Tokushima University / Educator and Researcher Directory --- Matsumoto, Toshio

Personal Web Page

https://researchmap.jp/read0007636 (researchmap)

Field of Study

○	Metabolic Pathology
○	Bone and Calcium Metabolism
○	Endocrinology

Subject of Study

○	代謝疾患に伴う血管障害の病因と治療に関する研究 (diabetes, atherosclerosis)
○	血液·骨髄増殖性疾患に伴う骨破壊の病態と治療に関する研究 (多発性骨髄腫, bone metastasis)
○	内分泌疾患の病因·診断および治療に関する分子医学的研究 (ホルモンの作用機序, 骨カルシウム代謝学)

Book / Paper

(See https://researchmap.jp/read0007636 (researchmap) for Published Book / Papers / Presentations.)

Book:

1.	Toshio Matsumoto : 骨代謝疾患, Medic Media, Apr. 2013.
2.	Itsuro Endo, Masahiro Abe and Toshio Matsumoto : 骨転移の分子標的治療薬, Dec. 2012.
3.	Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : テリパラチド皮下注製剤の骨形成促進作用とその使用法, MEDICAL VIEW CO., LTD., Jun. 2012.
4.	Kumiko Kagawa, Masahiro Abe and Toshio Matsumoto : がん骨転移治療―ビスフォスフォネート治療によるBone Management, SENTAN IGAKU-SHA, Mar. 2012.
5.	Shingen Nakamura, Masahiro Abe and Toshio Matsumoto : 新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に), Mar. 2012.
6.	Toshio Matsumoto : 内分泌疾患最近の動向, メディカル·ジャーナル社, 2011.
7.	Itsuro Endo and Toshio Matsumoto : 不動性骨粗鬆症, Oct. 2010.
8.	Itsuro Endo and Toshio Matsumoto : 新規開発中の治療薬, 医薬ジャーナル, 東京, Oct. 2010.
9.	Itsuro Endo and Toshio Matsumoto : 不動性骨粗鬆症, Oct. 2010.
10.	Masashi Akaike and Toshio Matsumoto : V 実験的研究 6．血管内皮障害―nitric oxideの観点から―, KINPODO, INC., Oct. 2010.
11.	Itsuro Endo and Toshio Matsumoto : ビタミンDの古典的作用-基礎と臨床からー, Jul. 2010.
12.	Itsuro Endo and Toshio Matsumoto : [Hormones and osteoporosis update. Vitamin D and bone]., Jul. 2009. (Summary) Calcium homeostasis is maintained by parathyroid hormone and vitamin D. Mechanisms of action of these calcium-regulating hormones have been extensively examined, and the intracellular signaling pathways as well as transcriptional regulation of their target genes have been elucidated. Epidemiological studies revealed the importance of vitamin D sufficiency, and efforts have been made to implement the diagnostic criteria for vitamin D insufficiency. As a therapeutic agent, a new active vitamin D analog with anti-fracture efficacy has been developed for the treatment of osteoporosis. (Keyword) Accidental Falls / Calcium / Drug Design / Homeostasis / Humans / Osteoporosis / RANK Ligand / Receptors, Calcitriol / Retinoid X Receptors / Signal Transduction / Transcription, Genetic / Vitamin D / Vitamin D Deficiency (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19567986 ● Search Scopus @ Elsevier (PMID): 19567986 (PubMed: 19567986)
13.	Sumiko Yoshida, Itsuro Endo and Toshio Matsumoto : 骨代謝 (ホルモンの病態異常と臨床検査) -- (各論多臓器,組織におけるホルモン相互間作用), IGAKU-SHOIN Ltd.Tokyo,Japan, 2008. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523669554734027776 (CiNii: 1523669554734027776)
14.	Masahiro Abe and Toshio Matsumoto : 第2章サイトカインによる生体調節機構 3)代謝, YODOSHA CO., LTD., Tokyo, Nov. 2005. (Keyword) 骨芽細胞分化 / canonical Wnt 経路 / Wnt 阻害因子 / sFRP-2 / 多発性骨髄腫
15.	Masahiro Abe and Toshio Matsumoto : A mechanism of bone destruction in multiple myeloma, Medical Review Co.,Ltd, Osaka, Nov. 2005. (Keyword) 骨髄腫 / 破骨細胞 / RANKL / MIP 1 / 骨芽細胞
16.	Masahiro Abe and Toshio Matsumoto : Bone Marrow in Cancer Metastasis, Shujunsha Co.Ltd., Tokyo, Jul. 2005. (Keyword) 骨転移 / 多発性骨髄腫 / 骨髄 / 破骨細胞 / 骨芽細胞
17.	Masahiro Abe and Toshio Matsumoto : 癌と骨組織との相互作用, Nakayama-Shoten Co., Ltd., Tokyo, Oct. 2004. (Keyword) multiple myeloma / osteoclast / RANKL / MIP-1 / osteoblast
18.	Toshihiro Hashimoto, Masahiro Abe and Toshio Matsumoto : [Biochemical markers in bone metastasis]., 癌と化学療法社, Tokyo, Jul. 2004. (Summary) Certain types of cancers have a strong propensity to metastasize to bone, which requires combination of multiple factors responsible for the different steps of metastasis. Bone metabolic markers are now widely used in clinical practice and give useful information on the ongoing bone metabolism, reflecting the activity of bone-resorbing osteoclasts and bone-forming osteoblasts. Bone markers have a potential as diagnostic tools for bone metastasis, and are useful in monitoring the response to anticancer as well as antiresorptive therapies. Since bone metabolic markers alone are insufficient for the diagnosis and assessment of bone metastasis, it is important to combine bone markers with tumor-related markers and imaging studies such as scintigraphy and MRI. More recently, soluble receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) have been implicated as markers for osteoclastogenic activity. Serum levels of these factors and/or their ratios may provide additional information on the severity of bone disease and the prognosis. (Keyword) bone metastasis / Bone markers / Osteoclastogenesis (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15272580 ● Summary page in Scopus @ Elsevier: 2-s2.0-3242671537 (PubMed: 15272580, Elsevier: Scopus)
19.	Toshihiro Hashimoto, Masahiro Abe and Toshio Matsumoto : 癌に伴う骨病変の病態と治療, Nankodo, Tokyo, Apr. 2004. (Keyword) bone metastasis / bone marker / bisphosphonate
20.	Yuichi Fujinaka and Toshio Matsumoto : 糖尿病最新の治療 2004-2006, Nankodo, Tokyo, Feb. 2004.
21.	Yuichi Fujinaka and Toshio Matsumoto : 糖尿病, 2000.
22.	Yuichi Fujinaka and Toshio Matsumoto : 糖尿病性昏睡, 2000.

Academic Paper (Judged Full Paper):

1.	Mai Kanai, Byambasuren Ganbaatar, Itsuro Endo, Yukiyo Ohnishi, Jumpei Teramachi, Hirofumi Tenshin, Yoshiki Higa, Masahiro Hiasa, Yukari Mitsui, Tomoyo Hara, Shiho Masuda, Hiroki Yamagami, Yuki Yamaguchi, Ken-ichi Aihara, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Toshio Matsumoto and Masahiro Abe : Inflammatory Cytokine-Induced Muscle Atrophy and Weakness Can Be Ameliorated by an Inhibition of TGF-β-Activated Kinase-1, International Journal of Molecular Sciences, 25, 11, 5715, 2024. (Summary) Chronic inflammation causes muscle wasting. Because most inflammatory cytokine signals are mediated via TGF-β-activated kinase-1 (TAK1) activation, inflammatory cytokine-induced muscle wasting may be ameliorated by the inhibition of TAK1 activity. The present study was undertaken to clarify whether TAK1 inhibition can ameliorate inflammation-induced muscle wasting. SKG/Jcl mice as an autoimmune arthritis animal model were treated with a small amount of mannan as an adjuvant to enhance the production of TNF-α and IL-1β. The increase in these inflammatory cytokines caused a reduction in muscle mass and strength along with an induction of arthritis in SKG/Jcl mice. Those changes in muscle fibers were mediated via the phosphorylation of TAK1, which activated the downstream signaling cascade via NF-κB, p38 MAPK, and ERK pathways, resulting in an increase in myostatin expression. Myostatin then reduced the expression of muscle proteins not only via a reduction in MyoD1 expression but also via an enhancement of Atrogin-1 and Murf1 expression. TAK1 inhibitor, LL-Z1640-2, prevented all the cytokine-induced changes in muscle wasting. Thus, TAK1 inhibition can be a new therapeutic target of not only joint destruction but also muscle wasting induced by inflammatory cytokines. (Keyword) Animals / MAP Kinase Kinase Kinases / Muscular Atrophy / Mice / cytokinesis / Muscle Weakness / Myostatin / Muscle Proteins / Tumor Necrosis Factor-alpha / NF-kappa B / inflammation / signal transduction / Tripartite Motif Proteins / Disease Models, Animal / Interleukin-1beta / phosphorylation / Muscle, Skeletal / Zearalenone (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms25115715 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38891908 ● Summary page in Scopus @ Elsevier: 2-s2.0-85195855255 (DOI: 10.3390/ijms25115715, PubMed: 38891908, Elsevier: Scopus)
2.	Marianna Ranieri, Ines Angelini, Mariagrazia DAgostino, Annarita Di Mise, Mariangela Centrone, Maria Venneri, Angela Ferrulli, Maria Mastrodonato, Grazia Tamma, Itsuro Endo, Seiji Fukumoto, Toshio Matsumoto and Giovanna Valenti : In vivo treatment with calcilytic of CaSR knock-in mice ameliorates renal phenotype reversing downregulation of the vasopressin-AQP2 pathway, The Journal of Physiology, 1-18, 2024. (Summary) High concentrations of urinary calcium counteract vasopressin action via the activation of the Calcium-Sensing Receptor (CaSR) expressed in the luminal membrane of the collecting duct cells, which impairs the trafficking of aquaporin-2 (AQP2). In line with these findings, we provide evidence that, with respect to wild-type mice, CaSR knock-in (KI) mice mimicking autosomal dominant hypocalcaemia, display a significant decrease in the total content of AQP2 associated with significantly higher levels of AQP2 phosphorylation at Ser261, a phosphorylation site involved in AQP2 degradation. Interestingly, KI mice also had significantly higher levels of phosphorylated p38MAPK, a downstream effector of CaSR and known to phosphorylate AQP2 at Ser261. Moreover, ATF1 phosphorylated at Ser63, a transcription factor downstream of p38MAPK, was significantly higher in KI. In addition, KI mice had significantly higher levels of AQP2-targeting miRNA137 consistent with a post-transcriptional downregulation of AQP2. In vivo treatment of KI mice with the calcilytic JTT-305, a CaSR antagonist, increased AQP2 expression and reduced AQP2-targeting miRNA137 levels in KI mice. Together, these results provide direct evidence for a critical role of CaSR in impairing both short-term vasopressin response by increasing AQP2-pS261, as well as AQP2 abundance, via the p38MAPK-ATF1-miR137 pathway. KEY POINTS: Calcium-Sensing Receptor (CaSR) activating mutations are the main cause of autosomal dominant hypocalcaemia (ADH) characterized by inappropriate renal calcium excretion leading to hypocalcaemia and hypercalciuria. Current treatments of ADH patients with parathyroid hormone, although improving hypocalcaemia, do not improve hypercalciuria or nephrocalcinosis. In vivo treatment with calcilytic JTT-305/MK-5442 ameliorates most of the ADH phenotypes of the CaSR knock-in mice including hypercalciuria or nephrocalcinosis and reverses the downregulation of the vasopressin-sensitive aquaporin-2 (AQP2) expression, providing direct evidence for a critical role of CaSR in impairing vasopressin response. The beneficial effect of calcilytic in reducing the risk of renal calcification may occur in a parathyroid hormone-independent action through vasopressin-dependent inhibition of cAMP synthesis in the thick ascending limb and in the collecting duct. The amelioration of most of the abnormalities in calcium metabolism including hypercalciuria, renal calcification, and AQP2-mediated osmotic water reabsorption makes calcilytic a good candidate as a novel therapeutic agent for ADH. (Keyword) calcium-sensing receptor / AQP2 (Link to Publication Site) ● Publication site (DOI): 10.1113/JP284233 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38367250 ● Search Scopus @ Elsevier (PMID): 38367250 ● Search Scopus @ Elsevier (DOI): 10.1113/JP284233 (DOI: 10.1113/JP284233, PubMed: 38367250)
3.	Yudai Joko, Yoko Yamamoto, Tatsuya Takemoto, Masahiro Abe, Toshio Matsumoto, Seiji Fukumoto and Shun Sawatsubashi : VDR is an essential regulator of hair follicle regression through the progression of cell death, Life Science Alliance, 6, 11, e202302014, 2023. (Summary) Vitamin D receptor (VDR) is essential for hair follicle homeostasis as its deficiency induces hair loss, although the mechanism involved remains unknown. Our research shows that, in -knockout mice, the hair cycle is halted during the catagen stage, preceding alopecia. In addition, in -knockout hair follicles, epithelial strands that normally regress during the catagen phase persist as "surviving epithelial strands." Single-cell RNA sequencing analysis suggests that these surviving epithelial strands are formed by cells in the lower part of the hair follicle. These findings emphasize the importance of the regression phase in hair follicle regeneration and establish VDR as a regulator of the catagen stage. (Keyword) Animals / Mice / Cell Death / Hair Follicle / Homeostasis / Mice, Knockout / Receptors, Calcitriol (Link to Publication Site) ● Publication site (DOI): 10.26508/lsa.202302014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37673445 ● Search Scopus @ Elsevier (PMID): 37673445 ● Search Scopus @ Elsevier (DOI): 10.26508/lsa.202302014 (DOI: 10.26508/lsa.202302014, PubMed: 37673445)
4.	Shiho Masuda, Tomoyo Hara, Hiroki Yamagami, Yukari Mitsui, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Harada, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura, Akio Kuroda, Itsuro Endo, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Vascular Endothelial Function Is Associated with eGFR Slope in Female and Non-Smoking Male Individuals with Cardiovascular Risk Factors: A Pilot Study on the Predictive Value of FMD for Renal Prognosis., Journal of Atherosclerosis and Thrombosis, 2023. (Summary) In individuals with cardiovascular risk factors, evaluation of vascular endothelial function enables prediction of renal prognosis in females and non-smoking males. (Tokushima University Institutional Repository) ● Metadata: 2011012 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.63987 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37081616 ● Search Scopus @ Elsevier (PMID): 37081616 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63987 (Tokushima University Institutional Repository: 2011012, DOI: 10.5551/jat.63987, PubMed: 37081616)
5.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Emiko Nakaue, Mariko Tanaka, Sooha Kim, Motosumi Nakagawa, Sou Shimizu, Kotaro Tanimoto, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : The Xanthine Oxidase Inhibitor Febuxostat Suppresses Adipogenesis and Activates Nrf2., Antioxidants, 12, 1, 2023. (Summary) Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in purine catabolism that acts as a novel regulator of adipogenesis. In pathological states, xanthine oxidoreductase activity increases to produce excess reactive oxygen species (ROS). The nuclear factor erythroid 2-related factor 2 (Nrf2) is a critical inducer of antioxidants, which is bound and repressed by a kelch-like ECH-associated protein 1 (Keap1) in the cytoplasm. The Keap1-Nrf2 axis appears to be a major mechanism for robust inducible antioxidant defenses. Here, we demonstrate that febuxostat, a xanthine oxidase inhibitor, alleviates the increase in adipose tissue mass in obese mouse models with a high-fat diet or ovariectomy. Febuxostat disrupts in vitro adipocytic differentiation in adipogenic media. Adipocytes appeared at day 7 in absence or presence of febuxostat were 160.8 ± 21.2 vs. 52.5 ± 12.7 (p < 0.01) in 3T3L1 cells, and 126.0 ± 18.7 vs. 55.3 ± 13.4 (p < 0.01) in 10T1/2 cells, respectively. Adipocyte differentiation was further enhanced by the addition of hydrogen peroxide, which was also suppressed by febuxostat. Interestingly, febuxostat, but not allopurinol (another xanthine oxidase inhibitor), rapidly induced the nuclear translocation of Nrf2 and facilitated the degradation of Keap1, similar to the electrophilic Nrf2 activator omaveloxolone. These results suggest that febuxostat alleviates adipogenesis under oxidative conditions, at least in part by suppressing ROS production and Nrf2 activation. Regulation of adipocytic differentiation by febuxostat is expected to inhibit obesity due to menopause or overeating. (Tokushima University Institutional Repository) ● Metadata: 2011068 (Link to Publication Site) ● Publication site (DOI): 10.3390/antiox12010133 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36670994 ● Search Scopus @ Elsevier (PMID): 36670994 ● Search Scopus @ Elsevier (DOI): 10.3390/antiox12010133 (Tokushima University Institutional Repository: 2011068, DOI: 10.3390/antiox12010133, PubMed: 36670994)
6.	Bingzi Dong, Masahiro Hiasa, Yoshiki Higa, Yukiyo Ohnishi, Itsuro Endo, Takeshi Kondo, Yuichi Takashi, Maria Tsoumpra, Risa Kainuma, Shun Sawatsubashi, Hiroshi Kiyonari, Go Shioi, Hiroshi Sakaue, Tomoki Nakashima, Shigeaki Kato, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : Osteoblast/osteocyte-derived interleukin-11 regulates osteogenesis and systemic adipogenesis., Nature Communications, 13, 1, 2022. (Summary) did not exhibit any abnormalities. We demonstrate that osteoblast/osteocyte-derived IL-11 controls both osteogenesis and systemic adiposity in response to mechanical loading, an important insight for our understanding of osteoporosis and metabolic syndromes. (Keyword) Animals / Mice / Adipogenesis / Interleukin-11 / Obesity / Osteoblasts / Osteocytes / Osteogenesis / Mice, Knockout (Tokushima University Institutional Repository) ● Metadata: 2011671 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41467-022-34869-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36424386 ● Search Scopus @ Elsevier (PMID): 36424386 ● Search Scopus @ Elsevier (DOI): 10.1038/s41467-022-34869-3 (Tokushima University Institutional Repository: 2011671, DOI: 10.1038/s41467-022-34869-3, PubMed: 36424386)
7.	Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Hiroki Yamagami, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma Heparin Cofactor II Activity Is Inversely Associated with Hepatic Fibrosis of Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus., Journal of Atherosclerosis and Thrombosis, 2022. (Summary) Plasma HCII activity was inversely associated with clinical hepatic fibrosis indices including FIB-4 index, NFS and APRI and with the prevalence of advanced hepatic fibrosis in patients with T2DM. The results suggest that HCII can serve as a novel biomarker for assessment of hepatic fibrosis of NAFLD in patients with T2DM. (Tokushima University Institutional Repository) ● Metadata: 2011020 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.63752 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244745 ● Search Scopus @ Elsevier (PMID): 36244745 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.63752 (Tokushima University Institutional Repository: 2011020, DOI: 10.5551/jat.63752, PubMed: 36244745)
8.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, Masahiro Hiasa, Hirofumi Tenshin, A Oda, A Seki, Y Inoue, Kotaro Tanimoto, Yoshiki Higa, M Oura, K Sogabe, Takeshi Harada, Ryohei Sumitani, T Maruhashi, H Yamagami, Y Sawa, Itsuro Endo, K Tsuneyama, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Aberrant upregulation of the endogenous PP2A inhibitor CIP2A is vital for myeloma cell growth and survival, International Journal of Myeloma, 12, 2, 14-23, 2022. (Summary) <p>The serine/threonine kinase TAK1 is constitutively overexpressed and auto-phosphorylated in multiple myeloma (MM) cells. Protein phosphatase 2A (PP2A) is a major serine/threonine phosphatase which dephosphorylates proteins phosphorylated by various serine/threonine kinases to regulate multiple cellular functions. We recently reported that the serine/threonine kinase TGF-β-activated kinase-1 (TAK1) is highly expressed and auto-phosphorylated to mediate critical growth and survival signaling in MM cells. We demonstrate here that regulation of PP2A activity inversely affects the phosphorylation levels of TAK1 in MM cells, and that MM cells aberrantly overexpress cancerous inhibitor of PP2A (CIP2A), an endogenous inhibitor for PP2A. <i>CIP2A</i> gene silencing as well as treatment with the CIP2A inhibitor TD52 potently induced MM cell death along with suppression of TAK1 expression in MM cells. These results suggest the critical role of PP2A inactivation via CIP2A upregulation in TAK1 phosphorylation and its protein expression and thereby MM cell growth and survival, posing the CIP2A-PP2A axis as an important therapeutic target.</p> (Keyword) multiple myeloma / TAK1 / CIP2A / PP2A (Tokushima University Institutional Repository) ● Metadata: 2009992 (Link to Publication Site) ● Publication site (DOI): 10.57352/ijm.12.2_14 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390573947533793024 ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.12.2_14 (Tokushima University Institutional Repository: 2009992, DOI: 10.57352/ijm.12.2_14, CiNii: 1390573947533793024)
9.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Takeshi Harada, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, Tomoyo Hara, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Mechanical unloading aggravates bone destruction and tumor expansion in myeloma., Haematologica, 107, 3, 744-749, 2022. (Keyword) Bone Resorption / Humans / Multiple Myeloma / Osteoclasts / Osteolysis (Tokushima University Institutional Repository) ● Metadata: 2009605 (Link to Publication Site) ● Publication site (DOI): 10.3324/haematol.2021.278295 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34788982 ● Search Scopus @ Elsevier (PMID): 34788982 ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2021.278295 (Tokushima University Institutional Repository: 2009605, DOI: 10.3324/haematol.2021.278295, PubMed: 34788982)
10.	Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masahiro Hiasa, Yusuke Inoue, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : TGF-β-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-α and RANKL expression., Clinical & translational immunology, 11, 1, 2022. (Summary) TAK1 inhibition with LLZ may become a novel treatment strategy to effectively alleviate inflammasome-mediated inflammation and RANKL-induced osteoclastic bone destruction in joints alongside its potent suppression of TNF-α and IL-6 production and proteinase-mediated pathological processes in RA. (Tokushima University Institutional Repository) ● Metadata: 2010099 (Link to Publication Site) ● Publication site (DOI): 10.1002/cti2.1371 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35079379 ● Search Scopus @ Elsevier (PMID): 35079379 ● Search Scopus @ Elsevier (DOI): 10.1002/cti2.1371 (Tokushima University Institutional Repository: 2010099, DOI: 10.1002/cti2.1371, PubMed: 35079379)
11.	Yuichi Takashi, Shun Sawatsubashi, Itsuro Endo, Yukiyo Ohnishi, Masahiro Abe, Munehide Matsuhisa, Daiji Kawanami, Toshio Matsumoto and Seiji Fukumoto : Skeletal FGFR1 signaling is necessary for regulation of serum phosphate level by FGF23 and normal life span., Biochemistry and Biophysics Reports, 27, 101107, 2021. (Summary) Fibroblast growth factor (FGF) 23 produced by the bone is the principal hormone to regulate serum phosphate level. Serum FGF23 needs to be tightly regulated to maintain serum phosphate in a narrow range. Thus, we hypothesized that the bone has some phosphate-sensing mechanism to regulate the production of FGF23. Previously we showed that extracellular phosphate induces the phosphorylation of FGF receptor 1 (FGFR1) and FGFR1 signaling regulates the expression of , whose product works to increase FGF23 production . In this study, we show the significance of FGFR1 in the regulated FGF23 production and serum phosphate level . We generated late-osteoblast/osteocyte-specific -knockout mice ( ) by crossing the and the floxed mouse lines. We evaluated serum phosphate and FGF23 levels, the expression of in the bone, the body weight and life span. A selective ablation of aborted the increase of serum active full-length FGF23 and the enhanced expression of in the bone by a high phosphate diet. These mice showed more pronounced hyperphosphatemia compared with control mice. In addition, these mice fed with a control diet showed body weight loss after 23 weeks of age and shorter life span. These results reveal a novel significance of FGFR1 signaling in the phosphate metabolism and normal life span. (Tokushima University Institutional Repository) ● Metadata: 2009203 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrep.2021.101107 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34458594 ● Search Scopus @ Elsevier (PMID): 34458594 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrep.2021.101107 (Tokushima University Institutional Repository: 2009203, DOI: 10.1016/j.bbrep.2021.101107, PubMed: 34458594)
12.	Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma Heparin Cofactor II Activity Is Inversely Associated with Albuminuria and Its Annual Deterioration in Patients with Diabetes., Journal of Diabetes Investigation, 2021. (Summary) The plasma HCII activity was inversely and specifically associated with glomerular injury in patients with diabetes. The results suggest that HCII can serve as a novel predictive factor for early-stage DKD development, as represented by albuminuria. (Tokushima University Institutional Repository) ● Metadata: 2009447 (Link to Publication Site) ● Publication site (DOI): 10.1111/jdi.13602 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34043882 ● Search Scopus @ Elsevier (PMID): 34043882 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13602 (Tokushima University Institutional Repository: 2009447, DOI: 10.1111/jdi.13602, PubMed: 34043882)
13.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Asuka Oda, Ariunzaya Bat-Erdene, Takeshi Harada, Shingen Nakamura, Mohannad Ashtar, Sou Shimizu, Masami Iwasa, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK1 is a pivotal therapeutic target for tumor progression and bone destruction in myeloma, Haematologica, 106, 5, 1401-1413, 2021. (Summary) Along with the tumor progression, the bone marrow microenvironment is skewed in multiple myeloma (MM), which underlies the unique pathophysiology of MM and confers aggressiveness and drug resistance in MM cells. TGF-β-activated kinase-1 (TAK1) mediates a wide range of intracellular signaling pathways. We demonstrate here that TAK1 is constitutively overexpressed and phosphorylated in MM cells, and that TAK1 inhibition suppresses the activation of NF-κB, p38MAPK, ERK and STAT3 to decrease the expression of critical mediators for MM growth and survival, including PIM2, MYC, Mcl-1, IRF4, and Sp1, along with a substantial reduction in the angiogenic factor VEGF in MM cells. Intriguingly, TAK1 phosphorylation was also induced along with upregulation of vascular cell adhesion molecule-1 (VCAM-1) in bone marrow stromal cells (BMSCs) in cocultures with MM cells, which facilitated MM cell-BMSC adhesion while inducing IL-6 production and receptor activator of nuclear factor κ-Β ligand (RANKL) expression by BMSCs. TAK1 inhibition effectively impaired MM cell adhesion to BMSCs to disrupt the support of MM cell growth and survival by BMSCs. Furthermore, TAK1 inhibition suppressed osteoclastogenesis enhanced by RANKL in cocultures of bone marrow cells with MM cells, and restored osteoblastic differentiation suppressed by MM cells or inhibitory factors for osteoblastogenesis overproduced in MM. Finally, treatment with the TAK1 inhibitor LLZ1640-2 markedly suppressed MM tumor growth and prevented bone destruction and loss in mouse MM models. Therefore, TAK1 inhibition may be a promising therapeutic option targeting not only MM cells but also the skewed bone marrow microenvironment in MM. (Keyword) Animals / Bone Marrow Cells / MAP Kinase Kinase Kinases / Mice / Multiple Myeloma / NF-kappa B / Osteoclasts / Osteolysis / RANK Ligand / Tumor Microenvironment (Tokushima University Institutional Repository) ● Metadata: 2009431 (Link to Publication Site) ● Publication site (DOI): 10.3324/haematol.2019.234476 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32273474 ● Search Scopus @ Elsevier (PMID): 32273474 ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2019.234476 (Tokushima University Institutional Repository: 2009431, DOI: 10.3324/haematol.2019.234476, PubMed: 32273474)
14.	Toshio Matsumoto and Itsuro Endo : RANKL as a target for the treatment of osteoporosis, Journal of Bone and Mineral Metabolism, 39, 1, 91-105, 2021. (Summary) Osteoporosis is characterized by compromised bone strength, predisposing to an increased risk of fracture. Because bone is constantly remodeled, and bone mass and structure are determined by the balance between bone resorption and bone formation, it is important to maintain normal bone turnover. Therefore, therapies that reduce bone resorption have been the mainstream of osteoporosis treatment. Receptor activator of nuclear factor-kappa B ligand (RANKL)-RANK signaling was found to play a pivotal role in the regulation of osteoclastic bone resorption, and inhibition of RANKL-RANK system has become an important therapeutic target for the treatment of osteoporosis. Denosumab, a fully human monoclonal anti-RANKL neutralizing antibody, is developed as a drug for the treatment of osteoporosis. This review summarized pharmacokinetic and pharmacodynamic properties of denosumab, clinical studies including phase 2 dose-ranging and its extension study, phase 3 fracture prevention study (FREEDOM) with extension up to 10 years, studies on male osteoporosis (ADAMO study), and on glucocorticoid-induced osteoporosis, along with relevant clinical studies in Japan. In addition, mechanism of denosumab action that can explain its long-term sustained effects, combination and sequential treatment as well as the problems in discontinuation of denosumab, and finally safety of denosumab therapy is discussed. (Keyword) osteoporosis / Bone / postmenopausal / Bone Density (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-020-01153-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33057808 ● Search Scopus @ Elsevier (PMID): 33057808 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-020-01153-7 (DOI: 10.1007/s00774-020-01153-7, PubMed: 33057808)
15.	Yuichi Takashi, Shu Wakino, Hitoshi Minakuchi, Masashi Ishizu, Akio Kuroda, Hisato Shima, Manabu Tashiro, Keiko Miya, Kazuyoshi Okada, Jun Minakuchi, Shu Kawashima, Munehide Matsuhisa, Toshio Matsumoto and Seiji Fukumoto : Circulating FGF23 is not associated with cardiac dysfunction, atherosclerosis, infection or inflammation in hemodialysis patients., Journal of Bone and Mineral Metabolism, 38, 1, 70-77, 2020. (Summary) Fibroblast growth factor (FGF) 23 is a bone-derived hormone regulating serum inorganic phosphate (Pi) concentration. FGF23 is also involved in the development of chronic kidney disease (CKD)-mineral and bone disorder. Serum FGF23 concentration begins to increase early in the progression of CKD and can be remarkably high in hemodialysis patients with end-stage renal disease. It has been reported that high FGF23 concentration is a risk factor for cardiac dysfunction, atherosclerosis, infection or systemic inflammation in CKD patients. FGF23 was also shown to induce cardiac hypertrophy directly acting on cardiomyocytes. However, it is still controversial whether high FGF23 is causing cardiac dysfunction, atherosclerosis, infection or systemic inflammation in CKD patients. In the current study, we investigated whether FGF23 concentration is associated with cardiac dysfunction, atherosclerosis, infection or systemic inflammation in Japanese hemodialysis patients. We recruited 119 hemodialysis patients and examined the association between serum FGF23 concentration and several parameters concerning mineral metabolism, cardiac dysfunction, atherosclerosis, infection, and systemic inflammation. Serum FGF23 concentration was independently associated with serum calcium and Pi concentration (β = 0.276, p < 0.001; β = 0.689, p < 0.001). However, serum FGF23 concentration was not associated with parameters of cardiac dysfunction, atherosclerosis, infection, and systemic inflammation, either. Our results do not support the hypothesis that high FGF23 in dialysis patients is the cause of cardiac dysfunction, atherosclerosis, infection or systemic inflammation. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-019-01027-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31420749 ● Search Scopus @ Elsevier (PMID): 31420749 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-019-01027-7 (DOI: 10.1007/s00774-019-01027-7, PubMed: 31420749)
16.	Toshio Matsumoto and Itsuro Endo : MInodronate, Bone, 137, 115432, 2020. (Summary) Minodronate is a heterocyclic nitrogen-containing bisphosphonate with high potency in inhibiting bone resorption, and is developed for clinical use in Japan. Minodronate has very high potency in inhibiting farnesyl pyrophosphate synthase, and shows lower affinity for bone matrix hydroxyapatite at both neutral and acidic pH. As a result, small amount of minodronate is deposited in bone but can exert strong anti-resorptive activity in vivo. In this review on minodronate, we summarize the mechanism of action, physico-chemical properties, effects on bone quality in animals, and effects on bone turnover, bone mineral density and fracture prevention, as well as safety in the treatment of patients with osteoporosis. (Keyword) osteoporosis / Bone / postmenopausal / Bone Density (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bone.2020.115432 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32422295 ● Search Scopus @ Elsevier (PMID): 32422295 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bone.2020.115432 (DOI: 10.1016/j.bone.2020.115432, PubMed: 32422295)
17.	Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masahiro Hiasa, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Shiroh Fujii, Ryohei Sumitani, Hirokazu Miki, Kengo Udaka, Mamiko Takahashi, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The Roles of ROS Generation in RANKL-Induced Osteoclastogenesis: Suppressive Effects of Febuxostat., Cancers, 12, 4, 2020. (Summary) Receptor activator of NF-κB ligand (RANKL), a critical mediator of osteoclastogenesis, is upregulated in multiple myeloma (MM). The xanthine oxidase inhibitor febuxostat, clinically used for prevention of tumor lysis syndrome, has been demonstrated to effectively inhibit not only the generation of uric acid but also the formation of reactive oxygen species (ROS). ROS has been demonstrated to mediate RANKL-mediated osteoclastogenesis. In the present study, we therefore explored the role of cancer-treatment-induced ROS in RANKL-mediated osteoclastogenesis and the suppressive effects of febuxostat on ROS generation and osteoclastogenesis. RANKL dose-dependently induced ROS production in RAW264.7 preosteoclastic cells; however, febuxostat inhibited the RANKL-induced ROS production and osteoclast (OC) formation. Interestingly, doxorubicin (Dox) further enhanced RANKL-induced osteoclastogenesis through upregulation of ROS production, which was mostly abolished by addition of febuxostat. Febuxostat also inhibited osteoclastogenesis enhanced in cocultures of bone marrow cells with MM cells. Importantly, febuxostat rather suppressed MM cell viability and did not compromise Dox's anti-MM activity. In addition, febuxostat was able to alleviate pathological osteoclastic activity and bone loss in ovariectomized mice. Collectively, these results suggest that excessive ROS production by aberrant RANKL overexpression and/or anticancer treatment disadvantageously impacts bone, and that febuxostat can prevent the ROS-mediated osteoclastic bone damage. (Tokushima University Institutional Repository) ● Metadata: 2007971 (Link to Publication Site) ● Publication site (DOI): 10.3390/cancers12040929 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32283857 ● Search Scopus @ Elsevier (PMID): 32283857 ● Search Scopus @ Elsevier (DOI): 10.3390/cancers12040929 (Tokushima University Institutional Repository: 2007971, DOI: 10.3390/cancers12040929, PubMed: 32283857)
18.	Maria Tsoumpra, Shun Sawatsubashi, Michihiro Imamura, Seiji Fukumoto, Shin'ichi Takeda, Toshio Matsumoto and Yoshitsugu Aoki : Dystrobrevin alpha gene is a direct target of the vitamin D receptor in muscle., Journal of Molecular Endocrinology, 64, 3, 195-208, 2020. (Summary) The biologically active metabolite of vitamin D, 1,25-dihydroxyvitamin D3 (VD3), exerts its tissue-specific actions through binding to its intracellular vitamin D receptor (VDR) which functions as a heterodimer with retinoid X receptor (RXR) to recognize vitamin D response elements (VDRE) and activate target genes. Upregulation of VDR in murine skeletal muscle cells occurs concomitantly with transcriptional regulation of key myogenic factors upon VD3 administration, reinforcing the notion that VD3 exerts beneficial effects on muscle. Herein we elucidated the regulatory role of VD3/VDR axis on the expression of dystrobrevin alpha (DTNA), a member of dystrophin-associated protein complex (DAPC). In C2C12 cells, Dtna and VDR gene and protein expression were upregulated by 1-50 nM of VD3 during all stages of myogenic differentiation. In the dystrophic-derived H2K-mdx52 cells, upregulation of DTNA by VD3 occurred upon co-transfection of VDR and RXR expression vectors. Silencing of MyoD1, an E-box binding myogenic transcription factor, did not alter the VD3-mediated Dtna induction, but Vdr silencing abolished this effect. We also demonstrated that VD3 administration enhanced the muscle-specific Dtna promoter activity in presence of VDR/RXR only. Through site-directed mutagenesis and chromatin immunoprecipitation assays, we have validated a VDRE site in Dtna promoter in myogenic cells. We have thus proved that the positive regulation of Dtna by VD3 observed during in vitro murine myogenic differentiation is VDR mediated and specific. The current study reveals a novel mechanism of VDR-mediated regulation for Dtna, which may be positively explored in treatments aiming to stabilize the DAPC in musculoskeletal diseases. (Link to Publication Site) ● Publication site (DOI): 10.1530/JME-19-0229 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31940280 ● Search Scopus @ Elsevier (PMID): 31940280 ● Search Scopus @ Elsevier (DOI): 10.1530/JME-19-0229 (DOI: 10.1530/JME-19-0229, PubMed: 31940280)
19.	Seiji Fukumoto, Satoshi Soen, Tetsuya Taguchi, Takashi Ishikawa, Hisashi Matsushima, Masakazu Terauchi, Shigeo Horie, Toshiyuki Yoneda, Toshitsugu Sugimoto and Toshio Matsumoto : Management manual for cancer treatment-induced bone loss (CTIBL): position statement of the JSBMR., Journal of Bone and Mineral Metabolism, 38, 2, 141-144, 2020. (Summary) Androgen deprivation therapy and aromatase inhibitors are known to cause a decrease in bone mineral density and an increase in fractures. Patients receiving these treatments have been shown to have a fracture risk equal to or greater than that of patients with osteoporosis with prevalent fractures. This manual was created to prevent fractures in patients with cancer treatment-induced bone loss with high fracture risks who cannot be treated under the current Japanese guideline for the prevention and treatment of osteoporosis. This manual recommends drug treatment for patients with BMD - 2.0 T score < - 1.5 with the family history of hip fracture or 15% or more 10-year probability of major osteoporotic fractures by FRAX; or in patients with BMD T score < - 2.0. It is important to verify whether the use of this manual can reduce fractures and improve the quality of life of patients with cancer treatment-induced bone loss by prospective studies. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-020-01087-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32020289 ● Search Scopus @ Elsevier (PMID): 32020289 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-020-01087-0 (DOI: 10.1007/s00774-020-01087-0, PubMed: 32020289)
20.	Seiji Fukumoto, Yuichi Takashi, Maria Tsoumpra, Shun Sawatsubashi and Toshio Matsumoto : How do we sense phosphate to regulate serum phosphate level?, Journal of Bone and Mineral Metabolism, 38, 1, 1-6, 2020. (Summary) Abnormal phosphate levels result in several pathological conditions such as rickets/osteomalacia and ectopic calcification indicating that there must be a system that regulates phosphate level within a narrow range. FGF23 has been shown to be an essential hormone regulating serum phosphate level. FGF23 binds to Klotho-FGF receptor complex to reduce serum phosphate level. Several reports suggested that FGF receptor is involved in the regulation of FGF23 production. It has been also shown that high extracellular phosphate can activate several intracellular signaling pathways. However, it has been unclear whether and how phosphate regulates FGF23 production in vivo. Our recent results indicate that high extracellular phosphate directly activates FGF receptor 1 and the downstream intracellular signaling enhances FGF23 production. Thus, there is a negative feedback system for the regulation of serum phosphate level involving FGF receptor and FGF23. We propose that FGF receptor works at least as one of phosphate sensors in the maintenance of serum phosphate level. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-019-01066-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31797064 ● Search Scopus @ Elsevier (PMID): 31797064 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-019-01066-0 (DOI: 10.1007/s00774-019-01066-0, PubMed: 31797064)
21.	Maria Tsoumpra, Seiji Fukumoto, Toshio Matsumoto, Shin'ichi Takeda, Matthew J. A. Wood and Yoshitsugu Aoki : Peptide-conjugate antisense based splice-correction for Duchenne muscular dystrophy and other neuromuscular diseases., EBioMedicine, 45, 630-645, 2019. (Summary) Duchenne muscular dystrophy (DMD) is an X-linked disorder characterized by progressive muscle degeneration, caused by the absence of dystrophin. Exon skipping by antisense oligonucleotides (ASOs) has recently gained recognition as therapeutic approach in DMD. Conjugation of a peptide to the phosphorodiamidate morpholino backbone (PMO) of ASOs generated the peptide-conjugated PMOs (PPMOs) that exhibit a dramatically improved pharmacokinetic profile. When tested in animal models, PPMOs demonstrate effective exon skipping in target muscles and prolonged duration of dystrophin restoration after a treatment regime. Herein we summarize the main pathophysiological features of DMD and the emergence of PPMOs as promising exon skipping agents aiming to rescue defective gene expression in DMD and other neuromuscular diseases. The listed PPMO laboratory findings correspond to latest trends in the field and highlight the obstacles that must be overcome prior to translating the animal-based research into clinical trials tailored to the needs of patients suffering from neuromuscular diseases. (Tokushima University Institutional Repository) ● Metadata: 2008029 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ebiom.2019.06.036 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31257147 ● Search Scopus @ Elsevier (PMID): 31257147 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ebiom.2019.06.036 (Tokushima University Institutional Repository: 2008029, DOI: 10.1016/j.ebiom.2019.06.036, PubMed: 31257147)
22.	Yuichi Takashi, Hidetaka Kosako, Shun Sawatsubashi, Yuka Kinoshita, Nobuaki Ito, Maria K. Tsoumpra, Masaomi Nangaku, Masahiro Abe, Munehide Matsuhisa, Shigeaki Kato, Toshio Matsumoto and Seiji Fukumoto : Activation of unliganded FGF receptor by extracellular phosphate potentiates proteolytic protection of FGF23 by its O-glycosylation, Proceedings of the National Academy of Sciences of the United States of America, 116, 23, 11418-11427, 2019. (Summary) Fibroblast growth factor (FGF) 23 produced by bone is a hormone that decreases serum phosphate (Pi). Reflecting its central role in Pi control, serum FGF23 is tightly regulated by serum Pi alterations. FGF23 levels are regulated by the transcriptional event and posttranslational cleavage into inactive fragments before its secretion. For the latter, O-glycosylation of FGF23 by gene product prevents the cleavage, leading to an increase in serum FGF23. However, the molecular basis of Pi sensing in the regulation of serum FGF23 remains elusive. In this study, we showed that high Pi diet enhanced the skeletal expression of , but not , with expected increases in serum FGF23 and Pi in mice. induction by high Pi was further observed in osteoblastic UMR 106 cells, and this was mediated by activation of the extracellular signal-regulated kinase (ERK) pathway. Through proteomic searches for the upstream sensor for high Pi, we identified one subtype of the FGF receptor (FGFR1c), which was phosphorylated by high Pi in the absence of FGFs. The mode of unliganded FGFR activation by high Pi appeared different from that of FGFR bound to a canonical FGFR ligand (FGF2) when phosphorylation of the FGFR substrate 2α and ERK was monitored. Finally, we showed that an FGFR inhibitor and conditional deletion of in osteoblasts/osteocytes abrogated high Pi diet-induced increases in serum FGF23 and femoral expression in mice. Thus, these findings uncover an unrecognized facet of unliganded FGFR function and illustrate a Pi-sensing pathway involved in regulation of FGF23 production. (Tokushima University Institutional Repository) ● Metadata: 2006656 (Link to Publication Site) ● Publication site (DOI): 10.1073/pnas.1815166116 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31097591 ● Search Scopus @ Elsevier (PMID): 31097591 ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.1815166116 (Tokushima University Institutional Repository: 2006656, DOI: 10.1073/pnas.1815166116, PubMed: 31097591)
23.	Dong Bingzi, Itsuro Endo, Ohnishi Yukoyo, Mitsui Yukari, Kiyoe Kurahashi, Mai Kanai, Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : Persistent Activation of Calcium-Sensing Receptor Suppresses Bone Turnover, Increases Microcracks, and Decreases Bone Strength., JBMR Plus, 3, 7, e10182, 2019. (Summary) Activating mutations of calcium-sensing receptor (CaSR) cause autosomal dominant hypocalcemia type 1 (ADH1). Patients with ADH1 exhibit similar features to patients with hypoparathyroidism, including reduced serum parathyroid hormone (PTH) and Ca with low bone turnover. Although persistent suppression of bone turnover may increase bone fragility, bone strength in ADH1 patients has been unclear. We created knock-in mice harboring the A843E activating mutation of CaSR, mimicking severe features of ADH1 patients. The severe form of ADH1 model mice showed smaller body and bone size with lower bone mineral density (BMD) and cortical area of the femur compared with age-matched wild-type (WT) mice. Bone strength in the femur was lower in ADH1 mice even after correction by bone geometry and/or BMD. Microcracks were markedly increased in ADH1 mice, but were rarely detected in WT mice. There was a negative correlation between bone strength corrected by bone geometry and/or BMD and microcrack number or density in ADH1 and WT mice. Among ADH1 mice, negative correlation was still observed between bone strength and microcrack number or density. Microcracks increased with age in ADH1 mice, and were negatively correlated with bone strength. Treatment with PTH(1-34) or a calcilytic, JTT-305, increased bone turnover, reduced microcracks, and increased bone strength to similar levels to those in WT mice. The increase in microcracks was associated with a reduction in bone strength in ADH1 mice, and aging aggravates these changes. These results demonstrate that activating mutation of CaSR causes reduction in PTH secretion with suppressed bone turnover, that reduced bone turnover is associated with an age-dependent increase in microcracks with a reduction in bone strength, and that both PTH(1-34) and calcilytic ameliorate all these changes in bone turnover and strength. It is suggested that fracture susceptibility may be increased in severe types of ADH1 patients especially in the elderly. © 2019 The Authors. published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research. (Link to Publication Site) ● Publication site (DOI): 10.1002/jbm4.10182 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31372589 ● Search Scopus @ Elsevier (PMID): 31372589 ● Search Scopus @ Elsevier (DOI): 10.1002/jbm4.10182 (DOI: 10.1002/jbm4.10182, PubMed: 31372589)
24.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Takeshi Harada, Shingen Nakamura, Ryota Amachi, Hirofumi Tenshin, Masami Iwasa, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pim-2 is a critical target for treatment of osteoclastogenesis enhanced in myeloma., British Journal of Haematology, 180, 4, 581-585, 2018. (Tokushima University Institutional Repository) ● Metadata: 2006078 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.14388 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27748523 ● Search Scopus @ Elsevier (PMID): 27748523 ● Search Scopus @ Elsevier (DOI): 10.1111/bjh.14388 (Tokushima University Institutional Repository: 2006078, DOI: 10.1111/bjh.14388, PubMed: 27748523)
25.	Shun Sawatsubashi, Yudai Joko, Seiji Fukumoto, Toshio Matsumoto and Shigeo S. Sugano : Development of versatile non-homologous end joining-based knock-in module for genome editing., Scientific Reports, 8, 1, 593, 2018. (Summary) CRISPR/Cas9-based genome editing has dramatically accelerated genome engineering. An important aspect of genome engineering is efficient knock-in technology. For improved knock-in efficiency, the non-homologous end joining (NHEJ) repair pathway has been used over the homology-dependent repair pathway, but there remains a need to reduce the complexity of the preparation of donor vectors. We developed the versatile NHEJ-based knock-in module for genome editing (VIKING). Using the consensus sequence of the time-honored pUC vector to cut donor vectors, any vector with a pUC backbone could be used as the donor vector without customization. Conditions required to minimize random integration rates of the donor vector were also investigated. We attempted to isolate null lines of the VDR gene in human HaCaT keratinocytes using knock-in/knock-out with a selection marker cassette, and found 75% of clones isolated were successfully knocked-in. Although HaCaT cells have hypotetraploid genome composition, the results suggest multiple clones have VDR null phenotypes. VIKING modules enabled highly efficient knock-in of any vectors harboring pUC vectors. Users now can insert various existing vectors into an arbitrary locus in the genome. VIKING will contribute to low-cost genome engineering. (Tokushima University Institutional Repository) ● Metadata: 2005550 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-18911-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29330493 ● Summary page in Scopus @ Elsevier: 2-s2.0-85043529637 (Tokushima University Institutional Repository: 2005550, DOI: 10.1038/s41598-017-18911-9, PubMed: 29330493, Elsevier: Scopus)
26.	Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Ryota Amachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Keiichiro Watanabe, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Kiyoe Kurahashi, Sumiko Yoshida, Kenichi Aihara, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition subverts the osteoclastogenic action of TRAIL while potentiating its antimyeloma effects., Blood Advances, 1, 24, 2124-2137, 2017. (Summary) Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) agonists induce tumor-specific apoptosis indicating that they may be an attractive therapeutic strategy against cancers, including multiple myeloma (MM). Osteoclastogenesis is highly induced in MM, which in turn enhances MM growth, thereby forming a vicious cycle between MM tumor expansion and bone destruction. However, the effects of TRAIL on MM-enhanced osteoclastogenesis remain largely unknown. Here, we show that TRAIL induced apoptosis in MM cells, but not in osteoclasts (OCs), and that it rather facilitated receptor activator of NF-B ligand-induced osteoclastogenesis along with upregulation of cellular FLICE inhibitory protein (c-FLIP). TRAIL did not induce death-inducing signaling complex formation in OCs, but formed secondary complex (complex II) with the phosphorylation of transforming growth factor -activated kinase-1 (TAK1), and thus activated NF-B signaling. c-FLIP knockdown abolished complex II formation, thus permitting TRAIL induction of OC cell death. The TAK1 inhibitor LLZ1640-2 abrogated the TRAIL-induced c-FLIP upregulation and NF-B activation, and triggered TRAIL-induced caspase-8 activation and cell death in OCs. Interestingly, the TRAIL-induced caspase-8 activation caused enzymatic degradation of the transcription factor Sp1 to noticeably reduce c-FLIP expression, which further sensitized OCs to TRAIL-induced apoptosis. Furthermore, the TAK1 inhibition induced antiosteoclastogenic activity by TRAIL even in cocultures with MM cells while potentiating TRAIL's anti-MM effects. These results demonstrated that osteoclastic lineage cells use TRAIL for their differentiation and activation through tilting caspase-8-dependent apoptosis toward NF-B activation, and that TAK1 inhibition subverts TRAIL-mediated NF-B activation to resume TRAIL-induced apoptosis in OCs while further enhancing MM cell death in combination with TRAIL. (Tokushima University Institutional Repository) ● Metadata: 2004899 (Link to Publication Site) ● Publication site (DOI): 10.1182/bloodadvances.2017008813 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29296860 ● Search Scopus @ Elsevier (PMID): 29296860 ● Search Scopus @ Elsevier (DOI): 10.1182/bloodadvances.2017008813 (Tokushima University Institutional Repository: 2004899, DOI: 10.1182/bloodadvances.2017008813, PubMed: 29296860)
27.	Takeshi Mitsuhashi, Ryoko Uemoto, Kazue Ishikawa, Sumiko Yoshida, Yasumasa Ikeda, Shusuke Yagi, Toshio Matsumoto, Masashi Akaike and Ken-ichi Aihara : Endothelial Nitric Oxide Synthase-Independent Pleiotropic Effects of Pitavastatin Against Atherogenesis and Limb Ischemia in Mice., Journal of Atherosclerosis and Thrombosis, 2017. (Summary) Pitavastatin exerts eNOS-independent protective effects against atherogenesis and hind-limb ischemia in mice, which may occur via modifications on key molecules such as AMPK and diverse molecules. (Tokushima University Institutional Repository) ● Metadata: 2008411 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.37747 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28592707 ● Search Scopus @ Elsevier (PMID): 28592707 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37747 (Tokushima University Institutional Repository: 2008411, DOI: 10.5551/jat.37747, PubMed: 28592707)
28.	Kiyoe Kurahashi, Seika Inoue, Sumiko Yoshida, Yasumasa Ikeda, Kana Morimoto, Ryoko Uemoto, Kazue Ishikawa, Takeshi Kondo, Tomoyuki Yuasa, Itsuro Endo, Masato Miyake, Seiichi Oyadomari, Toshio Matsumoto, Masahiro Abe, Hiroshi Sakaue and Ken-ichi Aihara : The Role of Heparin Cofactor in the Regulation of Insulin Sensitivity and Maintenance of Glucose Homeostasis in Humans and Mice., Journal of Atherosclerosis and Thrombosis, 2017. (Summary) The present studies provide evidence to support the idea that HC plays an important role in the maintenance of glucose homeostasis by regulating insulin sensitivity in both humans and mice. Stimulators of HC production may serve as novel therapeutic tools for the treatment of type 2 diabetes. (Tokushima University Institutional Repository) ● Metadata: 2004119 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.37739 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28502917 ● Search Scopus @ Elsevier (PMID): 28502917 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37739 (Tokushima University Institutional Repository: 2004119, DOI: 10.5551/jat.37739, PubMed: 28502917)
29.	Akio Kuroda, Tsuruo Miho, Aki Nanako, Takeshi Kondo, Oguro Yukari, Motoyuki Tamaki, Ken-ichi Aihara, Itsuro Endo, Toshio Matsumoto, Masahiro Abe and Munehide Matsuhisa : A Pirot study comparing the CGM-assessed glycemic profiles of patients with type 1 diabetes on insulin degludec and insulin glargine, Diabetology International, 8, 1, 112-115, 2017. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13340-016-0289-4 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85013200573 (DOI: 10.1007/s13340-016-0289-4, Elsevier: Scopus)
30.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Shingen Nakamura, Derek Hanson, Keiichiro Watanabe, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masami Iwasa, Itsuro Endo, Takeshi Kondo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Yoshiaki Kuroda, Hideaki Horikawa, Eiji Tanaka, Masahiro Abe and Toshio Matsumoto : A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration., Oncotarget, 7, 43, 70447-70461, 2016. (Summary) Myeloma (MM) cells and osteoclasts are mutually interacted to enhance MM growth while creating acidic bone lesions. Here, we explored acid sensing of MM cells and its role in MM cell response to acidic conditions. Acidic conditions activated the PI3K-Akt signaling in MM cells while upregulating the pH sensor transient receptor potential cation channel subfamily V member 1 (TRPV1) in a manner inhibitable by PI3K inhibition. The acid-activated PI3K-Akt signaling facilitated the nuclear localization of the transcription factor Sp1 to trigger the expression of its target genes, including TRPV1 and HDAC1. Consistently, histone deacetylation was enhanced in MM cells in acidic conditions, while repressing a wide variety of genes, including DR4. Indeed, acidic conditions deacetylated histone H3K9 in a DR4 gene promoter and curtailed DR4 expression in MM cells. However, inhibition of HDAC as well as either Sp1 or PI3K was able to restore DR4 expression in MM cells suppressed in acidic conditions. These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions. (Tokushima University Institutional Repository) ● Metadata: 2006189 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.11927 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27626482 ● Search Scopus @ Elsevier (PMID): 27626482 ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.11927 (Tokushima University Institutional Repository: 2006189, DOI: 10.18632/oncotarget.11927, PubMed: 27626482)
31.	Takeshi Harada, Hirokazu Miki, Q Cui, A Oda, Ryota Amachi, Jumpei Teramachi, A Bat-Erdene, K Sogabe, M Iwasa, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Sumiko Yoshida, I Endo, Ken-ichi Aihara, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Expansion of Th1-like V9V2T cells by new-generation IMiDs, lenalidomide and pomalidomide, in combination with zoledronic acid., Leukemia, 31, 1, 258-262, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1038/leu.2016.273 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27698446 ● Search Scopus @ Elsevier (PMID): 27698446 ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2016.273 (DOI: 10.1038/leu.2016.273, PubMed: 27698446)
32.	Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, Ohnishi Yukiyo, Dong Bingzi, Oguro Yukari, Kiyoe Kurahashi, Sumiko Yoshida, Yuichi Fujinaka, Akio Kuroda, Munehide Matsuhisa, Seiji Fukumoto, Toshio Matsumoto and Masahiro Abe : Serum carboxy-terminal telopeptide of type I collagen levels are associated with carotid atherosclerosis in patients with cardiovascular risk factors., Endocrine Journal, 63, 4, 397-404, 2016. (Summary) Carboxy-terminal telopeptide of type I collagen (ICTP) is generated through matrix metalloproteinase (MMP)-dependent type I collagen digestion, and has been widely utilized as a biomarker for bone turnover. The fact that atherosclerotic lesions are rich in both type I collagen and MMP-producing macrophages led to the hypothesis that serum ICTP concentrations may serve as a non-invasive clinical biomarker for atherosclerosis. Therefore, the association of serum ICTP concentrations with the maximum intima-media thickness (IMT) of carotid arteries, a surrogate index of systemic atherosclerosis, or brachial-ankle pulse wave velocity (baPWV) in patients with atherosclerotic risk factors was evaluated. A total of 52 male and 65 female (mean age: 62.8 yrs) patients without renal failure, malignancies or bone diseases known to affect serum ICTP concentrations were recruited. Patients with max IMTs ≥1.1 mm showed significantly higher serum ICTP concentrations compared with patients with max IMTs <1.1 mm (3.33 ± 0.97 vs 2.82 ± 0.65 ng/mL, p<0.05). Serum ICTP concentration was also positively correlated with max IMT (p<0.001) or baPWV values (p<0.05). Multivariate analyses also revealed that serum ICTP concentrations were correlated with max IMT (p<0.001; 95% CI 0.200 to 0.454). These results suggest that serum ICTP concentrations can be used as a non-invasive biomarker for systemic atherosclerosis. (Tokushima University Institutional Repository) ● Metadata: 2002903 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.EJ15-0589 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26877258 ● Summary page in Scopus @ Elsevier: 2-s2.0-84964267287 (Tokushima University Institutional Repository: 2002903, DOI: 10.1507/endocrj.EJ15-0589, PubMed: 26877258, Elsevier: Scopus)
33.	James Derek Hanson, Shingen Nakamura, Ryota Amachi, Masahiro Hiasa, Asuka Oda, Daisuke Tsuji, Kohji Itoh, Takeshi Harada, Kazuki Horikawa, Jumpei Teramachi, Hirokazu Miki, Toshio Matsumoto and Masahiro Abe : Effective impairment of myeloma cells and their progenitors by blockade of monocarboxylate transportation., Oncotarget, 6, 32, 33568-33586, 2015. (Summary) Cancer cells robustly expel lactate produced through enhanced glycolysis via monocarboxylate transporters (MCTs) and maintain alkaline intracellular pH. To develop a novel therapeutic strategy against multiple myeloma (MM), which still remains incurable, we explored the impact of perturbing a metabolism via inhibiting MCTs. All MM cells tested constitutively expressed MCT1 and MCT4, and most expressed MCT2. Lactate export was substantially suppressed to induce death along with lowering intracellular pH in MM cells by blockade of all three MCT molecules with -cyano-4-hydroxy cinnamate (CHC) or the MCT1 and MCT2 inhibitor AR-C155858 in combination with MCT4 knockdown, although only partially by knockdown of each MCT. CHC lowered intracellular pH and severely curtailed lactate secretion even when combined with metformin, which further lowered intracellular pH and enhanced cytotoxicity. Interestingly, an ambient acidic pH markedly enhanced CHC-mediated cytotoxicity, suggesting preferential targeting of MM cells in acidic MM bone lesions. Furthermore, treatment with CHC suppressed hexokinase II expression and ATP production to reduce side populations and colony formation. Finally, CHC caused downregulation of homing receptor CXCR4 and abrogated SDF-1-induced migration. Targeting tumor metabolism by MCT blockade therefore may become an effective therapeutic option for drug-resistant MM cells with elevated glycolysis. (Tokushima University Institutional Repository) ● Metadata: 2002753 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.5598 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26384349 ● Summary page in Scopus @ Elsevier: 2-s2.0-84946086135 (Tokushima University Institutional Repository: 2002753, DOI: 10.18632/oncotarget.5598, PubMed: 26384349, Elsevier: Scopus)
34.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Daiju Fukuda, HM Salim, Masayoshi Ishida, Tomomi Matsuura, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Toshio Matsumoto and Masataka Sata : Predictive factors for efficacy of dipeptidyl peptidase-4 inhibitors in patients with type 2 diabetes mellitus., Diabetes & Metabolism Journal, 39, 4, 342-347, 2015. (Summary) BACKGROUND: Predictive factors for the efficacy of dipeptidyl peptidase-4 (DPP-4) inhibitors for lowering glycosylated hemoglobin (HbA1c) remain unclear in patients with type 2 diabetes mellitus. The aim of this study is therefore to clarify predictive factors of the efficacy of DPP-4 inhibitors for lowering HbA1c after 12 months of treatment.METHODS: A total of 191 consecutive type 2 diabetic patients (male sex 55%, mean age, 68.3±35.8 years), who had been treated with DPP-4 inhibitors for 12 months, were enrolled in this study and evaluated retrospectively.RESULTS: After 12 months of DPP-4 inhibitor treatment, random blood glucose level, and HbA1c level, decreased from 167±63 to 151±49 mg/dL (P<0.01), and from 7.5%±1.3% to 6.9%±0.9% (P<0.01) respectively, without severe side effects. Multiple regression analysis showed that predictors of DPP-4 inhibitor treatment efficacy in lowering HbA1c level after 12 months were a decrease in HbA1c level after 3 months of treatment, a high baseline HbA1c level, a low baseline body mass index, and the absence of coronary artery disease.CONCLUSION: Most suitable candidates for treatment with DPP-4 inhibitors are diabetics who are not obese and do not have coronary artery disease. In addition, long-term efficacy of DPP-4 inhibitors can be predicted by decrement of HbA1c after 3 months of treatment. (Keyword) Coronary artery disease / diabetes mellitus / Dipeptidyl-peptidase IV inhibitors / Obese / Predictive factors (Tokushima University Institutional Repository) ● Metadata: 2000366 (Link to Publication Site) ● Publication site (DOI): 10.4093/dmj.2015.39.4.342 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26301197 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939780057 (Tokushima University Institutional Repository: 2000366, DOI: 10.4093/dmj.2015.39.4.342, PubMed: 26301197, Elsevier: Scopus)
35.	Seiji Fukumoto, Keiichi Ozono, Toshimi Michigami, Masanori Minagawa, Ryo Okazaki, Toshitsugu Sugimoto, Yasuhiro Takeuchi and Toshio Matsumoto : Pathogenesis and diagnostic criteria for rickets and osteomalacia-proposal by an expert panel supported by the Ministry of Health, Labour and Welfare, Japan, the Japanese Society for Bone and Mineral Research, and the Japan Endocrine Society., Journal of Bone and Mineral Metabolism, 33, 5, 467-473, 2015. (Summary) Rickets and osteomalacia are diseases characterized by impaired mineralization of bone matrix. Recent investigations have revealed that the causes of rickets and osteomalacia are quite variable. Although these diseases can severely impair the quality of life of affected patients, rickets and osteomalacia can be completely cured or at least respond to treatment when properly diagnosed and treated according to the specific causes. On the other hand, there are no standard criteria to diagnose rickets or osteomalacia nationally and internationally. Therefore, we summarize the definition and pathogenesis of rickets and osteomalacia, and propose diagnostic criteria and a flowchart for the differential diagnosis of various causes of these diseases. We hope that these criteria and the flowchart are clinically useful for the proper diagnosis and management of these diseases. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-015-0698-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26197863 ● Summary page in Scopus @ Elsevier: 2-s2.0-84940796363 (DOI: 10.1007/s00774-015-0698-7, PubMed: 26197863, Elsevier: Scopus)
36.	Bingzi Dong, Itsuro Endo, Yukiyo Ohnishi, Takeshi Kondo, Tomoka Hasegawa, Norio Amizuka, Hiroshi Kiyonari, Go Shioi, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : Calcilytic Ameliorates Abnormalities of Mutant Calcium-Sensing Receptor (CaSR) Knock-In Mice Mimicking Autosomal Dominant Hypocalcemia (ADH)., Journal of Bone and Mineral Research, 30, 11, 1980-1993, 2015. (Summary) Activating mutations of calcium-sensing receptor (CaSR) cause autosomal dominant hypocalcemia (ADH). ADH patients develop hypocalcemia, hyperphosphatemia, and hypercalciuria, similar to the clinical features of hypoparathyroidism. The current treatment of ADH is similar to the other forms of hypoparathyroidism, using active vitamin D3 or parathyroid hormone (PTH). However, these treatments aggravate hypercalciuria and renal calcification. Thus, new therapeutic strategies for ADH are needed. Calcilytics are allosteric antagonists of CaSR, and may be effective for the treatment of ADH caused by activating mutations of CaSR. In order to examine the effect of calcilytic JTT-305/MK-5442 on CaSR harboring activating mutations in the extracellular and transmembrane domains in vitro, we first transfected a mutated CaSR gene into HEK cells. JTT-305/MK-5442 suppressed the hypersensitivity to extracellular Ca(2+) of HEK cells transfected with the CaSR gene with activating mutations in the extracellular and transmembrane domains. We then selected two activating mutations locating in the extracellular (C129S) and transmembrane (A843E) domains, and generated two strains of CaSR knock-in mice to build an ADH mouse model. Both mutant mice mimicked almost all the clinical features of human ADH. JTT-305/MK-5442 treatment in vivo increased urinary cAMP excretion, improved serum and urinary calcium and phosphate levels by stimulating endogenous PTH secretion, and prevented renal calcification. In contrast, PTH(1-34) treatment normalized serum calcium and phosphate but could not reduce hypercalciuria or renal calcification. CaSR knock-in mice exhibited low bone turnover due to the deficiency of PTH, and JTT-305/MK-5442 as well as PTH(1-34) increased bone turnover and bone mineral density (BMD) in these mice. These results demonstrate that calcilytics can reverse almost all the phenotypes of ADH including hypercalciuria and renal calcification, and suggest that calcilytics can become a novel therapeutic agent for ADH. (Tokushima University Institutional Repository) ● Metadata: 2002739 (Link to Publication Site) ● Publication site (DOI): 10.1002/jbmr.2551 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25967373 ● Summary page in Scopus @ Elsevier: 2-s2.0-84945482381 (Tokushima University Institutional Repository: 2002739, DOI: 10.1002/jbmr.2551, PubMed: 25967373, Elsevier: Scopus)
37.	Itsuro Endo, Seiji Fukumoto, Keiichi Ozono, Noriyuki Namba, Daisuke Inoue, Ryo Okazaki, Mika Yamauchi, Toshitsugu Sugimoto, Masanori Minagawa, Toshimi Michigami, Masaki Nagai and Toshio Matsumoto : Nationwide survey of fibroblast growth factor 23 (FGF23)-related hypophosphatemic diseases in Japan: prevalence, biochemical data and treatment., Endocrine Journal, 62, 9, 811-816, 2015. (Summary) A nationwide epidemiologic survey of fibroblast growth factor 23 (FGF23)-related hypophosphatemic diseases was conducted in 2010 to clarify the prevalence and the clinical presentations of the disorders. A questionnaire inquiring the experience of patients with these diseases was sent to randomly selected hospitals throughout Japan. The estimated annual incidence of the diseases was 117 cases (95% CI 75 - 160), 55 males (95% CI 30 - 81) and 62 females (95% CI 40 - 84). Tumor-induced osteomalacia (TIO) and X-linked hypophosphatemic rickets (XLH) were the most prevalent causes of acquired and genetic FGF23-related hypophosphatemic diseases, respectively. The estimated incidence of XLH was about 1 in 20,000. We have also collected clinical data of the patients by a secondary survey. These patients showed FGF23 levels of above 30 pg/ml by intact assay in the presence of hypophosphatemia. While complete resection of responsible tumors improved biochemical abnormalities in patients with TIO, treatment with phosphate and/or active vitamin D3 did not normalize serum phosphate and tubular maximum transport of phosphate in patients with XLH. Our results suggest that there is no racial difference in the incidence of XLH. While FGF23 measurement is useful for the diagnosis of FGF23-related hypophosphatemic diseases, the better management is necessary especially for patients with genetic hypophosphatemic rickets caused by excessive actions of FGF23. (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.EJ15-0275 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26135520 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942935508 (DOI: 10.1507/endocrj.EJ15-0275, PubMed: 26135520, Elsevier: Scopus)
38.	Jin Temma, Munehide Matsuhisa, Toru Horie, Akio Kuroda, Hiroyasu Mori, Motoyuki Tamaki, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Toshio Matsumoto : Non-invasive Measurement of Skin Autofluorescence as a Beneficial Surrogate Marker for Atherosclerosis in Patients with Type 2 Diabetes, The Journal of Medical Investigation : JMI, 62, 3-4, 126-129, 2015. (Summary) Advanced glycation end-products (AGEs) are thought to play a major role in the pathogenesis of diabetic vascular complications. Skin autofluorescence (AF) was recently reported to represent tissue AGEs accumulation with a non-invasive method. The aim of the present study was to evaluate association between AF value and diabetic vascular complications, such as retinopathy, nephropathy and cervical atherosclerosis using the carotid intima-media thickness (IMT), an established marker of cardiovascular disease in patients with type 2 diabetes. A total of 68 patients with type 2 diabetes were enrolled in a cross-sectional manner. AGEs accumulation was measured with AF reader. Clinical parameters were collected at the time of AF and IMT measurement. Max-IMT was correlated with age and AF (r=0.407, p=0.001), but not with HbA1c, GA, and pentosidine. Also, AF was not correlated with HbA1c, GA and pentosidine, but was correlated with age (r=0.560, p<0.001), duration of diabetes (r=0.256, p<0.05). Multivariate regression analysis revealed that AF, but not age, was an independent determinant of max-IMT. In conclusion, AF might be a beneficial surrogate marker for evaluating carotid atherosclerosis in patients with type 2 diabetes non-invasively. J. Med. Invest. 62: 126-129, August, 2015. (Tokushima University Institutional Repository) ● Metadata: 2004454 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.62.126 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399335 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942054596 (Tokushima University Institutional Repository: 2004454, DOI: 10.2152/jmi.62.126, PubMed: 26399335, Elsevier: Scopus)
39.	Shusuke Yagi, M Fujimura, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, M Tada, Yuka Ueda, Takayuki Ise, Koji Yamaguchi, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Increase in serum triglyceride was associated with coronary plaque vulnerability in a patient with rheumatoid arthritis., Journal of Cardiology Cases, 10, 2, 54-57, 2014. (Summary) Rates of morbidity and mortality from cardiovascular disease are high in patients with rheumatoid arthritis (RA); however, the mechanisms and biomarkers that reflect coronary plaque vulnerability have not yet been established. We present a case of acute coronary syndrome (ACS) presumably caused by exacerbation of chronic inflammation of RA, in which an abrupt increase in serum triglyceride was seen on the day of onset of ACS but not during effort angina. This case suggests that RA patients with an abrupt increase in triglyceride need intensive care including anti-platelet and statin therapy for the prevention of coronary plaque rupture.<Learning objective: Triglyceride might be a sensitive biomarker of activated macrophages and plaque vulnerability in patients with RA. RA patients with an abrupt increase in triglyceride might need intensive care including anti-platelet and statin therapy for the prevention of coronary plaque rupture.> (Keyword) Acute coronary syndrome / Triglyceride / Tumor necrosis factor- / Biomarker (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jccase.2014.04.009 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84905378195 (DOI: 10.1016/j.jccase.2014.04.009, Elsevier: Scopus)
40.	Shusuke Yagi, Ken-ichi Aihara, Takeshi Kondo, Itsuro Endo, Junko Hotsuchi, Takayuki Ise, Takashi Iwase, Masashi Akaike, Toshio Matsumoto and Masataka Sata : High serum parathyroid hormone and calcium are risk factors for hypertension in Japanese patients., Endocrine Journal, 61, 7, 727-733, 2014. (Summary) Excess parathyroid hormone (PTH), known as primary hyperparathyroidism (pHPT), results in hypercalcemia and bone loss. Recent studies have shown that PTH is associated with the occurrence of hypertension in Western countries; however, controversy remains regarding high serum levels of PTH and calcium as risk factors for hypertension in Japanese patients. We retrospectively enrolled 114 consecutive Japanese patients who visited our hospital for examination and treatment of hypercalcemia and/or hypertension with serum calcium levels ≥ 9.8 mg/dL. To estimate the prevalence of hypertension, the patients were categorized according to calcium levels into hypercalcemic (10.2-13.4 mg/dL) and normocalcemic (9.8-10.1 mg/dL) groups, which were further categorized into high PTH (50-440 pg/mL) and low PTH (8-49 pg/mL) groups. The prevalence of hypertension was higher in patients with hypercalcemia than in patients with normocalcemia in both the high and low PTH groups. The prevalence of hypertension was higher in patients with high serum PTH levels than in patients with low serum PTH levels in both the hypercalcemic and normocalcemic groups. Logistic multiple regression analysis determined that serum calcium (P < 0.05) and PTH (P < 0.01) levels were positive contributors to hypertension. In conclusion, high serum levels of PTH and calcium are risk factors for hypertension in Japanese patients. (Keyword) parathyroid hormone / calcium / hypertension (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.EJ14-0004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24849536 ● CiNii @ National Institute of Informatics (CRID): 1390001206300211712 ● Summary page in Scopus @ Elsevier: 2-s2.0-84905190698 (DOI: 10.1507/endocrj.EJ14-0004, PubMed: 24849536, CiNii: 1390001206300211712, Elsevier: Scopus)
41.	Masashi Akaike, Ken-ichi Aihara, Hiroaki Yanagawa, Takashi Iwase, Sumiko Yoshida, Sato Chiho, Saijo Tomoka, Hiroaki Mikasa, Kashiwada Yoshizaki, Yoshihisa Takaishi, Koichiro Tsuchiya, Toshiaki Tamaki, Toshio Matsumoto and Masataka Sata : Efficacy and safety of Citrus sudachi peel in obese adults:A randomized, double-blind, pilot study, Functional Foods in Health and Disease, 4, 6, 276-284, 2014. (Link to Publication Site) ● Publication site (DOI): 10.31989/ffhd.v4i7.5 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85054855286 (DOI: 10.31989/ffhd.v4i7.5, Elsevier: Scopus)
42.	Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto, Sakamoto Wataru, Yogo Toshinobu and Kazunori Ishimura : Magnetically Responsive Smart Nanoparticles for Cancer Treatment with a Combination of Magnetic Hyperthermia and Remote-Control Drug Release, Theranostics, 4, 8, 834-844, 2014. (Summary) We report the synthesis of smart nanoparticles (NPs) that generate heat in response to an alternating current magnetic field (ACMF) and that sequentially release an anticancer drug (doxorubicin, DOX). We further study the in vivo therapeutic efficacy of the combination of magnetic hyperthermia (MHT) and chemotherapy using the smart NPs for the treatment of multiple myeloma. The smart NPs are composed of a polymer with a glass-transition temperature (T g) of 44°C, which contains clustered Fe3O4 NPs and DOX. The clustered Fe3O4 NPs produce heat when the ACMF is applied and rise above 44°C, which softens the polymer phase and leads to the release of DOX. The combination of MHT and chemotherapy using the smart NPs destroys cancer cells in the entire tumor and achieves a complete cure in one treatment without the recurrence of malignancy. Furthermore, the smart NPs have no significant toxicity. (Keyword) Animals / Body Weight / Drug Liberation / Female / Hyperthermia, Induced / Magnetic Phenomena / Mice / Nanoparticles / Neoplasms / Organ Size / Telemedicine (Tokushima University Institutional Repository) ● Metadata: 2000326 (Link to Publication Site) ● Publication site (DOI): 10.7150/thno.9199 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24955144 ● Summary page in Scopus @ Elsevier: 2-s2.0-84902517614 (Tokushima University Institutional Repository: 2000326, DOI: 10.7150/thno.9199, PubMed: 24955144, Elsevier: Scopus)
43.	Masahiro Hiasa, Jumpei Teramachi, A Oda, Ryota Amachi, T Harada, Shingen Nakamura, Hirokazu Miki, Shiroh Fujii, Kumiko Kagawa, Keiichiro Watanabe, Itsuro Endo, Y Kuroda, T Yoneda, Daisuke Tsuji, Michiyasu Nakao, Eiji Tanaka, Kenichi Hamada, Shigeki Sano, Kouji Itou, Toshio Matsumoto and Masahiro Abe : Pim-2 kinase is an important target of treatment for tumor progression and bone loss in myeloma., Leukemia, 2014. (Summary) Pim-2 kinase is overexpressed in multiple myeloma (MM) cells to enhance their growth and survival, and regarded as a novel therapeutic target in MM. However, the impact of Pim-2 inhibition on bone disease in MM remains unknown. We demonstrated here that Pim-2 expression was also upregulated in bone marrow stromal cells and MC3T3-E1 preosteoblastic cells in the presence of cytokines known as the inhibitors of osteoblastogenesis in MM, including interleukin-3 (IL-3), IL-7, tumor necrosis factor-, transforming growth factor- (TGF-) and activin A, as well as MM cell conditioned media. The enforced expression of Pim-2 abrogated in vitro osteoblastogenesis by BMP-2, which suggested Pim-2 as a negative regulator for osteoblastogenesis. Treatment with Pim-2 short-interference RNA as well as the Pim inhibitor SMI-16a successfully restored osteoblastogenesis suppressed by all the above inhibitory factors and MM cells. The SMI-16a treatment potentiated BMP-2-mediated anabolic signaling while suppressing TGF- signaling. Furthermore, treatment with the newly synthesized thiazolidine-2,4-dione congener, 12a-OH, as well as its prototypic SMI-16a effectively prevented bone destruction while suppressing MM tumor growth in MM animal models. Thus, Pim-2 may have a pivotal role in tumor progression and bone loss in MM, and Pim-2 inhibition may become an important therapeutic strategy to target the MM cell-bone marrow interaction.Leukemia advance online publication, 30 May 2014; doi:10.1038/leu.2014.147. (Link to Publication Site) ● Publication site (DOI): 10.1038/leu.2014.147 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24787487 ● Search Scopus @ Elsevier (PMID): 24787487 ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2014.147 (DOI: 10.1038/leu.2014.147, PubMed: 24787487)
44.	Masahiro Abe, Takeshi Harada and Toshio Matsumoto : Concise review: Defining and targeting myeloma stem cell-like cells., Stem Cells, 32, 5, 1067-1073, 2014. (Summary) Multiple myeloma (MM) remains incurable despite recent advances in the treatment of MM. Although the idea of MM cancer stem cells (CSCs) has been proposed for the drug resistance in MM, MM CSCs have not been properly defined yet. Besides clonotypic B cells, phenotypically distinct MM plasma cell fractions have been demonstrated to possess a clonogenic capacity, leading to long-lasting controversies regarding the cells of origin in MM or MM-initiating cells. However, MM CSCs may not be a static population and survive as phenotypically and functionally different cell types via the transition between stem-like and non-stem-like states in local microenvironments, as observed in other types of cancers. Targeting MM CSCs is clinically relevant, and different approaches have been suggested to target molecular, metabolic and epigenetic signatures, and the self-renewal signaling characteristic of MM CSC-like cells. (Keyword) Animals / Cell Differentiation / Clone Cells / Humans / Models, Biological / Multiple Myeloma / Neoplastic Stem Cells / Stem Cell Niche / Tumor Microenvironment (Link to Publication Site) ● Publication site (DOI): 10.1002/stem.1643 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24449391 ● Search Scopus @ Elsevier (PMID): 24449391 ● Search Scopus @ Elsevier (DOI): 10.1002/stem.1643 (DOI: 10.1002/stem.1643, PubMed: 24449391)
45.	Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto, Toshinari Kori and Kazunori Ishimura : Photostable Iodinated Silica/Porphyrin Hybrid Nanoparticles with Heavy-Atom Effect for Wide-Field Photodynamic/Photothermal Therapy Using Single Light Source, Advanced Functional Materials, 24, 4, 503-513, 2014. (Link to Publication Site) ● Publication site (DOI): 10.1002/adfm.201301771 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84892950115 (DOI: 10.1002/adfm.201301771, Elsevier: Scopus)
46.	Mizuho Kinouchi, Ken-ichi Aihara, Yuichi Fujinaka, Sumiko Yoshida, Yukari Ooguro, Kiyoe Kurahashi, Takeshi Kondo, Nanako Aki, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : Diabetic conditions differentially affect the endothelial function, arterial stiffness and carotid atherosclerosis., Journal of Atherosclerosis and Thrombosis, 21, 5, 486-500, 2014. (Summary) Aim: The levels of fasting and postprandial plasma glucose, HbA1c and other risk factors for atherosclerosis have distinct effects in patients with and those without diabetes mellitus. The aim of this study was to determine the impact of diabetic surrogate markers on the endothelial function, arterial stiffness and carotid atherosclerosis in individuals with and without diabetes. Methods: A total of 320 Japanese subjects(mean age: 61.2±12.1 years) were recruited in this study. Demographic, clinical and laboratory parameters, including 75 g OGTT(155 subjects) results, were examined. The endothelial function was evaluated according to the flow-mediated vasodilation of the brachial artery(%FMD). In addition, arterial stiffness was evaluated according to the brachial-ankle pulse wave velocity(baPWV), and carotid atherosclerotic changes were estimated according to the maximum intima-media thickness(max-IMT) and resistive index of the common carotid artery(CCA-RI). A multiple regression analysis was performed to identify independent determinants of these vascular surrogate markers. Results: None of the glucose-related parameters were associated with the %FMD. In contrast, the presence of T2DM, the HbA1c level and an increased plasma glucose level at 60 minutes during 75 g OGTT were associated with an increased baPWV. The HbA1c level was also correlated with an increased max-IMT. The fasting plasma glucose(FPG) level and the presence of T2DM correlated with an increased CCA-RI. In the subjects with T2DM, the protective effects of high-density lipoprotein cholesterol(HDL-C) on the %FMD and baPWV were abolished. Conclusions: Various glucose metabolism parameters have different effects the degree of arterial stiffness and presence of carotid atherosclerosis, but not the endothelial function, suggesting that pharmacological intervention has the potential to preserve the endothelial function in diabetic individuals. In addition, the presence of T2DM blunts the vascular protective effects of HDL-C on the endothelial function and progression of arterial stiffness. (Keyword) Type 2 diabetes / Endothelial function / Arterial stiffness / Carotid atherosclerosis (Tokushima University Institutional Repository) ● Metadata: 2002266 (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.20834 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24401746 ● CiNii @ National Institute of Informatics (CRID): 1390001204430842112 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901494272 (Tokushima University Institutional Repository: 2002266, DOI: 10.5551/jat.20834, PubMed: 24401746, CiNii: 1390001204430842112, Elsevier: Scopus)
47.	Takeshi Kondo, Akio Kuroda, 曽我部公子, 大黒由加里, 倉橋清衛, Motoyuki Tamaki, Mizuho Kinouchi, Sumiko Yoshida, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka, Munehide Matsuhisa and Toshio Matsumoto : Comparison of Continuous Glucose Monitoring (CGM) Values before and after Adrenalectomy in a Case of Adrenaline-producing Pheochromocytoma, Journal of the The Japan Diabetes Society, 57, 9, 729-735, 2014. (Summary) A 77-year-old woman was incidentally found to have a left adrenal mass measuring 2.5 cm in January 2012. The urine metanephrine concentration was 3.0 mg/day (normal range, 0.04-0.19 mg/day), and an iodine-131 metaiodobenzylguanidine (MIBG) scan showed uptake in the area of the left adrenal gland, leading to a diagnosis of pheochromocytoma. In addition, the patient had a history of diabetes mellitus for nine years, with gradually worsening blood glucose control since 2010. The patient was subsequently admitted to our hospital for perioperative care. On admission, her fasting blood glucose level was 121 mg/dl and her HbA1c level was 8.5 %. She was treated with basal-bolus insulin therapy during hospitalization and underwent adrenalectomy at the urology department after her glycemic control had improved. The total daily insulin dose was immediately decreased from 50 to 14 units after the adrenalectomy procedure. In addition, the mean glucose level on preoperative continuous glucose monitoring (CGM) had been 141 mg/dl with a standard deviation (SD) of 54. However, after the operation, the mean glucose level increased to 153 mg/dl while the SD decreased to 24; thus, the range of glycemic fluctuation markedly decreased after surgery. Therefore, excess endogenous adrenalin primarily contributed to the glycemic fluctuations observed in this patient with pheochromocytoma. (Keyword) 褐色細胞腫 / アドレナリン / 糖尿病 / CGM(持続血糖モニター) (Link to Publication Site) ● Publication site (DOI): 10.11213/tonyobyo.57.729 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204908593792 ● Summary page in Scopus @ Elsevier: 2-s2.0-84908507898 (DOI: 10.11213/tonyobyo.57.729, CiNii: 1390001204908593792, Elsevier: Scopus)
48.	Takeshi Harada, Shuji Ozaki, Asuka Oda, Daisuke Tsuji, Akishige Ikegame, Masami Iwasa, Kengo Udaka, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Yoshiaki Kuroda, Shigeto Kawai, Kouji Itou, Hisafumi Yamada-Okabe, Toshio Matsumoto and Masahiro Abe : Combination with a Defucosylated Anti-HM1.24 Monoclonal Antibody plus Lenalidomide Induces Marked ADCC against Myeloma Cells and Their Progenitors, PLoS ONE, 8, 12, e83905, 2013. (Summary) The immunomodulatory drug lenalidomide (Len) has drawn attention to potentiate antibody-dependent cellular cytotoxicity (ADCC)-mediated immunotherapies. We developed the defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317) overexpressed in multiple myeloma (MM) cells. In this study, we evaluated ADCC by YB-AHM and Len in combination against MM cells and their progenitors. YB-AHM was able to selectively kill via ADCC MM cells in bone marrow samples from patients with MM with low effector/target ratios, which was further enhanced by treatment with Len. Interestingly, Len also up-regulated HM1.24 expression on MM cells in an effector-dependent manner. HM1.24 was found to be highly expressed in a drug-resistant clonogenic "side population" in MM cells; and this combinatory treatment successfully reduced SP fractions in RPMI 8226 and KMS-11 cells in the presence of effector cells, and suppressed a clonogenic potential of MM cells in colony-forming assays. Collectively, the present study suggests that YB-AHM and Len in combination may become an effective therapeutic strategy in MM, warranting further study to target drug-resistant MM clonogenic cells. (Keyword) Aged / Aged, 80 and over / Antibodies, Monoclonal, Humanized / Antibody-Dependent Cell Cytotoxicity / Antigens, CD / Antineoplastic Combined Chemotherapy Protocols / Cell Line, Tumor / Drug Synergism / Female / GPI-Linked Proteins / Glycosylation / Humans / immunotherapy / Lenalidomide / Male / Middle Aged / Multiple Myeloma / Neoplastic Stem Cells / Side-Population Cells / Thalidomide / Up-Regulation (Tokushima University Institutional Repository) ● Metadata: 2002273 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0083905 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24386306 ● Summary page in Scopus @ Elsevier: 2-s2.0-84891280322 (Tokushima University Institutional Repository: 2002273, DOI: 10.1371/journal.pone.0083905, PubMed: 24386306, Elsevier: Scopus)
49.	弘世貴久, 渡邉隆宏, 綿田裕孝, 安孫子亜津子, 羽田勝計, 武部典子, 佐藤譲, 山口賢, 石原寿光, 前田朝美, 江藤一弘, 太田明雄, 田中逸, 武田貞二, 駒津光久, 卯木智, 前川聡, 伊藤裕進, 能宗伸輔, 廣峰義久, 川畑由美子, 池上博司, 寺前純吾, 花房俊昭, 富永貴元, 井上康, 谷澤幸生, Toshio Matsumoto, Akio Kuroda, Munehide Matsuhisa, 野見山崇, 柳瀬敏彦, 小林邦久, 近藤龍也, 荒木栄一, 石井則夫, 井形元雄, 久木留大介, 本島寛之 and 河盛隆造 : Effectiveness of miglitol combined with various types of insulin therapy for reducing the daily glycemic fluctuation on Japanese type 2 diabetic patients: Evaluation with self-monitoring blood glucose (SMBG), Therapeutic Research, 34, 12, 1503-1511, 2013. (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84893163294 (Elsevier: Scopus)
50.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Yuka Sumitomo-Ueda, Ryoko Uemoto, Kazue Ishikawa, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Yasuhiro Mouri, Matomo Sakari, Takahiro Matsumoto, Ken-ichi Takeyama, Masashi Akaike, Mitsuru Matsumoto, Masataka Sata, Kenneth Walsh, Shigeaki Kato and Toshio Matsumoto : Androgen receptor promotes sex-independent angiogenesis in response to ischemia and is required for activation of vascular endothelial growth factor receptor signaling., Circulation, 128, 1, 60-71, 2013. (Summary) These results document a physiological role of AR in sex-independent angiogenic potency and provide evidence of novel cross-talk between the androgen/AR signaling and VEGF/kinase insert domain protein receptor signaling pathways. (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCULATIONAHA.113.001533 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23723256 ● Search Scopus @ Elsevier (PMID): 23723256 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCULATIONAHA.113.001533 (DOI: 10.1161/CIRCULATIONAHA.113.001533, PubMed: 23723256)
51.	Shingen Nakamura, Hirokazu Miki, Shinsuke Kido, Ayako Nakano, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Keiichiro Watanabe, Takeshi Harada, Shiroh Fujii, Kyoko Takeuchi, Kumiko Kagawa, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Activating transcription factor 4, an ER stress mediator, is required for, but exce ssive ER stress suppresses osteoblastogenesis by bortezomib., International Journal of Hematology, 98, 1, 66-73, 2013. (Summary) Endoplasmic reticulum (ER) stress is induced in matrix-producing osteoblasts and plays an essential role in osteoblastogenesis. Although the bone anabolic activity of proteasome inhibitors has been demonstrated, the roles of ER stress induced by proteasome inhibition in osteoblastogenesis remain largely unknown. Here we show that bortezomib translationally increases protein levels of activating transcription factor 4 (ATF4), a downstream mediator of ER stress, in bone marrow stromal cells and MC3T3-E1 preosteoblastic cells. The suppression of ATF4 expression by siRNA abrogated osteocalcin expression and mineralized nodule formation by MC3T3-E1 cells induced by bortezomib, indicating a critical role for ATF4 in bortezomib-mediated osteoblastogenesis. However, bortezomib at 20 nM or higher abolished the mineralized nodule formation along with reductions in the expression of osteoblastogenesis mediators β-catenin and Osterix. Furthermore, at 50 nM, bortezomib induced the expression of C/EBP homologous protein (CHOP), suggesting activation of the ATF4-CHOP pro-apoptotic pathway. These results suggest that a low dose of bortezomib induces osteogenic activity, but that, in contrast, excessive ER stress caused by bortezomib at higher doses hampers osteoblastogenesis. Therefore, dosing schedules for proteasome inhibitors warrant further study to maximize anabolic actions without compromising anti-MM activity in patients with multiple myeloma (MM). (Keyword) 3T3 Cells / Activating Transcription Factor 4 / Animals / Antineoplastic Agents / Biological Markers / Bone Marrow Cells / Boronic Acids / Calcification, Physiologic / Cells, Cultured / Endoplasmic Reticulum Stress / Gene Expression Regulation / Gene Silencing / Humans / Mice / Multiple Myeloma / Neoplasm Proteins / Osteoblasts / Osteocalcin / Osteogenesis / Proteasome Inhibitors / Pyrazines / RNA, Small Interfering / Stromal Cells (Tokushima University Institutional Repository) ● Metadata: 2002143 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-013-1367-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23708974 ● Summary page in Scopus @ Elsevier: 2-s2.0-84880304849 (Tokushima University Institutional Repository: 2002143, DOI: 10.1007/s12185-013-1367-z, PubMed: 23708974, Elsevier: Scopus)
52.	Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura : Gold Nanoparticle Cluster/Plasmon-Enhanced Fluorescent Silica Core-Shell Nanoparticles for X-Ray Computed Tomography/Fluorescence Dual-Mode Imaging of Tumors, Chemical Communications, 49, 5334-5336, 2013. (Summary) Owing to the surface plasmon resonance-enhanced electromagnetic field, clustered gold nanoparticles-fluorescent silica core-shell nanoparticles became excited within the therapeutic window and fluoresced strongly in this window. The nanoparticles enabled tumor detection using fluorescence imaging and X-ray computed tomography. (Keyword) Animals / Fluorescence / Fluorescent Dyes / Gold / Mice / Nanoparticles / Neoplasms / Optical Imaging / Silicon Dioxide / Surface Plasmon Resonance / Tomography, X-Ray Computed (Link to Publication Site) ● Publication site (DOI): 10.1039/c3cc41876f (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23648868 ● Search Scopus @ Elsevier (PMID): 23648868 ● Search Scopus @ Elsevier (DOI): 10.1039/c3cc41876f (DOI: 10.1039/c3cc41876f, PubMed: 23648868)
53.	Koichiro Hayashi, Michihiro Nakamura, Wataru Sakamoto, Toshinobu Yogo, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura : "Superparamagnetic Nanoparticle Clusters for Cancer Theranostics Combining Magnetic Resonance Imaging and Hyperthermia Treatment, Theranostics, 3, 6, 366-376, 2013. (Summary) Superparamagnetic nanoparticles (SPIONs) could enable cancer theranostics if magnetic resonance imaging (MRI) and magnetic hyperthermia treatment (MHT) were combined. However, the particle size of SPIONs is smaller than the pores of fenestrated capillaries in normal tissues because superparamagnetism is expressed only at a particle size <10 nm. Therefore, SPIONs leak from the capillaries of normal tissues, resulting in low accumulation in tumors. Furthermore, MHT studies have been conducted in an impractical way: direct injection of magnetic materials into tumor and application of hazardous alternating current (AC) magnetic fields. To accomplish effective enhancement of MRI contrast agents in tumors and inhibition of tumor growth by MHT with intravenous injection and a safe AC magnetic field, we clustered SPIONs not only to prevent their leakage from fenestrated capillaries in normal tissues, but also for increasing their relaxivity and the specific absorption rate. We modified the clusters with folic acid (FA) and polyethylene glycol (PEG) to promote their accumulation in tumors. SPION clustering and cluster modification with FA and PEG were achieved simultaneously via the thiol-ene click reaction. Twenty-four hours after intravenous injection of FA- and PEG-modified SPION nanoclusters (FA-PEG-SPION NCs), they accumulated locally in cancer (not necrotic) tissues within the tumor and enhanced the MRI contrast. Furthermore, 24 h after intravenous injection of the NCs, the mice were placed in an AC magnetic field with H = 8 kA/m and f = 230 kHz (Hf = 1.8×10(9) A/m∙s) for 20 min. The tumors of the mice underwent local heating by application of an AC magnetic field. The temperature of the tumor was higher than the surrounding tissues by ≈6°C at 20 min after treatment. Thirty-five days after treatment, the tumor volume of treated mice was one-tenth that of the control mice. Furthermore, the treated mice were alive after 12 weeks; control mice died up to 8 weeks after treatment. (Tokushima University Institutional Repository) ● Metadata: 2000328 (Link to Publication Site) ● Publication site (DOI): 10.7150/thno.5860 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23781284 ● Summary page in Scopus @ Elsevier: 2-s2.0-84882252518 (Tokushima University Institutional Repository: 2000328, DOI: 10.7150/thno.5860, PubMed: 23781284, Elsevier: Scopus)
54.	Shuji Kato, Itsuro Endo, Mitsunori Fujimura, Rika Kuriwaka-Kido, Yuichi Fujinaka, Ken-ichi Aihara, Takashi Iwase, Daisuke Inoue, Masashi Akaike, Masahiro Abe and Toshio Matsumoto : Serum carboxy-terminal telopeptide of type I collagen (ICTP) as a surrogate marker for vulnerable plaques in atherosclerotic patients: A pilot study., Atherosclerosis, 229, 1, 182-185, 2013. (Summary) Evaluation of atherosclerotic plaques depends on invasive intravascular ultrasonography (IVUS). Carboxy-terminal telopeptide of type I collagen (ICTP) is produced by matrix metalloproteinase (MMP)-dependent digestion of type I collagen. Because vulnerable plaques are rich in type I collagen and MMPs from macrophages, we examined the association between serum ICTP and coronary plaques in patients with coronary disease. We recruited 46 men and 17 women without renal failure or bone diseases affecting serum ICTP, who underwent coronary IVUS. Serum ICTP levels were higher in patients with coronary plaques containing more than 10% necrotic core area than in patients with less than 10% necrotic core area. A positive correlation was found between serum ICTP and necrotic core area. Only serum ICTP was positively correlated with necrotic core area by multivariate analysis (p < 0.05). These results suggest that serum ICTP can be used as a non-invasive marker of vulnerable plaques in atherosclerotic patients. (Tokushima University Institutional Repository) ● Metadata: 2002141 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2013.03.030 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23639859 ● Search Scopus @ Elsevier (PMID): 23639859 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2013.03.030 (Tokushima University Institutional Repository: 2002141, DOI: 10.1016/j.atherosclerosis.2013.03.030, PubMed: 23639859)
55.	Sumiko Yoshida, Akio Kuroda, 新居沙央里, 松本友里, 近藤絵里, 安藝菜奈子, Itsuro Endo, Ken-ichi Aihara, 鈴木麗子, Toshio Matsumoto and Munehide Matsuhisa : The New Paradigm 722 Insulin Pump Can Achieve Good Glycemic Control with Carbohydrate Counting Alone : A Case Report of Type 1 Diabetes Mellitus, Journal of the The Japan Diabetes Society, 56, 4, 240-245, 2013. (Summary) インスリンポンプParadigm712は，インスリン作用時間(AIT)が8時間の設定のため，十分な食後血糖補正インスリン投与を提案しないが，新しいParadigm 722はAITを2~8時間に設定できる．そこで，Paradigm 722の食後血糖補正インスリン量の妥当性を検証した．症例は1型糖尿病の50歳代女性．入院の上インスリンリスプロでParadigm 722を導入，食事スキップで基礎インスリンを設定し，糖質/インスリン比を各食前(11，15，13)g/Uとしたカーボカウントのもと，AITを3時間，インスリン効果値を60mg/dl/Uと設定した．退院前1週間の食後2時間血糖補正の際，150mg/dlを目標にインスリン効果値を用いた補正による自己算出インスリン量とポンプでの自動算出インスリン量とを比較した．食後高血糖に対する補正インスリンは，14回中7回で自己算出量よりも自動算出量が適切であった．Paradigm 722による食後補正インスリン自動算出法は，自己算出法と同等で，これを用いることで良好な血糖管理が簡便になった．(著者抄録) (Keyword) インスリン作用 / 持続皮下インスリン注入療法 / カーボカウント / 1型糖尿病 (Link to Publication Site) ● Publication site (DOI): 10.11213/tonyobyo.56.240 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204909103744 ● Summary page in Scopus @ Elsevier: 2-s2.0-84878045431 (DOI: 10.11213/tonyobyo.56.240, CiNii: 1390001204909103744, Elsevier: Scopus)
56.	Hiroshi Hagino, Masataka Shiraki, Masao Fukunaga, Tetsuo Nakano, Kunio Takaoka, Yasuo Ohashi, Toshitaka Nakamura and Toshio Matsumoto : Number and severity of prevalent vertebral fractures and the risk of subsequent vertebral fractures in Japanese women with osteoporosis: results from the minodronate trial., Journal of Bone and Mineral Metabolism, 31, 5, 544-550, 2013. (Summary) The aim was to evaluate the risk of new vertebral fractures with the increasing number and severity of prevalent vertebral fractures in women who received placebo or minodronate in a post hoc analysis of a 2-year randomized, double-blind, placebo-controlled study. The subjects were women aged 55-80 years old with 1-5 fragility fractures between the T4 and L4 vertebrae and bone mineral density <80 % of the young adult mean. A total of 704 subjects were randomized to take minodronate 1 mg (n = 359) or placebo (n = 345) once a day for 24 months. In the placebo group, the risk of incident vertebral fractures during the 2-year observational period was significantly related to the number and severity of prevalent vertebral fractures at baseline. The number of prevalent vertebral fractures was an independent risk factor for incident vertebral fracture in multivariate analysis. The relative risk reductions of vertebral fractures by minodronate treatment were 45.2, 61.1, and 64.2 % for patients with 1, 2, and ≥3 prevalent vertebral fractures, respectively, and 87.8, 64.6, and 50.1 % for patients with mild, moderate, and severe prevalent vertebral fractures, respectively. In conclusion, the number of prevalent vertebral fractures is an independent risk factor for incident vertebral fracture and minodronate reduces the fracture risk even in patients at a higher risk for fracture. (Keyword) Aged / Aged, 80 and over / Bone Density Conservation Agents / Diphosphonates / Double-Blind Method / Female / Humans / Imidazoles / Middle Aged / Osteoporosis / Spinal Fractures (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-013-0439-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23529800 ● Summary page in Scopus @ Elsevier: 2-s2.0-84885429041 (DOI: 10.1007/s00774-013-0439-8, PubMed: 23529800, Elsevier: Scopus)
57.	Rika Kuriwaka-Kido, Shinsuke Kido, Yuka Miyatani, Yuji Ito, Takeshi Kondo, Takashi Omatsu, Bingzi Dong, Itsuro Endo, Ken-ichi Miyamoto and Toshio Matsumoto : Parathyroid hormone (1-34) counteracts the suppression of interleukin-11 expression by glucocorticoid in murine osteoblasts: a possible mechanism for stimulating osteoblast differentiation against glucocorticoid excess., Endocrinology, 154, 3, 1156-1167, 2013. (Summary) Glucocorticoid (GC) excess causes a rapid loss of bone with a reduction in bone formation. Intermittent PTH (1-34) administration stimulates bone formation and counteracts the inhibition of bone formation by GC excess. We have previously demonstrated that mechanical strain enhances interleukin (IL)-11 gene transcription by a rapid induction of FosB expression and protein kinase C (PKC)--mediated phosphorylation of phosphorylated mothers against decapentaplegic (Smad)-1. Because IL-11 suppresses the expression of dickkopf-1 and -2 and stimulates Wnt signaling, IL-11 appears to mediate at least a part of the effect of mechanical strain on osteoblast differentiation and bone formation. The present study was undertaken to examine the effect of PTH(1-34) and GCs on IL-11 expression in murine primary osteoblasts (mPOBs). PTH(1-34) treatment of mPOBs enhanced IL-11 expression in a time- and dose-dependent manner. PTH(1-34) also stimulated FosB expression and Smad1 phosphorylation, which cooperatively stimulated IL-11 gene transcription. PTH(1-34)-induced Smad1 phosphorylation was mediated via PKC and was abrogated in mPOBs from PKC knockout mice. Dexamethasone suppressed IL-11 gene transcription enhanced by PTH(1-34) without affecting FosB expression or Smad1 phosphorylation, and dexamethasone-GC receptor complex was bound to JunD, which forms heterodimers with FosB. High doses of PTH(1-34) counteracted the effect of dexamethasone on apoptosis of mPOBs, which was blunted by neutralizing anti-IL-11 antibody or IL-11 small interfering RNA. These results demonstrate that PTH(1-34) and GCs interact to regulate IL-11 expression in parallel with osteoblast differentiation and apoptosis and suggest that PTH(1-34) and dexamethasone may regulate osteoblast differentiation and apoptosis via their effect on IL-11 expression. (Keyword) Alkaline Phosphatase / Animals / Apoptosis / Cell Differentiation / Cells, Cultured / Dexamethasone / Gene Expression Regulation / Interleukin-11 / Mice / Osteoblasts / Osteocalcin / Osteoprotegerin / Parathyroid Hormone / Phosphorylation / Promoter Regions, Genetic / Protein Kinase C-delta / Proto-Oncogene Proteins c-fos / Proto-Oncogene Proteins c-jun / RANK Ligand / RNA, Messenger / RNA, Small Interfering / Receptors, Glucocorticoid / Signal Transduction / Smad1 Protein (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2013-1915 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23397032 ● Search Scopus @ Elsevier (PMID): 23397032 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2013-1915 (DOI: 10.1210/en.2013-1915, PubMed: 23397032)
58.	Akio Kuroda, Tetsuyuki Yasuda, Mitsuyoshi Takahara, Fumie Sakamoto, Ryuichi Kasami, Kazuyuki Miyashita, Sumiko Yoshida, Eri Kondo, Ken-ichi Aihara, Itsuro Endo, Taka-Aki Matsuoka, Hideaki Kaneto, Toshio Matsumoto, Iichiro Shimomura and Munehide Matsuhisa : Carbohydrate-to-Insulin Ratio Is Estimated from 300-400 Divided by Total Daily Insulin Dose in Type 1 Diabetes Patients Who Use the Insulin Pump., Diabetes Technology & Therapeutics, 14, 11, 1077-1080, 2012. (Summary) Abstract Background: To optimize insulin dose using insulin pump, basal and bolus insulin doses are widely calculated from total daily insulin dose (TDD). It is recommended that total daily basal insulin dose (TBD) is 50% of TDD and that the carbohydrate-to-insulin ratio (CIR) equals 500 divided by TDD. We recently reported that basal insulin requirement is approximately 30% of TDD. We therefore investigated CIR after adjustment of the proper basal insulin rate. Subjects and Methods: Forty-five Japanese patients with type 1 diabetes were investigated during several weeks of hospitalization. The patients were served standard diabetes meals (25-30 kcal/kg of ideal body weight). Each meal omission was done to confirm basal insulin rate. Target blood glucose level was set at 100 and 150 mg/dL before and 2 h after each meal, respectively. After the basal insulin rate was fixed and target blood glucose levels were achieved, TBD, CIR, TDD, and their products were determined. Results: Mean (±SD) blood glucose levels before and 2 h after meals were 121±47 and 150±61 mg/dL, respectively. TDD was 31.5±9.0 U, and TBD was 27.0±6.5% of TDD. CIR×TDD of breakfast was significantly lower than those of lunch and supper (288±73 vs. 408±92 and 387±83, respectively; P<0.01). Conclusions: CIR has diurnal variance and is estimated from the formula CIR=300/TDD at breakfast or CIR=400/TDD at lunch and supper in type 1 diabetes patients. These results indicate that the insulin dose has been underestimated by using previously established calculations. (Link to Publication Site) ● Publication site (DOI): 10.1089/dia.2012.0109 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23101953 ● Search Scopus @ Elsevier (PMID): 23101953 ● Search Scopus @ Elsevier (DOI): 10.1089/dia.2012.0109 (DOI: 10.1089/dia.2012.0109, PubMed: 23101953)
59.	Hiroshi Hagino, Toshiyuki Takano, Masao Fukunaga, Masataka Shiraki, Toshitaka Nakamura and Toshio Matsumoto : Eldecalcitol reduces the risk of severe vertebral fractures and improves the health-related quality of life in patients with osteoporosis., Journal of Bone and Mineral Metabolism, 31, 2, 183-189, 2012. (Summary) Eldecalcitol reduces the risk of vertebral fractures in comparison to alfacalcidol in osteoporotic patients under vitamin D repletion. The aim of this study was to evaluate the effects of eldecalcitol on the spinal location of incident vertebral fractures, the severity of the fractures, and the changes in health-related quality of life (HRQOL) compared with those of alfacalcidol. The post hoc analysis has been performed on the data from the three-year, double-blind, randomized, head-to-head clinical trial of eldecalcitol versus alfacalcidol conducted in Japan. A total of 1054 patients were enrolled and randomized to take 0.75 μg eldecalcitol or 1.0 μg alfacalcidol daily for 3 years. The incidence of vertebral fractures was re-evaluated based on the location on the spine (upper T4-T10; lower T11-L4). The severity of vertebral fractures was determined by the semi-quantitative method, and the change in HRQOL was analyzed by using the Medical Outcomes Study Short Form 36-item questionnaire. The incidence of vertebral fracture at the lower spine was less in the eldecalcitol group than in the alfacalcidol group (p = 0.029). The incidence of severe vertebral fracture (Grade 3) was 3.8 % in the eldecalcitol group and 6.7 % in the alfacalcidol group, demonstrated a significant difference between the 2 groups (p = 0.036). Both eldecalcitol and alfacalcidol improved HRQOL in osteoporotic patients. Although no significant differences in each HRQOL scores were observed between eldecalcitol and alfacalcidol during the observational period, overall improvement from baseline of HRQOL scores were clearly observed in the eldecalcitol group. In conclusion, the incidences of lower spinal vertebral fractures and severe vertebral fractures were reduced further by eldecalcitol compared to alfacalcidol in the 3-year clinical trial. Daily treatment with eldecalcitol is effective in improving HRQOL, possibly owing to the reduced risk of lower spinal vertebral fractures and/or severe vertebral fractures. (Keyword) Aged / Female / health / Humans / Incidence / Japan / Male / Osteoporosis / Prevalence / quality of life / Risk Factors / Spinal Fractures / vitamin D (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-012-0397-6 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84881473408 (DOI: 10.1007/s00774-012-0397-6, Elsevier: Scopus)
60.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Takashi Iwase, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya, Masataka Sata, Masashi Akaike, Shigeaki Kato, Toshio Matsumoto and Toshiaki Tamaki : Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway, The Journal of Biological Chemistry, 287, 41, 34256-34263, 2012. (Summary) We previously clarified that heparin cofactor II (HCII), a serine proteinase inhibitor, exerts various protective actions on cardiovascular diseases in both experimental and clinical studies. In the present study, we aimed to clarify whether HCII participates in the regulation of angiogenesis. Male heterozygous HCII-deficient (HCII(+/-)) mice and male littermate wild-type (HCII(+/+)) mice at the age of 12-16 weeks were subjected to unilateral hindlimb ligation surgery. Laser speckle blood flow analysis showed that blood flow recovery in response to hindlimb ischemia was delayed in HCII(+/-) mice compared with that in HCII(+/+) mice. Capillary number, arteriole number, and endothelial nitric-oxide synthase (eNOS), AMP-activated protein kinase (AMPK), and liver kinase B1 (LKB1) phosphorylation in ischemic muscles were decreased in HCII(+/-) mice. Human purified HCII (h-HCII) administration almost restored blood flow recovery, capillary density, and arteriole number as well as phosphorylation levels of eNOS, AMPK, and LKB1 in ischemic muscles of HCII(+/-) mice. Although treatment with h-HCII increased phosphorylation levels of eNOS, AMPK, and LKB1 in human aortic endothelial cells (HAECs), the h-HCII-induced eNOS phosphorylation was abolished by compound C, an AMPK inhibitor, and by AMPK siRNA. In a similar fashion, tube formation, proliferation, and migration of HAECs were also promoted by h-HCII treatment and were abrogated by pretreatment with compound C. HCII potentiates the activation of vascular endothelial cells and the promotion of angiogenesis in response to hindlimb ischemia via an AMPK-eNOS signaling pathway. These findings suggest that HCII is a novel therapeutic target for treatment of patients with peripheral circulation insufficiency. (Keyword) Heparin cofactor II (HCII) / vascular endothelial cells / angiogenesis (Tokushima University Institutional Repository) ● Metadata: 2012615 (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M112.353532 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22904320 ● Search Scopus @ Elsevier (PMID): 22904320 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M112.353532 (Tokushima University Institutional Repository: 2012615, DOI: 10.1074/jbc.M112.353532, PubMed: 22904320)
61.	Koichiro Hayashi, Michihiro Nakamura, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura : Near-Infrared Fluorescent Silica/Porphyrin Hybrid Nanorings for In Vivo Cancer Imaging, Advanced Functional Materials, 22, 17, 3539-3546, 2012. (Link to Publication Site) ● Publication site (DOI): 10.1002/adfm.201200219 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1002/adfm.201200219 (DOI: 10.1002/adfm.201200219)
62.	Tamotsu Kanbara, Hirotsugu Kurobe, Takashi Kitaichi, Mikio Sugano, Nakayama Taisuke, Hajime Kinoshita, Takashi Iwase, Akaike Masafumi, Masahiro Abe, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa : Autologous Peripheral Blood-Derived Mononuclear Cells Induced by Erythropoietin Improve Critical Ischemic Limbs., Annals of Vascular Diseases, 5, 1, 52-60, 2012. (Summary) Purpose: Efficient and secure collection of CD34+ cells are crucial for the angiogenic therapies. We have developed autologous peripheral blood-mononuclear cell (MNC) transplantation induced by erythropoietin (rhEPO) for critical ischemic limbs. Methods: Seven patients, including five with arteriosclerosis obliterans, one with Buerger's disease and one with progressive systemic sclerosis, underwent ten cell therapies. The first administration of rhEPO was performed two weeks before apheresis, and the second administration and blood donation were performed one week before apheresis to activate bone marrow. MNCs including CD34+ cells, isolated from peripheral blood by apheresis, were immediately injected intramuscularly into ischemic limbs. Results: The number of peripheral blood-CD34 + cells had significantly increased from 1.32 ± 0.83/microL, before the rhEPO induction, to 1.86 ± 0.94/microL, before the apheresis. The number of transplanted MNCs ranged between 0.5 × 10(9) and 16.5 × 10(9), and that of CD34+ cells, between 0.1 × 10(6) and 12.7 × 10(6), accounting for 0.02%-0.1% of MNCs. There were no serious complications. Finger ulcers with Buerger's disease were significantly improved one month after the transplantations, but the same or other ulcer(s) appeared 2-6 months later. Three patients had an improvement in rest pain, and one patient extended maximum pain-free walking distance. Conclusions: Erythropoietin-induced autologous peripheral blood-MNC transplantation is a useful and safe alternative for ischemic limbs. (Link to Publication Site) ● Publication site (DOI): 10.3400/avd.oa.11.00070 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23555486 ● Search Scopus @ Elsevier (PMID): 23555486 ● Search Scopus @ Elsevier (DOI): 10.3400/avd.oa.11.00070 (DOI: 10.3400/avd.oa.11.00070, PubMed: 23555486)
63.	Toshio Matsumoto and Itsuro Endo : Eldecalcitol for the treatment of osteoporosis., Drugs of Today, 48, 3, 189-196, 2012. (Summary) Eldecalcitol [1α,25-dihydroxy-2β-(3-hydroxypropyloxy)-vitamin D₃] is an analogue of 1α,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], bearing a hydroxypropyloxy residue at the 2β position. Eldecalcitol shows stronger effects than alfacalcidol to increase bone mineral density and reduce bone resorption markers in osteoporotic patients, and oral once-daily 0.75 μg eldecalcitol reduced vertebral fracture incidence by 26% compared to 1.0 μg alfacalcidol in a 3-year randomized, double-blind, active-comparator clinical trial. The effect of eldecalcitol on vertebral fracture incidence was sustained throughout the 3-year study period, and the annual incidence of vertebral fracture during the third year was significantly lower with eldecalcitol rather than with alfacalcidol treatment (3.9% vs 7.0%, respectively). Eldecalcitol also reduced the incidence of wrist fractures by 71% compared to alfacalcidol. Eldecalcitol is well tolerated and is not associated with serious side effects including sustained hypercalcemia. Eldecalcitol was approved for the treatment of osteoporosis in Japan in 2011. (Keyword) Adult / Aged / Animals / Bone Density / Bone Density Conservation Agents / Clinical Trials as Topic / Clinical Trials, Phase I as Topic / Clinical Trials, Phase II as Topic / Drug Evaluation, Preclinical / Drug Interactions / Female / Fractures, Bone / Humans / Middle Aged / Osteoporosis / Osteoporosis, Postmenopausal / Randomized Controlled Trials as Topic / Rats / Vitamin D (Link to Publication Site) ● Publication site (DOI): 10.1358/dot.2012.48.3.1745223 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22462038 ● Search Scopus @ Elsevier (PMID): 22462038 ● Search Scopus @ Elsevier (DOI): 10.1358/dot.2012.48.3.1745223 (DOI: 10.1358/dot.2012.48.3.1745223, PubMed: 22462038)
64.	Kumiko Kagawa, Ayako Nakano, Hirokazu Miki, Asuka Oda, Hiroe Amou, Kyoko Takeuchi, Shingen Nakamura, Takeshi Harada, Shiro Fujii, Kenichiro Yata, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Inhibition of TACE activity enhances the susceptibility of myeloma cells to TRAIL., PLoS ONE, 7, 2, 2012. (Summary) These results demonstrate that MM cells post-translationally down-modulate the cell surface expression of DR4 through ectodomain shedding by endogenous TACE, and that TACE inhibition is able to restore cell surface DR4 levels and the susceptibility of MM cells to TRAIL or an agonistic antibody against DR4. Thus, TACE may protect MM cells from TRAIL-mediated death through down-modulation of cell-surface DR4. It can be envisaged that TACE inhibition augments clinical efficacy of TRAIL-based immunotherapy against MM, which eventually becomes resistant to the present therapeutic modalities. (Keyword) ADAM Proteins / Blotting, Western / Cell Line, Tumor / Cell Survival / Flow Cytometry / HL-60 Cells / Humans / Multiple Myeloma / Receptors, TNF-Related Apoptosis-Inducing Ligand / Reverse Transcriptase Polymerase Chain Reaction / TNF-Related Apoptosis-Inducing Ligand / U937 Cells (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0031594 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22389670 ● Search Scopus @ Elsevier (PMID): 22389670 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0031594 (DOI: 10.1371/journal.pone.0031594, PubMed: 22389670)
65.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Takayuki Ise, Yasumasa Ikeda, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : ロスバスタチンによる脂質低下作用非依存的な形態的および機能的頸動脈硬化改善作用, Progress in Medicine, 32, 2, 315-320, 2012.
66.	Hirotsugu Kurobe, Ken-ichi Aihara, Higashida Mayuko, Hirata Yoichiro, Nishiya Masako, Matsuoka Yuki, Tamotsu Kanbara, Nakayama Taisuke, Hajime Kinoshita, Mikio Sugano, Eiki Fujimoto, Kurobe Ayako, Sugawara Noriko, Takashi Kitaichi, Masashi Akaike, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa : Ezetimibe monotherapy ameliorates vascular function in patients with hypercholesterolemia through decreasing oxidative stress., Journal of Atherosclerosis and Thrombosis, 18, 12, 1080-1089, 2011. (Summary) Ezetimibe, an inhibitor of cholesterol intestinal absorption, is a lipid lowering agent. However, anti-atherogenic effects of ezetimibe have not been fully elucidated. Therefore, the objective in this study was to clarify the vascular protective effects of ezetimibe in patients with hypercholesterolemia. Ezetimibe was administered to 20 patients with hypercholesterolemia (group E), and 20 age- and sex-matched patients with hypercholesterolemia were followed as controls (group C). Difference in metabolic profiles and cardiovascular surrogate markers before ezetimibe treatment and after 12 weeks of ezetimibe treatment were statistically evaluated. Ezetimibe treatment significantly reduced serum levels of low-density lipoprotein cholesterol (LDL-C) and malondialdehyde-modified low-density lipoprotein (MDA-LDL). In addition, the values of body mass index, body weight, waist circumference, plasma HbA1c and urinary albumin were significantly decreased in group E compared to those in group C. On the other hand, high-density lipoprotein cholesterol (HDL-C) and adiponectin levels were significantly increased in group E compared to those in group C. The values of brachial-ankle pulse wave velocity (ba-PWV), mean arterial blood pressure (m-ABP), and % of flow-mediated dilation (FMD) were significantly improved in group E. Furthermore, ultrasonic studies demonstrated amelioration of the vascular stiffness of common carotid arteries in group E but not in group C. These vascular protective effects of ezetimibe were statistically correlated with the decreased values of MDA-LDL and MDA-LDL-to-LDL-C ratio but not with those of LDL-C. Ezetimibe has a lipid lowering-independent vascular protective effect in patients with hypercholesterolemia through decreasing oxidative stress. (Keyword) Aged / Azetidines / Case-Control Studies / Endothelium, Vascular / Humans / Hypercholesterolemia / Lipids / Male / Middle Aged / oxidative stress (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.9548 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22027560 ● Search Scopus @ Elsevier (PMID): 22027560 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.9548 (DOI: 10.5551/jat.9548, PubMed: 22027560)
67.	Hirokazu Miki, Shingen Nakamura, Shuji Ozaki, A Oda, H Amou, Akishige Ikegame, Keiichiro Watanabe, Masahiro Hiasa, Q Cui, T Harada, Shiroh Fujii, A Nakano, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, A Sakai, Masahiro Abe and Toshio Matsumoto : KRN5500, a spicamycin derivative, exerts anti-myeloma effects through impairing both myeloma cells and osteoclasts., British Journal of Haematology, 155, 3, 328-339, 2011. (Summary) The spicamycin analogue KRN5500 alters glycoprotein processing and induces damage in the endoplasmic reticulum (ER)-Golgi apparatus in cancer cells. In the present study, we explored the cytotoxic effects of KRN5500 on multiple myeloma (MM) cells and the bone marrow microenvironment with special reference to ER stress. Cell proliferation assay showed that KRN5500 induced G1 arrest and apoptosis in MM cells in a time- and dose-dependent manner. KRN5500 enhanced ER stress independently of caspase activation in MM cells. This cell death was observed even in the presence of bone marrow stroma cells or osteoclasts. Notably, KRN5500 induced cell death also in osteoclasts. In vivo effects of KRN5500 were evaluated using two xenograft models established in severe combined immunodeficient (SCID) mice by either subcutaneous injection of RPMI 8226 cells or intra-bone injection of INA-6 cells to subcutaneously implanted rabbit bones (SCID-rab model). KRN5500 significantly inhibited tumour growth in both animal models, and decreased the number of osteoclasts, which resulted in prevention of bone destruction in the SCID-rab model. These results suggest that KRN5500 exerts anti-MM effects through impairing both MM cells and osteoclasts. Therefore, this unique mechanism of KRN5500 might be a useful therapeutic option in patients with MM. (Keyword) Animals / Apoptosis / Bone Marrow Cells / Caspases / Cell Line, Tumor / Cell Proliferation / Dose-Response Relationship, Drug / Female / G1 Phase / Humans / Mice / Mice, SCID / Multiple Myeloma / Osteoclasts / Purine Nucleosides / Rabbits / Random Allocation / Stromal Cells / Tumor Microenvironment / Xenograft Model Antitumor Assays (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2141.2011.08844.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21902681 ● Search Scopus @ Elsevier (PMID): 21902681 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2141.2011.08844.x (DOI: 10.1111/j.1365-2141.2011.08844.x, PubMed: 21902681)
68.	Toshio Matsumoto, Rika Kuriwaka-Kido, Takeshi Kondo, Itsuro Endo and Shinsuke Kido : Regulation of osteoblast differentiation by interleukin-11 via AP-1 and Smad signaling., Endocrine Journal, 59, 2, 91-101, 2011. (Summary) Mechanical stress and parathyroid hormone (PTH) are major stimulators, and aging and glucocorticoids excess are important suppressors of osteoblast differentiation. Mechanical stress and PTH stimulate interleukin (IL)-11 expression in cells of osteoblast lineage by enhancing transcription of IL-11 gene via an increase in intracellular Ca² . The elevated Ca² activates extracellular signal-regulated kinase (ERK) to enhance phosphorylation of cyclic AMP response element-binding protein (CREB), which binds to the fosB gene promoter and enhances FosB expression. FosB dimerizes with JunD on the IL-11 gene promoter to enhance its transcription. Both mechanical stress and PTH also stimulate phosphorylation of Smad1 via an activation of protein kinase C (PKC). Phosphorylated Smad1 binds to the IL-11 gene promoter and forms complex with FosB/JunD to further enhance IL-11 gene transcription. The increased IL-11 then suppresses expression of Wnt inhibitors, including Dickkopf 1 (Dkk1) and 2, and enhances Wnt signaling to stimulate osteoblast differentiation and inhibit adipocyte differentiation. The suppression of osteoblast differentiation by aging involves a decrease in IL-11 gene transcription by a reduction in JunD binding to the activator protein (AP)-1 site of the IL-11 gene promoter. Glucocorticoids inhibit transcriptional activation of IL-11 gene by an interaction of glucocorticoid-glucocorticoid receptor (GR) complex with FosB/JunD heterodimer. Thus, factors that enhance osteoblast differentiation stimulate, and those which suppress osteoblast differentiation inhibit IL-11 gene transcription, and IL-11 enhances Wnt signaling by suppressing expression of its inhibitors. These observations are consistent with the notion that IL-11 mediates stimulatory and inhibitory signals of osteoblast differentiation by affecting Wnt signaling. (Keyword) Adipocytes / Aging / Animals / Cell Differentiation / Gene Expression Regulation, Developmental / Humans / Interleukin-11 / Osteoblasts / Osteogenesis / Signal Transduction / Smad Proteins / Transcription Factor AP-1 / Wnt Signaling Pathway (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.EJ11-0219 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21931225 ● Search Scopus @ Elsevier (PMID): 21931225 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.EJ11-0219 (DOI: 10.1507/endocrj.EJ11-0219, PubMed: 21931225)
69.	Toshio Matsumoto, Masako Ito, Yasufumi Hayashi, Takako Hirota, Yusuke Tanigawara, Teruki Sone, Masao Fukunaga, Masataka Shiraki and Toshitaka Nakamura : A new active vitamin D3 analog, eldecalcitol, prevents the risk of osteoporotic fractures--a randomized, active comparator, double-blind study., Bone, 49, 4, 605-612, 2011. (Summary) Eldecalcitol is an analog of 1,25-dihydroxyvitamin D(3) that improves bone mineral density; however, the effect of eldecalcitol on the risk of fractures is unclear. The objective of this study is to examine whether eldecalcitol is superior to alfacalcidol in preventing osteoporotic fractures. This trial is registered with ClinicalTrials.gov, number NCT00144456. This 3 year randomized, double-blind, active comparator, superiority trial tested the efficacy of daily oral 0.75 g eldecalcitol versus 1.0 g alfacalcidol for prevention of osteoporotic fractures. 1054 osteoporotic patients 46 to 92 years old were randomly assigned 1:1 to receive eldecalcitol (n=528) or alfacalcidol (n=526). Patients were stratified by study site and serum 25-hydroxyvitamin D level. Patients with low serum 25-hydroxyvitamin D levels (<50 nmol/L) were supplemented with 400 IU/day vitamin D(3). Primary end point was incident vertebral fractures. Secondary end points included any non-vertebral fractures and change in bone mineral density and bone turnover markers. Compared with the alfacalcidol group, the incidence of vertebral fractures was lower in eldecalcitol group after 36 months of treatment (13.4 vs. 17.5%; hazard ratio, 0.74; predefined 90% confidence interval [CI], 0.56-0.97). Eldecalcitol reduced turnover markers and increased bone mineral density more strongly than alfacalcidol. Eldecalcitol reduced the incidence of three major non-vertebral fractures, which was due to a marked reduction in wrist fractures by a post-hoc analysis (1.1 vs. 3.6%; hazard ratio, 0.29; 95% CI, 0.11-0.77). Among the adverse events, the incidence of increase in serum and urinary calcium was higher in the eldecalcitol group, without any difference in glomerular filtration rate between the two groups. Eldecalcitol is more efficacious than alfacalcidol in preventing vertebral and wrist fractures in osteoporotic patients with vitamin D sufficiency, with a safety profile similar to alfacalcidol. (Keyword) Aged / Aged, 80 and over / Bone Density / Bone Remodeling / Cholecalciferol / Double-Blind Method / Female / Hormones / Humans / Incidence / Japan / Kaplan-Meier Estimate / Male / Middle Aged / Osteoporotic Fractures / Risk Factors / Spinal Fractures / Treatment Outcome / vitamin D (Tokushima University Institutional Repository) ● Metadata: 2000267 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bone.2011.07.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21784190 ● Summary page in Scopus @ Elsevier: 2-s2.0-80052278079 (Tokushima University Institutional Repository: 2000267, DOI: 10.1016/j.bone.2011.07.011, PubMed: 21784190, Elsevier: Scopus)
70.	Qu Cui, Hironobu Shibata, Asuka Oda, Hiroe Amou, Ayako Nakano, Kenichiro Yata, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Targeting myeloma-osteoclast interaction with V9V2 T cells., International Journal of Hematology, 94, 1, 63-70, 2011. (Summary) Multiple myeloma (MM) cells stimulate osteoclastogenesis, and osteoclasts (OCs) in turn enhance MM growth and drug resistance, resulting in a vicious cycle. V9V2 T cells exert potent anti-tumor effects, making T cell-based immunotherapies using these cells attractive candidates for currently incurable malignancies, such as MM. However, the impact of such treatments on the MM-OC interaction is largely unknown. We demonstrate here that V9V2 T cells expanded by zoledronic acid and IL-2 exerted potent cytotoxic effects on both MM cells and OCs, even in coculture settings, but showed no such effect on bone marrow stromal cells. V9V2 T cells marginally affected colony formation from normal hematopoietic progenitors, and furthermore migrated toward osteopontin and MIP-1, factors produced by the MM-OC interaction. These results suggest that V9V2 T cells expanded by zoledronic acid and IL-2 are able to migrate to MM bone lesions and preferentially target OCs as well as MM cells, thereby inhibiting both tumor expansion and bone destruction. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-011-0885-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21698356 ● Search Scopus @ Elsevier (PMID): 21698356 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0885-9 (DOI: 10.1007/s12185-011-0885-9, PubMed: 21698356)
71.	Ayako Nakano, Masahiro Abe, Asuka Oda, Hiroe Amou, Masahiro Hiasa, Shingen Nakamura, Hirokazu Miki, Takeshi Harada, Shirou Fujii, Kumiko Kagawa, Kyoko Takeuchi, Takashi Watanabe, Shuji Ozaki and Toshio Matsumoto : Delayed treatment with vitamin C and N-acetyl-L: -cysteine protects Schwann cells without compromising the anti-myeloma activity of bortezomib., International Journal of Hematology, 93, 6, 727-735, 2011. (Summary) Bortezomib-induced peripheral neuropathy (BIPN) emerges as a disabling adverse effect. As rat models for BIPN have demonstrated damage in nerve Schwann cells, we screened for cytoprotective agents to devise a method of rescuing Schwann cells from the cytotoxic effects of bortezomib without compromising its anti-myeloma effects. Schwann cells underwent macroautophagy along with cytoplasmic inclusion body and vacuole formation, and appeared much less susceptible to bortezomib-induced cytotoxicity than did myeloma cells. Vitamin C or N-acetyl-L: -cysteine (NAC) achieved near-complete rescue of Schwann cells treated with bortezomib at 30 nM or less, and these agents in combination are able to cooperatively inhibit the morphological changes and the cytotoxicity in Schwann cells with higher doses of bortezomib. The delayed addition of vitamin C and/or NAC after the exposure to bortezomib alleviated the cytotoxicity in Schwann cells but not myeloma cells. These results suggest that delayed treatment with these agents may be instrumental in prophylaxis of BIPN. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-011-0850-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21526377 ● Search Scopus @ Elsevier (PMID): 21526377 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-011-0850-7 (DOI: 10.1007/s12185-011-0850-7, PubMed: 21526377)
72.	J Asano, A Nakano, A Oda, H Amou, Masahiro Hiasa, Kyoko Takeuchi, H Miki, S Nakamura, T Harada, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Ken-ichiro Yata, A Sakai, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : The serine/threonine kinase Pim-2 is a novel anti-apoptotic mediator in myeloma cells., Leukemia, 2011. (Summary) Bone marrow stromal cells (BMSCs) and osteoclasts (OCs) confer multiple myeloma (MM) cell survival through elaborating factors. We demonstrate herein that IL-6 and TNF family cytokines, TNF, BAFF and APRIL, but not IGF-1 cooperatively enhance the expression of the serine/threonine kinase Pim-2 in MM cells. BMSCs and OCs upregulate Pim-2 expression in MM cells largely via the IL-6/STAT3 and NF-B pathway, respectively. Pim-2 short interfering RNA reduces MM cell viability in cocultures with BMSCs or OCs. Thus, upregulation of Pim-2 appears to be a novel anti-apoptotic mechanism for MM cell survival. Interestingly, the mammalian target of rapamycin inhibitor rapamycin further suppresses the MM cell viability in combination with the Pim-2 silencing. The Pim inhibitor (Z)-5-(4-propoxybenzylidene) thiazolidine-2, 4-dione and the PI3K inhibitor LY294002 cooperatively enhance MM cell death. The Pim inhibitor suppresses 4E-BP1 phosphorylation along with the reduction of Mcl-1 and c-Myc. Pim-2 may therefore become a new target for MM treatment.Leukemia advance online publication, 8 April 2011; doi:10.1038/leu.2011.60. (Tokushima University Institutional Repository) ● Metadata: 2002336 (Link to Publication Site) ● Publication site (DOI): 10.1038/leu.2011.60 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21475253 ● Search Scopus @ Elsevier (PMID): 21475253 ● Search Scopus @ Elsevier (DOI): 10.1038/leu.2011.60 (Tokushima University Institutional Repository: 2002336, DOI: 10.1038/leu.2011.60, PubMed: 21475253)
73.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Kazue Ishikawa, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Effect of low-dose (1 mg/day) pitavastatin on left ventricular diastolic function and albuminuria in patients with hyperlipidemia., The American Journal of Cardiology, 107, 11, 1644-1649, 2011. (Summary) The aim of the present study was to evaluate the factors that modulate the protective action of statins on cardiorenal function, regardless of the lipid-lowering effect. To treat abnormal serum lipid profiles, low-dose pitavastatin (1.0 mg/day) was administered to 65 hyperlipidemic patients. The exclusion criteria included left ventricular ejection fraction <40% and apparent renal disease. Age- and gender-matched patients with hyperlipidemia (n = 40) served as the controls. After 12 to 16 weeks of pitavastatin treatment, pitavastatin had decreased low-density lipoprotein cholesterol (from 143.5 ± 31.4 to 98.2 ± 19.4 mg/dl, p <0.01), triglycerides (from 157.7 ± 57.2 to 140.5 ± 60.7 mg/dl, p <0.01), E/e' (from 10.8 ± 6.2 to 9.0 ± 4.5, p <0.05), a parameter of left ventricular diastolic function, and albuminuria (from 47.6 ± 55.9 to 28.5 ± 40.0 mg/g creatinine, p <0.01). Furthermore, pitavastatin decreased serum transforming growth factor-1 (from 709 ± 242 to 550 ± 299 pg/ml, p <0.01), urinary 8-hydroxy-2'-deoxyguanosine (from 6.6 ± 4.1 to 5.0 ± 3.1 g/g creatinine, p <0.01), an oxidative stress marker, and increased urinary nitrate and nitrite (from 22.5 ± 14.6 to 29.4 ± 27.6 nmol/g creatinine, p <0.05). No such changes were observed in the controls. Multiple regression analysis in the pitavastatin group revealed the effect of pitavastatin on cardiorenal function was associated with suppression of oxidative stress, but not on low-density lipoprotein cholesterol reduction. In conclusion, pitavastatin decreases E/e' and albuminuria, which is associated with suppression of oxidative stress. (Keyword) Aged / Albuminuria / Case-Control Studies / Cholesterol, LDL / Diastole / Female / Humans / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Hyperlipidemias / Male / Middle Aged / Quinolines / Treatment Outcome / Triglycerides / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1016/j.amjcard.2011.01.054 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21458773 ● Search Scopus @ Elsevier (PMID): 21458773 ● Search Scopus @ Elsevier (DOI): 10.1016/j.amjcard.2011.01.054 (DOI: 10.1016/j.amjcard.2011.01.054, PubMed: 21458773)
74.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Yuka Sumitomo-Ueda, Sumiko Yoshida, Toshio Matsumoto and Masataka Sata : Bosentan improves systemic sclerosis-related peripheral circulation insufficiency., International Journal of Cardiology, 147, 3, 472-475, 2011. (Keyword) Adult / Aged / Blood Circulation / Female / Humans / Middle Aged / Pain Measurement / Raynaud Disease / Scleroderma, Systemic / Sulfonamides (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ijcard.2011.01.025 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21296436 ● Search Scopus @ Elsevier (PMID): 21296436 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijcard.2011.01.025 (DOI: 10.1016/j.ijcard.2011.01.025, PubMed: 21296436)
75.	Michihiro Nakamura, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura : One-pot synthesis and characterization of dual fluorescent thiol-organosilica nanoparticles as non-photoblinking quantum dots and their applications for biological imaging, Journal of Materials Chemistry, 21, 4689-4695, 2011. (Link to Publication Site) ● Publication site (DOI): 10.1039/C0JM04259E (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1039/C0JM04259E (DOI: 10.1039/C0JM04259E)
76.	Shunji Hashizume, Masashi Akaike, Hiroyuki Azuma, Kazue Ishikawa, Sumiko Yoshida, Yuka Ueda, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Ken-ichi Aihara, Masahiro Abe, Masataka Sata and Toshio Matsumoto : Activation of peroxisome proliferator-activated receptor α in megakaryocytes reduces platelet-derived growth factor-BB in platelets., Journal of Atherosclerosis and Thrombosis, 18, 2, 138-147, 2011. (Summary) Platelet-derived growth factor (PDGF)-BB plays a crucial role in atherosclerosis and vascular remodeling by promoting the migration and proliferation of vascular smooth muscle cells. The objective of this study was to clarify the pleiotropic effect of peroxisome proliferator-activated receptor α (PPARα) activators on PDGF-BB expression in megakaryocytes and platelets. The expression of PPARα in a human erythroleukemia (HEL) cells was clearly detected by reverse transcriptase-PCR and immunofluorescence microscopy. The expression level of PPARα in HEL cells was unchanged regardless of differentiation into megakaryocytic cells by treatment with phorbol 12-myristate 13 acetate (TPA). The TPA-induced expression of PDGF-B mRNA and PDGF-BB protein levels in culture media was significantly decreased by treatment with PPARα activators, Wy14643 and fenofibric acid, in a dose-dependent manner. PDGF-BB expression induced by inflammatory cytokines, including interleukin-1β or interleukin-6, was also significantly suppressed by treatment with PPARα activators. Immunohistochemistry of human bone marrow showed the expression of PPARα in both the nucleus and cytoplasm of megakaryocytes. In addition, PDGF-BB levels in platelets were significantly decreased from 1,800±870 to 1,470±840 pg/10(5) platelets (mean±SD, p<0.05) by treatment with 300 mg fenofibrate once daily for 4 weeks in 13 patients with dyslipidemia. Activation of PPARα in megakaryocytes reduces PDGF-BB expression in platelets. PPARα activators may exert vasculo-protective action through suppression of PDGF-BB production in a megakaryocyte/platelet pathway. (Keyword) Adult / Blood Platelets / cell differentiation / Cell Line, Tumor / Dyslipidemias / Female / Fenofibrate / gene expression / Humans / immunohistochemistry / Lipids / Male / Megakaryocytes / Middle Aged / PPAR alpha / Platelet-Derived Growth Factor / Pyrimidines / RNA, Messenger / Tetradecanoylphorbol Acetate (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.5868 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21060209 ● Search Scopus @ Elsevier (PMID): 21060209 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.5868 (DOI: 10.5551/jat.5868, PubMed: 21060209)
77.	Takayuki Ise, Ken-ichi Aihara, Yuka Ueda, Sumiko Yoshida, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Plasma heparin cofactor II activity is inversely associated with left atrial volume and diastolic dysfunction in humans with cardiovascular risk factors., Hypertension Research, 34, 2, 225-231, 2010. (Summary) Thrombin has a crucial role in cardiac remodeling through protease-activated receptor-1 activation in cardiac fibroblasts and cardiomyocytes. As heparin cofactor II (HCII) inhibits the action of tissue thrombin in the cardiovascular system, it is possible that HCII counteracts the development of cardiac remodeling. We investigated the relationships between plasma HCII activity and surrogate markers of cardiac geometry, including left atrial volume index (LAVI), relative wall thickness (RWT) and left ventricular mass index, and deceleration time (DcT) and the ratio of peak E velocity to early diastolic mitral annulus velocity (E/e' ratio) as surrogate markers of left ventricular diastolic dysfunction measured using echocardiography in 304 Japanese elderly individuals without systolic heart failure (169 men and 135 women; mean age: 65.4 ± 11.8 years). Mean plasma HCII activity in all participants was 95.8 ± 17.0% and there was no difference between the mean plasma HCII activities in males and females. Multiple regression analysis revealed that there were significant inverse relationships between plasma HCII activity and LAVI (coefficient: -0.2302, P<0.001), between HCII activity and RWT (coefficient: -0.0007, P<0.05), between HCII activity and DcT (coefficient: -0.5189, P<0.05) and between HCII activity and E/e' ratio (coefficient: -0.0558, P<0.01). Plasma HCII activity was independently and inversely associated with the development of cardiac remodeling, including cardiac concentric change, left atrial enlargement and left ventricular diastolic dysfunction. These findings suggest that cardiac tissue thrombin inactivation by HCII is a novel therapeutic target for cardiac remodeling and atherosclerosis. (Keyword) Aged / Cross-Sectional Studies / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Risk Factors / Ventricular Dysfunction / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.211 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21107326 ● Search Scopus @ Elsevier (PMID): 21107326 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2010.211 (DOI: 10.1038/hr.2010.211, PubMed: 21107326)
78.	Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Sumiko Yoshida, Yuka Sumitomo-Ueda, Ken-ichi Aihara, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Bosentan ameliorated exercise-induced pulmonary arterial hypertension complicated with systemic sclerosis., Internal Medicine, 49, 21, 2309-2312, 2010. (Summary) Pulmonary arterial hypertension (PAH) is a frequent complication in patients with systemic sclerosis. Bosentan is used in patients with symptomatic PAH; however, it has not been established whether or not bosentan ameliorates the progression of PAH in patients with no PAH-related symptoms. We present a case of systemic sclerosis with no PAH-related symptoms in which bosentan ameliorated exercise-induced PAH evaluated by 6-minute walk stress echocardiography, brachial flow-mediated dilation, and skin temperature of hands and feet. The results suggest that administration of bosentan in patients with early-stage PAH ameliorates pulmonary arterial vasodilatation through improvement of endothelial function. (Keyword) Exercise / Exercise Test / Female / Humans / Hypertension, Pulmonary / Middle Aged / Scleroderma, Systemic / Sulfonamides (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.49.3812 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21048365 ● CiNii @ National Institute of Informatics (CRID): 1390282679847104768 ● Search Scopus @ Elsevier (PMID): 21048365 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.49.3812 (DOI: 10.2169/internalmedicine.49.3812, PubMed: 21048365, CiNii: 1390282679847104768)
79.	Shinsuke Kido, Rika Kuriwaka-Kido, Yuka Umino-Miyatani, Itsuro Endo, Daisuke Inoue, Hisaaki Taniguchi, Yasumichi Inoue, Takeshi Imamura and Toshio Matsumoto : Mechanical stress activates Smad pathway through PKCδ to enhance interleukin-11 gene transcription in osteoblasts., PLoS ONE, 5, 9, 2010. (Summary) These results demonstrate that PKCδ-BR-Smads pathway plays an important role in the intracellular signaling in response to mechanical stress, and that a cross-talk between PKCδ-BR-Smads and ΔFosB/JunD pathways synergistically stimulates IL-11 gene transcription in response to mechanical stress. (Keyword) Animals / Bone Morphogenetic Proteins / Cell Line / Cells, Cultured / Humans / Interleukin-11 / Mice / Osteoblasts / Phosphorylation / Protein Binding / Protein Kinase C-delta / Signal Transduction / Smad Proteins / Stress, Mechanical / Transcription, Genetic (Tokushima University Institutional Repository) ● Metadata: 2000237 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0013090 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20927330 ● Search Scopus @ Elsevier (PMID): 20927330 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0013090 (Tokushima University Institutional Repository: 2000237, DOI: 10.1371/journal.pone.0013090, PubMed: 20927330)
80.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Sumiko Yoshida, Yuka Ueda, Yasumasa Ikeda, Kazue Ishikawa, Toshio Matsumoto and Masataka Sata : High plasma aldosterone concentration is a novel risk factor of cognitive impairment in patients with hypertension., Hypertension Research, 34, 1, 74-78, 2010. (Summary) Cognitive impairment leading to dementia is associated with high prevalence of hypertension, decreased quality of life and poor prognosis. Aldosterone is known as a risk factor for cardiovascular and cerebrovascular diseases. In addition, mineral corticoid receptors are abundantly expressed in the hippocampus, which plays a pivotal role in cognitive function; however, it has not been determined whether plasma aldosterone level is associated with cognitive impairment in patients with hypertension. We enrolled 68 patients with essential hypertension and assessed their cardiovascular risk factors, including blood pressure, hyperlipidemia, diabetes mellitus, obesity, smoking, history of cerebral infarction, renal function, parameters of inflammation, oxidative stress and nitric oxide bioavailability, a parameter of cerebral blood flow and carotid plaque by ultrasound examination, plasma renin activity and plasma aldosterone concentration (PAC). The mini-mental state examination (MMSE) was used to evaluate cognitive function. The relevance of cardiovascular risk factors and MMSE score was statistically evaluated. Multiple regression analysis showed that age (P<0.01), PAC (P<0.01) and history of cerebral infarction (P<0.05) were inversely and independently associated with MMSE score. Mineral corticoid receptor antagonists, including spironolactone and eplerenone, increased MMSE score in seven patients with hypertension, but not in the controls. In conclusion, increased PAC is associated with impaired cognitive function and mineral corticoid receptor blockade may protect against not only cardiovascular mortality, but also cognitive impairment in patients with hypertension.Hypertension Research advance online publication, 23 September 2010; doi:10.1038/hr.2010.179. (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.179 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20861841 ● Search Scopus @ Elsevier (PMID): 20861841 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2010.179 (DOI: 10.1038/hr.2010.179, PubMed: 20861841)
81.	Takako Taniguchi, Shinsuke Kido, Emiko Yamauchi, Masahiro Abe, Toshio Matsumoto and Hisaaki Taniguchi : Induction of endosomal/lysosomal pathways in differentiating osteoblasts as revealed by combined proteomic and transcriptomic analyses., FEBS Letters, 584, 18, 3969-3974, 2010. (Summary) We have analyzed proteome changes associated with bone-forming osteoblast differentiation by quantitative differential proteomic and transcriptomic analyses using in vitro differentiation model. Sixty nine proteins were found up-regulated (>2-fold) and 18 were down-regulated (<0.5-fold) at protein level. The mRNA levels of these proteins were then analyzed by quantitative real-time PCR combined with clustering analysis. The most prominent cluster with increased protein and mRNA levels contains endosomal and lysosomal proteins, demonstrating the drastic induction of degradative endosomal/lysosomal pathways in osteoblasts. Osteoblasts, therefore, are involved not only in the synthesis but also in the turnover of the extracellular matrix proteins such as collagens. (Keyword) Animals / cell differentiation / Gene Expression Profiling / Lysosomes / Mice / Mice, Inbred ICR / Osteoblasts / Plasmids / proteome / proteomics (Link to Publication Site) ● Publication site (DOI): 10.1016/j.febslet.2010.07.055 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20682313 ● Search Scopus @ Elsevier (PMID): 20682313 ● Search Scopus @ Elsevier (DOI): 10.1016/j.febslet.2010.07.055 (DOI: 10.1016/j.febslet.2010.07.055, PubMed: 20682313)
82.	Yuka Sumitomo-Ueda, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Yasumasa Ikeda, Ryoko Uemoto, Shusuke Yagi, Takashi Iwase, Kazue Ishikawa, Yoichiro Hirata, Masashi Akaike, Masataka Sata, Shigeaki Kato and Toshio Matsumoto : Heparin cofactor II protects against angiotensin II-induced cardiac remodeling via attenuation of oxidative stress in mice., Hypertension, 56, 3, 430-436, 2010. (Summary) Heparin cofactor II (HCII), a serine protease inhibitor, inhibits tissue thrombin action after binding with dermatan sulfate proteoglycans in the extracellular matrix of the vascular system. We previously reported that heterozygous HCII-deficient (HCII(+/-)) humans and mice demonstrate acceleration of vascular remodeling, including atherosclerosis. However, the action of HCII on cardiac remodeling never has been determined. HCII(+/+) and HCII(+/-) mice at age 25 weeks were infused with angiotensin II (Ang II; 2.0 mg/kg/d) for 2 weeks by an osmotic mini-pump. Echocardiography revealed acceleration of cardiac concentric remodeling in HCII(+/-) mice and larger left atrial volume in HCII(+/-) mice than in HCII(+/+) mice. Histopathologic studies showed more prominent interstitial fibrosis in both the left atrium and left ventricle in HCII(+/-) mice than in HCII(+/+) mice. Daily urinary excretion of 8-hydroxy-2'-deoxyguanosine, a parameter of oxidative stress, and dihydroethidium-positive spots, indicating superoxide production in the myocardium, were markedly increased in Ang II-treated HCII(+/-) mice compared to those in HCII(+/+) mice. Cardiac gene expression levels of atrial natriuretic peptides and brain natriuretic peptides, members of the natriuretic peptide family, Nox 4, Rac-1, and p67(phox) as components of NAD(P)H oxidase, and transforming growth factor-beta1 and procollagen III were more augmented in HCII(+/-) mice than in HCII(+/+) mice. However, administration of human HCII protein attenuated all of those abnormalities in Ang II-treated HCII(+/-) mice. Moreover, human HCII protein supplementation almost abolished cardiac fibrosis in Ang II-treated HCII(+/+) mice. The results indicate that HCII has a protective role against Ang II-induced cardiac remodeling through suppression of the NAD(P)H oxidase-transforming growth factor-beta1 pathway. (Keyword) Analysis of Variance / Angiotensin II / Animals / Atrial Natriuretic Factor / Cardiomegaly / Echocardiography / Fibrosis / Heart Atria / Heparin Cofactor II / Mice / Mice, Transgenic / Myocardium / Natriuretic Peptide, Brain / Oxidative Stress / Transforming Growth Factor beta1 / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.110.152207 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20660821 ● Summary page in Scopus @ Elsevier: 2-s2.0-77955984037 ● Summary page in Scopus @ Elsevier: 2-s2.0-78149260566 (DOI: 10.1161/HYPERTENSIONAHA.110.152207, PubMed: 20660821, Elsevier: Scopus, Elsevier: Scopus)
83.	Ryo Okazaki, Toshitsugu Sugimoto, Hiroshi Kaji, Yoshio Fujii, Masataka Shiraki, Daisuke Inoue, Itsuro Endo, Toshio Okano, Takako Hirota, Issei Kurahashi and Toshio Matsumoto : Vitamin D insufficiency defined by serum 25-hydroxyvitamin D and parathyroid hormone before and after oral vitamin D₃ load in Japanese subjects., Journal of Bone and Mineral Metabolism, 29, 1, 103-110, 2010. (Summary) Vitamin D insufficiency is a risk for both skeletal and nonskeletal health. However, some ambiguity remains about threshold serum 25(OH)D for vitamin D insufficiency. To determine the threshold serum 25(OH)D to maintain normal calcium availability without elevation in serum parathyroid hormone (PTH) among Japanese subjects with various calcium intakes, we conducted a multicenter prospective open-labeled study. We recruited 107 ambulatory subjects without disorders affecting vitamin D metabolism to whom oral vitamin D₃ 800 IU/day for 4 weeks or 1,200 IU/day for 8 weeks was given. Serum 25(OH)D, PTH, calcium, phosphate, and magnesium were measured before and after vitamin D₃ supplementation. Calcium intake was assessed by questionnaires. When all the data were combined, serum 25(OH)D was negatively correlated with PTH. The cubic spline curve between serum 25(OH)D and PTH indicated PTH reached its plateau between 35 and 40 pg/ml at 25(OH)D between 25 and 30 ng/ml. Vitamin D₃ supplementation increased serum 25(OH)D and decreased PTH. Change in PTH correlated positively with baseline serum 25(OH)D. From the regression analyses, baseline serum 25(OH)D above 28 ng/ml corresponded to the threshold level without reduction in PTH after vitamin D₃ supplementation. In multivariate regression analyses, age but not calcium intake was a significant determinant of PTH. We concluded that a serum 25(OH)D level of 28 ng/ml was identified as a threshold for vitamin D insufficiency necessary to stabilize PTH to optimal levels. (Keyword) Adult / Aged / Aged, 80 and over / Cholecalciferol / Female / Humans / Male / Middle Aged / Osteoporosis / Parathyroid Hormone / Prospective Studies / Vitamin D / Vitamin D Deficiency (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-010-0200-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20567864 ● Search Scopus @ Elsevier (PMID): 20567864 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-010-0200-5 (DOI: 10.1007/s00774-010-0200-5, PubMed: 20567864)
84.	Sumiko Yoshida, Ken-ichi Aihara, Hiroyuki Azuma, Ryoko Uemoto, Yuka Sumitomo-Ueda, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Susumu Nishio, Hiromi Kawano, Junko Miki, Hirotsugu Yamada, Yoichiro Hirata, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is inversely associated with sex-dependent diverse carotid atherosclerosis regardless of endothelial function., Atherosclerosis, 212, 1, 310-315, 2010. (Summary) BACKGROUND: Dehydroepiandrosterone sulfate (DHEAS) is thought to be associated with life expectancy and anti-aging. However, its biological significance in atherosclerosis remains controversial. Therefore, the aim of this study was to determine whether DHEAS is associated with development of carotid atherosclerosis in subjects with cardiovascular risk factors. SUBJECTS AND METHODS: A total of 419 Japanese individuals (208 males and 211 females) were recruited from Tokushima University Hospital, Japan. In all subjects, maximum intima-media thickness (max-IMT) in all carotid arteries, and mean-IMT and mean blood flow volume (BFV) in the common carotid arteries (CCA) were measured by ultrasonography; endothelial function was assessed by flow-mediated vasodilation of the brachial artery (%FMD). Serum DHEAS and classical cardiovascular risk factors were also evaluated. Statistical significance was determined by multiple regression analysis to elucidate independent determinants of max-IMT, mean-IMT, mean CCA-BFV, and %FMD. RESULTS: Serum DHEAS levels were higher in males than in females. Multiple regression analysis revealed that DHEAS was an independent negative factor for both max-IMT and mean-IMT in males but not in females. In contrast, DHEAS was the sole positive factor for mean CCA-BFV in females but not in males. In addition, there was no significant relationship between %FMD and DHEAS regardless of sex and other confounding factors. CONCLUSION: Although DHEAS is not involved in endothelial function, DHEAS is inversely associated with sex-dependent diverse carotid atherosclerosis such as increased max-IMT and mean-IMT in males and decreased CCA-BFV in females. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2010.05.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20627295 ● Search Scopus @ Elsevier (PMID): 20627295 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2010.05.011 (DOI: 10.1016/j.atherosclerosis.2010.05.011, PubMed: 20627295)
85.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, Takashi Sato, Kazue Ishikawa, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Yuka Ueda, Sumiko Yoshida, Hiroyuki Azuma, Kenneth Walsh, Toshiaki Tamaki, Shigeaki Kato and Toshio Matsumoto : Androgen receptor counteracts Doxorubicin-induced cardiotoxicity in male mice., Molecular Endocrinology, 24, 7, 1338-1348, 2010. (Summary) Doxorubicin (Dox) has been used as a potent anticancer agent, but serious cardiotoxicity precludes its use in a wide range of patients. We have reported that the androgen-androgen receptor (AR) system plays important roles in cardiac growth and protection from angiotensin II-induced cardiac remodeling. The present study was undertaken to clarify whether the androgen-AR system exerts a cardioprotective effect against Dox-induced cardiotoxicity. Male AR knockout (ARKO) and age-matched littermate male wild-type (WT) mice at 25 wk of age were given ip injections of Dox (20 mg/kg) or a vehicle. The survival rate and left ventricular function in Dox-treated male ARKO mice were reduced compared with those in Dox-treated male WT mice. Electron microscopic study showed prominent vacuole formation of myocardial mitochondria in Dox-treated male ARKO mice. Cardiac oxidative stress and apoptosis of cardiomyocytes were increased more prominently by Dox treatment in male ARKO mice than in male WT mice. In addition, Dox-induced reduction in the expression of cardiac mitochondria transcription factor A (Tfam) and phosphorylation of serine-threonine kinase (Akt) was more pronounced in male ARKO mice than in male WT mice. In cardiac myoblast cells, testosterone up-regulated Akt phosphorylation and Tfam expression and exerted an antiapoptotic effect against Dox-induced cardiotoxicity. Collectively, the results demonstrate that Dox-induced cardiotoxicity is aggravated in male ARKO mice via exacerbation of mitochondrial damage and superoxide generation, leading to enhanced apoptosis of cardiomyocytes. Thus, the androgen-AR system is thought to counteract Dox-induced cardiotoxicity partly through activation of the Akt pathway and up-regulation of Tfam to protect cardiomyocytes from mitochondrial damage and apoptosis. (Keyword) Androgens / Animals / Antineoplastic Agents / Apoptosis / Blotting, Western / Cell Line / Cell Survival / DNA-Binding Proteins / Doxorubicin / Echocardiography / High Mobility Group Proteins / Immunoprecipitation / In Situ Nick-End Labeling / Male / Mice / Mice, Knockout / Microscopy, Electron / Myocardium / Myocytes, Cardiac / Oxidative Stress / Phosphorylation / Protein-Serine-Threonine Kinases / Rats / Receptors, Androgen / Superoxides / Testosterone / Thiobarbituric Acid Reactive Substances / Ventricular Function, Left (Link to Publication Site) ● Publication site (DOI): 10.1210/me.2009-0402 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20501642 ● Search Scopus @ Elsevier (PMID): 20501642 ● Search Scopus @ Elsevier (DOI): 10.1210/me.2009-0402 (DOI: 10.1210/me.2009-0402, PubMed: 20501642)
86.	Shusuke Yagi, Masashi Akaike, Mitsunori Fujimura, Takehiko Kimura, Takeshi Nishiuchi, Takashi Iwase, Ken-ichi Aihara, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Congenital ventricular aneurysm as an unexpected complication of monomorphic premature ventricular contractions., Internal Medicine, 49, 10, 907-912, 2010. (Summary) Congenital ventricular diverticulum (CVD) in adults is a rare cardiac malformation, which includes fibrous type congenital ventricular aneurysm (CVA). CVA is often clinically asymptomatic and shows no abnormality in the electrocardiogram or chest X-ray. However, some cases of sudden death resulting from ventricular tachycardia, cardiac embolism or ventricular rupture have been reported. Therefore, physicians should perform further cardiac imaging studies to detect a CVA if ventricular arrhythmia originating from the left ventricle is observed. Here, we report two successfully followed cases of CVA which were diagnosed from premature ventricular contractions. (Keyword) congenital ventricular aneurysm / congenital ventricular diverticulum / ventricular arrythmia (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.49.3008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20467175 ● CiNii @ National Institute of Informatics (CRID): 1390001204871212928 ● Search Scopus @ Elsevier (PMID): 20467175 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.49.3008 (DOI: 10.2169/internalmedicine.49.3008, PubMed: 20467175, CiNii: 1390001204871212928)
87.	Michihiro Nakamura, Shuji Ozaki, Masahiro Abe, Hiroyuki Doi, Toshio Matsumoto and Kazunori Ishimura : Size-controlled synthesis, surface functionalization, and biological applications of thiol-organosilica particles., Colloids and Surfaces B:Biointerfaces, 79, 1, 19-26, 2010. (Summary) Thiol-organosilica particles of a narrow size distribution, made from 3-mercaptopropyltrimethoxysilane (MPMS), were prepared by means of a one-pot synthesis. We examined three synthetic conditions at high temperature (100 degrees C), including the Stöber synthesis and two entirely aqueous syntheses. Under all conditions, the sizes of MPMS particles were well controlled, and the average of the coefficient of variation for the size distribution was less than 20%. The incubation times required for formation of MPMS particles were shorter at high temperature than at low temperature. MPMS particles internally functionalized with fluorescent dye were also prepared by means of the same one-pot synthesis. On flow cytometry analysis these MPMS particles showed distinct peaks of scattering due to well-controlled sizes of particles as well as due to fluorescence signals. Real-time observation of interaction between fluorescent MPMPS particles and cultured cells could be observed under fluorescent microscopy with bright light. The surface of the as-prepared MPMS particles contained exposed mercaptopropyl residues, and the ability to adsorb proteins was at least 6 times higher than that of gold nanopaticles. In addition, fluorescein-labeled proteins adsorbed to the surface of the particles were quantitatively detected at the pg/ml level by flow cytometry. MPMS particles surface functionalized with anti-CD20 antibody using adsorption could bind with lymphoma cells expressing CD20 specifically. In this paper, we demonstrated the possibility of size-controlled thiol-organosilica particles for wild range of biological applications. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.colsurfb.2010.03.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20417071 ● Search Scopus @ Elsevier (PMID): 20417071 ● Search Scopus @ Elsevier (DOI): 10.1016/j.colsurfb.2010.03.008 (DOI: 10.1016/j.colsurfb.2010.03.008, PubMed: 20417071)
88.	Kyoko Takeuchi, Masahiro Abe, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Shinsuke Kido, Takeshi Harada, Osamu Tanaka, Hirokazu Miki, Shingen Nakamura, Ayako Nakano, Kumiko Kagawa, Kenichiro Yata, Shuji Ozaki and Toshio Matsumoto : Tgf-Beta inhibition restores terminal osteoblast differentiation to suppress myeloma growth., PLoS ONE, 5, 3, e9870, 2010. (Summary) BACKGROUND: Multiple myeloma (MM) expands almost exclusively in the bone marrow and generates devastating bone lesions, in which bone formation is impaired and osteoclastic bone resorption is enhanced. TGF-beta, a potent inhibitor of terminal osteoblast (OB) differentiation, is abundantly deposited in the bone matrix, and released and activated by the enhanced bone resorption in MM. The present study was therefore undertaken to clarify the role of TGF-beta and its inhibition in bone formation and tumor growth in MM. METHODOLOGY/PRINCIPAL FINDINGS: TGF-beta suppressed OB differentiation from bone marrow stromal cells and MC3T3-E1 preosteoblastic cells, and also inhibited adipogenesis from C3H10T1/2 immature mesenchymal cells, suggesting differentiation arrest by TGF-beta. Inhibitors for a TGF-beta type I receptor kinase, SB431542 and Ki26894, potently enhanced OB differentiation from bone marrow stromal cells as well as MC3T3-E1 cells. The TGF-beta inhibition was able to restore OB differentiation suppressed by MM cell conditioned medium as well as bone marrow plasma from MM patients. Interestingly, TGF-beta inhibition expedited OB differentiation in parallel with suppression of MM cell growth. The anti-MM activity was elaborated exclusively by terminally differentiated OBs, which potentiated the cytotoxic effects of melphalan and dexamethasone on MM cells. Furthermore, TGF-beta inhibition was able to suppress MM cell growth within the bone marrow while preventing bone destruction in MM-bearing animal models. CONCLUSIONS/SIGNIFICANCE: The present study demonstrates that TGF-beta inhibition releases stromal cells from their differentiation arrest by MM and facilitates the formation of terminally differentiated OBs, and that terminally differentiated OBs inhibit MM cell growth and survival and enhance the susceptibility of MM cells to anti-MM agents to overcome the drug resistance mediated by stromal cells. Therefore, TGF-beta appears to be an important therapeutic target in MM bone lesions. (Tokushima University Institutional Repository) ● Metadata: 2000254 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0009870 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20360846 ● Search Scopus @ Elsevier (PMID): 20360846 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0009870 (Tokushima University Institutional Repository: 2000254, DOI: 10.1371/journal.pone.0009870, PubMed: 20360846)
89.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Kazue Ishikawa, Takashi Iwase, Yasumasa Ikeda, Takeshi Soeki, Sumiko Yoshida, Yuka Sumitomo-Ueda, Toshio Matsumoto and Masataka Sata : Endothelial nitric oxide synthase-independent protective action of statin against angiotensin II-induced atrial remodeling via reduced oxidant injury., Hypertension, 55, 4, 918-923, 2010. (Summary) Activation of the renin-angiotensin system exacerbates atrial remodeling, leading to atrial fibrillation and thrombosis, especially in a condition with decreased NO bioavailability. Recently, it has been reported that statins reduce the incidence of atrial fibrillation through attenuation of atrial remodeling; however, the mechanisms have not been completely elucidated. Therefore, we aimed to clarify the beneficial effect of statin on atrial remodeling in condition with reduced NO bioavailability. Endothelial NO synthase(-/-) mice were sham operated or infused with angiotensin II (Ang II) via an osmotic minipump for 2 weeks, and Ang II-infused mice were divided into 3 treatment groups: pitavastatin, Tempol (a free radical scavenger), or vehicle. Echocardiography and electrocardiography showed that Ang II infusion caused left atrial enlargement and a high incidence of atrial fibrillation, whereas pitavastatin and Tempol prevented these abnormalities. In histological analysis, Ang II-induced atrial interstitial fibrosis, perivascular fibrosis, and cardiomyocyte hypertrophy were all attenuated by pitavastatin and Tempol. Immunohistochemical staining showed that Ang II downregulated thrombomodulin and tissue factor pathway inhibitor and upregulated tissue factor and plasminogen activator inhibitor 1 in the left atrium and that pitavastatin and Tempol corrected the thrombogenic condition. Moreover, pitavastatin and Tempol reduced Ang II-induced atrial superoxide production and atrial transforming growth factor-beta1 expression and Smad 2/3 phosphorylation. Atrial rac1-GTPase activity, known to activate NADPH oxidase, was attenuated by pitavastatin but not by Tempol. In conclusion, pitavastatin exerts endothelial NO synthase-independent protective actions against Ang II-induced atrial remodeling and atrial fibrillation with enhanced thrombogenicity through suppression of oxidant injury. (Keyword) Analysis of Variance / Angiotensin II / Animals / Antioxidants / Atrial Fibrillation / Blood Pressure / Blotting, Western / Cardiomegaly / Cyclic N-Oxides / Echocardiography / Fibrosis / Heart Atria / Heart Rate / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Male / Mice / Mice, Knockout / Myocytes, Cardiac / Nitric Oxide Synthase Type III / Oxidative Stress / Quinolines / Renin-Angiotensin System / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction / Smad2 Protein / Smad3 Protein / Spin Labels / Transforming Growth Factor beta1 (Link to Publication Site) ● Publication site (DOI): 10.1161/HYPERTENSIONAHA.109.146076 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20194307 ● Search Scopus @ Elsevier (PMID): 20194307 ● Search Scopus @ Elsevier (DOI): 10.1161/HYPERTENSIONAHA.109.146076 (DOI: 10.1161/HYPERTENSIONAHA.109.146076, PubMed: 20194307)
90.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, Takashi Iwase, Kazue Ishikawa, Sumiko Yoshida, Yuka Sumitomo-Ueda, Kenya Kusunose, Toshiyuki Niki, Koji Yamaguchi, Kunihiko Koshiba, Yoichiro Hirata, Munkhbaatar Dagvasumberel, Yoshio Taketani, Noriko Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Ezetimibe ameliorates metabolic disorders and microalbuminuria in patients with hypercholesterolemia., Journal of Atherosclerosis and Thrombosis, 17, 2, 173-180, 2010. (Summary) AIM: Ezetimibe, an inhibitor of Niemann-Pick C1-like 1 protein, has been shown to reduce the intestinal absorption of cholesterol. We investigated whether it also has beneficial effects on metabolic disorder and/or renal insufficiency in patients with hypercholesterolemia. METHODS: Ezetimibe was administered to 38 Japanese patients with hypercholesterolemia to obtain appropriate low-density lipoprotein cholesterol (LDL-chol) levels. Age- and sex-matched patients with hypercholesterolemia (n=38) were the controls. We evaluated the effects of ezetimibe before and 4 to 8 weeks after ezetimibe treatment. RESULTS: Ezetimibe significantly decreased LDL-chol levels and metabolic syndrome-related factors, including body weight, waist circumference, blood pressure; homeostasis model assessment insulin resistance (HOMA-IR), and urinary albumin excretion, were significantly reduced. In addition, it decreased the level of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-alpha, the urinary excretion of 8-hydroxy-2'-deoxyguanosine, a parameter of oxidative stress, and increased the urinary excretion of nitrate and nitrite (NOx). In the controls we observed no such changes. Excepting the decrease in the serum TNF-alpha level, the effects of ezetimibe were not correlated with decreased LDL-chol levels. CONCLUSION: Ezetimibe ameliorated the status of metabolic syndrome and microalbuminuria, reduced inflammation and oxidative stress, and increased nitric oxide bioavailability in a LDL-chol reduction-dependent and -independent manner. (Keyword) Aged / Albuminuria / Anticholesteremic Agents / Azetidines / C-Reactive Protein / Case-Control Studies / Cholesterol, LDL / Deoxyguanosine / Female / Humans / Hypercholesterolemia / Male / Metabolic Diseases / Metabolic Syndrome X / Middle Aged / Nitrates / Nitrites / Oxidative Stress / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.2378 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20150722 ● Search Scopus @ Elsevier (PMID): 20150722 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.2378 (DOI: 10.5551/jat.2378, PubMed: 20150722)
91.	Hajime Kinoshita, Tamotsu Kanbara, Hirotsugu Kurobe, Tatsuo Motoki, Mikio Sugano, Homare Yoshida, Takashi Kitaichi, Masataka Sata, Toshio Matsumoto and Tetsuya Kitagawa : Successful Implantations of Autologous Peripheral Blood-Derived Mononuclear Cells Pretreated by Erythropoietin and Blood Donation in a Patient with Buerger Disease and Intractable Finger Ulcers, Japanese Journal of Cardiovascular Surgery, 39, 1, 29-33, 2010. (Link to Publication Site) ● Publication site (DOI): 10.4326/jjcvs.39.29 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.4326/jjcvs.39.29 (DOI: 10.4326/jjcvs.39.29)
92.	Masatomo Mihara, Ken-ichi Aihara, Yasumasa Ikeda, Sumiko Yoshida, Mizuho Kinouchi, Kiyoe Kurahashi, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : Inhibition of thrombin action ameliorates insulin resistance in type 2 diabetic db/db mice., Endocrinology, 151, 2, 513-519, 2009. (Summary) The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr(-/-):db/db) mice. The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. It also reduced adipocyte size and macrophage infiltration into adipose tissue. The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation. (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2009-0661 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19966184 ● Search Scopus @ Elsevier (PMID): 19966184 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2009-0661 (DOI: 10.1210/en.2009-0661, PubMed: 19966184)
93.	Masahiro Hiasa, Masahiro Abe, Ayako Nakano, Asuka Oda, Hiroe Amou, Shinsuke Kido, Kyoko Takeuchi, Kumiko Kagawa, Kenichiro Yata, Toshihiro Hashimoto, Shuji Ozaki, Kenzo Asaoka, Eiji Tanaka, Keiji Moriyama and Toshio Matsumoto : GM-CSF and IL-4 induce dendritic cell differentiation and disrupt osteoclastogenesis through M-CSF receptor shedding by up-regulation of TNF-{alpha} converting enzyme (TACE), Blood, 114, 20, 4517-4526, 2009. (Summary) Monocytes give rise to macrophages, osteoclasts (OCs), and dendritic cells (DCs). M-CSF and RANK ligand induce OC differentiation from monocytes, while GM-CSF and IL-4 trigger monocytic differentiation into DCs. These two differentiation pathways occur in a mutually exclusive manner. However, regulatory mechanisms for the polarization of monocytic differentiation are still unclear. The present study was undertaken to clarify the mechanism of triggering the deflection of OC and DC differentiation from monocytes. GM-CSF and IL-4 abolished monocytic differentiation into OCs while inducing DC differentiation even in the presence of M-CSF and RANK ligand. GM-CSF and IL-4 in combination potently up-regulate TNF-alpha converting enzyme (TACE) expression and activity in monocytes, causing ectodomain shedding of the membrane-bound M-CSF receptor, resulting in the disruption of its phosphorylation by M-CSF as well as the induction of osteoclastogenesis from monocytes by M-CSF and RANK ligand. Interestingly, TACE inhibition robustly causes the resumption of the surface expression of M-CSF receptors on monocytes, which facilitates M-CSF-mediated phosphorylation of M-CSF receptors and macrophage/OC differentiation while impairing GM-CSF and IL-4-mediated DC differentiation from monocytes. These results reveal a novel proteolytic regulation of M-CSF receptor expression in monocytes to control M-CSF signaling and monocytic differentiation into macrophage/OC-lineage cells or DCs. (Keyword) ADAM Proteins / Blotting, Western / Cell Differentiation / Dendritic Cells / Fluorescent Antibody Technique / Granulocyte-Macrophage Colony-Stimulating Factor / Humans / Interleukin-4 / Macrophages / Monocytes / Osteoclasts / RANK Ligand / Receptor, Macrophage Colony-Stimulating Factor / Reverse Transcriptase Polymerase Chain Reaction / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1182/blood-2009-04-215020 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19762488 ● Search Scopus @ Elsevier (PMID): 19762488 ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2009-04-215020 (DOI: 10.1182/blood-2009-04-215020, PubMed: 19762488)
94.	Mitsunori Fujimura, Masashi Akaike, Takashi Iwase, Sumiko Yoshida, Yuka Sumitomo, Shusuke Yagi, Yasumasa Ikeda, Shunji Hashizume, Ken-ichi Aihara, Takeshi Nishiuchi, Yoshio Yasumura and Toshio Matsumoto : Decrease in plasma brain natriuretic peptide level in the early phase after the start of carvedilol therapy is a novel predictor of long-term outcome in patients with chronic heart failure., Acta Cardiologica, 64, 5, 589-595, 2009. (Summary) OBJECTIVE: The purpose of the present study was to determine whether change in plasma brain natriuretic peptide (BNP) level at an early phase of carvedilol therapy is a predictor of improvement in cardiac function and long-term prognosis in patients with systolic chronic heart failure (CHF). METHODS AND RESULTS: Neurohumoral factors and haemodynamics were examined in 64 patients with systolic CHF (left ventricular ejection fraction (LVEF) below 45%) before and one month (early phase) and 3 to 6 months (late phase) after the start of carvedilol therapy. These patients were followed up for a mean period of 57 months. Plasma BNP levels were already decreased in the early phase before improvement of LVEF in response to carvedilol therapy. Univariate and multivariate linear regression analyses showed that Delta log brain natriuretic peptide (BNP)E (= log BNP at baseline--log BNP at early phase) (P < 0.0001) was a significant independent predictor of improvement in LVEF in the late phase. Cardiac events occurred in I I patients during the follow-up period. In addition, multivariate Cox proportional hazards regression analysis showed that Delta log BNPE (P = 0.0045) and systolic blood pressure at baseline (P = -0.048) were significant independent predictors of the development of cardiac events. CONCLUSIONS: Decrease in plasma BNP level in the early phase of carvedilol therapy is a novel predictor of not only improvement of LVEF in the late phase but also prognosis in patients with systolic CHF. (Link to Publication Site) ● Publication site (DOI): 10.2143/AC.64.5.2042687 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20058503 ● Search Scopus @ Elsevier (PMID): 20058503 ● Search Scopus @ Elsevier (DOI): 10.2143/AC.64.5.2042687 (DOI: 10.2143/AC.64.5.2042687, PubMed: 20058503)
95.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Nobuyuki Takamori, Yasumasa Ikeda, Yuka Sumitomo, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Kazue Ishikawa, Masataka Sata, Tetsuya Kitagawa and Toshio Matsumoto : Heparin cofactor II is an independent protective factor against peripheral arterial disease in elderly subjects with cardiovascular risk factors., Journal of Atherosclerosis and Thrombosis, 16, 2, 127-134, 2009. (Summary) AIM: Heparin cofactor II (HCII) specifically inactivates thrombin action at the injured vascular wall. We have reported that HCII is a protective factor against coronary in-stent restenosis and carotid atherosclerosis; however, it is unclear whether there is any correlation between plasma HCII levels and the development of peripheral arterial disease (PAD). METHODS: Plasma HCII activity and the ankle brachial pressure index (ABI) were determined in 494 elderly subjects with cardiovascular risk factors. PAD was diagnosed by ABI below 0.9, and 62 subjects were diagnosed with PAD. The relationship between factors that affect cardiovascular events and the prevalence of PAD was statistically evaluated. RESULTS: Mean HCII activity in PAD subjects was significantly lower than in non-PAD subjects (87.5+/-19.7% v.s. 94.6+/-17.8%, p=0.009). Multivariate logistic regression analysis showed that age (odds ratio [OR]: 1.062, p=0.0016), current smoking (OR 3.028, p=0.002) and diabetes mellitus (OR 2.656, p=0.008) were independent and progressive determinants of PAD. In contrast, HCII was an independent inhibitory factor of PAD (OR: 0.982, p=0.048). CONCLUSIONS: Plasma HCII activity is inversely related to the prevalence of PAD. HCII may function as the sole protective factor against PAD in elderly people with cardiovascular risk factors. (Keyword) Aged / Aged, 80 and over / Cardiovascular Diseases / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Peripheral Vascular Diseases / Prevalence / Protective Agents / Risk Factors (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.E695 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19403987 ● Search Scopus @ Elsevier (PMID): 19403987 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.E695 (DOI: 10.5551/jat.E695, PubMed: 19403987)
96.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Yuka Ueda, Sumiko Yoshida, Takayuki Ise, Shusuke Yagi, Takashi Iwase, 近藤彰, 田村克也 and Toshio Matsumoto : アンジオテンシンII受容体拮抗薬バルサルタンのNO bioavailability改善効果に関する臨床的検討, Progress in Medicine, 29, 7, 1777-1782, 2009. (Summary) バルサルタンの降圧作用，動脈硬化抑制作用および糖代謝改善作用に一酸化窒素(NO)のバイオアベイラビリティの改善効果が関与しているか検討した．高血圧治療目的で通院加療中の42例を対象とした．バルサルタン投与にて，BMIやリポプロテイン(a)を含む脂質プロファイルに有意な変化は認めなかったが，収縮期血圧，脈圧，baPWVおよびHbA1cは有意に低下した．投与3ヵ月後には投与前と比較して，NOのバイオアベイラビリティのマーカーである血清硝酸/亜硝酸イオン(NOx)は約1.5倍に増加した．血清NOxの増加が，他の測定因子にどのように影響を与えているか，単変量および多変量解析を用いて解析し，血清NOxの増加量は収縮期血圧の低下と脈圧の減少との間においてそれぞれ有意な相関がみられた．また，HbA1cはバルサルタン投与3ヵ月後に有意に低下していたが，その変化はNOxの増加量と有意な相関がみられた． (Keyword) Nitrogen Oxides(血液) Glycosylated Hemoglobin A 降圧剤(治療的利用,薬理学) 高血圧(薬物療法) 生物学的利用率動脈硬化症-アテローム性(予防,診断) 経口投与一酸化窒素 Valsartan(治療的利用,薬理学) Angiotensin II Type 1 Receptor Blockers(治療的利用,薬理学) 脈波伝播速度ヒト中年(45~64) 高齢者(65~79) 男女
97.	Ken-ichi Kitazoe, Masahiro Abe, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Takeshi Harada, Ayako Nakano, Kyoko Takeuchi, Toshihiro Hashimoto, Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto : Valproic acid exerts anti-tumor as well as anti-angiogenic effects on myeloma., International Journal of Hematology, 89, 1, 45-57, 2008. (Summary) Multiple myeloma is still an incurable disease, most commonly occurring in the elderly. The myeloma-induced bone marrow microenvironment protects myeloma cells from drug-induced apoptosis. Therefore, the development of novel and tolerable therapeutic alternatives to overcome the drug resistance is an important clinical issue. Valproic acid (VPA), a safe and widely used anti-epileptic agent, is revisited as a class I- and IIa-specific histone deacetylase inhibitor. In the present study, we evaluated the effect as well as a mechanism of actions of VPA on myeloma cell growth and survival, with special reference to the myeloma-induced bone marrow microenvironment. VPA at therapeutic concentrations for epilepsy induced cell death in primary CD138-positive myeloma cells as well as myeloma cell lines, but not in CD138-negative bone marrow cells. VPA suppressed osteoclastogenesis as well as osteoclast-mediated myeloma cell growth. VPA also inhibited vascular tubule formation enhanced by co-cultures of myeloma cells and osteoclasts in concert with thalidomide. In addition, VPA induced both caspase-dependent and -independent cell death in myeloma cells, and potentiated the anti-myeloma effects of melphalan and dexamethasone. Collectively, VPA is suggested to exert multi-factorial anti-myeloma actions, and may serve as a safe adjuvant to be included in conventional chemotherapies against myeloma. (Keyword) Antineoplastic Combined Chemotherapy Protocols / Bone Marrow / cell proliferation and differentiation / Cell Survival / Coculture Techniques / Drug Synergism / Histone Deacetylase Inhibitors / Humans / Multiple Myeloma / Osteoclasts / Thalidomide / Tumor Cells, Cultured / Valproic Acid (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-008-0226-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19093163 ● Search Scopus @ Elsevier (PMID): 19093163 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-008-0226-9 (DOI: 10.1007/s12185-008-0226-9, PubMed: 19093163)
98.	Shusuke Yagi, Masahi Akaike, Mitsunori Fujimura, Takayuki Ise, Sumiko Yoshida, Yuka Sumitomo, Yasumasa Ikeda, Takashi Iwase, Ken-ichi Aihara, Hiroyuki Azuma, Atsushi Kurushima, Youichi Ichikawa, Tetsuya Kitagawa, Takehiko Kimura, Takeshi Nishiuchi and Toshio Matsumoto : Infective endocarditis caused by lactobacillus., Internal Medicine, 47, 12, 1113-1116, 2008. (Summary) Lactobacillus (LB) is a gram-positive rod-shaped bacterium that inhabits the oral cavity, gastrointestinal tract, vagina and nasal cavity. Although LB plays a role in the prevention of infections caused by pathogenic bacteria, it causes some critical infectious diseases such as infective endocarditis (IE). IE due to LB is rare; however, early diagnosis and early treatment are important because of its high mortality rate. We report the onset of IE after otologic treatment in a heavy drinker of alcohol, the second case of IE due to LB in Japan. (Keyword) Adult / Alcoholism / Endocarditis, Bacterial / Gram-Positive Bacterial Infections / Heart Valve Prosthesis Implantation / Humans / Immunocompromised Host / Lactobacillus / Male / Mitral Valve Insufficiency (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.47.0744 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18552468 ● Summary page in Scopus @ Elsevier: 2-s2.0-48049096600 ● Summary page in Scopus @ Elsevier: 2-s2.0-56349127735 (DOI: 10.2169/internalmedicine.47.0744, PubMed: 18552468, Elsevier: Scopus, Elsevier: Scopus)
99.	Seiji Fukumoto, Noriyuki Numba, Keiichi Ozono, Mika Yamauchi, Toshitsugu Sugimoto, Toshimi Michigami, Hiroyuki Tanaka, Daisuke Inoue, Masanori Minagawa, Itsuro Endo and Toshio Matsumoto : Causes and differential diagnosis of hypocalcemia--recommendation proposed by expert panel supported by ministry of health, labour and welfare, Japan, Endocrine Journal, 55, 5, 787-794, 2008. (Summary) Serum calcium (Ca) level is maintained within a narrow range mainly by actions of parathyroid hormone (PTH) and 1,25-dihydroxyvitmain D [1,25(OH)(2)D]. While it is not rare to encounter hypocalcemia in clinical practice, there is currently no practical guideline for the differential diagnosis of hypocalcemia. We therefore propose flowcharts for the differential diagnosis of hypocalcemia and hypoparathyroidism, especially PTH-deficient hypoparathyroidism in which many genetic or other causes have been identified recently. Hypocalcemia can be divided into two categories, hypocalcemia with low serum phosphate level, and one with normal to elevated serum phosphate level. Deficient actions of 1,25(OH)(2)D, loss of Ca into urine, and deposition of Ca in bone or soft tissues are main causes of hypocalcemia with low to low normal serum phosphate level. Hypocalcemia with high normal to high serum phosphate level includes chronic renal failure and hypoparathyroidism. Hypoparathyroidism is subdivided into PTH-deficient hypoparathyroidism and pseudohypoparathyroidism. Recent investigations identified several causes of PTH-deficient hypoparathyroidism, including genetic abnormalities and parathyroid autoantibodies, which should be differentiated from idiopathic hypoparathyroidism. Physical and laboratory findings, the time of the onset of diseases and accompanying illness can be clues for identifying causes of PTH-deficient hypoparathyroidism. (Keyword) Hypocalcemia / differential diagnosis (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.k08e-076 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18490837 ● Search Scopus @ Elsevier (PMID): 18490837 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.k08e-076 (DOI: 10.1507/endocrj.k08e-076, PubMed: 18490837)
100.	Itsuro Endo, Seiji Fukumoto, Keiichi Ozono, Noriyuki Namba, Hiroyuki Tanaka, Daisuke Inoue, Masanori Minagawa, Toshitsugu Sugimoto, Mika Yamauchi, Toshimi Michigami and Toshio Matsumoto : Clinical usefulness of measurement of fibroblast growth factor 23 (FGF23) in hypophosphatemic patients: proposal of diagnostic criteria using FGF23 measurement., Bone, 42, 6, 1235-1239, 2008. (Summary) Fibroblast growth factor 23 (FGF23) plays important roles in the development of hypophosphatemic diseases such as tumor-induced osteomalacia (TIO) and X-linked hypophosphatemic rickets/osteomalacia (XLH). However, clinical usefulness of measurement of FGF23 has not been established. The objective of this study is to examine the importance of FGF23 measurement in the diagnosis of hypophosphatemic diseases. Biochemical parameters concerning phosphate metabolism were analyzed in a cross-sectional study. 32 patients with TIO, 28 patients with XLH and 16 hypophosphatemic patients with other causes including vitamin D deficiency, Fanconi's syndrome and Cushing's syndrome were studied. In patients with TIO and XLH, FGF23 was above the upper limit of the reference range in most patients irrespective of medical treatment. The lowest FGF23 in these patients was 38.0 pg/ml. FGF23 in hypophosphatemic patients with other causes was undetectable (less than 3 pg/ml) in 12 patients and the highest FGF23 in this group was 23.9 pg/ml. Relationship between phosphate and FGF23 indicated that TIO and XLH are diseases with high FGF23 and hypophosphatemia judged by age-dependent reference ranges for serum phosphate. FGF23 measurement is useful for differential diagnosis of hypophosphatemic diseases caused by excess actions of FGF23 and other etiologies. High FGF23 with low phosphate judged by age-dependent reference ranges for phosphate establishes the diagnosis of diseases caused by excess actions of FGF23. (Keyword) Adolescent / Adult / Aged / Aged, 80 and over / Child / Child, Preschool / Cross-Sectional Studies / Familial Hypophosphatemic Rickets / Female / Fibroblast Growth Factors / Genetic Diseases, X-Linked / Humans / Hypophosphatemia / Infant / Male / Middle Aged / Osteomalacia / Phosphorus (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bone.2008.02.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18396126 ● Search Scopus @ Elsevier (PMID): 18396126 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bone.2008.02.014 (DOI: 10.1016/j.bone.2008.02.014, PubMed: 18396126)
101.	Toshiyuki Obata, Ichiro Yokota, Kazuhiro Yokoyama, Eiji Okamoto, Yoshiko Kanezaki, Yoshinori Tanaka, Hiroshi Maegawa, Kiyoshi Teshigawara, Fumiko Hirota, Tomoyuki Yuasa, Kazuhiro Kishi, Atsushi Hattori, Seiichi Hashida, Kazuhiko Masuda, Mitsuru Matsumoto, Toshio Matsumoto, Atsunori Kashiwagi and Yousuke Ebina : Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes mellitus., Diabetes, 56, 8, 2028-2035, 2007. (Summary) Insulin binds to the alpha-subunit of the insulin receptor (IRalpha) and subsequently exerts its effects in the cells. The soluble ectodomains of several receptors have been found to circulate in the plasma. Therefore, we hypothesized that soluble human insulin receptor (hIR) ectodomain (alpha-subunit and a part of beta-subunit) may exist in the plasma of diabetic patients. We identified soluble hIR ectodomain in human plasma by a two-step purification followed by immunoblotting and gel-filtration chromatography. Furthermore, we established an hIRalpha-specific enzyme-linked immunosorbent assay and measured the plasma IRalpha levels in patients with diabetes. We also investigated this phenomenon in streptozotocin-induced diabetic hIR transgenic mice. Soluble hIRalpha, but not intact hIRbeta or whole hIR, exists in human plasma. The plasma IRalpha levels were significantly higher in type 1 (2.00 +/- 0.60 ng/ml; n = 53) and type 2 (2.26 +/- 0.80; n = 473) diabetic patients than in control subjects (1.59 +/- 0.40 ng/ml; n = 123 (P < 0.001 vs. control). Plasma IRalpha level was positively correlated with blood glucose level, and 10-20% of the insulin in plasma bound to hIRalpha. In the in vivo experiments using diabetic hIR transgenic mice, hyperglycemia was confirmed to increase the plasma hIRalpha level and the half-life estimated to be approximately 6 h. We propose that the increased soluble IR ectodomain level appears to be a more rapid glycemic marker than A1C or glycoalbumin. (Keyword) Animals / Diabetes Mellitus / Diabetes Mellitus, Experimental / Diabetes Mellitus, Type 1 / Diabetes Mellitus, Type 2 / Enzyme-Linked Immunosorbent Assay / Humans / Mice / Mice, Transgenic / Receptor, Insulin / Solubility / Streptozocin (Link to Publication Site) ● Publication site (DOI): 10.2337/db07-0394 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17563065 ● Search Scopus @ Elsevier (PMID): 17563065 ● Search Scopus @ Elsevier (DOI): 10.2337/db07-0394 (DOI: 10.2337/db07-0394, PubMed: 17563065)
102.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Masataka Sata, Nobuyuki Takamori, Shusuke Yagi, Takashi Iwase, Yuka Sumitomo, Hirotaka Kawano, Takashi Yamada, Toru Fukuda, Takahiro Matsumoto, Keisuke Sekine, Takashi Sato, Yuko Nakamichi, Yoko Yamamoto, Kimihiro Yoshimura, Tomoyuki Watanabe, Takashi Nakamura, Akimasa Oomizu, Minoru Tsukada, Hideki Hayashi, Toshiki Sudo, Shigeaki Kato and Toshio Matsumoto : Strain-dependent embryonic lethality and exaggerated vascular remodeling in heparin cofactor II-deficient mice, The Journal of Clinical Investigation, 117, 6, 1514-1526, 2007. (Summary) Heparin cofactor II (HCII) specifically inhibits thrombin action at sites of injured arterial wall, and patients with HCII deficiency exhibit advanced atherosclerosis. However, the in vivo effects and the molecular mechanism underlying the action of HCII during vascular remodeling remain elusive. To clarify the role of HCII in vascular remodeling, we generated HCII-deficient mice by gene targeting. In contrast to a previous report, HCII(-/-) mice were embryonically lethal. In HCII(+/-) mice, prominent intimal hyperplasia with increased cellular proliferation was observed after tube cuff and wire vascular injury. The number of protease-activated receptor-1-positive (PAR-1-positive) cells was increased in the thickened vascular wall of HCII(+/-) mice, suggesting enhanced thrombin action in this region. Cuff injury also increased the expression levels of inflammatory cytokines and chemokines in the vascular wall of HCII(+/-) mice. The intimal hyperplasia in HCII(+/-) mice with vascular injury was abrogated by human HCII supplementation. Furthermore, HCII deficiency caused acceleration of aortic plaque formation with increased PAR-1 expression and oxidative stress in apoE-KO mice. These results demonstrate that HCII protects against thrombin-induced remodeling of an injured vascular wall by inhibiting thrombin action and suggest that HCII is potentially therapeutic against atherosclerosis without causing coagulatory disturbance. (Keyword) Animals / Base Sequence / Blood Vessels / DNA Primers / Embryo Loss / Female / Gene Targeting / Genes, Lethal / Genotype / Heparin Cofactor II / Heterozygote / Homozygote / Male / Mice / Mice, Inbred C57BL / knockout mice / Pregnancy (Link to Publication Site) ● Publication site (DOI): 10.1172/JCI27095 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17549254 ● Search Scopus @ Elsevier (PMID): 17549254 ● Search Scopus @ Elsevier (DOI): 10.1172/JCI27095 (DOI: 10.1172/JCI27095, PubMed: 17549254)
103.	Takao Mitsui, Makoto Kunishige, Michiko Ichimiya, Kana Shichijo, Itsuro Endo and Toshio Matsumoto : Beneficial effect of tacrolimus on myasthenia gravis with thymoma, The Neurologist, 13, 2, 83-86, 2007. (Summary) We examined the effect of tacrolimus on myasthenia gravis (MG). Five patients with thymoma and 5 patients without thymoma underwent prior thymectomy but showed persistent myasthenic symptoms. Oral administration with tacrolimus significantly improved MG scores 1, 3, and 6 months following the beginning of treatment in all patients (P < 0.05), and the improvement was significantly higher in the thymoma group compared with the nonthymoma group (P < 0.05). However, there was no significant change in antiacetylcholine receptor titers in either group. This indicates a particular application of immunosuppressive therapy for thymomatous MG following thymectomy. (Keyword) Administration, Oral / Adult / Aged / Autoantibodies / Autoimmunity / Female / Humans / Immunosuppressive Agents / Male / Middle Aged / Myasthenia Gravis / Receptors, Nicotinic / Tacrolimus / Thymoma / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1097/01.nrl.0000256352.77668.ef (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17351528 ● Search Scopus @ Elsevier (PMID): 17351528 ● Search Scopus @ Elsevier (DOI): 10.1097/01.nrl.0000256352.77668.ef (DOI: 10.1097/01.nrl.0000256352.77668.ef, PubMed: 17351528)
104.	Youichi Tanaka, Masahiro Abe, Masahiro Hiasa, Asuka Oda, Hiroe Amou, Ayako Nakano, Kyoko Takeuchi, Kenichi Kitazoe, Shinsuke Kido, Daisuke Inoue, Keiji Moriyama, Toshihiro Hashimoto, Shuji Ozaki and Toshio Matsumoto : Myeloma Cell-Osteoclast Interaction Enhances Angiogenesis Together with Bone Resorption: A Role for Vascular Endothelial Cell Growth Factor and Osteopontin, Clinical Cancer Research, 13, 3, 816-823, 2007. (Summary) Similar to osteoclastogenesis, angiogenesis is enhanced in the bone marrow in myeloma in parallel with tumor progression. We showed previously that myeloma cells and osteoclasts are mutually stimulated to form a vicious cycle to lead to enhance both osteoclastogenesis and tumor growth. The present study was undertaken to clarify whether myeloma cell-osteoclast interaction enhances angiogenesis and whether there is any mutual stimulation between osteoclastogenesis and angiogenesis. Myeloma cells and monocyte-derived osteoclasts were cocultured, and angiogenic activity produced by the cocultures was assessed with in vitro vascular tubule formation assays and human umbilical vascular endothelial cell (HUVEC) migration and survival. Osteoclastogenic activity was determined with rabbit bone cell cultures on dentine slices. Myeloma cells and osteoclasts constitutively secrete proangiogenic factors, vascular endothelial growth factor (VEGF) and osteopontin, respectively. A cell-to-cell interaction between myeloma cells and osteoclasts potently enhanced vascular tubule formation. Blockade of both VEGF and osteopontin actions almost completely abrogated such vascular tubule formation as well as migration and survival of HUVECs enhanced by conditioned medium from cocultures of myeloma cells and osteoclasts. Furthermore, these factors in combination triggered the production of osteoclastogenic activity by HUVEC. Osteoclast-derived osteopontin and VEGF from myeloma cells cooperatively enhance angiogenesis and also induce osteoclastogenic activity by vascular endothelial cells. These observations suggest the presence of a close link between myeloma cells, osteoclasts, and vascular endothelial cells to form a vicious cycle between bone destruction, angiogenesis, and myeloma expansion. (Keyword) Bone Resorption / Cell Movement / Cell Survival / Coculture Techniques / Culture Media, Conditioned / Disease Progression / Endothelium, Vascular / Humans / Monocytes / Multiple Myeloma / Neovascularization, Pathologic / Osteoclasts / Osteopontin / Umbilical Veins / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1158/1078-0432.CCR-06-2258 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17289872 ● Search Scopus @ Elsevier (PMID): 17289872 ● Search Scopus @ Elsevier (DOI): 10.1158/1078-0432.CCR-06-2258 (DOI: 10.1158/1078-0432.CCR-06-2258, PubMed: 17289872)
105.	近藤剛史, Itsuro Endo, 木内美瑞穂, Yuichi Fujinaka, Daisuke Inoue, 福本誠二, 大歯浩一, Kenji Endo, Natsuo Yasui, 長谷川匡, Hisanori Uehara, Yoshimi Bando and Toshio Matsumoto : 腫瘍性骨軟化症の一例, 日本内分泌学会雑誌, 83, 136-138, 2007.
106.	Masahiro Abe, Shinsuke Kido, Masahiro Hiasa, Nakano Ayako, Oda Asuka, Amou Hiroe and Toshio Matsumoto : BAFF and APRIL as osteoclast-derived survival factors for myeloma cells: a rationale for TACI-Fc tratment in patients with multiple myeloma., Leukemia, 20, 7, 1313-1315, 2006. (Keyword) B-Cell Activating Factor / Cell Survival / Humans / Immunoglobulin Fc Fragments / Multiple Myeloma / Osteoclasts / Transmembrane Activator and CAML Interactor Protein / Tumor Necrosis Factor Ligand Superfamily Member 13 (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.leu.2404228 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16617317 ● Search Scopus @ Elsevier (PMID): 16617317 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.leu.2404228 (DOI: 10.1038/sj.leu.2404228, PubMed: 16617317)
107.	Y. Kuroda, Takao Mitsui, M. Kunishige, Masayuki Shono, Masashi Akaike, H. Azuma and Toshio Matsumoto : Parkin enhances mitochondrial biogenesis in proliferating cells., Human Molecular Genetics, 15, 6, 883-895, 2006. (Summary) We describe a novel function of parkin, a RING protein, which is elaborately involved in mitochondrial biogenesis. Parkin was located within the mitochondrial organelle of proliferating cells. Anti-proliferative treatments released parkin from mitochondria to cytosol. Results of pharmacological treatments indicate that parkin was released from mitochondria when permeability transition pore was opened. The extra-mitochondrial localization was also observed in differentiated cells. In proliferating cells, transcription and replication of mitochondrial DNA was enhanced by parkin overexpression and attenuated by parkin suppression with siRNA. Parkin was associated with mitochondrial transcription factor A (TFAM) and enhanced TFAM-mediated mitochondrial transcription. These results indicate that parkin is involved in the regulation of mitochondrial transcription/replication other than the ubiquitin-mediated protein degradation system in proliferating cells. (Keyword) Parkin / mitochondria (Link to Publication Site) ● Publication site (DOI): 10.1093/hmg/ddl006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16449237 ● Search Scopus @ Elsevier (PMID): 16449237 ● Search Scopus @ Elsevier (DOI): 10.1093/hmg/ddl006 (DOI: 10.1093/hmg/ddl006, PubMed: 16449237)
108.	Ali Jalili, Shuji Ozaki, Tomoko Hara, Hironobu Shibata, Toshihiro Hashimoto, Masahiro Abe, Yasuhiko Nishioka and Toshio Matsumoto : Induction of HM1.24 peptide specific cytotoxic T lymphocytes by using peripheral-blood stem-cell harvests in patients with multiple myeloma, Blood, 106, 10, 3538-3545, 2005. (Summary) HM1.24 antigen is preferentially overexpressed in multiple myeloma (MM) cells but not in normal cells. To explore the potential of HM1.24 as a target for cellular immunotherapy, we selected 4 HM1.24-derived peptides that possess binding motifs for HLA-A2 or HLA-A24 by using 2 computer-based algorithms. The ability of these peptides to generate cytotoxic T lymphocytes (CTLs) was examined in 20 healthy donors and 6 patients with MM by a reverse immunologic approach. Dendritic cells (DCs) were induced from peripheral-blood mononuclear cells of healthy donors or peripheral-blood stem-cell (PBSC) harvests from patients with MM, and autologous CD8(+) T cells were stimulated with HM1.24 peptide-pulsed DCs. Both interferon-gamma-producing and cytotoxic responses were observed after stimulation with either HM1.24-126 or HM1.24-165 peptides in HLA-A2 or HLA-A24 individuals. The peptide-specific recognition of these CTLs was further confirmed by tetramer assay and cold target inhibition assay. Importantly, HM1.24-specific CTLs were also induced from PBSC harvests from patients with MM and these CTLs were able to kill MM cells in an HLA-restricted manner. These results indicate the existence of functional DCs and HM1.24-specific CTL precursors within PBSC harvests and provide the basis for cellular immunotherapy in combination with autologous PBSC transplantation in MM. (Keyword) Antigens, CD / Cell Line, Tumor / Dendritic Cells / Female / GPI-Linked Proteins / HLA-A Antigens / HLA-A2 Antigen / HLA-A24 Antigen / Hematopoietic Stem Cells / Humans / Interferon-gamma / Male / Membrane Glycoproteins / Multiple Myeloma / Peptides / Peripheral Blood Stem Cell Transplantation / T-Lymphocytes, Cytotoxic / Transplantation, Homologous (Link to Publication Site) ● Publication site (DOI): 10.1182/blood-2005-04-1438 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16037388 ● Search Scopus @ Elsevier (PMID): 16037388 ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2005-04-1438 (DOI: 10.1182/blood-2005-04-1438, PubMed: 16037388)
109.	Takashi Oshima, Masahiro Abe, Jin Asano, Tomoko Hara, Kenichi Kitazoe, Etsuko Sekimoto, Yoichi Tanaka, Hironobu Shibata, Toshihiro Hashimoto, Shuji Ozaki, Shinsuke Kido, Daisuke Inoue and Toshio Matsumoto : Myeloma cells suppress bone formation by secreting a soluble Wnt inhibitor, sFRP-2, Blood, 106, 9, 3160-3165, 2005. (Summary) Multiple myeloma (MM) develops devastating bone destruction with enhanced bone resorption and suppressed bone formation. In contrast to enhanced osteoclastogenesis, little is known about the mechanism of impaired bone formation in MM. Because a canonical Wingless-type (Wnt) signaling pathway has recently been shown to play an important role in osteoblast differentiation, we examined whether MM cells affect a canonical Wnt pathway to suppress bone formation. Conditioned media from RPMI8226 and U266 MM cell lines and primary MM cells suppressed in vitro mineralization as well as alkaline phosphatase activity in osteoblasts induced by bone morphogenetic protein 2 (BMP-2). These cell lines constitutively produced a soluble Wnt inhibitor, secreted Frizzled-related protein 2 (sFRP-2), but not other Wnt inhibitors including sFRP-1, sFRP-3, and dickkopf 1 (DKK-1) at the protein level. Most MM cells from patients with advanced bone destructive lesions also expressed sFRP-2. Furthermore, exogenous sFRP-2 suppressed osteoblast differentiation induced by BMP-2, and immunodepletion of sFRP-2 significantly restored mineralized nodule formation in vitro, suggesting a predominant role for MM cell-derived sFRP-2 in the impairment of bone formation by MM. Thus, in addition to enhanced osteolysis, MM cells also suppress bone formation at least in part through an inhibition of the canonical Wnt pathway by secreting sFRP-2. (Keyword) Animals / Antibodies / Bone Morphogenetic Protein 2 / Bone Morphogenetic Proteins / Calcification, Physiologic / Cell Differentiation / Genes, Reporter / Humans / Melanoma / Membrane Proteins / Mice / Osteoblasts / Osteogenesis / Solubility / Transforming Growth Factor beta / Tumor Cells, Cultured / Wnt Proteins (Link to Publication Site) ● Publication site (DOI): 10.1182/blood-2004-12-4940 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16030194 ● Search Scopus @ Elsevier (PMID): 16030194 ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2004-12-4940 (DOI: 10.1182/blood-2004-12-4940, PubMed: 16030194)
110.	Hironobu Shibata, Masahiro Abe, Kenji Hiura, Javier Wilde, Keiji Moriyama, Toshiaki Sano, Ken-ichi Kitazoe, Toshihiro Hashimoto, Shuji Ozaki, Shingo Wakatsuki, Shinsuke Kido, Daisuke Inoue and Toshio Matsumoto : Malignant B-lymphoid cells with bone lesions express receptor activator of nuclear factor-kappaB ligand and vascular endothelial growth factor to enhance osteoclastogenesis., Clinical Cancer Research, 11, 17, 6109-6115, 2005. (Summary) Receptor activator of nuclear factor-kappaB ligand (RANKL) is a key mediator of osteoclastogenesis. Because certain types of tumor cells aberrantly express RANKL, and because bone destruction also develops in B-cell lymphomas of bone origin, we investigated RANKL expression and the mechanisms of osteoclastogenesis in B-lymphoid neoplasms. Immunohistochemistry of bone specimens resected from patients with primary B-cell lymphoma of bone with bone destruction revealed that lymphoma cells express RANKL as well as vascular endothelial cell growth factor (VEGF). The tumor cells isolated from the bone specimens enhanced osteoclastogenesis in vitro. In contrast, B-cell lymphoma infiltrating to the bone marrow without bone destruction did not express RANKL. Both RANKL and VEGF were expressed by a portion of B-lymphoid cell lines, including Daudi and IM-9. These RANKL-expressing tumor cells enhanced osteoclastogenesis from RAW264.7 cells and human monocyte-derived preosteoclasts in the absence of stromal cells/osteoblasts in a RANKL-dependent manner. Furthermore, conditioned media from Daudi cells enhanced transmigration of preosteoclasts that was inhibited by anti-VEGF antibody, suggesting that tumor cell-derived VEGF mediates recruitment of osteoclast precursors. Moreover, cocultures of B-lymphoid cell lines with osteoclasts enhanced the growth of B-lymphoid cells. Some malignant B cells aberrantly express functional RANKL as well as VEGF to enhance osteoclastogenesis. The coexpression of RANKL and VEGF may also contribute to the close cellular interactions with osteoclastic cells, thereby forming a vicious cycle between osteoclastic bone destruction and tumor expansion in bone. (Keyword) Bone Neoplasms / Carrier Proteins / Cell Movement / Culture Media, Conditioned / Flow Cytometry / Humans / Immunoenzyme Techniques / Lymphoma, B-Cell / Membrane Glycoproteins / Osteoclasts / RANK Ligand / Receptor Activator of Nuclear Factor-kappa B / Stromal Cells / Tumor Cells, Cultured / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1158/1078-0432.CCR-05-0181 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16144909 ● Search Scopus @ Elsevier (PMID): 16144909 ● Search Scopus @ Elsevier (DOI): 10.1158/1078-0432.CCR-05-0181 (DOI: 10.1158/1078-0432.CCR-05-0181, PubMed: 16144909)
111.	Toshio Matsumoto, Takami Miki, Hiroshi Hagino, Toshitsugu Sugimoto, Sumiaki Okamoto, Takako Hirota, Yusuke Tanigawara, Yasufumi Hayashi, Masao Fukunaga, Masataka Shiraki and Toshitaka Nakamura : A New Active Vitamin D, ED-71, Increases Bone Mass in Osteoporotic Patients under Vitamin D Supplementation: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial, The Journal of Clinical Endocrinology and Metabolism, 90, 9, 5031-5036, 2005. (Summary) ED-71 has been shown to increase lumbar bone mineral density (BMD) in osteoporotic subjects. However, vitamin D insufficiency might have influenced the effect of ED-71 on BMD. Our objective was to examine whether ED-71 can increase BMD in osteoporotic patients under vitamin D supplementation. We conducted a randomized, double-blind, placebo-controlled clinical trial of 219 osteoporotic patients (49-87 yr of age). Interventions: Subjects were randomly assigned to receive placebo or 0.5, 0.75, or 1.0 microg/d ED-71 for 12 months. All the subjects received 200 or 400 IU/d vitamin D(3). We assessed changes in lumbar and hip BMD and bone turnover markers from baseline. Lumbar BMD increased with ED-71 treatment for 12 months (2.2, 2.6, and 3.1% from baseline and 2.9, 3.4, and 3.8% vs. placebo group in subjects receiving 0.5, 0.75, and 1.0 microg ED-71, respectively). Total hip BMD also increased with 0.75 and 1.0 microg ED-71 (-0.8, 0.6, and 0.9% from baseline and 0.1, 1.5, and 1.8% vs. placebo group in the 0.5, 0.75, and 1.0 microg ED-71 groups, respectively). Bone formation and resorption markers were suppressed by approximately 20% after 12 months of 0.75 and 1.0 microg ED-71 treatment. Transient hypercalcemia over 2.6 mmol/liter occurred in 7, 5, and 23% of subjects in the 0.5, 0.75, and 1.0 microg ED-71 groups, respectively, but none of them developed sustained hypercalcemia. These results demonstrate that ED-71 treatment at around 0.75 microg/d can effectively and safely increase lumbar and hip BMD in osteoporotic patients with vitamin D supplementation. (Keyword) Absorptiometry, Photon / Aged / Aged, 80 and over / Biological Markers / Bone Density / Bone Remodeling / Calcitriol / calcium / Dose-Response Relationship, Drug / Double-Blind Method / Female / Hip Joint / Hormones / Humans / Hypercalcemia / Lumbar Vertebrae / Male / Middle Aged / Osteoporosis / Patient Compliance / vitamin D (Link to Publication Site) ● Publication site (DOI): 10.1210/jc.2004-2552 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15972580 ● Summary page in Scopus @ Elsevier: 2-s2.0-24344474407 (DOI: 10.1210/jc.2004-2552, PubMed: 15972580, Elsevier: Scopus)
112.	Hiro Cgikakiyo, Makoto Kunishige, Hiide Yoshino, Atsuko Asano, Yuka Sumitomo, Itsuro Endo, Toshio Matsumoto and Takao Mitsui : Delayed motor and sensory neuropathy in a patient with brainstem encephalitis, Journal of the Neurological Sciences, 234, 1-2, 105-108, 2005. (Summary) Bickerstaff's brainstem encephalitis (BBE), Miller Fisher syndrome (MFS) and Guillain-Barré syndrome (GBS) are thought to be closely related and to form a continuous spectrum. However, chronic polyneuropathy in BBE has not been reported. We report the temporal profile of anti-ganglioside antibody titer in a case of BBE-like brainstem encephalitis complicated with chronic polyneuropathy. A 71-year-old Japanese woman presented with drowsiness and cerebellar ataxia in addition to mild weakness in distal limb muscles. Anti-GalNAc-GD1a IgG and anti-GalNAc-GM1b IgG antibodies were positive in her serum. Brain magnetic resonance imaging revealed high-intensity signals in the midbrain, pons, and middle cerebellar peduncles on T2-weighted images. Central nervous system manifestations improved after immunomodulating therapy that included prednisolone, plasmapheresis and intravenous immunoglobulin. Nevertheless, the distal muscle weakness was exacerbated when the anti-GalNAc-GD1a IgG titer was elevated. Nerve conduction study indicated motor and sensory neuropathy which was developed motor dominant axonal damage. These findings suggest that anti-ganglioside antibodies, including anti-GalNAc-GD1a IgG, may be involved in a common autoimmune mechanism in BBE-like brainstem encephalitis and chronic motor dominant axonal neuropathy. However, the fact that the latter manifestation exacerbated after the improvement of former one possibly indicates different thresholds of neurologic symptoms mediated by anti-ganglioside antibodies in the present patient. (Keyword) Aged / Autoantibodies / Blotting, Western / Brain Stem / Chromatography, Thin Layer / Encephalitis / Evoked Potentials, Motor / Evoked Potentials, Somatosensory / Female / Follow-Up Studies / Gangliosides / Humans / Immunoglobulin G / Magnetic Resonance Imaging / Neural Conduction / Penicillamine / Peripheral Nervous System Diseases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jns.2005.02.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15936038 ● Search Scopus @ Elsevier (PMID): 15936038 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jns.2005.02.011 (DOI: 10.1016/j.jns.2005.02.011, PubMed: 15936038)
113.	Yasumasa Ikeda, Ken-ichi Aihara, Takashi Sato, Masashi Akaike, Masanori Yoshizumi, Yuki Suzaki, Yuki Izawa-Ishizawa, Mitsunori Fujimura, Shunji Hashizume, Midori Kato, Shusuke Yagi, Toshiaki Tamaki, Hirotaka Kawano, Takahiro Matsumoto, Hiroyuki Azuma, Shigeaki Kato and Toshio Matsumoto : Androgen receptor gene knockout male mice exhibit impaired cardiac growth and exacerbation of angiotensin II-induced cardiac fibrosis., The Journal of Biological Chemistry, 280, 33, 29661-29666, 2005. (Summary) Androgen has anabolic effects on cardiac myocytes and has been shown to enhance left ventricular enlargement and function. However, the physiological and patho-physiological roles of androgen in cardiac growth and cardiac stress-induced remodeling remains unclear. We aimed to clarify whether the androgen-nuclear androgen receptor (AR) system contributes to the cardiac growth and angiotensin II (Ang II)-stimulated cardiac remodeling by using systemic AR-null male mice. AR knock-out (ARKO) male mice, at 25 weeks of age, and age-matched wild-type (WT) male mice were treated with or without Ang II stimulation (2.0 mg/kg/day) for 2 weeks. ARKO mice with or without Ang II stimulation showed a significant reduction in the heart-to-body weight ratio compared with those of WT mice. In addition, echocardiographic analysis demonstrated impairments of both the concentric hypertrophic response and left ventricular function in Ang II-stimulated ARKO mice. Western blot analysis of the myocardium revealed that activation of extracellular signal-regulated kinases (ERK) 1/2 and ERK5 by Ang II stimulation were lower in ARKO mice than those of WT mice. Ang II stimulation caused more prominent cardiac fibrosis in ARKO mice than in WT mice with enhanced expression of types I and III collagen and transforming growth factor-beta1 genes and with increased Smad2 activation. These results suggest that, in male mice, the androgen-AR system participates in normal cardiac growth and modulates cardiac adaptive hypertrophy and fibrosis during the process of cardiac remodeling under hypertrophic stress. (Keyword) Angiotensin II / Animals / blood pressure / Cardiomegaly / DNA-Binding Proteins / pulmonary fibrosis / Heart Rate / Male / Mice / Mice, Inbred C57BL / Mice, Inbred CBA / knockout mice / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / myocardium / RNA, Messenger / Receptors, Androgen / Smad2 Protein / Trans-Activators / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M411694200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15961403 ● Search Scopus @ Elsevier (PMID): 15961403 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M411694200 (DOI: 10.1074/jbc.M411694200, PubMed: 15961403)
114.	Takashi Iwase, Noritoshi Nagaya, Takafumi Fujii, Takefumi Itoh, Shinsuke Murakami, Toshio Matsumoto, Kenji Kangawa and Soichiro Kitamura : Comparison of angiogenic potency between mesenchymal stem cells and mononuclear cells in a rat model of hindlimb ischemia, Cardiovascular Research, 66, 3, 543-551, 2005. (Summary) OBJECTIVE: Mesenchymal stem cells (MSC) are pluripotent cells that differentiate into a variety of cells including endothelial cells and vascular smooth muscle cells. Although transplantation of bone marrow-derived mononuclear cells (MNC) has already been applied for the treatment of critical limb ischemia, little information is available regarding comparison of the angiogenic potency between MSC and MNC. Accordingly, we injected equal numbers of MSC or MNC in a rat model of hindlimb ischemia and compared their therapeutic potential. METHODS AND RESULTS: Immediately after creating hindlimb ischemia, rats were randomized to receive MSC transplantation (MSC group), MNC transplantation (MNC group), or vehicle infusion (Control group). Three weeks after transplantation, the laser Doppler perfusion index was significantly higher in the MNC group than in the Control group (0.69+/-0.1 vs. 0.57+/-0.06, P<0.01). Furthermore, there was a marked improvement in blood perfusion in the MSC group (0.81+/-0.08). Capillary density was highest in the MSC group. The number of transplanted cell-derived endothelial cells was higher in the MSC group than in the MNC group. Transplanted cell-derived vascular smooth muscle cells were detected only in the MSC group. In vitro, MSC were more tolerant to apoptotic stimulus (serum starvation and hypoxia) than MNC. CONCLUSIONS: MSC transplantation caused significantly greater improvement in hindlimb ischemia than MNC transplantation. Compared with MNC, MSC survived well under an ischemic environment, and differentiated into not only endothelial cells but also vascular smooth muscle cells. Thus, MSC transplantation may be a new therapeutic strategy for the treatment of severe peripheral vascular disease. (Keyword) Animals / apoptosis / Bone Marrow Transplantation / cell differentiation / Endothelial Cells / Hindlimb / ischemia / Laser-Doppler Flowmetry / Leukocytes, Mononuclear / Male / Mesenchymal Stem Cell Transplantation / Models, Animal / Muscle, Smooth, Vascular / Neovascularization, Physiologic / Peripheral Vascular Diseases / Random Allocation / Rats / Rats, Inbred Lew / Transplantation, Autologous (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cardiores.2005.02.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15914119 ● Summary page in Scopus @ Elsevier: 2-s2.0-19444380789 (DOI: 10.1016/j.cardiores.2005.02.006, PubMed: 15914119, Elsevier: Scopus)
115.	Hiroko Omori, Takao Mitsui, Makoto Kunishige, Itsuro Endo, Koji Takahashi and Toshio Matsumoto : Beneficial effect of tacrolimus on myasthenia gravis with thymoma, Clinical Neuropathology, 24, 4, 191-193, 2005. (Summary) We report a 53-year-old Japanese woman who had recurrent orbital myositis for 14 years. She exhibited mild muscle weakness in proximal limbs 13 years after the onset of orbital myositis. An electromyogram revealed myopathic potentials and denervation potentials in proximal limb muscles. Quadriceps biopsy showed infiltrates of mononuclear cells around intramuscular vessels and mild degenerative changes in muscle cells. These findings indicate that the present case belongs to the spectrum of localized nodular myositis. (Keyword) Adult / Chronic Disease / Electromyography / female / Humans / Muscle, Skeletal / Orbital Pseudotumor / Polymyositis / Recurrence (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16033136 ● Summary page in Scopus @ Elsevier: 2-s2.0-21844470000 (PubMed: 16033136, Elsevier: Scopus)
116.	Kana Shichijo, Takao Mitsui, Makoto Kunishige, Yukiko Kuroda, Kenjiro Masuda and Toshio Matsumoto : Involvement of mitochondria in myasthenia gravis complicated with dermatomyositis and rheumatoid arthritis: a case report, Acta Neuropathologica, 109, 5, 539-542, 2005. (Summary) We report a 57-year-old male with myasthenia gravis complicated with dermatomyositis and rheumatoid arthritis without evidence of thymoma. He showed prominent muscle wasting and weakness in the four extremities and trunk in addition to swallowing disturbance. He showed intolerance to exercise on a bicycle ergometer, and muscle biopsy specimens demonstrated ragged-red fibers. An anti-acetylcholine receptor (AChR) antibody was detected in his serum but no anti-mitochondrial M2 component antibody was found. In contrast, results of immunohistochemical study indicated that his serum sample reacted to muscle mitochondria as well as AChR. These results indicate the presence of an unidentified anti-mitochondrial antibody that may be involved in the development of mitochondrial dysfunction in skeletal muscle of the present patient. (Keyword) Anti-acetylcholine receptor antibody / immunohistochemistry / Anti-mitochondrial antibody / Mitochondrial dysfunction / Ragged-redfibers (Link to Publication Site) ● Publication site (DOI): 10.1007/s00401-005-0990-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15843907 ● Summary page in Scopus @ Elsevier: 2-s2.0-21344436854 (DOI: 10.1007/s00401-005-0990-z, PubMed: 15843907, Elsevier: Scopus)
117.	Midori Kato, Hiroyuki Azuma, Masashi Akaike, Takahiko Iuchi, Ken-ichi Aihara, Yasumasa Ikeda, Mitsunori Fujimura, Tomonori Yoshida, Hiroshi Yamaguchi, Shunji Hashizume and Toshio Matsumoto : Aspirin inhibits thrombin action on endothelial cells via up-regulation of aminopeptidase N/CD13 expression., Atherosclerosis, 183, 1, 49-55, 2005. (Summary) OBJECTIVE: We hypothesized that aspirin may exhibit its anti-atherosclerotic effects via mechanisms other than cyclooxygenase inhibition in platelets. METHODS AND RESULTS: Using enhanced subtraction hybridization analysis, we found in human umbilical vein endothelial cells (HUVECs) that aspirin up-regulates the expression of aminopeptidase N (APN/CD13) mRNA and its surface protein levels in a dose-dependent manner. Enzymatic activity of APN/CD13 on HUVECs was increased approximately 1.5-fold by 1 mmol L(-1) of aspirin, and treatment with bestatin, an inhibitor for APN/CD13 metalloprotease activity, attenuated the enhanced activities of APN/CD13. Since activated thrombin receptor is reported to be inactivated by APN/CD13 in vitro, protective actions of aspirin on HUVECs by thrombin stimulation were examined, resulting in the suppression of endothelin-1 and reactive oxygen species productions in HUVECs. These inhibitory actions of aspirin were partially abrogated by bestatin. CONCLUSIONS: Aspirin may exert its anti-atherothrombotic effects in part via the inhibition of thrombin action by up-regulating APN/CD13 on endothelial cells. (Keyword) Antigens, CD13 / Aspirin / Cells, Cultured / Endothelial Cells / Endothelin-1 / Endothelium, Vascular / Enzyme Induction / Fibrinolytic Agents / Genes, Reporter / Humans / Leucine / Protease Inhibitors / RNA, Messenger / reactive oxygen species / Subtraction Technique / Thrombin / Transcription, Genetic / Transfection / Umbilical Veins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2005.03.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16216591 ● Search Scopus @ Elsevier (PMID): 16216591 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2005.03.003 (DOI: 10.1016/j.atherosclerosis.2005.03.003, PubMed: 16216591)
118.	Hajime Nawata, Satoshi Soen, Ryoichi Takayanagi, Ikuo Tanaka, Kunio Takaoka, Masao Fukunaga, Toshio Matsumoto, Yasuo Suzuki, Hiroyuki Tanaka, Saeko Fujiwara, Takami Miki, Akira Sagawa, Yoshiki Nishizawa and Yoshiki Seino : Guidelines on the management and treatment of glucocorticoid-induced osteoporosis of the Japanese Society for Bone and Mineral Research(2004), Journal of Bone and Mineral Metabolism, 23, 2, 105-109, 2005. (Keyword) Steroid(glucocorticoid) / Osteoporosis / Guideline (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-004-0596-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15750687 ● Summary page in Scopus @ Elsevier: 2-s2.0-20944440967 (DOI: 10.1007/s00774-004-0596-x, PubMed: 15750687, Elsevier: Scopus)
119.	Toshio Matsumoto and Masahiro Abe : The Importance of Notch Signaling in Myeloma Cell-Osteoclast Interactions, BoneKEy Osteovision, 2, 2, 7-10, 2005. (Link to Publication Site) ● Publication site (DOI): 10.1138/20050148 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1138/20050148 (DOI: 10.1138/20050148)
120.	Takashi Iwase, Noritoshi Nagaya, Takafumi Fujii, Takefumi Itoh, Hatsue Ishibashi-Ueda, Masakazu Yamagishi, Kunio Miyatake, Toshio Matsumoto, Soichiro Kitamura and Kenji Kangawa : Adrenomedullin enhances angiogenic potency of bone marrow transplantation in a rat model of hindlimb ischemia, Circulation, 111, 3, 356-362, 2005. (Summary) BACKGROUND: Previous studies have shown that adrenomedullin (AM) inhibits vascular endothelial cell apoptosis and induces angiogenesis. We investigated whether AM enhances bone marrow cell-induced angiogenesis. METHODS AND RESULTS: Immediately after hindlimb ischemia was created, rats were randomized to receive AM infusion plus bone marrow-derived mononuclear cell (MNC) transplantation (AM+MNC group), AM infusion alone (AM group), MNC transplantation alone (MNC group), or vehicle infusion (control group). The laser Doppler perfusion index was significantly higher in the AM and MNC groups than in the control group (0.74+/-0.11 and 0.69+/-0.07 versus 0.59+/-0.07, respectively, P<0.01), which suggests the angiogenic potency of AM and MNC. Importantly, improvement in blood perfusion was marked in the AM+MNC group (0.84+/-0.08). Capillary density was highest in the AM+MNC group, followed by the AM and MNC groups. In vitro, AM inhibited MNC apoptosis, promoted MNC adhesiveness to a human umbilical vein endothelial cell monolayer, and increased the number of MNC-derived endothelial progenitor cells. In vivo, AM administration not only enhanced the differentiation of MNC into endothelial cells but also produced mature vessels that included smooth muscle cells. CONCLUSIONS: A combination of AM infusion and MNC transplantation caused significantly greater improvement in hindlimb ischemia than MNC transplantation alone. This effect may be mediated in part by the angiogenic potency of AM itself and the beneficial effects of AM on the survival, adhesion, and differentiation of transplanted MNCs. (Keyword) Adrenomedullin / Angiogenesis Inducing Agents / Animals / apoptosis / Bone Marrow Transplantation / Cell Adhesion / cell differentiation / Cell Movement / Cells, Cultured / Combined Modality Therapy / Endothelial Cells / Hindlimb / Humans / ischemia / Male / Myocytes, Smooth Muscle / Neovascularization, Physiologic / Peptides / Peripheral Vascular Diseases / Random Allocation / Rats / Rats, Inbred Lew / Stem Cells / Umbilical Veins / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000153352.29335.B9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15655128 ● Summary page in Scopus @ Elsevier: 2-s2.0-19944431981 (DOI: 10.1161/01.CIR.0000153352.29335.B9, PubMed: 15655128, Elsevier: Scopus)
121.	Tomonori Yoshida, Hiroyuki Azuma, Ken-ichi Aihara, Mitsunori Fujimura, Masashi Akaike, Takao Mitsui and Toshio Matsumoto : Vascular smooth muscle cell proliferation is dependent upon upregulation of mitochondrial transcription factor A (mtTFA) expression in injured rat carotid artery, Atherosclerosis, 178, 1, 39-47, 2005. (Summary) Consistent with the physiological response to increased energy demand in proliferating cells, the number of mitochondria is upregulated in synthetic states of vascular smooth muscle cells (VSMC) in atherosclerotic lesion. We hypothesized that mitochondrial transcription factor A (mtTFA), a prerequisite factor for the transcription and replication of mtDNA, may be upregulated in VSMC of injured rat carotid artery, and that inhibition of its expression can attenuate the intimal thickening. Changes of intimal thickening and mtTFA expression by a treatment with antisense oligodeoxynucleotides (ODN) for mtTFA were investigated in balloon-injured rat carotid artery model. The expression of mtTFA was upregulated as early as 3 h up to 7 days after balloon injury. Delivery of ansisense ODN for mtTFA from adventitia side to injured arterial wall caused a significant decrease in intima-to-media (I/M) ratio. Furthermore, the increase in immunoreactivity and mRNA expression of mtTFA in injured artery as well as the number of mitochondria in intimal VSMC was abrogated by antisense ODN treatment. These data demonstrate that expression of mtTFA is upregulated in intimal VSMC of injured rat carotid artery, and that suppression of mtTFA expression by antisense ODN can attenuate intimal thickening after balloon injury. (Keyword) Antisense oligodeoxynucleotide / Arterial injury / Intimal thickening / Dedifferentiation / Restenosis (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2004.08.029 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15585199 ● Search Scopus @ Elsevier (PMID): 15585199 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2004.08.029 (DOI: 10.1016/j.atherosclerosis.2004.08.029, PubMed: 15585199)
122.	M Kunishige, Takao Mitsui, I Endo and Toshio Matsumoto : Dermatomyositis associated with impairment in both muscle aerobic and anaerobic function, Clinical Neuropathology, 24, 1, 32-35, 2005. (Summary) We report a 50-year-old Japanese woman with dermatomyositis in whom an anti-mitochondrial antibody was detected. Muscle biopsy demonstrated periodic acid Schiff- (PAS) positive vacuoles in addition to infiltrates of mononuclear cells. Histochemical analysis showed reduced phosphorylase activity. An aerobic exercise test demonstrated that the concentrations of serum lactate and pyruvate were elevated before corticosteroid therapy but decreased after the therapy. On the other hand, in forearm ischemic exercise tests, the responses of serum lactate and pyruvate were attenuated before corticosteroid therapy but recovered after the therapy. These findings indicate that an inflammatory mechanism interfered with myophosphorylase activity and muscle aerobic function. (Keyword) dematomyositis / antimitochondrial antibody / myophosphorylase activity / corticosteroid therapy / muscle aerobic function (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15696782 ● Search Scopus @ Elsevier (PMID): 15696782 (PubMed: 15696782)
123.	山口普史, Yasumasa Ikeda, 藤村光則, 森岡将臣, 橋詰俊二, 加藤みどり, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Toshio Matsumoto, 稲山真美 and Masaki Hanibuchi : アミオダロン肺合併症との鑑別を要したマイコプラズマ肺炎合併拡張型心筋症の1例, Progress in Medicine, 25, Suppl.1, 1552-1556, 2005. (Summary) 52歳男.47歳時に拡張型心筋症と診断され,持続性心室頻拍でアミオダロン150mg/日を開始した.その後,心室頻拍が頻回となり,心臓電気生理学的検査で心室細動が誘発されたため除細動器植込み術を受け,アミオダロンは増量して継続していた.今回,乾性咳が出現し,胸部X線で左右下肺野にスリガラス状陰影を指摘された.検査所見では高度の炎症所見を認めたが,KL-6は正常範囲で,C型肝炎ウイルスとヒトT細胞性白血病ウイルスI型のキャリアであった.胸部CTでは両側下肺野を中心として壁の肥厚を伴う気管支拡張や小葉中心性の粒状・樹枝状の陰影が多発しており,周囲の肺野に淡い濃度上昇を認めた.アミオダロンの副作用か感染症かは判断できなかったが,アミオダロンは中止し,アンピシリンナトリウム・スルバクタムナトリウム合剤を開始すると共にサイトメガロウイルス高力価免疫グロブリン投与を行った.入院10日目にマイコプラズマ抗体異常高値が判明し,マイコプラズマ肺炎と診断しミノサイクリン100mg/日を開始した.その結果,炎症所見,画像所見は徐々に軽快し,アミオダロンも再開して退院となった (Keyword) Amiodarone(治療的利用,毒性・副作用) Minocycline(治療的利用) 胸部X線診断心筋症-拡張型(合併症) 鑑別診断 X線CT 肺炎-マイコプラズマ性(合併症,X線診断) 頻拍-心室性(薬物療法) 肺炎-細菌性(合併症,X線診断,薬物療法) 肺炎-間質性(化学的誘発,X線診断) 胸部CT ヒト中年(45~64) 男
124.	Naoki Kimura, Shigeto Kawai, Yasuko Kinoshita, Takahiro Ishiguro, Yumiko Azuma, Shuji Ozaki, Masahiro Abe, Masamichi Sugimoto, Yuichi Hirata, Tetsuro Orita, Hisafumi Okabe, Toshio Matsumoto and Masayuki Tsuchiya : 2D7 diabody bound to the α2 domain of HLA class I efficiently induces caspase-independent cell death against malignant and activated lymphoid cells, Biochemical and Biophysical Research Communications, 325, 4, 1201-1209, 2004. (Summary) A mouse monoclonal antibody (2D7 mAb), which specifically bound to the alpha2 domain of HLA class I, rapidly induces cell aggregation accompanied by weak cytotoxicity against ARH-77 cells, suggesting that 2D7 mAb had a potential for agonist antibody. In order to enhance this cytotoxicity, 2D7 mAb was engineered to be a small bivalent antibody fragment, 2D7 diabody. The resultant 2D7 diabody showed a strong cytotoxicity against ARH-77 cells. As a notable characteristic feature, the lethal effect of 2D7 diabody was quite rapid, mediated by a caspase-independent death pathway. Furthermore, 2D7 diabody also showed cytotoxicity against several leukemia and lymphoma cell lines, and mitogen-activated peripheral blood mononuclear cells (PBMC), but not for normal resting PBMC and adherent cell lines such as HUVEC. These results suggest that 2D7 diabody could be expected as a novel therapeutic antibody for hematological malignancies as well as inflammatory diseases. (Keyword) Agonist antibody / Diabody / HLA class I / cell death / Therapeutic antibody / Hematological malignancy (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2004.10.163 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15555554 ● Search Scopus @ Elsevier (PMID): 15555554 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2004.10.163 (DOI: 10.1016/j.bbrc.2004.10.163, PubMed: 15555554)
125.	Masayuki Iki, Takashi Akiba, Toshio Matsumoto, Harumi Nishino, Sadanobu Kagamimori, Yoshiko Kagawa and Hideo Yoneshima : Reference database of biochemical markers of bone turnover for the Japanese female population. Japanese Population-based Osteoporosis (JPOS) Study, Osteoporosis International, 15, 12, 981-991, 2004. (Summary) The present study was conducted as a part of the Japanese Population-based Osteoporosis (JPOS) Study to establish reference values on the biochemical markers of bone turnover in the general Japanese female population over an applicable age range. The study recruited 3250 women aged 15-79 years, randomly selected from five municipalities throughout Japan, and obtained measurements of serum osteocalcin (OC) and bone-specific alkaline phosphatase (BAP); free and total forms of immunoreactive deoxypyridinoline, free pyridinolines and type I collagen cross-linked C-terminal telopeptide (CTx) in urine; serum intact parathyroid hormone (PTH) and 1,25 dihydroxy vitamin D (1,25 (OH)2D); and bone density at the spine, hip and distal forearm. After excluding subjects with apparent or suggested abnormalities affecting bone mass, 2535 (78%) subjects were further analyzed. The authors presented 5-year age-specific mean values of the markers and mean marker levels derived from women aged 30-44 years with normal bone density as a healthy young adult reference. Values of the markers decreased with increasing age before the age of 40, increased steeply among subjects in their 50s, and remained elevated in the elderly. Serum calcium, phosphorus, PTH and 1,25 (OH)2D levels were higher in postmenopausal women than in premenopausal women. However, 1,25 (OH)2D was lower among early postmenopausal subjects. The levels of OC, BAP, CTx, PTH and 1,25(OH)2D were significantly greater for women with osteoporosis than for those without. The diagnostic value of the markers was limited as the sensitivity and specificity ranged from 55% to 60%. These findings will aid health professionals in the correct assessment of bone turnover status in Japanese women over a wide range of age. (Keyword) Age-related change / Biochemical markers of bone turnover / Japanese women / Menopause-related change / Population-based epidemiologic study / Random sample (Link to Publication Site) ● Publication site (DOI): 10.1007/s00198-004-1634-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15570414 ● Summary page in Scopus @ Elsevier: 2-s2.0-11244275482 (DOI: 10.1007/s00198-004-1634-1, PubMed: 15570414, Elsevier: Scopus)
126.	Daisuke Inoue, Shinsuke Kido and Toshio Matsumoto : Transcriptional Induction of FosB/FosB Gene by Mechanical Stress in Osteoblasts, The Journal of Biological Chemistry, 279, 48, 49795-49803, 2004. (Summary) Mechanical stress to bone plays a critical role in maintaining bone mass and strength. However, the molecular mechanism of mechanical stress-induced bone formation is not fully understood. In the present study, we demonstrate that FosB and its spliced variant DeltaFosB, which is known to increase bone mass by stimulating bone formation in vivo, is rapidly induced by mechanical loading in mouse hind limb bone in vivo and by fluid shear stress (FSS) in mouse calvarial osteoblasts in vitro both at the mRNA and protein levels. FSS induction of FosB/DeltaFosB gene expression was dependent on gadlinium-sensitive Ca(2+) influx and subsequent activation of ERK1/2. Analysis of the mouse FosB/DeltaFosB gene upstream regulatory region with luciferase reporter gene assays revealed that the FosB/DeltaFosB induction by FSS occurred at the transcriptional level and was conferred by a short fragment from -603 to -327. DNA precipitation assays and DNA decoy experiments indicated that ERK-dependent activation of CREB binding to a CRE/AP-1 like element (designated "CRE2") at the position of -413 largely contributed to the transcriptional effects of FSS. These results suggest that DeltaFosB participates in mechanical stress-induced intracellular signaling cascades that activate the osteogenic program in osteoblasts. (Keyword) Alternative Splicing / Animals / Base Sequence / Calcium / Cyclic AMP Response Element-Binding Protein / Extracellular Signal-Regulated MAP Kinases / Gadolinium / Mice / Molecular Sequence Data / Osteoblasts / Prostaglandins / Proto-Oncogene Proteins c-fos / RNA, Messenger / Stress, Mechanical (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M404096200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15383527 ● Summary page in Scopus @ Elsevier: 2-s2.0-9644303172 (DOI: 10.1074/jbc.M404096200, PubMed: 15383527, Elsevier: Scopus)
127.	M Kunishige, Takao Mitsui, B. H. Tan, H. N. Leong, T Takasaki, I Kurane, A Mihara and Toshio Matsumoto : Preferential gray matter involvement in dengue myelitis, Neurology, 63, 10, 1980-1981, 2004. (Keyword) infection (Link to Publication Site) ● Publication site (DOI): 10.1212/01.WNL.0000144194.29643.D0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15557535 ● Summary page in Scopus @ Elsevier: 2-s2.0-8844279149 (DOI: 10.1212/01.WNL.0000144194.29643.D0, PubMed: 15557535, Elsevier: Scopus)
128.	YUKIKO WATANABE, HIROSHI OHSHIMA, KOH MIZUNO, CHIHARU SEKIGUCHI, MASAO FUKUNAGA, KENJIRO KOHRI, JÖRN RITTWEGER, DIETER FELSENBERG, Toshio Matsumoto and TOSHITAKA NAKAMURA : Intravenous Pamidronate Prevents Femoral Bone Loss and Renal Stone Formation During 90-Day Bed Rest, Journal of Bone and Mineral Research, 19, 11, 1771-1778, 2004. (Summary) Long-term bed rest has potential risks of bone loss and renal stone formation. We examined the effects of resistive exercise and intravenous pamidronate on BMD, bone turnover, urinary calcium, and renal stone formation in 25 healthy males during 90-day bed rest. Pamidronate prevented femoral bone loss and renal stone formation, but resistive exercise showed little effects. Long-term bed rest increases the risks of bone loss and urinary stone formation. Resistive exercise increases bone formation, and bisphosphonates reduce bone resorption. However, the effects of muscle exercise and bisphosphonates have not been examined side-by-side. The objectives of this study are to compare the effects of pamidronate with resistive exercise on BMD and renal stone formation during prolonged bed rest. Twenty-five male white volunteers, 26-45 years of age, were randomly assigned to the control (n = 9), exercise (n = 9), and pamidronate (n = 7) groups and underwent 90-day 6 degrees head-down tilt bed rest. Exercise group performed squats and heel raises on a flywheel device for 30 minutes every 3 days. Pamidronate (60 mg) was administered intravenously 14 days before bed rest. BMD of the head, forearm, lumbar spine, and proximal femur; biochemical bone markers; calcium (Ca) metabolism; and abdominal radiographs were examined during 90 days of bed rest and 360 days of reloading. In controls, proximal femoral BMD decreased, and bone resorption markers and urinary Ca increased during bed rest, along with development of renal stones in two of nine subjects. Resistive exercise increased bone formation but was unable to prevent femoral BMD decrease and increases in bone resorption and urinary Ca during bed rest, with formation of renal stones in four of nine subjects. Pamidronate maintained femoral BMD, reduced bone resorption and urinary Ca, and completely prevented renal stone formation. Resistive exercise increased bone formation but could not reduce bone resorption and the risk of renal stones. In contrast, inhibition of bone resorption by pamidronate could preserve bone mineral and reduce the risk of renal stone formation during prolonged bed rest. (Keyword) Adult / Alkaline Phosphatase / Bed Rest / Biological Markers / Bone Density / Bone Diseases, Metabolic / Bone Remodeling / Bone Resorption / Bone and Bones / calcium / Diet / Diphosphonates / Exercise / Exercise Test / Humans / Infusions, Intravenous / Kidney Calculi / Male / Middle Aged / Supine Position / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1359/JBMR.040811 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15476576 ● Summary page in Scopus @ Elsevier: 2-s2.0-16644399512 (DOI: 10.1359/JBMR.040811, PubMed: 15476576, Elsevier: Scopus)
129.	Yukiho Tanimoto, Masahiko Yokozeki, Hiura Kenji, Kazuya Matsumoto, Hideki Nakanishi, Toshio Matsumoto, PJ Marie and Keiji Moriyama : A soluble form of fibroblast growth factor receptor 2 (FGFR2) with S252W mutation acts as an efficient inhibitor for the enhanced osteoblastic differentiation caused by FGFR2 activation In Apert syndrome., The Journal of Biological Chemistry, 279, 44, 45926-45934, 2004. (Keyword) BONE-MARROW CELLS / CROUZON-SYNDROME / TRANSCRIPTION FACTOR / SIGNALING PATHWAYS / COLLAGEN-SYNTHESIS / BIRTH PREVALENCE / CALVARIAL BONE / SKULL VAULT / GENE CAUSE / IN-VIVO (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M404824200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15310757 ● CiNii @ National Institute of Informatics (CRID): 1363107368427305088 ● Search Scopus @ Elsevier (PMID): 15310757 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M404824200 (DOI: 10.1074/jbc.M404824200, PubMed: 15310757, CiNii: 1363107368427305088)
130.	Makoto Kunishige, Takao Mitsui, Hiide Yoshino, Atsuko Asano, Miho Tsuruo, Itsuro Endo, Fumikazu Yagi and Toshio Matsumoto : Isolated cranial neuropathy associated with anti-glycolipid antibodies, Journal of the Neurological Sciences, 225, 1-2, 51-55, 2004. (Summary) We describe seven patients with isolated cranial neuropathy in whom serum anti-glycolipid antibodies were detected. Trigeminal sensory neuropathy was found in four patients, who had exhibited symptoms for 2 months to 4 years. The other three patients showed facial nerve palsy with or without ophthalmoparesis. Temporal profile analysis of anti-glycolipid antibodies revealed that titers of anti-glycolipid IgM antibodies against GM2 and LM1 gradually decreased in patients having chronic trigeminal sensory neuropathy. In patients with acute trigeminal sensory neuropathy, elevation of anti-LM1 antibody titers continued over 12 months although anti-GalNAc-GD1a antibody disappeared. On the other hand, titers of anti-glycolipid antibodies rapidly decreased in patients with acute facial nerve palsy with or without ophthalmoparesis. We conclude that anti-glycolipid antibodies may play an important role in the development of isolated cranial neuropathy in some patients. (Keyword) Neuropathy / glycolipid antibody (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jns.2004.06.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15465085 ● Summary page in Scopus @ Elsevier: 2-s2.0-4744372018 (DOI: 10.1016/j.jns.2004.06.017, PubMed: 15465085, Elsevier: Scopus)
131.	Masahiro Abe, Kenji Hiura, Javier Wilde, Atsushi Shioyasono, Keiji Moriyama, Toshihiro Hashimoto, Shinsuke Kido, Takashi Oshima, Hironobu Shibata, Shuji Ozaki, Daisuke Inoue and Toshio Matsumoto : Osteoclasts enhance myeloma cell growth and survival via cell-cell contact: a vicious cycle between bone destruction and myeloma expansion., Blood, 104, 8, 2484-2491, 2004. (Summary) Multiple myeloma (MM) expands in the bone marrow and causes devastating bone destruction by enhancing osteoclastic bone resorption in its vicinity, suggesting a close interaction between MM cells and osteoclasts (OCs). Here, we show that peripheral blood mononuclear cell-derived OCs enhanced growth and survival of primary MM cells as well as MM cell lines more potently than stromal cells, and that OCs protected MM cells from apoptosis induced by serum depletion or doxorubicin. OCs produced osteopontin (OPN) and interleukin 6 (IL-6), and adhesion of MM cells to OCs increased IL-6 production from OCs. In addition, IL-6 and OPN in combination enhanced MM cell growth and survival. However, the effects of OCs on MM cell growth and survival were only partially suppressed by a simultaneous addition of anti-IL-6 and anti-OPN antibodies and were completely abrogated by inhibition of cellular contact between MM cells and OCs. These results demonstrate that OCs enhance MM cell growth and survival through a cell-cell contact-mediated mechanism that is partially dependent on IL-6 and OPN. It is suggested that interactions of MM cells with OCs augment MM growth and survival and, thereby, form a vicious cycle, leading to extensive bone destruction and MM cell expansion. (Keyword) Animals / Antibodies / Cell Adhesion / Cell Division / Cell Survival / Cells, Cultured / Coculture Techniques / Culture Media, Serum-Free / Diphosphonates / Doxorubicin / Humans / Integrin alpha4beta1 / Integrin alphaVbeta3 / Interleukin-6 / Multiple Myeloma / Osteoclasts / Osteopontin / Rabbits / Sialoglycoproteins / Stromal Cells (Link to Publication Site) ● Publication site (DOI): 10.1182/blood-2003-11-3839 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15187021 ● Search Scopus @ Elsevier (PMID): 15187021 ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2003-11-3839 (DOI: 10.1182/blood-2003-11-3839, PubMed: 15187021)
132.	Yuichi Fujinaka, Sumiko Yoshida, 鈴木康博, Daisuke Inoue, Toshio Matsumoto, 影治照喜, Kazuhito Matsuzaki, 岡崎敏之, 里見淳一郎, 永廣信治, 隈晴二, 佐野壽昭, 新谷保実 and 福本礼 : 片側性副腎腫瘤を合併した Cushing 病の1例, ホルモンと臨床, 52, 135-140, 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572261549989833472 (CiNii: 1572261549989833472)
133.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Michiko Yamashita, Toshiki Sudo, Hideki Hayashi, Yoshihisa Yamada, Fuminari Endoh, Mitsunori Fujimura, Tomonori Yoshida, Hiroshi Yamaguchi, Shunji Hashizume, Midori Kato, Kimihiro Yoshimura, Yoko Yamamoto, Shigeaki Kato and Toshio Matsumoto : Disruption of nuclear vitamin D receptor gene causes enhanced thrombogenicity in mice, The Journal of Biological Chemistry, 279, 34, 35798-35802, 2004. (Summary) Vitamin D metabolites influence the expression of various genes involved in calcium homeostasis, cell differentiation, and regulation of the immune system. Expression of these genes is mediated by the activation of the nuclear vitamin D receptor (VDR). Previous studies have shown that a hormonally active form of vitamin D, 1alpha,25-dihydroxyvitamin D3, exerts anticoagulant effects in cultured monocytic cells. To clarify whether activation of VDR plays any antithrombotic actions in vivo, hemostatic/thrombogenic systems were examined in normocalcemic VDR knock-out (KO) mice on a high calcium diet and compared with wild type and hypocalcemic VDRKO mice that were fed a regular diet. Platelet aggregation was enhanced significantly in normocalcemic VDRKO mice compared with wild type and hypocalcemic VDRKO mice. Aortic endothelial nitric-oxide (NO) synthase expression and urinary NOx excretions were reduced in hypocalcemic VDRKO mice, but not in normocalcemic VDRKO mice. Northern blot and RT-PCR analyses revealed that the gene expression of antithrombin in the liver as well as that of thrombomodulin in the aorta, liver and kidney was down-regulated in hypo- and normocalcemic VDRKO mice. Whereas tissue factor mRNA expression in the liver and kidney was up-regulated in VDRKO mice regardless of plasma calcium level. Furthermore, VDRKO mice manifested an exacerbated multi-organ thrombus formation after exogenous lipopolysaccharide injection regardless of the calcemic conditions. These results demonstrate that activation of nuclear VDR elicits antithrombotic effects in vivo, and suggest that the VDR system may play a physiological role in the maintenance of antithrombotic homeostasis. (Keyword) FILTRATION PRESSURE METHOD / TISSUE-FACTOR / 1,25-DIHYDROXYVITAMIN D-3 / ANTITHROMBIN DEFICIENCY / WHOLE-BLOOD / EXPRESSION / cells / AGGREGATION / inhibition / ALOPECIA (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M404865200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15205460 ● CiNii @ National Institute of Informatics (CRID): 1362262945661168512 ● Summary page in Scopus @ Elsevier: 2-s2.0-4143096123 (DOI: 10.1074/jbc.M404865200, PubMed: 15205460, CiNii: 1362262945661168512, Elsevier: Scopus)
134.	A Ohno, Takao Mitsui, Itsuro Endo, Makoto Kunishige, Toshio Shigekiyo and Toshio Matsumoto : Dermatomyositis associated with Sjögren's syndrome: VEGF involvement in vasculitis, Clinical Neuropathology, 23, 4, 178-182, 2004. (Summary) Two patients with dermatomyositis complicated with Sjögren's syndrome (SjS), are reported. Both patients exhibited sensory-dominant polyneuropathy, compatible with neurologic involvement in SjS. Vascular endothelial growth factor (VEGF) levels were increased in their plasma. Histological examination demonstrated vasculitic changes in biopsied specimens of muscle and salivary glands from the patients, and VEGF was overexpressed in the vasculitic lesions. These findings suggest that VEGF overexpression was associated with the development of vasculopathy in skeletal muscle and salivary glands and possibly in the peripheral nervous system. (Keyword) Dermatomyositis / VEGF (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15328883 ● Search Scopus @ Elsevier (PMID): 15328883 (PubMed: 15328883)
135.	Yasushi Oshima, Yukiko Kuroda, Makoto Kunishige, Toshio Matsumoto and Takao Mitsui : OXIDATIVE STRESS-ASSOCIATED MITOCHONDRIAL DYSFUNCTION IN CORTICOSTEROID-TREATED MUSCLE CELLS, Muscle & Nerve, 30, 1, 49-54, 2004. (Summary) We analyzed the effects of corticosteroid on mitochondrial membrane potentials (DeltaPsi(m)), generation of reactive oxygen species (ROS), and apoptosis in a human rhabdomyosarcoma cell line, RD, and a dopaminergic neuroblastoma cell line, SH-SY5Y. The cell lines were cultured in the presence or absence of dexamethasone and superoxide dismutase (SOD) for up to 1 week. Dexamethasone treatment increased DeltaPsi(m), ROS generation, and apoptosis in proliferating RD cells. Treatment with SOD attenuated ROS generation and apoptosis, but not DeltaPsi(m). The increase in DeltaPsi(m) seemed to be the primary effect of dexamethasone on proliferating RD cells, which is probably mediated by mitochondrial transcription. In differentiated RD cells, but not differentiated SH-SY5Y cells, dexamethasone treatment showed a delayed effect of interfering with the DeltaPsi(m) and increasing ROS generation and apoptosis. Since these changes disappeared in the presence of SOD, dexamethasone primarily induced ROS generation, resulting in apoptosis. We speculate that this mechanism provides the basis of a pathophysiological model of corticosteroid myopathy. (Keyword) apoptosis / corticosteroid myopathy / dexamethasone / mitochondrial membrane potentials / reactive oxygen species / superoxide dismutase (Link to Publication Site) ● Publication site (DOI): 10.1002/mus.20036 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15221878 ● Summary page in Scopus @ Elsevier: 2-s2.0-3042771402 (DOI: 10.1002/mus.20036, PubMed: 15221878, Elsevier: Scopus)
136.	Ken-ichi Aihara, Hiroyuki Azuma, Nobuyuki Takamori, Yasuhiko Kanagawa, Masashi Akaike, Mitsunori Fujimura, Tomonori Yoshida, Shunji Hashizume, Midori Kato, Hiroshi Yamaguchi, Shuji Kato, Yasumasa Ikeda, Tomoko Arase, Akira Kondo and Toshio Matsumoto : Heparin cofactor II is a novel protective factor against carotid atherosclerosis in elderly individuals., Circulation, 109, 22, 2761-2765, 2004. (Summary) Thrombin plays a crucial role in atherothrombotic changes. Because heparin cofactor II (HCII) inhibits thrombin actions after binding to dermatan sulfate at injured arterial walls, HCII may negatively regulate thrombin actions in vascular walls. We hypothesized that plasma HCII activity is a preventive factor against atherosclerotic changes, especially in elderly individuals who already have atherosclerotic vascular injuries. Maximum plaque thickness (MPT) in the carotid artery was measured by ultrasonography in 306 Japanese elderly individuals (154 men and 152 women; age, 40 to 91 years; 68.9+/-11.1 years, mean+/-SD). The relevance of cardiovascular risk factors including plasma HCII activity to the severity of MPT was statistically evaluated. Plasma HCII activity decreased with age. Simple linear regression analysis after adjustments for age and sex showed that lipoprotein(a), glycosylated hemoglobin A1c, and presence of diabetes mellitus significantly contributed to an increase in MPT values (r=0.119, P<0.05; r=0.196, P<0.001; and r=0.227, P<0.0001, respectively). In contrast, high-density lipoprotein (HDL) cholesterol and HCII activity were negatively correlated with MPT values (r=-0.117, P<0.05, and r=-0.202, P<0.0005, respectively). Multiple regression analysis revealed that plasma HCII activity and HDL cholesterol independently contributed to the suppression of MPT values and that the antiatherogenic contribution of HCII activity was stronger than that of HDL cholesterol (P<0.001 and P<0.05, respectively). These results suggest that HCII can be a novel and independent antiatherogenic factor. Moreover, HCII is a stronger predictive factor than HDL cholesterol against carotid atherosclerosis in elderly individuals. (Keyword) Adult / Aged / Aged, 80 and over / aging / Antithrombins / Cardiovascular Diseases / Carotid Artery Diseases / Female / Heparin Cofactor II / Humans / Male / Middle Aged / Regression Analysis / Risk Factors / Severity of Illness Index (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000129968.46095.F3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15148272 ● Search Scopus @ Elsevier (PMID): 15148272 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000129968.46095.F3 (DOI: 10.1161/01.CIR.0000129968.46095.F3, PubMed: 15148272)
137.	Makoto Kunishige, Takao Mitsui, Yukiko Kuroda, Sumiko Yoshida, Masaaki Kosaka and Toshio Matsumoto : Expanding phenotype and clinical heterogeneity in patients with identical mutation of the parkin gene., European Neurology, 51, 3, 183-185, 2004. (Keyword) Blotting, Southern / brain disease / Cerebellar Ataxia / DNA Mutational Analysis / Exons / Family Health / Female / Heterozygote / Humans / magnetic resonance imaging / Male / Middle Aged / Mutation / Parkinsonian Disorders / Phenotype / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Ubiquitin-Protein Ligases (Link to Publication Site) ● Publication site (DOI): 10.1159/000077671 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15073448 ● Search Scopus @ Elsevier (PMID): 15073448 ● Search Scopus @ Elsevier (DOI): 10.1159/000077671 (DOI: 10.1159/000077671, PubMed: 15073448)
138.	Toshihiro Hashimoto, Masahiro Abe, Takashi Oshima, Hironobu Shibata, Shuji Ozaki, Daisuke Inoue and Toshio Matsumoto : Ability of myeloma cells to secrete macrophage inflammatory protein (MIP)-1α and MIP-1β correlates with lytic bone lesions in patients with multiple myeloma, British Journal of Haematology, 125, 1, 38-41, 2004. (Summary) Macrophage inflammatory protein (MIP)-1alpha and MIP-1beta have been identified as candidates for multiple myeloma (MM)-derived bone-resorbing factors. To validate the clinical relevance of these observations, we investigated correlations between the ability of MM cells to secrete these chemokines and the extent of MM bone lesions as well as levels of biochemical bone markers in patients with MM. Patients with multiple bone lesions exhibited higher MIP-1alpha and MIP-1beta secretion from MM cells along with elevated urinary deoxypyridinoline (Dpd), without significant elevation of serum bone-specific alkaline phosphatase (BALP) or osteocalcin compared with those with minimal bone lesions. MIP-1alpha and MIP-1beta levels correlated positively with urinary Dpd and serum BALP but not with serum osteocalcin. These results provide further evidence for a causal role of MIP-1alpha and MIP-1beta in the development of lytic bone lesions, and suggest that MM cells suppress osteoblastic bone formation to cause an imbalance of bone turnover and development of destructive bone lesions. (Keyword) multiple myeloma / chemokines / bone disease (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2141.2004.04864.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15015966 ● Search Scopus @ Elsevier (PMID): 15015966 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2141.2004.04864.x (DOI: 10.1111/j.1365-2141.2004.04864.x, PubMed: 15015966)
139.	Yoshiko Kanezaki, Toshiyuki Obata, Rie Matsushima, Asako Minami, Tomoyuki Yuasa, Kazuhiro Kishi, Yoshimi Bando, Hisanori Uehara, Keisuke Izumi, Tasuku Mitani, Mitsuru Matsumoto, Yukari Takeshita, Yutaka Nakaya, Toshio Matsumoto and Yousuke Ebina : KATP Channel Knockout Mice Crossbred with Transgenic Mice Expressing a Dominant-Negative Form of Human Insulin Receptor have Glucose Intolerance but not Diabetes, Endocrine Journal, 51, 2, 133-144, 2004. (Summary) Impaired insulin secretion and insulin resistance are thought to be two major causes of type 2 diabetes mellitus. There are two kinds of diabetic model mice: one is a K(ATP) channel knockout (Kir6.2KO) mouse which is defective in glucose-induced insulin secretion, and the other is a transgenic mouse expressing the tyrosine kinase-deficient (dominant-negative form of) human insulin receptor (hIR(KM)TG), and which has insulin resistance in muscle and fat. However, all of these mice have no evidence of overt diabetes. To determine if the double mutant Kir6.2KO/hIR(KM)TG mice would have diabetes, we generated mutant mice by crossbreeding, which would show both impaired glucose-induced insulin secretion and insulin resistance in muscle and fat. We report here that: 1) blood glucose levels of randomly fed and 6 h fasted double mutant (Kir6.2KO/hIR(KM)TG) mice were comparable with those of wild type mice; 2) in intraperitoneal glucose tolerance test (ipGTT), Kir6.2KO/hIR(KM)TG mice had an impaired glucose tolerance; and 3) during ipGTT, insulin secretion was not induced in either Kir6.2KO/hIR(KM)TG or Kir6.2KO mice, while the hIR(KM)TG mice showed a more prolonged insulin secretion than did wild type mice; 4) hyperinsulinemic euglycemic clamp test revealed that Kir6.2KO, Kir6.2KO/hIR(KM)TG and hIR(KM)TG mice, showed decreased whole-body glucose disposal compared with wild type mice; 5) Kir6.2KO, but not Kir6.2KO/hIR(KM)TG mice had some obesity and hyperleptinemia compared with wild type mice. Thus, the defects in glucose-induced insulin secretion (Kir6.2KO) and an insulin resistance in muscle and fat (hIR(KM)TG) were not sufficient to lead to overt diabetes. (Keyword) Adipose Tissue / Animals / Blood Glucose / Enzyme Activation / Epididymis / Fasting / Genes, Dominant / Genotype / Glucose / Glucose Clamp Technique / Glucose Intolerance / Glucose Tolerance Test / Humans / Insulin / Leptin / Liver / Male / Mice / Mice, Knockout / Mice, Transgenic / Organ Size / Postprandial Period / Potassium Channels, Inwardly Rectifying / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Receptor, Insulin (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.51.133 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15118262 ● Search Scopus @ Elsevier (PMID): 15118262 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.51.133 (DOI: 10.1507/endocrj.51.133, PubMed: 15118262)
140.	Masashi Akaike, Hiroyuki Azuma, 石川雅康, 井上利彦, 遠藤武徳, 岡崎誠司, 小島章裕, 佐藤幸一, 田村克也, 田村隆一, 長楽雅仁, 中平晴仁, 林郁郎, 日浅光春, 藤村光則, 松本直也, 宮恵子, 山口普史, 吉田健三, 渡部滋夫 and Toshio Matsumoto : 日本動脈硬化学会による診療ガイドラインからみた高コレステロール血症治療の動向とその問題点, Progress in Medicine, 24, 3, 767-772, 2004.
141.	Daisuke Inoue and Toshio Matsumoto : Reduced AP-1 mediated transcription of interleukin-11 gene in marrow stromal cells as a mechanism of senile Osteoprosis: lessons from SAMP6, International Congress Series, 1260, C, 61-65, 2004. (Keyword) senile osteoporosis / Bone formation / Stromal cells / interleukin-11 / Promoter / AP-1 (Link to Publication Site) ● Publication site (DOI): 10.1016/S0531-5131(03)01692-3 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85023117101 (DOI: 10.1016/S0531-5131(03)01692-3, Elsevier: Scopus)
142.	Nobuyuki Takamori, Hiroyuki Azuma, Midori Kato, Shunji Hashizume, Ken-ichi Aihara, Masashi Akaike, Katsuya Tamura and Toshio Matsumoto : High plasma heparin cofactor II activity is associated with reduced incidence of in-stent restenosis after percutaneous coronary intervention, Circulation, 109, 4, 481-486, 2004. (Summary) Thrombin plays an important role in the development of atherosclerosis and restenosis after percutaneous coronary intervention. Because heparin cofactor II (HCII) inhibits thrombin action in the presence of dermatan sulfate, which is abundantly present in arterial wall, HCII may affect vascular remodeling by modulating thrombin action. We hypothesized that patients with high plasma HCII activity may show a reduced incidence of in-stent restenosis (ISR). Sequential coronary arteries (n=166) with NIR stent (Boston Scientific Corp) implantation in 134 patients were evaluated before, immediately after, and at 6 months after percutaneous coronary intervention. Patients were divided into the following groups: high HCII (> or =110%, 45 lesions in 36 patients), normal HCII (> or =80% and <110%, 81 lesions in 66 patients), and low HCII (<80%, 40 lesions in 32 patients). Percent diameter stenosis at follow-up in the high-HCII group (18.7%) was significantly lower (P=0.046) than that in the normal-HCII group (30.3%) or the low-HCII group (29.0%). The ISR rate in the high-HCII group (6.7%) was significantly lower than that in the low-HCII group (30.0%) (P=0.0039). Furthermore, multivariate analysis demonstrated that high plasma HCII activity is an independent factor in reducing the incidence of angiographic restenosis (odds ratio, 0.953/1% increase of HCII; 95% CI, 0.911 to 0.998). The results demonstrate that HCII may have a hitherto unrecognized effect in inhibiting ISR. The effect of HCII may be mediated by inactivating thrombin in injured arteries, thereby inhibiting vascular smooth muscle cell migration and proliferation. (Keyword) cardiovascular diseases / angioplasty / atherosclerosis / thrombin / dermatan sulfate (Link to Publication Site) ● Publication site (DOI): 10.1161/01.CIR.0000109695.39671.37 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14744972 ● Search Scopus @ Elsevier (PMID): 14744972 ● Search Scopus @ Elsevier (DOI): 10.1161/01.CIR.0000109695.39671.37 (DOI: 10.1161/01.CIR.0000109695.39671.37, PubMed: 14744972)
143.	Yukiko Hiasa, Makoto Kunishige, Takao Mitsui, Shunsuke Kondo, Rika Kuriwaka, Shizuka Shigekiyo, Takanori Kanematsu, Nobuo Satake, Yoshimi Bando, Akira Kondo, Itsuro Endo, Yasushi Oshima and Toshio Matsumoto : Complicated paraneoplastic neurological syndromes: a report of two patients with small cell or non-small cell lung cancer, Clinical Neurology and Neurosurgery, 106, 12, 47-49, 2003. (Summary) Paraneoplastic neurological syndromes are frequently associated in patients with small cell lung cancer (SCLC) and antineuronal antibodies are involved in the autoimmune mechanism. Multiple syndromes are sometimes complicated in a single patient with SCLC. However, little is known about non-SCLC-associated neurological manifestations. We report two patients with complicated paraneoplastic neurological syndromes. Patient 1 showed paraneoplastic limbic encephalitis (PLE), paraneoplastic sensory neuropathy (PSN) and Lambert-Eaton myasthenic syndrome (LEMS) associated with SCLC. Patient 2 developed opsoclonus-ataxia and probable PLE associated with non-SCLC. Analysis of various antineuronal antibodies revealed that anti-Hu and P/Q-type voltage-gated calcium channel (VGCC) antibodies were positive in Patient 1 but any antibodies were not in Patient 2. Brain MRI demonstrated high intensity signals in temporal lobes particularly on fluid-attenuated inversion recovery (FLAIR) or diffusion-weighted images. These findings suggest that complicated paraneoplastic neurological syndromes occur in non-SCLC as well as SCLC and that unidentified antineuronal autoantibodies may underlie the pathophysiology. (Keyword) paraneoplastic neurological syndromes / lung cancer (Link to Publication Site) ● Publication site (DOI): 10.1016/s0303-8467(03)00059-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14643918 ● Search Scopus @ Elsevier (PMID): 14643918 ● Search Scopus @ Elsevier (DOI): 10.1016/s0303-8467(03)00059-3 (DOI: 10.1016/s0303-8467(03)00059-3, PubMed: 14643918)
144.	Naoko Matsui, Takao Mitsui, Itsuro Endo, Yasushi Oshima, Makoto Kunishige and Toshio Matsumoto : Dermatomyositis with peripheral nervous system involvement: activation of vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR) in vasculitic lesions, Internal Medicine, 42, 12, 1233-1239, 2003. (Summary) We describe two cases of dermatomyositis (DM) with nervous system involvement. Polyneuropathy was observed in both patients, and cerebral vasculitis was suspected in one patient. Histological examination of biopsied specimens of skeletal muscles, skin and sural nerves revealed vasculitis. Furthermore, vascular endothelial growth factor (VEGF) and VEGF receptors (VEGFRs) were overexpressed in vasculitic lesions. Although, VEGF and VEGFRs were not detected in biopsied specimens of skeletal muscle from normal subjects, they were observed in one of two patients with DM who did not exhibit neuropathy. These findings suggest the possibility that VEGF overproduction is associated with development of vasculitis in some cases of DM complicated with peripheral neuropathy. (Keyword) DErmatomyositis / VEGF (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.42.1233 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14714966 ● Search Scopus @ Elsevier (PMID): 14714966 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.42.1233 (DOI: 10.2169/internalmedicine.42.1233, PubMed: 14714966)
145.	Itsuro Endo, Daisuke Inoue, Takao Mitsui, Yoshifumi Umaki, Masashi Akaike, Tatsuya Yoshizawa, Shigeaki Kato and Toshio Matsumoto : Deletion of Vitamin D Receptor Gene in Mice Results in Abnormal Skeletal Muscle Development with Deregulated Expression of Myoregulatory Transcription Factors, Endocrinology, 144, 12, 5138-5144, 2003. (Keyword) D RESPONSE SEQUENCE / PARATHYROID-HORMONE / 1,25-DIHYDROXYVITAMIN-D3 RECEPTORS / metabolism / RICKETS / FALLS / RAT / identification / OSTEOMALACIA / MECHANISMS (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2003-0502 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12959989 ● Search Scopus @ Elsevier (PMID): 12959989 ● Search Scopus @ Elsevier (DOI): 10.1210/en.2003-0502 (DOI: 10.1210/en.2003-0502, PubMed: 12959989)
146.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, 山口普史, Yasumasa Ikeda, 加藤茂明 and Toshio Matsumoto : ビタミンD-ビタミンD受容体システムは生体における血液凝固調節因子である, 第25回日本血栓止血学会学術集会, 14, 5, 420, 2003. (Keyword) *Vitamin D(薬理学) 遺伝子発現血液凝固 Calcitriol Receptors Thrombomodulin マウス動物
147.	Yuichi Fujinaka, 福永絵里, 鈴木康博, Daisuke Inoue and Toshio Matsumoto : 重篤な内分泌異常，骨代謝異常を認めた重症潰瘍性大腸炎の一例, Folia endocrinologica Japonica, 79, 0, 51-54, 2003. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1571417124898099968 (CiNii: 1571417124898099968)
148.	Takao Mitsui, Yoshifumi Umaki, Masakazu Nagasawa, Masashi Akaike, Satoshi Ohtsuka, Masaaki Odomi, Kenji Aki and Toshio Matsumoto : Motor neuron involvement in a patient with long-term corticosteroid administration, Internal Medicine, 42, 9, 862-866, 2003. (Summary) An asthmatic patient with corticosteroid treatment for 45 years presented with slowly progressive limb muscle atrophy. His muscle symptoms were involved in four limbs and tongue, and deep tendon reflexes were exaggerated. Biopsied muscle pathology indicated the presence of neurogenic muscular atrophy in combination with corticosteroid myopathy. Furthermore, 8-hydroxy-deoxyguanosine (8-OH-dG) was prominently increased in mitochondrial and nuclear DNA. An aerobic exercise test demonstrated remarkable serum lactate elevation, which was attenuated by the administration of coenzyme Q10. These findings are consistent with the assumption that long-term corticosteroid administration potentially induces not only myopathy but also motor neuron involvement as in mitochondrial diseases. (Keyword) asthma / corticosteroid myopathy / denervation / neurogenic muscular atrophy / mitochondria (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.42.862 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14518677 ● CiNii @ National Institute of Informatics (CRID): 1390282679843291136 ● Search Scopus @ Elsevier (PMID): 14518677 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.42.862 (DOI: 10.2169/internalmedicine.42.862, PubMed: 14518677, CiNii: 1390282679843291136)
149.	Yoshiko Kanezaki, Rie Matsushima, Toshiyuki Obata, Yutaka Nakaya, Toshio Matsumoto and Yousuke Ebina : Injection of the Insulin receptor alpha subunit increases blood glucose levels in mice, Biochemical and Biophysical Research Communications, 309, 3, 572-577, 2003. (Summary) Using the expression vector of the truncated human insulin receptor (hIR), we have constructed a stable Chinese hamster ovary (CHO) cell line which secretes the His-tagged alpha subunit (insulin-binding domain) of hIR into medium. To examine characteristics of the His-tagged hIRalpha, we purified the protein secreted from the CHO cells. The His-tagged hIRalpha was glycosylated and processed a dimer. The molecule bound insulin with an affinity similar to that of the intact hIR. The His-tagged full length of hIR was autophosphorylated by insulin stimulation in CHO cells. Injection of the purified His-tagged hIRalpha into veins of mice increased in the concentration of blood glucose within 30 min. The intraperitoneal glucose tolerance test (ipGTT) done after injection of the purified His-tagged hIRalpha showed evidence of a marked hyperglycemia. These findings provide direct evidence that the presence of hIRalpha in the blood stream inhibits insulin actions by binding with plasma insulin. (Keyword) insulin receptor / His-tagged alpha subunit / insulin binding / blood glucose concentration / EXTRACELLULAR DOMAIN / cells / ECTODOMAIN / EXPRESSION / identification / GLYCOSYLATION / BACULOVIRUS / SECRETION / antibody / kinase (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2003.08.028 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12963028 ● Search Scopus @ Elsevier (PMID): 12963028 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2003.08.028 (DOI: 10.1016/j.bbrc.2003.08.028, PubMed: 12963028)
150.	Makoto Kunishige, Takao Mitsui, Masashi Akaike, Masakazu Kawajiri, Masayuki Shono, Hisaomi Kawai and Toshio Matsumoto : Overexpressions of myoglobin and antioxidant enzymes in ragged-red fibers of skeletal muscle from patients with mitochondrial encephalomyopathy, Muscle & Nerve, 28, 4, 484-492, 2003. (Summary) To determine the relationship between myoglobin (Mb) and the defense system against reactive oxygen species in various myopathies, we performed immunohistochemical analyses of Mb and various antioxidant enzymes, including manganese superoxide dismutase (Mn-SOD), copper zinc SOD (CuZn-SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Biopsied muscle specimens were obtained from patients with chronic progressive external ophthalmoplegia (CPEO), Kearns-Sayre syndrome (KSS), Duchenne muscular dystrophy (DMD), and polymyositis (PM). In patients with CPEO/KSS, stainings of Mb, SOD, CAT, and GSH-Px in nonatrophic ragged-red fibers (RRFs) were more intense than those in non-RRFs. These pronounced stainings corresponded to ragged-red lesions. The staining intensities of these antioxidant enzymes were significantly correlated with that of Mb (P < 0.001). Atrophic RRFs in specimens from patients with CPEO/KSS showed intense stainings of these antioxidant enzymes but not intense staining of Mb. In specimens from patients with DMD/PM, the antioxidant enzymes but not Mb were overexpressed in degenerative fibers. These results suggest that oxidative stress is associated with Mb expression specifically in mitochondrial diseases. The antioxidant enzymes seem to be upregulated to protect against muscle damage in nonatrophic RRFs. However, the Mb-mediated oxidative damage may become more extensive and result in further mitochondrial dysfunction and progressive atrophy of RRF with impaired upregulation of Mb. (Keyword) catalase / glutathione peroxidase / oxgen radical / ragged-red fibers / superoxide dismutase (Link to Publication Site) ● Publication site (DOI): 10.1002/mus.10466 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14506721 ● Search Scopus @ Elsevier (PMID): 14506721 ● Search Scopus @ Elsevier (DOI): 10.1002/mus.10466 (DOI: 10.1002/mus.10466, PubMed: 14506721)
151.	Emiko Tohjima, Daisuke Inoue, Nobuchika Yamamoto, Shinsuke Kido, Yuji Ito, Shuji Kato, Yasuhiro Takeuchi, Seiji Fukumoto and Toshio Matsumoto : Decreased AP-1 activity and interleukin-11 expression by bone marrow stromal cells may be associated with impaired bone formation in aged mice, Journal of Bone and Mineral Research, 18, 8, 1461-1470, 2003. (Summary) Expression of an osteogenic cytokine, IL-11, is decreased in SAMP6. We show here that IL-11 transcription largely depends on AP-1 transcription factors, activities of which are decreased in SAMP6 as well as aged ICR mice. Therefore, diminished AP-1 activity and the resultant decline in IL-11 expression may play a role in impaired bone formation in the aged. Evidence suggests that impaired osteoblastogenesis contributes to aging-associated osteopenia. The P6 strain of senescence-accelerated mice (SAM) is an animal model of senile osteoporosis, which exhibits low bone mass caused by impaired bone formation. Bone marrow stromal cells from SAMP6 show decreased osteoblastogenesis and increased adipogenesis. We previously demonstrated that these abnormalities of SAMP6 stromal cells may be attributed to decreased expression of interleukin (IL)-11. In this study, we attempted to determine the molecular mechanism of decreased IL-11 expression by SAMP6 stromal cells by cloning and analyzing the mouse IL-11 gene promoter. We found that two tandem activating protein-1 (AP-1) sites that reside immediately upstream of TATA box play critical roles in IL-11 gene transcription. Gel shift analysis showed that binding activity to the IL-11 AP-1 sites was reduced in SAMP6 stromal cell nuclear extracts. Among multiple components of AP-1 transcription factors, Jun D binding was particularly decreased. Furthermore, decreased Jun D binding and IL-11 expression by stromal cells was also observed in aged mice of the ICR strain. Therefore, decreased AP-1 activity and a resultant decline in IL-11 expression by bone marrow stromal cells may play a role in impaired bone formation in the aged. (Keyword) senile osteoporosis / senescence-accelerated mice / interleukin-11 / promoter / activating protein-1 (Link to Publication Site) ● Publication site (DOI): 10.1359/jbmr.2003.18.8.1461 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12929935 ● Summary page in Scopus @ Elsevier: 2-s2.0-2142650270 (DOI: 10.1359/jbmr.2003.18.8.1461, PubMed: 12929935, Elsevier: Scopus)
152.	Mitsunori Fujimura, Masashi Akaike, Midori Kato, Nobuyuki Takamori, Masahiro Abe, Takeshi Nishiuchi, Hiroyuki Azuma and Toshio Matsumoto : Aggressive antiplatelet therapy before coronary stent implantation in acute coronary syndrome with essential thrombocythemia--a case report, Angiology, 54, 4, 485-490, 2003. (Summary) A 52-year-old man was admitted to the hospital because of unstable angina pectoris. Coronary angiography revealed severe stenosis at a proximal site of the left anterior descending artery. Essential thrombocythemia (ET) was diagnosed on the basis of findings of marked thrombocytosis (106 x 10(4)/microL) and an increased number of immature megakaryocytes in the bone marrow. Because hyperaggregability of platelets was demonstrated by an ex vivo platelet aggregation assay and by elevated plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), antiplatelet therapy with aspirin and ticlopidine and cytoreduction therapy with hydroxyurea were started. This combination treatment resulted in a decrease in the platelet count to less than 60 x 10(4)/microL and decreases in plasma levels of both beta-TG and PF4 to almost normal values. Percutaneous coronary angioplasty and stenting were then performed successfully without thrombotic complications. These findings suggest that combination therapy with antiplatelet and cytoreduction agents before catheter intervention is useful for the prevention of thrombotic complications in patients with acute coronary syndrome associated with essential thrombocythemia. (Keyword) Acute Disease / Angina, Unstable / Aspirin / Combined Modality Therapy / Coronary Stenosis / Humans / Hydroxyurea / Male / Middle Aged / Platelet Aggregation Inhibitors / Stents / Thrombocythemia, Essential / Ticlopidine (Link to Publication Site) ● Publication site (DOI): 10.1177/000331970305400414 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12934770 ● Search Scopus @ Elsevier (PMID): 12934770 ● Search Scopus @ Elsevier (DOI): 10.1177/000331970305400414 (DOI: 10.1177/000331970305400414, PubMed: 12934770)
153.	Nami Inoue, Makoto Kunishige, Sumiko Yoshida, Yasushi Oshima, Yoshiaki Ohnishi, Yasuhiro Kuroda, Atsuko Asano, Hiide Yoshino, Toshio Matsumoto and Takao Mitsui : Dissociation between titer of anti-ganglioside antibody and severity of symptoms in a case of Guillain-Barre syndrome with treatment-related fluctuation, Journal of the Neurological Sciences, 210, 1-2, 105-108, 2003. (Summary) Since plasma exchange (PE) and intravenous immunoglobulin (i.v.Ig) have been widely used in treatment for Guillain-Barré syndrome (GBS), early relapse and treatment-related fluctuation have been a potential problem, but little is known about the mechanism of relapse and fluctuation. We describe a patient who had GBS with treatment-related fluctuation. A 37-year-old Japanese man exhibited acute distal-dominant weakness in upper limbs after upper respiratory infection. His cranial nerve system was normal and muscle weakness was limited to upper limbs. Anti-GT1a IgG was strongly positive and anti-GQ1b IgG was also detected in his serum. Muscle weakness responded well to double-filtration plasmapheresis (DFPP) followed by i.v.Ig, but relapsed 45 days after the initial treatment. Although repeated treatments were effective, the patient showed additional minor deterioration twice. Motor nerve conduction velocities (MCVs) corresponded to the muscle weakness, but elevated level of cerebrospinal fluid (CSF) protein remained and anti-ganglioside antibody titers steadily decreased throughout the clinical course. These findings indicate that the clinical fluctuation was not due to changes in the production of anti-ganglioside antibodies but presumably to the transient beneficial effects of DFPP/i.v.Ig and the outlasting inflammatory response in peripheral nerves. (Keyword) Anti-GT1a antibody / anti-GQ1b antibody / acute inflammatory demyelinating / Intravenous immunoglobulin / Plasma exchange (Link to Publication Site) ● Publication site (DOI): 10.1016/S0022-510X(03)00031-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12736098 ● Search Scopus @ Elsevier (PMID): 12736098 ● Search Scopus @ Elsevier (DOI): 10.1016/S0022-510X(03)00031-5 (DOI: 10.1016/S0022-510X(03)00031-5, PubMed: 12736098)
154.	新谷保実, Sumiko Yoshida, 鈴木康博, 加藤修司, Yuichi Fujinaka, Daisuke Inoue, Toshio Matsumoto, 宮恵子, 長田淳一 and 小阪昌明 : 絶食試験後の食事再開時に著しい高血糖をきたしたBulimia nervosaの1例, ホルモンと臨床, 51, 6, 575-579, 2003. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523951030056638720 (CiNii: 1523951030056638720)
155.	T Shigekiyo, O Fujino, Y Kanagawa and Toshio Matsumoto : Prekallikrein (PK) Tokushima: PK deficiency caused by a Gly401-->Glu mutation, Journal of Thrombosis and Haemostasis, 1, 6, 1314-1316, 2003. (Keyword) DNA Mutational Analysis / Humans / Male / Middle Aged / Mutation, Missense / Pedigree / Prekallikrein (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1538-7836.2003.00154.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12871337 ● Summary page in Scopus @ Elsevier: 2-s2.0-2142656304 (DOI: 10.1046/j.1538-7836.2003.00154.x, PubMed: 12871337, Elsevier: Scopus)
156.	Shinsuke Kido, Daisuke Inoue, Kenji Hiura, Wilde Javier, Yuji Ito and Toshio Matsumoto : Expression of RANK is dependent upon differentiation into the macrophage/osteoclast lineage: induction by 1alpha,25-dihydroxyvitamin D3 and TPA in a human myelomonocytic cell line, HL60, Bone, 32, 6, 621-629, 2003. (Summary) Receptor activator of nuclear factor (RANK) is a member of the tumor necrosis factor receptor superfamily indispensable for osteoclast differentiation. However, little is known about the regulatory mechanism of RANK expression. In the present study, RANK expression during macrophage/osteoclast differentiation was investigated using a human myelomonocytic cell line, HL60, capable of differentiating into mature osteoclasts under appropriate conditions. RANK mRNA expression was barely detectable in growing HL60 cells. We found that treatment with 1alpha,25-dihydroxyvitamin D(3) and TPA resulted in an apparent induction of RANK mRNA and protein in association with differentiation into the macrophage/osteoclast lineage. Induction of RANK was time and dose dependent and lineage specific. Moreover, RANK induction was blocked by an RNA polymerase II inhibitor, suggesting an involvement of a transcriptional mechanism. The induced RANK was functional as it was able to bind RANK ligand and activate NF-kappaB. In the induced HL60 cells expressing both c-Fms and RANK, RANK mRNA expression was further enhanced by RANKL, but not by macrophage colony-stimulating factor. These results suggest a positive feedback regulation of RANK expression by its own intracellular signaling. The in vitro system described here may be a useful model to elucidate the regulatory mechanism of RANK expression and its role in human osteoclastogenesis. (Keyword) osteoclasts / vitamin D / growth factors-others (Link to Publication Site) ● Publication site (DOI): 10.1016/S8756-3282(03)00049-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12810169 ● Summary page in Scopus @ Elsevier: 2-s2.0-0142093039 (DOI: 10.1016/S8756-3282(03)00049-8, PubMed: 12810169, Elsevier: Scopus)
157.	Soichi Honda, Chisato Kosugi, Shozo Yamada, Toshiaki Sano, Toshio Matsumoto, Mitsuo Itakura and Katsuhiko Yoshimoto : Human Pituitary Adenomas Infrequently Contain Inactivation of Retinoblastoma 1 Gene and Activation of Cyclin Dependent Kinase 4 Gene., Endocrine Journal, 50, 3, 309-318, 2003. (Summary) Components of cyclinD1/cyclin-dependent kinase 4 (CDK4)/p16INK4a/pRb pathway are the frequent target of many tumor types. We examined the role of retinoblastoma susceptibility gene (RB1) and the CDK4 gene in human pituitary tumorigenesis. For the RB1 gene, pRb expression and loss of heterozygosity (LOH) on 13q in pituitary adenomas were analysed. Immunostaining of pRb revealed lack of expression in 1 of 29 pituitary adenomas. In 4 of 31 pituitary adenomas, allelic imbalances including LOH of RB1 on 13q14 were detected. Three of 4 pituitary adenomas, in which one adenoma lacked pRb expression, had a common LOH region at least from D13S219 on 13q12.3-q13 to D13S265 on 13q31-32. Interphase fluorescence in situ hybridization with a probe of RB1 showed 2 copies of RB1 gene suggesting that mitotic recombination events, not deletion or chromosome loss, led to LOH in the 3 pituitary adenomas analyzed. All 27 exons, intron-exon boundaries, and essential promoter region of RB1 gene were then sequenced in genomic DNA from 4 pituitary adenomas with allelic imbalance on 13q14 including one adenoma without pRb expression and 3 adenomas with pRb expression. Any somatic mutations, insertions, or microdeletions in the RB1 gene were not detected in 4 pituitary adenomas. Methylation sensitive (MS)-polymerase chain reaction (PCR) and bisulfite sequencing analysis revealed hypomethylated status of CpG islands in the promoter region of the RB1 genes of 4 pituitary adenomas. In addition, activating mutations of CDK4 gene, which is a component of cyclinD1/CDK4/p16INK4a/pRb pathway, were not detected in 31 pituitary adenomas. Based on these results, it is concluded that somatic mutations of the RB1 gene or CDK4 gene do not appear to play a major role in pituitary tumorigenesis. This supports the presence of potential tumor suppressor gene(s) on 13q12.3-q13 to 13q31-32 in pituitary adenomas. (Keyword) Adenoma / Adult / Aged / Chromosomes, Human, Pair 13 / Cyclin-Dependent Kinase 4 / Cyclin-Dependent Kinases / DNA Methylation / Female / Gene Expression Regulation, Neoplastic / Genes, Retinoblastoma / Humans / Immunohistochemistry / In Situ Hybridization, Fluorescence / Loss of Heterozygosity / Male / Middle Aged / Mutation / Pituitary Neoplasms / Polymerase Chain Reaction / Promoter Regions, Genetic / Proto-Oncogene Proteins (Tokushima University Institutional Repository) ● Metadata: 2004870 (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.50.309 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12940460 ● Search Scopus @ Elsevier (PMID): 12940460 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.50.309 (Tokushima University Institutional Repository: 2004870, DOI: 10.1507/endocrj.50.309, PubMed: 12940460)
158.	Takahiko Iuchi, Masashi Akaike, Takao Mitsui, Yasushi Ohshima, Yasumi Shintani, Hiroyuki Azuma and Toshio Matsumoto : Glucocorticoid Excess Induces Superoxide Production in Vascular Endothelial Cells and Elicits Vascular Endothelial Dysfunction, Circulation Research, 92, 1, 81-87, 2003. (Summary) Glucocorticoid (GC) excess often elicits serious adverse effects on the vascular system, such as hypertension and atherosclerosis, and effective prophylaxis for these complications is limited. We sought to reveal the mechanism underlying GC-induced vascular complications. Responses in forearm blood flow to reactive hyperemia in 20 GC-treated patients were significantly decreased to 43+/-8.9% (mean+/-SEM) from the values obtained before GC therapy (130+/-14%). An administration of vitamin C almost normalized blood flow responses. In human umbilical vein endothelial cells (HUVECs), production of hydrogen peroxide was increased up to 166.5+/-3.3% of control values by 10(-7) mol/L dexamethasone (DEX) treatment (P<0.01). Concomitant with DEX-induced hydrogen peroxide production, intracellular amounts of peroxynitrite significantly increased and those of nitric oxide (NO) decreased, respectively (P<0.01). Immunoblotting analysis using anti-nitrotyrosine antibody showed that peroxynitrite formation was increased in DEX-treated HUVECs. Using inhibitors against metabolic pathways for generation of reactive oxygen species (ROS), we identified that the major production sources of ROS by DEX treatment were mitochondrial electron transport chain, NAD(P)H oxidase, and xanthine oxidase. These findings suggest that GC excess causes overproduction of ROS and thereby perturbs NO availability in the vascular endothelium, leading to vascular complications in patients with GC excess. (Keyword) Glucocorticoid / reactive oxygen species / nitric oxide / vascular endothelial function (Link to Publication Site) ● Publication site (DOI): 10.1161/01.RES.0000050588.35034.3C (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12522124 ● Search Scopus @ Elsevier (PMID): 12522124 ● Search Scopus @ Elsevier (DOI): 10.1161/01.RES.0000050588.35034.3C (DOI: 10.1161/01.RES.0000050588.35034.3C, PubMed: 12522124)
159.	新谷保実, 加藤修司, Yuichi Fujinaka, Daisuke Inoue, 宮恵子 and Toshio Matsumoto : 血糖コントロールに解離して糖化蛋白が異常高値を示した胃切除後糖尿病患者の1例, 内分泌・糖尿病科, 16, 4, 389-394, 2003.
160.	新谷保実, Yuichi Fujinaka, 高橋幸志, 伊藤祐司, 加藤修司, Daisuke Inoue, Toshio Matsumoto, Nobuhiro Kurita, Seiki Tashiro, Yoshimi Bando, Toshiaki Sano and 宮恵子 : 空腹時の血漿インスリン濃度は常に低値で，グルカゴンにより著明なインスリン分泌反応が誘導されたインスリノーマの1例, 糖尿病, 46, 8, 679-684, 2003.
161.	Yuichi Fujinaka, Daisuke Inoue and Toshio Matsumoto : 重篤な骨粗鬆症および内分泌異常を認めた潰瘍性大腸炎の1例, 治療学, 37, 12, 1315-1319, 2003.
162.	Yasuhiro Takeuchi, Sumiyo Watanabe, Genichiro Ishii, Shu Takeda, Konosuke Nakayama, Seiji Fukumoto, Yasuyuki Kaneta, Daisuke Inoue, Toshio Matsumoto, Kenichi Harigaya and Toshiro Fujita : Interleukin-11 as a Stimulatory Factor for Bone Formation Prevents Bone Loss with Advancing Age in Mice*, The Journal of Biological Chemistry, 277, 50, 49011-49018, 2002. (Summary) Cytokines in interleukin (IL)-11 subfamily participate in the regulation of bone cell proliferation and differentiation. We report here positive effects of IL-11 on osteoblasts and bone formation. Overexpression of human IL-11 gene in transgenic mice resulted in the stimulation of bone formation to increase cortical thickness and strength of long bones, and in the prevention of cortical bone loss with advancing age. Bone resorption and osteoclastogenesis were not affected in IL-11 transgenic mice. In experiments in vitro, IL-11 stimulated transcription of the target gene for bone morphogenetic protein (BMP) via STAT3, leading to osteoblastic differentiation in the presence of BMP-2, but inhibited adipogenesis in bone marrow stromal cells. These results indicate that IL-11 is a stimulatory factor for osteoblastogenesis and bone formation to conserve cortical bone, possibly by enhancing BMP actions in bone. IL-11 may be a new therapeutic target for senile osteoporosis. (Keyword) aging / Animals / Base Sequence / Bone Development / Bone Marrow Cells / Bone Morphogenetic Proteins / Bone Resorption / Cells, Cultured / Chromans / DNA Primers / Humans / Interleukin-11 / Male / Mice / Mice, Transgenic / Recombinant Proteins / Thiazoles / Thiazolidinediones / Transcription, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M207804200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12384500 ● CiNii @ National Institute of Informatics (CRID): 1360292618612506624 ● Summary page in Scopus @ Elsevier: 2-s2.0-0037073709 (DOI: 10.1074/jbc.M207804200, PubMed: 12384500, CiNii: 1360292618612506624, Elsevier: Scopus)
163.	Itsuro Endo, Takao Mitsui and Toshio Matsumoto : Diurnal fluctuation of edema synchronized with plasma VEGF concentration in patient with POEMS syndrome., Internal Medicine, 41, 12, 1196-1198, 2002. (Summary) A case of POEMS syndrome in a 49-year-old Japanese woman is reported. The patient exhibited prominent edema in her legs at night, but her edema usually improved by the following morning. The plasma concentrations of VEGF in the patient showed diurnal fluctuations; plasma VEGF levels peaked at night and decreased in the daytime. Immunocytochemical study demonstrated the expression of VEGF in IgA- and λ-positive plasma cells in bone marrow. The results indicate that VEGF was produced at least by plasma cells and that VEGF production was regulated by circadian rhythm in synchronization with the development of edema.(Internal Medicine 41: 1196-1198, 2002) (Keyword) POEM / VEGF (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.41.1196 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679844545664 ● Summary page in Scopus @ Elsevier: 2-s2.0-0036971959 (DOI: 10.2169/internalmedicine.41.1196, CiNii: 1390282679844545664, Elsevier: Scopus)
164.	Yasushi Oshima, Takao Mitsui, H Yoshino, Itsuro Endo, Makoto Kunishige, A Asano and Toshio Matsumoto : Central motor conduction in patients with anti-ganglioside antibody associated neuropathy syndromes and hyperreflexia, Journal of Neurology, Neurosurgery, and Psychiatry, 73, 5, 568-573, 2002. (Summary) Several serum antibodies against gangliosides are diagnostically important, particularly in Guillain-Barré syndrome (GBS), Miller Fisher syndrome (MFS), and multifocal motor neuropathy (MMN). Although hyperreflexia is an atypical symptom in these disorders, it has been found in some patients with GBS, MFS, and MMN. The aim of the study was to determine whether hyperreflexia corresponds to corticospinal tract dysfunction in these patients. The study examined central and peripheral motor conduction in patients with hyperreflexia who exhibited acute paralysis (group 1, n=5), acute ataxia and ophthalmoplegia (group 2, n=7), or chronic paralysis with conduction block (group 3, n=2). The clinical symptoms are similar to those in patients with GBS, MFS, and MMN, respectively, and serum anti-ganglioside antibodies were found to be positive in all patients. Using magnetic and electrical stimulation techniques, central and peripheral motor conduction were compared in patients in groups 1, 2, and 3 and patients with GBS (n=7), MFS (n=8), and MMN (n=6). Central motor conduction times (CMCTs) in patients in groups 1, 2, and 3 were significantly delayed compared with those in patients with GBS, MFS, and MMN (p<0.01, p<0.05, p<0.05, respectively), and the delayed CMCTs significantly improved in the recovery periods (p<0.01, p<0.01, p<0.05, respectively). However, motor conduction velocity, compound muscle action potential, and F wave conduction velocity were not significantly different between the patients. These findings indicate that corticospinal tract is functionally involved in patients with anti-ganglioside antibody associated neuropathy syndromes and hyperreflexia (Keyword) anti-ganglioside antibody / neuropathy syndromes and hyperreflexia (Link to Publication Site) ● Publication site (DOI): 10.1136/jnnp.73.5.568 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12397153 ● Search Scopus @ Elsevier (PMID): 12397153 ● Search Scopus @ Elsevier (DOI): 10.1136/jnnp.73.5.568 (DOI: 10.1136/jnnp.73.5.568, PubMed: 12397153)
165.	Eri Fukunaga, Makoto Kunishige, Takao Mitsui, Itsuro Endo, Yasushi Oshima, Yukiko Kuroda, S Hara and Toshio Matsumoto : Severe dermatomyositis with rhabdomyolysis and paralytic ileus: a case successfully treated with plasmapheresis and intravenous immunoglobulin, European Journal of Neurology, 9, 6, 697-698, 2002. (Keyword) dermatomyositis / lntravenous immunoglobulin (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1468-1331.2002.00447_10.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12453096 ● Search Scopus @ Elsevier (PMID): 12453096 ● Search Scopus @ Elsevier (DOI): 10.1046/j.1468-1331.2002.00447_10.x (DOI: 10.1046/j.1468-1331.2002.00447_10.x, PubMed: 12453096)
166.	Masahiro Abe, Kenji Hiura, Javier Wilde, Keiji Moriyama, Toshihiro Hashimoto, Shuji Ozaki, Shingo Wakatsuki, Masaaki Kosaka, Shinsuke Kido, Daisuke Inoue and Toshio Matsumoto : Role for macrophage inflammatory protein (MIP)-1α and MIP-1β in the development of osteolytic lesions in multiple myeloma, Blood, 100, 6, 2195-2202, 2002. (Summary) Multiple myeloma (MM) cells cause devastating bone destruction by activating osteoclasts in the bone marrow milieu. However, the mechanism of enhanced bone resorption in patients with myeloma is poorly understood. In the present study, we investigated a role of C-C chemokines, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta, in MM cell-induced osteolysis. These chemokines were produced and secreted by a majority of MM cell lines as well as primary MM cells from patients. Secretion of MIP-1alpha and MIP-1beta correlated well with the ability of myeloma cells to enhance osteoclastic bone resorption both in vitro and in vivo as well as in MM patients. In osteoclastogenic cultures of rabbit bone cells, cocultures with myeloma cells as well as addition of myeloma cell-conditioned media enhanced both formation of osteoclastlike cells and resorption pits to an extent comparable to the effect of recombinant MIP-1alpha and MIP-1beta. Importantly, these effects were mostly reversed by neutralizing antibodies against MIP-1alpha and MIP-1beta, or their cognate receptor, CCR5, suggesting critical roles of these chemokines. We also demonstrated that stromal cells express CCR5 and that recombinant MIP-1alpha and MIP-1beta induce expression of receptor activator of nuclear factor-kappaB (RANK) ligand by stromal cells, thereby stimulating osteoclast differentiation of preosteoclastic cells. These results suggest that MIP-1alpha and MIP-1beta may be major osteoclast-activating factors produced by MM cells. (Keyword) Animals / Bone Neoplasms / Bone Resorption / Carrier Proteins / Chemokine CCL3 / Chemokine CCL4 / Coculture Techniques / Culture Media, Conditioned / Humans / Macrophage Inflammatory Proteins / Membrane Glycoproteins / Multiple Myeloma / Osteoclasts / Osteolysis / Paracrine Communication / RANK Ligand / Rabbits / Receptor Activator of Nuclear Factor-kappa B / Receptors, CCR5 / Stromal Cells / Tumor Cells, Cultured (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12200385 ● Summary page in Scopus @ Elsevier: 2-s2.0-0037105599 (PubMed: 12200385, Elsevier: Scopus)
167.	Masashi Akaike, Hiroyuki Azuma, Ayako Kagawa, Kazuya Matsumoto, Ikuro Hayashi, Katsuya Tamura, Takeshi Nishiuchi, Takahiko Iuchi, Nobuyuki Takamori, Ken-ichi Aihara, Tomonori Yoshida, Yasuhiko Kanagawa and Toshio Matsumoto : Effect of Aspirin Treatment on Serum Concentrations of Lipoprotein(a) in Patients with Atherosclerotic Diseases, Clinical Chemistry, 48, 9, 1454-1459, 2002. (Summary) Increased serum lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerosis. We previously reported that aspirin reduced Lp(a) production by cultured hepatocytes via the reduction of apolipoprotein(a) [apo(a)] gene transcription. We evaluated both the effect of aspirin treatment (81 mg/day) on serum Lp(a) concentrations and the correlation between the degree of reduction in serum Lp(a) and the type of apo(a) isoform in 70 patients with coronary artery disease or cerebral infarction. Aspirin lowered serum Lp(a) concentrations to approximately 80% of the baseline values in patients with high Lp(a) concentrations (>300 mg/L). The percentage of decrease in serum Lp(a) was larger in patients with high Lp(a) than in patients with low Lp(a) (<300 mg/L), irrespective of apo(a) isoform size. The decreases in serum Lp(a) in high Lp(a) patients with both the high-molecular-weight and the low-molecular-weight isoforms were positively correlated with the baseline Lp(a) concentrations. Because the secretory efficiencies of apo(a) in the same isoform are likely to be similar, the difference in serum Lp(a) concentrations in patients having the same apo(a) isoform depends on the transcriptional activity of the apo(a) gene. These findings suggest that aspirin decreases serum Lp(a) concentrations via a decrease in apo(a) gene transcription more effectively in patients with high transcriptional activity of this gene. (Keyword) Arteriosclerosis / Aspirin / Cerebral Infarction / Coronary Disease / Female / Humans / Hypolipidemic Agents / Lipoprotein(a) / Male / Middle Aged / Protein Isoforms (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12194922 ● Search Scopus @ Elsevier (PMID): 12194922 (PubMed: 12194922)
168.	Takao Mitsui, Yoshifumi Umaki, Masakazu Nagasawa, Masashi Akaike, Kenji Aki, Hiroyuki Azuma, Shuji Ozaki, Masaaki Odomi and Toshio Matsumoto : Mitochondrial damage in patients with long-term corticosteroid therapy: development of oculoskeletal symptoms similar to mitochondrial disease, Acta Neuropathologica, 104, 3, 260-266, 2002. (Summary) Two patients with long-term corticosteroid administration sporadically developed limb muscle wasting followed by ophthalmoplegia, and the skeletal muscle pathology revealed ragged-red fibers (RRFs) with abnormal mitochondria, in addition to the findings of corticosteroid myopathy. The oculoskeletal symptoms of the present cases resemble those of chronic progressive external ophthalmoplegia, a type of mitochondrial disease. The ocular muscles have more RRFs than limb muscles, and large multiple deletions of mitochondrial DNA was detected in ocular and limb muscles of the two patients by PCR but not by Southern blotting. Immunohistochemistry demonstrated that 8-hydroxy-deoxyguanosine (8-OH-dG) and 4-hydroxy-2-nonenal were intensely stained in skeletal muscles of these patients particularly in RRFs. High-performance liquid chromatography with electrochemical detection analysis revealed an increase in 8-OH-dG from mitochondrial DNA. These findings may suggest that long-term corticosteroid administration potentially induces oxidative stress-mediated mitochondrial damage, resulting in the development of the oculoskeletal symptoms in some patients. (Keyword) Aldehydes / Anti-Inflammatory Agents / Deoxyguanosine / Diagnosis, Differential / Exercise Test / Female / Gene Deletion / Humans / Lactic Acid / Male / Middle Aged / Mitochondria, Muscle / Oculomotor Muscles / Ophthalmoplegia, Chronic Progressive External / Prednisolone / Superoxide Dismutase / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1007/s00401-002-0553-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12172911 ● Search Scopus @ Elsevier (PMID): 12172911 ● Search Scopus @ Elsevier (DOI): 10.1007/s00401-002-0553-5 (DOI: 10.1007/s00401-002-0553-5, PubMed: 12172911)
169.	Masahiro Abe, Yasumi Shintani, Yuzuru Eto, Kazuyo Harada, Masaaki Kosaka and Toshio Matsumoto : Potent induction of activin A secretion from monocytes and bone marrow stromal fibroblasts by cognate interaction with activated T cells, Journal of Leukocyte Biology, 72, 2, 347-352, 2002. (Summary) Activin A is a multifunctional cytokine essential for cell differentiation and apoptosis including erythroid cell differentiation in the bone marrow. In addition, activin A is induced by inflammation and exerts anti-inflammatory effects. However, the mechanism of activin A induction is still unclear, especially by inflammatory processes. Here we show that activin A secretion from monocytes and bone marrow stromal fibroblasts, its major sources in the bone marrow, is markedly enhanced by cognate interaction with activated T cells. This process is mediated by CD40/CD40 ligand interaction as well as concomitantly secreted T cell-derived cytokines, granulocyte macrophage-colony stimulating factor, and interferon-gamma. Furthermore, stromal fibroblasts as well as monocytes provide a costimulatory signal to anti-CD3-treated T cells via CD80 and CD86 to maintain the enhanced activin A production. These findings suggest that activin A is potently induced in the bone marrow and may play a role in the suppression of inflammatory or immune processes. (Keyword) CD40 / CD28 / costimulation / GM-CSF / IFN-γ (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12149426 ● Summary page in Scopus @ Elsevier: 2-s2.0-0036698295 (PubMed: 12149426, Elsevier: Scopus)
170.	Takao Mitsui, Hiroyuki Azuma, Masakazu Nagasawa, Takahiko Iuchi, Masashi Akaike, Masaaki Odomi and Toshio Matsumoto : Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle, Journal of Neurology, 249, 8, 1004-1009, 2002. (Summary) Corticosteroid myopathy is a major clinical problem in patients undergoing chronic corticosteroid treatment and shows insidious and progressive muscle atrophy in proximal limbs. Although several mechanisms underlying the pathophysiology of muscle injury have been postulated, precise pathogenesis is still not clear. We evaluated the mitochondrial functions in patients receiving corticosteroids compared with those in healthy controls or patients not receiving corticosteroids. The serum levels and total production of lactate were investigated by an aerobic exercise test using a bicycle ergometer. Mitochondrial respiratory activities and oxidative damage in biopsied skeletal muscles were also studied. The results of aerobic exercise tests revealed a significant overproduction of lactate in patients treated with corticosteroids ( p < 0.005), which was positively correlated with total corticosteroid doses administered ( p < 0.0001). In these patients, mitochondrial enzyme activity in complex I was significantly decreased ( p < 0.05) and oxidative damage of biopsied skeletal muscle was remarkable both in mitochondrial and nuclear DNAs ( p < 0.001). The results suggest that chronic corticosteroid administration induces mitochondrial dysfunction and oxidative damage in skeletal muscles, which may be the pathogenesis, at least in part, of corticosteroid-induced myopathy. (Keyword) Corticosteroid myopathy / Mitochondrial respiratory activity / oxidative damage / aerobic exercise / biopsied skeletal muscle (Link to Publication Site) ● Publication site (DOI): 10.1007/s00415-002-0774-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12195445 ● Search Scopus @ Elsevier (PMID): 12195445 ● Search Scopus @ Elsevier (DOI): 10.1007/s00415-002-0774-5 (DOI: 10.1007/s00415-002-0774-5, PubMed: 12195445)
171.	Yoshifumi Umaki, Takao Mitsui, Itsuro Endo, Masashi Akaike and Toshio Matsumoto : Apoptosis-related changes in skeletal muscle of patients with mitochondreal disease., Acta Neuropathologica, 103, 2, 163-170, 2002. (Summary) Much interest has recently been shown in apoptosis-mediated roles in the pathophysiology of mitochondrial diseases, because mitochondrial defects are implicated in a wide variety of degenerative diseases. We investigated whether apoptotic events occurred in skeletal muscles of patients with mitochondrial diseases, including chronic progressive external ophthalmoplegia (CPEO), Kearns-Sayer syndrome (KSS), and mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). In a immunohistochemical study, stainings for 8-hydroxy-deoxyguanosine (8-OH-dG), 4-hydroxy-nonenal (4-HNE), Mn-SOD, Bcl-2, cytochrome c, DNase I and Bcl-x L showed a pronounced granular distribution in the cytochrome c oxidase (COX)-negative ragged-red fibers (RRFs). On the other hand, the signals for Bax, p53, Fas and caspase 3 were not obviously increased in RRFs. In situ labeling of DNA breaks demonstrated preferential signals not only in myonuclei but also in subsarcolemmal regions of RRFs, indicating that mitochondrial as well as myonuclear DNA is fragmented in RRFs. An immunoblotting study demonstrated that cytochrome c was increased in the cytosol of diseased muscles and that DNase I was increased in mitochondria, compared to that of normal muscles. No difference was observed between protein bands at 20 kDa corresponding to caspase 3 in diseased and normal muscles. These findings demonstrate that these mitochondrial diseases harbor unique apoptosis-related changes that differ from caspase 3-dependent apoptosis. It is thought that these changes are induced by superoxide overproduction and cytochrome c release resulting from an inherent mitochondrial defect and that the events are associated with DNase I activation. (Keyword) mitochondrial diseases / skeletal muscles (Link to Publication Site) ● Publication site (DOI): 10.1007/s004010100446 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11810183 ● Search Scopus @ Elsevier (PMID): 11810183 ● Search Scopus @ Elsevier (DOI): 10.1007/s004010100446 (DOI: 10.1007/s004010100446, PubMed: 11810183)
172.	Toshio Matsumoto, N Nagata, N Horikoshi, I Adachi and Y Ohashi : Comparative study of incadronate and elcatonin in patients with malignancy-associated hypercalcaemia, The Journal of International Medical Research, 30, 3, 230-243, 2002. (Summary) The clinical usefulness of incadronate was compared with elcatonin in 26 patients with malignancy-associated hypercalcaemia. Data from 21 and 24 patients could be used to assess efficacy and safety, respectively. Eleven patients were given a single 10-mg intravenous infusion of incadronate and 10 received twice-daily intramuscular injections of 40 IU of elcatonin for 7 consecutive days. After treatment, corrected serum calcium levels decreased significantly in both groups. The anti-hypercalcaemic effect of elcatonin was characterized by its rapid onset, with serum calcium levels reduced 1 day after administration. In contrast, the anti-hypercalcaemic effect of incadronate was more sustained but only became apparent a few days after infusion. Evaluation of symptoms revealed significantly greater improvement rates in the incadronate group compared with the elcatonin group. Adverse drug reactions were observed in three patients in the incadronate group, i.e. mild and transient fever in two cases and exacerbation of disturbance of consciousness in one case. These findings suggest that incadronate produces more marked and sustained hypocalcaemic effects than elcatonin, and that co-administration of these two drugs may yield both rapid and sustained control of malignancy-associated hypercalcaemia. (Keyword) incadronate / elcatonin / Bisphosphonate / malignancy-associated hypercalcaemia / hypercalcaemia / Calcitonin (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12166339 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035988465 (PubMed: 12166339, Elsevier: Scopus)
173.	Ryo Okazaki, Daisuke Inoue, Minako Shibata, Mieko Saika, Shinsuke Kido, Hikari Ooka, Hirofumi Tomiyama, Yoshikazu Sakamoto and Toshio Matsumoto : Estrogen Promotes Early Osteoblast Differentiation and Inhibits Adipocyte Differentiation in Mouse Bone Marrow Stromal Cell Lines that Express Estrogen Receptor (ER) α or ß, Endocrinology, 143, 6, 2349-2356, 2002. (Keyword) LIGAND-INDEPENDENT ACTIVATION / TRANSCRIPTIONAL ACTIVATION / MORPHOGENETIC PROTEINS / gene expression / GROWTH-FACTORS / MESSENGER-RNA / ADIPOGENESIS / OSTEOPOROSIS / MICE / SEX (Link to Publication Site) ● Publication site (DOI): 10.1210/endo.143.6.8854 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12021200 ● Search Scopus @ Elsevier (PMID): 12021200 ● Search Scopus @ Elsevier (DOI): 10.1210/endo.143.6.8854 (DOI: 10.1210/endo.143.6.8854, PubMed: 12021200)
174.	Rika Kuriwaka, Takao Mitsui, Soichiro Fujiwara, Yoshihiko Nishida and Toshio Matsumoto : Loss of postural reflexes in long-term occupational solvent exposure, European Neurology, 47, 2, 85-87, 2002. (Summary) Inhalation of organic solvents has long been known to damage various nervous systems, including cerebellum, brainstem, and pyramidal tract. However, little is known about the damage of the dopaminergic system. We report two patients with occupational long-term solvent exposure who developed postural instability without other features of parkinsonism. The concentration of HVA in CSF was decreased and the retropulsion was dramatically improved after the administration of levodopa. These findings indicate that the nigrostriatal dopaminergic neurons were disturbed by chronic solvent exposure, resulting in the loss of postural reflexes. (Keyword) postural reflexes / solvent exposure / dopaminergic neurons / Levodopa / Parkinsonism (Link to Publication Site) ● Publication site (DOI): 10.1159/000047958 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11844896 ● Summary page in Scopus @ Elsevier: 2-s2.0-0036178096 (DOI: 10.1159/000047958, PubMed: 11844896, Elsevier: Scopus)
175.	Naoko Yagishita, Yoko Yamamoto, Tatsuya Yoshizawa, Keisuke Sekine, Yoshikatsu Uematsu, Hisashi Murayama, Yumiko Nagai, Wojciech Krezel, Pierre Chambon, Toshio Matsumoto and Shigeaki Kato : Aberrant Growth Plate Development in VDR/RXR Double Null Mutant Mice, Endocrinology, 142, 12, 5332-5341, 2001. (Summary) VDR forms heterodimers with one of three RXRs, RXR alpha, RXR beta, and RXR gamma, and it is thought that RXR ligands can also modulate the trans-activation function of VDR/RXR heterodimers. In the present study we generated VDR/RXR gamma double null mutant mice to examine the convergent actions of vitamin D and vitamin A signaling and to explore the possibility of a functionally redundant VDR. Although RXR gamma(-/-) mice exhibited no overt abnormalities, VDR(-/-)/RXR gamma(-/-) mice appeared similar to VDR(-/-) mice, showing features typical of vitamin D-dependent rickets type II, including growth retardation, impaired bone formation, hypocalcemia, and alopecia. However, compared to VDR(-/-) mice, growth plate development in VDR(-/-)/RXR gamma(-/-) mutant mice was more severely impaired. Normalizing mineral ion homeostasis through dietary supplementation with high calcium and phosphorous effectively prevented rachitic abnormalities, except for disarranged growth plates in VDR(-/-)/RXR gamma(-/-) mutant mice, and alopecia in both VDR(-/-) and VDR(-/-)/RXR gamma(-/-) mutant mice. Histological analysis of VDR(-/-)/RXR gamma(-/-) growth plates revealed that development of the hypertrophic chondrocytes was selectively impaired. Thus, our findings indicated that the combined actions of VDR- and RXR gamma-mediated signals are essential for the normal development of growth plate chondrocytes, and raised the possibility that a functionally redundant VDR is present on chondrocytes as a heterodimer with RXR gamma. (Keyword) Animals / apoptosis / Bone and Bones / Chondrocytes / Diet / Growth Plate / homeostasis / Hypertrophy / Mice / knockout mice / Minerals / Osteoclasts / Phenotype / Receptors, Calcitriol / Receptors, Retinoic Acid / Retinoid X Receptors / Transcription Factors (Link to Publication Site) ● Publication site (DOI): 10.1210/endo.142.12.8544 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11713233 ● Summary page in Scopus @ Elsevier: 2-s2.0-17944374451 (DOI: 10.1210/endo.142.12.8544, PubMed: 11713233, Elsevier: Scopus)
176.	Masahiro Abe, Yasumi Shintani, Yuzuru Eto, Kazuyo Harada, Yuichi Fujinaka, Masaaki Kosaka and Toshio Matsumoto : Interleukin-1 β enhances and interferon-γ suppresses activin A actions by reciprocally regulating activin A and follistatin secretion from bone marrow stromal fibroblasts, Clinical and Experimental Immunology, 126, 1, 64-68, 2001. (Summary) Activin A is a multi-functional cytokine with a potent stimulation on erythroid cell differentiation in the bone marrow. The actions of activin A are determined by a balance of the levels of activin A and its inhibitor, follistatin (FS). However, the regulation of its actions in the bone marrow has been unclear. Here we show that bone marrow-derived stromal fibroblasts are the major source of activin A and FS in the bone marrow, and that the production of activin A is enhanced by interleukin-1beta (IL-1beta) and lipopolysaccharide (LPS), whereas interferon-gamma (IFN-gamma) inhibits the secretion of activin A by stromal fibroblasts. Concomitantly, IL-1beta as well as LPS inhibits and IFN-gamma stimulates FS secretion from stromal fibroblasts. Thus, these cytokines potently regulate activin A actions by reciprocal modulation of activin A and FS secretion from stromal fibroblasts. Because activin A exhibits anti-inflammatory effects in various tissues, up-regulation of activin A actions by IL-1beta and endotoxin in the bone marrow may play a protective role against inflammatory processes as well as anaemia. The present results also suggest that the inhibitory effect of IFN-gamma on erythropoiesis is mediated at least in part by a suppression of activin A actions in bone marrow. (Keyword) activin A / follistatin / stroma / IL-1β / IFN-γ (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1365-2249.2001.01644.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11678900 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034781894 (DOI: 10.1046/j.1365-2249.2001.01644.x, PubMed: 11678900, Elsevier: Scopus)
177.	Y Kuroda, Takao Mitsui, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : Homozygous deletion mutation of the parkin gene in patients with atypical parkinsonism, Journal of Neurology, Neurosurgery, and Psychiatry, 71, 2, 231-234, 2001. (Summary) Autosomal recessive juvenile parkinsonism (AR-JP) is characterised by homogenous clinical features and selective degeneration of nigral neurons. Recent progress in molecular genetic analyses of AR-JP has led to the identification of a novel ubiquitin-like protein, parkin, whose precise function still remains to be elucidated. Two unrelated Japanese families had levodopa unresponsive parkinsonism complicated with cerebellar and pyramidal tract dysfunction. Genetic analysis of the parkin gene and mRNA in both families disclosed identical mutations with large deletions extending from exons 3 to 4. These results suggest that the parkin protein possesses an important function not only in the substantia nigra but also in extranigral neurons of the CNS and that the phenotype of multiple system dysfunction can also be a complication in patients with AR-JP due to variations in sites of or changes in functions by parkin mutation. (Keyword) AR-JP / parkin / multiple system degeneration / deletion mutation (Link to Publication Site) ● Publication site (DOI): 10.1136/jnnp.71.2.231 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11459900 ● Search Scopus @ Elsevier (PMID): 11459900 ● Search Scopus @ Elsevier (DOI): 10.1136/jnnp.71.2.231 (DOI: 10.1136/jnnp.71.2.231, PubMed: 11459900)
178.	Toshihiro Hashimoto, Makoto Takishita, Masaki Kosaka, Toshiaki Sano and Toshio Matsumoto : Superantigens and autoantigens may be involved in the pathogenesis of gastric mucosa-associated lymphoid tissue lymphoma, International Journal of Hematology, 74, 2, 197-204, 2001. (Summary) To clarify the origin of tumor cells and the possible role of antigens in the pathogenesis of mucosa-associated lymphoid tissue lymphoma (MALTL) of the stomach, we analyzed the DNA sequences of the immunoglobulin (Ig) variable region gene from tumor cells of 4 patients with low-grade and 2 patients with high-grade MALTL associated with Helicobacter pylori infection. There were few somatic mutations in the Ig variable region gene, but intraclonal variations were observed in 2 of the 4 low-grade MALTL cases. In the remaining 2 low-grade MALTL and 1 of the 2 high-grade MALTL cases, somatic mutations and intraclonal variations were evident. In contrast, somatic mutations in the Ig variable region gene were prominent, but intraclonal variation was absent in the other high-grade MALTL cases. The deduced amino acid sequences of the antigen-binding fragments (Fab) from 2 MALTL cases revealed homology with anti-thyroglobulin antibodies, 3 MALTL cases with lupus anti-DNA antibodies, and 1 MALTL case with a rheumatoid factor. Furthermore, the heavy-chain variable region 3 (V(H)3) family genes were used in 5 of the 6 MALTL cases and had conserved amino acid residues for binding to staphylococcal protein A (SpA), a superantigen of B cells. Considering that another superantigen, protein Fv, competes for binding to Fab with SpA and has been shown to play a major role in immune defenses against gut pathogens, SpA and possibly protein Fv may contribute to the development of MALTL. Thus, these observations suggest that most gastric MALTLs arise from memory B cells that are preliminarily activated by superantigens and autoantigens. (Keyword) mucosa-associated lymphoid tissue lymphoma / immunoglobulin gene / staphylococcal protein A / protein Fv / Superantigen (Link to Publication Site) ● Publication site (DOI): 10.1007/BF02982005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11594522 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035434226 (DOI: 10.1007/BF02982005, PubMed: 11594522, Elsevier: Scopus)
179.	Masahiro Abe, Y Shintani, Y Eto, K Harada, Y Fujinaka, M Kosaka and Toshio Matsumoto : Interleukin 1β enhances and interferon-γ suppresses activin A actions by reciprocally regulating activin A and follistatin secretion from bone marrow stromal fibroblasts, Clinical and Experimental Immunology, 126, 64-68, 2001. (Keyword) IFN-γ / activin / follistain / stroma / IL-1β
180.	Mieko Saika, Daisuke Inoue, Shinsuke Kido and Toshio Matsumoto : 17β-Estradiol stimulates expression of osteoprotegerin by a mouse stromal cell line, ST-2, via estrogen receptor-α, Endocrinology, 142, 6, 2205-2212, 2001. (Summary) Osteoprotegerin (OPG) is a recently identified member of the tumor necrosis factor (TNF) receptor superfamily that regulates bone mass through an inhibitory action on osteoclast differentiation and function. To determine its potential roles of OPG in pathological changes in bone metabolism caused by estrogen deficiency, we investigated effects of estrogen on OPG expression by a mouse stromal cell line, ST-2, in vitro. Treatment of ST-2 cells with 17beta-E(2) resulted in up-regulation of OPG expression at both the messenger RNA and protein levels. The effect was time and dose dependent and steroid specific. The stimulatory action of 17beta-E(2) on OPG expression appeared to be mediated by the estrogen receptor-alpha (ERalpha) subtype because stable overexpression of ERalpha, but not of ERbeta, enhanced the OPG induction by 17beta-E(2). Moreover, estrogen withdrawal after 5-day pretreatment, mimicking the event occurring in vivo at menopause, dramatically diminished the expression of OPG. These findings suggest that down-regulation of OPG after estrogen withdrawal contributes to the enhanced osteoclastic bone resorption and bone loss after menopause by enhancing RANK ligand-RANK system that lies downstream of a large number of bone-resorbing cytokines. (Keyword) Animals / Cell Line / Dose-Response Relationship, Drug / Estradiol / Estrogen Receptor alpha / gene expression / Glycoproteins / Humans / Kinetics / Mice / Osteoprotegerin / RNA, Messenger / Receptors, Cytoplasmic and Nuclear / Receptors, Estrogen / Receptors, Tumor Necrosis Factor / Stromal Cells (Link to Publication Site) ● Publication site (DOI): 10.1210/endo.142.6.8220 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11356664 ● Summary page in Scopus @ Elsevier: 2-s2.0-85047681459 (DOI: 10.1210/endo.142.6.8220, PubMed: 11356664, Elsevier: Scopus)
181.	Ken-ichi Aihara, Hiroyuki Azuma, Yasumasa Ikeda, Masashi Akaike, Masahiro Abe, Takashi Sugihara and Toshio Matsumoto : Successful combination therapy--flunarizine,pentoxifylline, and cholestyramine--for spur cell anemia, International Journal of Hematology, 73, 3, 351-355, 2001. (Summary) Spur cell anemia, a hemolytic anemia observed in patients with alcoholic cirrhosis, is characterized by unusual erythrocyte morphology and an increased ratio of free cholesterol to phospholipid in the erythrocyte membrane. The prognosis of spur cell anemia is usually extremely poor, however, we describe here a patient with spur cell anemia who was successfully treated with combination therapy consisting of flunarizine, pentoxifylline, and cholestyramine. Initial therapy with flunarizine alone for 6 weeks did not significantly decrease the number of spur cells on peripheral blood smears. So pentoxifylline was added to the regimen. The patient recovered from the anemia, showed remarkable improvement with regard to the hyperbilirubinemia, and the changes were accompanied by a significant decrease in the number of spur cells in peripheral blood smears. To correct the hypercholesterolemia, cholestyramine was added to the regimen, which resulted in a reduction in the serum level of free cholesterol and an increase in the molar ratio of free cholesterol to phospholipid in erythrocyte membrane. However, 6 months later a skin eruption developed that was considered an adverse reaction to the drugs, so the flunarizine and pentoxifylline were discontinued. With cholestyramine therapy alone, the remission of spur cell anemia was maintained for more than 11 months. These observations suggest that non-invasive combination therapy with flunarizine, pentoxifylline, and cholestyramine is effective and valuable in the treatment of patients with spur cell anemia. (Keyword) Spur cell anemia / Free cholesterol / Hepatosplenomegaly / Pentoxifylline / Cholestyramine (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11345202 ● Search Scopus @ Elsevier (PMID): 11345202 (PubMed: 11345202)
182.	Aya Nakano, Takao Mitsui, Itsuro Endo, Y Takeda, Shuji Ozaki and Toshio Matsumoto : Solitary plasmacytoma with VEGF overproduction: report of a patient with polyneuropathy, Neurology, 56, 6, 818-819, 2001. (Keyword) Plasmacytoma / VEGF (Link to Publication Site) ● Publication site (DOI): 10.1212/wnl.56.6.818 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11274332 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035957252 (DOI: 10.1212/wnl.56.6.818, PubMed: 11274332, Elsevier: Scopus)
183.	Yasushi Oshima, Takao Mitsui, Itsuro Endo, Yoshifumi Umaki and Toshio Matsumoto : Corticospinal tract involvement in a variant of Guillain-Barré syndrome, European Neurology, 46, 1, 39-42, 2001. (Summary) To determine the involvement of the corticospinal tract in Guillain-Barré syndrome (GBS), we examined central motor conduction in patients with GBS-like symptoms and hyperreflexia using a magnetic stimulation technique. The subjects were 3 patients who exhibited ascending muscle weakness 2-4 weeks after preceding infections. Deep tendon reflexes were exaggerated in all four limbs of the 3 patients. The results of cerebrospinal fluid examinations revealed protein elevation without pleocytosis. The serum anti-GM(1) antibody titer was elevated in 2 patients. The results of nerve conduction study revealed axonal motor neuropathy and normal F-wave conduction. Central motor conduction time (CMCT) in patients with hyperreflexia was significantly delayed compared to that in patients with GBS and areflexia (p < 0.001), and the delayed CMCTs were significantly improved in the recovery periods (p < 0.001). Although hyperreflexia is a controversial symptom in patients with GBS, these findings indicate that there is functional corticospinal tract involvement in patients with a GBS variant. (Keyword) Guillain-Barré syndrome (Link to Publication Site) ● Publication site (DOI): 10.1159/000050754 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11455182 ● Search Scopus @ Elsevier (PMID): 11455182 ● Search Scopus @ Elsevier (DOI): 10.1159/000050754 (DOI: 10.1159/000050754, PubMed: 11455182)
184.	Yasuhiko Kanagawa, Toshio Shigekiyo, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : Molecular mechanism of type I congenital heparin cofactor (HC) II deficiency caused by a missense mutation at reactive P2 site: HC II Tokushima, Thrombosis and Haemostasis, 85, 1, 101-107, 2001. (Summary) We found a 66-year-old Japanese patient with type I congenital heparin cofactor (HC) II deficiency manifesting multiple atherosclerotic lesions. To investigate the molecular pathogenesis of our patient, we performed sequencing analysis and expressed recombinant human wild-type and mutant HC II molecules in COS-1 and CHO-K1 cells. Sequencing analysis following amplification of each of all 5 exons and its flanking region showed a single C to T transition at nucleotide position 12,854 in exon 5, which changed a Pro443 codon (CCG) to Leu codon (CTG). Because this mutation generates a new Bhv I site, the Bbv I digestion pattern of the PCR-amplified exon 5 fragments from each family member was analyzed. In all cases, the patterns were consistent with the activities and antigen levels of plasma HC I1 in those members. Transient transfection, metabolic labeling and pulse-chase experiments followed by immunoprecipitation analysis showed that the recombinant mutant HC II molecules were secreted from COS-1 cells in reduced amounts compared with the wild-type, and that an enhanced intracellular association of the mutant molecules with a chaperone, GRP78/BiP, was observed in CHO-K1 cells. Northern blot analysis indicated that the mutant HC I1 mRNA was transcribed at a similar level as that of wild-type. Immunohistochemical staining of the transfected cells revealed that COS-1 cells expressing the mutant HC II molecules were stained mainly in the perinuclear area. We conclude that the impaired secretion of the mutant HC II molecules, due to intracellular degradation, is the molecular pathogenesis of type I congenital HC II deficiency caused by a Pro443 to Leu mutation at reactive P2 site. (Keyword) heparin cofactor II / thrombosis / thrombin / transfection / chaperone (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11204559 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035171975 (PubMed: 11204559, Elsevier: Scopus)
185.	Masashi Akaike, 井内貴彦, 加藤みどり, 吉田智則, 橋詰俊二, 高森信行, 藤村光則, 金川泰彦, Hiroyuki Azuma and Toshio Matsumoto : 冠動脈疾患の予防ならびに治療の観点からみた高コレステロール血症治療の現状とその問題点, 診断と治療, 89, 3, 527-532, 2001. (Keyword) 冠動脈疾患 / 高コレステロール血症 / 一次予防 / 二次予防 / 高脂血症診療ガイドライン
186.	Takamasa Ohnishi, Eiji Takeda, Shiro Yogita, Hidenori Miyake, Takafumi Kinoshita, Yoshiyasu Terashima, Toshio Matsumoto and Seiki Tashiro : Effects of alendronate on bone metastases and hypercarcemia after surgery for hepatocellular carcinoma, Japanese Journal of Clinical Oncology, 30, 9, 410-413, 2000. (Summary) Alendronate, a bisphosphonate compound, lowers serum calcium in patients with cancer-associated hypercalcemia through its inhibitory effect on bone resorption and as a result symptoms associated with hypercalcemia improve. This study was carried out to investigate the effects of alendronate in patients with hypercalcemia due to bone metastasis of hepatocellular carcinoma (HCC). Two patients were evaluated. Their corrected serum calcium and alpha-fetoprotein (AFP) levels and their computed tomography (CT), bone scintigraphy and magnetic resonance imaging (MRI) findings were evaluated before and during alendronate treatment. After treatment, not only the corrected serum calcium levels but also AFP levels and bone pain decreased; in addition, the regression of the metastatic focus was noted in the MRI analysis. These tumor inhibitory effects of alendronate have not been reported in HCC before; and alendronate might serve to prevent bone metastases in patients with HCC. In conclusion, two patients who developed hypercalcemia associated with bone metastasis after surgery for HCC were treated with alendronate and they experienced alleviation of the pain due to bone metastasis, improvement of their quality of life and a marked decrease in AFP levels with tumor regression. (Keyword) Aged / Alendronate / Bone Neoplasms / Carcinoma, Hepatocellular / Female / Humans / Hypercalcemia / Liver Neoplasms / Male (Link to Publication Site) ● Publication site (DOI): 10.1093/jjco/hyd105 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11095140 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033661348 (DOI: 10.1093/jjco/hyd105, PubMed: 11095140, Elsevier: Scopus)
187.	Takao Mitsui, Masakazu Kawajiri, Makoto Kunishige, Takenori Endo, Masashi Akaike, Kenji Aki and Toshio Matsumoto : Functional association between nicotinic acetylcholine receptor and sarcomeric proteins via actin and desmin filaments, Journal of Cellular Biochemistry, 77, 4, 584-595, 2000. (Keyword) acetylcholine receptor / sarcomeric protein / actin / desmin / ATPase
188.	Ayako Kagawa, Hiroyuki Azuma, Masashi Akaike, Yasuhiko Kanagawa and Toshio Matsumoto : Aspirin Reduces Apolipoprotein(a) (Apo(a)) Production in Human Hepatocytes by Suppression of Apo(a) Gene Transcription, The Journal of Biological Chemistry, 274, 48, 34111-34115, 1999. (Summary) High serum lipoprotein(a) (Lp(a)) is a risk factor for vascular disorders. Our preliminary observations suggest that, in some patients with coronary heart disease with high serum Lp(a) levels, administration of aspirin reduced Lp(a) levels. Therefore, we aimed to analyze the effects of aspirin on the production of apo(a), the expression of apolipoprotein(a) (apo(a)) mRNA and the transcriptional activity of apo(a) gene promoter. Aspirin (5 mM) reduced the apo(a) levels in culture medium of human hepatocytes and suppressed apo(a) mRNA expression to 73% and 85% of the controls, respectively. Aspirin also reduced the transcriptional activity of apo(a) gene transfected into HepG2 hepatoma cells in a dose-dependent manner, with a maximal effect at 5 mM (44.3 +/- 1.5% of the control). Sodium salicylate (5 mM) also reduced apo(a) gene transcription, whereas indomethacin (10 microM) had no effect. Deletion analysis of apo(a) gene promoter showed that promoter region extending from -30 to +138 is critical for the effect of aspirin. Furthermore, enhanced production, mRNA expression, and gene transcription of apo(a) by interleukin-6 were also inhibited by aspirin. These results demonstrate that aspirin reduces apo(a) production from hepatocytes via reduction of the transcriptional activity of apo(a) gene with suppression of apo(a) mRNA expression. The suppression of apo(a) production by aspirin may at least in part play a role in the anti-atherogenic effect of aspirin in vascular disorders. (Keyword) Apolipoproteins A / Aspirin / Gene Expression Regulation / Humans / Indomethacin / Interleukin-6 / Liver / Luciferases / Promoter Regions, Genetic / RNA, Messenger / Recombinant Fusion Proteins / Sodium Salicylate / Transcription, Genetic / Tumor Cells, Cultured (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.274.48.34111 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10567380 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033607536 (DOI: 10.1074/jbc.274.48.34111, PubMed: 10567380, Elsevier: Scopus)
189.	Ryuzo Tani, Shuji Ozaki, Masaaki Kosaka, Soichiro Fujiwara, Hironobu Shibata, Shingo Wakatsuki and Toshio Matsumoto : Fas ligand-induced apoptosis of hepatocytes in natural killer cell leukaemia, British Journal of Haematology, 106, 3, 709-712, 1999. (Summary) Neoplastic natural killer (NK) cells overexpress Fas ligand (FasL), which may cause damage of Fas-bearing tissues. We report a patient with NK cell leukaemia who developed liver injury after pharyngitis. The NK leukaemic cells expressed functional FasL. In addition to soluble FasL, serum levels of interleukin-6 and interferon-gamma were increased dramatically when liver injury was aggravated. Moreover, hepatocytes expressed Fas and apoptotic hepatocytes were detected in the portal areas. These findings are consistent with the notion that inflammatory cytokines enhance the sensitivity to FasL and trigger apoptosis of hepatocytes in NK cell malignancies. (Keyword) natural killer cell / Fas / Fas ligand / apoptosis / liver (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10468861 ● Summary page in Scopus @ Elsevier: 2-s2.0-0032846765 (PubMed: 10468861, Elsevier: Scopus)
190.	Masashi Akaike, Hiroyuki Azuma, Ayako Kagawa, Yasuhiko Kanegawa, Ken-ichi Aihara, Madoka Matsuyama, Takahiko Iuchi, Nobuyuki Takamori, Tomonori Yoshida, Toshio Matsumoto, 松本和也, Ikuro Hayashi, Katsuya Tamura and Takeshi Nishiuchi : Effect of Aspirin Treatment on Serum Levels of Lipoprotein(a), --- Analysis From the Apolipoprotein(a)Isoforms ---, Shikoku Acta Medica, 55, 3, 109-114, 1999. (Keyword) Lipoprotein(a) / Apolipoprotein(a) / Aspirin / Apo(a)Isoform / Lp(a) Phenotype (Tokushima University Institutional Repository) ● Metadata: 2005307 (Tokushima University Institutional Repository: 2005307)
191.	Shuji Ozaki, Masaaki Kosaka, Yuji Wakahara, Yasuko Ozaki, Masayuki Tsuchiya, Yasuo Koishihara, Tetsuya Goto and Toshio Matsumoto : Humanized anti-HM1.24 antibody mediates myeloma cell cytotoxicity that is enhanced by cytokine stimulation of effector cells, Blood, 93, 11, 3922-3930, 1999. (Summary) To develop a new immunotherapy for multiple myeloma, we have generated a monoclonal antibody (MoAb) that detects a human plasma cell-specific antigen, HM1.24. Our previous study has shown that mouse anti-HM1.24 MoAb inhibits the proliferation of human myeloma cells implanted into severe combined immunodeficiency mice. In this report, we evaluated the antitumor activity of the humanized anti-HM1.24 MoAb (IgG1kappa), which was constructed by grafting the complementarity-determining regions. In contrast to the parent mouse MoAb, humanized anti-HM1.24 MoAb mediated antibody-dependent cellular cytotoxicity (ADCC) against both myeloma cell lines and myeloma cells from patients in the presence of human peripheral blood mononuclear cells (PBMCs). The PBMCs from untreated myeloma patients exhibited ADCC activity as efficiently as those of healthy donors. Although decreased ADCC activity of PBMCs was observed in patients who responded poorly to conventional chemotherapy, it could be significantly augmented by the stimulation with interleukin-2 (IL-2), IL-12, or IL-15. There was a strong correlation between the percentage of CD16(+) cells and ADCC activity in the PBMCs of myeloma patients. Moreover, peripheral blood stem cell collections from myeloma patients contained higher numbers of CD16(+) cells than PBMCs and exhibited ADCC activity that was enhanced by IL-2. These results indicate that humanized anti-HM1.24 MoAb has potential as a new therapeutic strategy in multiple myeloma and that treatment of effector cells with immunomodulating cytokines can restore the effect of humanized anti-HM1.24 MoAb in patients with diminished ADCC activity. (Keyword) Adult / Aged / Aged, 80 and over / Animals / Antibodies, Monoclonal / Antigens, CD / Antigens, Differentiation, B-Lymphocyte / Cytotoxicity, Immunologic / Female / GPI-Linked Proteins / Hematopoietic Stem Cell Mobilization / Humans / immunotherapy / Interleukin-12 / Interleukin-15 / Interleukin-2 / Male / Membrane Glycoproteins / Mice / Middle Aged / Multiple Myeloma (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10339501 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033151528 (PubMed: 10339501, Elsevier: Scopus)
192.	Tomoko Hara, Shuji Ozaki, Masaaki Kosaka, Soichiro Fujiwara, Yuji Wakahara, Hideko Endo, shingo Wakatsuki and Toshio Matsumoto : Biclonal lymphoplasmacytic immunocytoma associated with Crohn's disease, Internal Medicine, 38, 6, 500-503, 1999. (Summary) A 33-year-old man with a 4-year history of Crohn's disease presented with marked ascites and an abdominal tumor. Two M-protein peaks, immunoglobulin (Ig) G-kappa and IgA-kappa, were detected in the serum. Neoplastic lymphoplasmacytic cells were infiltrated in the bone marrow and ascites. Histological examination of the abdominal tumor showed marked proliferation of lymphoplasmacytic cells that were positive for either IgG or IgA. Moreover, DNA sequences of the expressed IgG and IgA genes were different in the complementarity-determining region 3. These results suggest that chronic inflammation in Crohn's disease contributes to the simultaneous development of biclonal lymphoplasmacytic immunocytoma of the small intestine. (Keyword) malignant lymphoma / biclonal gammopathy / immunoglobulin gene (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.38.500 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10411357 ● Search Scopus @ Elsevier (PMID): 10411357 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.38.500 (DOI: 10.2169/internalmedicine.38.500, PubMed: 10411357)
193.	M. Kawajiri, Takao Mitsui, Masayuki Shono and Toshio Matsumoto : Quantitative analysis of immunofluorescent signals for dystrophin, beta-dystroglycan and myosin skeletal muscle by epifluorescence microscopy., Biotech-Histochem, 74, 2, 92-97, 1999. (Keyword) immunofluorescent / myosin / muscle
194.	Hisaomi Kawai, Masashi Akaike, Makoto Kunishige, Toshio Inui, Katsuhito Adachi, Chiyomi Kimura, Masakazu Kawajiri, Yoshihiko Nishida, Itsuro Endo, Setsuko Kashiwagi, Hiroshi Nishino, Tsutomu Fujiwara, Shiro Okuno, Carinne Roudaut, Isabelle Richard, Jacques S. Beckmann, Kazuo Miyoshi and Toshio Matsumoto : Clinical, pathological, and genetic features of limb-girdle muscular dystrophy type 2A with new calpain 3 gene mutations in seven patients from three Japanese families, Muscle & Nerve, 21, 11, 1493-1501, 1998. (Summary) We report on the clinical, pathological, and genetic features of 7 patients with limb-girdle muscular dystrophy type 2A (LGMD2A) from three Japanese families. The mean age of onset was 9.7+/-3.1 years (mean+/-SD), and loss of ambulance occurred at 38.5+/-2.1 years. Muscle atrophy was predominant in the pelvic and shoulder girdles, and proximal limb muscles. Muscle pathology revealed dystrophic changes. In two families, an identical G to C mutation at position 1080 the in calpain 3 gene was identified, and a frameshift mutation (1796insA) was found in the third family. The former mutation results in a W360R substitution in the proteolytic site of calpain 3, and the latter in a deletion of the Ca2+-binding domain. (Keyword) limb-girdle muscular dystrophy type 2A / calpain 3 gene / mutation / protease / clinical feature / pathology (Link to Publication Site) ● Publication site (DOI): 10.1002/(SICI)1097-4598(199811)21:11<1493::AID-MUS19>3.0.CO;2-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9771675 ● Search Scopus @ Elsevier (PMID): 9771675 ● Search Scopus @ Elsevier (DOI): 10.1002/(SICI)1097-4598(199811)21:11<1493::AID-MUS19>3.0.CO;2-1 (DOI: 10.1002/(SICI)1097-4598(199811)21:11<1493::AID-MUS19>3.0.CO;2-1, PubMed: 9771675)
195.	Shuji Ozaki, Masaaki Kosaka, Masafumi Harada, Hiromu Nishitani, Masaaki Odomi and Toshio Matsumoto : Radioimmunodetection of human myeloma xenografts with a monoclonal antibody directed against a plasma cell specific antigen, HM1.24, Cancer, 82, 11, 2184-2190, 1998. (Keyword) monoclonal antibody / multiple myeloma / F(ab')2 fragment / plasma cell / severe combined immunodeficiency mouse
196.	Shuji Ozaki, Koji Ogasahara, Masaaki Kosaka, Toshi Inoshita, Shingo Wakatsuki, Hisanori Uehara and Toshio Matsumoto : Hepatosplenic gamma delta T-cell lymphoma associated with hepatitis B virus infection, The Journal of Medical Investigation : JMI, 44, 3-4, 215-217, 1998. (Summary) Hepatitis B virus (HBV) infection has been implicated in the development of hepatocellular and hematopoietic malignancies. We describe a patient with chronic hepatitis B who developed hepatosplenic gamma delta T-cell lymphoma. A 45-year-old woman presented with marked hepatosplenomegaly and hepatic failure during the course of chronic hepatitis B. Peripheral blood examination revealed 57% abnormal lymphoid cells which expressed the gamma delta T-cell receptor. The cytogenetic analysis of tumor cells showed an abnormal karyotype; 47, XX, -13, +2mar in all 20 metaphases examined. A clonal rearrangement of the T-cell receptor genes was demonstrated by Southern blot analysis, showing monoclonal expansion of tumor cells. A liver biopsy specimen showed fibrosis of the portal areas and sinusoidal infiltration of tumor cells. HBV infection was documented by the presence of IgG anti-HBc and anti-HBs antibodies in serum. Although HBV-DNA was not detected in tumor cells by polymerase chain reaction analysis, there is a possibility that proliferation of gamma delta T cells in response to HBV infection played a role in the pathogenesis of hepatosplenic gamma delta T-cell lymphoma. (Keyword) hepatosplenic lymphoma / gamma delta T-cell / hepatitis B virus / chronic hepatitis / hepatosplenomegaly (Tokushima University Institutional Repository) ● Metadata: 2003867 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9597812 ● Search Scopus @ Elsevier (PMID): 9597812 (Tokushima University Institutional Repository: 2003867, PubMed: 9597812)
197.	Shuji Ozaki, Masaaki Kosaka, Shingo Wakatsuki, Masahiro Abe, Yasuo Koishihara and Toshio Matsumoto : Immunotherapy of multiple myeloma with a monoclonal antibody directed against a plasma cell-specific antigen, HM1.24, Blood, 90, 8, 3179-3186, 1997.
198.	板東浩, 藤中真一, 斎藤晴比古, 島健二, 斎藤史郎, Mitsuo Itakura, Toshio Matsumoto, Masamichi Kuwajima, Ken Saito, 川島周, 鶴尾美穂, 杉本紀子, 杉本順子, 清水寛, 江藤和子, 桜井えつ, 近藤彰, 林健司, 福島康江, 赤池瞳, 岩田坤, 住友辰次, 小川紘一, 松村光博, 矢野勇人, 川内茂徳, 福田克之, 竹田勝則, 筒井芳彦, 橋本吉弘, 米田弘, 土橋孝之, 溝渕樹, 石川雅康, 木村建彦, 大倉敏裕, 高田幸伸, 高橋秀夫, 石川由子, 曽根佳世子, 阿部多賀子, 和田美智子 and 十枝紀巳代 : Current micro-and Macroangiopathic Complication of Diabetic Patients by Primary Care Physicians on Multicenter-study, 日本プライマリ·ケア学会誌, 20, 1, 46-51, 1997. (Keyword) diabetes mellitus / Macroangiopathy / Complication / Microangiopathy / epidemiology (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572824500135153920 (CiNii: 1572824500135153920)

Academic Paper (Unrefereed Paper):

1.	Shingen Nakamura, Masahiro Abe and Toshio Matsumoto : Part7. 2. 新規治療薬の開発と臨床応用の可能性を探る (抗RANKL抗体などを中心に). がん骨転移治療ビスフォスフォネート治療によるBone Management, 先端医学者高橋俊二編集, 206-214, 2012.
2.	Itsuro Endo, Masahiro Abe and Toshio Matsumoto : 骨転移の分子標的治療薬骨転移のバイオロジーとマネージメント, 医薬ジャーナル社米田俊之編集, 215-224, 2012.
3.	Naoko Matsui, Takao Mitsui, Yasushi Ohshima, Kenji Yokoi, Makoto Kunishige, Fumikazu Yagi, Steven Vernino, Toshio Matsumoto and Ryuji Kaji : Anti-neuronal antibodies in acute pandysautonomia., Internal Medicine, 49, 1, 73-77, 2010. (Summary) We encountered two patients with acute pandysautonomia who subacutely exhibited extensive autonomic dysfunction after antecedent infections. Although these patients had been suffering from autonomic disturbance for several months, they both had a good clinical course after plasma exchange and intravenous immunoglobulin therapy. Thin-layer chromatography (TLC)-immunostaining did not demonstrate any antibodies against gangliosides, but immunoblot analysis showed antibodies against a neuroblastoma cell line, SH-SY5Y, in serum samples. Furthermore, ganglionic acetylcholine receptor autoantibodies were detected in one patient. These findings suggest that neuronal antibodies against the autonomic nervous system play an important role in the pathogenesis of acute pandysautonomia. (Keyword) Aged / Autoantibodies / Autoimmune Diseases of the Nervous System / Autonomic Nervous System Diseases / Humans / Immunoblotting / Immunoglobulins, Intravenous / Male / Neurons / Plasma Exchange / Receptors, Cholinergic (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.49.2788 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20046006 ● CiNii @ National Institute of Informatics (CRID): 1390001204871227136 ● Search Scopus @ Elsevier (PMID): 20046006 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.49.2788 (DOI: 10.2169/internalmedicine.49.2788, PubMed: 20046006, CiNii: 1390001204871227136)
4.	Takashi Iwase, Hirotsugu Kurobe, Shusuke Yagi, 原朋子, 長楽雅仁, 藤村光則, Shuji Ozaki, Masashi Akaike, 安部正博, Yutaka Masuda, Hiroyuki Azuma, Toshio Matsumoto and Tetsuya Kitagawa : 末梢単核球細胞を用いた抹消動脈閉塞症に対する新たな血管新生治療の試み, Shikoku Acta Medica, 62, 3,4, 137-141, 2006. (Tokushima University Institutional Repository) ● Metadata: 2001080 (Tokushima University Institutional Repository: 2001080)
5.	七條加奈, 関本悦子, 三原愛, 大田加与, 田中洋一, 大島隆志, 柴田泰伸, Toshihiro Hashimoto, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and 若槻真吾 : Successful treatment of relapsed/refractory Hodgkin's lymphoma with tandem transplantation, The Journal of the Japanese Society of Internal Medicine, 93, 10, 2210-2212, 2004. (Keyword) Hodgkin lymphoma / tandem transplantation (Link to Publication Site) ● Publication site (DOI): 10.2169/naika.93.2210 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282681418731648 ● Search Scopus @ Elsevier (DOI): 10.2169/naika.93.2210 (DOI: 10.2169/naika.93.2210, CiNii: 1390282681418731648)
6.	Masahiro Abe, Toshio Matsumoto and 小阪昌明 : Effect of bisphosphonate on myeloma bone disease, The Japanese Journal of Clinical Hematology, 43, 5, 349-352, 2002. (Keyword) Bisphosphonate / Osteolysis / osteoclast / Bone metabolism (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680010754944 (CiNii: 1390282680010754944)

Review, Commentary:

1.	Itsuro Endo and Toshio Matsumoto : 副甲状腺腫瘍の臨床研究の現状と展望, 日本臨床, 78, suppl 4, 544-548, Sep. 2020.
2.	Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : [The pathology, diagnosis and therapy on osteoporosis]., Nihon Rinsho. Japanese Journal of Clinical Medicine, 72, 10, 1774, Oct. 2014. (Summary) The increase of elderly population in Japan suggests the importance of the prevention of osteoporotic fracture. Falls and fractures account for around 10% of the causes for requiring care services in Japan. The Japanese criteria for initiating pharmacological treatment to prevent fragility fracture were revised in 2011. There are many kinds of anti-osteoporosis drugs including bisphosphonates, SERM, teriparatide, and denosumab that have been proven to reduce fractures. Thus, it is important to select drugs appropriate for each osteoporotic patients considering the mechanisms of drug action, their efficacy and side effects. In this article, we review pathophysiology, diagnosis and treatment of osteoporosis. (Keyword) Aged / Female / Humans / Male / Middle Aged / Osteoporosis (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25509801 ● Search Scopus @ Elsevier (PMID): 25509801 (PubMed: 25509801)
3.	Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : 骨粗鬆症の病態，診断，治療, 日本臨床, 72, 10, 1774-1779, Oct. 2014.
4.	Itsuro Endo and Toshio Matsumoto : 副甲状腺機能低下症, 内科, 113, 6, 1571-1573, Jun. 2014.
5.	Itsuro Endo and Toshio Matsumoto : 副甲状腺機能亢進症, 内科, 113, 6, 1568-1570, Jun. 2014.
6.	Itsuro Endo and Toshio Matsumoto : RANKL, The Medical Frontline, 69, 2, 257-261, Feb. 2014.
7.	Itsuro Endo and Toshio Matsumoto : チアマゾール, 重要薬マニュアル, 158-159, Jan. 2014.
8.	Itsuro Endo and Toshio Matsumoto : レボチロキシンナトリウム, 重要薬マニュアル, 156-157, Jan. 2014.
9.	Itsuro Endo and Toshio Matsumoto : テリパラチド(遺伝子組換え，合成), 重要薬マニュアル, 154-155, Jan. 2014.
10.	Itsuro Endo and Toshio Matsumoto : ラロキシフェン, 重要薬マニュアル, 152-153, Jan. 2014.
11.	Itsuro Endo and Toshio Matsumoto : エルデカルシトール, 重要薬マニュアル, 150-151, Jan. 2014.
12.	Itsuro Endo and Toshio Matsumoto : ミノドロン酸水和物, 重要薬マニュアル, 148-149, Jan. 2014.
13.	Itsuro Endo and Toshio Matsumoto : リセドロン酸ナトリウム, 重要薬マニュアル, 146-147, Jan. 2014.
14.	Itsuro Endo and Toshio Matsumoto : アレンドロ酸ナトリウム, 重要薬マニュアル, 144-145, Jan. 2014.
15.	Itsuro Endo and Toshio Matsumoto : 骨粗鬆症・甲状腺機能異常治療薬, 重要薬マニュアル, 140-143, Jan. 2014.
16.	鈴木麗子, 大和光, Kazuyoshi Kawazoe, Ken-ichi Aihara, Itsuro Endo, 安芸菜奈子, 倉橋清衛, Toshio Matsumoto, Akio Kuroda and Munehide Matsuhisa : インスリン注射により生じた皮下硬血を有する患者の実態調査とその介入の有用性の検討, Practice, 31, 6, 815-821, 2014.
17.	Itsuro Endo and Toshio Matsumoto : [Bone Structural Properties and Bone Strength. Bone architecture and strength on unloading]., Clinical Calcium, 23, 7, 1013-1019, Jul. 2013. (Summary) The bone loss due to space flight or prolonged bed rest observes early stage of unloading and causes both decreased bone formation and increased bone resorption. Mechanical unloading induced not only both tarbecular and cortical bone loss but also greater decline bone structure in weight-bearing bone. These findings and further examination concern about pathophysiolosy will allow for better understanding of unloading-associated bone loss and for development of effective countermeasures. (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23811590 ● Search Scopus @ Elsevier (PMID): 23811590 (PubMed: 23811590)
18.	Itsuro Endo and Toshio Matsumoto : ビスホスホネート, The Lipid, 24, 4, 73-78, Apr. 2013.
19.	Itsuro Endo and Toshio Matsumoto : 新しい骨粗鬆症治療薬, Internal Medicine, 111, 4, 671-676, Apr. 2013.
20.	Itsuro Endo and Toshio Matsumoto : 開発中の薬剤, Hormone Frontier in Gynecology, 20, 3, 51-56, Mar. 2013.
21.	Itsuro Endo and Toshio Matsumoto : 現在開発中あるいは今後開発される予定の骨粗鬆症治療薬にはどのようなものがありますか?, 骨粗鬆症治療, 12, 2, 67-70, Feb. 2013.
22.	Itsuro Endo and Toshio Matsumoto : BSAP(骨型ALP), Nihon Rinsho. Japanese Journal of Clinical Medicine, 71, supple, 258-260, 2013.
23.	Itsuro Endo and Toshio Matsumoto : [Space flight/bedrest immobilization and bone. Bisphosphonate and the loss of bone mineral due to space flight or prolonged bed rest]., Clinical Calcium, 22, 12, 1863-1870, Dec. 2012. (Summary) Bone mass and strength are maintained by appropriate weight bearing. The loss of bone mineral due to space flight or prolonged bed rest has been recognized by space scientists and physicians. In spite of the wealth of knowledge obtained thus far, many questions remain unanswered regarding the mechanism of bone loss as well as the factors affecting these skeletal processes. Bisphosphonates have a potential to become countermeasures against space flight-induced or disuse osteoporosis. In this review, the effect and the possible role of biphosphonates on the prevention and treatment of unloading-induced osteoporosis are summarized and future prospects are discussed. (Keyword) Bed Rest / Bone and Bones / Calcification, Physiologic / Diphosphonates / Humans / Space Flight / Time Factors (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23187079 ● Search Scopus @ Elsevier (PMID): 23187079 (PubMed: 23187079)
24.	Itsuro Endo and Toshio Matsumoto : 副甲状腺, 内分泌代謝専門医ガイドブック, 56-57, Nov. 2012.
25.	Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : ビスホスホネート製剤, Medicina, 49, 11, 348-350, Nov. 2012.
26.	Itsuro Endo and Toshio Matsumoto : 活性型ビタミンD3およびその誘導体, Medical Practice, 29, 11, 1949-1953, Nov. 2012.
27.	Itsuro Endo and Toshio Matsumoto : Effect of vitamin D on bone and immune system, Journal of Clinical and Experimental Medicine, 242, 9, 751-757, Sep. 2012. (Keyword) ビタミンD充足域 / 転倒抑止効果 / 骨免疫学 / 免疫調節作用 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522825130715932416 (CiNii: 1522825130715932416)
28.	Itsuro Endo and Toshio Matsumoto : 新規活性型ビタミンD誘導体エルデカルシトールの副作用としての高Ca血症・高Ca尿症の頻度や程度は従来の活性型ビタミンD3製剤とは違いますか?, ファーマナビゲーター活性型ビタミンD3製剤編, 326-331, Jul. 2012.
29.	Itsuro Endo and Toshio Matsumoto : エルデカルシトールの使用上の注意点, ファーマナビゲーター活性型ビタミンD3製剤編, 294-301, Jul. 2012.
30.	Itsuro Endo and Toshio Matsumoto : エルデカルシトールの開発の経緯, ファーマナビゲーター活性型ビタミンD3製剤編, 260-269, Jul. 2012.
31.	Itsuro Endo and Toshio Matsumoto : 活性型ビタミンD3製剤の治療上の注意点, ファーマナビゲーター活性型ビタミンD3製剤編, 252-259, Jul. 2012.
32.	Itsuro Endo and Toshio Matsumoto : ビタミンDの代謝, ファーマナビゲーター活性型ビタミンD3製剤編, 26-33, Jul. 2012.
33.	Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Effects of Statins on Cardiorenal Syndrome., International Journal of Vascular Medicine, 2012, 162545, Jun. 2012. (Summary) Cardiovascular disease and renal disease have a close relationship that forms a vicious cycle as a cardiorenal syndrome (CRS). Oxidative stress, endothelial dysfunction, and vascular inflammation could be therapeutic targets when the renin-angiotensin-aldosterone system is activated by accumulation of conventional cardiovascular risk factors; however, a strategy for management of CRS has not been established yet. Statins, HMG-CoA reductase inhibitors, have not only cholesterol-lowering effects but also pleiotropic effects on cardiovascular systems, including anti-inflammatory and antioxidant effects and improvement of nitric oxide bioavailability. Since recent studies have indicated that statins have beneficial effects on chronic kidney disease and heart failure as well as coronary artery disease in cholesterol-lowering-dependent/independent manners, treatment with statins might be a successful strategy for preventing deterioration of CRS. (Tokushima University Institutional Repository) ● Metadata: 2012649 (Link to Publication Site) ● Publication site (DOI): 10.1155/2012/162545 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22792467 ● Search Scopus @ Elsevier (PMID): 22792467 ● Search Scopus @ Elsevier (DOI): 10.1155/2012/162545 (Tokushima University Institutional Repository: 2012649, DOI: 10.1155/2012/162545, PubMed: 22792467)
34.	Itsuro Endo and Toshio Matsumoto : [New approved drugs for osteoporosis in Japan]., Clinical Calcium, 22, 6, 870-876, Jun. 2012. (Summary) These 2 years, we had had new therapeutic options for osteoporotic patients, for example minodoronate, bazedoxifene, teriparatide and eldecalcitol in Japan. Minodoronate and eldecalcitol came from Japan and they had many clinical evidences on Japanese patients. Teriparatide is a powerful anabolic agent for bone, had been provided as daily or weekly subcutaneous injection. These reagents may become helpful drug for osteoporotic patients. This review shows the character and clinical evidences of these drugs. (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22653027 ● Search Scopus @ Elsevier (PMID): 22653027 (PubMed: 22653027)
35.	Itsuro Endo and Toshio Matsumoto : 副甲状腺疾患, Medical Practice, 29, 171-178, May 2012.
36.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masashi Akaike and Toshio Matsumoto : Effects of androgens on cardiovascular remodeling., The Journal of Endocrinology, Apr. 2012. (Summary) Androgens, the male sex hormones, exert various biological effects on many target organs through the transcriptional effects of the nuclear androgen receptor (AR). ARs are expressed not only in classical target organs, such as the brain, genital organs, bone, and skeletal muscles, but also in the cardiovascular system. Because the female sex hormones estrogens are well known to protect against cardiovascular disease, sex has been considered to have a significant clinical impact on cardiovascular mortality. However, the influence of androgens on the cardiovascular system has not been fully elucidated. To clarify this issue, we analyzed the effects of administration of angiotensin II and doxorubicin, an anticancer agent, in a loading model in male wild-type and AR-deficient mice. In this review, we focus on the actions of androgens as potential targets for the prevention of cardiovascular diseases in males. (Link to Publication Site) ● Publication site (DOI): 10.1530/JOE-12-0126 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22493003 ● Search Scopus @ Elsevier (PMID): 22493003 ● Search Scopus @ Elsevier (DOI): 10.1530/JOE-12-0126 (DOI: 10.1530/JOE-12-0126, PubMed: 22493003)
37.	Itsuro Endo and Toshio Matsumoto : 骨粗鬆症治療薬, The Japanese journal of clinical and experimental medicine, 89, 4, 461-465, Apr. 2012.
38.	Itsuro Endo and Toshio Matsumoto : 抗スクレロスチン抗体, 骨粗鬆症治療, 11, 3, 47-51, Mar. 2012.
39.	Itsuro Endo and Toshio Matsumoto : 骨粗鬆症治療薬としてのビタミンD製剤の位置づけ-新規薬剤の承認を受けて, 腎と骨代謝, 25, 3, 243-249, Mar. 2012.
40.	Kumiko Kagawa, Masahiro Abe and Toshio Matsumoto : がん治療における骨の管理の重要性がん骨転移治療ビスフォスフォネート治療によるBone Management, 先端医学者高橋俊二編集, 16-21, 2012.
41.	Itsuro Endo and Toshio Matsumoto : [Frontiers in vitamin D; basic research and clinical application. Eldecalcitol: the effect on bones and calcium metabolism]., Clinical Calcium, 21, 11, 103-110, Nov. 2011. (Summary) Eldecalcitol is a new active vitamin D compound, bearing a hydroxypropyloxy residue at the 2-position of 1, 25 (OH) D . In ovariectomized rats, eldecalcitol increased vertebral bone mass and bone strength by inhibiting bone resorption and maintaining bone formation. In randomized, placebo-controlled, double-blinded clinical trial for osteoporotic subjects, eldecalcitol increased lumber vertebral and hip bone mineral density independent of vitamin D status. Furthermore, in patients with osteoporosis, eldecalcitol treatment was associated with a lower risk of vertebral and wrist fractures, with greater decrease in bone turnover markers compared with alfacalcidol. The incidence of adverse events was similar between the two treatments. Therefore, eldecalcitol can become a new treatment of choice for osteoporosis. (Keyword) Animals / Bone Density / Bone Density Conservation Agents / Bone Remodeling / Bone Resorption / Bone and Bones / Calcium / Disease Models, Animal / Dose-Response Relationship, Drug / Female / Fractures, Bone / Fractures, Spontaneous / Humans / Osteogenesis / Osteoporosis, Postmenopausal / Ovariectomy / Rats / Vitamin D (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22040826 ● Search Scopus @ Elsevier (PMID): 22040826 (PubMed: 22040826)
42.	Itsuro Endo and Toshio Matsumoto : 続発性骨粗鬆症, 診断と治療, 99, 10, 1661-1667, Oct. 2011. (Keyword) secondary osteoporosis
43.	Itsuro Endo and Toshio Matsumoto : 骨粗鬆症, 医学スーパーラーニングスリーズ内分泌・糖尿病内科学, 129-134, Sep. 2011.
44.	Itsuro Endo and Toshio Matsumoto : Progress and perspectives in bone research, Nihon Rinsho. Japanese Journal of Clinical Medicine, 69, 7, 1175-1180, Jul. 2011. (Keyword) osteoporosis / bone metabolism (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291854804514048 ● Summary page in Scopus @ Elsevier: 2-s2.0-80051602471 (CiNii: 1520291854804514048, Elsevier: Scopus)
45.	Itsuro Endo and Toshio Matsumoto : 癌と関連した高カルシウム血症, 腎と透析, 71, 5, 662-666, May 2011. (Keyword) PTHrP / cytokine / hypercalcemia
46.	Itsuro Endo and Toshio Matsumoto : Parathyroid neoplasms: a state and view of clinical research, Nihon Rinsho. Japanese Journal of Clinical Medicine, 69, 455-460, Mar. 2011. (Keyword) parathyroid / neoplasm (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21834160 ● CiNii @ National Institute of Informatics (CRID): 1524232504690824960 ● Summary page in Scopus @ Elsevier: 2-s2.0-80052524491 (PubMed: 21834160, CiNii: 1524232504690824960, Elsevier: Scopus)
47.	Itsuro Endo and Toshio Matsumoto : ビタミンD新規合成誘導体の展望, THE BONE, 25, 3, 135-139, Mar. 2011. (Keyword) vitamin D analogue
48.	Itsuro Endo and Toshio Matsumoto : PTHの生理作用, 骨粗鬆症治療, 10, 2, 10-14, Feb. 2011. (Keyword) PTH
49.	Itsuro Endo and Toshio Matsumoto : 電解質異常の診断の進め方-Ca, P, Mg-, Mebio, 28, 1, 27-33, Jan. 2011.
50.	Itsuro Endo and Toshio Matsumoto : [Eldecalcitol (ED-71)]., Clinical Calcium, 21, 1, 53-58, Jan. 2011. (Summary) ED-71 is a new vitamin D receptor ligand, bearing a hydroxypropoxy substituent at the 2β-position of 1α, 25 (OH) (2)D(3). In ovariectomized rats, ED-71 increased vertebral bone mass and bone strength by inhibiting bone resorption and maintaining bone formation. In randomized, placebo-controlled, double-blinded clinical trial for osteoporotic subjects, ED-71 increased lumber vertebral and hip bone mineral density independently vitamin D status. Furthermore, ED-71 may have a better osteoprotective effect than alfacalcidol and suggest that ED-71 may serve as a new generation of active vitamin D with anti-fracture efficacy in osteiporotic subjects. (Keyword) Animals / Bone Density / Bone Resorption / Dose-Response Relationship, Drug / Female / Fractures, Bone / Humans / Lumbar Vertebrae / Osteogenesis / Osteoporosis / Randomized Controlled Trials as Topic / Rats / Stimulation, Chemical / Vitamin D (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21187594 ● Search Scopus @ Elsevier (PMID): 21187594 (PubMed: 21187594)
51.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, Masashi Akaike and Toshio Matsumoto : Transforming Growth Factor-1 as a Common Target Molecule for Development of Cardiovascular Diseases, Renal Insufficiency and Metabolic Syndrome., Cardiology Research and Practice, 2011, 175381, Dec. 2010. (Summary) Transforming growth factor-1 (TGF-1) is a polypeptide member of the transforming growth factor superfamily of cytokines. It is a secreted protein that performs many cellular functions including control of cell growth, cell proliferation, cell differentiation and apoptosis. In the cardiovascular system, TGF-1 plays pivotal roles in the pathogenesis of hypertension, restenosis after percutaneous coronary intervention, atherosclerosis, cardiac hypertrophy and heart failure. In addition, TGF-1 has been shown to be increased in adipose tissue of obese subjects with insulin resistance. Furthermore, TGF-1 is a potent initiator of proliferation of renal mesangial cells leading to chronic kidney disease. Some currently available agents can manipulate TGF-1 expression leading to amelioration of cardiovascular diseases. Thus, an understanding of interactions between chronic kidney disease and metabolic syndrome and the development of cardiovascular diseases is an important issue, and attention should be given to TGF-1 as a crucial factor for regulation and modulation of those pathological conditions. (Link to Publication Site) ● Publication site (DOI): 10.4061/2011/175381 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21234356 ● Search Scopus @ Elsevier (PMID): 21234356 ● Search Scopus @ Elsevier (DOI): 10.4061/2011/175381 (DOI: 10.4061/2011/175381, PubMed: 21234356)
52.	Itsuro Endo and Toshio Matsumoto : [Secondary osteoporosis UPDATE. Drugs under development for metabolic bone disease]., Clinical Calcium, 20, 5, 700-708, May 2010. (Summary) For the treatment of osteoporosis, anti-resorptive agents including bisphosphonates and raloxifene are widely used. As new anti-resorptive drugs, anti-RANKL antibody and cathepsin K inhibitor are under development. Among bone anabolic agents, daily subcutaneous injection of teriparatide will soon become available in Japan. In addition, new anabolic agents such as calcilitycs and anti-sclerostin antibody are under clinical or preclinical development for the treatment of osteoporosis. (Keyword) Anabolic Agents / Bone Density Conservation Agents / Bone Diseases, Metabolic / Cathepsins / Diphosphonates / Drug Discovery / Humans / Osteoporosis / RANK Ligand / Raloxifene / Selective Estrogen Receptor Modulators / Teriparatide (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20445281 ● Search Scopus @ Elsevier (PMID): 20445281 (PubMed: 20445281)
53.	Itsuro Endo and Toshio Matsumoto : Drugs for osteoporosis under development, Clinic All-Round, 59, 4, 599-605, Apr. 2010. (Keyword) 抗RANKL抗体 / カテプシンK阻害薬 / Ca感知受容体拮抗薬 / 抗スクレロスチン抗体 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522825130679651584 (CiNii: 1522825130679651584)
54.	Itsuro Endo and Toshio Matsumoto : 骨粗鬆症の臨床, 糖尿病・代謝・内分泌 Annual Review 2010, 246-255, Jan. 2010.
55.	Itsuro Endo and Toshio Matsumoto : 電解質異常の診断の進め方ーCa, P, Mg-, Mebio, 28, 1, 27-33, Jan. 2010.
56.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Heparin Cofactor II as a Novel Vascular Protective Factor Against Atherosclerosis., Journal of Atherosclerosis and Thrombosis, 16, 5, 523-531, Sep. 2009. (Summary) Heparin cofactor II (HCII) specifically inhibits thrombin action at the site of vascular wall injury. We encountered a congenital HCII deficiency patient with advanced multiple atherosclerotic lesions. This patient led us to conduct clinical studies to examine the role of HCII against atherosclerosis. We found that the incidence of in-stent restenosis after percutaneous coronary intervention, severity of carotid atherosclerosis and prevalence of peripheral arterial disease are inversely associated with plasma HCII activity. In order to clarify the vascular protective action of HCII, we generated HCII- deficient mice by gene targeting. In contrast to a previous study, HCII(-/-) mice were embryonically lethal. In HCII(+/-) mice, accelerated intimal hyperplasia and frequent thrombosis were observed after cuff or wire injury of femoral arteries. The number of protease-activated receptor-1 (PAR-1) -positive cells and the gene expression levels of inflammatory cytokines and chemokines were increased in the thickened vascular walls of HCII(+/-) mice. The accelerated intimal hyperplasia in HCII+/- mice with vascular injury was attenuated by human HCII administration. Furthermore, HCII deficiency exaggerated aortic plaque formation with increased oxidative stress in apolipoprotein E(-/-) mice. These results demonstrate that HCII protects against thrombin-induced vascular remodeling in both humans and mice and suggest that HCII is a predictive biomarker and therapeutic target for atherosclerosis. (Keyword) Animals / atherosclerosis / Female / Heparin Cofactor II / Humans / knockout mice / knockout mice / Recombinant Proteins (Link to Publication Site) ● Publication site (DOI): 10.5551/jat.1552 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19729870 ● Search Scopus @ Elsevier (PMID): 19729870 ● Search Scopus @ Elsevier (DOI): 10.5551/jat.1552 (DOI: 10.5551/jat.1552, PubMed: 19729870)
57.	Yuichi Fujinaka and Toshio Matsumoto : メタボリックシンドロームと骨粗鬆症, Keywordで学ぶメタボリックシンドローム, 2008.
58.	Masashi Akaike and Toshio Matsumoto : NO bioavailability, CLINICAL CALCIUM, 17, 6, 864-870, 2007.
59.	Ken-ichi Aihara, Hiroyuki Azuma and Toshio Matsumoto : Vitamin D-vitamin D receptor system regulates antithrombogenicity in vivo., Clinical Calcium, 16, 7, 1173-1179, Jul. 2006. (Summary) Although it has been well documented that vitamin D receptor (VDR) activation influences the expression of various genes involved in calcium homeostasis and cell differentiation, the physiological role of VDR action in hemostasis remains unclear. We studied thrombogenicity in normocalcemic VDR knock-out (KO) mice on a high calcium diet in comparison with that in wild-type mice and that in hypocalcemic VDRKO mice fed a regular diet. Platelet aggregation was significantly enhanced in normocalcemic VDRKO mice. Aortic endothelial nitric-oxide (NO) synthase expression and urinary NOx excretion were reduced in hypocalcemic VDRKO mice but not in normocalcemic VDRKO mice. The gene expression of antithrombin in the liver and that of thrombomodulin in the aorta, liver and kidney were down-regulated in hypo- and normocalcemic VDRKO mice, whereas tissue factor gene expression in the liver and kidney was up-regulated in VDRKO mice regardless of plasma calcium level. Furthermore, VDRKO mice manifested an exacerbated multi-organ thrombus formation after exogenous lipopolysaccharide injection regardless of the calcemic conditions. These results demonstrate that the vitamin D-VDR system plays a pivotal role in antithrombogenicity in vivo. (Keyword) Animals / Antithrombins / Blood Coagulation / Down-Regulation / Hypocalcemia / Lipopolysaccharides / Liver / knockout mice / Mice, Knockout / nitric oxide / Nitric Oxide Synthase Type III / Receptors, Calcitriol / Thrombomodulin / Thromboplastin / Vitamin D (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16816478 ● Search Scopus @ Elsevier (PMID): 16816478 (PubMed: 16816478)
60.	Yuichi Fujinaka and Toshio Matsumoto : トピックス: メタボリックシンドロームと骨粗鬆症, The Medical Frontline, 61, 6, 1421-1427, Jun. 2006.
61.	Ken-ichi Aihara, Yasumasa Ikeda and Toshio Matsumoto : 【慢性心不全の分子機構新しい治療戦略を求めて】性ステロイドと心保護作用, Cardioangiology, 59, 6, 579-584, 2006. (Keyword) Androgens / *Estrogens(薬理学) / Androgen Receptors / Estrogen Receptors / 心不全 / ノックアウトマウス / 心室リモデリング / マウス / 動物
62.	Masashi Akaike and Toshio Matsumoto : 血管内皮細胞に対するステロイドの影響と大腿骨頭壊死, 整形外科, 48, 25-29, 2005.
63.	Ken-ichi Aihara, Masashi Akaike, Daisuke Inoue, Hiroyuki Azuma and Toshio Matsumoto : 副甲状腺機能亢進症, ホルモンと臨床, 52, 5, 93(483)-96(486), May 2004.
64.	新谷保実, Yuichi Fujinaka and Toshio Matsumoto : 検査値異常から読む病態と診断計画, 臨床医, 28, 1586-1589, 2002.
65.	Toshio Matsumoto, Masashi Akaike and Daisuke Inoue : 内分泌疾患, Internal Medicine, 86, 6, 1119-1127, Dec. 2000.
66.	Toshio Matsumoto and Masashi Akaike : 骨と脈管系との関わり, 骨と骨代謝, 12, 4, 319-323, 1999.
67.	Yuichi Fujinaka, 新谷保実 and Toshio Matsumoto : 癌遺伝子と癌抑制遺伝子ヒト癌と癌遺伝子・癌抑制遺伝子, New Horizon for Medicine, 30, 7, 1999-2004, 1998.

Proceeding of International Conference:

1.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Takeshi Harada, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, Tomoyo Hara, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Mechanical unloading promotes bone destruction and myeloma tumor expansion, Cancer and bone society young investigator symposium, Online, Feb. 2022.
2.	Hirofumi Tenshin, Takeshi Harada, Yusuke Inoue, Jumpei Teramachi, Masahiro Hiasa, Sou Shimizu, Emiko Nakaue, Kotaro Tanimoto, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Targeting SLAMF7 to disrupt myeloma-osteoclast interaction: elotuzumabs ADCC activity with Th1-like gamma delta T cells towards osteoclasts and myeloma cells., Cancer and bone society young investigator symposium, Feb. 2022.
3.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The anti-SLAMF7 elotuzumab enhances ADCC activity with Th1-like γδT cells towards osteoclasts and myeloma cells., The European Calcified Tissue Society 2021 Digital Congress 2021, web, Mar. 2021.
4.	Itsuro Endo and Toshio Matsumoto : Does Romosozumab increase cardiovascular events? Analysis of early post-marketing phase vigilance in Japan, Japan Bone Academy, Tokyo, Nov. 2020.
5.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Eiji Tanaka, Kotaro Tanimoto, Sou Shimizu, Masahiro Oura, Kimiko Sogabe, Masahiro Abe, Toshio Matsumoto and Itsuro Endo : The novel therapeutic approaches with TAK1 inhibition against the aberrant NLRP3 inflammasome activation in rheumatoid arthritis, ECTS 2020 Digital Congress, Oct. 2020.
6.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Ashtar Mohannad, Kotaro Tanimoto, Soh Shimizu, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The role of NLRP3 inflammasome activation in joint inflammation and destruction in rheumatoid arthritis: novel therapeutic approaches with TAK1 inhibition., 29th Australian and New Zealand Bone and Mineral Society Annual Scientific Meeting, Oct. 2019.
7.	Maria Tsoumpra, Michihiro Imamura, Yoshitaka Mizobe, Shin'ichi Takeda, Yoshitsugu Aoki, Seiji Fukumoto and Toshio Matsumoto : The vitamin D - vitamin D receptor axis positively regulates the expression of dystrobrevin alpha during murine myogenic differentiation, ASBMR 2019, Orlando, Sep. 2019.
8.	Mai Kanai, Itsuro Endo, Yasuko Takahashi, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : Establishment of model mice of FGF23-related hypophosphatemia induced by iron solution administration, ASBMR 2019, Orlando, Sep. 2019.
9.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Ashtar Mohannad, Kotaro Tanimoto, Masami Iwasa, Bat-Erdene Ariunzaya, Takeshi Harada, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition effectively alleviates joint inflammation as well as bone destruction in rheumatoid arthritis: Suppression of NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption, American Society for Bone and Mineral Society Annual meeting 2019, Orlando, Florida, USA,, Sep. 2019.
10.	Jumpei Teramachi, Soh Shimizu, Hirofumi Tenshin, Bat-Erdene Ariunzaya, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Takeshi Harada, Mohannad Ashtar, Kotaro Tanimoto, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : A progressive auto-amplification loop in TAK1 expression and activation in MM cells., ASBMR 2019,, Orlando, Florida, USA., Sep. 2019.
11.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Ashtar Mohannad, Kotaro Tanimoto, Masami Iwasa, Bat-Erdene Ariunzaya, Takeshi Harada, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition effectively alleviates joint inflammation as well as bone destruction in rheumatoid arthritis: Suppression of NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption., ASBMR 2019,, Orlando, Florida, USA., Sep. 2019.
12.	Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Iwasa Masami, Takeshi Harada, Bat-Erdene Ariunzaya, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Peri-implantitis and the role of Febuxostat in osteoclast differentiation., AEEDC Dubai World Orthodontic Conference, Dubai, UAE, Feb. 2019.
13.	Bingzi Dong, Itsuro Endo, Yukiyo Ohnishi, Zhengju Fu, Toshio Matsumoto and Yangang Wang : Calcilytic, calcium-sensing receptor antagonist, enhances bone remodeling and increases bone mineral density without increasing urinary calcium excretion., ASBMR 2018 Annual Meeting, Mnrtial, QU, Oct. 2018.
14.	Yuichi Takashi, Yuka Kinoshita, Nobuaki Ito, Shun Sawatsubashi, Hidetaka Kosako, Masahiro Abe, Munehide Matsuhisa, Toshio Matsumoto and Seiji Fukumoto : FGF receptor 1c works as a phosphate-sensor to regulate FGF23 production, ASBMR 2018 Annual Meeting Registration Confirmation, Sep. 2018.
15.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Disruption of a progressive vicious cycle between myeloma tumor growth and bone destruction by TAK1 inhibition, ASBMR 2018 Annual Meeting, Montreal, Sep. 2018.
16.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Ashtar Mohannad, Kotaro Tanimoto, Iwasa Masami, Bat-Erdene Ariunzaya, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Opposite effects of TRAIL on the Sp-1-c-FLIP survival pathway in myeloma cells and osteoclasts., ASBMR 2018 Annual Meeting, Montreal, Sep. 2018.
17.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Tatsuji Haneji, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction, 8th International Workshop on Advances in the Molecular Pharmacology and Therapeutics of Bone and other Musculoskeletal Diseases and Cancer and Bone Society 2018 Meeting, Oxford, Jun. 2018.
18.	Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Apoptosis inducer TRAIL stimulates osteoclast differentiation and survival via TAK1 activation., 1st International Conference of Biophysical Technology in Dentistry (+10th International Scientific Meeting in Dentistry),, Makassar, Indonesia., Apr. 2018.
19.	Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Apoptosis inducer TRAIL stimulates osteoclast differentiation and survival via TAK1 activation., The 4th ASEAN plus Tokushima Joint International Conference, Bali, Indonesia, Dec. 2017.
20.	Itsuro Endo, Dong Bingzi, Ohnishi Yukiyo, Kondo Takeshi, Masahiro Hiasa, Jumpei Teramachi, Toshio Matsumoto, Masahiro Abe, Seiji Fukumoto and Tatsuji Haneji : Decreased bone strength induced by persistent activation of calcium-sensing receptor, American Society for Bone and Mineral Research (ASBMR) 2017 Annual Meeting, Denver, Sep. 2017.
21.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition impairs myeloma cell-bone marrow interaction to reduce myeloma tumor growth and bone destruction, American Society for Bone and Mineral Research (ASBMR) 2017 Annual Meeting, Denver, Sep. 2017.
22.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction, International Society for Experimental Hematology 46th Annual Scientific Meeting, Frankfurt, Aug. 2017.
23.	Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Masahiro Hiasa, A Baterdene, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Osteoclasts utilize TRAIL for their NF-B activation, but TAK1 inhibition resumes TRAIL-induced apoptosis in osteoclasts., Australian and New Zealand Bone and Mineral Society 2017, Brisbane, Australia., Jun. 2017.
24.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Akihito Yamamoto, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK1 inhibition on myeloma tumor progression and bone destruction, Cancer and Bone Society Conference 2017, Indianapolis, May 2017.
25.	Ryota Amachi, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Jumpei Teramachi, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Osteoblast Creates a Non-permissive Niche for Myeloma Cells, 95th General Session & Exhibition of the IADR program book, San Francisco, Mar. 2017.
26.	Hirofumi Tenshin, Jumpei Teramachi, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : TRAIL Stimulates Osteoclast Differentiation and Survival via TAK1 Activation., 95th General Session & Exhibition of the IADR program book, San Francisco, Mar. 2017.
27.	Kiyoe Kurahashi, Itsuro Endo, Nakamura Maiko, Ohnishi Yukiyo, Takeshi Kondo, Aizawa Shinichi, Toshio Matsumoto, Seiji Fukumoto and Masahiro Abe : Glucose intolerance induced by persistent activation of calcium-sensing receptor, American Society for Bone and Mineral Research 2016 Annual Meeting, Atlanta, Sep. 2016.
28.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kiyoe Kurahashi, Takeshi Kondo, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : TAK-1 inhibition disrupts Pim-2-associated and Pim-2-independent key signaling pathways to effectively suppress tumor growth and restore bone formation in myeloma, American Society for Bone and Mineral Research 2016 Annual Meeting, Atlanta, Sep. 2016.
29.	Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Bingzi Dong, Masahiro Hiasa, Keiichiro Watanabe, Ryota Amachi, S Nakamura, H Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Osteoclasts utilize an apoptosis-inducer TRAIL as a stimulator for osteoclastogenesis Critical roles of the TAK-1-Pim-2 signaling induced by RANK ligand and TRAIL., ANZBMS 2016 Annual Meeting, Gold Coast, Aug. 2016.
30.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of TAK-1 inhibition on tumor growth and bone destruction in myeloma, 21st Congress European Hematology Association, Copenhagen, Jun. 2016.
31.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Derek Hanson, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Pim inhibition suppresses osteoclastogenesis and tumor growth in myeloma, 57th ASH Annual Meeting and Exposition, Orlando, Dec. 2015.
32.	Hirofumi Tenshin, Jumpei Teramachi, A Oda, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, S Nakamura, H Miki, I Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAIL is not a proapoptotic but rather anti-apoptotic mediator for osteoclasts to stimulate their differentiation and survival, ASBMR 2015 Annual Meeting, Seattle, Oct. 2015.
33.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Asuka Oda, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Up-regulation of the pH sensor TRPV1 in myeloma cells and their adaption to an acidic microenvironment, ASBMR 2015 Annual Meeting, Seattle, Oct. 2015.
34.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pivotal role of TAK-1 in tumor growth and bone destruction in myeloma: Therapeutic impact of TAK-1 inhibition, American Society for Bone and Mineral Research 2015 Annual Meeting, Oct. 2015.
35.	Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, nishi Oh Yukiyo, Bingzi Dong, Kiyoe Kurahashi, Sumiko Yoshida, Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, Masahiro Abe, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Serum carboxy-terminal telopeptide of type I collagen, as a marker for systemic atherosclerosis, ANZBMS 2015 Annual Meeting, Hobart, Sep. 2015.
36.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : Saturated Fatty Acids Predominantly Activate PERK Pathway via Altered Composition of the Endoplasmic Reticulum Membrane, and Reduce Insulin Secretion in Pancreatic Cell by Translation Attenuation, 75th ADA scientific sessions, Jun. 2015.
37.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kumiko Kagawa, Hirokazu Miki, Shiroh Fujii, Keiichiro Watanabe, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Critical role of Pim-2 in NF-B-mediated suppression of osteoblastogenesis and stimulation of osteoclastogenesis: Therapeutic impact of Pim inhibition on myeloma bone disease., 2014 ASBMR Annual Meeting, Houston, Sep. 2014.
38.	Akio Kuroda, 鶴尾美穂, Takeshi Kondo, 安芸奈菜子, 大黒由加里, Itsuro Endo, Ken-ichi Aihara, Motoyuki Tamaki, Toshio Matsumoto and Munehide Matsuhisa : Comparison of insulin Glargine with Insulin Degludec in Type 1 Diabetes Patients., 第74回アメリカ糖尿病学会, Jun. 2014.
39.	Akiko Hata, Yosuke Shikama, Nanako Aki, Chisato Kosugi, Hiroya Kobayashi, Masashi Miyoshi, Takayuki Nakao, Ayako Tamura, Takako Ichihara, Takako Minagawa, Yumi Kuwamura, Toshio Matsumoto and Makoto Funaki : Serum Adipocyte Fatty Acid-binding Protein Is Related to the Development of Metabolic Syndrome in Japanese Male Workers, Diabetes, 63, Suppl.1, A.388, Jun. 2014.
40.	Dong Bingzi, Takeshi Kondo, Itsuro Endo, 大西幸代, 尾松卓, Masahiro Abe, 相澤慎一 and Toshio Matsumoto : educed bone formation and increased adiposity with insulin resistance in interleukin-11 deficient mice, European Calcified Tissue Society Annual Meeting 2014, Prague, May 2014.
41.	Ken-ichi Aihara, Sumiko Yoshida, Uemoto Ryoko, Ishikawa Kazue and Toshio Matsumoto : Plasma Heparin Cofactor II Activities are Inversely Associated with Aberrant Glucose Metabolism in Humans and Mice, American Heart Associations Scientific Sessions 2013 Dallas, Texas, Nov. 2013.
42.	Ryota Amachi, Masahiro Abe, Masahiro Hiasa, Keiichiro Watanabe, S Fujii, T Harada, H Miki, S Nakamura, I Endo, Eiji Tanaka and Toshio Matsumoto : Acidic conditions epigenetically repress the TRAIL receptor DR4 in myeloma cells to confer their resistance to TRAIL, ASBMR 2013 Annual Meeting,, Baltimore, Oct. 2013.
43.	Keiichiro Watanabe, Masahiro Abe, H Mori, Ryota Amachi, Masahiro Hiasa, T Harada, S Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto : Potent induction of bone formation in myeloma bone lesions by the cathepsin K inhibitor KK1-300-01 in combination with the proteasome inhibitor bortezomib, ASBMR 2013 Annual Meeting,, Baltimore, Oct. 2013.
44.	Akio Kuroda, Takeshi Kondo, Ken-ichi Aihara, Itsuro Endo, T Yasuda, H Kaneto, T Matsuoka, Toshio Matsumoto and Munehide Matsuhisa : The characteristics of type 1 diabetes patients who use insulin pump with square-wave bolus insulin., 73th America Diabetes Association (poster), Jun. 2013.
45.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda and Toshio Matsumoto : Androgen receptor promotes angiogenesis in response to ischemia via activation of VEGF receptor signaling pathway regardless of sex, ENDO 2013;The Endocrine Society's 95th Annual Meeting & Expo, San Francisco, Jun. 2013.
46.	Ken-ichi Aihara, Sumiko Yoshida, Ryoko Uemoto, Kazue Ishikawa and Toshio Matsumoto : Plasma Heparin Cofactor II Activities are Inversely Associated with Aberrant Glucose Metabolism in Humans and Mice., American Heart Association, Scientific Sessions 2013, Dallas, Jun. 2013.
47.	Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, H Mori, Itsuro Endo, Eiji Tanaka and Toshio Matsumoto : Induction of bone formation in myeloma osteolytic lesions by cathepsinK inhibition, Kyoto, Apr. 2013.
48.	Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, Hirokazu Miki, Shingen Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : An acidic milieu suppersses histone acetylation in myeloma cells to down-regulate the TRAIL receptor DR4 expression., Kyoto, Apr. 2013.
49.	Itsuro Endo, Toshio Matsumoto and 福本誠二 : FGF(), 厚生労働省科学研究費補助金難治性疾患克服研究事業ホルモン受容機構異常に関する調査研究平成24年度班会議東京都 2013年1月, Jan. 2013.
50.	Harada Takeshi, Ozaki Shuji, Oda Asuka, Iwasa Masami, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe, Shibata Hironobu, Akishige Ikegame, Daisuke Tsuji, Ito Kohji, Ri Masaki, Iida Shinsuke, Shiotsu Yukimasa, Kawai Shigeto, Yamada-Okabe Hisafumi and Toshio Matsumoto : Combination therapy of a defucosylated anti-HM1.24 monoclonal antibody plus Ienalidomide induces marked antibody-dependent cellular cytotoxicity and inhibits the clonogenic potential of myeloma cancer stem-like cells. Atlanta, Dec. 2012., The 54th Annual Meeting of the American Society of Hamatology, Dec. 2012.
51.	T Harada, Shuji Ozaki, A Oda, M Iwasa, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe, Hirofumi Shibata, Akishige Ikegame, Daisuke Tsuji, Kouji Itou, M Ri, S Iida, Y Shiotsu, S Kawai, H Yamada-Okabe and Toshio Matsumoto : Combination Therapy of a Defucosylated Anti-HM1.24 Monoclonal Antibody Plus Lenalidomide Induces Marked Antibody-Dependent Cellular Cytotoxicity and Inhibits the Clonogenic Potential of Myeloma Cancer Stem-Like Cells., 54th ASH Annual Meeting and Exposition, USA, Atlanta, Dec. 2012.
52.	Ryota Amachi, Masahiro Abe, Ryota Amachi, Keiichiro Watanabe, S Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto : An acidic milieu suppresses DR4 editing to cause myeloma resistance to TRAIL, ASEAN plus and Tokushima Joint International Conference, Yogjakarta, Indonesia, Dec. 2012.
53.	Masahiro Abe, Masahiro Hiasa, Watanabe ken-ichiro, Nakamura Shingen, Harada Takeshi, Itsuro Endo and Toshio Matsumoto : Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition, 12th CIBD International Meeting on Cancer Induced Bone Disease (CIBD) Lyon, Nov. 2012, Nov. 2012.
54.	Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Harada Takeshi, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition, 12th Int'l Meeting on Cancer Induced Bone Disease, Lyon, Nov. 2012.
55.	Ken-ichi Aihara, Sumiko Yoshida, Mizuho Kinouchi, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : Diabetes Spoils the Favorable Effect of HDL-Cholesterol on Endothelial Function in the Elderly with Cardiovascular Risk Factors, American Heart Association Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
56.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Androgen Receptor is Required for Cellular Survival and Angiogenesis in Response to Ischemia via Activation of VEGF Receptor Signaling Pathway Regardless of Sex, American Heart Association Scientific Session 2012, Nov. 2012.
57.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masataka Sata, Masashi Akaike, Toshio Matsumoto and Toshiaki Tamaki : Heparin Cofactor II Promotes Angiogenesis in Response to Ischemic Hindlimb via an AMPK-eNOS-dependent Manner, American Heart Association Scientific Sessions 2012, Nov. 2012.
58.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Eicosapentaenoic acid administration ameliorates cardiac remodeling in humans and protects against Ang II-induced cardiovascular remodeling via attenuation of oxidative stress in mice., American Heart Association Scientific Sessions 2012, ロサンゼルス, Nov. 2012.
59.	Masahiro Hiasa, Ryota Amachi, Keiichiro Watanabe, Harada Takeshi, Fujii Shirou, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Pim-2 suppresses BMP-2 signaling as a common inhibitory mediator of osteoblastogenesis in myeloma, ASBMR 2012 Anuual Meeting, Minneapolis, Oct. 2012.
60.	Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, S Fujii, S Nakamura, H Miki, K Kagawa, H Mori, I Endo, Eiji Tanaka and Toshio Matsumoto : Restoration of bone formation in myeloma osteolytic lesions by the cathepsin K inhibitor KK1-300-01, 34th ASBMR meeting, Minneapolis, MN, USA., Oct. 2012.
61.	Masahiro Hiasa, Masahiro Abe and Toshio Matsumoto : RelB attenuates the activation of the classical NF-kB pathway to facilitate osteoblastogenesis, Sep. 2012.
62.	Masahiro Hiasa, Masahiro Abe, Rieko Arakaki, Akiko Yamada, Kenzo Asaoka, Toshio Matsumoto, Yoshio Hayashi and Naozumi Ishimaru : RelB attenuates the activation of the classical NF-κB pathway to facilitate osteoblastogenesis, ANZBMS Annual Scientific Meeting, Perth, Sep. 2012.
63.	Takeshi Kondo, Omatsu Takashi, Dong Bingzi, Ohnishi Yukiyo, Aizawa Shin-ichi, Itsuro Endo and Toshio Matsumoto : Interleukin(IL)-11 is required for mechanical stress-induced bone formation, Australian and New Zealand Bone and Mineral Society, Gold Coast, Sep. 2012.
64.	Keiichiro Watanabe, Masahiro Abe, Hiroyo Mori, Ryota Amachi, Masahiro Hiasa, T Harada, S Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto : The cathepsin K inhibitor KK1-300-01 prevents bone destruction and resumes bone formation in myeloma osteolytic lesions, Australian & New Zealand Bone & Mineral Society 22th Annual Scientific Meeting with 1st Asia-Pacific Bone and Mineral Research meeting, Perth, Australia., Sep. 2012.
65.	Akio Kuroda, YASUDA TETSUYUKI, TAKAHARA MITSUYOSHI, SAKAMOTO FUMIE, KASAMI RYUUICHI, MIYASHITA KAZUYUKI, MATSUOKA TAKA-AKI, Sumiko Yoshida, KONDO ERI, Itsuro Endo, Ken-ichi Aihara, KANETO HIDEAKI, Toshio Matsumoto, SHIMOMURA IICHIRO and Munehide Matsuhisa : Carbohydrate-to-Insulin Ratio is Calculated to be 300-400 Divided by Total Daily Insulin Dose in Type 1 Diabetic Patients Who Are on Insulin Pump Therapy, American Diabetes Association 72nd Scieentific Sessions, Philadelphia, Jun. 2012.
66.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Masashi Akaike and Toshio Matsumoto : Heparin cofactor II, a serine protease inhibitor, is a novel regulating factor for glucose metabolism and albuminuria, Keystone Symposia: Complications of Diabetes: Mechanisms of Injury and Failure of Repair, Mar. 2012.
67.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Shuhei Tomita, Masataka Sata, Masashi Akaike, Shigeki Kato, Toshio Matsumoto and Toshiaki Tamaki : Heparin Cofactor Promotes Angiogenesis via an AMPK-eNOS Signaling Pathway, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
68.	Keiichiro Watanabe, Masahiro Abe, M Kawatani, Masahiro Hiasa, A Kawano, T Jinno, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, H Osada and Toshio Matsumoto : Aggravation of myeloma growth and drug resistance by an acidic created in myeloma-osteoclast interaction., ASBMR 2011 Annual Meeting, San Diego, Sep. 2011.
69.	Masahiro Hiasa, nakano ayako, Keiichiro Watanabe, C Qu, T Harada, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Kumiko Kagawa, Kyoko Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition., ASBMR 2011 Annual Meeting, San Diego, Sep. 2011.
70.	Masahiro Hiasa, nakano ayako, Keiichiro Watanabe, C Qu, T Harada, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Kumiko Kagawa, Kyoko Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Dual effects of Pim inhibition on myeloma: induction of bone formation and tumor suppression., IOF-ANZBMS 2011 Annual Meeting, Gold Coast, Sep. 2011.
71.	Takeshi Kondo, Takashi Omatsu, Yukiyo Ohnishi, Toshio Matsumoto and Itsuro Endo : Interleukin-11 is required for the maintenance of axial bone mass in mice., International Osteoporosis Foundation Annual Meeting 2011, Sep. 2011. (Keyword) IL-11 / bone formation
72.	Itsuro Endo, Seiji Fukumoto and Toshio Matsumoto : FGF23-related hypophosphatemic diseases in Japan., oint Meeting of International Bone and Mineral Society and The Japanese Society of Bone Mineral Research, Jul. 2011.
73.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : An Acidic Mileu Created In Myeloma-Osteoclast Interaction Enhances Tumor Growth, but Triggers Anti-Myeloma Activity of Reveromycin A, a Novel Anti-Resorptive Agent, 52th American Society of Hematology, Orlando, Dec. 2010.
74.	Cui Qu, Masahiro Abe, Miki Hirokazu, Shingen Nakamura, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Nakano Ayako, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : Lenalidomide In Combination with Zoledronic Acid Restores the Activation and Anti-Myeloma Effects of γδT Cells Attenuated by the Bone Marrow Microenvironment, 52th American Society of Hematology, Orlando, Dec. 2010.
75.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Androgen receptor is essential for cell survival and neovascularization after ischemia., American Heart Association Scientific Sessions 2010, Chicago, Nov. 2010.
76.	Itsuro Endo, Toshio Matsumoto and Ken-ichi Aihara : Serum ICTP can be a surrogate marker of coronary unstable plaques, ASBMR annual meeting, Tronto, Canada, Oct. 2010.
77.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : A Novel Anti-resorptive Agent, Reveromycin A, Ameliorates Bone Destruction and Tumor Growth in Myeloma, ASBMR 2010 Annual Meeting, Toronto, Oct. 2010.
78.	Masahiro Hiasa, Masahiro Abe, nakano ayako, oda aska, amo hiroe, Keiichiro Watanabe, Shingen Nakamura, miki hirokazu, Kyoko Takeuchi, Kumiko Kagawa, Shuji Ozaki, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto : Bone Marrow Stromal Cells Suppress TACE-mediated M-CSFR and RANK Shedding to Facilitate Osteoclastogenesis and Suppress DC Differentiation from Monocytes., ASBMR 2010 Annual Meeting, Toronto, Oct. 2010.
79.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Androgen receptor participants in ischemia-induced tissue damage and angiogenesis in male mice, 23rd Scientific Meeting of the International Society of Hypertension Vancouver, Vancouver, Sep. 2010.
80.	Masahiro Abe, Masahiro Hiasa, Nakano A, Shingen Nakamura, Miki H, Qu C, Keiichiro Watanabe, Harada T, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : TIMP-3 up-regulation facilitates osteoclastogenesis and suppresses DC differentiation from monocytes in the bone marrow microenvironment in myeloma, 10th International Conference Cancer-induced Bone Disease, Sep. 2010. (Keyword) Sheffield (United Kingdom)
81.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : The novel anti-resorptive agent reveromycin A ameliorates bone destruction and tumor growth in myeloma, 10th International Conference Cancer-induced Bone Disease, Sheffield (United Kingdom), Sep. 2010.
82.	Masahiro Hiasa, Masahiro Abe, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto : Stroma inhibit DC differentiation through the suppression of M-CSFR shedding, 88th IADR, Barcelona, Jul. 2010.
83.	Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Sumiko Yoshida, Yasumasa Ikeda, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Plasma heparin cofactor II activity is an independent determinant for cardiac remodeling in subjects with cardiovascular risk factors, 20th International Society for Heart Research(ISHR), Kyoto, May 2010.
84.	Ken-ichi Aihara, Yuka Ueda, Takayuki Ise, Sumiko Yoshida, Yasumasa Ikeda, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Heparin cofactor II is a novel anticardiac remodeling factor against angiotensin II excess, 20th International Society for Heart Research(ISHR), Kyoto, May 2010.
85.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Exacerbation of cell survival and impaired neovascularization after hindlimb ischemia in male androgen receptor null mice, 20th International Society for Heart Research(ISHR), Kyoto, May 2010.
86.	Ken-ichi Aihara, Sumiko Yoshida, Kurahashi Kiyoe, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : Increased serum triglyceride is associated with left ventricular diastolic dysfunction., 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
87.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Suzuki Reiko, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
88.	Masahiro Hiasa, Masahiro Abe, I Endo, A Nakano, Shuji Ozaki, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto : Myeloma-bone marrow stromal cell interaction enhances osteoclastogenesis and suppresses dendritic cell differentiation from monocytes, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
89.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, Takashi Iwase, Masashi Akaike, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Hirata Yoichiro, Suzuki Reiko, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
90.	Ken-ichi Aihara, Sumiko Yoshida, Yuka Ueda, Uemoto Ryoko, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Rosuvastatin attenuates left ventricular mass even in subjects without cardiac hypertrophy, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
91.	Ken-ichi Aihara, Sumiko Yoshida, Kurahashi Kiyoe, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : Increased serum triglyceride is associated with left ventricular diastolic dysfunction, 14th International Congress of Endocrinology, Kyoto, Japan, Mar. 2010.
92.	Akishige Ikegame, Shuji Ozaki, Daisuke Tsuji, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Ayako Nakano, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, Masahiro Abe, Kouji Itou and Toshio Matsumoto : A recombinant HLA class I-specifi single-chain Fv diabody can target cancer stem cell-like side population cells in multiple myeloma, 51th Annual Meeting of the American Society of Hematolog, New Orleans, Louisiana, USA, Dec. 2009.
93.	Yuka Ueda, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Exacerbation of Angiotensin ll-induced Cardiac Remodeling through Enhancement of NADPH oxidase-TGF- 1 Pathway in Heparin Cofactor ll-Deficient Mice, Scientific Sessions 2009, American Heart Association, Florida, Nov. 2009.
94.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Shusuke Yagi, Yasumasa Ikeda, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Nishio Susumu, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is an endothelial function-independent protective factor against carotid atherosclerosis., Scientific Sessions 2009, American Heart Association, Florida, Nov. 2009.
95.	Ken-ichi Aihara, Mizuho Kinouchi, Yuichi Fujinaka, Sumiko Yoshida, Yuka Ueda, Kurahashi Kiyoe, Itsuro Endo, Uemoto Ryoko, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Albuminuria is an independent aggravating factor for visceral fat obesity regardless of diabetes mellitus: a study using abdominal CT scan imaging, Scientific Sessions 2009, American Heart Association, Florida, Nov. 2009.
96.	Masahiro Hiasa, Masahiro Abe, A Nakano, Kyoko Takeuchi, K Watanabe, Kumiko Kagawa, Ken-ichiro Yata, Kenzo Asaoka, Eiji Tanaka and Toshio Matsumoto : Bone marrow stromal cells inhibit dendritic cell differentiation and facilitate osteoclastogenesis in myeloma through the suppression of M-CSF receptor shedding in monocytes, 第26回内藤コンファレンス, Nov. 2009.
97.	S Nakamura, Masahiro Abe, Cui Qui, A Nakano, Oda A., Amou H., Ikegame A., Harada T., Masahiro Hiasa, H Miki, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto : Facilitation of Osteoblast Differentiation by ATF-4 Accumulation through Proteasome Inhibition., ASH Annual Meeting, Nov. 2009.
98.	Itsuro Endo, Onishi Yukiyo, Kido Rika, Kurahashi Kiyoe, Ito Yuuji, Yuichi Fujinaka, Ken-ichi Aihara, Sumiko Yoshida, Masahiro Abe, Fukumoto S and Toshio Matsumoto : A new calcilytic compound,JTT-305,inhibits enhanced signaling by activating mutations of calcium-sensing receptor in autosomal dominant hypocalcemia (ADH), ASBMR 31st Annual Meeting, Denver, Sep. 2009.
99.	A Nakano, Asano J., Masahiro Abe, Masahiro Hiasa, S Nakamura, H Miki, Kumiko Kagawa, Kyoko Takeuchi, Ken-ichiro Yata, Itsuro Endo, Shuji Ozaki and Toshio Matsumoto : Up-regulation of Pim-2 in myeloma cells by an interaction with bone marrow microenvironment enhances myeloma cell survival via stimulating Bad phosphorylation, ASBMR Annual Meeting, Denver, Sep. 2009.
100.	Masahiro Abe, A Oda, Shinsuke Kido, A Nakano, Masahiro Hiasa, H Amou, S Nakamura, Kyoko Takeuchi, H Miki, Kumiko Kagawa, Ken-ichiro Yata, Shuji Ozaki, Itsuro Endo and Toshio Matsumoto : Bortezomib, a proteasome inhibitor with anti-myeloma activity, stimulates osteoblast differentiation by enhancing ATF4 accumulation in osteoblastic cells., ASBMR Annual Meeting, Denver, Sep. 2009.
101.	Shusuke Yagi, Masashi Akaike, Takashi Iwase, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, S Yoshida, Y Sumitomo, Ken-ichi Aihara, Toshio Matsumoto and Masataka Sata : Bosentan, an Endothelin Receptor Antagonist, Exerts Protective Actions against Systemic Sclerosis-related Peripheral Circulation Insufficiency., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
102.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, S Yoshida, Y Sumitomo, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Pitavastatin Exerts LDL Cholesterol Reduction-independent Protective Action for Cardiac and Renal Function in Patients with Dyslipidemia., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
103.	Shusuke Yagi, Masashi Akaike, Ken-ichi Aihara, S Yoshida, Y Sumitomo, Kenya Kusunose, T Niki, Y Hirata, Koji Yamaguchi, Kunihiko Koshiba, Takashi Iwase, N Tomita, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Toshio Matsumoto and Masataka Sata : Plasma Aldosterone Concentration is Associated with Cognitive Impairement in Patients with Hypertension., 73th Annual scientific meeting of the Japanese circulation society, Mar. 2009.
104.	Ken-ichiro Yata, Masahiro Abe, Oda A., Amou H., takeuchi K., Masahiro Hiasa, Nakano A., Miki H., Nakamura S., Tanaka O., Kumiko Kagawa, Shuji Ozaki and Toshio Matsumoto : Anti-myeloma effects of γδ T cells are hampered by bone marrow stromal cells but resumed by stromal cell-derived osteoblasts, Annual Meeting of the American Society of Hematology, San Francisco, Dec. 2008.
105.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Increased serum triglyceride but not LDL cholesterol is associated with left ventricular diastolic dysfunction., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
106.	Takayuki Ise, Ken-ichi Aihara, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Ishikawa Kazue, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Plasma Heparin Cofactor II Activity Is Inversely Associated with Left Atrial Volume and Left Ventricular Diastolic Dysfunction., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
107.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is an antivascular remodeling factor in elderly individuals., Scientific Sessions 2008, American Heart Association, New Orleans, Nov. 2008.
108.	Takashi Iwase, Hirotsugu Kurobe, Masashi Akaike, Shunji Nakano, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Ken-ichi Aihara, Shuji Ozaki, Masahiro Abe, Natsuo Yasui, Toshio Matsumoto, Tetsuya Kitagawa and Masataka Sata : Erythropoietin administration with autologous blood donation - a novel strategy to enhance mobilization of circulating progenitor cells, American Heart Association Sessions 2008, New Orleans, Nov. 2008.
109.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, Ishikawa Kazue, Sumitomo Yuka, Sumiko Yoshida, Takashi Iwase, Toshio Matsumoto and Masataka Sata : Pitavastatin, an HMG-CoA Reductase Inhibitor, Prevents Glucocorticoid-induced Hypertension through Ameliorating Imbalance of Oxidative Stress and Nitric Oxide Production, American Heart Association Sessions 2008, New Orleans, Nov. 2008.
110.	Masahiro Abe, Masahiro Hiasa, Oda A., Amou H., takeuchi K., Tanaka O., Nakamura S., Miki H., Kumiko Kagawa, Ken-ichiro Yata, Shuji Ozaki, Kido S. and Toshio Matsumoto : Bone marrow stromal cells up-regulate M-CSF receptor in monocytes to disrupt dendritic cell differentiation while facilitating osteoclastogenesis in myeloma, ASBMR, Montreal, Sep. 2008.
111.	Takeuchi K., Masahiro Abe, Oda A., Amou H., Masahiro Hiasa, Tanaka O., Nakamura S., Miki H., Kumiko Kagawa, Ken-ichiro Yata, Hashimoto T., Shuji Ozaki, Kido S. and Toshio Matsumoto : TGF-β Suppresses Adipocytic Differentiation and Enhances Accumulation of Stromal Cells in Myeloma Bone Lesions, ASBMR, Montreal, Sep. 2008.
112.	Masahiro Abe, Masahiro Hiasa, Kido S., Oda A., Amou H., takeuchi K., Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto : TACE up-regulation in monocytes by GM-CSF and IL-4 disrupts myeloma cell-induced osteoclastogenesis while inducing dendritic cell differentiation, International Meeting on Cancer Induced Bone Disease, Scotland, Jun. 2008.
113.	Masashi Akaike, Ken-ichi Aihara, Shusuke Yagi, Yasumasa Ikeda, Ishikawa Kazue, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Takashi Iwase and Toshio Matsumoto : Pitavastatin, an HMG-CoA Reductase Inhibitor, Prevents Glucocorticoid-induced Hypertension through Increased Nitric Oxide Production as a Pleiotropic Effect on Vascular Endothelial Cells, Hypertension 2008 18th Scientific Meeting of the European Society of Hypertension 22nd Scientific Meeting of the International Society of Hypertension, Berlin, Jun. 2008.
114.	Takashi Iwase, Masashi Akaike, Shunji Nakano, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Ken-ichi Aihara, Natsuo Yasui and Toshio Matsumoto : Single erythropoietin administration with autologous blood donation - a novel strategy to enhance mobilization of endothelial progenitor cells, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
115.	Sumitomo Yuka, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Acceleration of angiotensin II-induced cardiac remodeling through enhancement of oxidative stress in heparin cofactor II knockout mice, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
116.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Dehydroepiandrosterone sulfate regulates carotid blood flow in elderly individuals, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
117.	Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Serum Lipid Disorder is Associated with Left Ventricular Diastolic Dysfunction in Elderly Individuals, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
118.	Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : The active form of vitamin D, 1,25(OH)2D3, prevents vascular remodeling and glucose intolerance in elderly individuals, 22nd Scientific Meeting of the International Society of Hypertension 2008, Berlin, Germany, Berlin, Jun. 2008.
119.	Takako Miyamoto, Shinsuke Kido, Masahiro Abe, Toshio Matsumoto and Hisaaki Taniguchi : Expression Profiling by Quantitative and Large-scale Proteomics in Differentiating Osteoblasts, HUPO 5th Annual World Congress, Los Angeles, Nov. 2006.
120.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Sumitomo Yuka, Masataka Sata, Kato Shigeaki and Toshio Matsumoto : Heparin Cofactor II Deficiency Causes Accelerated Thrombosis and Atherosclerosis in Mice, American Heart Association Scientific Sessions 2006, Chicago, USA, Nov. 2006.
121.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Fujimura Mitsunori, Hashizume Shunji, Takashi Iwase, Shusuke Yagi, Kondo Akira, Hiroyuki Azuma and Toshio Matsumoto : Valsartan Enhances Nitric Oxide Bioavailability and Reduces Arterial Stiffness in Patients with Essential Hypertension, The 21st Scientific Meeting of the International Society of Hypertension, 2006, Fukuoka, Japan, Oct. 2006.
122.	Takako Miyamoto, Shinsuke Kido, Toshio Matsumoto and Hisaaki Taniguchi : Proteomic Analysis of Osteoblast Differentiation, 20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB Congress, Kyoto, Jul. 2006.
123.	Hirotsugu Kurobe, Yuki Izawa, Y Fukuhara, Tamotsu Kanbara, A Kurushima, Ken-ichi Aihara, Masashi Akaike, Masashi Kano, Takashi Kitaichi, Yutaka Masuda, Hiroyuki Azuma, Toshiaki Tamaki, Toshio Matsumoto, Tetsuya Kitagawa, Shuhei Tomita and Masanori Yoshizumi : HIF-ARNT transcriptional system in Tcells has a pivotal role in vascular inflammation and remodeling, XIL International Symposium on Atherosclerosis, Italy, Jun. 2006.
124.	Yutaka Masuda, H Kurobe, Takashi Kitaichi, Masashi Kano, A Kurushima, Tetsuya Kitagawa, T Iwase, Masashi Akaike, M Abe and Toshio Matsumoto : Erythropoietin induced peripheral stem cell transplantation for severe ischemic limbs, The 14th Annual Meeting of the Asian Society for Cardiovascular Surgery, Osaka, Jun. 2006.
125.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Fujimura Mitsunori, Shusuke Yagi, Hashizume Shunji, Yasumasa Ikeda, Takashi Iwase, Takamori Nobuyuki, Tetsuya Kitagawa and Toshio Matsumoto : Plasma Heparin Cofactor II Activity is a Predictor for Incidence of Peripheral Arterial Disease in Patients with Cardiovascular Risk Factors, XIV International Symposium on Atherosclerosis, 2006 Rome, Italy, Jun. 2006.
126.	Ken-ichi Aihara, Mihara Masatomo, Hiroyuki Azuma, Masashi Akaike, Takaya Matsushita, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Hashizume Shunji, Fujimura Mitsunori and Toshio Matsumoto : Argatroban, a synthetic thrombin antagonist, can reduce insulin resistance though thrombin inactivation in the db/db mouse model of type 2 diabetes mellitus, XIV International Symposium on Atherosclerosis, 2006 Rome, Italy, Jun. 2006.
127.	Hirotsugu Kurobe, Yuki Izawa, Yayoi Fukuhara, Tamotsu Kanbara, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Tetsuya Kitagawa, Toshiaki Tamaki, Toshio Matsumoto, Masaki Ueno, Shuhei Tomita and Masanori Yoshizumi : T Cell-specific HIF-1α-deficient Mice, but Not ARNT-deficient Mice, Exhibit Exacerbated Inflammation and Vascular Remodeling in Response to Cuff Injury, American Heart Association 2005 Scientifc Sessions, Dallas, Nov. 2005.
128.	Takamori Nobuyuki, Masashi Akaike, Ken-ichi Aihara, Hirono Akira, Yamaguchi Hiroshi, Hiroyuki Azuma, Tamura Katsuya and Toshio Matsumoto : Plasma Heparin Cofactor II Activities Predict Cardiovascular Risk in Patients with Coronary Heart Disease, American Heart Associations Scientific Sessions 2005, Dallas, USA, Nov. 2005.
129.	Ali Jalili, Shuji Ozaki, Tomoko Hara, Etsuko Sekimoto, Yoichi Tanaka, Takashi Ohshima, Hironobu Shibata, Toshihiro Hashimoto, Masahiro Abe, Yasuhiko Nishioka and Toshio Matsumoto : Generation of HM1.24-specific cytotoxic T lymphocytes from peripheral blood stem cell harvests of patients with multiple myeloma, 46th Annual Meeting: American Society of Hematology, San Francisco, Dec. 2004.
130.	Atsushi Shioyasono, Yasuo Oba, Hiura Kenji, Masahiro Abe, Toshio Matsumoto and Keiji Moriyama : MIP-1alpha is upregulated during experimental tooth movement, IADR 82nd General Session, Honolulu, Mar. 2004.
131.	Ken-ichi Aihara, Takamori Nobuyuki, Yasuhiko Kanagawa, Masashi Akaike, Fujimura Mitsunori, Yoshida Tomonori, Hashizume Shunji, Kato Midori, Yasumasa Ikeda, Hiroyuki Azuma and Toshio Matsumoto : Heparin cofactor II is inversely related to the severity of carotid atherosclerosis, American Heart Association, Scientific Sessions 2003 Orland Florida USA, Nov. 2003.

Proceeding of Domestic Conference:

1.	Shinsuke Kido, 中川航司, 遠藤逸郎, 坂田雅映, 橋本由衣, Sawako Tatsumi, Toshio Matsumoto and Ken-ichi Miyamoto : 糖尿病症骨症の発症機序の解析:終末糖化産物(AGEs)にんよるCanonical, 第1回骨バイオサイエンス研究会,
2.	Emiko Nakaue, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada, Yusuke Inoue, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : プロテアソーム阻害薬による骨髄腫骨病変部選択的骨形成誘導活性の検討, 第40回日本骨代謝学会学術集会, 141, Jul. 2022.
3.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : キサンチンオキシダーゼ(XO)阻害薬febuxostatによる脂肪細胞分化と骨芽細胞分化の制御機構, 第40回日本骨代謝学会学術集会, Jul. 2022.
4.	TANAKA Mariko, Masahiro Hiasa, Kotaro Tanimoto, Hirofumi Tenshin, Sou Shimizu, Yoshiki Higa, Emiko Nakaue, KIMU Suha, Jumpei Teramachi, Takeshi Harada, Shingen Nakamura, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動は骨髄腫骨病変部DPP-4発現増加と骨髄腫の腫瘍進展・髄外播種を加速させる, 第40回日本骨代謝学会学術集会, Jul. 2022.
5.	Takeshi Harada, Hirofumi Tenshin, Yusuke Inoue, Ryohei Sumitani, Emiko Nakaue, Jumpei Teramachi, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Production of SLAMF7 by osteoclasts and development of novel treatment targeting SLAMF7 against myeloma bone disease, 第40回日本骨代謝学会学術集会, Jul. 2022.
6.	Shun Sawatsubashi, 池戸葵, Toshio Matsumoto, 今井祐記 and Seiji Fukumoto : Functional analysis of vitamin D-dependent rickets type II model mouse introducing the human disease-related point mutations., 日本骨代謝学会学術集会プログラム抄録集, 40, 119, Jul. 2022.
7.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Kotaro Tanimoto, Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Critical role of the xanthine oxidase-ROS axis in perturbation of bone marrow milieu in myeloma, International Journal of Myeloma, 12, 3, 149, May 2022.
8.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Kotaro Tanimoto, Yoshiki Higa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The critical roles of the TAK1-CIP2A axis in MM cell growth and survival and osteoclastogensis, 第83回日本血液学会学術集会, BPA-3-3, Sep. 2021.
9.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, 大浦雅弘, Kimiko Sogabe, Itsuro Endo, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Critical roles of the XO-ROS axis in the pathology of bone loss in myeloma, 第83回日本血液学会学術集会, BPA-3-4, Sep. 2021.
10.	Hirofumi Tenshin, 寺町順平日浅雅博小田明日香原田武志, Masahiro Hiasa, 小田明日香, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Eiji Tanaka, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : NLRP3 inflammasome aggravates osteoclastic bone destruction in myeloma, 日本血液学会学術集会83回 Page 83回 Page OS2-4B-4(2021.09), Sep. 2021.
11.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Extraosseous dissemination of myeloma by mechanical unloading, 日本血液学会学術集会83回 Page 83回 Page OS2-11C-3(2021.09), Sep. 2021.
12.	Mai Kanai, 大西幸代, Tomoyo Hara, Itsuro Endo, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : TAK1 阻害による炎症性サイトカイン誘導性筋萎縮の改善, 第94回日本内分泌学会学術総会, Apr. 2021.
13.	Shun Sawatsubashi, Risa Kainuma, Toshio Matsumoto and Seiji Fukumoto : 栄養代謝状態が調節するグルココルチコイド受容体の転写制御機構の解明, Folia endocrinologica Japonica, 97, 1, 271, Apr. 2021.
14.	Shun Sawatsubashi, NISHIMURA Koichi, Toshio Matsumoto and Seiji Fukumoto : ヒストンシャペロンDEKによる核内構造体形成メカニズムの解明, 日本生化学会大会(Web), 94, 554, 2021.
15.	NISHIMURA Koichi, Shun Sawatsubashi, Toshio Matsumoto and Seiji Fukumoto : SWI/SNF複合体のIDRによる相分離を介した核内受容体AF-1領域との相互作用解析, 日本生化学会大会(Web), 94, 643, 2021.
16.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Kotaro Tanimoto, Yoshiki Higa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 骨髄腫細胞のPP2A阻害因子CIP2A発現誘導を介するTAK1活性化増強機構, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 149, Oct. 2020.
17.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Mohannad Ashtar, Sou Shimizu, Yoshiki Higa, Jumpei Teramachi, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動は骨吸収と骨髄腫進展を促進させる, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 149, Oct. 2020.
18.	Hirofumi Tenshin, Mohannad Ashtar, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する:Xanthine oxidase阻害剤febuxostatの治療効果．, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020.
19.	Itsuro Endo, 近藤剛史, Kiyoe Kurahashi, Toshio Matsumoto, Masahiro Abe and Seiji Fukumoto : 家族歴を有するFGF23関連低リン血症性骨軟化症の一例, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 150, Oct. 2020.
20.	Hirofumi Tenshin, アシテルモハナッド, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, 比嘉佳基, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する Xanthine oxidase阻害剤febuxostatの治療効果, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020. (Keyword) Xanthine Oxidase(拮抗物質・阻害物質) / reactive oxygen species / 抗腫瘍剤(毒性・副作用) / 骨吸収(化学的誘発,薬物療法,実験的) / cell differentiation / osteoclast / 破骨細胞分化因子 / Febuxostat(治療的利用) / RAW264.7細胞 / マウス / animal
21.	Shun Sawatsubashi, Toshio Matsumoto and Seiji Fukumoto : 栄養情報が調節するグルココルチコイド受容体の転写制御機構の解析, 第93回日本内分泌学会学術総会, 96, 1, 238, Jul. 2020.
22.	三井由香里, 飯塚裕斗, 田中智明, Itsuro Endo, Kiyoe Kurahashi, Sumiko Yoshida, 山口佑樹, 山上紘規, 藤中雄一, 森本佳奈, 白神敦久, Seiji Fukumoto and Toshio Matsumoto : CRH負荷試験による副腎皮質機能低下症·不全症カットオフ値策定の試み, 第93回日本内分泌学会学術総会, 96, 1, 251, Jul. 2020.
23.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 木内美瑞穂, 安井沙耶, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : TIR(Time-In-Range)とHbA1cとの関連∼HbA1cと組み合わせる血糖管理方法∼, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
24.	森岡隆子, Akio Kuroda, 鶴尾美穂, 堀筋冨士子, 秋田賢子, 松本幸恵, Tomoyuki Yuasa, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 予測低血糖自動注入停止型インスリンポンプが有効だった高齢1型糖尿病例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
25.	斎村玉緒, Akio Kuroda, 鶴尾美穂, 福井健壮, 掘貫理恵, 藤原敏孝, Tomoyuki Yuasa, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 脳悪性リンパ腫を発症した2がた糖尿病の1例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
26.	Yuichi Takashi, Shun Sawatsubashi, Itsuro Endo, Masahiro Abe, Munehide Matsuhisa, Toshio Matsumoto and Seiji Fukumoto : FGFR1は血中FGF23濃度を制御するリン感知受容体である, 第38回日本骨代謝学会学術集会, Oct. 2019.
27.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Bat-Erdene Ariunzaya, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害は関節リウマチにおけるNLRP3インフラマソーム誘導性の炎症および骨破壊を抑制する, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 190, Oct. 2019.
28.	Kotaro Tanimoto, Masahiro Hiasa, Akihiko Iwasa, Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masami Iwasa, 小田明日香, 曾我部公子, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる．, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Oct. 2019.
29.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害は関節リウマチにおけるNLRP3インフラマソーム誘導性の炎症および骨破壊を抑制する．, 第37回日本骨代謝学会学術集会, Oct. 2019.
30.	谷本幸太朗, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masami Iwasa, 小田明日香, Kimiko Sogabe, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる, 第37回日本骨代謝学会学術集会, Oct. 2019.
31.	Norio Iinuma, Seiji Fukumoto, Yukari Uemura, Shiro Tanaka, Saeko Fujiwara, Toshio Matsumoto and Hajime Orimo : 各年齢における骨粗鬆症患者の新規骨折発生に影響する因子-A-TOP研究登録の患者データを活用した解析(第2報)-, 第21回日本骨粗鬆症学会, Oct. 2019.
32.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Soh Shimizu, Ashtar Mohannad, Takeshi Harada, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption in rheumatoid arthritis : the therapeutic roles of TAK1 inhibition, 16th Meeting of Bone Biology Forum, Aug. 2019.
33.	Mai Kanai, 松岡飛翔, Itsuro Endo, 大西幸代, Yuichi Takashi, Kiyoe Kurahashi, Sumiko Yoshida, Ken-ichi Aihara, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : 鉄製剤投与によるFGF23関連低リン血症モデル作成の試み, 第92回日本内分泌学会学術総会, 95, 1, 422, May 2019.
34.	Yuichi Takashi, Hidetaka Kosako, Shun Sawatsubashi, Yuka Kinoshita, 伊東伸朗, Masahiro Abe, Munehide Matsuhisa, Shigeaki Kato, Toshio Matsumoto and Seiji Fukumoto : FGFR1はFGF23濃度調節を媒介するリン感知受容体である, 第92回日本内分泌学会学術総会, 95, 1, 333, May 2019.
35.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, Mizuho Kinouchi, Kimiko Sogabe, 加部一行, 瀬尾浩二, Masaharu Nishi, Naoya Matsumoto, Yasuhiko Kanagawa, Masahiro Abe, Toshio Matsumoto, 寺澤敏秀 and Munehide Matsuhisa : リブレ使用糖尿病患者の検討, 日本糖尿病学会中国四国地方会第56回総会, Oct. 2018.
36.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Takeshi Harada, Iwasa Masami, Shiroh Fujii, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Masahiro Oura, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Mechanisms of TAK1 over-activation in myeloma cells and TAK1-mediated myeloma growth and bone destruction, 第80回日本血液学会学術集会, Oct. 2018.
37.	Ashtar Mohannad, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Iwasa Masami, Takeshi Harada, Ariunzaya Erdene Bat, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Roles of ROS in induction of bone disease and cancer treatment-induced bone loss in myeloma., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
38.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Iwasa Masami, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Inverse regulation of c-FLIP-mediated survival in myeloma cells and osteoclasts by TRAIL., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
39.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Oda Asuka, Mohannad Ashtar, Ariunzaya Bat-Erdene, Iwasa Masami, Kimiko Sogabe, Oura Masahiro, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Impact of denervation-induced paralysis and mechanical unloading on tumor expansion in myeloma., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
40.	Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Kotaro Tanimoto, Ariunzaya Bat-Erdene, Mohannad Ashtar, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Kimiko Sogabe, Oura Masahiro, Shiroh Fujii, Kumiko Kagawa, Oda Asuka, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The effects of cathepsin K inhibition on osteocytes: its role in bone restoration in MM bone disease., The 80th Annual Meeting of the Japanese Society of Hematology, Oct. 2018.
41.	Yuichi Takashi, Masashi Ishizu, Shu Wakino, 水口斉, 島久登, 田代学, 宮恵子, 水口潤, Akio Kuroda, Toshio Matsumoto, Munehide Matsuhisa and Seiji Fukumoto : 血液透析患者における心不全・動脈硬化・感染のリスク因子としてのFGF23, 第18回日本内分泌学会四国支部学術集会, Sep. 2018.
42.	Itsuro Endo, 大西幸代, Kiyoe Kurahashi, Jumpei Teramachi, Masahiro Hiasa, Hirofumi Tenshin, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : カルシウム感知受容体活性型変異マウスにおける骨強度の低下, 第36回日本骨粗鬆症学会各術集会, Jul. 2018.
43.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition impairs myeloma cell-bone marrow interaction to reduce myeloma growth and bone destruction, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2018.
44.	Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : カテプシンK阻害による多発性骨髄腫骨病変部の骨量回復プロセスにおける骨細胞の役割．, 第36回日本骨代謝学会学術集会, Jul. 2018.
45.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害はTRAILによる破骨細胞活性化作用を遮断させると同時にTRAILの抗骨髄腫作用を増強する, 第36回日本骨代謝学会学術集会, Jul. 2018.
46.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1による破骨細胞に対するTRAILの生存・細胞死シグナル制御機構．, 第4回日本骨免疫学会, Jun. 2018.
47.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Mohannad Ashtar, Ariunzaya Bat-Erdene, Masami Iwasa, Kimiko Sogabe, 大浦雅弘, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 神経切断による麻痺と免荷の骨髄腫の進展への影響．, 第4回日本骨免疫学会, Jun. 2018.
48.	Itsuro Endo, Dong Bingzi, Ohnishi Yukiyo, Sumiko Yoshida, Ken-ichi Aihara, 相澤慎一, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : 常染色体優性低Ca血症1型モデルマウスにおける骨強度の低下, 第91回日本内分泌学会学術総会, Apr. 2018.
49.	斎村玉緒, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 加部一行, Mizuho Kinouchi, Sumiko Yoshida, Hiroki Yamagami, Takeshi Kondo, 西正晴, 松本直也, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : フラッシュグルコースモニタリングシステムにより施設入所可能となった高齢1型糖尿病の一例, 日本糖尿病学会中国四国地方会第55回総会抄録集, Nov. 2017.
50.	鶴尾美穂, Toshio Matsumoto, Akio Kuroda, Tomoyuki Yuasa, 加部一行, Takeshi Kondo, Mizuho Kinouchi, 井野口卓, Hiroki Yamagami, 松本直也, 西正晴, 寺澤敏秀, Masahiro Abe and Munehide Matsuhisa : SLADHを発症した高齢1型糖尿病の一例, 日本糖尿病学会中国四国地方会第55回総会抄録集, Nov. 2017.
51.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Masami Iwasa, Masahiro Oura, Yusaku Maeda, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Disruption of myeloma cell-bone marrow interaction by TAK-1 inhibition, 第80回日本血液学会学術集会, Oct. 2017.
52.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Ariunzaya Baterdene, Masami Iwasa, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAILは破骨細胞を活性化させるが，TAK1阻害により骨髄腫細胞とともに破骨細胞にもTRAILのアポトーシス誘導活性が惹起できる, The 35th Annual Meeting of the Japanese Society for Bone and Mineral Research (oral talk), Jul. 2017.
53.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Baterdene Ariunzaya, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1阻害はTRAILの抗骨髄腫作用を増強するともに骨吸収促進活性を抑制活性に変換する．, 第42回日本骨髄腫学会, May 2017.
54.	天知良太, Shingen Nakamura, Masahiro Hiasa, 小田明日香, バットエルデネアリウンザヤ, Jumpei Teramachi, Hirofumi Tenshin, Keiichiro Watanabe, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 骨形成誘導による骨髄腫細胞のエネルギー代謝の抑制, 第42回日本骨髄腫学会学術集会, May 2017.
55.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, Takeshi Kondo, Mizuho Kinouchi, Naoko Matsui, 細井恵美子, Masahiro Abe, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : γグロブリン療養後に一過性のGAD抗体価上昇がみられた糖尿病の一例, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
56.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 30. 天真寛文, 寺町順平, 小田明日香, 天知良太, , ,破骨細胞系細胞はアポトーシス誘引因子TRAILを生存促進・破骨細胞形成誘導因子として利用する:TAK1-Pim-2経路の役割, 第19回日本癌と骨病変研究会, Nov. 2016.
57.	斎村玉緒, 鶴尾美穂, Akio Kuroda, Takeshi Kondo, Tomoyuki Yuasa, Mizuho Kinouchi, Masahiro Abe, Toshio Matsumoto, 寺澤敏秀 and Munehide Matsuhisa : インスリンポンプの院内検定の試み, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
58.	Jumpei Teramachi, Hiroshi Mori, Yasuo Ochi, Ryota Amachi, Asuka Oda, Masahiro Hiasa, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Potent induction of bone formation by anti-resorptive cathepsin K inhibitor in myeloma., The 77th Annual Meeting of the Japanese Society of Hematology, Oct. 2016.
59.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TAK1 inhibition subverts TRAIL-mediated osteoclastogenesis., 第77回日本血液学会学術集会,, Oct. 2016.
60.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, 小田明日香, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shiroh Fujii, 遠藤逸郎, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Mechanism of the TRPV1 up-regulatation in myeloma cells and adaptation to an acidic microenvironment., 第77回日本血液学会学術集会,, Oct. 2016.
61.	Keiichiro Watanabe, Jumpei Teramachi, Ryota Amachi, 小田明日香, Hirofumi Tenshin, 岩浅正美, Masahiro Hiasa, Shingen Nakamura, 遠藤逸郎, 川谷誠, 長田裕之, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Amelotin gene expression is temporarily being upregulated at the initiation of apoptosis induced by TGFb1 in mouse gingival epithelial cells, 第77回日本血液学会学術集会,, Oct. 2016.
62.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Kiyoe Kurahashi, Takeshi Kondo, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK-1 inhibition disrupts Pim-2-associated and Pim-2-independent key signaling pathways to effectively suppress tumor growth and restore bone formation in myeloma, 第78回日本血液学会学術集会, Oct. 2016.
63.	Keiichiro Watanabe, Jumpei Teramachi, Ryota Amachi, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, 川谷誠, 長田裕之, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : リベロマイシンAによる酸性環境での骨髄腫細胞の治療抵抗性の克服, 日本骨代謝学会学術集会プログラム抄録集 (1349-0761)34回 Page183(2016.07), 183, Jul. 2016.
64.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 破骨細胞はTAK1の発現誘導を介しアポトーシスを抑制しTRAILにより成熟活性化される, 日本骨代謝学会学術集会プログラム抄録集 (1349-0761)34回 Page183(2016.07), 183, Jul. 2016.
65.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Hirofumi Tenshin, Ryota Amachi, 原田武志, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : 骨髄腫腫瘍進展と骨破壊病変形成におけるTAK1-Pim-2経路の役割, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2016.
66.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, 原田武志, Hirofumi Tenshin, Shingen Nakamura, Ryota Amachi, Shiroh Fujii, Keiichiro Watanabe, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pim-2は骨髄腫における破骨細胞形成促進の必須媒介因子である, 第41回日本骨髄腫学会学術集会, May 2016.
67.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAILは破骨細胞に細胞死を誘導せず，破骨細胞分化・生存を促進する., 第41回日本骨髄腫学会, May 2016.
68.	布村俊幸, Sumiko Yoshida, Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa, Toshio Matsumoto and Masahiro Abe : 副腎に接する神経線維腫を合併したレックリングハウゼン病の1例, 第114回日本内科学会四国地方会, May 2016.
69.	橋本晶慶, 鶴尾美穂, 秋田賢子, 森岡隆子, Akio Kuroda, Tomoyuki Yuasa, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Masahiro Abe, Munehide Matsuhisa and 寺澤敏秀 : 糖尿病教室のスタッフ間の相互評価による改善効果, 第59回日本糖尿病学会年次学術集会, May 2016.
70.	Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida and Toshio Matsumoto : グルココルコイド過剰誘導酸化ストレスの臨床的評価とeNOSの有無におけるピタバスタチンの虚血臓器保護効果機構の差異, 平成27年度第1回班会議, Dec. 2015.
71.	鶴尾美穂, Akio Kuroda, Takeshi Kondo, Tomoyuki Yuasa, Mizuho Kinouchi, Masahiro Abe, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : Sensor Angmented Pump(SAP)療法が有効であった高齢1型糖尿病の1例, 第53回日本糖尿病学会中国四国地方会, Oct. 2015.
72.	森岡隆子, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT2阻害薬が著効したprader, 第53回日本糖尿病学会中国四国地方会米子コンベンションセンター, Oct. 2015.
73.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, A Oda, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, H Miki, Kumiko Kagawa, Shiroh Fujii, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Mechanism of the TRPV1 up-regulatation in myeloma cells and adaptation to an acidic microenvironment, 第77回日本血液学会学術集会, Oct. 2015.
74.	Keiichiro Watanabe, Jumpei Teramachi, H Mori, Y Ochi, Ryota Amachi, A Oda, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, H Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Potent induction of bone formation by anti-resorptive cathepsin K inhibitor in myeloma, 第77回日本血液学会学術集会, Oct. 2015.
75.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Potent suppression of osteoclastogenesis in myeloma by Pim inhibition, 第77回日本血液学会学術集会, Oct. 2015.
76.	Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Keiichiro Watanabe, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Tumor reduction and bone restoration in myeloma by TAK-1 inhibition, 第77回日本血液学会学術集会, Oct. 2015.
77.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Hirofumi Tenshin, Ryota Amachi, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : Pim阻害による骨髄種骨病変の治療:破骨細胞形成の抑制, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2015.
78.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Hirofumi Tenshin, Ryota Amachi, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : 骨髄腫腫瘍進展と骨破壊病変形成における TAK-1の枢軸的役割, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Jul. 2015.
79.	Ken-ichi Aihara, Sumiko Yoshida, 上元良子, 石川カズ江 and Toshio Matsumoto : 内因性血清尿酸値およびフェブキソスタットによる頸動脈硬化への影響, 第47回日本動脈硬化学会総会・学術集会, Jul. 2015.
80.	Sumiko Yoshida, Yasumasa Ikeda, Ken-ichi Aihara and Toshio Matsumoto : 心血管病におけるアンドロゲン-AR系の役割, 第33回内分泌代謝学サマーセミナー, Jul. 2015.
81.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : TRAILは破骨細胞分化・生存を促進する:TAK-1による生と死の運命制御, 第1回日本骨免疫学会, 137, Jul. 2015.
82.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, 小田明日香, Hirofumi Tenshin, Keiichiro Watanabe, Shingen Nakamura, Kumiko Kagawa, Hirokazu Miki, Shiroh Fujii, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 酸環境での骨髄腫細胞のDR4発現抑制:酸によるエピジェネティックな遺伝子発現制御, 第1回日本骨免疫学会, 108, Jul. 2015.
83.	Ryota Amachi, Masahiro Hiasa, Jumpei Teramachi, 小田明日香, Keiichiro Watanabe, Hirofumi Tenshin, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Takeshi Kondo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 酸性環境での骨髄腫細胞のTRPV1の発現亢進と酸環境への適応, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 165, Jul. 2015.
84.	Hirofumi Tenshin, Jumpei Teramachi, 小田明日香, Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : アポトーシス誘導因子TRAILによる破骨細胞分化・生存の促進, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 164, Jul. 2015.
85.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masashi Akaike, Toshiaki Tamaki and Toshio Matsumoto : 心血管疾患における男性ホルモンの意義, 第15回日本抗加齢医学会総会シンポジウム「知って得するテストステロンアップデート」, May 2015.
86.	後藤廣平, 鶴尾美穂, Akio Kuroda, 伊澤真弓, Mizuho Kinouchi, Takeshi Kondo, Tomoyuki Yuasa, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT2阻害薬の強化インスリン療法への併用効果の検討, 第58回日本糖尿病学会年次学術集会口演, May 2015.
87.	Ken-ichi Aihara, Sumiko Yoshida, 大黒由加里, Motoyuki Tamaki, Takeshi Kondo, 倉橋清衛, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : ARB基盤高血圧治療の長期心腎保護効果における糖尿病の影響, 第58回総会日本糖尿病学会年次学術集会, May 2015.
88.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 膵β細胞での脂肪毒性における小胞体ストレス応答の役割の解明, 第58回日本糖尿病学会年次学術集会, May 2015.
89.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, 原田武志, Ryota Amachi, Hirofumi Tenshin, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Pim阻害による骨髄腫骨吸収亢進の抑制, 第40回日本骨髄腫学会学術集会, May 2015.
90.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, 原田武志, Ryota Amachi, Hirofumi Tenshin, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : TAK-1は骨髄腫腫瘍進展と骨破壊病変形成の枢軸的な媒介因子である, 第40回日本骨髄腫学会学術集会, May 2015.
91.	Ken-ichi Aihara, Sumiko Yoshida, 大黒由加里, 倉橋清衛, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : 本態性高血圧患者におけるアンジオテンシンII受容体拮抗薬単独およびカルシウム拮抗薬併用による長期心筋保護効果の検証, 第88回日本内分泌学会学術総会, Apr. 2015.
92.	Motoyuki Tamaki, 藤谷与士夫, 原朱美, 福中彩子, 荻原健, 宮塚健, Akio Kuroda, Toshio Matsumoto, 河盛隆造, Munehide Matsuhisa and 綿田裕孝 : 糖尿病発症・進展に関わる新規メカニズムの解明, 第88回日本内分泌学会学術総会シンポジウム, Apr. 2015.
93.	Bingzi Dong, Itsuro Endo, Takeshi Kondo, 大西幸代, Hiroshi Sakaue, 相澤慎一, Masahiro Abe and Toshio Matsumoto : Interleukin-11は脂肪細胞分化を抑制する, 第88回日本内分泌学会, Apr. 2015.
94.	Takeshi Kondo, Itsuro Endo, 大黒由加里, 倉橋清衛, Motoyuki Tamaki, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 遠位尿細管性アシドーシスの確定診断としてアミノレバンRは有用である．, 第112回日本内科学会総会・講演会, Apr. 2015.
95.	大黒由加里, Akio Kuroda, Motoyuki Tamaki, 倉橋清衛, Takeshi Kondo, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Toshio Matsumoto and Munehide Matsuhisa : 皮下注射による強化インスリン療養中の1型糖尿病患者における基礎インスリン比率の検討, 第250回徳島医学会学術集会(大塚講堂), Feb. 2015.
96.	Akio Kuroda, Takeshi Kondo, 安田哲行, 高原充佳, Ken-ichi Aihara, Itsuro Endo, 金藤秀明, 下村伊一郎, Toshio Matsumoto and Munehide Matsuhisa : インスリンポンプ療法での追加インスリン注入時間を規定する因子の検討, 第14回日本先進糖尿病治療研究会(あわぎんホール), Dec. 2014.
97.	大黒由加里, Akio Kuroda, Motoyuki Tamaki, 倉橋清衛, Takeshi Kondo, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Toshio Matsumoto and Munehide Matsuhisa : 皮下注射による強化インスリン療法1型糖尿病患者における基礎インスリン比率の検討, 第12回1型糖尿病研究会(イーグレ姫路), Nov. 2014.
98.	倉橋清衛, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, Ryosuke Sato, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸は膵β細胞の小胞体膜の組成を変化させ，PERK 経路の活性化による翻訳抑制を介してインスリン分泌を低下させる, 第9回臨床ストレス応答学会大会, Nov. 2014.
99.	Jumpei Teramachi, Masahiro Hiasa, 原田武志, Ryota Amachi, Kumiko Kagawa, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Therapeutic impact of Pim inhibition on myeloma bone disease: blockade of NF-B-mediated suppression of osteoblastogenesis and stimulation of osteoclastogenesis, 日本血液学会, Oct. 2014.
100.	浅井廣平, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 伊澤真弓, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT阻害薬の臨床効果の検討, 日本糖尿病学会中国四国地方会第52回総会, Oct. 2014.
101.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 松本直也, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT2阻害薬が著効したPrader Willi syndrome 合併糖尿病の1例, 日本糖尿病学会中国四国地方会第52回総会, Oct. 2014.
102.	荒木迪子, Motoyuki Tamaki, Akio Kuroda, 大黒由加里, 倉橋清衛, Takeshi Kondo, Ken-ichi Aihara, Itsuro Endo, 安芸菜奈子, Toshio Matsumoto and Munehide Matsuhisa : 2型糖尿病患者におけるeGFRの妥当性について, 日本糖尿病学会中国四国地方会第52回総会, Oct. 2014.
103.	Ken-ichi Aihara, Sumiko Yoshida, 大黒由加里, 倉橋清衛, Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : アンジオテンシン受容体拮抗薬およびカルシウム拮抗薬併用による心筋リモデリング抑制の長期効果, 第37日本高血圧学会総会, Oct. 2014.
104.	Motoyuki Tamaki, 荒木迪子, 野崎綾音, 大黒由加里, 倉橋清衛, Takeshi Kondo, Ken-ichi Aihara, Itsuro Endo, 安芸菜奈子, Toshio Matsumoto, Munehide Matsuhisa and Akio Kuroda : 肥満2型糖尿病患者のeGFRは24hrCCrと比較して過小評価されている, 第29回日本糖尿病合併症学会, Oct. 2014.
105.	森本佳奈, Ken-ichi Aihara, 大黒由加里, 倉橋清衛, Takeshi Kondo, Motoyuki Tamaki, 安藝菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : 多剤併用降圧療法と臓器障害モニタリングにより長期にわたり心腎大血管障害の改善が得られた加速型高血圧-悪性高血圧の1例, 第14回日本内分泌学会四国支部学術集会, Sep. 2014.
106.	白川光雄, 本田壮一, Katsuhiko Yoshimoto and Toshio Matsumoto : 抗ランクル抗体を投与した原発性副甲状腺機能亢進症の1例, 第14回日本内分泌学会四国地方会徳島, Sep. 2014.
107.	Ryota Amachi, Masahiro Hiasa, Keiichiro Watanabe, Jumpei Teramachi, 小田明日香, Keiichiro Watanabe, Shingen Nakamura, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 酸が惹起する骨髄腫細胞の酸感受と生存シグナルの悪循環, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 225, Jul. 2014.
108.	Dong Bingzi, Itsuro Endo, Takeshi Kondo, 大西幸代, Masahiro Abe, Seiji Fukumoto, 網塚憲生, 長谷川智香, 相澤慎一 and Toshio Matsumoto : 常染色体優性低Ca血症モデルマウスに対するcalcilyticsの効果, 第32回日本骨代謝学会学術集会, Jul. 2014.
109.	Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Ryota Amachi, Shingen Nakamura, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Pim-2キナーゼはTNF-αによる骨芽細胞分化抑制および破骨細胞形成促進の必須媒介因子である:Pim阻害薬の骨髄腫骨病変改善効果, 第32回日本骨代謝学会学術集会, Jul. 2014.
110.	Itsuro Endo, Masahiro Abe and Toshio Matsumoto : 骨転移に対するdenosumab療法:低Ca血症発現の実態と対策, 第32回日本骨代謝学会, Jul. 2014.
111.	Itsuro Endo, Masahiro Abe and Toshio Matsumoto : 骨転移に対するdenosumab療法, 第32回日本骨代謝学会学術集会, Jul. 2014.
112.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, 上元良子, 石川カズ江, Masashi Akaike and Toshio Matsumoto : 動脈硬化および虚血に対するeNOS非依存的なピタバスタチンの臓器保護効果の検討, 第46回日本動脈硬化学会総会・学術集会, Jul. 2014.
113.	Ken-ichi Aihara, 大黒由加里, 倉橋清衛, Takeshi Kondo, Mizuho Kinouchi, Itsuro Endo, Toshio Matsumoto, Motoyuki Tamaki, Akio Kuroda and Munehide Matsuhisa : エゼチミブとコレスチミドの併用で脂質プロフィルが改善した多発性筋炎合併家族性高コレステロール血症へテロ接合体の一例, 第110回日本内科学会四国地方会, Jun. 2014.
114.	森本佳奈, Ken-ichi Aihara, 大黒由加里, 倉橋清衛, Mizuho Kinouchi, Motoyuki Tamaki, 安藝菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : 多剤併用降圧療法により長期的な心・腎・大血管障害の改善が得られた高レニン性高血圧症の1例, 第3回臨床高血圧フォーラム, May 2014.
115.	大黒由加里, Akio Kuroda, Motoyuki Tamaki, 倉橋清衛, Takeshi Kondo, Mizuho Kinouchi, 近藤絵里, Sumiko Yoshida, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 皮下注射による強化インスリン療法1型糖尿病患者における基礎インスリン比率の検討, 第57回日本糖尿病学会年次学術集会口演, May 2014.
116.	松本幸恵, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 秋田賢子, Mizuho Kinouchi, Takeshi Kondo, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 糖尿病患者の考える指示エネルギー量，指示主食量の調査とその介入, 第57回日本糖尿病学会年次学術集会口演, May 2014.
117.	松本幸恵, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 秋田賢子, Mizuho Kinouchi, Takeshi Kondo, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 糖尿病患者の考える指示エネルギー量，指示主食量の調査とその介入, 第57回日本糖尿病学会年次学術集会, May 2014.
118.	Akiko Hata, Yosuke Shikama, 安藝菜奈子, Chisato Kosugi, 小林寛也, 三好雅士, 中尾隆之, Ayako Tamura, Takako Ichihara, Takako Minagawa, Yumi Kuwamura, Toshio Matsumoto and Makoto Funaki : 徳島県における血清脂肪細胞特異的脂肪酸結合蛋白質とメタボリックシンドローム発症との関連, Journal of the The Japan Diabetes Society, Vol.57, Suppl.1, May 2014.
119.	Itsuro Endo, Dong Bingzi, 長谷川智香, 網塚憲生, Seiji Fukumoto and Toshio Matsumoto : Ca感知受容体関連疾患の最新の知見とその治療, 第87回日本内分泌学会, Apr. 2014.
120.	Ken-ichi Aihara, Mizuho Kinouchi, 大黒由加里, 倉橋清衛, Takeshi Kondo, 安藝菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : 生活習慣病治療薬が血管内皮機能に及ぼす影響の検証, 第111回日本内科学会講演会, Apr. 2014.
121.	菅澤典子, 中山泰介, Hirotsugu Kurobe, 宅見央子, 東口文治, Hajime Kinoshita, Mikio Sugano, Tamotsu Kanbara, Eiki Fujimoto, Ken-ichi Aihara, Takashi Kitaichi, Toshio Matsumoto and Tetsuya Kitagawa : 動脈硬化病巣進展に対する糖転移ヘスペリジンの抑制効果についての検討, 第44回日本心臓血管外科学会学術総会, Feb. 2014.
122.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Sachiko Matsumoto, Daiju Fukuda, 松浦朋美, Takayuki Ise, Koji Yamaguchi, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Michio Shimabukuro, Toshio Matsumoto and Masataka Sata : DPP-4阻害薬の血糖降下作用に対する有効性予測因子, 第248回徳島医学会学術集会, Feb. 2014.
123.	森本佳奈, Ken-ichi Aihara, 大黒由加里, 倉橋清衛, Takeshi Kondo, Mizuho Kinouchi, Motoyuki Tamaki, 安芸菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : 6年間にわたる多剤併用降圧療法が心・腎・大血管障害の改善に寄与した高レニン性高血圧症の1例, 第248回徳島医学会学術集会, Feb. 2014.
124.	大黒由加里, Takeshi Kondo, 倉橋清衛, 安芸菜奈子, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 下垂体の経時的な変化を捉えたシーハン症候群の一例, 第23回臨床内分泌代謝Update, Jan. 2014.
125.	Hwa In, Akio Kuroda, Yuu Tamaki, Masato Tagi, Hiroki Moriguchi, Toshio Matsumoto, Yuichi Fujinaka, 安藝宏信, Tomiaki Morikawa and Munehide Matsuhisa : ITを活用した徳島県糖尿病医療連携システム構築のこころみ, 日本先進糖尿病治療研究会雑誌, 9, 47, Jan. 2014.
126.	Akio Kuroda, Takeshi Kondo, 安田哲行, 高原充佳, Ken-ichi Aihara, Itsuro Endo, 金藤秀明, 下村伊一郎, Toshio Matsumoto and Munehide Matsuhisa : インスリンポンプ療法での追加インスリン注入時間を規定する因子の検討, 第13回日本先進糖尿病治療研究会, Nov. 2013.
127.	大和光, 瀧川稲子, Akiko Matsumura, 山田静恵, 谷佳子, Ken-ichi Aihara, Toshio Matsumoto, Hwa In, Akio Kuroda and Munehide Matsuhisa : 徳島大学病院における糖尿病透析予防指導の有用性の検討, 日本糖尿病学会中国四国地方会第51回総会, Nov. 2013.
128.	大黒由加里, Takeshi Kondo, Akio Kuroda, 倉橋清衛, Mizuho Kinouchi, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 過剰基礎インスリン量が不適切な間食摂取に関連したインスリンポンプ使用1型糖尿病の2例, 日本糖尿病学会中国四国地方会第51回総会, Nov. 2013.
129.	松本幸恵, Akio Kuroda, 秋田賢子, 鶴尾美穂, Mizuho Kinouchi, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 主食の摂取状況調査, 日本糖尿病学会中国四国地方会第51回総会, Nov. 2013.
130.	Takeshi Kondo, 大黒由加里, Akio Kuroda, 倉橋清衛, Mizuho Kinouchi, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : テストステロン補充で速やかにインスリン抵抗性が改善した汎下垂体機能低下症合併糖尿病例, 日本糖尿病学会中国四国地方会第51回総会, Nov. 2013.
131.	Ken-ichi Aihara, Mizuho Kinouchi, 大黒由加里, Takeshi Kondo, 倉橋清衛, 安藝菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : メタボリックシンドロームおよび糖尿病の有無が血管内皮機能に及ぼす影響, 日本糖尿病学会中国四国地方会第51回総会, Nov. 2013.
132.	Takeshi Kondo, 大黒由加里, Akio Kuroda, 倉橋清衛, Mizuho Kinouchi, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : テストステロン補充で速やかにインスリン抵抗性が改善した汎下垂体機能低下症合併糖尿病例, 日本糖尿病学会中国四国地方会第51回総会, Nov. 2013.
133.	Ken-ichi Aihara, Mizuho Kinouchi, Sumiko Yoshida, 大黒由加里, 倉橋清衛, Takeshi Kondo, 安藝菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : 糖代謝異常の血管機能評価に及ぼす効果, 第36回日本高血圧学会総会, Oct. 2013.
134.	Keiichiro Watanabe, Masahiro Abe, H Mori, K Udaka, M Iwasa, D Hanson, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, Shingen Nakamura, H Miki, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka and Toshio Matsumoto : Bone restoration and tumor suppression in myeloma by cathepsin K inhibition with Bortezomib, 第75回日本血液学会学術集会, Oct. 2013.
135.	Ryota Amachi, Keiichiro Watanabe, Masahiro Hiasa, Masahiro Abe, Toshio Matsumoto and Eiji Tanaka : 酸性環境が骨髄腫細胞の破骨細胞活性に及ぼす影響, 第72回日本矯正歯科学会大会プログラム・抄録集, Oct. 2013.
136.	Kiyoe Kurahashi, 森智子, 野村明利, Atsushi Ogura, 津川和江, 宮本千伸, Masato Miyake, Miho Oyadomari, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸は小胞体膜の流動性低下によるPERK経路の活性化を介して膵β細胞におけるインスリン分泌を低下させる, 第86回日本生化学会大会, Sep. 2013.
137.	Kiyoe Kurahashi, 森智子, Akitoshi Nomura, Atsushi Ogura, 津川和江, 宮本千伸, Masato Miyake, Miho Oyadomari, Toshio Matsumoto and Seiichi Oyadomari : ポスター発表飽和脂肪酸は小胞体膜の流動性低下によるPERK経路の活性化を介して膵β細胞におけるインスリン分泌を低下させる, 第86回日本生化学会大会, Sep. 2013.
138.	大黒由加里, Takeshi Kondo, Shiroh Fujii, Shingen Nakamura, 倉橋清衛, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 著名な汎血球減少と肝筋逸脱酵素高値を呈した神経性食欲不振症の一例, 第13回日本内分泌学会四国支部学術集会, Sep. 2013.
139.	Takeshi Kondo, 岩佐昌美, 大黒由加里, 倉橋清衛, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 不動が惹起した高カルシウム血症で頻回の意識障害を来たした一例, 第13回日本内分泌学会四国支部学術集会, Sep. 2013.
140.	鈴木麗子, 大和光, 瀧川稲子, Ken-ichi Aihara, Itsuro Endo, 安芸菜奈子, 倉橋清衛, Toshio Matsumoto, Akio Kuroda and Munehide Matsuhisa : フットケア外来におけるインスリン皮下硬結の実態調査と皮下硬血患者への介入の結果報告, 第13回日本糖尿病情報学会年次学術集会, Aug. 2013.
141.	本田壮一, 小原聡彦, 橋本崇代, Katsuhiko Yoshimoto and Toshio Matsumoto : 長期臥床の入院患者の増加—骨粗鬆症—, 第247回徳島医学会学術集会, Aug. 2013.
142.	Mizuho Kinouchi, Ken-ichi Aihara, Sumiko Yoshida, 大黒由加里, 倉橋清衛, Takeshi Kondo, 安藝菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : 臨床血管機能における糖代謝異常の影響の解析, 第247回徳島医学会学術集会, Aug. 2013.
143.	Ken-ichi Aihara, Mizuho Kinouchi, Sumiko Yoshida, 岩佐昌美, 倉橋清衛, Takeshi Kondo, 安藝菜奈子, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Toshio Matsumoto : Evaluation for influence of diabetes on clinical vascular function, 第45回日本動脈硬化学会総会・学術集会, Jul. 2013.
144.	Ken-ichi Aihara, Toshio Matsumoto, Munehide Matsuhisa and 大和光 : 血管年齢を正確に知ってアンチエイジング!, 第13回日本抗加齢医学会総会, Jun. 2013.
145.	Michihiro Nakamura, Koichiro Hayashi, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura : 有機シリカ・マルチ蛍光ナノプローブによるSeamless蛍光イメーシング, 第8回日本分子イメージング学会学術集会, May 2013.
146.	Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : An acdic milieu confers the resistance to TRAIL in myeloma cells through the PI3K-Akt-mediated epigenetic down-regulation of the TRAIL receptor DR4, International Bone and Mineral Society 2013, May 2013.
147.	Keiichiro Watanabe, Masahiro Abe, H Mori, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto : Induction of cathepsin K induce bone formation in myeloma osteolytic lesions, International Bone and Mineral Society 2013, May 2013.
148.	鈴木麗子, 瀧川稲子, 大和光, 菊恵木田, Ken-ichi Aihara, Itsuro Endo, 安芸菜奈子, 倉橋清衛, Toshio Matsumoto, Akio Kuroda and Munehide Matsuhisa : フットケア外来におけるインスリン皮下硬結の実態調査と皮下硬結患者への介入の有用性検討, 第56回日本糖尿病学会年次学術集会, May 2013.
149.	藤島周子, 森岡隆子, 高田妙子, 岩谷沙紀, 斎村玉緒, 秋田賢子, 松本幸恵, Takeshi Kondo, Sumiko Yoshida, Tomoyuki Yuasa, 鶴尾美穂, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 当院の参加型糖尿病教室の取り組み, 第56回日本糖尿病学会年次学術集会, May 2013.
150.	伊澤真弓, Akio Kuroda, 上野裕子, 堀筋富士子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : インスリン注入器に関する患者の意識調査, 第56回日本糖尿病学会年次学術集会, May 2013.
151.	Kiyoe Kurahashi, 三浦直子, 宮本千伸, 津川和江, 森智子, Miho Oyadomari, Masato Miyake, Atsushi Ogura, Toshio Matsumoto and Seiichi Oyadomari : 膵β細胞における飽和脂肪酸による脂肪毒性に小胞体膜流動性の低下とPERK経路が影響する, 第56回日本糖尿病学会年次学術集会, May 2013.
152.	鶴尾美穂, Akio Kuroda, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : インスリン治療患者に対するチーム医療で行う段階的糖尿病療養指導の試み, 第56回日本糖尿病学会年次学術集会, May 2013.
153.	Akio Kuroda, 鶴尾美穂, Ken-ichi Aihara, Itsuro Endo, 安芸菜奈子, Sumiko Yoshida, Takeshi Kondo, Toshio Matsumoto and Munehide Matsuhisa : 1型糖尿病患者におけるインスリングラルギンからインスリンデグルデッグへの同量での切り替え:CGMSを用いた検討, 第56回日本糖尿病学会年次学術集会, May 2013.
154.	Takeshi Kondo, Akio Kuroda, Sumiko Yoshida, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 頻回インスリン療法による厳格な血糖管理下におけるシダグリプチン併用のインスリン所要量現象効果の検討, 第56回日本糖尿病学会年次学術集会ポスター, May 2013.
155.	奥村滋子, Akio Kuroda, 片田英子, 澤井敏子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 運転中の低血糖についての意識調査, 第56回日本糖尿病学会年次学術集会, May 2013.
156.	Akiko Hata, Yukiko Bandou, Yosuke Shikama, 安藝菜奈子, Chisato Kosugi, 西村美穂, 阿部房代, 佐藤美子, 中奥真理子, 片山りか, 赤松康代, Tohru Sakai, Emi Shuto, Rie Tsutsumi, Ayako Tamura, Takako Ichihara, Takako Minagawa, Yumi Kuwamura, 中尾隆之, 三好雅士, Hiroki Moriguchi, Yuu Tamaki, Toshio Matsumoto and Makoto Funaki : 徳島県におけるadiponectinや高感度CRPとメタボリックシンドロームとの関連, Journal of the The Japan Diabetes Society, Vol.56, Suppl.1, S.208, May 2013.
157.	Takeshi Kondo, Akio Kuroda, 曽我部公子, Sumiko Yoshida, 安藝菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 術前後で持続血糖測定(CGM)を比較しえたアドレナリン優位褐色細胞腫の1例, 第56回日本糖尿病学会年次学術集会, May 2013.
158.	Takeshi Kondo, 尾松卓, 董冰子, 大西幸代, 相澤慎一, Itsuro Endo and Toshio Matsumoto : インターロイキン(IL)-11は骨形成促進に必要である, 第86回日本内分泌学会学術集会, Apr. 2013.
159.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Matomo Sakari, Takahiro Matsumoto, Masashi Akaike, Masataka Sata and Toshio Matsumoto : アンドロゲン受容体は性差非依存的にVEGF受容体を介して虚血反応性血管新生を促進する, 第86回日本内分泌学会学術総会, Apr. 2013.
160.	秦明子, Yukiko Bandou, Yosuke Shikama, 安藝菜奈子, Chisato Kosugi, 西村美穂, 阿部房代, 佐藤美子, 中奥真理子, 片山りか, 赤松康代, 丹下幸子, Tohru Sakai, Emi Shuto, Rie Tsutsumi, Ayako Tamura, Takako Ichihara, Takako Minagawa, Yumi Kuwamura, Yumi Kuwamura, Takayuki Nakao, Masashi Miyoshi, Hiroki Moriguchi, Yuu Tamaki, Toshio Matsumoto and Makoto Funaki : 徳島県におけるadiponectinや高感度CRPとメタボリックシンドロームとの関連, Journal of the The Japan Diabetes Society, 56, Apr. 2013.
161.	松本和久, Sumiko Yoshida, Ken-ichi Aihara, 岩佐昌美, Takeshi Kondo, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, 安芸菜奈子, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : 膵臓の鉄過剰沈着とインスリン分泌不全を呈した無セルロプラスミン血症合併糖尿病の1例, 第86回日本内分泌学会学術総会, Apr. 2013.
162.	三橋威史, Ken-ichi Aihara, Sumiko Yoshida, 上元良子, 石川カズ江 and Toshio Matsumoto : 粥状動脈硬化モデルにおけるピタバスタチンの臓器保護効果の検討, 第86回日本内分泌学会学術総会, Apr. 2013.
163.	松本和久, Ken-ichi Aihara, Sumiko Yoshida, Mizuho Kinouchi, Takeshi Kondo, 倉橋清衛, 安藝菜奈子, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : 膵臓の鉄過剰沈着とインスリン分泌不全を呈した無セルロプラスミン血症合併糖尿病の1例, 第86回日本内分泌学会学術総会, Apr. 2013.
164.	Ken-ichi Aihara, Sumiko Yoshida, 上元良子, 石川カズ江, Masashi Akaike and Toshio Matsumoto : 重症下肢虚血壊死に対するピタバスタチンの組織保護効果に関する検討, 第86回日本内分泌学会学術総会, Apr. 2013.
165.	Ryota Amachi, Keiichiro Watanabe, Shiroh Fujii, T Harada, H Miki, S Nakamura, A Oda, Masahiro Hiasa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : An acdic milieu suppresses histone acetylation in myeloma cells to down-regulate the TRAIL receptor DR4 expression, 14th International Myeloma Workshop, Apr. 2013.
166.	Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, T Harada, Shiroh Fujii, S Nakamura, H Miki, K Kagawa, I Endo, Eiji Tanaka and Toshio Matsumoto : Induction of bone formation in myeloma osteolytic lesions by cathepsin K inhibition, 14th International Myeloma Workshop, Apr. 2013.
167.	曽我部公子, Takeshi Kondo, Akio Kuroda, Sumiko Yoshida, Nanako Kataoka, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 術前後で持続血糖測定(CGM)を比較しえた褐色細胞腫の一例, 第22回臨床内分泌代謝Update, Jan. 2013.
168.	牟田口惇, Takeshi Kondo, Itsuro Endo, Sumiko Yoshida, Nanako Kataoka, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 尿細管性アシドーシスの診断にアミノレバンが有用であった一例, 第22回臨床内分泌代謝Update, Jan. 2013.
169.	幸田舞子, Takeshi Kondo, Itsuro Endo, Sumiko Yoshida, Nanako Kataoka, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 悪性症候群様の症状から診断されたACTH分泌低下症の一例, 第22回臨床内分泌代謝Update, Jan. 2013.
170.	Itsuro Endo, Toshio Matsumoto and 福本誠二 : FGF23関連低リン血症性疾患の全国疫学調査(最終報告), 厚生労働科学研究費補助金難治疾患克服研究事業ホルモン受容機構異常に関する調査研究, Jan. 2013.
171.	Kiyoe Kurahashi, 森智子, Hiroshi Inoue, Atsushi Ogura, 津川和江, Masato Miyake, Hiroshi Inoue, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸による膵β細胞のインスリン分泌低下には小胞体膜流動性の変化による小胞体ストレスが関与し，PERK経路の活性化により改善される, 第85回日本生化学会大会, Dec. 2012.
172.	Hirokazu Miki, Shingen Nakamura, 竹内恭子, 原田武志, 岩佐昌美, Shiroh Fujii, Kumiko Kagawa, Masahiro Abe and Toshio Matsumoto : 赤芽球癆を合併した多中心性Castleman病の1例, 日本内科学会第107回四国地方会, Dec. 2012.
173.	松崎苑美, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Takeshi Kondo, Itsuro Endo, Toshio Matsumoto, Nanako Kataoka, Akio Kuroda and Munehide Matsuhisa : 血栓性微小血管障害症様の病態を示したメタボリックシンドロームの1例, 第107回日本内科学会四国地方会, Dec. 2012.
174.	佐埜弘樹, Ken-ichi Aihara, Sumiko Yoshida, Takeshi Kondo, 倉橋清衛, Itsuro Endo, Toshio Matsumoto, Akio Kuroda, Munehide Matsuhisa and Nanako Kataoka : 正常MRI所見を示し，ADH放出障害が主因と考えられた中枢性尿崩症の1例, 日本内科学会第107回四国地方会, Dec. 2012.
175.	Akio Kuroda, 新居沙央里, Sumiko Yoshida, 近藤絵里, Itsuro Endo, Ken-ichi Aihara, 松本友里, Nanako Kataoka, Toshio Matsumoto and Munehide Matsuhisa : 新たなインスリンポンプParadigm722によってカーボカウントのみで血糖管理が可能となった1症例, 第12回日本先進糖尿病治療学会研究会, Dec. 2012.
176.	Akio Kuroda, 高原充佳, 安田哲行, 松岡孝昭, Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara, Sumiko Yoshida, Toshio Matsumoto, 下村伊一郎, 金藤秀明 and Munehide Matsuhisa : 日本人1型糖尿病患者における「500ルールとは?」, 第12回日本先進糖尿病治療研究会, Dec. 2012.
177.	Toshio Matsumoto : 新時代の骨粗鬆症治療, 第85回日本内分泌学会学術総会ランチョンセミナー12, Dec. 2012.
178.	Sumiko Yoshida, Takeshi Kondo, 倉橋清衛, Itsuro Endo, Ken-ichi Aihara, 高島啓, Koji Yamaguchi and Toshio Matsumoto : 難治性冠攣縮性狭心症を合併した無痛性甲状腺炎の1例, 第55回日本甲状腺学会学術集会, 88, 2, 516, Nov. 2012. (Keyword) Thiamazole(治療的利用) Thyroxine(治療的利用) 狭心症-異型(合併症,薬物療法) 甲状腺炎-自己免疫性(合併症,画像診断,薬物療法) Nicorandil(治療的利用) *甲状腺炎-無痛性(合併症,画像診断,薬物療法) ヒト中年(45~64) 男
179.	幸田舞子, Takeshi Kondo, Akio Kuroda, Sumiko Yoshida, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : シタグリプチン投与によりインスリン所要量の減少効果が得られた高齢2型糖尿病の一例, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
180.	Takeshi Kondo, Akio Kuroda, 曽我部公子, Sumiko Yoshida, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 術前後で持続血糖測定(CGM)を比較しえたアドレナリン優位褐色細胞腫の一例, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
181.	Takeshi Kondo, Akio Kuroda, 曽我部公子, Sumiko Yoshida, 安芸菜奈子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : アドレナリン優位の褐色細胞腫の術前後で持続血糖測定(CGM)により血糖変動を比較した一例, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
182.	伊澤真弓, Akio Kuroda, 上野裕子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : インスリン注入器に関する患者の意識調査, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
183.	幸田舞子, Takeshi Kondo, Akio Kuroda, Sumiko Yoshida, Nanako Kataoka, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : シタグリプチン投与によりインスリン所要量の減少効果が得られた高齢2型糖尿病の一例, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
184.	岩佐昌美, Akio Kuroda, Sumiko Yoshida, Takeshi Kondo, Nanako Kataoka, Itsuro Endo, Ken-ichi Aihara, 福島泰江, Munehide Matsuhisa and Toshio Matsumoto : 血糖管理基準を満たすために分割食を必要としなかった2型糖尿病合併妊娠の1例, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
185.	奥村滋子, Akio Kuroda, 片田英子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, 松本直也, 笠松哲司, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 運転中の低血糖についての意識調査, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
186.	小田直輝, 悦子李, 松本真弓, 高松典道, Hirokazu Miki and Toshio Matsumoto : 輸血後7日目にIgG抗E抗体を酵素法にて強く検出した一症例, 第45回中四国支部医学検査学会, Nov. 2012.
187.	小田直輝, 悦子李, 松本真弓, 高松典道, Hirokazu Miki and Toshio Matsumoto : 輸血後7日目にIgG抗E抗体を酵素法にて強く検出した一症例, 第45回中四国支部医学検査学会, Nov. 2012.
188.	Itsuro Endo, 大薗卓也, 斉藤光恵, Toshio Matsumoto and Masahiro Abe : 骨転移に対するdenosumab 120mg皮下注後の重症低Ca血症発現の実態, 癌と骨代謝研究会, Nov. 2012.
189.	Shiroh Fujii, Masahiro Abe, Ryota Amachi, Keiichiro Watanabe, Masahiro Hiasa, 竹内恭子, 岩佐昌美, 原田武志, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Toshio Matsumoto : Pim inhibition preferentially induces anti-myeloma activity in an acidic milien, 第74回日本血液学会学術集会, Oct. 2012.
190.	Masahiro Hiasa, Masahiro Abe, Kumiko Kagawa, Hirokazu Miki, Shingen Nakamura, Harada Takeshi, Fujii Shirou, Keiichiro Watanabe, Ryota Amachi, Kenzo Asaoka and Toshio Matsumoto : Pim-2 acts as a common downstream mediator to suppress bone formation in myeloma., 第74回に本血液学会, Oct. 2012.
191.	Ryota Amachi, Masahiro Abe, Keiichiro Watanabe, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto : An acidic milieu suppresses DR4 editing and induces p22 c-FLIP to cause myeloma resistance to TRAIL, 第74回日本血液学会学術集会, Oct. 2012.
192.	Toshio Matsumoto : 骨粗鬆症治療の進歩, 第26回日本臨床内科医学会教育講演, Oct. 2012.
193.	Toshio Matsumoto : 骨粗鬆症治療の進歩と高齢者の骨折予防, 平成24年度日本内科学会生涯教育講演会, Sep. 2012.
194.	Toshio Matsumoto : 宇宙飛行に伴う骨量減少とその防止対策, 市民公開講演会「震災後の我が国における宇宙開発のあり方」, Sep. 2012.
195.	悦子李, 瀧本朋美, 松本真弓, Kazuhisa Maeda, Shuji Ozaki, Hirokazu Miki and Toshio Matsumoto : 血液型検査から無症候性の低ガンマグロブリン血症が判明し，周産期の感染予防に貢献し得た一例, 第57回日本輸血・細胞治療学会中国四国地方会, Sep. 2012.
196.	Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, Takeshi Kondo, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : 高尿酸血症は頸動脈プラークおよび血管抵抗を亢進させる, 第35回日本高血圧学会総会, 423, Sep. 2012. (Keyword) 頸動脈疾患血管抵抗動脈硬化症-アテローム性高尿酸血症 *動脈硬化プラークヒト男女
197.	白河綾, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Takeshi Kondo, Itsuro Endo, 安藝菜奈子, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : 副腎不全症状を呈し，診断に苦慮した両側副腎B細胞リンパ腫の1例, 第12回日本内分泌学会四国支部学術集会, Sep. 2012.
198.	原田武志, Shuji Ozaki, 岩佐昌美, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, 柴田泰伸, 重清俊雄, 岡田直人, 長尾多美子, 鈴木麗子, Shoji Sakiyama, Masahiro Abe and Toshio Matsumoto : 徳島県のエイズ拠点病院におけるHIV感染症及び後天性免疫不全症候群の現状, 第245回徳島県医学会学術総会, Jul. 2012.
199.	Toshio Matsumoto : RANKLシグナルと癌の骨病変, 第30回日本骨代謝学会学術集会ランチョンセミナー9, Jul. 2012.
200.	Keiichiro Watanabe, Masahiro Abe, Ryota Amachi, Masahiro Hiasa, Shingen Nakamura, 遠藤逸郎, 森裕史, Eiji Tanaka and Toshio Matsumoto : カテプシンK 阻害剤KK1-300-01 は骨髄腫骨病変部の骨破壊を抑制し骨形成を惹起する, 第30回日本骨代謝学会学術大会, 217, Jul. 2012.
201.	Toshio Matsumoto : 骨代謝治療薬としての新規活性型ビタミンD製剤の位置づけ, 第30回日本骨代謝学会集会シンポジウム4, Jul. 2012.
202.	Toshio Matsumoto : 宇宙飛行に伴う骨量減少とその防止対策, 第30回日本骨代謝学会学術集会JAXA共催シンポジウム, Jul. 2012.
203.	Toshio Matsumoto : 骨代謝治療薬としての新規活性型ビタミンD製剤の位置づけ, 第30回日本骨代謝学会集会シンポジウム4, Jul. 2012.
204.	Ken-ichi Aihara, Sumiko Yoshida and Toshio Matsumoto : シンポジウム11 心・血管病の性差:血管形態と機能解析からみた頸動脈硬化の性差と副腎アンドロゲンDHEASの抗動脈硬化作用, 第44回日本動脈硬化学会・学術総会/ヒルトン福岡シーホーク, Jul. 2012.
205.	Ken-ichi Aihara, Sumiko Yoshida and Toshio Matsumoto : 血管形態と機能解析からみた頸動脈硬化の性差と副腎アンドロゲンDHEASの抗動脈硬化作用, 第44回日本動脈硬化学会総会・学術集会: シンポジウム11 心・血管病の性差, Jul. 2012.
206.	Masahiro Hiasa, Masahiro Abe, Rieko Arakaki, Akiko Yamada, Kenzo Asaoka, Toshio Matsumoto, Yoshio Hayashi and Naozumi Ishimaru : RelB antagonizes the classical NF-κB pathway and its suppression of osteoblastogenesis, 第30回日本骨代謝学会, Jul. 2012.
207.	Sumiko Yoshida, Ken-ichi Aihara, Mizuho Kinouchi, 近藤絵里, Itsuro Endo and Toshio Matsumoto : Diabetes abolishes protective effect of HDL-cholesterol against endothelial dysfunction., 第44回日本動脈硬化学会総会・学術集会, Jul. 2012.
208.	Toshio Matsumoto : ビスホスホネート治療の新たな展開, 第30回骨代謝学会学術集会ランチョンセミナー, Jul. 2012.
209.	Takeshi Kondo, 尾松卓, 董冰子, 大西幸代, 相澤慎一, Itsuro Endo and Toshio Matsumoto : インターロイキン(IL)-11は力学的負荷による骨形成促進に必要である, 第30回日本骨代謝学会学術総会, Jul. 2012.
210.	尾松卓, Takeshi Kondo, 董冰子, 大西幸代, Itsuro Endo and Toshio Matsumoto : PKCδは骨再構築系の制御に重要である, 第30回日本骨代謝学会学術総会, Jul. 2012.
211.	Ryota Amachi, Masahiro Abe, Keiichiro Watanabe, Shingen Nakamura, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto : 酸性環境は骨髄腫細胞にDR4 の発現抑制とcFLIP の活性化を惹起しTRAIL に対する抵抗性を獲得させる, 第30回日本骨代謝学会学術集会, 259, Jul. 2012.
212.	Itsuro Endo, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Nanako Kataoka, Takeshi Kondo, 近藤絵里, Ken-ichi Aihara, Toshio Matsumoto, Akio Kuroda and Munehide Matsuhisa : Werner症候群に伴う糖尿病の治療経過, 第106回日本内科学会四国地方会, Jun. 2012.
213.	Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Takeshi Kondo, 近藤絵里, Nanako Kataoka, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : インクレチン関連薬を用いた周術期血糖管理の有用性, 第106回日本内科学会四国地方会, Jun. 2012.
214.	大黒由加里, Shingen Nakamura, 岩佐昌美, 原田武志, Shiroh Fujii, Kumiko Kagawa, Masahiro Abe, Toshio Matsumoto and Hirokazu Miki : 腰痛と副腎不全症状で発症した両側副腎原発DLBCLの1例, 日本内科学会第106回四国地方会, Jun. 2012.
215.	李悦子, 瀧本朋美, 松本真弓, 石井博之, 福森泰雄, Shuji Ozaki, 竹内恭子 and Toshio Matsumoto : 亜型遺伝子AelおよびAx03を同時に保有していた非常にまれな亜型症例, 第60回日本輸血・細胞治療学会総会, May 2012.
216.	Michihiro Nakamura, Koichiro Hayashi, Aziz Awaad, Hirokazu Miki, Shuji Ozaki, Masahiro Abe, Toshio Matsumoto and Kazunori Ishimura : 有機シリカ粒子技術を用いた近赤外蛍光ナノプローブの作製とユニバーサル蛍光イメージング, 第7回日本分子イメージング学会学術集会, May 2012.
217.	Toshio Matsumoto : 骨粗鬆症の進歩, 中外骨粗鬆症セミナー, May 2012.
218.	鶴尾美穂, 寺澤敏秀, 木戸里佳, Sumiko Yoshida, Tomoyuki Yuasa, Takeshi Kondo, 笠松哲司, 近藤絵里, Mizuho Kinouchi, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and Masashi Akaike : 粥状動脈硬化病変を呈した高Lp(a)血症合併糖尿病の姉妹例, 第55回日本糖尿病学会年次学術集会, May 2012.
219.	上野裕子, 堀筋富士子, 森岡隆子, 鶴尾美穂, Tomoyuki Yuasa, 木戸里佳, Sumiko Yoshida, Mizuho Kinouchi, Takeshi Kondo, 近藤絵里, 笠松哲司, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : サイトローテーションシート(SLS)を使用したインスリン自己注射の指導, 第55回日本糖尿病学会年次学術集会, May 2012.
220.	秋田賢子, 鶴尾美穂, 木戸里佳, Sumiko Yoshida, 近藤絵里, Mizuho Kinouchi, Takeshi Kondo, 笠松哲司, Tomoyuki Yuasa, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : カーボカウントを導入した高齢1型糖尿病の3例, 第55回日本糖尿病学会年次学術集会, May 2012.
221.	倉橋清衛, Taiji Ito, Akitoshi Nomura, 宮本千伸, 津川和江, 森智子, Miho Oyadomari, Toshio Matsumoto and Seiichi Oyadomari : 膵β細胞におけるグルコース応答性インスリン分泌低下に小胞体膜の流動性変化と小胞体ストレスが応答が影響する, 第55回日本糖尿病学会学術集会, May 2012.
222.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペントエン酸は酸化ストレス抑制を介して心臓リモデリングを抑制する, 日本高血圧学会第1回臨床高血圧フォーラム, May 2012. (Keyword) Eicosapentaenoic Acid(薬理学,治療的利用) 疾患モデル(動物) 心臓血管疾患(超音波診断,病理学,予防) 酸化ストレス BALB Cマウス心室リモデリング(予防) ヒトマウス動物男女
223.	Ken-ichi Aihara, Sumiko Yoshida, Masashi Akaike and Toshio Matsumoto : 血管内皮機能制御における血圧関連指標の意義, 日本高血圧学会第1回臨床高血圧フォーラム, May 2012.
224.	Jun Huang, Shinji Abe, Yuki Morita, Shuji Ozaki, Masatoshi Kishuku, Kazuo Minakuchi, Masaki Hanibuchi, Toshio Matsumoto, Saburo Sone and Yasuhiko Nishioka : Antibody-dependent cellular cytotoxicity against mesothelioma cells mediated by anti-HM 1.24 antibodies, 第52回日本呼吸器学会学術講演会, Apr. 2012.
225.	大黒由加里, Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, Takeshi Kondo, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Nanako Kataoka, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : 摂食障害による著明な低K血症を呈した視床下部性ACTH分泌低下症の1例, 第85回日本内分泌学会学術総会, Apr. 2012.
226.	Takeshi Kondo, 尾松卓, 董冰子, 大西幸代, 相澤慎一, Itsuro Endo and Toshio Matsumoto : インターロイキン(IL)-11は力学的負荷およびPTHによる骨量増加に必要である, 第85回日本内分泌学会学術総会, Apr. 2012.
227.	Toshio Matsumoto : 骨粗鬆症診断の進歩と今後の展望, 第85回日本内分泌学会学術総会, Apr. 2012.
228.	Sumiko Yoshida, Ken-ichi Aihara, 近藤絵里, 倉橋清衛, Takeshi Kondo, Mizuho Kinouchi, Itsuro Endo, Toshio Matsumoto, Nanako Kataoka, Akio Kuroda and Munehide Matsuhisa : 糖尿病はHDLコレステロールによる血管内皮機改善効果を減弱させる, 第85回日本内分泌学会学術総会, Apr. 2012.
229.	Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, Takeshi Kondo, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Nanako Kataoka, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : ヘパリンコファクターⅡは耐糖能制御因子である, 第85回日本内分泌学会学術総会, Apr. 2012.
230.	Sumiko Yoshida, Yuichi Fujinaka, Ken-ichi Aihara, 鈴木麗子, Mizuho Kinouchi, 近藤絵里, 安藝菜奈子, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : 当院検診受診者における耐糖能異常の特徴, 第109回日本内科学会総会・講演会, Apr. 2012.
231.	Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, Takeshi Kondo, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : 尿酸は形態および機能的頸動脈硬化症進展のリスク因子である, 第109回日本内科学会総会・講演会, Apr. 2012.
232.	原田武志, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 中野綾子, Kumiko Kagawa, 竹内恭子, Masahiro Abe and Toshio Matsumoto : 徳島県における多発性骨髄腫の治療成績の検討, 第109回日本内科学会総会・講演会, Apr. 2012.
233.	Toshio Matsumoto : あなたの骨は，大丈夫?, 第85回日本内分泌学会学術総会市民公開講座, Apr. 2012.
234.	Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, Takeshi Kondo, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : 尿酸は形態および機能的頸動脈硬化症進展のリスク因子である, 第109回日本内科学会総会・講演会, Apr. 2012. (Keyword) 危険因子頸動脈疾患(診断) 動脈硬化症(診断) *Uric Acid(血液) 頸動脈内膜中膜肥厚度ヒト
235.	原田武志, Shuji Ozaki, 小田明日香, 天羽宏枝, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 中野綾子, Kumiko Kagawa, 竹内恭子, Masahiro Abe, 柴田泰伸 and Toshio Matsumoto : Lenalidomide 治療中の多発性骨髄腫患者におけるCRP上昇の検討, 第51回日本血液学会中国四国地方会, Mar. 2012.
236.	Kumiko Kagawa, 原田武志, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 竹内恭子, Masahiro Abe and Toshio Matsumoto : 遺伝子組み替えヒトトロンボモジュリン投与中に硬膜下血腫を来した同腫骨髄移植2症例, 第34回日本造血細胞移植学会, Feb. 2012.
237.	Kumiko Kagawa, 原田武志, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, 竹内恭子, Masahiro Abe and Toshio Matsumoto : 遺伝子組み換えヒトトロンボモジュリン投与中に硬膜下血腫を来した同腫骨髄移植2症例, 第34回日本造血細胞移植学会, Feb. 2012.
238.	立花綾香, 田岡志保, 荻野寛隆, 高橋真美子, Ken-ichi Aihara, Sumiko Yoshida, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa, 福森智治 and Toshio Matsumoto : 低血圧で推移したvon Hippel-Lindau 病・褐色細胞腫の1手術例, 第21回臨床内分泌代謝Update in Hamamatsu, Jan. 2012.
239.	田岡志保, 立花綾香, 荻野寛隆, 高橋真美子, Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, 倉橋清衛, Itsuro Endo, Toshio Matsumoto, Nanako Kataoka, Akio Kuroda and Munehide Matsuhisa : 周術期血糖管理にリラグルチドが有用であった2型糖尿病患者の2例, 第21回臨床内分泌代謝Update in Hamamatsu, Jan. 2012.
240.	Shinsuke Kido, 橋本由衣, 藤原真理奈, Itsuro Endo, Hiroko Segawa, Sawako Tatsumi, Toshio Matsumoto and Ken-ichi Miyamoto : 糖尿病に併存する腎障害・骨障害の発症及び進展におけるFGF23の関与, 第15回日本病態栄養学会年次学術集会, Jan. 2012.
241.	Itsuro Endo, 福本誠二 and Toshio Matsumoto : FGF23関連性低リン血症性疾患の全国疫学調査最終報告, 厚生労働科学研究費補助金ホルモン受容機構異常に関する調査研究平成23年度研究報告会, Jan. 2012.
242.	Masahiro Hiasa, Rieko Arakaki, Akiko Yamada, Ritsuko 徳永律子 Oura, Masahiro Abe, Toshio Matsumoto, Yoshio Hayashi, Naozumi Ishimaru and Kenzo Asaoka : A novel role of NF-B relB in bone remodeling., 第40回日本免疫学会学術集会, Nov. 2011.
243.	Akio Kuroda, 新居沙央理, Sumiko Yoshida, 近藤絵里, Itsuro Endo, Ken-ichi Aihara, 松本友里, Nanako Kataoka, Toshio Matsumoto and Munehide Matsuhisa : 新たなインスリンポンプParadigm722によってカーボカウントのみで血糖管理が可能となった1症例, 第11回日本先進糖尿病治療研究会, Nov. 2011.
244.	橋本由衣, Shinsuke Kido, 藤原真理奈, 近藤剛史, Hiroko Segawa, Itsuro Endo, Sawako Tatsumi, Toshio Matsumoto and Ken-ichi Miyamoto : 糖尿病合併症発症におけるFGF23/Klothoの関与, 第44回日本栄養食糧学会中四国支部大会, Nov. 2011.
245.	Keiichiro Watanabe, Masahiro Abe, Q Cui, Masahiro Hiasa, M Kawatani, T Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, A Nakano, K Kagawa, K Takeuchi, H Osada, Eiji Tanaka and Toshio Matsumoto : Targeting an acidic microenvironment by reveromycin A to overcome drug resistance to myeloma cells and ameliorate bone disease., 第36回日本骨髄腫研究会総会, Nov. 2011.
246.	木戸里佳, 鶴尾美穂, Akio Kuroda, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司, Toshio Matsumoto, Munehide Matsuhisa and 寺沢敏秀 : カーボカウント併用CS11療法が有効であった高齢発症1型糖尿病症例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
247.	新居沙央里, Akio Kuroda, Sumiko Yoshida, 近藤絵里, Itsuro Endo, Ken-ichi Aihara, 松本友里, Nanako Kataoka, Munehide Matsuhisa and Toshio Matsumoto : 新たなインスリンポンプParadigm722によりカーボカウントのみで血糖管理が可能となった1例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
248.	堀筋富士子, 森岡隆子, 片田英子, 鶴尾美穂, 木戸里佳, Tomoyuki Yuasa, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺沢敏秀 : サイトローテーションシート(SLS)を使用したインスリン自己注射の指導, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
249.	秋田賢子, 木戸里佳, 鶴尾美穂, Sumiko Yoshida, Mizuho Kinouchi, Tomoyuki Yuasa, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺沢敏秀 : カーボカウントを導入した高齢1型糖尿病の3例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
250.	Mizuho Kinouchi, Ken-ichi Aihara, Yuichi Fujinaka, 鈴木麗子, Sumiko Yoshida, 近藤絵里, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : 内臓脂肪肥満とアルブミン尿の連関に関する検討, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
251.	鶴尾美穂, 寺沢敏秀, 木戸里佳, Tomoyuki Yuasa, Sumiko Yoshida, 笠松哲司, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and Masashi Akaike : 粥状動脈硬化病変を呈した糖尿病合併高Lp(a)血症の姉妹例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
252.	鈴木麗子, 大和光, 菊恵木田, Ken-ichi Aihara, Itsuro Endo, Nanako Kataoka, 近藤絵里, Toshio Matsumoto, Akio Kuroda and Munehide Matsuhisa : フットケア外来におけるインスリン皮下硬結の実態調査, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
253.	田岡志保, Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, Itsuro Endo and Toshio Matsumoto : 心血管リスク因子を有する成人の血管内皮機能制御因子に関する臨床的検討, 第34回日本高血圧学会総会, Oct. 2011. (Keyword) HDL Cholesterol(血液) LDL Cholesterol(血液) 危険因子血管内皮心臓血管疾患(病因) ヒト中年(45~64) 高齢者(65~79) 男女
254.	Ken-ichi Aihara, Sumiko Yoshida and Toshio Matsumoto : 頸動脈エコー法による心血管リスク評価のための血管形態と機能解析, 第34回日本高血圧学会総会, Oct. 2011.
255.	Ken-ichi Aihara, Sumiko Yoshida and Toshio Matsumoto : Evaluation for cardiovascular risk by multi-method carotid artery ultrasound examinations, 第34回日本高血圧学会総会パネルディスカッション: 非侵襲的血管指標の有用性と課題, Oct. 2011.
256.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペントエン酸の酸化ストレス抑制を介したアンジオテンシンII刺激による心血管リモデリング抑制効果の検討, 第34回日本高血圧学会総会, Oct. 2011.
257.	Masahiro Hiasa, Masahiro Abe, 中野綾子, Kyoko Takeuchi, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Eiji Tanaka, Kenzo Asaoka, Ken-ichiro Yata and Toshio Matsumoto : Pimキナーゼ阻害による腫瘍進展と骨破壊の抑制, 第73回日本血液学会, Oct. 2011.
258.	Yuichi Fujinaka, Mizuho Kinouchi, Chisato Kosugi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Hisaaki Taniguchi and Toshio Matsumoto : Wntシグナル抑制因子sFRP4の肥満・糖代謝との関連性についての検討, 第32回日本肥満学会, Sep. 2011. (Keyword) シグナルトランスダクション癌原遺伝子蛋白質肥満糖代謝脂肪細胞分化 Wnt Proteins SFRP4 Protein ヒト
259.	Ken-ichi Aihara, Yuichi Fujinaka, 鈴木麗子, Mizuho Kinouchi, Sumiko Yoshida, 近藤絵里, Nanako Kataoka, 倉橋清衛, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : 慢性腎臓病と内臓脂肪蓄積病態の連関, 第32回日本肥満学会, Sep. 2011.
260.	Sumiko Yoshida, Yuichi Fujinaka, Ken-ichi Aihara, 鈴木麗子, Mizuho Kinouchi, 近藤絵里, Nanako Kataoka, 倉橋清衛, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa and Toshio Matsumoto : メタボリックシンドローム検診受診者における耐糖能異常の検討, 第32回日本肥満学会, Sep. 2011.
261.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda and Toshio Matsumoto : 心血管臓器におけるアンドロゲン作用の意義, 第11回日本内分泌学会四国支部学術集会高知, Sep. 2011.
262.	Ken-ichi Aihara, Sumiko Yoshida, 近藤絵里, 倉橋清衛, Takeshi Kondo, Mizuho Kinouchi, Itsuro Endo, Toshio Matsumoto, Nanako Kataoka, Akio Kuroda and Munehide Matsuhisa : 慢性腎臓病におけるエイコサペンタエン酸の意義に関する臨床的検討, 第11回日本内分泌学会四国支部学術集会, Sep. 2011.
263.	Masahiro Hiasa, A Nakano, Keiichiro Watanabe, C Qu, T Harada, S Fujii, H Miki, S Nakamura, K Kagawa, K Takeuchi, Eiji Tanaka, Kenzo Asaoka, Shuji Ozaki, Toshio Matsumoto and Masahiro Abe : Prevention of tumor growth and bone destruction in myeloma by Pim kinase inhibition, Bone Biology Forum, 19-21st Aug, 2011, Shizuoka., Aug. 2011.
264.	Ken-ichi Aihara, Sumiko Yoshida, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, 久岡白陽花, 平田陽一郎, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Eicosapentaenoic acid-to-arachidonic acid ratio is inversely associated with albuminuria in individuals with cardiovascular risk factors, 第75回日本循環器学会総会・学術集会パシフィコ横浜, Aug. 2011.
265.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Eicosapentaenoic acid protects against angiotensin II-induced cardiovascular remodeling via attenuation of oxidative stress., 第75回日本循環器学会総会・学術集会パシフィコ横浜, Aug. 2011.
266.	山田諭, Kojiro Nagai, 上田恵理子, Taichi Murakami, Motokazu Matsuura, Seiji Kishi, Hideharu Abe, Toshio Doi, 遠藤逸郎 and Toshio Matsumoto : 活性型ビタミンD3外用剤による高カルシウム血症由来の腎機能障害の一例, 日本腎臓学会雑誌, 53, 6, 815, Aug. 2011.
267.	Masashi Akaike, Koichiro Tsuchiya, Yoshiki Kashiwada, Yoshihisa Takaishi, Toshiaki Tamaki, Takashi Iwase, Masataka Sata, Ken-ichi Aihara, Sumiko Yoshida, Toshio Matsumoto, 佐藤千穂, 西条伴香 and Hiroaki Yanagawa : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果 ∼探索的臨床試験による検討∼, 第243回徳島医学会学術集会公開シンポジウム, Jul. 2011.
268.	Masashi Akaike, Koichiro Tsuchiya, Yoshiki Kashiwada, Yoshihisa Takaishi, Toshiaki Tamaki, Takashi Iwase, Masataka Sata, Ken-ichi Aihara, 吉田守実子, Toshio Matsumoto, 佐藤千穂, 西条伴香 and Hiroaki Yanagawa : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果-探索的臨床試験による検討-, 第243回徳島医学会学術集会, Jul. 2011.
269.	Itsuro Endo, 福本誠二 and Toshio Matsumoto : FGF23-relared hypophosphtemic disease in Japan, 第29回日本骨代謝学会学術集会, Jul. 2011. (Keyword) FGF23 / rickets / hypophosphatemia
270.	Masahiro Hiasa, Masahiro Abe, 中野綾子, Keiichiro Watanabe, Shingen Nakamura, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto : Pimキナーゼの阻害は骨芽細胞分化を促進し，骨髄腫骨病変の形成と腫瘍進展を抑制する, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 178, Jul. 2011.
271.	Keiichiro Watanabe, Masahiro Abe, 川谷誠, Masahiro Hiasa, Shingen Nakamura, Eiji Tanaka, 長田裕之 and Toshio Matsumoto : リベロマイシンAによる酸性環境がもたらす骨髄腫薬剤耐性の克服と骨病変形成の抑制, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 208, Jul. 2011.
272.	Seiichi Oyadomari, Kiyoe Kurahashi, Taiji Ito, 森智子, 村橋玲那, Miho Oyadomari and Toshio Matsumoto : 小胞体ストレス応答による小胞体膜恒常性の破綻は膵β細胞の脂肪毒性の原因となる, 第54回日本糖尿病学会学術総会, May 2011.
273.	木戸里佳, Mizuho Kinouchi, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司, Toshio Matsumoto, Munehide Matsuhisa, 鶴尾美穂 and 寺沢敏秀 : カーボカウント併用CSⅡ療法が用効であった高齢発症1型糖尿病の2症例, 第54回日本糖尿病学会年次学術集会, May 2011.
274.	森岡隆子, 上野裕子, 堀筋富士子, 澤井敏子, 藤島周子, 奥村滋子, 伊澤真弓, 片田英子, 秋田賢子, 木戸里佳, Sumiko Yoshida, Mizuho Kinouchi, 笠松哲司, Tomoyuki Yuasa, 鶴尾美穂, 寺沢敏秀, Munehide Matsuhisa and Toshio Matsumoto : インスリン治療を行っている高齢糖尿病患者の療養指導について, 第54回日本糖尿病学会年次学術集会, May 2011.
275.	高島啓, Koji Yamaguchi, 坂東左知子, 林修司, 久岡白陽花, 冨田紀子, 竹内秀和, Toshiyuki Niki, Kenya Kusunose, Yoshio Taketani, Takashi Iwase, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Sumiko Yoshida, Toshio Matsumoto and Masataka Sata : 甲状腺機能亢進症と腰痛が発症の誘因と考えられた難治性冠攣縮性狭心症の1例, 第98回日本循環器学会中国・四国合同地方会, May 2011.
276.	Sumiko Yoshida, 大政暁, Ken-ichi Aihara, 倉橋清衛, Takeshi Kondo, Nanako Kataoka, Itsuro Endo, Yuichi Fujinaka, Munehide Matsuhisa and Toshio Matsumoto : 強化インスリン療法からGLP-1アナログ製剤少量投与に変更し，良好な血糖コントロールが得られた1例, 第104回日本内科学会四国地方会, May 2011.
277.	津川愛, Ken-ichi Aihara, Sumiko Yoshida, Itsuro Endo, Yuichi Fujinaka, Munehide Matsuhisa and Toshio Matsumoto : DPP-4阻害薬シタグリプチンの臨床効果の特徴に関する検討, 第84回日本内分泌学会学術総会, Apr. 2011.
278.	原知也, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Takeshi Kondo, Mizuho Kinouchi, Nanako Kataoka, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : 血清エイコサペンタエン酸/アラキドン酸比は心血管リスクを有する高齢者のCKDリスクマーカーである, 第84回日本内分泌学会学術総会, Apr. 2011.
279.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : フェノフィブラートはアンジオテンシンⅡ負荷による高血圧と心筋リモデリングを抑制する, 第84回日本内分泌学会学術総会, Apr. 2011.
280.	Yuichi Fujinaka, 倉橋清衛, Mizuho Kinouchi, Sumiko Yoshida, Nanako Kataoka, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : トリロスタン投与により内分泌学的な寛解状態が得られた異所性ACTH症候群一例, 第84回日本内分泌学会学術総会, Apr. 2011.
281.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, 佐藤隆史, Masashi Akaike, Toshiaki Tamaki, 加藤茂明 and Toshio Matsumoto : 心血管リモデリングにおける男性ホルモンの作用, 第84回日本内分泌学会学術集会シンポジウム「心血管病を内分泌・代謝面から考察する」, Apr. 2011.
282.	Itsuro Endo, Seiji Fukumoto and Toshio Matsumoto : FGF23関連低リン血症性疾患に対する全国疫学調査, 第84回日本内分泌学会学術総会, Apr. 2011.
283.	安積麻衣, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Nanako Kataoka, Itsuro Endo and Toshio Matsumoto : 2型糖尿病患者に対する強化インスリン療法は左室リモデリングを改善する, 第84回日本内分泌学会学術総会, Apr. 2011.
284.	Itsuro Endo, 福本誠二 and Toshio Matsumoto : FGF23関連低リン血症性疾患に関する全国疫学調査, 第84回日本内分泌学会学術総会, Apr. 2011. (Keyword) FGF23 / 低リン血症
285.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 石川カズ江, Sumiko Yoshida, Yuka Ueda, Takashi Iwase, Masataka Sata and Toshio Matsumoto : グルココルチコイド誘発性血管内皮細胞障害に対するアルドステロン受容体拮抗薬の効果, 第84回日本内分泌学会学術総会, Apr. 2011.
286.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペントエン酸は酸化ストレス抑制を介してアンジオテンシンⅡ刺激による心血管リモデリングを抑制する, 第84回日本内分泌学会学術総会, Apr. 2011.
287.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 虚血ストレスによる骨格筋アポトーシスおよび血管新生におけるアンドロゲン受容体の意義, 第84回日本内分泌学会学術総会, Apr. 2011.
288.	Hirotsugu Kurobe, Ken-ichi Aihara, 平田陽一郎, 西矢昌子, 中山泰介, Tatsuo Motoki, Mikio Sugano, Tamotsu Kanbara, Takashi Kitaichi, Masashi Akaike, Masataka Sata, Tetsuya Kitagawa and Toshio Matsumoto : エゼチミブ投与による脂質代謝および血管機能改善効果の検討, 第84回日本内分泌学会学術総会, Apr. 2011.
289.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida, Takashi Iwase, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Masataka Sata, Toshio Matsumoto and Toshiaki Tamaki : Heparin cofactor II enhances vascular endothelial cells function and angiogenesis, 第75回日本循環器学会総会・学術集会, Mar. 2011.
290.	近藤剛史, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : hCG,FSH製剤の併用によりパートナーの妊娠が確認された低ゴナドトロピン性男性性腺機能低下症の一例, 第20回臨床内分泌Update, Jan. 2011.
291.	門田宗之, Yuichi Fujinaka, 廣野友理, 倉橋清衛, Mizuho Kinouchi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Toshio Matsumoto : 低ナトリウム血症で発症したトルコ鞍部腫瘍の一例, 第20回臨床内分泌代謝Update, Jan. 2011.
292.	坂田雅映, Shinsuke Kido, 橋本由衣, Sawako Tatsumi, Hiroko Segawa, Toshio Matsumoto and Ken-ichi Miyamoto : FGF23/Klothoを介した新たな腎尿細管リン・カルシウム代謝調節機構の解明, 第14回日本病態栄養学会年次学術集会, Jan. 2011.
293.	Masahiro Hiasa, Masahiro Abe, 中野綾子, Keiichiro Watanabe, Shingen Nakamura, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto : Pimキナーゼの阻害は骨芽細胞分化を促進し，骨髄腫骨病変の形成と腫瘍進展を抑制する, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 178, 2011. (Keyword) 癌原遺伝子蛋白質(拮抗物質・阻害物質); 骨芽細胞; 骨疾患(病因,実験的); 骨髄腫(合併症,実験的); 細胞分化; Protein-Serine-Threonine Kinases(拮抗物質・阻害物質) / Mouse Pim2 Protein(拮抗物質・阻害物質) / マウス; 動物
294.	Keiichiro Watanabe, Masahiro Abe, 川谷誠, Masahiro Hiasa, Shingen Nakamura, Eiji Tanaka, 長田裕之 and Toshio Matsumoto : リベロマイシンAによる酸性環境がもたらす骨髄腫薬剤耐性の克服と骨病変形成の抑制, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 208, 2011. (Keyword) Pyrans; Spiro Compounds; 骨疾患; 骨髄腫; 抗腫瘍剤耐性 / Reveromycin A
295.	Keiichiro Watanabe, Masahiro Abe, Cui Qu, Kawatani Makoto, Masahiro Hiasa, Nakano Ayako, Jinno Tadashi, Harada Takeshi, Shiroh Fujii, Shingen Nakamura, Miki Hirokazu, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki, Eiji Tanaka, Osada Hiroyuki and Toshio Matsumoto : Reveromycin A prevents bone destruction and suppresses tumor growth in myeloma, 第72回日本血液学会, Dec. 2010.
296.	Kiyoe Kurahashi, Taiji Ito, 森智子, 村橋玲那, Miho Oyadomari, Toshio Matsumoto and Seiichi Oyadomari : 小胞体ストレス応答を介した膵β細胞における脂肪毒性メカニズムの解析, 第22回分子糖尿病学シンポジウム, Dec. 2010.
297.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : アンドロゲン受容体は虚血後骨格筋細胞のアポトーシスと血管新生を制御する, 第18回日本血管生物医学会学術集会, Dec. 2010.
298.	安積麻衣, Ken-ichi Aihara, Sumiko Yoshida, Toshio Matsumoto and Itsuro Endo : 糖尿病患者の心筋リモデリングおよび左室機能におけつ強化インスリン療法の効果, 第12回徳島臨床脈管研究会, Nov. 2010.
299.	近藤剛史, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto and Ken-ichi Aihara : hCG, FSH製剤の併用によりパートナーの妊娠が確認された低ゴナドトロピン性男性性腺機能低下症の一例, 第16回徳島内分泌研究会, Nov. 2010.
300.	Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : hCG, FSH製剤の併用によりパートナーの妊娠が確認された低ゴナドトロピン性男性性腺機能低下症の一例, 第103回日本内科学会四国地方会, Nov. 2010.
301.	木戸里佳, Shinsuke Kido, Itsuro Endo and Toshio Matsumoto : メカニカルストレスによる骨代謝制御, 第25回日本整形外科学会基礎学術集会, Oct. 2010.
302.	Hirotsugu Kurobe, Ken-ichi Aihara, 西矢昌子, 佐藤光代, 西尾進, 中山泰介, Tatsuo Motoki, Mikio Sugano, Tamotsu Kanbara, Takashi Kitaichi, Toshio Matsumoto and Tetsuya Kitagawa : エゼチミブ投与による脂質代謝および血管機能改善効果の検討, 第51回日本脈管学会総会, 50, Suppl., S153, Oct. 2010. (Keyword) LDL Cholesterol(血液) 運動療法血管内皮血流速度脂質代謝食事療法ランダム化比較試験 Ezetimibe(治療的利用) *脈波伝播速度ヒト
303.	Masashi Akaike, Shusuke Yagi, Ken-ichi Aihara, 石川カズ江, Yasumasa Ikeda, Sumiko Yoshida, Yuka Ueda, Takashi Iwase, Toshio Matsumoto and Masataka Sata : ピタバスタチンによる血管内皮細胞での一酸化窒素合成酵素の発現亢進作用とその機序の検討, 第33回日本高血圧学会総会, 390, Oct. 2010. (Keyword) 血管内皮高血圧(薬物療法) Pitavastatin(治療的利用,薬理学) 内皮細胞 *Nitric Oxide Synthase Type III ヒト
304.	Kumiko Kagawa, Jinno Tasashi, Harada Kakeshi, Cui Qu, Keiichiro Watanabe, Masahiro Hiasa, Oda Asuka, Amo Hiroe, Akishige Ikegame, Miki Hirokazu, Shiroh Fujii, Nakano Ayako, Kyoko Takeuchi, Shuji Ozaki, Masahiro Abe and Toshio Matsumoto : Sensitization of hematopietic malignant cells to TRAIL with bortezomib and a TACE inhibitor, 第72回日本血液学会, Sep. 2010.
305.	Shingen Nakamura, Masahiro Abe, Cui Qu, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Miki Hirokazu, Nakano Ayako, Oda Asuka, Amo Hiroe, Jinno Tasashi, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : Bortezomib-induced osteoblast differentiation is hampered by excessive ER stress, 第72回日本血液学会, Sep. 2010.
306.	Masahiro Hiasa, Masahiro Abe, 中野綾子, 小田明日香, 天羽宏枝, Kyoko Takeuchi, Kumiko Kagawa, Shingen Nakamura, 三木浩和, Ken-ichiro Yata, Keiichiro Watanabe, Shuji Ozaki, Kenzo Asaoka, Eiji Tanaka and Toshio Matsumoto : Bone marrow stromal cells supress TACE activity in monocytes to induce osteoclastogenesis, 第72回日本血液学会, Sep. 2010.
307.	Cui Qu, Masahiro Abe, Miki Hirokazu, Shingen Nakamura, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, Nakano Ayako, Jinnno Tadashi, Harada Takeshi, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : Bone marrow stromal cells attenuate gama delta T, 第72回日本血液学会, Sep. 2010.
308.	Masahiro Hiasa, Masahiro Abe, Toshio Matsumoto and Kenzo Asaoka : 骨髄間質細胞は単球のTACE活性を抑制し樹状細胞分化を抑制し破骨細胞分化を誘導する, 第3回ナノ・バイオメディカル学会大会, Sep. 2010.
309.	安積麻衣, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Nanako Kataoka, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto and Munehide Matsuhisa : 2型糖尿病患者の左室拡張障害に対する強化インスリン療法の効果, 第10回日本内分泌学会四国支部学術集会, Sep. 2010.
310.	Yuichi Fujinaka, 倉橋清衛, Sumiko Yoshida, Mizuho Kinouchi, Nanako Kataoka, Itsuro Endo, Ken-ichi Aihara, Toshio Matsumoto, Minako Saito, Daisuke Fukumoto and 大島康志 : インスリングルリジンの少量投与が有効であった即時型インスリンアレルギーの一例, 第10回日本内分泌学会四国支部学術集会, Sep. 2010.
311.	Masahiro Hiasa, Masahiro Abe, 中野綾子, 小田明日香, 天羽宏枝, Kyoko Takeuchi, Kumiko Kagawa, Shingen Nakamura, 三木浩和, Ken-ichiro Yata, Keiichiro Watanabe, Shuji Ozaki, Kenzo Asaoka, Eiji Tanaka and Toshio Matsumoto : 骨髄間質細胞は，単球のTACE活性を抑制し樹状細胞分化を抑制し破骨細胞文化を誘導する, 第28回日本骨代謝学会, Jul. 2010.
312.	Keiichiro Watanabe, Masahiro Abe, Kawatani Makoto, Masahiro Hiasa, Shingen Nakamura, Eiji Tanaka, 長田裕之 and Toshio Matsumoto : リベロマイシンAは骨髄腫骨破壊病変の形成と腫瘍進展を抑制する, 第28回日本骨代謝学会, Jul. 2010.
313.	Shingen Nakamura, Masahiro Abe, Cui Qu, Keiichiro Watanabe, Akishige Ikegame, Masahiro Hiasa, 三木浩和, 中野綾子, 小田明日香, 天羽宏枝, 神野雅, 原田武志, Shiroh Fujii, Kumiko Kagawa, Kyoko Takeuchi, Shuji Ozaki and Toshio Matsumoto : ボルテゾミブによる骨芽細胞分化の促進は過剰な小胞体ストレスによって抑制される, 第28回日本骨代謝学会, Jul. 2010.
314.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : A role of androgen receptor in ischemia-induced tissue damage and angiogenesis in male, 第42回日本動脈硬化学会総会・学術集会長良川国際会議場, Jul. 2010.
315.	Y. Sumiko, Ken-ichi Aihara, T. Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : A role of androgen receptor in iscchemia-induced tissue damage and angiogenesis in male., 第42回日本動脈硬化学会総会・学術集会, Jul. 2010.
316.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : アンドロゲンーアンドロゲン受容体系は下肢虚血における組織傷害防御と血管新生に必須である, 2010 年度(第 52 回)日本老年医学会学術集会神戸国際会議場・神戸商工会議所・神戸ポートピアホテル, Jun. 2010.
317.	Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Nanako Kataoka, Itsuro Endo, Yuichi Fujinaka, Ken-ichi Aihara and Toshio Matsumoto : ピオグリタゾンが著効したWerner症候群の1例, 第102回日本内科学会四国地方会, May 2010.
318.	Ken-ichi Aihara, Yuichi Fujinaka, Sumiko Yoshida, Itsuro Endo and Toshio Matsumoto : 血管内皮機能と頸動脈硬化症の連関に関する検討, 第102回日本内科学会四国地方会, May 2010.
319.	中川航司, Shinsuke Kido, 遠藤逸郎, 坂田雅映, 橋本由衣, 佐々木祥平, Sawako Tatsumi, Toshio Matsumoto and Ken-ichi Miyamoto : 糖尿病性骨症の発症機序の解明:終末糖化産物(AGEs)によるCanonical Wnt経路抑制機序の解析, 第64回日本栄養・食糧学会大会, May 2010.
320.	倉橋清衛, Mizuho Kinouchi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : 抗副腎薬投与により内因性コルチゾールの低下とともにACTHの劇的な低下が得られた異所性ACTH症候群の一例, 第83回日本内分泌学会学術総会, 86, 1, 144, Mar. 2010. (Keyword) ACTH Hydrocortisone Mitotane(治療的利用) 異所性ACTH産生症候群(薬物療法) *Trilostane(治療的利用) ヒト高齢者(65~79) 女
321.	Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto, Takashi Iwase, Masashi Akaike and Masataka Sata : ロスバスタチンによる心筋リモデリング抑制効果の検討, 第83回日本内分泌学会学術総会, Mar. 2010.
322.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Accelerated cellular apoptosis and impaired angiogenesis after hindlimb ischemia in male mice lacking androgen receptor, 第74回日本循環器学会総会・学術集会国立京都国際会館, Mar. 2010.
323.	Hirotsugu Kurobe, 浦田将久, Yayoi Fukuhara, Tamotsu Kanbara, Ken-ichi Aihara, Masashi Akaike, Yousuke Takahama, Toshiaki Tamaki, Toshio Matsumoto, Shuhei Tomita and Tetsuya Kitagawa : 血管リモデリング時の転写因子HIF-1αの役割 (第110回日本外科学会定期学術集会), Journal of Japan Surgical Society, 111, 2, 701, Mar. 2010. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572543027394884480 (CiNii: 1572543027394884480)
324.	倉橋清衛, Ken-ichi Aihara, Sumiko Yoshida, Itsuro Endo and Toshio Matsumoto : 強化インスリン療法による2型糖尿病患者の左室リモデリングおよび拡張能改善効果に関する検討, 第240回徳島医学会学術集会, Feb. 2010.
325.	阿部容子, Itsuro Endo, Ken-ichi Aihara and Toshio Matsumoto : 重症低血糖昏睡および肺炎をきたした神経性食思不振症の救命症例, 第240回徳島医学会学術集会, Feb. 2010.
326.	Itsuro Endo and Toshio Matsumoto : FGF23関連低リン血症性くる病・骨軟化症の第一次全国調査, 厚生労働科学研究費補助金ホルモン受容機構異常に関する調査研究, Jan. 2010.
327.	木戸里佳, Yuichi Fujinaka, 寺澤敏秀, Mizuho Kinouchi, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司, Toshio Matsumoto and 鶴尾美穂 : インスリン治療中に副腎不全および粘液水腫を合併し，意識障害を伴う低血糖を繰り返した一例, 第101回日本内科学会四国地方会, Nov. 2009.
328.	Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : 強化インスリン療法による血糖コントロールの改善により左室拡張能の改善がみられた3例, 第101回日本内科学会四国地方会, Nov. 2009.
329.	Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : 家族内集積が疑われた緩徐進行1型糖尿病の一例, 第47回に本糖尿病学会中国四国地方会, Nov. 2009.
330.	Sumiko Yoshida, Yuichi Fujinaka, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Ken-ichi Aihara and Toshio Matsumoto : SPIDDMが疑われる1型糖尿病の家族内集積例, 第47回日本糖尿病学会中国四国地方会, Nov. 2009.
331.	Yuichi Fujinaka, Ken-ichi Aihara, 鈴木麗子, Mizuho Kinouchi, Sumiko Yoshida, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : メタボリックシンドローム検診における糖代謝異常の検討, 第47回日本糖尿病学会中国四国地方会, Nov. 2009.
332.	Daisuke Tsuji, Shuji Ozaki, Akishige Ikegame, 伊藤良和, 徳田美幸, 岡野和真, Masahiro Abe, Toshio Matsumoto and Kouji Itou : ヒト多発性骨髄腫由来ガン幹細胞の単離及び性質決定, 第82回日本生化学会大会, Oct. 2009.
333.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Hirotsugu Yamada, Masataka Sata and 西尾進 : 副腎アンドロゲンDHEASの抗動脈硬化作用における性差の検討, 第32回日本高血圧学会学術集会, Oct. 2009.
334.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, 鈴木麗子, 倉橋清衛, Itsuro Endo, Shusuke Yagi, Takashi Iwase, 平田陽一郎, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 内臓脂肪蓄積制御に関わる因子の臨床的検討, 第32回日本高血圧学会総会, 196, Oct. 2009. (Keyword) LDL Cholesterol 危険因子 *腹腔内脂肪(X線診断) ヒト中年(45~64) 高齢者(65~79) 男女
335.	Sumiko Yoshida, Ken-ichi Aihara, 伊勢孝之, 上田由佳, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 副腎アンドロゲンDHEASの抗動脈硬化作用における性差の検討, 第32回日本高血圧学会総会, Oct. 2009.
336.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Sumiko Yoshida, Yuka Ueda, Shusuke Yagi, Takashi Iwase, Toshio Matsumoto and Masataka Sata : ミネラルコルチコイド受容体を介したグルココルチコイド過剰による血管内皮細胞障害作用, 第32回日本高血圧学会総会, 244, Oct. 2009. (Keyword) Glucocorticoids 血管内皮細胞系 Mineralocorticoid Receptors 内皮細胞ヒト
337.	倉橋清衛, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka, Toshio Matsumoto, Shinya Watanabe and Tetsuro Ohmori : 脳波の徐波化を伴う重症低血糖昏睡を来たした神経性食思不振症の一例, 第9回日本内分泌学会四国支部学術集会, Sep. 2009.
338.	Yuichi Fujinaka, Ken-ichi Aihara, 鈴木麗子, Mizuho Kinouchi, Sumiko Yoshida, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : 当院メタボリックシンドローム検診における糖代謝異常の検討．, 第239回徳島医学会学術総会, Aug. 2009.
339.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, Sumiko Yoshida, 倉橋清衛, Itsuro Endo, Yuka Ueda, 平田陽一郎, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Influence of lipid profile on endothelial function in subjects with cardiovascular risk factors, 第41回日本動脈硬化学会総会・学術集会, Jul. 2009.
340.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Regular use of rosuvastatin attenuates carotid atherosclerosis regardless of LDL cholesterol lowering effect, 第41回日本動脈硬化学会総会・学術集会, Jul. 2009.
341.	Itsuro Endo, 大西幸代, 木戸里佳, 倉橋清衛, Sumiko Yoshida, Yuichi Fujinaka, Ken-ichi Aihara, Masahiro Abe, 福本誠二 and Toshio Matsumoto : 新規calcilytics，JTT305は常染色体優性低Ca血症におけるCa感知受容体活性型変異シグナルを抑制する, 第27回日本骨代謝学会学術集会, 195, Jul. 2009. (Keyword) シグナルトランスダクション染色体異常低カルシウム血症(薬物療法) 変異 *Calcium-Sensing Receptors(拮抗物質・阻害物質)
342.	倉橋清衛, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 一酸化炭素中毒にて急性心筋梗塞を発症した2型糖尿病の1例, 第100回日本内科学会四国地方会, May 2009.
343.	Itsuro Endo, 藤村光則, Sumiko Yoshida, 栗若里佳, Shinsuke Kido, Takashi Iwase, Daisuke Inoue, Ken-ichi Aihara, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : 冠動脈不安定プラーク予測因子としてのICTP, 第82回日本内分泌学会学術総会, 85, 1, 283, Apr. 2009. (Keyword) 生物学的マーカー Peptide Fragments(血液) 冠状動脈硬化症(診断) 動脈硬化症-アテローム性(診断) Collagen Type I(血液) *ICTP (Collagen Type I C-Terminal Telopeptides)(血液) ヒト男女
344.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, 住友由佳, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Toshio Matsumoto and Masataka Sata : グルココルチコイド誘発性血管内皮細胞障害におけるミネラルコルチコイド受容体の関与, 第82回日本内分泌学会学術総会, 85, 1, 373, Apr. 2009. (Keyword) Glucocorticoids(毒性・副作用) 血管内皮培養細胞 Mineralocorticoid Receptors(薬理学) 内皮細胞ヒト
345.	Sumiko Yoshida, Ken-ichi Aihara, 西尾進, 倉橋清衛, Itsuro Endo, Yuichi Fujinaka, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, Hirotsugu Yamada, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 副腎アンドロゲンDHEASは血管内皮機能非依存的に頸動脈硬化を抑制する, 第82回日本内分泌学会学術総会, 85, 1, 366, Apr. 2009. (Keyword) 頸動脈疾患血管内皮動脈硬化症 Dehydroepiandrosterone Sulfate(薬理学) ヒト男女
346.	Ken-ichi Aihara, Yuichi Fujinaka, Sumiko Yoshida, 鈴木麗子, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : 尿中アルブミンは内臓脂肪蓄積の強力な増悪因子である, 第82回日本内分泌学会学術総会, 85, 1, 337, Apr. 2009. (Keyword) Albumins(尿) 危険因子腹腔内脂肪ヒト中年(45~64) 高齢者(65~79) 男女
347.	Ken-ichi Aihara, Yuichi Fujinaka, Sumiko Yoshida, 鈴木麗子, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : 内臓脂肪増大因子に関する臨床的検討, 第106回日本内科学会総会・講演会, 98, Suppl., 233, Apr. 2009. (Keyword) 危険因子心臓血管疾患(病因) メタボリックシンドローム(合併症) *腹腔内脂肪ヒト男女
348.	Sumiko Yoshida, Ken-ichi Aihara, 倉橋清衛, Itsuro Endo, Yuichi Fujinaka, 住友由佳, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase and Masashi Akaike : DHEASは血管内皮機能に依存せず動脈硬化を抑制する(頸動脈エコーを用いた臨床的検討), 第106回日本内科学会総会・講演会, 98, Suppl., 139, Apr. 2009. (Keyword) 頸動脈(超音波診断) 超音波診断動脈硬化症(超音波診断) Dehydroepiandrosterone Sulfate(薬理学,血液) ヒト男女
349.	Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto, Takashi Iwase, Masashi Akaike and Masataka Sata : ロスバスタチンによる心筋リモデリング抑制効果の検討, 第83回日本内分泌学会学術総会国立京都国際会館, Mar. 2009.
350.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, Sumitomo Yuka, Shusuke Yagi, Takashi Iwase, Kurahashi Kiyoe, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Increased serum triglyceride but not LDL cholesterol is associated with left ventricular diastolic dysfunction., 第73回日本循環器学会総会・学術集会, Mar. 2009.
351.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, 倉橋清衛, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Dehydroepiandrosterone sulfate is an antivascular remodeling factor, 第73回日本循環器学会総会・学術集会, Mar. 2009.
352.	住友由佳, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : Heparin Cofactor II-deficient Mice Exert Exacerbation of Angiotensin II-induced Cardiac Remodeling through Enhancement of NADPH oxidase - TGF- 1 Pathway, 第73回日本循環器学会総会・学術集会, Mar. 2009.
353.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Sumiko Yoshida, 住友由佳, Shusuke Yagi, Takashi Iwase, Toshio Matsumoto and Masataka Sata : Glucocorticoid Excess Causes Vascular Endothelial Cell Dysfunction through Activation of Mineral Corticoid Receptor, 第73回日本循環器学会総会・学術集会, Mar. 2009.
354.	Tomoyuki Yuasa, Toshiyuki Obata, Ichiro Yokota, Eiji Okamoto, Yoshiko Kanezaki, Hiroshi Maegawa, Fumiko Hirota, Kazuhiro Kishi, Seiichi Hashida, Hisao Nagaya, Ogura Yuko, Masuda Kazuhiko, Mitsuru Matsumoto, Toshio Matsumoto, Atsunori Kashiwagi and Yousuke Ebina : Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes., International Symposium on Diabetes - Kickoff of Hannover-Tokushima Research Communiation, Mar. 2009.
355.	倉橋清衛, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : 甲状腺機能低下症の経過中にGraves眼症を来した一例, 第19回臨床内分泌代謝Up date, Mar. 2009.
356.	Sumiko Yoshida, Yuichi Fujinaka, 倉橋清衛, Itsuro Endo, Ken-ichi Aihara, Toshio Matsumoto, 松本真一 and 大島康志 : 重症筋無力症を合併したグレーブス眼症の一例, 第19回臨床内分泌代謝Up date, Mar. 2009.
357.	倉橋清衛, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : PEG-IFN-α2bおよびリバビリン治療後に劇症1型糖尿病をふくむ多彩な自己免疫疾患を発症した2例, 第99回日本内科学会四国地方会, Nov. 2008.
358.	Masahiro Hiasa, Masahiro Abe, 竹内恭子, Ken-ichiro Yata, Kumiko Kagawa, 三木浩和, Shuji Ozaki, Kenzo Asaoka and Toshio Matsumoto : 骨髄間質細胞は単球のM-CSFR発現を増強し単球由来樹状細胞分化を抑制し骨髄腫細胞による破骨細胞分化を促進する, 日本骨代謝学会・学術総会, Oct. 2008.
359.	竹内恭子, Masahiro Abe, Masahiro Hiasa, 田中修, 中村信元, 三木浩和, Kumiko Kagawa, Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto : 骨髄腫骨病変部由来TGF-βは，脂肪細胞分化を抑制し骨髄内に間質細胞を誘導する, 日本骨代謝学会・学術総会, Oct. 2008.
360.	Itsuro Endo, 藤村光則, Sumiko Yoshida, 栗若里佳, Shinsuke Kido, Takashi Iwase, Daisuke Inoue, Ken-ichi Aihara, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : 冠動脈不安定プラーク予測因子としてのICTP, 第26回日本骨代謝学会学術集会, 194, Oct. 2008. (Keyword) Peptide Fragments(血液) 冠状動脈硬化症 Collagen Type I(血液) ICTP (Collagen Type I C-Terminal Telopeptides)(血液) ヒト男女
361.	竹内恭子, Masahiro Abe, Masahiro Hiasa, 田中修, 中村信元, 三木浩和, Kumiko Kagawa, Ken-ichiro Yata, Shuji Ozaki and Toshio Matsumoto : TGF-βによる間質細胞からの脂肪細胞分化の抑制, 日本血液学会, Oct. 2008.
362.	Ken-ichiro Yata, Masahiro Abe, Masahiro Hiasa, 竹内恭子, 田中修, 中村信元, 三木浩和, Kumiko Kagawa, Shuji Ozaki and Toshio Matsumoto : 骨髄腫細胞と間質細胞の共存は単球M-CSFR発現増強を介し単球分化を破骨細胞側に偏らせる, 日本血液学会, Oct. 2008.
363.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, 住友由佳, 倉橋清衛, Itsuro Endo, Yuichi Fujinaka, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 左室拡張能に対する脂質代謝異常の意義, 第31回日本高血圧学会総会, Oct. 2008.
364.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 副腎アンドロゲンDHEASは頚動脈血流の制御因子である, 第31回日本高血圧学会学術集会, Oct. 2008.
365.	住友由佳, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Takeshi Soeki, Masashi Akaike and Masataka Sata : ヘパリンコファクターⅡは抗酸化ストレス作用を介してアンジオテンシンIIによる心房および心室のリモデリングを抑制する, 第31回日本高血圧学会総会, Oct. 2008.
366.	Masashi Akaike, Shusuke Yagi, Ken-ichi Aihara, 石川カズ江, Yasumasa Ikeda, Sumiko Yoshida, 住友由佳, Takashi Iwase, 阿部純一, Toshio Matsumoto and Masataka Sata : ピタバスタチンはERK5-KLF2経路の活性化を介して血管内皮細胞での一酸化窒素合成酵素の発現を亢進する, 第31回日本高血圧学会総会, Oct. 2008.
367.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 副腎アンドロゲンDHEASの血管への作用(頚動脈エコーを用いた臨床的検討), 第13回武田高血圧シンポジウム, Oct. 2008.
368.	Itsuro Endo, 倉橋清衛, Sumiko Yoshida, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : IFN-α2bおよびリバビリン治療後に劇症1型糖尿病，下垂体機能低下症，尋常性乾癬を発症した1例, 第8回内分泌学会四国支部学術集会, Sep. 2008.
369.	倉橋清衛, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : 甲状腺乳頭癌を合併した原発性副甲状腺機能亢進症の一例, 第8回内分泌学会四国支部学術集会, Sep. 2008.
370.	Masahiro Hiasa, Masahiro Abe, Kenzo Asaoka and Toshio Matsumoto : inhibition of osteoclastgenesis by ectodomain shedding of M-CSF receptor, 17, Aug. 2008.
371.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : 脂質代謝異常による左室拡張障害の臨床的検討, 第40回日本動脈硬化学会総会, 249, Jul. 2008. (Keyword) 脂質異常症(合併症) / 左心室機能障害(病因) / Homo sapiens / male / female
372.	Sumiko Yoshida, Ken-ichi Aihara, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : 副腎アンドロゲンの頸動脈硬化抑制作用に関する検討, 第40回日本動脈硬化学会総会, 253, Jul. 2008. (Keyword) Androgens(治療的利用) / 頸動脈疾患(予防) / 頸動脈疾患(予防) / 動脈硬化症(予防) / 副腎 / Homo sapiens / male / female
373.	Shusuke Yagi, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, 住友由佳, Yasumasa Ikeda, 岩瀬俊, Takeshi Soeki, Masashi Akaike and Toshio Matsumoto : ピタバスタチンはRac-1を介した酸化ストレス制御によりeNOS非依存的にアンジオテンシンIIによる心房リモデリングを抑制する, 第40回日本動脈硬化学会総会, 203, Jul. 2008. (Keyword) Angiotensin II 抗酸化剤(治療的利用) 心房動脈硬化症(薬物療法) 酸化ストレス rac GTP-Binding Proteins 心室リモデリング *Pitavastatin(治療的利用) マウス動物
374.	Sumiko Yoshida, Itsuro Endo, 倉橋清衛, Mizuho Kinouchi, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : カルバマゼピンでビタミンD欠乏と下垂体機能検査異常を呈した1例, 第98回日本内科学会四国地方会, Jun. 2008.
375.	Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : インスリン強化療法導入による血糖コントロールの改善により左室機能障害の回復をみた糖尿病性心筋症の2例, 第98回日本内科学会四国地方会, Jun. 2008.
376.	Sumiko Yoshida, Ken-ichi Aihara, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : 頸動脈血行動態における副腎アンドロゲンの臨床的意義, 第81回日本内分泌学会学術総会, 84, 1, 202, May 2008. (Keyword) Androgens(血液) 頸動脈 *副腎血行力学ヒト成人(19~44) 男女
377.	Ken-ichi Aihara, Sumiko Yoshida, Takayuki Ise, 住友由佳, Shusuke Yagi, Takashi Iwase, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : 左室拡張能における脂質代謝異常の影響に関する検討, 第81回日本内分泌学会学術総会, 84, 1, 222, May 2008. (Keyword) 脂質異常症左心室機能ヒト成人(19~44) 男女
378.	Takeshi Kondo, 小島直, Takayuki Ise, Mizuho Kinouchi, Sumiko Yoshida, 栗若里佳, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : 進行性の頭蓋骨陥凹と骨粗鬆症を来たした一例, 第81回日本内分泌学会学術総会, 83, 4, 834, May 2008. (Keyword) 骨粗鬆症(合併症) 骨発育異常(合併症) 鑑別診断頭蓋骨ヒト成人(19~44) 女
379.	三原正朋, Ken-ichi Aihara, Yuichi Fujinaka, Chisato Kosugi, Mizuho Kinouchi, Masashi Akaike and Toshio Matsumoto : トロンビンによるインスリン抵抗性制御機構の解析, 第52回日本糖尿病学会年次学術集会, 51, Suppl.1, S-126, May 2008. (Keyword) Thrombin(治療的利用) インスリン抵抗性(薬物療法) 3T3-L1細胞マウス動物
380.	Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, 住友由佳, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : 1α 25 dihydroxyvitamin D3 is a protective factor against vascular remodeling and glucose tolerance in elderly individuals, 第72回日本循環器学会学術集会, Mar. 2008.
381.	住友由佳, Ken-ichi Aihara, Takayuki Ise, Sumiko Yoshida, Shusuke Yagi, Takashi Iwase, 石川カズ江, Masashi Akaike and Toshio Matsumoto : Angiotensin II-induced cardiac remodeling is exacerbated with increased oxidative stress in heparin cofactor II-deficient mice., 第72回日本循環器学会総会・学術集会, Mar. 2008.
382.	Masashi Akaike, Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Takayuki Ise, Sumiko Yoshida, 住友由佳, Takashi Iwase, Abe Jun-ichi and Toshio Matsumoto : HMG-CoA Reductase Inhibitor Pitavastatin Increases the Expression of Endothelial NOS through Activation of ERK5-KLF2 Pathway in Vascular Endothelial Cells, 第72回日本循環器学会学術集会, Mar. 2008.
383.	Itsuro Endo, Takeshi Kondo, Mizuho Kinouchi, Sumiko Yoshida, Ken-ichi Aihara, Yuichi Fujinaka, 樫原茂 and Toshio Matsumoto : IFN-α2bおよびリバビリン治療後に甲状腺機能異常と劇症1型類似の糖尿病を発症した1例, 第97回日本内科学会四国地方会, Dec. 2007.
384.	Takeshi Kondo, Ken-ichi Aihara, Takayuki Ise, Mizuho Kinouchi, Sumiko Yoshida, Itsuro Endo, Yuichi Fujinaka and Toshio Matsumoto : 心腎障害の改善にACE阻害薬とARBの併用が有効であった高レニン性高血圧症の1例, 第97回日本内科学会四国地方会, Dec. 2007.
385.	住友由佳, Ken-ichi Aihara, Takayuki Ise, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : レニン・アンジオテンシン活性下におけるヘパリンコファクターIIの心筋リモデリングへの影響, 第30回日本高血圧学会総会, 170, Oct. 2007. (Keyword) Angiotensins Heparin Cofactor II Renin 心室リモデリングマウス動物
386.	Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, Takayuki Ise, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : Pitavastatinはangiotensin IIによる心腎障害をeNOS非依存性にrac1抑制による酸化ストレス抑制を介して改善する, 第30回日本高血圧学会総会, 205, Oct. 2007. (Keyword) Angiotensin II 心臓疾患(実験的) 腎臓疾患(実験的) 酸化ストレスノックアウトマウス rac GTP-Binding Proteins Pitavastatin(薬理学) マウス動物
387.	Masashi Akaike, Ken-ichi Aihara, Shusuke Yagi, Yasumasa Ikeda, 石川カズ江, 住友由佳, Takashi Iwase and Toshio Matsumoto : グルココルチコイド誘発性高血圧に対するピタバスタチンの効果とその機序の検討, 第30回日本高血圧学会総会プログラム, 210, Oct. 2007. (Keyword) Glucocorticoids 高血圧(薬物療法,実験的) C57BLマウス Pitavastatin(治療的利用,薬理学) マウス動物オス
388.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, Takayuki Ise, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : 血管リモデリング制御因子としての活性化ビタミンD, 第30回日本高血圧学会総会, 260, Oct. 2007. (Keyword) Vitamin D(治療的利用) 動脈硬化症(薬物療法,診断) *血管リモデリングヒト男女
389.	Ken-ichi Aihara, Sumiko Yoshida, Takeshi Kondo, 栗若里佳, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Shusuke Yagi, 住友由佳, Masashi Akaike and Toshio Matsumoto : 活性型ビタミンDは血漿アンチトロンビン活性の制御に関与する, 日本内分泌学会第7回四国支部学術集会, 83, 4, 834, Sep. 2007. (Keyword) Antithrombins(血液) Calcitriol(治療的利用,薬理学) ヒト中年(45~64) 高齢者(65~79) 男女
390.	Takeshi Kondo, 小島直, Takayuki Ise, Mizuho Kinouchi, Sumiko Yoshida, 栗若里佳, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : 進行性の頭蓋骨陥凹と骨粗鬆症を来たした一例, 日本内分泌学会第7回四国支部学術集会, 83, 4, 834, Sep. 2007. (Keyword) 骨粗鬆症(合併症) 骨発育異常(合併症) 鑑別診断頭蓋骨ヒト成人(19~44) 女
391.	Shinji Kawahito, Akio Iseki, Hiroshi Kitahata, Takashi Kawano, Kaori Takata, Tamotsu Kanbara, Toshio Matsumoto, Tetsuya Kitagawa and Shuzo Oshita : バージャー病に対する自己単核球細胞移植による血管新生治療, 第41回日本ペインクリニック学会, Jul. 2007.
392.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : 活性化ビタミンDは臨床的動脈硬化抑制因子である, 第39回日本動脈硬化学会総会・学術集会, 250, Jul. 2007. (Keyword) Calcitriol(血液) 断面研究動脈硬化症(予防) ヒト中年(45~64) 高齢者(65~79) 男女
393.	Itsuro Endo, Takeshi Kondo, Mizuho Kinouchi, Sumiko Yoshida, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : Carbamazepineで著明な骨量減少と下垂体検査異常を呈した一例, 第80回日本内分泌学会学術総会, 83, 3, 784, Jun. 2007. (Keyword) Carbamazepine(毒性・副作用) 甲状腺機能低下症(化学的誘発,診断) *骨密度ヒト高齢者(65~79) 男
394.	Itsuro Endo, Takeshi Kondo, 重清友理, Mizuho Kinouchi, Ken-ichi Aihara, Yuichi Fujinaka, Daisuke Inoue, Eiji Kudo, 福本誠二 and Toshio Matsumoto : 低リン血症性骨軟化症を来した腫瘍合併の成人2症例, 第80回日本内分泌学会学術総会, 83, 1, 156, Jun. 2007. (Keyword) 線維芽細胞増殖因子巨細胞腫(合併症,画像診断) 骨軟化症(合併症) MRI 低リン血症(合併症) 腫瘍性低リン血症性骨軟化症(合併症) 線維芽細胞増殖因子-23 ヒト中年(45~64) 高齢者(65~79) 男女
395.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Takeshi Kondo, 重清友理, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Masashi Akaike and Toshio Matsumoto : 活性化ビタミンDの抗動脈硬化作用に関する臨床的検討, 第80回日本内分泌学会学術総会, 83, 1, 159, Jun. 2007. (Keyword) Calcitriol(治療的利用,薬理学) 動脈硬化症(薬物療法,診断) Maxacalcitol(血液) ヒト中年(45~64) 高齢者(65~79) 男女
396.	Takeshi Kondo, Itsuro Endo, Mizuho Kinouchi, Ken-ichi Aihara, Yuichi Fujinaka, Toshio Matsumoto, 福本誠二, Kenji Endo, Hisanori Uehara and Shoichiro Takao : 腫瘍性骨軟化症の1例, 第96回日本内科学会四国地方会, May 2007.
397.	Takashi Iwase, 住友由佳, Shusuke Yagi, Yasumasa Ikeda, Ken-ichi Aihara, Shuji Ozaki, Masashi Akaike, Masahiro Abe, Toshio Matsumoto and Tetsuya Kitagawa : エリスロポイエチンを用いた新たな血管新生療法の試み, 第104回日本内科学会総会・講演会, 96, Suppl., 133, Apr. 2007. (Keyword) Erythropoietin(治療的利用) 血液成分除去法動脈閉塞性疾患(治療) *末梢血幹細胞移植ヒト
398.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Hiroyuki Azuma and Toshio Matsumoto : 活性化ビタミンDによる血管リモデリング制御作用, 第104回日本内科学会総会・講演会, 96, Suppl., 194, Apr. 2007. (Keyword) Vitamin D(治療的利用) 動脈閉塞性疾患(診断,薬物療法) 末梢血管疾患(診断,薬物療法) 血管リモデリングヒト中年(45~64) 高齢者(65~79) 男女
399.	Itsuro Endo, Takeshi Kondo, Mizuho Kinouchi, Sumiko Yoshida, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : carbamazepineで著明な骨量減少と下垂体検査異常を呈した一例, 第17回臨床内分泌代謝Update, Mar. 2007.
400.	Shusuke Yagi, Ken-ichi Aihara, Yasumasa Ikeda, 住友由佳, Takashi Iwase, Masashi Akaike and Toshio Matsumoto : PitavastatinはAngiotensin IIによる心血管リモデリングと腎障害をeNOS非依存性に抑制する, 第36回日本心脈管作動物質学会, 30, 1, 24, Feb. 2007. (Keyword) Angiotensin II(毒性・副作用) 腎臓疾患(実験的,化学的誘発) 経口投与酸化ストレス心室リモデリング Pitavastatin(薬理学) 血管リモデリング *Nitric Oxide Synthase Type III マウス動物
401.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, 住友由佳, Shusuke Yagi, Takashi Iwase, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体システムによる血管リモデリング制御機構の解析, 第36回日本心脈管作動物質学会, 30, 1, 35, Feb. 2007. (Keyword) Androgens Angiotensin II Androgen Receptors 酸化ストレス一酸化窒素 *血管リモデリングマウス動物オス
402.	Masashi Akaike, Ken-ichi Aihara, Yasumasa Ikeda, 石川カズ江, Shusuke Yagi, 住友由佳, Takashi Iwase and Toshio Matsumoto : ピタバスタチンは血管内皮機能の改善を介してグルココルチコイド過剰による高血圧を予防する, 第36回日本心脈管作動物質学会, 30, 1, 39, Feb. 2007. (Keyword) Dexamethasone(毒性・副作用) Glucocorticoids(毒性・副作用) 血管内皮高血圧(予防,化学的誘発,実験的) Pitavastatin(治療的利用,薬理学) マウス動物オス
403.	Ken-ichi Aihara, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Takashi Iwase, Hiroyuki Azuma, 加藤茂明, Masashi Akaike and Toshio Matsumoto : ApoE欠損マウスにおける血漿ヘパリンコファクターII活性の低下は酸化ストレスを増大させ粥状動脈硬化を促進させる, 第36回日本心脈管作動物質学会, 30, 1, 41, Feb. 2007. (Keyword) Apolipoproteins E Heparin Cofactor II 動脈硬化症-アテローム性(実験的) 免疫組織化学酸化ストレスノックアウトマウスマウス動物
404.	Masahiro Hiasa, Masahiro Abe, Toshihiro Hashimoto, Shuji Ozaki, Daisuke Inoue, Shinsuke Kido, Keiji Moriyama and Toshio Matsumoto : GM-CSFとIL-4は単球のM-CSF破骨細胞分化を抑制し樹状細胞分化を誘導する, Journal of Japanese Society of Bone Morphometry, 16, 3, 66, Dec. 2006. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573668925326077696 (CiNii: 1573668925326077696)
405.	多田真理枝, 住友由佳, Takashi Iwase, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Toshio Matsumoto and Hirotsugu Yamada : 心不全症状を繰り返した心尖部肥大型心筋症の一例, 第89回日本循環器学会四国地方会, Dec. 2006.
406.	宮本貴子, 木戸慎介, Masahiro Abe, Toshio Matsumoto and Hisaaki Taniguchi : Differential Proteomicsによる骨芽細胞分化の解析, 第24回日本骨代謝学会, Jul. 2006.
407.	Hirotsugu Kurobe, Yuki Izawa, Yayoi Fukumura, Tamotsu Kanbara, Atsushi Kurushima, Ken-ichi Aihara, Masashi Akaike, Masashi Kano, Takashi Kitaichi, Yutaka Masuda, Hiroyuki Azuma, Toshiaki Tamaki, Toshio Matsumoto, Tetsuya Kitagawa, Shuhei Tomita and Masanori Yoshizumi : HIF-ARNT transcriptional system in T cells has a pivotal role in vascular in flammation and remodeling., 第70回日本循環器学会学術総会, Mar. 2006.
408.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Mitsunori Fujimura, Syusuke Yagi, Syunji Hashizume, Yasumasa Ikeda, Takashi Iwase, Nobuyuki Takamori, Tetsuya Kitagawa and Toshio Matsumoto : Plasma Heparin Cofactor II Activity is Inversely Associated with Prevalence of Peripheral Arterial Disease in Elderly individuals., 第70回日本循環器学会学術総会, Mar. 2006.
409.	Ken-ichi Aihara, Mihara Masatomo, Azuma Hiroyuki, Masashi Akaike, Takaya Matsushita, Yasumasa Ikeda, Shusuke Yagi, Takashi Iwase, Hashizume Shunji, Fujimura Mitsunori and Toshio Matsumoto : Thrombin inactivation by synthetic thrombin antagonist argatroban ameliorates insulin resistance in type 2 diabetic db/db mice, The 70th Anniversary Annual Scientific Meetings of the Japanese Circulation Society, Mar. 2006.
410.	Hirotsugu Kurobe, Shuhei Tomita, Yuki Izawa, 福原弥生, Tamotsu Kanbara, Ken-ichi Aihara, Masashi Akaike, Tetsuya Kitagawa, Toshio Matsumoto, Masanori Yoshizumi and Toshiaki Tamaki : T細胞特異的HIF1αKOマイスではカフモデルにて血管リモデリングが促進される, 第15回日本循環薬理学会, Nov. 2005.
411.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, 藤村光則, Shusuke Yagi, 橋詰俊二, Yasumasa Ikeda, Takashi Iwase, Tetsuya Kitagawa and Toshio Matsumoto : ヘパリンコファクターIIは末梢動脈閉塞症に対する独立した防御因子である, 第28回日本血栓止血学会学術集会, Nov. 2005.
412.	Atsushi Shioyasono, Yasuo Oba, Hiasa Masahiro, Masahiro Abe, Toshio Matsumoto and Keiji Moriyama : Expression of chemokines in the periodontal tissue during tooth movement, 第64回日本矯正歯科学会大会, Oct. 2005.
413.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, Masataka Sata, Yasumasa Ikeda, 藤村光則, 橋詰俊二, Takashi Iwase, Shusuke Yagi, 大水章正, 塚田稔, Tetsuya Kitagawa, 加藤茂明 and Toshio Matsumoto : 新規血管リモデリング抑制因子ヘパリンコファクターIIの臨床および分子生物学的解析, 第13回日本血管生物医学会, Oct. 2005.
414.	田中洋一, Masahiro Abe, Masahiro Hiasa, Toshihiro Hashimoto, Shinsuke Kido, Daisuke Inoue, Shuji Ozaki, Keiji Moriyama and Toshio Matsumoto : 骨髄腫細胞，破骨細胞と血管内皮細胞の細胞間相互作用:腫瘍進展，骨破壊と血管新生の促進, 第23回日本骨代謝学会学術集会, Jul. 2005.
415.	田中洋一, Masahiro Abe, 日浅雅博, Toshihiro Hashimoto, 木戸慎介, Daisuke Inoue, Shuji Ozaki, Keiji Moriyama and Toshio Matsumoto : 骨髄腫細胞，破骨細胞と血管内皮細胞の細胞間相互作用:腫瘍進展，骨破壊と血管新生の促進, 第23回日本骨代謝学会学術集会, Jul. 2005.
416.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, 藤村光則, Yasumasa Ikeda, 橋詰俊二, Hiroyuki Azuma and Toshio Matsumoto : Pitavastatinは,Angiotensin IIによるマウス冠動脈リモデリングを抑制する, 第37回日本動脈硬化学会総会, 232, Jul. 2005. (Keyword) Angiotensin II 心臓血管疾患(診断,外科的療法,実験的) *Pitavastatin(薬理学) 血管リモデリング頸動脈内膜中膜肥厚度マウス動物
417.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, 藤村光則, 橋詰俊二, 大水正章, 塚田稔, 加藤茂明 and Toshio Matsumoto : 新規血管リモデリング抑制因子ヘパリンコファクターIIの分子生物学的解析, 第37回日本動脈硬化学会総会, 233, Jul. 2005. (Keyword) *Heparin Cofactor II 遺伝子発現血管疾患(病理学,実験的) 分子生物学血管リモデリングマウス動物
418.	Ken-ichi Aihara, 三原正朋, Yasumasa Ikeda, Shusuke Yagi, 藤村光則, 橋詰俊二, Takaya Matsushita, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : トロンビン作用の阻害は2型糖尿病モデルdb/dbマウスのインスリン抵抗性を改善する, 第78回日本内分泌学会総会学術集会, 81, 1, 190, Jul. 2005. (Keyword) Thrombin(拮抗物質・阻害物質) *インスリン抵抗性糖尿病-2型(診断,実験的) Argatroban(薬理学) メタボリックシンドローム(病因) マウス動物
419.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, Shusuke Yagi, Takashi Iwase, 橋詰俊二, 藤村光則, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体システムはドキソルビシンによる心筋酸化ストレスに対して防御的に作用する, 第78回日本内分泌学会総会学術集会, 81, 2, 548, Jul. 2005. (Keyword) Androgens(薬理学) Doxorubicin(毒性・副作用) Androgen Receptors(薬理学) 心筋疾患(実験的,化学的誘発) 心臓ミトコンドリア酸化ストレスノックアウトマウスマウス動物オス
420.	Shusuke Yagi, Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Takashi Iwase, 橋詰俊二, 藤村光則, Hiroyuki Azuma and Toshio Matsumoto : Pitavastatinは,Angiotensin IIによるマウス冠動脈および心筋リモデリングを抑制する, 第78回日本内分泌学会総会学術集会, 81, 2, 564, Jul. 2005. (Keyword) Angiotensin II 冠血管 C57BLマウス心室リモデリング *Pitavastatin(薬理学) 冠状動脈マウス動物
421.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Masataka Sata, Fujimura MItsunori, Hashizume Shunji, Yasumasa Ikeda, Shusuke Yagi, Kawano Hirotaka, Yamada Takashi, Fukuda Tohru, Sekine Keisuke, Sato Takashi, Nakamichi Yuko, Yamamoto Yoko, Yoshimura Kimihiro, Watanabe Tomoyuki, Nakamura Takashi, Ohmizu Akira, Tsukada Minoru, Shigeaki Kato and Toshio Matsumoto : Heparin cofactor II is required for fetal development and attenuates cuff-injured vascular remodeling in mice, The 37th Japan Atherosclerosis Society Annual Meeting, Jul. 2005.
422.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Hirotsugu Kurobe, 藤村光則, Shusuke Yagi, 橋詰俊二, Yasumasa Ikeda, Tetsuya Kitagawa and Toshio Matsumoto : ヘパリンコファクターIIは末梢動脈閉塞性病変進展に対する新規抑制因子である, 第102回日本内科学会総会・講演会, 94, Suppl., 228, Apr. 2005. (Keyword) Heparin Cofactor II 血圧測定動脈閉塞性疾患(診断) 足関節上腕血圧比ヒト中年(45~64) 高齢者(65~79)
423.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Kato Midori, Fujimura Mitsunori, Hashizume Shunji, Shusuke Yagi, Hiroyuki Azuma and Toshio Matsumoto : Angiotensin II Antagonist Valsartan Ameliorates Nitric Oxide Bioavailability and Arterial Stiffness Accompanied with The Reduction of Blood Pressure and Pulse Pressure in Elderly Hypertensives, 第69回日本循環器学会総会・学術集会, Mar. 2005.
424.	Ken-ichi Aihara, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi and Toshio Matsumoto : Arterial Cuff Injury Causes Enhanced Neointimal Formation and Increased Adventitial Area in Heterozygous Heparin Cofactor II Deficient Mice, 第69回日本循環器学会総会・学術集会, Mar. 2005.
425.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, 藤村光則, Shusuke Yagi, 橋詰俊二, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体系は生体の心筋防御機構である, 第42回日本臨床分子医学会学術総会, 78, 2005. (Keyword) Androgens Angiotensin II Androgen Receptors 心筋心室リモデリングマウス動物オス
426.	Yasuhiko Nishioka, Wang Wei, Shuji Ozaki, Toshio Matsumoto and Saburo Sone : 肺癌におけるHM1.24抗原発現と抗HM1.24抗体による抗体療法の可能性, 第17回日本バイオセラピィ学会ワークショップ3抗体療法と臨床応用, Nov. 2004.
427.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, 藤村光則, 橋詰俊二, Shusuke Yagi, 加藤茂明 and Toshio Matsumoto : ヘパリンコファクターII欠乏マウスにおける血管リモデリング異常の解析, 第27回日本血栓止血学会学術集会, Nov. 2004.
428.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, Yasumasa Ikeda, 周藤俊樹, 加藤茂明 and Toshio Matsumoto : ビタミンD-ビタミンD受容体システムによる血液凝固調節作用の解析, 第77回日本内分泌学会学術総会, 80, 1, 138, Jun. 2004. (Keyword) Thromboplastin *Vitamin D(薬理学) 遺伝子発現血液凝固血小板凝集 Calcitriol Receptors マウス動物
429.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, 森岡将臣, 加藤みどり, 橋詰俊二, 山口普史, 藤村光則, 吉田智則, Hiroyuki Azuma, 加藤茂明 and Toshio Matsumoto : アンドロゲン-アンドロゲン受容体システムは生体における心筋肥大及び心筋線維化の調節因子である, 第77回日本内分泌学会学術総会, 80, 1, 96, Jun. 2004. (Keyword) Androgens Androgen Receptors 心筋疾患 *心筋症-肥大性(診断,病理学,実験的) 線維症ノックアウトマウス心筋線維症(診断,病理学,実験的) マウス動物
430.	山口普史, 七條加奈, Takaya Matsushita, Yasumasa Ikeda, 森岡将臣, 加藤みどり, 橋詰俊二, 藤村光則, 吉田智則, Ken-ichi Aihara, Daisuke Inoue, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : 拡張型心筋症様病態を呈したCushing病の一例, Circulation journal : official journal of the Japanese Circulation Society, 68, 0, 828, Apr. 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573387451866119936 (CiNii: 1573387451866119936)
431.	Yasumasa Ikeda, 山口普史, 七條加奈, 森岡将臣, 加藤みどり, 橋詰俊二, 吉田智則, 藤村光則, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Toshio Matsumoto, 木村建彦 and 西内健 : Torsade de pointesを合併した汎下垂体機能低下症の一例, Circulation journal : official journal of the Japanese Circulation Society, 68, 0, 828, Apr. 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1571135652052441728 (CiNii: 1571135652052441728)
432.	橋詰俊二, Yasumasa Ikeda, 加藤みどり, 山口普史, 吉田智則, 藤村光則, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : 核内受容体PPARαの活性化は巨核球/血小板内PDGF-BBの産生を抑制する, 第36回日本動脈硬化学会総会, 196, 2004. (Keyword) 血小板由来増殖因子巨核球血小板培養腫瘍細胞白血病-急性赤芽球性細胞質受容体と核内受容体ペルオキシソーム増殖因子活性化受容体ヒト in vitro
433.	Ken-ichi Aihara, 高森信行, Yasuhiko Kanagawa, 藤村光則, 加藤みどり, 橋詰俊二, Yasumasa Ikeda, 田村克也, 近藤彰, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : ヘパリンコファクターIIの動脈硬化抑制作用に関する臨床的検討, 第41回日本臨床分子医学会学術総会, 55, 2004. (Keyword) Heparin Cofactor II Serine Proteinase Inhibitors(血液) ステント動脈硬化症血管平滑筋細胞増殖 Cofactor ヒト
434.	山口普史, Yasumasa Ikeda, 橋詰俊二, 加藤みどり, 吉田智則, 藤村光則, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : 遺伝性出血性末梢血管拡張症9家系における臨床病型と遺伝子変異に関する解析, 第25回日本血栓止血学会学術集会, 14, 5, 456, Nov. 2003. (Keyword) 遺伝性疾患出血変異 *毛細血管拡張症-遺伝性出血性(診断,遺伝学) 遺伝学的検査骨形成因子受容体I型ヒト
435.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, 高森信行, Yasuhiko Kanagawa, 藤村光則, 吉田智則, 橋詰俊二, 加藤みどり, 山口普史, Yasumasa Ikeda, 加藤修司, 荒瀬友子, 近藤彰 and Toshio Matsumoto : ヘパリンコファクターIIは高齢者における新規動脈硬化抑制因子である, 第25回日本血栓止血学会学術集会, 14, 5, 439, Nov. 2003. (Keyword) Antithrombins *Heparin Cofactor II(薬理学) HDL Cholesterol 動脈硬化症(診断,予防) 高齢者 Lipoprotein(a) ヒト中年(45~64) 高齢者(65~79) 高齢者(80~) 男女
436.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Fujimura Mitsunori, Sudo Toshiki, Hayashi Hideki, Yamada Yoshihisa, Yoshida Tomonori, Yamaguchi Hiroshi, Hashizume Shunji, Kato Midori and Toshio Matsumoto : Vitamin D/Vitamin D Receptor System Regulates Antithrombogenicity in vivo, 第68回日本循環器学会総会学術集会, Mar. 2003.
437.	Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Toshio Matsumoto, Michiko Yamashita, Yoshimura Kimihiro and Imagawa Jun-ichi : Elevated blood pressure with a cardiovascular remodeling in mice lacking vitamin D receptor, 第66回日本循環器学会総会・学術集会, Apr. 2002.
438.	Masashi Akaike, Hiroyuki Azuma, 香川礼香, 井内貴彦, 藤村光則, 橋詰俊二, 高森信行, 吉田智則, Ken-ichi Aihara, Yasuhiko Kanagawa, Toshio Matsumoto, Kazuya Matsumoto, 林郁郎, 田村克也 and 西内健 : 血中リポ蛋白(a)濃度に及ぼすアスピリンの影響 : アポリポ蛋白(a)アイソフォーム解析を用いた検討, 第64回日本循環器学会学術集会, 64, 0, 427, Mar. 2000. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570291227165355136 (CiNii: 1570291227165355136)
439.	高森信行, 橋詰俊二, Yasuhiko Kanagawa, Ken-ichi Aihara, 吉田智則, 井内貴彦, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : ヘパリンコファクターIIと動脈硬化発症の関連性, 第21回日本血栓止血学会学術集会, 10, 5, 393, Nov. 1999. (Keyword) Heparin Heparin Cofactor II(生理学) 動脈硬化症 Cofactor ヒト中年(45~64) 高齢者(65~) 男女
440.	Yasuhiko Kanagawa, Ken-ichi Aihara, 高森信行, 吉田智則, 井内貴彦, Masashi Akaike, 重清俊雄, Hiroyuki Azuma and Toshio Matsumoto : Pro443からLeuへの変異を有する先天性ヘパリンコファクター(HC)II欠乏症の分子機構の解明, 第21回日本血栓止血学会学術集会, 10, 5, 355, Nov. 1999. (Keyword) Heparin(欠損・欠乏) 血液蛋白質障害(発生学・遺伝学) 変異 Cofactor ヒト
441.	Masashi Akaike, 井内貴彦, 高森信行, Ken-ichi Aihara, 吉田智則, Yasuhiko Kanagawa, Itsuro Endo, Takao Mitsui, Hiroyuki Azuma, 重清俊雄 and Toshio Matsumoto : 先天性ヘパリンコファクターII(HC II)欠乏症でみられた多発性動脈病変 : 動脈硬化症の進展におけるHCIIの臨床的意義の検討, 第63回日本循環器学会学術集会, 63, 1, 645, Mar. 1999. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1574231876839482624 (CiNii: 1574231876839482624)
442.	Masashi Akaike, Hiroyuki Azuma, 香川礼香, Yasuhiko Kanagawa, Ken-ichi Aihara, 井内貴彦, 高森信行, 吉田智則, Toshio Matsumoto and Kazuya Matsumoto : 高リポ蛋白(a)血症に及ぼすaspirinの影響アポリポ蛋白(a)アイソフォームとの関連, Shikoku Acta Medica, 55, 2, 82, 1999. (Keyword) Apolipoproteins A Aspirin 高リポ蛋白質血症蛋白質アイソフォームヒト (Tokushima University Institutional Repository) ● Metadata: 2005300 (Tokushima University Institutional Repository: 2005300)
443.	Masashi Akaike, Yasuhiko Kanagawa, 香川礼香, 吉田智則, Ken-ichi Aihara, Hiroyuki Azuma, Toshio Matsumoto and Kazuya Matsumoto : 高Lp(a)血症に及ぼすaspirinの影響 Lp(a)アイソフォーム解析を用いた検討, The Journal of the Japanese Society of Internal Medicine, 88, 139, 1999. (Keyword) Aspirin(薬理学) Lipoprotein(a)(血液,薬物影響,代謝性障害) ヒト
444.	Yasuhiko Kanagawa, 重清俊雄, Ken-ichi Aihara, 松山まどか, 香川礼香, 宮本和正, 井内貴彦, Masashi Akaike, Hiroyuki Azuma and Toshio Matsumoto : 先天性ヘパリンコファクターII(HCII)欠乏症1家系の遺伝子解析, 第20回日本血栓止血学会学術集会, 9, 4, 315, Nov. 1998. (Keyword) Heparin Cofactor II(欠損・欠乏) 血液蛋白質障害配列分析ヒト

Products:

1.	Itsuro Endo and Toshio Matsumoto : ビスホスホネートの分子種と骨親和性, ビスホスホネートエビデンスブック, Oct. 2013.

Et cetera, Workshop:

1.	Jumpei Teramachi, Hirofumi Tenshin, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : 骨髄腫特異的抗腫瘍活性と骨再生をもたらす新規分子標的薬の開発, 2018 先端医学交流セミナー, Aug. 2018.
2.	Sumiko Yoshida, Ken-ichi Aihara, Masashi Akaike and Toshio Matsumoto : ステロイド性大腿骨頭壊死症予防に向けた，大量グルココルチコイドによる酸化ストレスおよび血管内皮機能の変化と，ピタバスタチンの臨床的有効性の検討, 特発性大腿骨頭壊死症の治療法確立と革新的予防法開発にむけた全国学術研究, Aug. 2016.
3.	Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida and Toshio Matsumoto : グルココルコイド過剰誘導酸化ストレスの臨床的評価とeNOSの有無におけるピタバスタチンの虚血臓器保護効果機構の差異, 厚生労働科学研究費補助金平成27年度第1回班会議, Aug. 2015.
4.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, Ryosuke Sato, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸は膵β細胞の小胞体膜の組成を変化させ，PERK 経路の活性化による翻訳抑制を介してインスリン分泌を低下させる, 第26回分子糖尿病学シンポジウム, Dec. 2014.
5.	Kiyoe Kurahashi, 森智子, 宮本千伸, 津川和江, Miho Oyadomari, Kazuna Takahara, Ryosuke Sato, 木村千寿子, Masato Miyake, Toshio Matsumoto and Seiichi Oyadomari : 飽和脂肪酸による膵β細胞の小胞体膜の組成変化は，PERK経路活性化を遷延させ翻訳抑制を介してインスリン分泌を低下させる, 第9回小胞体ストレス研究会, Jul. 2014.
6.	Ryota Amachi, Masahiro Abe, Keiichiro Watanabe, Kumiko Kagawa, Shiroh Fujii, 原田武志, Hirokazu Miki, Keiichiro Watanabe, 小野明日香, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto : 骨髄腫の酸性環境はTRAIL受容体発現をエピジェネティックに抑制し，TRAIL抵抗性をもたらす, 第20回徳島骨代謝研究会, Nov. 2013.
7.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, 上元良子, 石川カズ江 and Toshio Matsumoto : 心血管ストレス制御におけるアンドロゲン受容体機能の性差, 第4回テストステロン研究会, Nov. 2013.
8.	Dong Bingzi, Takeshi Kondo, Itsuro Endo, Yukiyo Ohnishi, Takashi Omatsu, Shin-ichi Yoshizawa, Hiroshi Sakaue and Toshio Matsumoto : Interleukin-11 controls bone and adipose tissue mass by regulating osteoblastic and adipogenic differentiation, 4th Bone BioScience Meeting, Jun. 2013.
9.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : 虚血耐性における性差非依存性のアンドロゲン受容体作用, 第5回核内受容体・ホルモン研究会, Mar. 2013.
10.	Dong Bingzi, Itsuro Endo, Takeshi Kondo, Yukiyo Ohnishi, Masahiro Abe, Shin-ichi Yoshizawa, Seiji Fukumoto and Toshio Matsumoto : The Effect of calcilytics on activating mutation of calcium-sensing repceptor knock-in mice model of autosomal dominant hypocalcemia, 骨とCaクラスターミニリトリート, Feb. 2013.
11.	Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida and Toshio Matsumoto : Pitavastatinは血管内皮機能障害を背景にした重症虚血誘導組織壊死を抑制する, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成24 年度第2回班会議, Jan. 2013.
12.	Toshio Matsumoto : 骨代謝の調節機構と骨粗鬆症制御機構とその異常, 第5回分子内分泌代謝学セミナー, Dec. 2012.
13.	Toshio Matsumoto : 骨粗鬆症治療の新たな展開, 骨粗鬆症治療講演会, Nov. 2012.
14.	Toshio Matsumoto : 腫瘍と骨の相互作用多発性骨髄腫と骨微少環境, 第15回最新医学研究会, Nov. 2012.
15.	Takeshi Kondo, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara and Toshio Matsumoto : 当院で経験したSITSHの2例, 第18回徳島内分泌研究会, Nov. 2012.
16.	Toshio Matsumoto : 新時代の骨粗鬆症治療, 運動器疾患フォーラムin Osaka, Nov. 2012.
17.	Toshio Matsumoto : 骨粗鬆症診断Update, 第10回骨粗鬆症フォーラム, Nov. 2012.
18.	Itsuro Endo, 大薗卓也, 齋藤光恵, 久保田由紀子, Masahiro Abe and Toshio Matsumoto : 骨転移に対するdenosumab 120mg 皮下注後の重傷低Ca血症発現の実態, 第15回癌と骨病変研究会, Nov. 2012.
19.	Keiichiro Watanabe, Masahiro Abe and Toshio Matsumoto : リベロマイシンAによる酸性環境がもたらす骨髄腫薬剤耐性の克服と骨病変形成の制御, 第15回癌と骨病変研究会, Nov. 2012.
20.	Toshio Matsumoto : 骨粗鬆症の病態と治療Update, 沖縄県臨床整形外科医会第13回教育研修会, Oct. 2012.
21.	Toshio Matsumoto : 新時代の骨粗鬆症治療, 出雲整形外科学術講演会, Oct. 2012.
22.	Toshio Matsumoto : 骨カルシウム代謝異常症の病態と診断, 第13回名古屋エンドクリン治療研究会, Sep. 2012.
23.	Toshio Matsumoto : 骨粗鬆症の治療戦略とエディロール, 姫路内科医会学術講演会, Sep. 2012.
24.	Toshio Matsumoto : 骨粗鬆症の病態と治療, 腰痛セミナーin城南 2012, Sep. 2012.
25.	Toshio Matsumoto : ビタミンDと骨粗鬆症治療, 第26回ROD-21研究会, Sep. 2012.
26.	Toshio Matsumoto : 生活習慣病・ステロイド過剰と骨粗鬆症, 第20回筑後骨代謝・骨粗鬆症研究会, Aug. 2012.
27.	Toshio Matsumoto : 癌の骨病変に対する治療戦略, 癌領域の骨代謝を考える会, Aug. 2012.
28.	Keiichiro Watanabe, Ryota Amachi, Masahiro Hiasa, Shingen Nakamura, Itsuro Endo, Hiroshi Mori, Eiji Tanaka and Toshio Matsumoto : The cathepsinK inhibitor ONO-KK1-300-01 (ONO-KK1) prevents bone destruction and restores bone formation in myeloma bone lesions, Bone Seminar, Aug. 2012.
29.	Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida and Toshio Matsumoto : 血管内皮機能障害を背景にした重症虚血誘導組織壊死に対するpitavastatinの効果, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成24 年度第1回班会議, Aug. 2012.
30.	Toshio Matsumoto : ビスホスホネートと骨粗鬆症治療, 島原市医師会学術講演会, Jul. 2012.
31.	Ryota Amachi, Masahiro Abe, Keiichiro Watanabe, Kumiko Kagawa, 藤井志郎, 原田武志, Hirokazu Miki, Shingen Nakamura, 小田明日香, Masahiro Hiasa, Eiji Tanaka and Toshio Matsumoto : 酸環境は骨髄腫細胞のTRAILに対する抵抗性を増強する, 第3回骨バイオサイエンス研究会, Jul. 2012.
32.	Toshio Matsumoto : 骨代謝の調節機構と骨粗鬆症, 愛媛大学大学院消化器・代謝生物学コースフォーラム第34回愛媛内分泌代謝疾患懇話会, Jul. 2012.
33.	Toshio Matsumoto : 骨粗鬆症治療Update, 八王子市医師会学術講演会, Jul. 2012.
34.	Toshio Matsumoto : 骨粗鬆症の病態と治療Update, 第12回中高年女性の予防医学研究会イブニングセミナー, Jul. 2012.
35.	Toshio Matsumoto : 腫瘍と骨の相互作用多発性骨髄腫と骨微少環境, 内分泌・代謝セミナー, Jul. 2012.
36.	Toshio Matsumoto : 骨粗鬆症治療の進歩と宇宙飛行に伴う骨量減少の予防宇宙で骨量減少, 整形外科長良リバーサイドフォーラム, Jun. 2012.
37.	Toshio Matsumoto : 力学的負荷による骨量代謝制御, Chiba OsteoBiology Seminar, Jun. 2012.
38.	Toshio Matsumoto : 生活習慣病と骨代謝, 糖尿病の先端研究を臨床に応用するための研究会, Jun. 2012.
39.	Toshio Matsumoto : 骨粗鬆症の進歩, 佐賀県骨粗鬆症学術講演会, Jun. 2012.
40.	Sumiko Yoshida, Ken-ichi Aihara and Toshio Matsumoto : 心腎連関病態におけるEPA;エイコサペントエン酸の臨床的意義, 第10回徳島リスクファクター研究会, Jun. 2012.
41.	Toshio Matsumoto : 生活習慣病・ステロイド過剰と骨粗鬆症, 北九州PTH治療講演会, May 2012.
42.	Toshio Matsumoto : エビスタ最新の話題, Evista Web Conference, May 2012.
43.	Toshio Matsumoto : 腫瘍と骨の相互作用多発性骨髄腫と骨微少環境, 学術講演会「骨バイオロジーの行方」, May 2012.
44.	Toshio Matsumoto : 骨粗鬆症の進歩, みやぎ骨粗鬆症学術講演会, Apr. 2012.
45.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : アンドロゲン受容体は，虚血ストレスに対する骨格筋アポトーシス防御および血管新生に必須である, 第4回核内受容体研究会, Apr. 2012.
46.	Toshio Matsumoto : 骨粗鬆症の新たな展開, 千葉骨と関節フォーラム, Apr. 2012.
47.	Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida and Toshio Matsumoto : 酸化ストレス抑制作用を介したグルココルチコイド誘発性血管内皮細胞障害治療, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成23 年度第2回班会議, Dec. 2011.
48.	Sumiko Yoshida, 近藤絵里, 倉橋清衛, Mizuho Kinouchi, Nanako Kataoka, Itsuro Endo, Ken-ichi Aihara, Toshio Matsumoto, Akio Kuroda and Munehide Matsuhisa : 当科での1型糖尿病に対するインスリンポンプ療法導入経験, 第17回徳島内分泌研究会, Nov. 2011.
49.	Masahiro Hiasa, Masahiro Abe, 中野綾子, Keiichiro Watanabe, Kyoko Takeuchi, Kumiko Kagawa, Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, 原田武志, Shuji Ozaki, Eiji Tanaka, Kenzo Asaoka and Toshio Matsumoto : Pimキナーゼの阻害による骨髄腫の進展抑制, 癌と骨病変研究会, Nov. 2011.
50.	Masashi Akaike, Ken-ichi Aihara, Sumiko Yoshida and Toshio Matsumoto : グルココルチコイド誘発性血管内皮細胞障害に対する酸化ストレス抑制の意義, 厚生労働科学研究費補助金難治性疾患克服研究事業特発性大腿骨頭壊死症調査研究班平成23 年度第1回班会議, Aug. 2011.
51.	Keiichiro Watanabe, Masahiro Abe, 崔衢, 川谷誠, Masahiro Hiasa, 長田裕之, Eiji Tanaka and Toshio Matsumoto : A novel anti-resorptive agent, reveromycin A, ameliorates bone destruction and tumor growth in myeloma, 第2回骨バイオサイエンス研究会, Jul. 2011.
52.	Sumiko Yoshida, 倉橋清衛, Takeshi Kondo, Nanako Kataoka, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka and Toshio Matsumoto : 当院での原発性アルドステロン症に対するエプレレノンの効果, Meet the Specialist, Mar. 2011.
53.	Sumiko Yoshida, Ken-ichi Aihara, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : アンドロゲン受容体は，虚血ストレスに対する骨格筋アポトーシス防御および血管新生に必須である, 第3回核内受容体研究会帝人ファーマ株式会社, Mar. 2011.
54.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : エイコサペンタエン酸の心血管リモデリング抑制効果の検討, 第3回Tokushima Young Investigators Conference, Mar. 2011.
55.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : EPAによる心血管リモデリング抑制効果の検討, 第30回心血管セミナー, Jan. 2011.
56.	Masahiro Hiasa, Masahiro Abe, 中野綾子, 小田明日香, 天羽宏枝, Kyoko Takeuchi, Kumiko Kagawa, Shingen Nakamura, 三木浩和, Ken-ichiro Yata, Keiichiro Watanabe, Shuji Ozaki, Kenzo Asaoka, Eiji Tanaka and Toshio Matsumoto : 骨髄間質細胞は，単球のTACE活性を抑制し樹状細胞分化を抑制し破骨細胞文化を誘導する, 第17回徳島骨代謝研究会, Nov. 2010.
57.	Keiichiro Watanabe, Masahiro Abe, 崔衢, 川谷誠, 長田裕之, Eiji Tanaka and Toshio Matsumoto : リベロマイシンAの骨髄腫骨病変と腫瘍進展抑制作用, 第1回骨バイオサイエンス研究会, Jun. 2010.
58.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 虚血および血管新生におけるアンドロゲン作用の検討, 興和学術講演会, May 2010.
59.	Ken-ichi Aihara, Sumiko Yoshida, Yasumasa Ikeda, Masashi Akaike, 加藤茂明 and Toshio Matsumoto : 心血管ストレスに対するandrogen-androgen 受容体系の役割, 第2回核内受容体研究会, Mar. 2010.
60.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Yasumasa Ikeda, 倉橋清衛, Mizuho Kinouchi, Itsuro Endo, Yuichi Fujinaka, Takashi Iwase, Masashi Akaike, Masataka Sata and Toshio Matsumoto : 下肢虚血モデルを用いたアンドロゲン受容体による虚血臓器保護効果の検討, 第15回徳島内分泌研究会, Nov. 2009.
61.	Tomoyuki Yuasa, Toshiyuki Obata, Ichiro Yokota, 岡本英治, Hisao Nagaya, Seiichi Hashida, 前川聡, Atsunori kasiwagi, Mitsuru Matsumoto, Toshio Matsumoto, Kazuhiro Kishi and Yousuke Ebina : 可溶性インスリン受容体細胞外ドメイン(sIRα)は高血糖に相関して血中濃度が高まる, 第7回 1型糖尿病研究会, Nov. 2009.
62.	Itsuro Endo, 大西幸代, 木戸里佳, 倉橋清衛, Yuichi Fujinaka, Ken-ichi Aihara, Sumiko Yoshida, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : Ca感知受容体機能に及ぼすcalcilyticsの作用, 第3回瀬戸内フォーラム, Aug. 2009.
63.	倉橋清衛, Shingen Nakamura, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Yuichi Fujinaka, Toshio Matsumoto, Shusuke Yagi, Takashi Iwase, Masashi Akaike and Masataka Sata : 一酸化炭素中毒を契機に発見された急性心筋梗塞の一例, 第9回徳島総合診療研究会, Jul. 2009.
64.	Ken-ichi Aihara, Yuichi Fujinaka, Mizuho Kinouchi, 鈴木麗子, Sumiko Yoshida, 倉橋清衛, Itsuro Endo and Toshio Matsumoto : 内蔵脂肪蓄積因子の臨床的検討ーメタボリックシンドローム検診から見えたことー, 第7回徳島リスクファクター研究会, Jun. 2009.
65.	Itsuro Endo, Sumiko Yoshida, 栗若里佳, Shinsuke Kido, Ken-ichi Aihara, Yuichi Fujinaka, 藤村光則 and Toshio Matsumoto : 冠動脈不安定ブラーク予測因子としてのICTP, 第3回徳島Vascular Endocrinology conference, Mar. 2009.
66.	Ken-ichiro Yata, Masahiro Abe, 竹内恭子, Masahiro Hiasa, 中野綾子, 三木浩和, 田中修, 中村信元, Kumiko Kagawa, Shuji Ozaki and Toshio Matsumoto : 骨髄間質細胞はγδT細胞による抗骨髄腫効果を減弱させる, 日本骨髄腫研究会総会, Nov. 2008.
67.	Tomoyuki Yuasa, Toshiyuki Obata, Ichiro Yokota, Eiji Okamoto, Yoshiko Kanezaki, Hiroshi Maegawa, Fumiko Hirota, Kazuhiro Kishi, Seiichi Hashida, Hisao Nagaya, Ogura Yuko, Masuda Kazuhiko, Mitsuru Matsumoto, Toshio Matsumoto, Atsunori Kashiwagi and Yousuke Ebina : Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes., The 1st Insulin Resistance in Metabolic Disease Forum, Aug. 2008.
68.	Ken-ichi Aihara, Hiroyuki Azuma, Masashi Akaike, Yasumasa Ikeda, Shusuke Yagi, 住友由佳, Sumiko Yoshida, Takayuki Ise, Takashi Iwase and Toshio Matsumoto : 新規血管リモデリング抑制因子ヘパリンコファクターIIの分子生物学的解析, 第9回四国循環器研究会, Sep. 2007.

Report:

1.	Itsuro Endo and Toshio Matsumoto : ホルモン受容機構異常に関する調査研究平成22年度研究報告書, 厚生労働科学研究費補助金(難治疾患克服研究事業), 15-16, May 2011.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Role and mechanism of action of IL-11 on the regulation of bone and adipose tissue interaction (Project/Area Number: 16H05327 )
Elucidation of molecular mechanism of the regulation of skeletal homeostasis, and development of new therapeutic approaches against skeletal disorders (Project/Area Number: 25293215 )
Relationships among skeletal, adipose and vasclar regulatory system, and elucidation of pathogensis caused by disturbances of these systems (Project/Area Number: 20249050 )
Molecular mechanic sum of the regulation and dies regulation of bone homeostasis and Development of therapeutic approaches (Project/Area Number: 17209035 )
Identification and clinical application of osteoclast-derived growth factors for myeloma (Project/Area Number: 15591010 )
Differentiation-inducing signals in osteoblasts and its application for development of bone anabolic therapy (Project/Area Number: 14370329 )
Roles for MIP-1α and β in the development of osteolytic lesions in multiple myeloma (Project/Area Number: 13671067 )
Development of immunotherapy targeting neoplastic lymphocyte-specific antigen (2D7) against hematological malignancies (Project/Area Number: 13557082 )
骨格系の制御に関わる転写因子と骨粗鬆症におけるその異常 (Project/Area Number: 12137207 )
骨格系の制御プログラムと疾患 (Project/Area Number: 11897003 )
Role and clinical significance of heparin cofactor II as an anti-atherosclerotic factor (Project/Area Number: 11838011 )
Mechanism of signal transduction that regulates osteoclast differentiation and its abnormalities in bone distructive diseases (Project/Area Number: 11470227 )
Development of novel agents using the method of modulating the transcriptional activity of apo (a) gene (Project/Area Number: 10557105 )
Development of a new therapeutic approach for senile osteoporosis using bone matrix deoorin (Project/Area Number: 06557055 )
Pathogenesis of Metastatic Bone Lesion and Development of Methods for Its Diagnosis and Treatment (Project/Area Number: 06454343 )
Role of matrix proteins in the local regulation of bone metabolism and its abonomalities in osteoporosis (Project/Area Number: 06454336 )
Cell Biological Investigation of Disturbances in Bone Cell Functions with their Application to the Treatment of Osteoporosis (Project/Area Number: 03454217 )
Purification of prostate-derived bone growth factor and its application to the treatment of osteoporosis (Project/Area Number: 02557111 )
Hypercalcemic Factors in ATL (Project/Area Number: 62570537 )
情報伝達系不全による病態に関する研究 (Project/Area Number: 62440047 )
ビタミンD作用の発現に関する研究-24,25水酸化ビタミンD_3等の役割について (Project/Area Number: 61570541 )
Disorders of calcium metabolism (Project/Area Number: 59440052 )
Search by Researcher Number (20157374)

Professor Emeritus : Matsumoto, Toshio

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)