Details of a Researcher - OGASAWARA Noriko

Papers - OGASAWARA Noriko

Division display 61 - 80 of about 99 ／ All the affair displays >>

視聴覚障害者の人工内耳装用の現状

海﨑文, 新谷朋子, 才川悦子, 小笠原徳子, 吉野真代, 今野綾美, 北川可恵, 氷見徹夫

ＡＵＤＩＯＬＯＧＹＪＡＰＡＮ ( 一般社団法人日本聴覚医学会 ) 57 ( 5 ) 293 - 294 2014

DOI CiNii

当院で人工内耳手術を行った小児進行性難聴例の検討

髙橋希, 才川悦子, 新谷朋子, 小笠原徳子, 海﨑文, 吉野真代, 今野綾美, 北川可恵

ＡＵＤＩＯＬＯＧＹＪＡＰＡＮ ( 一般社団法人日本聴覚医学会 ) 57 ( 5 ) 283 - 284 2014

DOI CiNii

Humulone suppresses replication of respiratory syncytial virus and release of IL-8 and RANTES in normal human nasal epithelial cells

Jun Fuchimoto, Takashi Kojima, Tamaki Okabayashi, Tomoyuki Masaki, Noriko Ogasawara, Kazufumi Obata, Kazuaki Nomura, Satoshi Hirakawa, Naoyuki Kobayashi, Tatsuro Shigyo, Shin-ichi Yokota, Nobuhiro Fujii, Hiroyuki Tsutsumi, Tetsuo Himi, Norimasa Sawada

MEDICAL MOLECULAR MORPHOLOGY ( SPRINGER JAPAN KK ) 46 ( 4 ) 203 - 209 2013.12 [Refereed]

Respiratory syncytial virus (RSV) is the major infectious agent causing serious respiratory tract inflammation in infants and young children. However, an effective vaccine and anti-viral therapy for RSV infection have not yet been developed. Hop-derived bitter acids have potent pharmacological effects on inflammation. Therefore, we investigated the effects of humulone, which is the main constituent of hop bitter acids, on the replication of RSV and release of the proinflammatory cytokine IL-8 and chemokine RANTES in RSV-infected human nasal epithelial cells (HNECs). We found that humulone prevented the expression of RSV/G-protein, formation of virus filaments and release of IL-8 and RANTES in a dose-dependent manner in RSV-infected HNECs. These findings suggest that humulone has protective effects against the replication of RSV, the virus assembly and the inflammatory responses in HNECs and that it is a useful biological product for the prevention and therapy for RSV infection.

DOI PubMed

Solitary fibrous tumor of the head and neck in a child: Case report and review of the literature

Ogasawara Noriko, Kikuchi Keisuke, Yoshioka Iwao, Yamashita Keiji, Himi Tetsuo

Journal of Pediatric Surgery Case Reports ( Elsevier Inc. ) 1 ( 8 ) 194 - 196 2013

DOI

Regulation of Tight Junctions in Upper Airway Epithelium

Takashi Kojima, Mitsuru Go, Ken-ichi Takano, Makoto Kurose, Tsuyoshi Ohkuni, Jun-ichi Koizumi, Ryuta Kamekura, Noriko Ogasawara, Tomoyuki Masaki, Jun Fuchimoto, Kazufumi Obata, Satoshi Hirakawa, Kazuaki Nomura, Takashi Keira, Ryou Miyata, Nobuhiro Fujii, Hiroyuki Tsutsumi, Tetsuo Himi, Norimasa Sawada

BIOMED RESEARCH INTERNATIONAL ( HINDAWI PUBLISHING CORPORATION ) 2013 947072 2013 [Refereed]

The mucosal barrier of the upper respiratory tract including the nasal cavity, which is the first site of exposure to inhaled antigens, plays an important role in host defense in terms of innate immunity and is regulated in large part by tight junctions of epithelial cells. Tight junction molecules are expressed in both M cells and dendritic cells as well as epithelial cells of upper airway. Various antigens are sampled, transported, and released to lymphocytes through the cells in nasal mucosa while they maintain the integrity of the barrier. Expression of tight junction molecules and the barrier function in normal human nasal epithelial cells (HNECs) are affected by various stimuli including growth factor, TLR ligand, and cytokine. In addition, epithelial-derived thymic stromal lymphopoietin (TSLP), which is a master switch for allergic inflammatory diseases including allergic rhinitis, enhances the barrier function together with an increase of tight junction molecules in HNECs. Furthermore, respiratory syncytial virus infection in HNECs in vitro induces expression of tight junction molecules and the barrier function together with proinflammatory cytokine release.. is paper summarizes the recent progress in our understanding of the regulation of tight junctions in the upper airway epithelium under normal, allergic, and RSV-infected conditions.

DOI PubMed

Hop water extract inhibits double-stranded RNA-induced thymic stromal lymphopoietin release from human nasal epithelial cells

Jun Fuchimoto, Takashi Kojima, Naoyuki Kobayashi, Tsuyoshi Ohkuni, Noriko Ogasawara, Tomoyuki Masaki, Kazufumi Obata, Kazuaki Nomura, Atsushi Kondoh, Tatsuro Shigyo, Tetsuo Himi, Norimasa Sawada

AMERICAN JOURNAL OF RHINOLOGY & ALLERGY ( OCEAN SIDE PUBLICATIONS INC ) 26 ( 6 ) 433 - 438 2012.11 [Refereed]

Background: Thymic stromal lymphopoietin (TSLP) acts as a master switch for allergic inflammation and plays a key role in allergic diseases, including allergic rhinitis. Double-stranded RNA (dsRNA) recognized by Toll-like receptor 3 (TLR3) strongly activates TSLP release from human nasal epithelial cells (HNECs). Hop (Humulus lupulus L.) extracts have been shown to have potent pharmacologic effects on inflammation. Methods: To investigate whether a hop water extract (HWE) prevents TSLP release from HNECs, human telomerase reverse transcriptase (hTERT)-transfected HNECs, used as a model of normal HNECs, were pretreated with HWE before treatment with the TLR3 ligand Polyinosine-polycytidylic acid (poly[I:C]). Results: In the hTERT-transfected HNECs, treatment with HWE significantly reduced poly(I:C)-induced production and release of TSLP in a dose-dependent manner, as well as dexamethasone. Treatment with the protein kinase C (PKC) inhibitor GF109203X and NF-kappa B inhibitor IMD-0354 also reduced poly(I:C)-induced TSLP release from hTERT-transfected HNECs. Treatment with HWE efficiently prevented up-regulation of PKC activity by 12-O-tetradecanoyl phorbol-13-acetate but not NF-kappa B activity induced by IL-1 beta in hTERT-transfected HNECs. Conclusion: Our results clearly indicated that HWE inhibited dsRNA-induced production and release of TSLP via a PKC signal pathway in HNECs and it may have potent preventive effects against allergic rhinitis.

DOI PubMed

ヒト鼻粘膜上皮細胞を用いたcurcuminによるRSvirusの複製阻害およびタイト結合発現誘導のメカニズム解析

小幡和史, 小島隆, 正木智之, 渕本潤, 平川賢史, 野村一顕, 高澤啓, 小笠原徳子, 氷見徹夫, 澤田典均

日本病理学会会誌 ( (一社)日本病理学会 ) 101 ( 1 ) 280 - 280 2012.03

Altered expression of claudin-1, claudin-7, and tricellulin regardless of human papilloma virus infection in human tonsillar squamous cell carcinoma

Atsushi Kondoh, Ken-Ichi Takano, Takashi Kojima, Tsuyoshi Ohkuni, Ryuta Kamekura, Noriko Ogasawara, Mitsuru Go, Norimasa Sawada, Tetsuo Himi

ACTA OTO-LARYNGOLOGICA ( INFORMA HEALTHCARE ) 131 ( 8 ) 861 - 868 2011.08 [Refereed]

Conclusions: Altered expression of claudin-1, claudin-7, and tricellulin in early tonsillar squamous cell carcinoma (SCC) independent of human papilloma virus (HPV) infection may lead to tumor progression. Objectives: Integral tight junction proteins, the claudins and tricellulin, play a crucial role in all tissues. HPV is significantly associated with tonsillar SCC. We sought to determine the expression of claudin-1, claudin-7, and tricellulin in HPV-infected and HPV-free tonsillar SCC. Methods: Twenty-eight tonsillar SCCs were studied by immunohistochemical analysis and real-time reverse transcription polymerase chain reaction with in situ hybridization analysis. Results: Compared with normal tissues, claudin-1 was strongly expressed, whereas claudin-7 and tricellulin were weakly expressed or were absent in primary SCC and metastatic lymph nodes. Claudin-7 and tricellulin were markedly reduced at all stages of tumor development. In situ hybridization analysis showed no correlation between HPV infection and altered expression of the tight junction proteins.

DOI PubMed

A nuclear factor-kappa B signaling pathway via protein kinase C delta regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells

Tomoyuki Masaki, Takashi Kojima, Tamaki Okabayashi, Noriko Ogasawara, Tsuyoshi Ohkuni, Kazufumi Obata, Akira Takasawa, Masaki Murata, Satoshi Tanaka, Satoshi Hirakawa, Jun Fuchimoto, Takafumi Ninomiya, Nobuhiro Fujii, Hiroyuki Tsutsumi, Tetsuo Himi, Norimasa Sawada

MOLECULAR BIOLOGY OF THE CELL ( AMER SOC CELL BIOLOGY ) 22 ( 13 ) 2144 - 2156 2011.07 [Refereed]

Respiratory syncytial virus (RSV) is the major cause of bronchitis, asthma, and severe lower respiratory tract disease in infants and young children. The airway epithelium, which has a well-developed barrier regulated by tight junctions, is the first line of defense during respiratory virus infection. In upper airway human nasal epithelial cells (HNECs), however, the primary site of RSV infection, the mechanisms of replication and budding of RSV, and the epithelial cell responses, including the tight junctional barrier, remain unknown. To investigate the detailed mechanisms of replication and budding of RSV in HNECs and the epithelial cell responses, we established an RSV-infected model using human telomerase reverse transcriptase-transfected HNECs. We first found that the expression and barrier function of tight junction molecules claudin-4 and occludin were markedly induced together with production of proinflammatory cytokines interleukin 8 and tumor necrosis factor-alpha in HNECs after RSV infection, and the induction of tight junction molecules possibly contributed to budding of RSV. Furthermore, the replication and budding of RSV and the epithelial cell responses in HNECs were regulated via a protein kinase C delta/hypoxia-inducible factor-1 alpha/nuclear factor-kappa B pathway. The control of this pathway in HNECs may be useful not only for prevention of replication and budding of RSV, but also in therapy for RSV-induced respiratory pathogenesis.

DOI PubMed

Epithelial barrier and antigen uptake in lymphoepithelium of human adenoids

Noriko Ogasawara, Takashi Kojima, Mitsuru Go, Ken-Ichi Takano, Ryuta Kamekura, Tsuyoshi Ohkuni, Jun-Ichi Koizumi, Tomoyuki Masaki, Jun Fuchimoto, Kazufumi Obata, Makoto Kurose, Tomoko Shintani, Norimasa Sawada, Tetsuo Himi

ACTA OTO-LARYNGOLOGICA ( INFORMA HEALTHCARE ) 131 ( 2 ) 116 - 123 2011.02 [Refereed]

Invasion of antigens through the mucosal surface can be prevented by the common mucosal immune system, including Peyer's patches (PPs) and nasopharyngeal-associated lymphoreticular tissue (NALT). The adenoids (nasopharyngeal tonsils) comprise one of the NALTs and constitute the major part of Waldeyer's lymphoid ring in humans. However, the role of the lymphoepithelium, including M cells and dendritic cells (DCs), in the adenoids is unknown compared with the epithelium of PPs. NALTs also have unique functions such as the barrier of epithelial cells and uptake of antigens by M cells and DCs, and may play a crucial role in airway mucosal immune responses. The lymphoepithelium of adenoids has well-developed tight junctions that play an important role in the barrier function, the same as nasal epithelium but not palatine tonsillar epithelium. Tight junction molecules are expressed in both M cells and DCs as well as epithelial cells, and various antigens may be sampled, transported, and released to lymphocytes through the cells while they maintain the integrity of the epithelial barrier. This review summarizes the recent progress in our understanding of how M cells and DCs control the epithelial barrier in the adenoids.

DOI PubMed

Poly(I:C) reduces expression of JAM-A and induces secretion of IL-8 and TNF-alpha via distinct NF-kappa B pathways in human nasal epithelial cells

Tsuyoshi Ohkuni, Takashi Kojima, Noriko Ogasawara, Tomoyuki Masaki, Jun Fuchimoto, Ryuta Kamekura, Jun-ichi Koizumi, Shingo Ichimiya, Masaki Murata, Satoshi Tanaka, Tetsuo Himi, Norimasa Sawada

TOXICOLOGY AND APPLIED PHARMACOLOGY ( ACADEMIC PRESS INC ELSEVIER SCIENCE ) 250 ( 1 ) 29 - 38 2011.01 [Refereed]

Human nasal epithelium is an important physical barrier and innate immune defense protecting against inhaled substances and pathogens. Toll-like receptor (TLR) signaling, which plays a key role in the innate immune response, has not been well characterized in human nasal epithelial cells (HNECs), including the epithelial tight junctional barrier. In the present study, mRNAs of TLR1-10 were detected in hTERT-transfected HNECs, which can be used as an indispensable and stable model of normal HNECs, similar to primary cultured HNECs. To investigate the changes of tight junction proteins and the signal transduction pathways via TLRs in HNECs in vitro, hTERT-transfected HNECs were treated with TLR2 ligand P(3)CSK(4), TLR3 ligand poly(I:C), TLR4 ligand LPS, TLR7/8 ligand CL097, TLR8 ligand ssRNA40/LyoVec, and TLR9 ligand ODN2006. In hTERT-transfected HNECs, treatment with poly(I:C) significantly reduced expression of the tight junction protein JAM-A and induced secretion of proinflammatory cytokines IL-8 and TNF-alpha. Both the reduction of JAM-A expression and the induction of secretion of IL-8 and TNF-alpha after treatment with poly(I:C) were modulated by distinct signal transduction pathways via EGFR. PI3K, and p38 MAPK and finally regulated by a TLR3-mediated NF-kappa B pathway. The control of TLR3-mediated signaling pathways in HNECs may be important not only in infection by viral dsRNA but also in autoimmune diseases caused by endogenous dsRNA released from necrotic cells. (C) 2010 Elsevier Inc. All rights reserved.

DOI PubMed

Mucosal Immune Barrier and Antigen-Presenting System in Human Nasal Epithelial Cells

Tetsuo Himi, Ken-ichi Takano, Noriko Ogasawara, Mitsuru Go, Makoto Kurose, Jun-ichi Koizumi, Ryuta Kamekura, Atsushi Kondo, Tsuyoshi Ohkuni, Tomoyuki Masaki, Takashi Kojima, Norimasa Sawada, Hiroyuki Tsutsumi

RECENT ADVANCES IN TONSILS AND MUCOSAL BARRIERS OF THE UPPER AIRWAYS ( KARGER ) 72 28 - + 2011 [Refereed]

The upper respiratory tract including the nasal cavity, which is the first site of invading antigen exposure, plays a crucial role in host defense via the mucosal immune response. The epithelium of nasal mucosa forms a continuous barrier against a wide variety of exogenous antigens. The epithelial barrier function is regulated in large part by the apical-most intercellular junction, referred to as the tight junction. Antigen-presenting cells, particularly dendritic cells (DCs), are known to play an important role in human nasal mucosa. Recently, the author and colleagues discovered a new mechanism for pathogen uptake in the nasal mucosa, by which DCs open the tight junctions between epithelial cells and send dendrites outside the epithelium to directly sample the pathogen. In order to preserve the integrity of the epithelial barrier and penetrate beyond well-developed epithelial tight junctions, DCs express tight junction proteins. We also found that these DCs are activated by nasal epithelial-derived TSLP induced by stimuli such as cytokines and Toll-like receptor ligands. In this lecture, I will talk about the novel mechanisms in host defense in terms of innate immunity of the nasal mucosa from the point of view of the mucosal barrier function. Copyright (C) 2011 S. Karger AG, Basel

DOI PubMed

Carbon ion radiotherapy as an initial treatment in an unresectable head and neck soft tissue tumor

Noriko Ogasawara, Naoki Hyakushima, Keisuke Kikuchi, Tomonori Nagaya, Iwao Yoshioka, Masao Murakami, Yoshio Hishikawa

Practica Oto-Rhino-Laryngologica 104 ( 12 ) 899 - 903 2011 [Refereed]

Soft tissue tumor is a rare disease in the head and neck regions which is difficult to diagnose and treat. We report on a case of unresectable soft tissue tumor in the head and neck. The patient was a 41-year-old man who noticed some swelling on the right side of his neck which had started three months prior to presenting. A tumor was found in the right neck surrounding his common carotid artery which was judged unresectable because of its location and size. The differentiated diagnosis between a synovial sarcoma and a malignant peripheral nerve sheath tumor (MPNST) was difficult. The patient underwent carbon ion radiotherapy as an initial treatment in the Hyogo Ion Beam Medical Center. There was a partial response from the tumor in his neck tumor, but it metastasized to the lung and bone and the patient died of pulmonary failure nine months after the initial treatment.

DOI

c-Jun N-Terminal Kinase Is Largely Involved in the Regulation of Tricellular Tight Junctions via Tricellulin in Human Pancreatic Duct Epithelial Cells

Takashi Kojima, Jun Fuchimoto, Hiroshi Yamaguchi, Tatsuya Ito, Akira Takasawa, Takafumi Ninomiya, Shin Kikuchi, Noriko Ogasawara, Tsuyoshi Ohkuni, Tomoyuki Masaki, Koichi Hirata, Tetsuo Himi, Norimasa Sawada

JOURNAL OF CELLULAR PHYSIOLOGY ( WILEY-LISS ) 225 ( 3 ) 720 - 733 2010.12 [Refereed]

Tricellulin (TRIC) is a tight junction protein at tricellular contacts where three epithelial cells meet, and it is required for the maintenance of the epithelial barrier. To investigate whether TRIC is regulated via a c-Jun N-terminal kinase (JNK) pathway, human pancreatic HPAC cells, highly expressed at tricellular contacts, were exposed to various stimuli such as the JNK activators anisomycin and 12-O-tetradecanoylphorbol 13-acetate (TPA), and the proinflammatory cytokines IL-1 beta, TNF alpha, and IL-1 alpha. TRIC expression and the barrier function were moderated by treatment with the JNK activator anisomycin, and suppressed not only by inhibitors of JNK and PKC but also by siRNAs of TRIC. TRIC expression was induced by treatment with the PKC activator TPA and proinflammatory cytokines IL-1 beta, TNF alpha, and IL-1 alpha, whereas the changes were inhibited by a JNK inhibitor. Furthermore, in normal human pancreatic duct epithelial cells using hTERT-transfected primary cultured cells, the responses of TRIC expression to the various stimuli were similar to those in HPAC cells. TRIC expression in tricellular tight junctions is strongly regulated together with the barrier function via the JNK transduction pathway. These findings suggest that JNK may be involved in the regulation of tricellular tight junctions including TRIC expression and the barrier function during normal remodeling of epithelial cells, and prevent disruption of the epithelial barrier in inflammation and other disorders in pancreatic duct epithelial cells. J. Cell. Physiol. 225: 720-733, 2010. (C) 2010 Wiley-Liss, Inc.

DOI PubMed

ヒト鼻粘膜上皮細胞における新規タイト結合分子tricellulinの発現調節

大國毅, 小島隆, 小笠原徳子, 正木智之, 澤田典均, 氷見徹夫

日本鼻科学会会誌 ( (一社)日本鼻科学会 ) 49 ( 3 ) 425 - 425 2010.07

PPAR gamma agonists upregulate the barrier function of tight junctions via a PKC pathway in human nasal epithelial cells

Noriko Ogasawara, Takashi Kojima, Mitsuru Go, Tsuyoshi Ohkuni, Jun-ichi Koizumi, Ryuta Kamekura, Tomoyuki Masaki, Masaki Murata, Satoshi Tanaka, Jun Fuchimoto, Tetsuo Himi, Norimasa Sawada

PHARMACOLOGICAL RESEARCH ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD ) 61 ( 6 ) 489 - 498 2010.06 [Refereed]

Peroxisome proliferator activated (PPAR)gamma plays a critical role in the control of not only adipocyte differentiation, lipid metabolism and immunity but also the barrier functions of epithelial and endothelial cells. In the present study, to investigate effects of PPAR gamma agonists on the tight junctional barrier of human nasal epithelial cells (HNECs), hTERT-transfected HNECs, which highly express both PPAR gamma and tight junction proteins, were treated with the PPAR gamma agonists rosiglitazone and troglitazone. Treatment with the PPAR gamma agonists enhanced the barrier function of hTERT-transfected HNECs together with the upregulation of tight junction molecules claudin-1 and -4, occludin, and tricellulin at the transcriptional level. A significant increase of tight junction strands was also observed after treatment with rosiglitazone. Treatment with PPAR gamma agonists induced the activity of phospho-PKC in hTERT-transfected HNECs. The upregulation of the tight junction molecules in hTERT-transfected HNECs by rosiglitazone was inhibited by not only PPAR gamma antagonists GW9662 and T0070907, but also the panPKC inhibitor GF109203X. These findings suggest that PPAR gamma agonists upregulate the barrier function of tight junctions of human nasal epithelial cells via a PKC signaling pathway and could be novel drugs for protection against inhaled substances and pathogens in the airway epithelium of human nasal mucosa. (C) 2010 Elsevier Ltd. All rights reserved.

DOI PubMed

Toll様受容体刺激によるヒト鼻粘膜上皮細胞タイト結合分子発現変化について

大國毅, 小島隆, 小笠原徳子, 正木智之, 澤田典均, 氷見徹夫

日本耳鼻咽喉科学会会報 ( (一社)日本耳鼻咽喉科頭頸部外科学会 ) 113 ( 4 ) 405 - 405 2010.04

RSウイルス感染ヒト鼻粘膜上皮細胞におけるタイト結合の誘導

正木智之, 小島隆, 大國毅, 小笠原徳子, 氷見徹夫, 村田雅樹, 田中敏, 澤田典均

日本病理学会会誌 ( (一社)日本病理学会 ) 99 ( 1 ) 191 - 191 2010.03

Thymic stromal lymphopoietin induces tight junction protein claudin-7 via NF-kappa B in dendritic cells

Ryuta Kamekura, Takashi Kojima, Akira Takashima, Jun-ichi Koizumi, Noriko Ogasawara, Mitsuru Go, Ken-ichi Takano, Masaki Murata, Satoshi Tanaka, Shingo Ichimiya, Tetsuo Himi, Norimasa Sawada

HISTOCHEMISTRY AND CELL BIOLOGY ( SPRINGER ) 133 ( 3 ) 339 - 348 2010.03 [Refereed]

Epithelial-derived thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine that triggers dendritic cell (DC)-mediated Th2-type inflammatory responses. The activated DCs can penetrate the epithelium to directly take up antigen without compromising the barrier function. Although it is reported that DCs express tight junction molecules and can establish tight junction-like structures with adjacent epithelial cells to preserve the epithelial barrier, the regulation of expression of tight junction molecules in DCs remains unknown. In the present study, to investigate the mechanical regulation of expression of tight junction molecules in DCs, XS52 DCs that was a long-term DC line established from the epidermis of a newborn BALB/c mouse, were treated with TSLP or toll-like receptor (TLR) ligands. In XS52 cells, tight junction molecules claudin-1, -3, -4, -6, -7, -8, and occludin were detected. mRNA expression of TSLP receptor and all these tight junction molecules was significantly increased in activated XS52 cells after treatment with TSLP. In addition, expression of claudin-7 protein was increased in dose- and time-dependent manner. In XS52 cells, which express TLR2, TLR3, TLR4, and TLR7, but not TLR9, expression of claudin-7 protein was also increased after treatment with ligands of TLR2, TLR4 or TLR7/8, Pam(3)Cys-Ser-(Lys)(4), LPS, or CL097. The NF-kappa B inhibitor IMD-0354 prevented upregulation of claudin-7 after treatment with TSLP or TLR ligands. These findings indicate that TSLP induces expression of tight junction protein claudin-7 in DCs via NF-kappa B as well as via TLRs and may control tight junctions of DCs to preserve the epithelial barrier during allergic inflammation.

DOI PubMed

鼻粘膜上皮細胞における自然免疫toll like receptorによるタイト結合分子発現調節

大國毅, 小島隆, 小笠原徳子, 正木智之, 澤田均典, 氷見徹夫

アレルギーの臨床 ( (株)北隆館 ) 30 ( 1 ) 88 - 89 2010.01

　 PREV - NEXT 　

<OGASAWARA Noriko>

Papers - OGASAWARA Noriko