Faculty Profiles - OZAKI Toshifumi

MISC - OZAKI Toshifumi

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Rupture of flexor tendon as the complication of volar distal radius plate

KANAZAWA Tomoko

54 ( 2 ) 385 - 386 2011.3

The use of external fixation during internal fixation for distal radius fractures

HASEI Jo

54 ( 2 ) 387 - 388 2011.3

軟部肉腫の治療成績はどこまで改善したか滑膜肉腫の治療成績と新規治療法の提案

中紀文, 竹中聡, 星学, 松峯昭彦, 戸口田淳也, 和田卓郎, 馬場一郎, 尾崎敏文, 上田孝文, 岩本幸英, 吉川秀樹

日本整形外科学会雑誌 85 ( 2 ) S38 - S38 2011.2

Evaluation of the accuracy of the stem position of cementless total hip arthroplasty with computed tomography-based navigation system

Orthopedic surgery 62 ( 1 ) 13 - 17 2011.1

Separation of the perivascular basement membrane provides a conduit for inflammatory cells in a mouse spinal cord injury model. International journal

Tomoyuki Takigawa, Tomoko Yonezawa, Teruhito Yoshitaka, Jun Minaguchi, Masae Kurosaki, Masato Tanaka, Yoshikazu Sado, Aiji Ohtsuka, Toshifumi Ozaki, Yoshifumi Ninomiya

Journal of neurotrauma 27 ( 4 ) 739 - 51 2011

Language：English

Spinal cord injury results in disruption of the cord microstructure, which is followed by inflammation leading to additional deterioration. Perivascular basement membranes are a component of the spinal cord microstructure that lies between blood vessels and astrocytes. The impact of disrupting the basement membrane structure on the expansion of inflammation has not been fully examined. The objective of this study was to clarify the relationship between damage to basement membranes and inflammation after spinal cord injury. Immunohistochemical analyses of the perivascular extracellular matrix were performed in a mouse spinal cord injury model. In normal tissue, the perivascular basement membrane was a single-layer structure produced by both endothelial cells and surrounding astrocytes. After spinal cord injury, however, the perivascular basement membrane often separated into an inner endothelial basement membrane and an outer parenchymal basement membrane. The altered basement membranes formed during the acute phase (within 7 days after spinal cord injury). During the subacute phase of injury, numerous monocytes and macrophages accumulated in the space between the separated basement membranes and infiltrated into the parenchyma where astrocytic endfeet were displaced. Infiltration of inflammatory cells from the injury core was attenuated coincident with the appearance of the glia limitans and glial scar. Furthermore, the outer parenchymal basement membrane was connected to the basement membrane of the glia limitans surrounding the injury core. Our data suggest that structurally altered basement membranes facilitate expansion of secondary inflammation during the subacute phase of spinal cord injury.

DOI： 10.1089/neu.2009.1111

PubMed

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Preclinical evaluation of telomerase-specific oncolytic virotherapy for human bone and soft tissue sarcomas. International journal

Tsuyoshi Sasaki, Hiroshi Tazawa, Jo Hasei, Toshiyuki Kunisada, Aki Yoshida, Yuuri Hashimoto, Shuya Yano, Ryosuke Yoshida, Futoshi Uno, Shunsuke Kagawa, Yuki Morimoto, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

Clinical cancer research : an official journal of the American Association for Cancer Research 17 ( 7 ) 1828 - 38 2011

Language：English

PURPOSE: Tumor-specific replication-selective oncolytic virotherapy is a promising antitumor therapy for induction of cell death in tumor cells but not of normal cells. We previously developed an oncolytic adenovirus, OBP-301, that kills human epithelial malignant cells in a telomerase-dependent manner. Recent evidence suggests that nonepithelial malignant cells, which have low telomerase activity, maintain telomere length through alternative lengthening of telomeres (ALT). However, it remains unclear whether OBP-301 is cytopathic for nonepithelial malignant cells. Here, we evaluated the antitumor effect of OBP-301 on human bone and soft tissue sarcoma cells. EXPERIMENTAL DESIGN: The cytopathic activity of OBP-301, coxsackie and adenovirus receptor (CAR) expression, and telomerase activity were examined in 10 bone (OST, U2OS, HOS, HuO9, MNNG/HOS, SaOS-2, NOS-2, NOS-10, NDCS-1, and OUMS-27) and in 4 soft tissue (CCS, NMS-2, SYO-1, and NMFH-1) sarcoma cell lines. OBP-301 antitumor effects were assessed using orthotopic tumor xenograft models. The fiber-modified OBP-301 (termed OBP-405) was used to confirm an antitumor effect on OBP-301-resistant sarcomas. RESULTS: OBP-301 was cytopathic for 12 sarcoma cell lines but not for the non-CAR-expressing OUMS-27 and NMFH-1 cells. Sensitivity to OBP-301 was dependent on CAR expression and not on telomerase activity. ALT-type sarcomas were also sensitive to OBP-301 because of upregulation of human telomerase reverse transcriptase (hTERT) mRNA following virus infection. Intratumoral injection of OBP-301 significantly suppressed the growth of OST and SYO-1 tumors. Furthermore, fiber-modified OBP-405 showed antitumor effects on OBP-301-resistant OUMS-27 and NMFH-1 cells. CONCLUSIONS: A telomerase-specific oncolytic adenovirus is a promising antitumor reagent for the treatment of bone and soft tissue sarcomas.

DOI： 10.1158/1078-0432.CCR-10-2066

PubMed

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屈筋腱障害予防を目的とした橈骨遠位端骨折用掌側ロッキングプレートの設置位置の検討

近藤秀則, 今谷潤也, 清水弘毅, 中道亮, 妹尾則孝, 尾崎敏文

日本手外科学会雑誌 = The journal of Japanese Society for Surgery of the Hand 27 ( 3 ) 252 - 255 2010.12

P1-246 腎機能低下MRSA患者に対するバンコマイシン含有セメントビーズの有用性(一般演題ポスター発表,薬物動態・TDM・投与設計,臨床から学び臨床へと還元する医療薬学)

川上恭弘, 浅海浩二, 尾崎敏文, 千堂年昭

日本医療薬学会年会講演要旨集 20 328 - 328 2010.10

Open Reduction for Residual Subluxation after Developmental Dislocation of the Hip

ENDO Hirosuke

19 ( 2 ) 367 - 373 2010.10

Evaluation for the short-term results and the operative indication of Chiari pelvic osteotomy

ENDO Hirosuke

36 54 - 59 2010.10

Less invasive intrapelvic approach (Stoppa modification) in the treatment of acetabular fractures and pelvic ring injuries

NODA T., OZAKI T., TAKAGI Y., OGAWA K., YAGATA Y., UEDA Y.

32 ( 3 ) 522 - 526 2010.9

T細胞特異的SOCS5過剰発現はマウス抗II型コラーゲン抗体関節炎において関節炎を遷延させる

高畑智宏, 松川昭博, 西田圭一郎, 尾崎敏文

日本整形外科学会雑誌 84 ( 8 ) S1145 - S1145 2010.8

Surgical treatment of metastatic bone tumors

Orthopedic surgery 61 ( 8 ) 919 - 926 2010.7

The role of thallium-201 and pentavalent dimercapto succinic acid (DMSA) for staging cartilaginous tumors

Orthopedic surgery 61 ( 8 ) 787 - 792 2010.7

Epigenetic Regulation in Chondrogenesis

Takayuki Furumatsu, Toshifumi Ozaki

ACTA MEDICA OKAYAMA 64 ( 3 ) 155 - 161 2010.6

Language：English Publishing type：Book review, literature introduction, etc. Publisher：OKAYAMA UNIV MED SCHOOL

Epigenetics is an essential mechanism to control gene expression and fundamental cellular processes. DNA methylation in CpG-rich promoters correlates with gene silencing. Histone modification including histone acetylation and deacetylation determines the stability of the chromatin structure. Condensed chromatin (heterochromatin), which has a higher-order histone-DNA structure, prevents the access of transcriptional activators to their target genes. The fundamental unit of eukaryotic chromatin consists of 146 bp of DNA wrapped around a histone octamer. Posttranslational modifications of the histone tail and the chromatin remodeling complex disrupt histone-DNA contacts and induce nucleosome mobilization. Histone acetylation of specific lysine residues in the histone tail plays a crucial role in epigenetic regulation. Histone acetylation is a dynamic process regulated by the antagonistic actions of 2 families of enzymes - the histone acetyltransferases (HATs) and the histone deacetylases (HDACs). The balance between histone acetylation and deacetylation serves as a key epigenetic mechanism for transcription factor-dependent gene expression and the developmental process. We review emerging evidence that DNA methylation, histone acetylation modified by HAT and/or HDAC, and transcription factor-associated molecules contribute to a mechanism that can alter chromatin structure, gene expression, and cellular differentiation during chondrogenesis.

Web of Science

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Evaluation of venous return of proximal femoral fractures using fracture table

TERAMOTO H., INOUE A., NAKANISHI K., NARAZAKI S., YAMANE K., NODA T., OZAKI T.

32 ( 2 ) 377 - 380 2010.5