3 and Reh cells developed paraplegia 21 days after inoculation. All died by day 26-27, The leukemic cells were localized to bone marrow and around the spinal cord, with no infiltration into peripheral blood, spleen, liver, thymus, or lymph nodes. SCID mice inoculated with Rho V14-transfected KM3 cells showed a 5-day reduction in the time to paraplegia and death compared with SCID mice inoculated with hygromycin-resistance gene-transfected KM3 (hyg(r)) cells. In addition, the mice inoculated with Rho V14 cells showed leukemic cell infiltration, not only into bone marrow and around the spinal cord but also into peripheral blood, liver, and spleen. There were no in vitro or in vivo differences in growth rates of Rho V14 and hyg(r) cells. However, the Rho V14 cells showed markedly increased cell adhesion compared to the hygr cells.
Conclusion. Results suggest that Rho activation accelerates human leukemic cell invasion via augmentation of cell adhesion. (C) 2000 International Society for Experimental Hematology, Published by Elsevier Science Inc.

　 Previous page - Next page 　