記述言語：英語   掲載種別：研究論文（学術雑誌）  

Ectopic bone formation in mice is the gold standard for evaluation of osteogenic constructs. By regular procedures, usually only 4 constructs can be accommodated per mouse, limiting screening power. Combinatorial cassettes (combi-cassettes) hold up to 19 small, uniform constructs from the time of surgery, through time in vivo, and subsequent evaluation. Two types of bone tissue engineering constructs were tested in the combi-cassettes: i) a cell-scaffold construct containing primary human bone marrow stromal cells with hydroxyapatite/tricalcium phosphate particles (hBMSCs + HA/TCP) and ii) a growth factor-scaffold construct containing bone morphogenetic protein 2 in a gelatin sponge (BMP2+GS). Measurements of bone formation by histology, bone formation by X-ray microcomputed tomography (μCT) and gene expression by quantitative polymerase chain reaction (qPCR) showed that constructs in combi-cassettes were similar to those created by regular procedures. Combi-cassettes afford placement of multiple replicates of multiple formulations into the same animal, which enables, for the first time, rigorous statistical assessment of: 1) the variability for a given formulation within an animal (intra-animal variability), 2) differences between different tissue-engineered formulations within the same animal and 3) the variability for a given formulation in different animals (inter-animal variability). Combi-cassettes enable a more high-throughput, systematic approach to in vivo studies of tissue engineering constructs.

DOI： 10.1016/j.biomaterials.2018.09.035

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Understanding the mechanisms that control cutaneous wound healing is crucial to successfully manage repair of damaged skin. The goal of the current study was to uncover novel extracellular matrix (ECM) components that control the wound healing process. Full thickness skin defects were created in mice and used to show CCN4 up-regulation during wound-healing as early as 1 day after surgery, suggesting a role in inflammation and subsequent dermal migration and proliferation. To determine how CCN4 could regulate wound healing we used Ccn4-KO mice and showed they had delayed wound closure accompanied by reduced expression of Col1a1 and Fn mRNA. Boyden chamber assays using Ccn4-deficient dermal fibroblasts showed they have reduced migration and proliferation compared to WT counterparts. To confirm CCN4 has a role in proliferation and migration of dermal cells, siRNA knockdown and transduction of CCN4 adenoviral transduction were used and resulted in reduced or enhanced migration of human adult dermal fibroblast (hADF) cells respectively. The induced migration of the dermal fibroblasts by CCN4 appears to work via α5β1 integrin receptors that further stimulates down-stream ERK/JNK signaling. The regulation of CCN4 by TNF-α prompted us look further at their potential relationship. Treatment of hADFs with CCN4 and TNF-α alone or together showed CCN4 counteracted the inhibition of TNF-α on COL1A1 and FN mRNA expression and the stimulation of TNF-α on MMP-1 and MMP3 mRNA expression. CCN4 appeared to counterbalance the effects of TNF-α by inhibiting downstream NF-κB/p-65 signaling. Taken together we show CCN4 stimulates dermal fibroblast cell migration, proliferation and inhibits TNF-α stimulation, all of which could regulate wound healing.

DOI： 10.1016/j.matbio.2018.01.004

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記述言語：日本語   出版者・発行元：岐阜大学医学教育開発研究センター  

岡山大学歯学部は、平成26年に岡山大学が採択された文部科学省課題解決型高度医療人材養成プログラム選定事業「健康寿命社会を担う歯科医学教育改革-死生学や地域包括ケアモデルを導入した医科歯科連携教育体制の構築-」の中で、岡山大学病院で展開されているチーム医療の現場を体験する「高度医療支援・周術期口腔機能管理実習」を必須科目として開講している。本実習は、単なる知識の習得ではなく、チーム医療の現場で専門性をもって積極的に対応できる歯科医療人養成を目的としており、現在は岡山大学の学生だけでなく、上記事業の連携大学からの学生受け入れも行っている。本実習は、チーム医療の現場を実際に経験させるだけでなく、学生にがん手術予定の患者及び患者家族をエスコートするという役割を与えたことで、学習内容が印象に残り、医療職としてのプロフェッショナリズムを育む可能性があることが示唆された。(著者抄録)

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掲載種別：研究論文（学術雑誌）  

Objective: Increased Wisp1 expression was previously reported in experimental and human osteoarthritis (OA). Moreover, adenoviral overexpression of Wisp1 in naïve mouse knee joints resulted in early OA-like cartilage lesions. Here, we determined how the matricellular protein WISP1 is involved in the pathology that occurs in the complex osteoarthritic environment with aging and experimental OA in wild type (WT) and Wisp1−/− mice. Methods: WT and Wisp1−/− mice were aged or experimental OA was induced with intraarticular collagenase injection, destabilization of the medial meniscus (DMM) or anterior cruciate ligament transection (ACLT). Joint pathology was assessed using histology and microCT. Protease expression was evaluated with qRT-PCR and activity was determined by immunohistochemical staining of the aggrecan neoepitope NITEGE. Protease expression in human end-stage OA synovial tissue was determined with qRT-PCR after stimulation with WISP1. Results: With aging, spontaneous cartilage degeneration in Wisp1−/− was not decreased compared to their WT controls. However, we observed significantly decreased cartilage degeneration in Wisp1−/− mice after induction of three independent experimental OA models. While the degree of osteophyte formation was comparable between WT and Wisp1−/− mice, increased cortical thickness and reduced trabecular spacing was observed in Wisp1−/− mice. In addition, we observed decreased MMP3/9 and ADAMTS4/5 expression in Wisp1−/− mice, which was accompanied by decreased levels of NITEGE. In line with this, stimulation of human OA synovium with WISP1 increased the expression of various proteases. Conclusions: WISP1 plays an aggravating role in the development of post-traumatic experimental OA.

DOI： 10.1016/j.joca.2017.07.012

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Analysis of CCN4 function in bone was assessed using both gain and loss of function approaches. In mice this was done by genetic engineering and homologous recombination to create mice with complete ablation of the protein. For human skeletal cells adenoviral gene transfer and shRNA were used for gain and loss of function respectively. Here we describe procedures used to make and then analyze osteogenic and osteoclastic cells with or without CCN4 to determine its role in osteogenic differentiation.

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The small proteoglycan biglycan (Bgn) is highly expressed in the organic matrix of bone and plays a role in bone formation. Previous work implicated Bgn in vessel growth during bone healing [1]. By infusing barium sulfate (BaSO4) into WT and Bgn-deficient mice we discovered the positive effect of Bgn in modulating angiogenesis during fracture healing. Using micro-computed tomography angiography we found significant differences in the vessel size and volume among other parameters. To further understand the mechanistic basis for this, we explored the relationship between Bgn and the anti-angiogenic protein endostatin. Immunohistochemistry (IHC) showed co-localization of Bgn and endostatin in regions of bone formation, with increased endostatin staining in Bgn-KO compared to WT at 14 days post-fracture. To further elucidate the relationship between Bgn and endostatin, an endothelial cell tube formation assay was used. This study showed that endothelial cells treated with endostatin had significantly decreased vessel length and vessel branches compared to untreated cells, while cells treated with endostatin and Bgn at a 1:1 M ratio had vessel length and vessel branches comparable to untreated cells. This indicated that Bgn was able to mitigate the inhibitory effect of endostatin on endothelial cell growth. In summary, these results suggest that Bgn is needed for proper blood vessel formation during fracture healing, and one mechanism by which Bgn impacts angiogenesis is through inhibition of endostatin.

DOI： 10.1016/j.matbio.2016.03.008

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The CCN family of proteins plays important roles in development and homeostasis of bone and cartilage. To understand the role of CCN4 in chondrogenesis, human bone marrow stromal cells (hBMSCs) were transduced with CCN4 adenovirus (adCCN4) or siRNA to CCN4 (siCCN4) in the presence or absence of transforming growth factor-β3 (TGF-β3). Overexpression of CCN4 enhanced TGF-β3-induced SMAD2/3 phosphorylation and chondrogenesis of hBMSCs in an in vitro assay using a micromass culture model. On the other hand, knockdown of CCN4 inhibited the TGF-β3-induced SMAD2/3 phosphorylation and synthesis of cartilage matrix in micromass cultures of hBMSCs. Immunoprecipitation-western blot analysis revealed that CCN4 bound to TGF-β3 and regulated the ability of TGF-β3 to bind to hBMSCs. In vivo analysis confirmed there was a significant decrease in the gene expression levels of chondrocyte markers in cartilage samples from Ccn4-knock out (KO) mice, compared to those from wild type (WT) control. In order to investigate the regenerative properties of the articular cartilage in Ccn4-KO mice, articular cartilage defects were surgically performed in the knee joints of young mice, and the results showed that the cartilage was partially repaired in WT mice, but not in Ccn4-KO mice. In conclusion, these results show, for the first time, that CCN4 has a positive influence on chondrogenic differentiation by modulating the effects of TGF-β3.

DOI： 10.1016/j.bone.2015.11.007

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

WISP1/CCN4 (hereafter referred to as WISP1), a member of the CCN family, is found in mineralized tissues and is produced by osteoblasts and their precursors. In this study, Wisp1-deficient (Wisp1(-/-)) mice were generated. Using dual-energy x-ray absorptiometry, we showed that by 3 months, the total bone mineral density of Wisp1(-/-) mice was significantly lower than that of WT mice. Further investigation by micro-computed tomography showed that female Wisp1(-/-) mice had decreased trabecular bone volume/total volume and that both male and female Wisp1(-/-) mice had decreased cortical bone thickness accompanied by diminished biomechanical strength. The molecular basis for decreased bone mass in Wisp1(-/-) mice arises from reduced bone formation likely caused by osteogenic progenitors that differentiate poorly compared with WT cells. Osteoclast precursors from Wisp1(-/-) mice developed more tartrate-resistant acid phosphatase-positive cells in vitro and in transplants, suggesting that WISP1 is also a negative regulator of osteoclast differentiation. When bone turnover (formation and resorption) was induced by ovariectomy, Wisp1(-/-) mice had lower bone mineral density compared WT mice, confirming the potential for multiple roles for WISP1 in controlling bone homeostasis. Wisp1(-/-) bone marrow stromal cells had reduced expression of β-catenin and its target genes, potentially caused by WISP1 inhibition of SOST binding to LRP6. Taken together, our data suggest that the decreased bone mass found in Wisp1(-/-) mice could potentially be caused by an insufficiency in the osteodifferentiation capacity of bone marrow stromal cells arising from diminished Wnt signaling, ultimately leading to altered bone turnover and weaker biomechanically compromised bones.

DOI： 10.1074/jbc.M114.628818

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Matrix proteoglycans such as biglycan (Bgn) dominate skeletal tissue and yet its exact role in regulating bone function is still unclear. In this paper we describe the potential role of (Bgn) in the fracture healing process. We hypothesized that Bgn could regulate fracture healing because of previous work showing that it can affect normal bone formation. To test this hypothesis, we created fractures in femurs of 6-week-old male wild type (WT or Bgn+/0) and Bgn-deficient (Bgn-KO or Bgn-/0) mice using a custom-made standardized fracture device, and analyzed the process of healing over time. The formation of a callus around the fracture site was observed at both 7 and 14 days post-fracture in WT and Bgn-deficient mice and immunohistochemistry revealed that Bgn was highly expressed in the fracture callus of WT mice, localizing within woven bone and cartilage. Micro-computed tomography (μCT) analysis of the region surrounding the fracture line showed that the Bgn-deficient mice had a smaller callus than WT mice. Histology of the same region also showed the presence of less cartilage and woven bone in the Bgn-deficient mice compared to WT mice. Picrosirius red staining of the callus visualized under polarized light showed that there was less fibrillar collagen in the Bgn-deficient mice, a finding confirmed by immunohistochemistry using antibodies to type I collagen. Interestingly, real time RT-PCR of the callus at 7 days post-fracture showed a significant decrease in relative vascular endothelial growth factor A (VEGF) gene expression by Bgn-deficient mice as compared to WT. Moreover, VEGF was shown to bind directly to Bgn through a solid-phase binding assay. The inability of Bgn to directly enhance VEGF-induced signaling suggests that Bgn has a unique role in regulating vessel formation, potentially related to VEGF storage or stabilization in the matrix. Taken together, these results suggest that Bgn has a regulatory role in the process of bone formation during fracture healing, and further, that reduced angiogenesis could be the molecular basis.

DOI： 10.1016/j.matbio.2013.12.004

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Prostate cancer (PC) is a leading cause of death in men however the factors that regulate its progression and eventual metastasis to bone remain unclear. Here we show that WISP1/CCN4 expression in prostate cancer tissues was up-regulated in early stages of the disease and, further, that it correlated with increased circulating levels of WISP1 in the sera of patients at early stages of the disease. WISP1 was also elevated in the mouse prostate cancer model TRAMP in the hypoplastic diseased tissue that develops prior to advanced carcinoma formation. When the ability of anti-WISP1 antibodies to reduce the spread of PC3-Luc cells to distant sites was tested it showed that twice weekly injections of anti-WISP1 antibodies reduced the number and overall size of distant tumors developed after intracardiac (IC) injection of PC3-Luc cells in mice. The ability of antibodies against WISP1 to inhibit growth of PC3-Luc cancer cells in mice was also evaluated and showed that twice weekly injections of anti-WISP1 antibodies reduced local tumor growth when examined in xenografts. To better understand the mechanism of action, the migration of PC3-Luc cells through membranes with or without a Matrigel™ barrier showed the cells were attracted to WISP1, and that this attraction was inhibited by treatment with anti-WISP1 antibodies. We also show the expression of WISP1 at the bone-tumor interface and in the stroma of early grade cancers suggested WISP1 expression is well placed to play roles in both fostering growth of the cancer and its spread to bone. In summary, the up-regulation of WISP1 in the early stages of cancer development coupled with its ability to inhibit spread and growth of prostate cancer cells makes it both a potential target and an accessible diagnostic marker for prostate cancer.

DOI： 10.1371/journal.pone.0071709

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

CCN2 (also known as connective tissue growth factor) interacts with several growth factors involved in endochondral ossification via its characteristic four modules and modifies the effect of such growth factors. Presently we investigated whether CCN2 interacts with fibroblast growth factor 2 (FGF2). Solid-phase binding assay, immunoprecipitation-Western blot analysis, and surface plasmon resonance (SPR) spectroscopy revealed that the C-terminal module of CCN2 (CT) directly bound to FGF2 with a dissociation constant of 5.5 nm. Next, we examined the combinational effects of CCN2 and FGF2 on the proliferation of and matrix metalloproteinase (MMP)-9 and -13 productions by cultured chondrocytes. FGF2 promoted not only the proliferation but also the production of MMP9 and -13, however, combined of FGF2 with CT module nullified the enhancement of both MMP productions and proliferation. To clarify the mechanism, we investigated the binding of CCN2 or its CT module to FGF receptor 1. As a result, we found that CCN2 bound to FGF receptor 1 with a dissociation constant of 362 nm, whereas the CT module did not. In addition, when we tested FGF signaling in chondrocytic HCS-2/8 cells stimulated by the combination of FGF2 with CT module, the level of ERK1/2, p38 MAPK, and c-Jun N-terminal kinase phosphorylation was decreased compared with that found with FGF2 alone. These findings suggest that CCN2 may regulate the proliferation and matrix degradation of chondrocytes by forming a complex with FGF2 as a novel modulator of FGF2 functions.

DOI： 10.1210/en.2011-0234

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Both CCN family 2/connective tissue growth factor (CCN2/CTGF) and bone morphogenetic protein (BMP)-2 play an important role in cartilage metabolism. We evaluated whether or not CCN2 would interact with BMP-2, and examined the combination effect of CCN2 with BMP-2 (CCN2-BMP-2) on the proliferation and differentiation of chondrocytes. Immunoprecipitation-western blotting analysis, solid-phase binding assay and surface plasmon resonance (SPR) spectroscopy showed that CCN2 directly interacted with BMP-2 with a dissociation constant of 0.77 nM as evaluated by SPR. An in vivo study revealed that CCN2 was co-localized with BMP-2 at the pre-hypertrophic region in the E18.5 mouse growth plate. Interestingly, CCN2-BMP-2 did not affect the BMP-2/CCN2-induced phosphorylation of p38 MAPK but caused less phosphorylation of ERK1/2 in cultured chondrocytes. Consistent with these results, cell proliferation assay showed that CCN2-BMP-2 stimulated cell growth to a lesser degree than by either CCN2 or BMP-2 alone, whereas the expression of chondrocyte marker genes and proteoglycan synthesis, representing the mature chondrocytic phenotype, was increased collaboratively by CCN2-BMP-2 treatment in cultured chondrocytes. These findings suggest that CCN2 may regulate the proliferating and differentiation of chondrocytes by forming a complex with BMP-2 as a novel modulator of BMP signalling.

DOI： 10.1093/jb/mvn159

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掲載種別：研究論文（学術雑誌）  

Vascular endothelial growth factor (VEGF) is essential for establishing vascularization and regulating chondrocyte development and survival. We have demonstrated that VEGF regulates the expression of CCN2/connective tissue growth factor (CCN2/CTGF) an essential mediator of cartilage development and angiogenesis, suggesting that CCN2 functions in down-stream of VEGF, and that VEGF function is mediated in part by CCN2. On the other hand, the phenotype of Ccn2 mutant growth plates, which exhibit decreased expression of VEGF in the hypertrophic zone, indicates that Vegf expression is dependent on Ccn2 expression as well. Therefore, we investigated the molecular mechanisms underlying the induction of VEGF by CCN2 using a human chondrocytic cell line, HCS-2/8. Hypoxic stimulation (5% O2) of HCS-2/8 cells increased VEGF mRNA levels by ∼ 8 fold within 6 h as compared with the cells cultured under normoxia. In addition, VEGF expression was further up-regulated under hypoxia in HCS-2/8 cells transfected with a Ccn2 expression plasmid. Hypoxia-inducible factor (HIF)-1α mRNA and protein levels were increased by stimulation with recombinant CCN2 (rCCN2). Furthermore, the activity of a VEGF promoter that contained a HIF-1 binding site was increased in HCS-2/8, when the cells were stimulated by rCCN2. These results suggest that CCN2 regulates the expression of VEGF at a transcriptional level by promoting HIF-1α activity. In fact, HIF-1α was detected in the nuclei of proliferative and pre-hypertrophic chondrocytes of wild-type mice, whereas it was not detected in Ccn2 mutant chondrocytes in vivo. This activation cascade from CCN2 to VEGF may therefore play a critical role in chondrocyte development and survival. © 2008 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bone.2008.08.125

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

われわれの教室では、高齢者の歯列欠損補綴に際し、欠損や口腔内の問題により患者がどのような障害をきたしているかを理解し、個々の患者の全身状態、高齢者特有の社会的背景、精神的・心理的特徴を考慮に入れた臨床決断を行うための思考能力を開発することを目標としたチュートリアル教育を行った。対象は、平成17年度岡山大学歯学部4年次生57名である。チュートリアル演習を行うため、これらの学生を少人数のグループ(7〜8名)に分けた。次に、グループ単位で歯列欠損を有する高齢患者の診療を見学させ、医療面接によりその患者に生じている医学的、精神・社会的な問題や苦悩について実際に質問、抽出させた。この患者見学を起点とし、本患者の問題点や苦悩を解決するための方策について、270分×5回の問題発見解決型チュートリアル演習を行った。毎回の学習後に各グループ構成員に対して本学習の行動目標に当たる9項目:思考能力(4項目)、分析力(1項目)、概念を創出する力(2項目)、学習態度(2項目)について4段階で評価し、各項目の中央値の経時的変化を本学習の効果として評価した。その結果、評価した9項目すべてにおいて、結果の中央値が演習最終日までの期間に有意に上昇し、個々の患者の全身状態、高齢者特有の社会的背景、精神的・心理的特徴を考慮に入れた臨床決断を行うという本学習目標に対応して教育効果が得られたことが示された。(著者抄録)

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記述言語：日本語   出版者・発行元：岡山歯学会  

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Mechanical stress plays an important role in the cartilage metabolism. The aim of this study is to determine the influence of mechanical load magnitude and frequency on cartilage metabolism in terms of the expression of hypertrophic chondrocyte-specific gene product 24/connective tissue growth factor/CCN family 2 (Hcs24/CTGF/CCN2), as an essential mediator of extracellular matrix (ECM) production. When a human chondrocytic cell line, HCS-2/8 was exposed to uni-axial cyclic mechanical force (6% elongation, 10 times/min) only for 30 min, the expression level of Hcs24/CTGF/CCN2 (CCN2) increased, and c-Jun N-terminal protein kinase (JNK) was activated. These findings suggest that stretch-induced CCN2 may be mediated by the JNK pathway. When HCS-2/8 cells were subjected to cyclic tension force at 15 kPa, 30 cycles/min, which has been reported to be a degradation force for HCS-2/8 cells, the expressions of CCN2 and aggrecan were inhibited, and such expressions remained unchanged in rabbit hyaline costal cartilage cells. However, these expressions increased in rabbit meniscus tissue cells. These findings suggest that the sensitivity of mechanical stretch may be different depending on the type of cells. Furthermore, CCN2 was co-localized with aggrecan in this meniscus tissue region exposed to mechanical stress in vivo. These findings suggest that CCN2 induced by mechanical stress may therefore play some role in meniscus growth and regeneration.

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記述言語：日本語   出版者・発行元：(NPO)日本口腔科学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(株)ジェフコーポレーション  

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記述言語：日本語   出版者・発行元：(一社)日本老年歯科医学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(一社)日本老年歯科医学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：日本結合組織学会  

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記述言語：日本語   出版者・発行元：(一社)日本歯科医学教育学会  

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記述言語：日本語   出版者・発行元：(一社)日本骨代謝学会  

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記述言語：日本語   出版者・発行元：(一社)日本骨代謝学会  

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記述言語：日本語   出版者・発行元：(公社)日本補綴歯科学会  

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記述言語：日本語   出版者・発行元：(公社)日本補綴歯科学会  

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記述言語：日本語   出版者・発行元：(公社)日本補綴歯科学会  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：WILEY-BLACKWELL  

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記述言語：日本語   出版者・発行元：(一社)歯科基礎医学会  

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記述言語：日本語   出版者・発行元：(公社)日本補綴歯科学会  

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J-GLOBAL

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：WILEY-BLACKWELL  

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記述言語：日本語   出版者・発行元：(公社)日本生化学会  

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記述言語：日本語   出版者・発行元：(一社)日本骨代謝学会  

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記述言語：日本語   出版者・発行元：(公社)日本生化学会  

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記述言語：日本語   出版者・発行元：(一社)日本骨代謝学会  

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記述言語：日本語   出版者・発行元：岡山歯学会  

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記述言語：日本語   出版者・発行元：(公社)日本補綴歯科学会  

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J-GLOBAL

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記述言語：日本語   出版者・発行元：(公社)日本生化学会  

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記述言語：日本語   出版者・発行元：(一社)日本老年歯科医学会  

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記述言語：日本語   出版者・発行元：(一社)日本骨代謝学会  

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記述言語：日本語   出版者・発行元：(一社)日本骨代謝学会  

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開催年月日： 2019年8月3日 - 2019年8月4日

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：東京  

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開催年月日： 2019年2月16日 - 2019年2月17日

記述言語：日本語   会議種別：ポスター発表  

開催地：岡山  

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開催年月日： 2019年1月21日

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：岡山  

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開催年月日： 2018年12月1日 - 2021年12月2日

記述言語：日本語   会議種別：ポスター発表  

開催地：新潟  

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開催年月日： 2018年12月1日 - 2018年12月2日

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：新潟  

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開催年月日： 2018年8月29日

記述言語：日本語   会議種別：口頭発表（招待・特別）  

開催地：岡山  

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開催年月日： 2018年7月27日 - 2018年7月28日

記述言語：日本語   会議種別：ポスター発表  

開催地：福島  

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開催年月日： 2018年7月

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：郡山  

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開催年月日： 2018年1月

記述言語：日本語  

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開催年月日： 2017年11月10日 - 2017年11月11日

記述言語：日本語   会議種別：ポスター発表  

開催地：札幌  

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開催年月日： 2017年11月10日 - 2017年11月11日

記述言語：日本語   会議種別：ポスター発表  

開催地：札幌  

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開催年月日： 2017年11月10日 - 2017年11月11日

記述言語：日本語   会議種別：ポスター発表  

開催地：札幌  

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開催年月日： 2017年9月

記述言語：日本語  

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開催年月日： 2017年8月26日 - 2017年8月27日

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：山口  

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開催年月日： 2017年7月28日 - 2017年7月29日

記述言語：日本語   会議種別：ポスター発表  

開催地：松本  

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開催年月日： 2017年7月28日 - 2017年7月29日

記述言語：日本語   会議種別：ポスター発表  

開催地：松本  

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開催年月日： 2017年7月28日 - 2017年7月29日

記述言語：日本語   会議種別：口頭発表（一般）  

開催地：松本  

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開催年月日： 2017年7月

記述言語：日本語  

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開催年月日： 2017年7月

記述言語：日本語  

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開催年月日： 2017年7月

記述言語：日本語  

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開催年月日： 2017年6月14日 - 2017年6月16日

記述言語：日本語   会議種別：ポスター発表  

開催地：名古屋  

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開催年月日： 2017年6月

記述言語：日本語  

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開催年月日： 2016年7月

記述言語：日本語  

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開催年月日： 2016年7月

記述言語：日本語  

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開催年月日： 2016年7月

記述言語：日本語  

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開催年月日： 2016年7月

記述言語：日本語  

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開催年月日： 2016年6月

記述言語：日本語  

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開催年月日： 2013年9月

記述言語：日本語  

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開催年月日： 2013年5月

記述言語：日本語  

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開催年月日： 2010年12月

記述言語：日本語  

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開催年月日： 2009年7月

記述言語：日本語  

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開催年月日： 2009年

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開催年月日： 2009年

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開催年月日： 2008年11月

記述言語：日本語  

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開催年月日： 2008年10月

記述言語：日本語  

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開催年月日： 2008年6月

記述言語：日本語  

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開催年月日： 2008年4月

記述言語：日本語  

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開催年月日： 2008年

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開催年月日： 2007年11月

記述言語：日本語  

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開催年月日： 2007年9月

記述言語：日本語  

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開催年月日： 2007年6月

記述言語：日本語  

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開催年月日： 2007年6月

記述言語：日本語  

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開催年月日： 2007年

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開催年月日： 2006年

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