Tokushima University / Educator and Researcher Directory --- Endo, Itsuro

Field of Study

○	Medicine

Subject of Study

○

Book / Paper

Book:

1.	Takeshi Kondo and Itsuro Endo : 脱水, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2024.
2.	Takeshi Kondo and Itsuro Endo : 口渇, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2024.
3.	Tomoyo Hara and Itsuro Endo : 成長障害, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2024.
4.	Kiyoe Kurahashi and Itsuro Endo : るいそう, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2024.
5.	Itsuro Endo : 肥満・肥満症, IGAKU-SHOIN Ltd.Tokyo,Japan, Tokyo, Mar. 2024.
6.	Itsuro Endo : 代謝疾患, 医学出版社, Tokyo, Mar. 2024.
7.	Itsuro Endo : 内分泌疾患, 医学出版社, Tokyo, Mar. 2024.
8.	Itsuro Endo : 活性型ビタミンD3製剤, 羊土社, Tokyo, Nov. 2023.
9.	Itsuro Endo : 骨粗鬆症におけるロモソズマブの適応と注意点は?, 株式会社診断と治療社, Jun. 2023.
10.	Itsuro Endo : 画像で副甲状腺腫大を確認できない原発性副甲状腺機能亢進症の治療方針は?, 株式会社診断と治療社, Tokyo, Jun. 2023.
11.	Itsuro Endo : 低ホファターゼ症，骨形成不全症，軟骨異栄養症, 診断と治療社, May 2023.
12.	Itsuro Endo : 骨形成マーカー, NIPPONRINSHOSHA Co.,Ltd., Tokyo, Jan. 2023.
13.	Itsuro Endo : 活性型ビタミンD製剤を処方するときの注意点は?, 日本医事新報社, Aug. 2022.
14.	Sumiko Yoshida, 原倫世, 山口佑樹, Takeshi Kondo, 遠藤ふうり, 筒井康継, 桝田志保, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe, Kohhei Nakajima and Masahiro Abe : 急速に腫瘍が増大し悪性転化が疑われたCushing病の1例, Jun. 2019.
15.	Itsuro Endo : ロモソズマブ:骨粗鬆症への効果発現のメカニズムについて教えてください, 株式会社診断と治療社, Tokyo, Sep. 2016.
16.	Itsuro Endo : 骨組織を標的とした新しい診断・治療法, Medical Review Co.,Ltd, Feb. 2016.
17.	Itsuro Endo : 活性型ビタミンD, 最新医学社, Jan. 2016.
18.	Itsuro Endo : 2型糖尿病と骨折リスク, Jun. 2015.
19.	Itsuro Endo : 骨粗鬆症の薬物療法，活性型ビタミンD3薬, Iyaku Journal Co., Ltd., Feb. 2015.
20.	Takeshi Kondo and Itsuro Endo : 甲状腺機能異常症, JOHNS 耳鼻咽喉科薬物療法, JOHNS 耳鼻咽喉科薬物療法, 2015.
21.	Takeshi Kondo and Itsuro Endo : 甲状腺機能異常症, TOKYO IGAKUSHA, 2015.
22.	Masahiro Abe and Itsuro Endo : 高カルシウム血症, Iyaku Journal Co., Ltd., Mar. 2013.
23.	Itsuro Endo, Masahiro Abe and Toshio Matsumoto : 骨転移の分子標的治療薬, Dec. 2012.
24.	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.
25.	Itsuro Endo and Toshio Matsumoto : 不動性骨粗鬆症, Oct. 2010.
26.	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.
27.	Itsuro Endo and Toshio Matsumoto : 不動性骨粗鬆症, Oct. 2010.
28.	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.
29.	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)
30.	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)

Academic Paper (Judged Full Paper):

1.	Tomoyo Hara, Takeshi Watanabe, Hiroki Yamagami, Kosuke Miyataka, Saya Yasui, Takahito Asai, Yohsuke Kaneko, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Soichi Honda, Akira Kondo, Munehide Matsuhisa and Ken-ichi Aihara : Development of Liver Fibrosis Represented by the Fibrosis-4 Index Is a Specific Risk Factor for Tubular Injury in Individuals with Type 2 Diabetes, Biomedicines, Vol.12, No.8, 1789, 2024. (Summary) Although hyperglycemia and hypertension are well-known risk factors for glomerular injury in individuals with type 2 diabetes (T2D), specific risk factors for tubular injury remain unclear. We aimed to clarify the differences between risk factors for glomerular injury and risk factors for tubular injury in individuals with T2D. We categorized 1243 subjects into four groups based on urinary biomarkers, including the albumin-to-creatinine ratio (uACR) and L-type fatty acid-binding protein-to-creatinine ratio (uL-ABPCR) as a normal (N) group (uACR < 30 mg/gCr and uL-FABPCR < 5 μg/gCr; n = 637), a glomerular specific injury (G) group (uACR ≥ 30 mg/gCr and uL-FABPCR < 5 μg/gCr; n = 248), a tubular specific injury (T) group (uACR < 30 mg/gCr and uL-FABPCR ≥ 5 μg/gCr; n = 90), and a dual injury (D) group (uACR ≥ 30 mg/gCr and uL-FABPCR ≥ 5 μg/gCr; n = 268). Logistic regression analysis referencing the N group revealed that BMI, current smoking, and hypertension were risk factors for the G group, creatinine (Cr) and Fibrosis-4 (FIB-4) index were risk factors for the T group, and BMI, hypertension, HbA1c, Cr, and duration of diabetes were risk factors for the D group. While hypertension was a distinct specific risk factor for glomerular injury, the FIB-4 index was a specific contributor to the prevalence of tubular injury. On the other hand, the logistic regression analysis revealed that the hepatic steatosis index (HSI) did not show any significant association with the G group, T group, or D group. Taken together, the development of liver fibrosis rather than liver steatosis is an inherent threat relating to tubular injury in individuals with T2D. (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines12081789 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39200252 ● Summary page in Scopus @ Elsevier: 2-s2.0-85202596205 (DOI: 10.3390/biomedicines12081789, PubMed: 39200252, Elsevier: Scopus)
2.	Mamiko Takahashi, Shin Kondo, Kumiko Kagawa, Masafumi Nakamura, Yusaku Maeda, Ryohei Sumitani, Hikaru Yagi, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Itsuro Endo, Masahiro Abe and Shingen Nakamura : Skeletal muscle mass during chemotherapy for haematological malignancies: a retrospective study., BMJ Supportive & Palliative Care, Vol.14, No.2, 195-199, 2024. (Summary) This study investigated whether baseline or alteration in muscle mass affects complications during chemotherapy or overall survival (OS) in haematological malignancies. Skeletal Muscle Index (SMI) was evaluated by bioimpedance analysis before and after chemotherapy in patients with haematological malignancies, and the association between muscle mass and clinical data was retrospectively analysed. Exactly 104 patients were enrolled, with a mean age of 62.2 years. SMI was 7.85 and 6.08 in male and female patients under 65 years and 7.10 and 5.92 over 65 years, before chemotherapy, respectively. Lower baseline SMI was not correlated with worse OS in total patients (p=0.915). After a median measurement interval of 30 days after chemotherapy (n=67), body weight and SMI decreased by 2.73% and 2.87% (mean), respectively. The decrease in body weight correlated with the loss of trunk muscle mass (R=0.2107) but was more strongly associated with the loss of lower limbs muscle mass (R=0.3985). The muscle mass of lower limbs significantly decreased in lymphoma patients who experienced febrile neutropenia (-0.42% vs -6.04%, p=0.040). OS significantly decreased in lymphoma patients with loss of lower limbs muscle ≥2.8% (p=0.0327). Muscle loss occurred following anticancer treatments, significantly contributing to worse outcomes. Body composition assessment and relevant multimodal prevention of muscle loss may be vital for patients receiving chemotherapy for haematological malignancies. (Keyword) Humans / Male / Female / Retrospective Studies / Middle Aged / Hematologic Neoplasms / Muscle, Skeletal / Aged / Adult / Antineoplastic Agents / Aged, 80 and over / Body Composition / Sarcopenia (Tokushima University Institutional Repository) ● Metadata: 119635 (Link to Publication Site) ● Publication site (DOI): 10.1136/spcare-2024-004870 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38569748 ● Search Scopus @ Elsevier (PMID): 38569748 ● Search Scopus @ Elsevier (DOI): 10.1136/spcare-2024-004870 (Tokushima University Institutional Repository: 119635, DOI: 10.1136/spcare-2024-004870, PubMed: 38569748)
3.	Minae Hosoki, HORI Taiki, KANEKO Yohsuke, Kensuke Mori, Saya Yasui, Seijiro Tsuji, Hiroki Yamagami, Saki Kawata, Tomoyo Hara, Shiho Masuda, Yukari Mitsui, Kiyoe Kurahashi, Takeshi Harada, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : Causes of In-Hospital Death and Pharmaceutical Associations with Age of Death during a 10-Year Period (2011-2020) in Individuals with and without Diabetes at a Japanese Community General Hospital., Journal of Clinical Medicine, Vol.13, No.5, 1283, 2024. (Summary) Since diabetes and its complications have been thought to exaggerate cardiorenal disease, resulting in a short lifespan, we investigated causes of death and lifespans in individuals with and without diabetes at a Japanese community general hospital during the period from 2011 to 2020. Causes of death and age of death in individuals with and those without diabetes were compared, and associations between medications used and age of death were statistically analyzed. A total of 2326 deaths were recorded during the 10-year period. There was no significant difference between the mean ages of death in individuals with and those without diabetes. Diabetic individuals had higher rates of hepato-pancreatic cancer and cardio-renal failure as causes of death. The prescription rates of antihypertensives, antiplatelets, and statins in diabetic individuals were larger than those in non-diabetic individuals. Furthermore, the use of sulfonyl urea or glinides and insulin was independently and inversely associated with the age of death. In conclusion, individuals with diabetes were treated with comprehensive pharmaceutical interventions and had life spans comparable to those of individuals without diabetes. This study's discovery of an inverse relationship between the use of insulin secretagogues or insulin and the age of death suggests that the prevention of life-threatening hypoglycemia is crucial for individuals with diabetes. (Tokushima University Institutional Repository) ● Metadata: 119252 (Link to Publication Site) ● Publication site (DOI): 10.3390/jcm13051283 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38592103 ● Search Scopus @ Elsevier (PMID): 38592103 ● Search Scopus @ Elsevier (DOI): 10.3390/jcm13051283 (Tokushima University Institutional Repository: 119252, DOI: 10.3390/jcm13051283, PubMed: 38592103)
4.	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)
5.	Tomoko Maruhashi, Hirokazu Miki, Kimiko Sogabe, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : Acute suppression of translation by hyperthermia enhances anti-myeloma activity of carfilzomib, International Journal of Hematology, Vol.119, No.3, 291-302, 2024. (Summary) Hyperthermia is a unique treatment option for cancers. Multiple myeloma (MM) remains incurable and innovative therapeutic options are needed. We investigated the efficacy of hyperthermia and carfilzomib in combination against MM cells. Although MM cell lines exhibited different susceptibilities to pulsatile carfilzomib treatment, mild hyperthermia at 43℃ induced MM cell death in all cell lines in a time-dependent manner. Hyperthermia and carfilzomib cooperatively induced MM cell death even under suboptimal conditions. The pro-survival mediators PIM2 and NRF2 accumulated in MM cells due to inhibition of their proteasomal degradation by carfilzomib; however, hyperthermia acutely suppressed translation in parallel with phosphorylation of eIF2α to reduce these proteins in MM cells. Recovery of β5 subunit enzymatic activity from its immediate inhibition by carfilzomib was observed at 24 h in carfilzomib-insusceptible KMS-11, OPM-2, and RPMI8226 cells, but not in carfilzomib-sensitive MM.1S cells. However, heat treatment suppressed the recovery of β5 subunit activity in these carfilzomib-insusceptible cells. Therefore, hyperthermia re-sensitized MM cells to carfilzomib. Our results support the treatment of MM with hyperthermia in combination with carfilzomib. Further research is warranted on hyperthermia for drug-resistant extramedullary plasmacytoma. (Keyword) Humans / Multiple Myeloma / Oligopeptides / Hyperthermia, Induced (Tokushima University Institutional Repository) ● Metadata: 119321 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03706-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38252236 ● Search Scopus @ Elsevier (PMID): 38252236 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03706-8 (Tokushima University Institutional Repository: 119321, DOI: 10.1007/s12185-023-03706-8, PubMed: 38252236)
6.	Kimiko Sogabe, Shingen Nakamura, Yoshiki Higa, Hirokazu Miki, Asuka Oda, Tomoko Maruhashi, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Masafumi Nakamura, Yusaku Maeda, Tomoyo Hara, Hiroki Yamagami, Shiroh Fujii, Kumiko Kagawa, Shuji Ozaki, Kiyoe Kurahashi, Itsuro Endo, Ken-ichi Aihara, Emiko Nakaue, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada and Masahiro Abe : Acute accumulation of PIM2 and NRF2 and recovery of β5 subunit activity mitigate multiple myeloma cell susceptibility to proteasome inhibitors., International Journal of Hematology, Vol.119, No.3, 303-315, 2024. (Summary) Resistance to proteasome inhibitors (PIs) has emerged as an important clinical issue. We investigated the mechanisms underlying multiple myeloma (MM) cell resistance to PIs. To mimic their pharmacokinetic/pharmacodynamic (PK/PD) profiles, MM cells were treated with bortezomib and carfilzomib for 1 h at concentrations up to 400 and 1,000 nM, respectively. Susceptibility to these PIs markedly varied among MM cell lines. Pulsatile treatments with PIs suppressed translation, as demonstrated by incorporation of puromycin at 24 h in PI-susceptible MM.1S cells, but not PI-resistant KMS-11 cells. Inhibition of β5 subunit activity decreased at 24 h in KMS-11 cells, even with the irreversible PI carfilzomib, but not under suppression of protein synthesis with cycloheximide. Furthermore, the proteasome-degradable pro-survival factors PIM2 and NRF2 acutely accumulated in MM cells subjected to pulsatile PI treatments. Accumulated NRF2 was trans-localized into the nucleus to induce the expression of its target gene, HMOX1, in MM cells. PIM and Akt inhibition restored the anti-MM effects of PIs, even against PI-resistant KMS-11 cells. Collectively, these results suggest that increased synthesis of β5 proteasome subunit and acute accumulation of PIM2 and NRF2 reduce the anti-MM effects of PIs. (Keyword) Humans / Proteasome Inhibitors / NF-E2-Related Factor 2 / Multiple Myeloma / Proteasome Endopeptidase Complex / Drug Resistance, Neoplasm / Cell Line, Tumor / Bortezomib / Antineoplastic Agents / Proto-Oncogene Proteins / Protein Serine-Threonine Kinases (Tokushima University Institutional Repository) ● Metadata: 119384 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03705-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38245883 ● Search Scopus @ Elsevier (PMID): 38245883 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03705-9 (Tokushima University Institutional Repository: 119384, DOI: 10.1007/s12185-023-03705-9, PubMed: 38245883)
7.	Hiroki Yamagami, Tomoyo Hara, Saya Yasui, Minae Hosoki, Taiki Hori, Yousuke Kaneko, Yukari Mitsui, Kiyoe Kurahashi, Takeshi Harada, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Cross-Sectional and Longitudinal Associations between Skin Autofluorescence and Tubular Injury Defined by Urinary Excretion of Liver-Type Fatty Acid-Binding Protein in People with Type 2 Diabetes., Biomedicines, Vol.11, No.11, 3020, 2023. (Summary) = 0.026). In conclusion, SAF is positively correlated with uL-FABP but not with uACR in people with T2D. Thus, there is a possibility that SAF can serve as a novel predictor for the development of diabetic tubular injury. (Keyword) skin autofluorescence / type 2 diabetes / diabetic kidney disease / albuminuria / tubular injury / L-FABP (Tokushima University Institutional Repository) ● Metadata: 119108 (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines11113020 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38002020 ● CiNii @ National Institute of Informatics (CRID): 1050581224891895040 ● Summary page in Scopus @ Elsevier: 2-s2.0-85178346619 (Tokushima University Institutional Repository: 119108, DOI: 10.3390/biomedicines11113020, PubMed: 38002020, CiNii: 1050581224891895040, Elsevier: Scopus)
8.	Saya Yasui, Yousuke Kaneko, Hiroki Yamagami, Minae Hosoki, Taiki Hori, Akihiro Tani, Tomoyo Hara, Kiyoe Kurahashi, Takeshi Harada, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Hiroyasu Mori, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Takeshi Soeki and Ken-ichi Aihara : Dehydroepiandrosterone Sulfate, an Adrenal Androgen, Is Inversely Associated with Prevalence of Dynapenia in Male Individuals with Type 2 Diabetes., Metabolites, Vol.13, No.11, 1129, 2023. (Summary) Dehydroepiandrosterone sulfate (DHEAS) is thought to be associated with life expectancy and anti-aging. Although skeletal muscle disorders are often found in diabetic people, the clinical significance of DHEAS in skeletal muscle remains unclear. Therefore, we aimed to determine whether DHEAS is associated with the development of skeletal muscle disorders in individuals with type 2 diabetes (T2D). A cross-sectional study was conducted in 361 individuals with T2D. Serum DHEAS levels, skeletal muscle mass index (SMI), handgrip strength (HS), and gait speed (GS) were measured in the participants. Pre-sarcopenia, sarcopenia, and dynapenia were defined according to the definitions of the AWGS 2019 criteria. DHEAS level was positively associated with HS but not with SMI or GS after adjustment of confounding factors. Multiple logistic regression analyses in total subjects showed that DHEAS level had an inverse association with the prevalence of dynapenia but not with the prevalence of pre-sarcopenia or sarcopenia. Furthermore, a significant association between DHEAS level and dynapenia was found in males but not in females. ROC curve analysis indicated that cutoff values of serum DHEAS for risk of dynapenia in males was 92.0 μg/dL. Therefore, in male individuals with T2D who have low serum levels of DHEAS, adequate exercise might be needed to prevent dynapenia. (Tokushima University Institutional Repository) ● Metadata: 119107 (Link to Publication Site) ● Publication site (DOI): 10.3390/metabo13111129 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37999225 ● CiNii @ National Institute of Informatics (CRID): 1050862699868605952 ● Summary page in Scopus @ Elsevier: 2-s2.0-85178271509 (Tokushima University Institutional Repository: 119107, DOI: 10.3390/metabo13111129, PubMed: 37999225, CiNii: 1050862699868605952, Elsevier: Scopus)
9.	Hiroyasu Mori, 谷口諭, 玉木悠, 野村友美, 鈴木麗子, Akio Kuroda, 明比祐子, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, 白神敦久, 田蒔基行, 天満仁, 長島伸光, 比木武 and Munehide Matsuhisa : 2型糖尿病患者のPersonal Health Recordを用いたセルフモニタリングに自動支援メッセージが与える効果:探索的ランダム化比較試験, 日本糖尿病インフォマティクス学会誌, Vol.22, No.2, 7-18, 2023.
10.	Masahiro Oura, Takeshi Harada, Asuka Oda, Jumpei Teramachi, Atsushi Nakayama, Ryohei Sumitani, Yusuke Inoue, Yusaku Maeda, Kimiko Sogabe, Maruhashi Tomoko, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Shingen Nakamura, Tomoyo Hara, Hiroki Yamagami, Kiyoe Kurahashi, Itsuro Endo, Hiroo Hasegawa, Hiroshi Fujiwara and Masahiro Abe : Therapeutic efficacy of the resorcylic acid lactone LL-Z1640-2 for adult T-cell leukaemia/lymphoma, eJHaem, Vol.4, No.3, 667-678, 2023. (Summary) Adult T-cell leukaemia/lymphoma (ATL) remains incurable. The NF-κB and interferon regulatory factor 4 (IRF4) signalling pathways are among the critical survival pathways for the progression of ATL. TGF-β-activated kinase 1 (TAK1), an IκB kinase-activating kinase, triggers the activation of NF-κB. The resorcylic acid lactone LL-Z1640-2 is a potent irreversible inhibitor of TAK1/extracellular signal-regulated kinase 2 (ERK2). We herein examined the therapeutic efficacy of LL-Z1640-2 against ATL. LL-Z1640-2 effectively suppressed the in vivo growth of ATL cells. It induced in vitro apoptosis and inhibited the nuclear translocation of p65/RelA in ATL cells. The knockdown of strongly induced ATL cell death while downregulating MYC. LL-Z1640-2 as well as the NF-κB inhibitor BAY11-7082 decreased the expression of IRF4 and MYC at the protein and mRNA levels, indicating the suppression of the NF-κB-IRF4-MYC axis. The treatment with LL-Z1640-2 also mitigated the phosphorylation of p38 MAPK along with the expression of CC chemokine receptor 4. Furthermore, the inhibition of STAT3/5 potentiated the cytotoxic activity of LL-Z1640-2 against IL-2-responsive ATL cells in the presence of IL-2. Therefore, LL-Z1640-2 appears to be an effective treatment for ATL. Further studies are needed to develop more potent compounds that retain the active motifs of LL-Z1640-2. (Link to Publication Site) ● Publication site (DOI): 10.1002/jha2.758 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37601887 ● Search Scopus @ Elsevier (PMID): 37601887 ● Search Scopus @ Elsevier (DOI): 10.1002/jha2.758 (DOI: 10.1002/jha2.758, PubMed: 37601887)
11.	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: 118250 (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: 118250, DOI: 10.5551/jat.63987, PubMed: 37081616)
12.	Emiko Nakaue, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Takeshi Harada, Asuka Oda, Yusuke Inoue, Sou Shimizu, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Eiji Tanaka and Masahiro Abe : Mechanisms of preferential bone formation in myeloma bone lesions by proteasome inhibitors., International Journal of Hematology, 2023. (Summary) Proteasome inhibitors (PIs) can preferentially restore bone in bone-defective lesions of patients with multiple myeloma (MM) who respond favorably to these drugs. Most prior in vitro studies on PIs used continuous exposure to low PI concentrations, although pharmacokinetic analysis in patients has shown that serum concentrations of PIs change in a pulsatile manner. In the present study, we explored the effects of pulsatile treatment with PIs on bone metabolism to simulate in vivo PI pharmacokinetics. Pulsatile treatment with bortezomib, carfilzomib, or ixazomib induced MM cell death but only marginally affected the viability of osteoclasts (OCs) with F-actin ring formation. Pulsatile PI treatment suppressed osteoclastogenesis in OC precursors and bone resorption by mature OCs. OCs robustly enhanced osteoblastogenesis in cocultures with OCs and MC3T3-E1 pre-osteoblastic cells, indicating OC-mediated coupling to osteoblastogenesis. Importantly, pulsatile PI treatment did not impair robust OC-mediated osteoblastogenesis. These results suggest that PIs might sufficiently reduce MM cell-derived osteoblastogenesis inhibitors to permit OC-driven bone formation coupling while suppressing OC differentiation and activity in good responders to PIs. OC-mediated coupling to osteoblastogenesis appears to be a predominant mechanism for preferential occurrence of bone regeneration at sites of osteoclastic bone destruction in good responders. (Tokushima University Institutional Repository) ● Metadata: 118380 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03601-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37039914 ● Search Scopus @ Elsevier (PMID): 37039914 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03601-2 (Tokushima University Institutional Repository: 118380, DOI: 10.1007/s12185-023-03601-2, PubMed: 37039914)
13.	Taiki Hori, Shingen Nakamura, Hiroki Yamagami, Saya Yasui, Minae Hosoki, Tomoyo Hara, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Harada, Akio Kuroda, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Phase angle and extracellular water-to-total body water ratio estimated by bioelectrical impedance analysis are associated with levels of hemoglobin and hematocrit in patients with diabetes., Heliyon, Vol.9, No.4, 2023. (Summary) PhA and ECW/TBW but not SMI were associated with levels of Hgb and Hct in patients with diabetes. Therefore, aberrant values of PhA and ECW/TBW suggest a risk of anemia in diabetic patients. (Tokushima University Institutional Repository) ● Metadata: 118251 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.heliyon.2023.e14724 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37057050 ● Search Scopus @ Elsevier (PMID): 37057050 ● Search Scopus @ Elsevier (DOI): 10.1016/j.heliyon.2023.e14724 (Tokushima University Institutional Repository: 118251, DOI: 10.1016/j.heliyon.2023.e14724, PubMed: 37057050)
14.	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, Vol.12, No.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: 118313 (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: 118313, DOI: 10.3390/antiox12010133, PubMed: 36670994)
15.	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, Vol.13, No.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: 118940 (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: 118940, DOI: 10.1038/s41467-022-34869-3, PubMed: 36424386)
16.	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: 118258 (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: 118258, DOI: 10.5551/jat.63752, PubMed: 36244745)
17.	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, Vol.12, No.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: 117150 (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: 117150, DOI: 10.57352/ijm.12.2_14, CiNii: 1390573947533793024)
18.	Asami Okada, Misuzu Yamada-Yamashita, Yukari Tominaga, Kyoka Jo, Hiroyasu Mori, Reiko Suzuki, Masashi Ishizu, Motoyuki Tamaki, Yuko Akehi, Yuichi Takashi, Daisuke Koga, Eisuke Shimokita, Fuminori Tanihara, Kiyoe Kurahashi, Sumiko Yoshida, Yukari Mitsui, Shiho Masuda, Itsuro Endo, Ken-ichi Aihara, Shoji Kagami, Masahiro Abe, Kevin Ferreri, Yoshio Fujitani, Munehide Matsuhisa and Akio Kuroda : Novel method utilizing bisulfite conversion with dual amplification-refractory mutation system polymerase chain reaction to detect circulating pancreatic β-cell cfDNA., Journal of Diabetes Investigation, Vol.13, No.7, 1140-1148, 2022. (Summary) We developed a novel method for detecting unmethylated insulin DNA in circulation that can be performed using a conventional real-time PCR system. This method would be useful for analyzing dynamic profiles of β-cells in human disease such as type 1 diabetes. (Tokushima University Institutional Repository) ● Metadata: 117206 (Link to Publication Site) ● Publication site (DOI): 10.1111/jdi.13806 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35396829 ● Search Scopus @ Elsevier (PMID): 35396829 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13806 (Tokushima University Institutional Repository: 117206, DOI: 10.1111/jdi.13806, PubMed: 35396829)
19.	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, Vol.107, No.3, 744-749, 2022. (Keyword) Bone Resorption / Humans / Multiple Myeloma / Osteoclasts / Osteolysis (Tokushima University Institutional Repository) ● Metadata: 116715 (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: 116715, DOI: 10.3324/haematol.2021.278295, PubMed: 34788982)
20.	Yukari Mitsui, Akio Kuroda, Masashi Ishizu, Hiroyasu Mori, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Yuko Akehi, Ken-ichi Aihara, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : Basal insulin requirement in patients with type 1 diabetes depends on the age and body mass index., Journal of Diabetes Investigation, Vol.13, No.2, 292-298, 2022. (Summary) T (Tokushima University Institutional Repository) ● Metadata: 116546 (Link to Publication Site) ● Publication site (DOI): 10.1111/jdi.13547 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33740836 ● Search Scopus @ Elsevier (PMID): 33740836 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13547 (Tokushima University Institutional Repository: 116546, DOI: 10.1111/jdi.13547, PubMed: 33740836)
21.	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, Vol.11, No.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: 117260 (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: 117260, DOI: 10.1002/cti2.1371, PubMed: 35079379)
22.	Yukari Mitsui, Yuto Iizuka, Tomoaki Tanaka, Tomoyo Hara, Shiho Masuda, Yukiyo Ohnishi, Mai Kanai, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Kondo, Toshiko Kanezaki, Yasumi Shintani, Hiroki Yamagami, Hiroyuki Yamaguchi, Yuichi Fujinaka, Kana Morimoto, Atsuhisa Shirakami, Ken-ichi Aihara, Seiji Fukumoto, Masahiro Abe and Itsuro Endo : An attempt to create a treatment algorithm of central adrenal insufficiency using CRH test, DHEA-S and clinical evaluation., The Journal of Medical Investigation : JMI, Vol.69, No.3.4, 287-293, 2022. (Summary) Objective : To examine diagnostic performance of corticotropin-releasing hormone (CRH) test combined with baseline dehydroepiandrosterone sulfate (DHEA-S) in patients with a suspect of central adrenal insufficiency. Methods : Patients (n=215) requiring daily or intermittent hydrocortisone replacement, or no replacement were retrospectively checked with their peak cortisol after CRH test and baseline DHEA-S. Results : None of 106 patients with the peak cortisol · 17.5 g /L after CRH test required replacement, and all 64 patients with the peak cortisol < 10.0 g /L required daily replacement. Among 8 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S below the reference range, 6 patients required daily replacement and 1 patient was under intermittent replacement. Among 37 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S within the reference range, 10 and 6 patients were under intermittent and daily replacement, respectively. Conclusions : No patients with the peak cortisol · 17.5 g /L required hydrocortisone replacement, and all patients with the peak cortisol below 10.0 g /L required daily replacement. Careful clinical evaluation was required to determine requirement for replacement in patients with 10.0 g /L the peak cortisol < 17.5 g /L even in combination with baseline DHEA-S. J. Med. Invest. 69 : 287-293, August, 2022. (Keyword) Adrenal Insufficiency / Adrenocorticotropic Hormone / Algorithms / Corticotropin-Releasing Hormone / Dehydroepiandrosterone Sulfate / Humans / Hydrocortisone / Retrospective Studies (Tokushima University Institutional Repository) ● Metadata: 117738 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.287 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244782 ● CiNii @ National Institute of Informatics (CRID): 1390575263318485248 ● Summary page in Scopus @ Elsevier: 2-s2.0-85139886801 (Tokushima University Institutional Repository: 117738, DOI: 10.2152/jmi.69.287, PubMed: 36244782, CiNii: 1390575263318485248, Elsevier: Scopus)
23.	Asami Okada, Misuzu Yamada, Hiroyasu Mori, 明比祐子, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Akio Kuroda : 循環血中遊離 DNA を用いた膵β細胞傷害の新規検出法の確立, Shikoku Acta Medica, Vol.77, No.5,6, 249-245, 2021. (Summary) In people with type1 diabetes(T1D), biomarkers that can sensitively and quantitatively evaluate injury of pancreatic beta cell are required in order to predict the onset of the disease at an early stage and to provide interventions to prevent the progression of the disease. We developed a new method for quantifying pancreatic beta cell-derived insulin DNA in circulation that combines bisulfite conversion and Amplification Refractory Mutation System(ARMS)PCR, which can be performed using a conventional real-time PCR system. We applied this method to T1D patients and healthy adults, both could be detected in about 30% of cases. The results in healthy adults indicate that this method may have sensitivity to detect the turnover of pancreatic beta cells at physiological conditions. In post-onset T1D patients, there were many negatives because the amount of residual pancreatic beta cells was extremely small. However, in some cases with a short duration of the disease, pancreatic beta cell-derived insulin DNA was detected in negative correlation between the duration of the disease, that suggested the residual pancreatic beta cells continue to be slowly destroyed. It was demonstrated that the time course of pathophysiology in T1D could be understood using this method. (Keyword) Insulin / DNA methylation / RT-PCR / Type1 diabetes / cell-free DNA (Tokushima University Institutional Repository) ● Metadata: 117138 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050292317645976448 (Tokushima University Institutional Repository: 117138, CiNii: 1050292317645976448)
24.	木村蘭子, Kiyoe Kurahashi, 細木美苗, 辻誠士郎, 三井由加里, Sumiko Yoshida, 明比祐子, Itsuro Endo, Seiji Fukumoto and Masahiro Abe : 繰り返す脆弱性骨折を契機に発見されたクッシング症候群の一例, Shikoku Acta Medica, Vol.77, No.5-6, 269-274, 2021. (Summary) A 38-year-old woman had suffered from an avulsion fracture of the left cuboid bone, a rib fracture, a fatigue fracture of the left second metatarsal bone and a pubic fracture within the last 4 years. She also realized that her face was getting rounded and became aware of edema on extremities. She had repeated fragile fractures before menopause and was referred to our department on suspicion of secondary osteoporosis. The patients showed physical signs of moon face, central obesity, and abdominal violaceous striae. Cushing's syndrome was suspected, therefore confirmatory studies were performed. Circadian variation of cortisol : serum cortisol19．3μg/dL(at7:00), 21．4μg/dL(at23:00), urinary free cortisol :247．4μg/24h, ACTH :2．5pg/mL. Low-dose(1mg) dexamethasone did not suppress cortisol level(18．9μg/dL). Based on these findings, we diagnosed as Cushing's syndrome and glucocorticoid excess seemed to be the cause of secondary osteoporosis. Abdominal CT identified a 2．7 cm tumor in the left adrenal gland, and in-phase T1‐weighted MRI showed decreased signal compared to out-phase, suggesting an adrenocortical adenoma. She underwent laparoscopic left adrenalectomy. Postoperative fasting serum cortisol decreased to2．2 μg/dL, and glucocorticoid replacement therapy was started. It is necessary to find out any secondary causes for premenopausal women with fragility fractures. It is well known that endocrine disorders including Cushing's syndrome are the most frequent associated diseases in patients with premenopausal osteoporosis. Cushing's syndrome should be considered as a causative disease in premenopausal women with osteoporosis. (Keyword) Cushing syndrome / fragility fracture / Premenopausal woman (Tokushima University Institutional Repository) ● Metadata: 116832 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050573637786980224 (Tokushima University Institutional Repository: 116832, CiNii: 1050573637786980224)
25.	吉川紘平, 金子遥祐, 辻誠士郎, 河田沙紀, 川原綾香, 森建介, 遠藤ふうり, Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Masahiro Abe and Munehide Matsuhisa : TIA様症状を契機に診断されたインスリノーマの1例, Shikoku Acta Medica, Vol.77, No.5-6, 275-280, 2021. (Summary) We report the case of a67-year-old woman who had symptoms suggestive of a transient ischemic attack(TIA), such as lightheadedness and transient visual changes before meals for 4 months. She experienced altered consciousness before lunch and was taken to the emergency room2weeks ago. She had repeated hypoglycemia with a blood glucose level of 31 mg/dL. Insulin secretion was not suppressed, with an immunoreactive insulin level of 14．0 μU/mL and connecting peptide immunoreactivity of 1．83 ng/mL for occasional blood glucose levels of 49 mg/dL. Dynamic CT revealed a 17‐mm mass enhanced during the arterial phase in the pancreatic uncinate process, suggestive of a pancreatic neuroendocrine tumor. A selective arterial secretagogue(calcium)injection test revealed the localization of insulinoma in the head of the pancreas. Therefore, pancreatoduodenectomy was performed. Hyperglycemia occurred after the surgery, and it was judged that the insulinoma was resected. This case showed TIA-like symptoms without signs of sympathetic overdrive associated with hypoglycemia. Thus, the diagnosis was delayed. Insulinoma may present with symptoms of neuroglycopenia but not autonomic activity due to hypoglycemia. Insulinoma should be distinguished in patients with unknown neurological symptoms since neuroglycopenia caused by insulinoma is diverse. (Keyword) Insulinoma / Hypoglycemia / Neuroglycopenia / Transient ischemic attack (Tokushima University Institutional Repository) ● Metadata: 116831 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520292182331094144 (Tokushima University Institutional Repository: 116831, CiNii: 1520292182331094144)
26.	川原綾香, Kiyoe Kurahashi, 工藤千晶, 鎌田基夢, Shinsuke Katoh, Yukiko Tomioka, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, Sumiko Yoshida, Ken-ichi Aihara, Itsuro Endo, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 歩行不能だったが，多職種の高度な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例, Shikoku Acta Medica, Vol.76, No.5-6, 317-322, 2021. (Summary) A 48-year-old man who weighed 216 kg was significantly overweight with a body mass index (BMI)of 75．6kg/m2, and was unable to walk due to disuse syndrome. Because of the psychological and social problems in the background, a psychological examination was performed and the staff took time to build a trusting relationship with the patient, taking into account his characteristics. With diet and rehabilitation, he was able to lose weight to 124kg and BMI 43．9kg/m2 over 600 days, and was able to walk with assistive devices and defecate by himself. The patient was discharged from our hospital after a series of multidisciplinary meetings with medical, nursing, welfare, and governmental agencies to create an environment for home recuperation. The reasons for the improvement to enable him to be discharged from the hospital were due to the multi-disciplinary meetings among the staff inside and outside the hospital, information sharing and advanced coordination, and smooth communication with the patient by taking into account his characteristics from a psychological standpoint. (Keyword) Sever obesity / disuse syndrome / Patient-specific care / Multidisciplinary team (Tokushima University Institutional Repository) ● Metadata: 115801 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050568937749256704 (Tokushima University Institutional Repository: 115801, CiNii: 1050568937749256704)
27.	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, Vol.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: 116283 (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: 116283, DOI: 10.1016/j.bbrep.2021.101107, PubMed: 34458594)
28.	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: 116545 (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: 116545, DOI: 10.1111/jdi.13602, PubMed: 34043882)
29.	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, Vol.106, No.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: 116529 (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: 116529, DOI: 10.3324/haematol.2019.234476, PubMed: 32273474)
30.	桝田志保, Sumiko Yoshida, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由加里, Kiyoe Kurahashi, Itsuro Endo, 轟貴史 and Masahiro Abe : Delayed diagnosis of thyroid storm in an elderly patient: A case report, Japanese Journal of Geriatrics, Vol.58, No.1, 158-163, 2021. (Summary) <p>A 70-year-old woman was hospitalized for diarrhea, vomiting, loss of appetite, fatigue, and dyspnea on exertion for the past 3 weeks and treated with intravenous fluid for dehydration. She was receiving prednisolone for polymyositis. She did not have a history of thyroid disease. On day 4 of hospitalization, the patient was diagnosed with congestive heart failure and tachycardiac atrial fibrillation, and treatment with a diuretic agent was initiated. On day 7 of hospitalization, a clinical laboratory evaluation revealed that the level of free thyroxine was 9.95 ng/dL, free triiodothyronine was >30 pg/mL, and thyroid-stimulating hormone was <0.01 μU/mL, and the patient was initially diagnosed with thyrotoxicosis because of Graves' disease. She showed restlessness and had a fever of 39 °C, tachycardia of ≥140 beats/min, pulmonary edema, and frequent diarrhea, all of which were consistent with the symptoms of thyroid storm. Her general condition gradually improved with comprehensive treatment of thyroid storm comprising thiamazole, potassium iodide, hydrocortisone, and landiolol. A reassessment revealed that the patient had already had thyrotoxicosis and thyroid storm on admission. Thyroid storm is a potentially fatal disease that must be urgently addressed; however, its symptoms are difficult to distinguish from those caused by other diseases. Furthermore, elderly individuals may not exhibit typical symptoms of thyroid storm, so the diagnosis is difficult. In this case, the diagnosis was delayed because of the absence of typical symptoms of thyroid storm and the influence of a pre-existing medical condition and medication.</p> (Keyword) Thyroid storm / Graves' disease / Atrial fibrillation / Heart failure / Takotsubo cardiomyopathy (Link to Publication Site) ● Publication site (DOI): 10.3143/geriatrics.58.158 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390568772520282112 ● Search Scopus @ Elsevier (DOI): 10.3143/geriatrics.58.158 (DOI: 10.3143/geriatrics.58.158, CiNii: 1390568772520282112)
31.	Toshio Matsumoto and Itsuro Endo : RANKL as a target for the treatment of osteoporosis, Journal of Bone and Mineral Metabolism, Vol.39, No.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)
32.	Yumi Kuwamura, Sumiko Yoshida, Kiyoe Kurahashi, 澄川真珠子, Eijiro Sakamoto, Akio Kuroda, Ken-ichi Aihara, Makoto Funaki, Hiromichi Yumoto, Hirokazu Uemura, 岡本美鈴, 大和光, Munehide Matsuhisa, Itsuro Endo and Sachi Kishida : 糖尿病患者の口腔保健行動アセスメントツールを用いた看護支援プログラムの評価, Journal of the The Japan Diabetes Society, Vol.63, No.Supplement, S117, 2020. (Keyword) diabetes mellitus / oral health behaviors / assessment / 看護支援
33.	Toshio Matsumoto and Itsuro Endo : MInodronate, Bone, Vol.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)
34.	Yumi Kuwamura, Sumiko Yoshida, Kiyoe Kurahashi, Masuko Sumikawa, Eijiro Sakamoto, Ken-ichi Aihara, Hiromichi Yumoto, Akio Kuroda, Itsuro Endo, Toshiyuki Yasui and Sachi Kishida : Modified diabetes oral health assessment tool (M-DiOHAT©) for nurses and their association with efficacy beliefs and outcome expectancies in patients with diabetes, JNI : The Journal of Nursing Investigation, Vol.18, No.1, 13-26, 2020. (Keyword) diabetes mellitus / assessment / nursing / oral health behaviors (Tokushima University Institutional Repository) ● Metadata: 114058 (Link to Publication Site) ● Publication site (DOI): 10.32273/jni.JNI_018_013 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.32273/jni.JNI_018_013 (Tokushima University Institutional Repository: 114058, DOI: 10.32273/jni.JNI_018_013)
35.	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, Vol.12, No.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: 115041 (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: 115041, DOI: 10.3390/cancers12040929, PubMed: 32283857)
36.	Hiroya Matsuda, Kiyoe Kurahashi, Furi Endo, Shiho Masuda, Yukari Mitsui, Sumiko Yoshida, Yuko Akehi, Itsuro Endo and Seiji Fukumoto : A case of isolated ACTH deficiency that required 6 months for the diagnosis from onset., Shikoku Acta Medica, Vol.75, No.1, 2, 69-74, 2019. (Summary) A 53-year-old man noticed anorexia, nausea, and arthralgia of the upper limbs in April, 201X. Since these symptoms persisted, he visited general hospital and clinic and was examined for blood chemistry, ECG, echocardiography and so on. However, he did not get a definitive diagnosis and was followed up with drip infusion of saline. The symptoms did not subside and fatigue and syncope with hypotension developed. Furthermore, he also suffered weight loss of 10 kg in few months and was referred to our hospital for more detailed examinations in October, 201X. Upon the initial examination, all his symptoms matched those of adrenal insufficiency and notable decreases of both plasma ACTH and serum cortisol level were observed. Prompt glucocorticoid supplementation improved his symptoms and the abnormal laboratory data immediately. He was diagnosed adrenal insufficiency due to isolated ACTH deficiency from the results of CRH loading test and insulin tolerance test. Since most of the symptoms and laboratory findings are non-specific, diagnosis of adrenal insufficiency is often delayed. However, adrenal insufficiency could worsen when the patient is under stress (e.g. infection) and often be life-threatening. Glucocorticoid replacement therapy should be initiated as soon as the diagnosis is confirmed. Furthermore, educating patients and his families plays a very important role in the management of chronic adrenal insufficiency, in particular to the prevention of adrenal crisis. (Keyword) isolated ACTH deficiency / adrenal insufficiency / anorexia / nausea / arthralgia (Tokushima University Institutional Repository) ● Metadata: 113765 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845763703567104 (Tokushima University Institutional Repository: 113765, CiNii: 1050845763703567104)
37.	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, Vol.3, No.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)
38.	Hiroyasu Mori, Akio Kuroda, Masashi Ishizu, Mami Ohishi, Yuichi Takashi, Yinhua Otsuka, Satoshi Taniguchi, Motoyuki Tamaki, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Yuko Akehi and Munehide Matsuhisa : Association of accumulated advanced glycation end-products with a high prevalence of sarcopenia and dynapenia in patients with type 2 diabetes., Journal of Diabetes Investigation, 2019. (Summary) Advanced glycation end-products (AGEs), which are a major cause of diabetic vascular complications, accumulate in various tissues under chronic hyperglycemic conditions, as well as with aging in patients with diabetes. The loss of muscle mass and strength, so-called sarcopenia and dynapenia, has recently been recognized as a diabetic complication. However, the influence of accumulated AGEs on muscle mass and strength remains unclear. The present study aimed to evaluate the association of sarcopenia and dynapenia with accumulated AGEs in patients with type 2 diabetes. We recruited 166 patients with type 2 diabetes aged 30 years (mean age 63.2 ± 12.3 years; body mass index 26.3 ± 4.9 kg/m ; glycated hemoglobin 7.1 ± 1.1%). Skin autofluorescence as a marker of AGEs, limb skeletal muscle mass index, grip strength, knee extension strength and gait speed were assessed. Sarcopenia and dynapenia were observed in 7.2 and 13.9% of participants, respectively. Skin autofluorescence was significantly higher in patients with sarcopenia and dynapenia. Skin autofluorescence was the independent determinant for skeletal muscle mass index, grip strength, knee extension strength, sarcopenia and dynapenia. Accumulated AGEs could contribute to reduced muscle mass and strength, leading to sarcopenia and dynapenia in patients with type 2 diabetes. (Tokushima University Institutional Repository) ● Metadata: 114022 (Link to Publication Site) ● Publication site (DOI): 10.1111/jdi.13014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30677242 ● Search Scopus @ Elsevier (PMID): 30677242 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13014 (Tokushima University Institutional Repository: 114022, DOI: 10.1111/jdi.13014, PubMed: 30677242)
39.	Shusuke Yagi, Itsuro Endo, Taichi Murakami, Tetsuya Hida, Yousuke Yamamoto, Tomohiro Soga, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Daiju Fukuda, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Shinji Kawahito and Masataka Sata : Adult onset of Immunoglobulin A vasculitis - A case report,, The Journal of Medical Investigation : JMI, Vol.66, No.3,4, 344-346, 2019. (Summary) Immunoglobulin A vasculitis (IgAV), formerly known as Henoch-Schönlein purpura, primarily occurs during childhood between the ages of 3 and 15 years and is the most common form of systemic vasculitis in children ; its occurrence in adults has been rarely reported. Such low incidence could be attributable to either under-diagnosis or misdiagnosis. Thus, not only pediatricians but also physicians should be able to diagnose IgAV accurately to manage the patients appropriately and avoid its associated complications. In addition, treatment of adult onset IgAV with renal involvement has not been fully established yet. We describe here a case of adult onset IgAV complicated by proteinuria and pharyngitis, which was cured by no specific treatment. J. Med. Invest. 66 : 344-346, August, 2019. (Keyword) Acetaminophen / Adult / Factor XIII / Humans / Immunoglobulin A / Male / Pharyngitis / Proteinuria / Purpura, Schoenlein-Henoch (Tokushima University Institutional Repository) ● Metadata: 114166 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.344 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31656302 ● Search Scopus @ Elsevier (PMID): 31656302 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.66.344 (Tokushima University Institutional Repository: 114166, DOI: 10.2152/jmi.66.344, PubMed: 31656302)
40.	Ariunzaya Bat-Erdene, Shingen Nakamura, Asuka Oda, Masami Iwasa, Jumpei Teramachi, Mohannad Ashtar, Takeshi Harada, Hirokazu Miki, Hirofumi Tenshin, Masahiro Hiasa, Shiroh Fujii, Kimiko Sogabe, Masahiro Oura, Kengo Udaka, Kumiko Kagawa, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : Class 1 HDAC and HDAC6 inhibition inversely regulates CD38 induction in myeloma cells via interferon-α and ATRA., British Journal of Haematology, 2018. (Tokushima University Institutional Repository) ● Metadata: 113393 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.15673 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30474853 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057280798 (Tokushima University Institutional Repository: 113393, DOI: 10.1111/bjh.15673, PubMed: 30474853, Elsevier: Scopus)
41.	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, Vol.180, No.4, 581-585, 2018. (Tokushima University Institutional Repository) ● Metadata: 112935 (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: 112935, DOI: 10.1111/bjh.14388, PubMed: 27748523)
42.	Shiroh Fujii, Shingen Nakamura, Asuka Oda, Hirokazu Miki, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Harada, Kumiko Kagawa, Michiyasu Nakao, Shigeki Sano and Masahiro Abe : Unique anti-myeloma activity by thiazolidine-2,4-dione compounds with Pim inhibiting activity., British Journal of Haematology, Vol.180, No.2, 246-258, 2018. (Summary) Proviral Integrations of Moloney virus 2 (PIM2) is overexpressed in multiple myeloma (MM) cells, and regarded as an important therapeutic target. Here, we aimed to validate the therapeutic efficacy of different types of PIM inhibitors against MM cells for their possible clinical application. Intriguingly, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a reduced PIM2 protein levels and impaired MM cell survival preferentially in acidic conditions, in contrast to other types of PIM inhibitors, including AZD1208, CX-6258 and PIM447. SMI-16a also suppressed the drug efflux function of breast cancer resistance protein, minimized the sizes of side populations and reduced in vitro colony-forming capacity and in vivo tumourigenic activity in MM cells, suggesting impairment of their clonogenic capacity. PIM2 is known to be subject to ubiquitination-independent proteasomal degradation. Consistent with this, the proteasome inhibitors bortezomib and carfilzomib increased PIM2 protein levels in MM cells without affecting its mRNA levels. However, SMI-16a mitigated the PIM2 protein increase and cooperatively enhanced anti-MM effects in combination with carfilzomib. Collectively, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a uniquely reduce PIM2 protein in MM cells, which may contribute to their profound efficacy in addition to their immediate kinase inhibition. Their combination with proteasome inhibitors is envisioned. (Keyword) Animals / Antineoplastic Agents / Cell Line, Tumor / Cell Survival / Cell Transformation, Neoplastic / Disease Models, Animal / Humans / Hydrogen-Ion Concentration / Mice / Multiple Myeloma / Proteasome Inhibitors / Protein-Serine-Threonine Kinases / Proteolysis / Proto-Oncogene Proteins / Thiazolidinediones (Tokushima University Institutional Repository) ● Metadata: 112752 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.15033 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29327347 ● Summary page in Scopus @ Elsevier: 2-s2.0-85040344893 (Tokushima University Institutional Repository: 112752, DOI: 10.1111/bjh.15033, PubMed: 29327347, Elsevier: Scopus)
43.	Hirokazu Miki, Shingen Nakamura, Asuka Oda, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kiyoe Kurahashi, Sumiko Yoshida, Kumiko Kagawa, Itsuro Endo, Aihara Kenichi, Mariko Ikuo, Kouji Itou, Koichiro Hayashi, Michihiro Nakamura and Masahiro Abe : Effective impairment of myeloma cells and their progenitors by hyperthermia., Oncotarget, Vol.9, No.12, 10307-10316, 2017. (Summary) Multiple myeloma (MM) remains incurable, and MM-initiating cells or MM progenitors are considered to contribute to disease relapse through their drug-resistant nature. In order to improve the therapeutic efficacy for MM, we recently developed novel superparamagnetic nanoparticles which selectively accumulate in MM tumors and extirpate them by heat generated with magnetic resonance. We here aimed to clarify the therapeutic effects on MM cells and their progenitors by hyperthermia. Heat treatment at 43°C time-dependently induced MM cell death. The treatment upregulated endoplasmic reticulum (ER) stress mediators, ATF4 and CHOP, while reducing the protein levels of Pim-2, IRF4, c-Myc and Mcl-1. Combination with the proteasome inhibitor bortezomib further enhanced ER stress to potentiate MM cell death. The Pim inhibitor SMI-16a also enhanced the reduction of the Pim-2-driven survival factors, IRF4 and c-Myc, in combination with the heat treatment. The heat treatment almost completely eradicated "side population" fractions in RPMI8226 and KMS-11 cells and suppressed their clonogenic capacity as determined by colony formation and tumorigenic capacity in SCID mice. These results collectively demonstrated that hyperthermia is able to impair clonogenic drug-resistant fractions of MM cells and enhance their susceptibility to chemotherapeutic drugs. (Tokushima University Institutional Repository) ● Metadata: 113059 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.23121 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29535808 ● Summary page in Scopus @ Elsevier: 2-s2.0-85041952629 (Tokushima University Institutional Repository: 113059, DOI: 10.18632/oncotarget.23121, PubMed: 29535808, Elsevier: Scopus)
44.	Shusuke Yagi, Ken-ichi Aihara, Takeshi Kondo, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Daiju Fukuda, Yutaka Nakaya, Kin-Ichiro Suwaki, Takashi Takeji, Toshihiro Wada, Masdan Hotimah Salim, Saori Hama, Tomomi Matsuura, Takayuki Ise, Kenya Kusunose, Koji Yamaguchi, Takeshi Tobiume, Hirotsugu Yamada, Takeshi Soeki, Tetsuzo Wakatsuki, Munehide Matsuhisa, Michio Shimabukuro, Masashi Akaike and Masataka Sata : Predictors for the Treatment Effect of Sodium Glucose Co-transporter 2 Inhibitors in Patients with Type 2 Diabetes Mellitus., Advances in Therapy, Vol.35, No.1, 124-134, 2017. (Summary) Predictors for the effect of sodium glucose co-transporter 2 (SGLT2) inhibitors at lowering hemoglobin A1c (HbA1c) levels in type 2 diabetes mellitus patients remain unclear. We therefore aimed to elucidate these predictors in type 2 diabetes patients after 3 months of SGLT2 treatment. A total of 302 consecutive type 2 diabetes patients who had been treated with SGLT2 inhibitors as monotherapy or add-on therapy to existing antidiabetic treatments were enrolled retrospectively. After excluding 27 patients whose HbA1c levels could not be evaluated 3 months after treatment, the glucose-lowering effects of SGLT2 inhibitors were assessed in 275 patients by measuring HbA1c levels before and 3 months after treatment. The predictors for changes in HbA1c levels after 3 months of treatment were evaluated. SGLT2 inhibitor treatment for 3 months decreased HbA1c levels from 7.8 ± 1.2% to 7.4 ± 1.0% (p < 0.0001). A multiple regression analysis showed that the independent determinants for SGLT2 inhibitor treatment effect included decreased HbA1c levels after 1 month of treatment, high baseline HbA1c levels, and a high estimated glomerular filtration rate (eGFR). We show that type 2 diabetes patients who received the greatest glucose-lowering effect with SGLT2 inhibitor treatment were those with preserved renal function (high baseline eGFR) and high baseline HbA1c levels. Moreover, SGLT2 inhibitor treatment efficacy could be predicted by the patients' initial response to treatment. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12325-017-0639-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29185199 ● Summary page in Scopus @ Elsevier: 2-s2.0-85035102977 (DOI: 10.1007/s12325-017-0639-z, PubMed: 29185199, Elsevier: Scopus)
45.	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, Vol.1, No.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: 111724 (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: 111724, DOI: 10.1182/bloodadvances.2017008813, PubMed: 29296860)
46.	Kiyoe Kurahashi, Itsuro Endo, Takeshi Kondo, Kana Morimoto, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Kohhei Nakajima, Yoshifumi Mizobuchi, Shinji Nagahiro, Masahiro Abe and Seiji Fukumoto : Remarkable Shrinkage of a Growth Hormone (GH)-secreting Macroadenoma Induced by Somatostatin Analogue Administration: A Case Report and Literature Review., Internal Medicine, Vol.56, No.18, 2455-2461, 2017. (Summary) Acromegaly is caused by excessive growth hormone secretion, usually from pituitary adenomas. Somoatostatin analogues are widely used as primary or adjunctive therapy in the management of acromegaly. In this report, we present a case with remarkable shrinkage of a tumor after relatively short-term octreotide long-acting release (LAR) administration. During the 30-month follow-up after starting octreotide LAR, there was no recurrence of acromegaly with remarkable shrinkage of the tumor on pituitary magnetic resonance imaging. A literature review of the predictors for tumor shrinkage after the administration of somatostatin analogues in patients with acromegaly is also discussed in relation to this case. (Tokushima University Institutional Repository) ● Metadata: 114396 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.8223-16 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28824054 ● Summary page in Scopus @ Elsevier: 2-s2.0-85029653591 (Tokushima University Institutional Repository: 114396, DOI: 10.2169/internalmedicine.8223-16, PubMed: 28824054, Elsevier: Scopus)
47.	Jun Okazaki, Naoki Muguruma, Shinji Kitamura, Tetsuo Kimura, Koichi Okamoto, Hiroshi Miyamoto, Kazuhiro Kishi, Yoshimi Bando, Takeshi Kondo, Itsuro Endo, Masahiro Abe and Tetsuji Takayama : Paraneoplastic hypocalcemia developed in gastric cancer accompanied by osteoblastic metastasis, Internal Medicine, Vol.56, No.11, 1345-1349, 2017. (Summary) Paraneoplastic syndromes are generally defined as clinical disorders associated with malignant diseases, and hypocalcemia associated with cancer is a rare condition. A woman in her 60s was referred to our hospital for the further examination of massive ascites due to carcinoma of unknown primary origin. She complained of numbness around her lips, and marked hypocalcemia of 5.0 mg/dL was noted. After two courses of chemotherapy, computed tomography showed a decrease in the ascites, and her serum calcium level increased. Although hypocalcemia is a very rare condition in patients with gastric cancer, serum calcium values should be evaluated when neurological symptoms are observed. (Keyword) Adult / Aged / Female / Humans / Hypocalcemia / Middle Aged / Neoplasm Metastasis / Osteoblasts / Paraneoplastic Syndromes / Stomach Neoplasms / Tomography, X-Ray Computed / Treatment Outcome / Young Adult (Tokushima University Institutional Repository) ● Metadata: 114393 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.56.8545 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28566596 ● Summary page in Scopus @ Elsevier: 2-s2.0-85020067897 (Tokushima University Institutional Repository: 114393, DOI: 10.2169/internalmedicine.56.8545, PubMed: 28566596, Elsevier: Scopus)
48.	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: 110925 (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: 110925, DOI: 10.5551/jat.37739, PubMed: 28502917)
49.	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, Vol.8, No.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)
50.	Sakiya Yoshimoto, Kojiro Nagai, Eriko Shibata, Sayo Ueda, Hiroyuki Ono, Masanori Tamaki, Kenji Nishimura, Fumiaki Obata, Taizo Inagaki, Masanori Minato, Fumi Kishi, Motokazu Matsuura, Naoko Matsui, Itsuro Endo, Michael Hann, Seiji Kishi, Taichi Murakami, Hideharu Abe and Toshio Doi : Influential factors on serum albumin concentration in hospitalized chronic kidney disease patients., The Journal of Medical Investigation : JMI, Vol.64, No.1.2, 146-152, 2017. (Summary) SAC was affected by not only proteinuria, but also postural change, physical activity, and food in CKD patients. SAC should be analyzed by standardizing a patient's condition during phlebotomy. J. Med. Invest. 64: 146-152, February, 2017. (Tokushima University Institutional Repository) ● Metadata: 111103 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.146 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373613 ● Summary page in Scopus @ Elsevier: 2-s2.0-85016409577 (Tokushima University Institutional Repository: 111103, DOI: 10.2152/jmi.64.146, PubMed: 28373613, Elsevier: Scopus)
51.	Takeshi Kondo, Itsuro Endo, Yukari Ooguro, Kana Morimoto, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Masahiro Abe and Seiji Fukumoto : Suppression of the Hypothalamic-pituitary-adrenal Axis by Maximum Androgen Blockade in a Patient with Prostate Cancer., Internal Medicine, Vol.55, No.24, 3623-3626, 2016. (Summary) A 78-year-old Japanese man showed suppression of the hypothalamic-pituitary-adrenal axis during maximum androgen blockade (MAB) therapy including chlormadinone acetate (CMA) for prostate cancer. After stopping the MAB therapy, both the basal ACTH level and the response to CRH recovered. While no reports have indicated that CMA suppresses the hypothalamic-pituitary-adrenal axis in patients with prostate cancer, CMA has been shown to inhibit this axis in animals. These observations suggest that we must monitor the hypothalamic-pituitary-adrenal axis in patients treated with CMA, especially under stressful conditions. (Keyword) Adrenal Glands / Adrenocorticotropic Hormone / Aged / Androgen Antagonists / Animals / Antineoplastic Agents / Chlormadinone Acetate / Corticotropin-Releasing Hormone / Diabetes Mellitus, Type 2 / Humans / Hypothalamo-Hypophyseal System / Male / Pituitary-Adrenal System / Prostatic Neoplasms / Treatment Outcome (Tokushima University Institutional Repository) ● Metadata: 114392 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.55.7359 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27980263 ● Summary page in Scopus @ Elsevier: 2-s2.0-85007140325 (Tokushima University Institutional Repository: 114392, DOI: 10.2169/internalmedicine.55.7359, PubMed: 27980263, Elsevier: Scopus)
52.	Ariunzaya Bat-Erdene, Hirokazu Miki, Asuko Oda, Shingen Nakamura, Jumpei Teramachi, Ryota Amachi, Hirofumi Tenshin, Masahiro Hiasa, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kimiko Sogabe, Kumiko Kagawa, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara and Masahiro Abe : Synergistic targeting of Sp1, a critical transcription factor for myeloma cell growth and survival, by panobinostat and proteasome inhibitors., Oncotarget, Vol.7, No.48, 79064-79075, 2016. (Summary) Panobinostat, a pan-deacetylase inhibitor, synergistically elicits cytotoxic activity against myeloma (MM) cells in combination with the proteasome inhibitor bortezomib. Because precise mechanisms for panobinostat's anti-MM action still remain elusive, we aimed to clarify the mechanisms of anti-MM effects of panobinostat and its synergism with proteasome inhibitors. Although the transcription factor Sp1 was overexpressed in MM cells, the Sp1 inhibitor terameprocol induced MM cell death in parallel with reduction of IRF4 and cMyc. Panobinostat induced activation of caspase-8, which was inversely correlated with reduction of Sp1 protein levels in MM cells. The panobinostat-mediated effects were further potentiated to effectively induce MM cell death in combination with bortezomib or carfilzomib even at suboptimal concentrations as a single agent. Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation. The synergistic Sp1 reduction markedly suppressed Sp1-driven prosurvival factors, IRF4 and cMyc. Besides, the combinatory treatment reduced HDAC1, another Sp1 target, in MM cells, which may potentiate HDAC inhibition. Collectively, caspase-8-mediated post-translational Sp1 degradation appears to be among major mechanisms for synergistic anti-MM effects of panobinostat and proteasome inhibitors in combination. (Tokushima University Institutional Repository) ● Metadata: 109988 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.12594 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27738323 ● Search Scopus @ Elsevier (PMID): 27738323 ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.12594 (Tokushima University Institutional Repository: 109988, DOI: 10.18632/oncotarget.12594, PubMed: 27738323)
53.	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, Vol.7, No.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: 113048 (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: 113048, DOI: 10.18632/oncotarget.11927, PubMed: 27626482)
54.	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, Vol.63, No.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: 109666 (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: 109666, DOI: 10.1507/endocrj.EJ15-0589, PubMed: 26877258, Elsevier: Scopus)
55.	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, Vol.30, No.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: 109486 (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: 109486, DOI: 10.1002/jbmr.2551, PubMed: 25967373, Elsevier: Scopus)
56.	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, Vol.62, No.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)
57.	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, Vol.62, No.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: 111266 (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: 111266, DOI: 10.2152/jmi.62.126, PubMed: 26399335, Elsevier: Scopus)
58.	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, Vol.61, No.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)
59.	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)
60.	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, Vol.21, No.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: 106061 (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: 106061, DOI: 10.5551/jat.20834, PubMed: 24401746, CiNii: 1390001204430842112, Elsevier: Scopus)
61.	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, Vol.57, No.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)
62.	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, Vol.229, No.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: 105936 (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: 105936, DOI: 10.1016/j.atherosclerosis.2013.03.030, PubMed: 23639859)
63.	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, Vol.56, No.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)
64.	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, Vol.154, No.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)
65.	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, Vol.14, No.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)
66.	Toshio Matsumoto and Itsuro Endo : Eldecalcitol for the treatment of osteoporosis., Drugs of Today, Vol.48, No.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)
67.	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, Vol.32, No.2, 315-320, 2012.
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, Vol.59, No.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.	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: 106134 (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: 106134, DOI: 10.1038/leu.2011.60, PubMed: 21475253)
70.	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, Vol.5, No.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 (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 (DOI: 10.1371/journal.pone.0013090, PubMed: 20927330)
71.	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, Vol.29, No.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)
72.	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, Vol.55, No.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)
73.	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, Vol.42, No.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)
74.	Takao Mitsui, Makoto Kunishige, Michiko Ichimiya, Kana Shichijo, Itsuro Endo and Toshio Matsumoto : Beneficial effect of tacrolimus on myasthenia gravis with thymoma, The Neurologist, Vol.13, No.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)
75.	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, Vol.83, 136-138, 2007.
76.	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, Vol.234, No.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)
77.	Hiroko Omori, Takao Mitsui, Makoto Kunishige, Itsuro Endo, Koji Takahashi and Toshio Matsumoto : Beneficial effect of tacrolimus on myasthenia gravis with thymoma, Clinical Neuropathology, Vol.24, No.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)
78.	K Yamaguchi, H Shibuya, K Sasaki, K Takashima, Yasushi Sato, Y Arimura, Tetsuji Takayama, Itsuro Endo, Y Shinomura, Y Niitsu and K Hirata : Clinical evaluation of laparoscopy-assisted distal gastrwctomy for early gastric cancer., Tumor Research, Vol.40, 37-45, 2005.
79.	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, Vol.225, No.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)
80.	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, Vol.23, No.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)
81.	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, Vol.106, No.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)
82.	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, Vol.42, No.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)
83.	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, Vol.144, No.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)
84.	Itsuro Endo, Takao Mitsui and Toshio Matsumoto : Diurnal fluctuation of edema synchronized with plasma VEGF concentration in patient with POEMS syndrome., Internal Medicine, Vol.41, No.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)
85.	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, Vol.73, No.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)
86.	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, Vol.9, No.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)
87.	Yoshifumi Umaki, Takao Mitsui, Itsuro Endo, Masashi Akaike and Toshio Matsumoto : Apoptosis-related changes in skeletal muscle of patients with mitochondreal disease., Acta Neuropathologica, Vol.103, No.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)
88.	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, Vol.56, No.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)
89.	Yasushi Oshima, Takao Mitsui, Itsuro Endo, Yoshifumi Umaki and Toshio Matsumoto : Corticospinal tract involvement in a variant of Guillain-Barré syndrome, European Neurology, Vol.46, No.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)
90.	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, Vol.21, No.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)

Academic Paper (Unrefereed Paper):

1.	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.

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, Vol.78, No.suppl 4, 544-548, Sep. 2020.
2.	Itsuro Endo : 活性型ビタミンD3製剤とその誘導体, 診断と治療, Vol.108, No.9, 1193-1197, Sep. 2020. (Keyword) ビタミンD不足症・欠乏症 / 転倒抑制効果 / 高カルシウム血症 / 高カルシウム尿症 / ビタミン D ブソクショウ・ケツボウショウ / テントウヨクセイコウカ / コウカルシウムケッショウ / コウカルシウムニョウショウ (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390576745218874496 (CiNii: 1390576745218874496)
3.	Itsuro Endo : 活性型ビタミンD, 糖尿病・内分泌代謝科, Vol.50, No.suppl 5, 153-158, Jul. 2020.
4.	Toshiyuki Yasui and Itsuro Endo : 糖尿病, 臨床婦人科産科, Vol.74, No.4, 132-138, Apr. 2020.
5.	Itsuro Endo : 骨粗鬆症薬物療法:活性型ビタミンD3, 副甲状腺・骨代謝疾患診療マニュアル改訂第2版, 146-147, May 2019.
6.	Itsuro Endo : 低リン血症の鑑別診断, 副甲状腺・骨代謝疾患診療マニュアル改訂第2版, 47-49, May 2019.
7.	Itsuro Endo : 骨粗鬆症治療の標的分子としてのsclerostinとは?, リウマチ科, Vol.60, No.6, 646-650, Dec. 2018.
8.	Itsuro Endo : 抗RANKL抗体, 糖尿病と骨粗鬆症, 162-166, Aug. 2018.
9.	Itsuro Endo : FSA and obesity, osteoporosis, Clinical Calcium, Vol.28, No.7, 941-945, Jun. 2018. (Summary) It is well known that the rise of FSH is a hallmark of menopause associated with osteoporosis and visceral adiposity. Recent days, Zahidi's group reported that blocking FSH signals prevents bone loss in ovariectomized mice by inhibiting bone resorption and stimulating bone synthesis. The same research group also showed that blocking FSH action reduces body fat volume by promoting beige fat thermogenesis. These findings open new doors for novel and complementary treatments addressing post-menopausal osteoporosis and metabolic diseases. (Keyword) Animals / Body Weight / Calcium / Female / Follicle Stimulating Hormone / Mice / Obesity / Osteoporosis (Link to Publication Site) ● Publication site (DOI): 10.20837/4201807941 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29950547 ● Search Scopus @ Elsevier (PMID): 29950547 ● Search Scopus @ Elsevier (DOI): 10.20837/4201807941 (DOI: 10.20837/4201807941, PubMed: 29950547)
10.	Itsuro Endo : 低リン血症, 内分泌代謝科専門医研修ガイドブック, 109-111, May 2018.
11.	Itsuro Endo : 薬物の分野でトピックとなっている論文のレビュー, The Journal of Japan Osteoporosis Society, Vol.3, No.4, 61-65, Oct. 2017. (Keyword) 骨粗鬆症 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523388080956353536 (CiNii: 1523388080956353536)
12.	Itsuro Endo : 活性型ビタミンD製剤を処方するときの注意点は?, もう悩まない骨粗鬆症診療, 176-180, Apr. 2017. (Keyword) 骨粗鬆症
13.	Itsuro Endo : [Calcilytic drugs:Feature and future.], Clinical Calcium, Vol.27, No.4, 547-552, Mar. 2017. (Summary) Calcium-sensing receptor(CaSR)is highly expressed in parathyroid, kidney, bone, and small and large intestines to regulate Ca homeostasis. Calcilytics are allosteric antagonists of CaSR, and stimulate endogenous PTH release. Several calcilytics have been evaluated as anabolic therapies for postmenopausal osteoporosis but clinical development of all of them has been abandoned because the lacked clinical efficacy. Calcilytics might be repurposed for new indications like autosomal dominant hypocalcemia or other disorders. (Keyword) Animals / calcium / Clinical Trials as Topic / Drug Evaluation, Preclinical / Humans / Osteoporosis / Receptors, Calcium-Sensing (Link to Publication Site) ● Publication site (DOI): 10.20837/4201704077 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28336831 ● Search Scopus @ Elsevier (PMID): 28336831 ● Search Scopus @ Elsevier (DOI): 10.20837/4201704077 (DOI: 10.20837/4201704077, PubMed: 28336831)
14.	Itsuro Endo : エルデカルシトールー骨形成あるいは骨吸収マーカーはどちらを測定すべきかー, Bone Joint Nerve, Vol.7, No.2, 2017.
15.	Itsuro Endo : 選択枝の広がった骨粗鬆症治療, medical practice, Vol.33, No.11, 1801-1807, Nov. 2016.
16.	Itsuro Endo : デノスマブの安全性, ファーマナビゲーターRANKL抗体編, 308-319, Sep. 2016.
17.	Itsuro Endo : ロモソズマブ投与中の留意点について教えてください, 骨粗鬆症治療薬クリニカルクエスチョン100, 144, Sep. 2016.
18.	Itsuro Endo : ロモソズマブ基本投与法と場合別投与法について教えてください, 骨粗鬆症治療薬クリニカルクエスチョン100, 142-143, Sep. 2016.
19.	Itsuro Endo : ロモソズマブ骨密度改善や骨折抑制に対する効果について教えてください, 骨粗鬆症治療薬クリニカルクエスチョン100, 141, Sep. 2016.
20.	Itsuro Endo : ロモソズマブ骨粗鬆症への効果発現のメカニズムについて教えてください, 骨粗鬆症治療薬クリニカルクエスチョン100, 139-140, Sep. 2016.
21.	Itsuro Endo : テリパラチドと活性型ビタミンD3製剤併用の安全性と有効性は?, Clinical Questionで学ぶ骨粗鬆症治療の安全対策, 82-83, Jul. 2016.
22.	Itsuro Endo : 尿路結石患者に対して活性型ビタミンD3製剤の投与は適切か?, Clinical Questionで学ぶ骨粗鬆症治療の安全対策, 79-81, Jul. 2016.
23.	Itsuro Endo : 活性型ビタミンD3製剤とカルシウム製剤の併用療法の功罪は?, Clinical Questionで学ぶ骨粗鬆症治療の安全対策, 76-78, Jul. 2016.
24.	Itsuro Endo : 糖尿病と骨折, 糖尿病診療マスター, Vol.14, No.4, 288-294, Apr. 2016.
25.	Itsuro Endo : カテプシンK阻害薬による骨粗鬆症の治療, Endocrinology, Diabetology & Metabolism, Vol.42, No.3, 208-211, Mar. 2016. (Keyword) cathepsin K inhibitors / type Ⅰ collagen / odanacatib (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522262180481466624 (CiNii: 1522262180481466624)
26.	Itsuro Endo : 成長障害, 内科診断学第3版, 245-251, Feb. 2016.
27.	Itsuro Endo : 骨組織を標的とした新しい診断・治療法, 骨・臓器ネットワークとオステオサイト, 109-116, Feb. 2016.
28.	Itsuro Endo : Epidemiology of FGF23-related hypophosophatemic diseases, Clinical Calcium, Vol.26, No.2, 45-52, Feb. 2016. (Summary) Through the studies of patients with hypophosphatemic rickets/osteomalacia, fibroblast growth factor 23(FGF23)has emerged as a humoral factor that reduces serum phosphate. Discovery of FGF23 as an essential regulator of phosphate homeostasis has markedly improved our understanding of phosphate homeostasis and hypophosphatemic or hyperphosphatemic disorders. A nationwide epidemiologic survey of FGF23-related hypophosphatemic diseases indicated that the patients showed FGF23 levels of above 30 pg/mL by intact assay in the presence of hypophosphatemia. The survey also showed that prevalence and biochemical data before and after treatment of the diseases. Novel therapeutic methods for these disorders may be developed by elucidation of the mechanism of action of FGF23. (Keyword) Animals / Biomarkers / Extracellular Matrix Proteins / Fibroblast Growth Factors / Homeostasis / Humans / Hypophosphatemia / Mice / Mutation / PHEX Phosphate Regulating Neutral Endopeptidase / Phosphates / Phosphoproteins / Phosphoric Diester Hydrolases / Prevalence / Pyrophosphatases / Rickets, Hypophosphatemic (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26813502 ● Summary page in Scopus @ Elsevier: 2-s2.0-84964950510 (PubMed: 26813502, Elsevier: Scopus)
29.	Itsuro Endo : 活性型ビタミンD製剤, 骨粗しょう症診断と治療のABC, 165-171, Jan. 2016.
30.	Itsuro Endo : [Bone and Nutrition. A prospect of calcium sensing receptor]., Clinical Calcium, Vol.25, No.7, 1029-1036, Jul. 2015. (Summary) Following the discovery of the calcium-sensing receptor (CaSR) in 1993, its pivotal role in disorders of calcium homeostasis was demonstrated. Compelling evidence suggests that the CaSR plays multiple roles extending well beyond not only regulating the level of extracellular Ca(2+), but also controlling diverse and crucial roles in human physiology and pathophysiology. This review covers current knowledge of the role of the CaSR in disorders of calcium homeostasis (familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism, autosomal dominant hypocalcemia, primary and secondary hyperparathyroidism, hypercalcemia of malignancy) as well as unrelated diseases such as breast and colorectal cancer, Alzheimer's disease and pancreatitis. In addition, it examines the use or potential use of CaSR agonists or antagonists in the management of disorders as diverse as hyperparathyroidism and Alzheimer's disease. (Keyword) Alzheimer Disease / Animals / Breast Neoplasms / Calcium / Calcium Metabolism Disorders / Colorectal Neoplasms / Female / Homeostasis / Humans / Male / Mice / Molecular Targeted Therapy / Mutation / Pancreatitis / Receptors, Calcium-Sensing (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26119316 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942636157 (PubMed: 26119316, Elsevier: Scopus)
31.	Itsuro Endo : 2型糖尿病と骨折リスク, ファーマナビゲーター糖尿病と骨代謝編, Vol.0, No.0, 96-105, Jun. 2015.
32.	Itsuro Endo : 骨吸収抑制薬と活性型ビタミンDの併用療法, Clinical Calcium, Vol.25, No.3, 111-117, Mar. 2015.
33.	Itsuro Endo : Current Topics on Vitamin D. Combined therapy of anti-resorptive drug and active vitamin D, Clinical Calcium, Vol.25, No.3, 433-438, Mar. 2015. (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25716817 ● Summary page in Scopus @ Elsevier: 2-s2.0-84942789767 (PubMed: 25716817, Elsevier: Scopus)
34.	Itsuro Endo : 画像で副甲状腺腫大を確認できない原発性副甲状腺機能亢進症の治療方針は?, 内分泌代謝疾患Clinical Question100, 76-77, Dec. 2014.
35.	Itsuro Endo : 画像で副甲状腺を確認できない原発性副甲状腺機能亢進症の治療方針は?, 内分泌疾患CLINICASL QUESTION 100, Vol.0, No.0, 76-7, Dec. 2014.
36.	Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : [The pathology, diagnosis and therapy on osteoporosis]., Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.72, No.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)
37.	Itsuro Endo : [Metabolic bone and joint diseases]., Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.72, No.10, 1785, Oct. 2014. (Summary) Metabolic bone and joint diseases in adults include osteomalacia, rheumatoid arthritis, gouty arthritis. Recently, the newest molecular biology procedures and the clinical observation studies can produce good results for understanding of these diseases. From this perspective, the author introduced updated information of the pathophysiology, the latest diagnostic criteria and the therapy of these diseases. (Keyword) Aged / Arthritis, Gouty / Arthritis, Rheumatoid / Humans / Osteomalacia (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25509803 ● Search Scopus @ Elsevier (PMID): 25509803 (PubMed: 25509803)
38.	Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : 骨粗鬆症の病態，診断，治療, 日本臨床, Vol.72, No.10, 1774-1779, Oct. 2014.
39.	Itsuro Endo : 代謝性骨・関節疾患, 日本臨床, Vol.72, No.10, 1785-1791, Oct. 2014.
40.	Itsuro Endo : 不動(長期臥床，麻痺)に伴う骨粗鬆症, THE BONE, Vol.28, No.3, 75-80, Sep. 2014.
41.	Itsuro Endo : グルココルチコイドによるIL-11を介する骨芽細胞制御とPTHの影響, Clinical Calcium, Vol.13, No.2, 43-50, Sep. 2014. (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25177004 ● Search Scopus @ Elsevier (PMID): 25177004 (PubMed: 25177004)
42.	Itsuro Endo : グルココルチコイドによるIL-11を介する骨芽細胞制御とPTHの影響, CLINICAL CALCIUM, Vol.24, No.9, 43-50, Sep. 2014.
43.	Itsuro Endo : 糖尿病と骨折リスク, 月刊糖尿病, Vol.6, No.72, 25-32, Aug. 2014. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521980706056658944 (CiNii: 1521980706056658944)
44.	Itsuro Endo : 糖尿病と骨折リスク, 月刊糖尿病, Vol.6, No.7, 25-32, Aug. 2014.
45.	Itsuro Endo : Wntシグナルによる骨形成の制御とスクレロスチン, Current Therapy, Vol.32, No.10, 87, Jun. 2014.
46.	Itsuro Endo : ステロイド骨粗鬆症に対する活性型ビタミンDの効果, 整形・災害外科, Vol.57, No.7, 883-890, Jun. 2014.
47.	Itsuro Endo : ステロイド骨粗鬆症に対する活性型ビタミンDの効果, Orthopeadics and Traumatology, Vol.57, No.7, 883, Jun. 2014.
48.	Itsuro Endo and Toshio Matsumoto : 副甲状腺機能低下症, 内科, Vol.113, No.6, 1571-1573, Jun. 2014.
49.	Itsuro Endo and Toshio Matsumoto : 副甲状腺機能亢進症, 内科, Vol.113, No.6, 1568-1570, Jun. 2014.
50.	Itsuro Endo : 内分泌疾患とは, Dental Outlook, 141, May 2014.
51.	Itsuro Endo : ロモソズマブによる骨粗鬆症治療の可能性, Endocrinology, Diabetology & Metabolism, Vol.40, No.3, 228-232, Mar. 2014. (Keyword) romosozumab / sclerostin / Wnt/β-catenin pathway / osteoporosis (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291855712202240 (CiNii: 1520291855712202240)
52.	Itsuro Endo : α-Klotho, 骨粗鬆症治療, Vol.13, No.2, 59-62, Feb. 2014.
53.	Itsuro Endo and Toshio Matsumoto : RANKL, The Medical Frontline, Vol.69, No.2, 257-261, Feb. 2014.
54.	Itsuro Endo : RANKL, The Medical Frontline, Vol.69, No.2, 257-261, Feb. 2014.
55.	Itsuro Endo and Toshio Matsumoto : チアマゾール, 重要薬マニュアル, 158-159, Jan. 2014.
56.	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.
57.	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.
58.	Itsuro Endo and Toshio Matsumoto : ラロキシフェン, 重要薬マニュアル, 152-153, Jan. 2014.
59.	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.
60.	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.
61.	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.
62.	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.
63.	Itsuro Endo : 抗スクレロスチン抗体による骨形成促進と骨粗鬆症治療, Clinical Calcium, Vol.24, No.1, 69-73, Jan. 2014.
64.	Itsuro Endo : 抗スクレロスチン抗体による骨形成促進と骨粗鬆症治療, CLINICAL CALCIUM, Vol.24, No.1, 69-74, Jan. 2014.
65.	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.
66.	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, Vol.31, No.6, 815-821, 2014.
67.	Itsuro Endo and Toshio Matsumoto : [Bone Structural Properties and Bone Strength. Bone architecture and strength on unloading]., Clinical Calcium, Vol.23, No.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)
68.	Itsuro Endo and Toshio Matsumoto : ビスホスホネート, The Lipid, Vol.24, No.4, 73-78, Apr. 2013.
69.	Itsuro Endo and Toshio Matsumoto : 新しい骨粗鬆症治療薬, Internal Medicine, Vol.111, No.4, 671-676, Apr. 2013.
70.	Itsuro Endo and Toshio Matsumoto : 開発中の薬剤, Hormone Frontier in Gynecology, Vol.20, No.3, 51-56, Mar. 2013.
71.	Itsuro Endo : カテプシンK阻害薬による骨粗鬆症治療, リウマチ科, Vol.49, No.3, 328-331, Mar. 2013.
72.	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, Vol.12, No.2, 67-70, Feb. 2013.
73.	Itsuro Endo : 腫瘍とリン, 腎と骨代謝, Vol.26, No.1, 57-64, Jan. 2013.
74.	Itsuro Endo and Toshio Matsumoto : BSAP(骨型ALP), Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.71, No.supple, 258-260, 2013.
75.	Itsuro Endo : プライマリ・ケアとしての骨粗鬆症診療活性型ビタミンD3, 治療, Vol.94, No.12, 2066-2070, Dec. 2012.
76.	Itsuro Endo : 活性型ビタミンD (特集プライマリ・ケアとしての骨粗鬆症診療 : 骨折予防に向けた骨粗鬆症治療), The Journal of Therapy, Vol.94, No.12, 2066-2069, Dec. 2012. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523669553308030080 (CiNii: 1523669553308030080)
77.	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, Vol.22, No.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)
78.	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.
79.	Takeshi Kondo, Itsuro Endo and Toshio Matsumoto : ビスホスホネート製剤, Medicina, Vol.49, No.11, 348-350, Nov. 2012.
80.	Itsuro Endo and Toshio Matsumoto : 活性型ビタミンD3およびその誘導体, Medical Practice, Vol.29, No.11, 1949-1953, Nov. 2012.
81.	Itsuro Endo and Toshio Matsumoto : Effect of vitamin D on bone and immune system, Journal of Clinical and Experimental Medicine, Vol.242, No.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)
82.	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.
83.	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.
84.	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.
85.	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.
86.	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.
87.	Itsuro Endo and Toshio Matsumoto : [New approved drugs for osteoporosis in Japan]., Clinical Calcium, Vol.22, No.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)
88.	Itsuro Endo and Toshio Matsumoto : 副甲状腺疾患, Medical Practice, Vol.29, 171-178, May 2012.
89.	Itsuro Endo : PTH replacement therapy on hypoparathyroidism, Endocrinology, Diabetology & Metabolism, Vol.34, No.5, 453-456, May 2012. (Keyword) parathyroid hormone (PTH) / teriparatide / hypoparathyroidism (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1523106603335357696 (CiNii: 1523106603335357696)
90.	Itsuro Endo : テリパラチド連日皮下注製剤の骨形成促進作用と使用法, Mebio, Vol.29, No.5, 76-82, May 2012.
91.	Itsuro Endo and Toshio Matsumoto : 骨粗鬆症治療薬, The Japanese journal of clinical and experimental medicine, Vol.89, No.4, 461-465, Apr. 2012.
92.	Itsuro Endo and Toshio Matsumoto : 抗スクレロスチン抗体, 骨粗鬆症治療, Vol.11, No.3, 47-51, Mar. 2012.
93.	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, Vol.25, No.3, 243-249, Mar. 2012.
94.	Itsuro Endo and Toshio Matsumoto : [Frontiers in vitamin D; basic research and clinical application. Eldecalcitol: the effect on bones and calcium metabolism]., Clinical Calcium, Vol.21, No.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)
95.	Itsuro Endo and Toshio Matsumoto : 続発性骨粗鬆症, 診断と治療, Vol.99, No.10, 1661-1667, Oct. 2011. (Keyword) secondary osteoporosis
96.	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.
97.	Itsuro Endo and Toshio Matsumoto : Progress and perspectives in bone research, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.69, No.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)
98.	Itsuro Endo and Toshio Matsumoto : 癌と関連した高カルシウム血症, 腎と透析, Vol.71, No.5, 662-666, May 2011. (Keyword) PTHrP / cytokine / hypercalcemia
99.	Itsuro Endo : 微少重力と骨障害 (特集続発性骨粗鬆症UPDATE : 内分泌疾患との関連), ホルモンと臨床, Vol.59, No.4, 417-422, Apr. 2011.
100.	Itsuro Endo : 微少重力と骨障害, ホルモンと臨床, Vol.59, No.4, 101-106, Apr. 2011.
101.	Itsuro Endo and Toshio Matsumoto : Parathyroid neoplasms: a state and view of clinical research, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.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)
102.	Itsuro Endo and Toshio Matsumoto : ビタミンD新規合成誘導体の展望, THE BONE, Vol.25, No.3, 135-139, Mar. 2011. (Keyword) vitamin D analogue
103.	Itsuro Endo : 骨粗鬆症薬としてのビタミンD, Medical Science Digest, Vol.37, No.3, 94-97, Mar. 2011. (Keyword) vitamin D analogue / bone metabolism
104.	Itsuro Endo and Toshio Matsumoto : PTHの生理作用, 骨粗鬆症治療, Vol.10, No.2, 10-14, Feb. 2011. (Keyword) PTH
105.	Itsuro Endo and Toshio Matsumoto : 電解質異常の診断の進め方-Ca, P, Mg-, Mebio, Vol.28, No.1, 27-33, Jan. 2011.
106.	Itsuro Endo and Toshio Matsumoto : [Eldecalcitol (ED-71)]., Clinical Calcium, Vol.21, No.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)
107.	Itsuro Endo : 骨粗鬆症薬の使い方の実際ビタミンD誘導体, Medical Practice, Vol.27, No.6, 1017-1022, Jun. 2010.
108.	Itsuro Endo and Toshio Matsumoto : [Secondary osteoporosis UPDATE. Drugs under development for metabolic bone disease]., Clinical Calcium, Vol.20, No.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)
109.	Itsuro Endo and Toshio Matsumoto : Drugs for osteoporosis under development, Clinic All-Round, Vol.59, No.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)
110.	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.
111.	Itsuro Endo and Toshio Matsumoto : 電解質異常の診断の進め方ーCa, P, Mg-, Mebio, Vol.28, No.1, 27-33, Jan. 2010.

Proceeding of International Conference:

1.	Hiroki Yamagami, Tomoyo Hara, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Analysis of clinical factors involved in AGE accumulation in people with type 2 diabetes, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Jul. 2023.
2.	Yosuke Kaneko, Saya Yasui, Minae Hosoi, Akihiro Tani, Hiroki Yamagami, Hiroyasu Mori, Tomoyo Hara, Yukari Mitsui, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Akio Kuroda, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Takeshi Soeki, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Dehydroepiandrosterone sulfate and skeletal muscle disorders in patients with type 2 diabetes, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Tokyo, Jul. 2023.
3.	Yumi Kuwamura, Kiyoe Kurahashi, Sumiko Yoshida, Hiromichi Yumoto, Maki Hosoki, Yukihiro Momota, Ken-ichi Aihara, Masuko Sumikawa, Hirokazu Uemura, Munehide Matsuhisa and Itsuro Endo : Evaluation of Nursing Educational Material on Oral Health Behavior of Persons with Diabetes: Part 3 -- Physicians' Survey, International Diabetes Federation Western Pacific Congress 2023 /15th Scientific Meeting of Asian Association for the study of Diabetes, Kyoto, Japan, Jul. 2023.
4.	Tomoyo Hara, Hiroki Yamagami, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Clinical factors and glycemic control in Japanese people with type 2 diabetes treated with weekly Dulaglutide at a dose of 0.75 mg, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, Jul. 2023.
5.	Minae Hosoki, Hiroki Yamagami, Taiki Hori, Saya Yasui, Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Masahiro Abe and Ken-ichi Aihara : Pharmaceutical Influences on In-hospital Death in Patients with and Those without Diabetes at a Japanese General Hospital, The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022.
6.	Shiho Masuda, Tomoyo Hara, Hiroki Yamagami, Mitsui Yukari, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Evaluation of Vascular Function for Prediction of Renal Prognosis in Japanese Patients with Lifestyle-Related Diseases, The 29th Scientific Meeting of the International Society of Hypertension, Oct. 2022.
7.	Tomoyo Hara, Mitsui Yukari, Masuda Shiho, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma heparin cofactor activity is inversely associated with the development NAFLD in patients with diabetes, American Diabetes Association 82nd Scientific Sessions, Jun. 2022.
8.	Hiroki Yamagami, Yasui Saya, Hosoki Minae, Hori Taiki, Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Masahiro Abe and Ken-ichi Aihara : Skin autofluorescence is associated with tubular injury represented by urinary excretion of liver-type fatty acid-binding protein in patients with diabetes, American Diabetes Association 82nd Scientific Sessions, Jun. 2022.
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 promotes bone destruction and myeloma tumor expansion, Cancer and bone society young investigator symposium, Online, Feb. 2022.
10.	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.
11.	Tomoyo Hara, Mitsui Yukari, Masuda Shiho, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Heparin cofactor II prevents the development of albuminuria in patients with diabetes, EASD 2021 57th Annual Meeting, Sep. 2021.
12.	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.
13.	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.
14.	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.
15.	Tomoyo Hara, H Yamagami, Y Mitsui, S Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma heparin cofactor activity is inversely associated with the development NAFLD in patients with diabetes, American Diabetes Association 80th Scientific Session, Chicago, Jun. 2020.
16.	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.
17.	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.
18.	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.
19.	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.
20.	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.
21.	Yumi Kuwamura, Sumiko Yoshida, Kiyoe Kurahashi, Masuko Sumikawa, Eijiro Sakamoto, Akio Kuroda, Hikari Yamato, Misuzu Okamoto, Hirokazu Uemura, Daisuke Hinode, Hiromichi Yumoto, Ken-ichi Aihara, Makoto Funaki, Munehide Matsuhisa, Itsuro Endo and Sachi Kishida : Oral health behaviors of outpatients with diabetes based on the Revised Diabetes Oral Health Assessment Tool for nurses, Journal of Diabetes Investigation, Vol.10, No.Supplement1, 26, Sendai-City, Miyagi Prefecture, May 2019. (Keyword) oral health behaviors / diabetes nursing / assessment
22.	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.
23.	Itsuro Endo, Bingzi Dong, Yukiyo Ohnishi, Yukari Ooguro, Kurahashi Kiyoe, Hiasa Masahiro, Junpei Teramachi, Tenshin Hirofumi, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : Persistent activation of calcium-sensing receptor increases microcrack and decreases bone strength, ASBMR 2018 Annual Meeting, Mnrtial, QU, Oct. 2018.
24.	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.
25.	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.
26.	Yumi Kuwamura, Sumiko Yoshida, Kiyoe Kurahashi, Masuko Sumikawa, Eijiro Sakamoto, Ken-ichi Aihara, Hiromichi Yumoto, Munehide Matsuhisa, Itsuro Endo, Toshiyuki Yasui and Sachi Kishida : The Relationship Between the Modified Diabetes Oral Health Assessment Tool© for Nurses, Self-Efficacy Scale, and Outcome Expectancy Scale for Self-Care of Patients with Periodontal Disease, 2nd Technological Competency as Caring in the Health Sciences 2018, 63, Aug. 2018. (Keyword) nurse / diabetes mellitus / oral health / self-efficacy / outcome expectancy
27.	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.
28.	Akio Kuroda, Misuzu Yamada, Yukari Tominaga, Reiko Suzuki, Motoyuki Tamaki, Yuko Akehi, Yuichi Takashi, Daisuke Otsuka, Eisuke Shimokita, Fuminori Tanihara, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe, Kevin Ferreri and Munehide Matsuhisa : Detection of pancreatic beta cell DNA in the circulation using the amplification refractory mustation system PCR, American Diabetes Association 78th Scientific Sessions, Orlando, Jun. 2018.
29.	Munehide Matsuhisa, Hiroyasu Mori, Mami Ohishi, Masashi Ishizu, Reiko Suzuki, Ineko Takikawa, Satoshi Taniguchi, Motoyuki Tamaki, Yuko Akehi, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Akio Kuroda : The risk factors for rapid decline of renal function in Japanese patients with diabetes mellitus, American Diabetes Association 78th Scientific Sessions, Orlando, Jun. 2018.
30.	Sumiko Yoshida, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : Changes of oxidative stress markers in patient of diabetes educational hospitalization., The Endocrine Society's Annual Meeting 2018, Chicago, Mar. 2018.
31.	Kana Morimoto, Masuda Shiho, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Sumiko Yoshida, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Akehi Yuko, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa and Ken-ichi Aihara : Identification of clinical determinants for coefficient of variation of - intervals in patients with type 2 diabetes., International Conference on Diabetes and Its Complications 2017, Baltimore, Nov. 2017. (Keyword) therapy / 合併症
32.	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.
33.	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.
34.	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.
35.	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.
36.	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.
37.	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.
38.	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.
39.	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.
40.	Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Analysis of sodium restriction-induced blood pressure reduction in hospitalized patients with type 2 diabetes mellitus, The 10th Congress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases, Tokyo, Jul. 2016.
41.	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.
42.	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.
43.	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.
44.	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.
45.	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.
46.	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.
47.	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.
48.	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.
49.	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.
50.	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.
51.	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.
52.	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.
53.	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.
54.	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.
55.	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.
56.	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.
57.	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.
58.	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
59.	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.
60.	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.
61.	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.
62.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Mizuho Kinouchi and Itsuro Endo : Rosuvastatin exerts an LDL cholesterol reduction-independent protective effect against carotid atherosclerosis, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
63.	Sumiko Yoshida, Ken-ichi Aihara, Yuka Ueda, Mizuho Kinouchi and Itsuro Endo : Dehydroepiandrosterone sulfate is an endothelial function-indipendent anti-atherogenic factor, 14th International Congress of Endocrinology, Kyoto, Mar. 2010.
64.	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.
65.	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.
66.	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.
67.	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.
68.	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.
69.	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.
70.	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.
71.	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.
72.	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.
73.	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.

Proceeding of Domestic Conference:

1.	Ken-ichi Aihara, Tomoyuki Yuasa, Shingen Nakamura, 村井純平, 岡本恵暢, KANEKO Yohsuke, 森建介, 細木美苗, HORI Taiki, 河田沙紀, 辻誠士郎, 安井沙耶, Hiroki Yamagami, Tomoyo Hara, Toshiki Otoda and Itsuro Endo : 来院時心肺停止・死亡転帰患者の臨床背景における糖尿病有無の影響に関する検討, 第24回日本内分泌学会四国支部学術集会, Sep. 2024.
2.	秋澤聡秀, Tomoyo Hara, 坂尾祐佳子, 佐藤寛子, 浅井孝仁, 安井沙耶, Hiroki Yamagami, Takeshi Soeki and Itsuro Endo : 高クロール血症を契機に診断に至った市販鎮痛薬による慢性ブロム中毒の1例, 第269回徳島医学会学術集会, Jul. 2024.
3.	Tomoyo Hara, 横田海友, 清水一磨, 浅井孝仁, Hiroki Yamagami, 三井由加里, 桝田志保, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 心血管疾患リスクを有する患者における可溶型DPP-4/CD26と動脈硬化指標との連関解析, 第56回日本動脈硬化学会総会, Jul. 2024.
4.	Tomoyo Hara, 横田海友, 清水一磨, 浅井孝仁, Hiroki Yamagami, 三井由加里, 桝田志保, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 糖尿病患者における可溶型DPP-4/CD26と動脈硬化指標との関連, 第67日本糖尿病学会学術集会, May 2024.
5.	遠藤裕美, Tomoyo Hara, 清水一磨, 吉田麻衣子, 浅井孝仁, Hiroki Yamagami, Ryo Kanamura, Kiyoe Kurahashi and Itsuro Endo : 早期に治療介入できた免疫関連有害事象による1型糖尿病の1例, 第268回徳島医学会学術集会, Mar. 2024.
6.	浅井孝仁, Tomoyo Hara, 清水一磨, 吉田麻衣子, 山上絋規, 三井由加里, Kiyoe Kurahashi, Akio Kuroda, Munehide Matsuhisa and Itsuro Endo : ランレオチドを投与した14症例の糖代謝への影響に関する検討, 第33回臨床内分泌代謝Update, Nov. 2023.
7.	Tomoyo Hara, 清水一磨, 浅井孝仁, 吉田麻衣子, Hiroki Yamagami, 三井由加里, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 2型糖尿病患者の非アルコール性脂肪性肝疾患における尿中可溶性ウロキナーゼ型プラスミノーゲン活性化受容体の臨床的意義, 第38回日本糖尿病合併症学会, Oct. 2023.
8.	MIMA Shunsuke, Hiroyuki Yamasaki, BANDO Mayu, Shinji Nagasaka, Yutaro Yamashita, Kazuhide Mineda, Yoshiro Abe, Sumiko Yoshida, Itsuro Endo, Munehide Matsuhisa, Masahiro Takaiwa and Ichiro Hashimoto : 糖尿病患者の歩行時における足底圧・せん断応力と足底部皮下組織量の研究, 第32回日本形成外科学会基礎学術集会, Oct. 2023.
9.	清水一磨, Hiroki Yamagami, Tomoyo Hara, 答島悠貴, 浅井孝仁, 三井由加里, Kiyoe Kurahashi, Munehide Matsuhisa and Itsuro Endo : 診断に7年間を要したTSH産生下垂体micro adenomaの一例, 第33回臨床内分泌代謝Update, Oct. 2023.
10.	Tomoyo Hara, Hiroki Yamagami, 三井由加里, Kiyoe Kurahashi, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo and Ken-ichi Aihara : 2 型糖尿病患者における血圧・血糖管理目標達成下での腎糸球体・尿細管障害のリスク因子の検討, 第45回日本高血圧学会総会, Sep. 2023.
11.	Kim SooHa, Jumpei Teramachi, Masahiro Hiasa, Hirofumi Tenshin, Emiko Nakaue, TANAKA Mariko, NAKAGAWA Motosumi, Itsuro Endo, Takeshi Harada, Eiji Tanaka and Masahiro Abe : Molecular mechanisms for generation of non-permissive niche for myeloma cells by activated osteoblasts., The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 173, Jul. 2023.
12.	Sumiko Yoshida, Akio Kuroda, Munehide Matsuhisa and Itsuro Endo : 糖尿病血糖管理入院における尿Titin N-terminal Fragmentの変化の検討, 第66回日本内分泌学会学術総会, Jun. 2023.
13.	Hiroki Yamagami, Tomoyo Hara, Yuki Tohjima, Takahito Asai, 三井由加里, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : 2型糖尿病患者のSkin autofluorscenceを規定する因子の検討, 第96回日本内分泌学会学術総会, Jun. 2023.
14.	答島悠貴, Tomoyo Hara, 浅井孝仁, Hiroki Yamagami, 三井由加里, 倉橋衛清, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 当院におけるインスリングラルギン/リキシセナチド(iGlarLixi)導入症例の臨床背景および効果の検討, 第66回日本糖尿病学会年次学術集会, May 2023.
15.	Hiroki Yamagami, Tomoyo Hara, Yuki Tohjima, Takahito Asai, 三井由加里, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : 2型糖尿病患者のAGEs蓄積に関わる臨床的因子の解析, 第66回日本糖尿病学会年次学術集会, May 2023.
16.	Yuki Tohjima, Tomoyo Hara, Takahito Asai, Hiroki Yamagami, 三井由加里, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 当院におけるインスリングラルギン/リキシセナチド (iGlarLixi)導入症例の臨床背景および効果の検討, 第66回日本糖尿病学会年次学術集会, May 2023.
17.	Tomoyo Hara, Yuki Tohjima, Takahito Asai, Hiroki Yamagami, 三井由加里, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 糖尿病患者における腎糸球体および尿細管障害特異的なリスク因子の臨床的検討, 第66回日本糖尿病学会年次学術集会, May 2023.
18.	古賀鈴奈, 吉田菜々花, IWAGAKI Yuma, Itsuro Endo, Kensaku Aki and Eiji Hosoi : 漢方薬の NK 様培養細胞 KHYG-1活性に及ぼす影響 - IFN-γ-, 第46回徳島県医学検査学会, Dec. 2022.
19.	吉田菜々花, 古賀鈴奈, IWAGAKI Yuma, Itsuro Endo, Kensaku Aki and Eiji Hosoi : 漢方薬の NK 様培養細胞 KHYG-1活性に及ぼす影響 - グランザイムB -, 第46回徳島県医学検査学会, Dec. 2022.
20.	吉良瑠里子, IWAGAKI Yuma, Itsuro Endo, Kensaku Aki and Eiji Hosoi : 血液型遺伝子プロモーター領域におけるメチル化と H抗原発現および HmRNA 発現量に関する検討, 第46回徳島県医学検査学会, Dec. 2022.
21.	Yuki Tohjima, 三井由加里, 浅井孝仁, Tomoyo Hara, Hiroki Yamagami, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Akio Kuroda, Masahiro Abe and Munehide Matsuhisa : レパグリニドとクロピドグレルの併用による遷延性低血糖を認めた一例, 日本糖尿病学会中国四国地方会第60回総会, Nov. 2022.
22.	Tomoyo Hara, Kiyoe Kurahashi, Hirofumi Hamano, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : デュラグルチド使用中患者の HbA1c管理に影響を与える因子の検討, 日本糖尿病学会中国四国地方会第60回総会, Nov. 2022.
23.	答島悠貴, Tomoyo Hara, 浅井孝仁, Hiroki Yamagami, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo and Seiji Fukumoto : 低ALP血症を契機として，ALPL遺伝子解析を行い診断に至った成人型低ホスファターゼ血症の一例, 第22回日本内分泌学会四国支部学術集会, Sep. 2022.
24.	Tomoyo Hara, 浅井孝仁, 答島悠貴, Hiroki Yamagami, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Seiji Fukumoto and Itsuro Endo : 授乳中にPTHrP上昇による高Ca血症を呈した一例, 第22回日本内分泌学会四国支部学術集会, Sep. 2022.
25.	三井由加里, Akio Kuroda, Tomoyo Hara, Hiroki Yamagami, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : 持続皮下インスリン注入療法下 1 型糖尿病合併妊娠における分娩直後のインスリン投与設定変更の提案, 第22回日本糖尿病インフォマティクス学会年次学術集会, Aug. 2022.
26.	Shiho Masuda, Tomoyo Hara, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 生活習慣病患者のeGFR年間変化量予測における血管内皮機能の意義, 第54回日本動脈硬化学会総会・学術集会, Jul. 2022.
27.	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.
28.	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.
29.	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.
30.	Tomoyo Hara, 山上紘規, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 糖尿病患者における血漿Heparin Cofactor II活性とNAFLD病態指標の連関解析, 第8回肝臓と糖尿病・代謝研究会, Jun. 2022.
31.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, 小田明日香, Sou Shimizu, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Takeshi Harada and Masahiro Abe : TAK1 阻害は骨髄腫の細胞間相互作用による骨破壊と薬剤耐性を改善する, 第47回日本骨髄腫学会学術集会, May 2022.
32.	Sumiko Yoshida, 辻誠一郎, Kiyoe Kurahashi, 宮恵子, 島久登, 田代学, 井上朋子, 水口潤, 中村信元, Akio Kuroda, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : 透析患者における新型コロナワクチン抗体と糖尿病の関連の検討, 第 65 回日本糖尿病学会年次学術集会, May 2022.
33.	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, Vol.12, No.3, 149, May 2022.
34.	Emiko Nakaue, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Ryohei Sumitani, 丸橋朋子, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka and Masahiro Abe : The impact of pulsatile proteasome inhibitor on bone metabolism, International Journal of Myeloma, Vol.12, No.3, 152, May 2022. (Keyword) 骨髄腫-多発性(薬物療法,病理学) / 骨組織リモデリング / パルス療法(薬物療法) / Proteasome Inhibitors(治療的利用,薬理学) / Homo sapiens
35.	Sumiko Yoshida, 辻誠士郎, Kiyoe Kurahashi, 宮恵子, 島久登, 田代学, 井上朋子, 水口潤, Shingen Nakamura, Akio Kuroda, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : 透析患者における新型コロナワクチン抗体と糖尿病の関連の検討, Journal of the The Japan Diabetes Society, Vol.65, No.Suppl.1, S-165, Apr. 2022. (Keyword) 血液透析ウイルス抗体腎不全-慢性(治療) 糖尿病性腎症(治療) 予防接種 COVID-19ワクチン(治療的利用) *Tozinameran(治療的利用) ヒト男女
36.	Sumiko Yoshida, 辻誠士郎, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, Tomoyo Hara, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : 精神疾患とうつ尺度が減量入院効果に及ぼす影響, 第41回日本肥満学会・第38回日本肥満症治療学会, Mar. 2022.
37.	辻誠士郎, Sumiko Yoshida, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, Tomoyo Hara, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : 行動療法を重視した2週間の減量入院後の減量効果の検討, 第41回日本肥満学会・第38回日本肥満症治療学会, Mar. 2022.
38.	辻誠士郎, Sumiko Yoshida, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, Tomoyo Hara, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : 行動療法を重視した2週間の減量入院後の減量効果の検討, 第42回日本肥満学会第39回日本肥満症治療学会学術集会, Mar. 2022.
39.	Sumiko Yoshida, 辻誠士郎, 金子遥祐, 森建介, 河田沙紀, 川原綾香, 遠藤ふうり, Tomoyo Hara, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : 精神疾患とうつ尺度が減量入院効果に及ぼす影響, 第42回日本肥満学会第39回日本肥満症治療学会学術集会, Mar. 2022.
40.	Tomoyo Hara, 河田沙紀, 川原綾香, 金子遥祐, 森建介, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Seiji Fukumoto and Masahiro Abe : 低Mg血症によるPTH分泌不全により著明な低Ca血症を来した一例, 第33回日本老年医学会四国地方会, Jan. 2022. (Keyword) 副甲状腺
41.	森建介, Kiyoe Kurahashi, 河田沙紀, 川原綾香, 金子遥祐, 高丸利加子, Sumiko Yoshida, Itsuro Endo, Yasuhiko Nishioka and Masahiro Abe : 失語症のため治療説明に難渋し方針決定が遅れた異所性ACTH症候群の1例, 第33回日本老年医学会四国地方会, Jan. 2022.
42.	辻誠士郎, Sumiko Yoshida, 宮恵子, 島久登, 田代学, 井上朋子, 水口潤, Shingen Nakamura, Itsuro Endo and Masahiro Abe : 65歳以上の透析患者における新型コロナワクチン抗体価の検討, 第33回日本老年医学会四国地方会, Jan. 2022.
43.	藤原一成, 張拓未, 田中翔, 野村侑香, Itsuro Endo and Hirokazu Miki : 多発性骨髄腫に対するカルフィルゾミブの使用経験ー心血管合併症および生理機能検査に関する後方視的検討ー, 第45回徳島県医学検査学会, Dec. 2021.
44.	Sho Tanaka, Takumi Hari, Kazuki Fujiwara, Yuka Nomura, MATSUDA Wako, NAGAI Teruyuki, 大西幸代, Tomoyo Hara, Kiyoe Kurahashi, Ganbaatar Byambasuren, Mai Kanai and Itsuro Endo : ミトコンドリア移植による乳癌新規治療法開発の試み, 第45回徳島県医学検査学会, Dec. 2021.
45.	NAGAI Teruyuki, MATSUDA Wako, 大西幸代, Tomoyo Hara, Kiyoe Kurahashi, Ganbaatar Byambasuren, Mai Kanai and Itsuro Endo : 健常ミトコンドリア産生工場としての間葉系幹細胞, 第45回徳島県医学検査学会, Dec. 2021.
46.	Mai Kanai, Itsuro Endo, 平田有紀奈, 西尾進 and Kenya Kusunose : イバブラジン投与における心機能への効果について~心エコー図検査を用いた短期間パイロット研究~, 第45回徳島県医学検査学会, Dec. 2021.
47.	宮武大輔, 岩垣侑真, 豊田剛志, 曽根淳美, Itsuro Endo, Kensaku Aki and Eiji Hosoi : 血液型遺伝子プロモーター領域におけるメチル化とH抗原発現およびHmRNA発現量に関する検討, 第45回徳島県医学検査学会, Dec. 2021.
48.	山元美礼, 岩垣侑真, 豊田剛志, 曽根淳美, Itsuro Endo, Kensaku Aki and Eiji Hosoi : 漢方薬のNK様培養細胞KHYG-1活性に及ぼす影響, 第45回徳島県医学検査学会, Dec. 2021.
49.	青山理央, 川原綾香, Kiyoe Kurahashi, Tomoyo Hara, Sumiko Yoshida, Akio Kuroda, Munehide Matsuhisa, Munehide Matsuhisa, Seiji Fukumoto, Itsuro Endo and Masahiro Abe : 1型糖尿病とバセドウ病を同時に診断した1例, 日本内科学会第125回四国地方会, Dec. 2021.
50.	高岡俊, 金子遥祐, 辻誠士郎, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Masahiro Abe and Seiji Fukumoto : レンバチニブで破壊性甲状腺炎をきたし，医原性副腎皮質機能低下症による副腎不全が顕在化した一例, 日本内科学会第125回四国地方会, Dec. 2021.
51.	Shiho Masuda, Tomoyo Hara, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 生活習慣病患者におけるeGFR年間変化量と血管内皮機能の連関解析, 第6回日本糖尿病・生活習慣病ヒューマンデータ学会, Dec. 2021.
52.	Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 糖尿病患者における血漿Heparin Cofactor II活性とNAFLD病態指標の連関, 第6回日本糖尿病・生活習慣病ヒューマンデータ学会, Dec. 2021. (Keyword) ヘパリンコファクターII / NAFLD / diabetes
53.	山口佑樹, Itsuro Endo, 藤井由加里, 林亜紀, 近藤朱音, 森根幹生, 岩崎泰正 and 前田和寿 : 妊娠を契機に増悪した腎性尿崩症の1例, 第31回臨床内分泌代謝Update, Nov. 2021.
54.	河田沙紀, Tomoyo Hara, Sumiko Yoshida, 川原綾香, Yohsuke Kaneko, Kensuke Mori, 遠藤ふうり, 辻誠士郎, 三井由加里, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Masahiro Abe and Seiji Fukumoto : アルドステロンを含む3種のホルモン産生副腎皮質癌の一例, 第32回臨床内分泌代謝Update, Nov. 2021.
55.	平岡栞名, Tomoyo Hara, 河田沙紀, 川原綾香, Yohsuke Kaneko, Kensuke Mori, 遠藤ふうり, 辻誠士郎, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Yoshimi Bando, Itsuro Endo and Seiji Fukumoto : アドレナリン優位の上昇を示したパラガングリオーマの1例, 第31回臨床内分泌代謝Update, Nov. 2021.
56.	河田沙紀, Tomoyo Hara, Sumiko Yoshida, 川原綾香, 金子遥祐, 森建介, 遠藤ふうり, 辻誠士郎, 三井由加里, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Masahiro Abe and Seiji Fukumoto : アルドステロンを含む3種のホルモン産生性副腎皮質癌の一例, 第31回臨床内分泌代謝Update, Nov. 2021.
57.	森建介, 辻誠士郎, Sumiko Yoshida, 河田沙紀, 川原綾香, 金子遥祐, 細木美苗, 遠藤ふうり, Tomoyo Hara, 三井由加里, Kiyoe Kurahashi, Itsuro Endo, Seiji Fukumoto and Masahiro Abe : 10cmの右大腿部腫瘤を原因とする腫瘍性骨軟化症の1例, 第31回臨床内分泌Update, Nov. 2021.
58.	Sumiko Yoshida, 河田沙紀, 川原綾香, 金子遥祐, 森建介, 遠藤ふうり, 辻誠士郎, Tomoyo Hara, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Masahiro Abe and Seiji Fukumoto : 新型コロナワクチン投与後に発症した亜急性甲状腺炎の1例, 第64回日本甲状腺学会学術集会, Nov. 2021.
59.	川原綾香, Kiyoe Kurahashi, 河田沙紀, 金子遥祐, 遠藤ふうり, Tomoyo Hara, 辻誠士郎, Sumiko Yoshida, Akio Kuroda, Itsuro Endo and Munehide Matsuhisa : 肝膿瘍とサイトメガロウイルス胃炎を合併した2型糖尿病の一例, 日本糖尿病学会中国四国地方会第59回総会, Oct. 2021.
60.	金子遥祐, Tomoyo Hara, 河田沙紀, 川原綾香, 遠藤ふうり, 辻誠士郎, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, Itsuro Endo and Munehide Matsuhisa : PD-1抗体が1型糖尿病発症に関与したと考えられる非典型的な3例(29文字), 日本糖尿病学会中国四国地方会第59回総会, Oct. 2021.
61.	河田沙紀, Kiyoe Kurahashi, 川原綾香, 金子遥祐, 遠藤ふうり, Tomoyo Hara, 辻誠士郎, Sumiko Yoshida, Akio Kuroda, Itsuro Endo and Munehide Matsuhisa : 糖尿病ケトアシドーシスが改善後にケトーシスが再燃した2型糖尿病の1例, 日本糖尿病学会中国四国地方会第59回総会, Oct. 2021.
62.	Asami Okada, Misuzu Yamada, Hiroyasu Mori, 明比祐子, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Akio Kuroda : 1型糖尿病患者における膵β細胞傷害の定量化の試み, 日本糖尿病学会中国四国地方会第59回総会, Oct. 2021.
63.	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.
64.	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.
65.	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.
66.	川原綾香, Tomoyo Hara, 平岡栞名, 辻誠士郎, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Masahiro Abe and Seiji Fukumoto : 前立腺癌の副腎転移が123I-MIBGシンチグラフィ陽性を示した1例, 第21回日本内分泌学会四国支部学術集会, Sep. 2021.
67.	金子遥祐, Kiyoe Kurahashi, 水口槙子, Sumiko Yoshida, 明比祐子, Itsuro Endo and Seiji Fukumoto : 急速に右動眼神経麻痺が悪化したが，速やかに外科治療を行い寛解しえた13歳のクッシング病の一例, 第21回日本内分泌学会四国支部学術集会, Sep. 2021.
68.	Asami Okada, Misuzu Yamada, Hiroyasu Mori, 明比祐子, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa and Akio Kuroda : 循環血中遊離DNAを用いた膵β細胞障害の新規検出法の確立, 第263回徳島医学会学術集会, Aug. 2021.
69.	吉川紘平, 金子遥祐, 辻誠士郎, 河田沙紀, 川原綾香, 森健介, 遠藤ふうり, 原倫世, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, 明比祐子, Itsuro Endo, Munehide Matsuhisa, Masahiro Abe and Seiji Fukumoto : TIA様発作を契機に診断されたインスリノーマの一例, 第263回徳島医学会, Aug. 2021.
70.	辻誠士郎, Sumiko Yoshida, 平岡栞名, Kohsuke Miyataka, Minae Hosoki, Tomoyo Hara, 三井由加里, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Masahiro Abe and Munehide Matsuhisa : 行動療法を中心とした2週間の減量入院プログラムの退院後の減量効果, 第64回日本糖尿病学会年次学術集会, May 2021.
71.	Tomoyo Hara, 平岡栞名, Minae Hosoki, Kohsuke Miyataka, 辻誠士郎, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo and Ken-ichi Aihara : 糖尿病患者のアルブミン尿増加に関わる臨床因子の横断および縦断解析, 第9回日本高血圧学会臨床高血圧フォーラム, May 2021.
72.	遠藤理子, Kiyoe Kurahashi, 平岡栞名, 細木美苗, 宮高紘輔, 辻誠士郎, Sumiko Yoshida, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : 慢性膵炎の急性増悪を繰り返し，仮性脾動脈瘤の急速な増大を認めた一例, 第124回日本内科学会四国地方会(WEB開催), May 2021.
73.	Hirokazu Miki, Shingen Nakamura, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Masateru Kondo, Naoto Okada, Yoshimi Bando, Itsuro Endo and Masahiro Abe : The importance of retaining physical functions to prevent SRE in multiple myeloma., 第46回日本骨髄腫学会学術集会, May 2021.
74.	Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo and Munehide Matsuhisa : 血漿 Heparin Cofactor \|\| 活性とNAFLD病態指標の連関解析, 第94回日本内分泌学会学術総会, Apr. 2021.
75.	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.
76.	Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : 血漿Heparin Cofactor II活性とNAFLD病態指標の連関解析, 第94回日本内分泌学会学術総会, Apr. 2021.
77.	Mai Kanai, 長井輝幸, Itsuro Endo, 大西幸代, 原倫世, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, 瀬部真由, Hiroshi Sakaue, Seiji Fukumoto, 松本俊夫 and 安倍正博 : TAK1阻害による炎症性サイトカイン誘導性骨格筋萎縮の改善, Folia endocrinologica Japonica, Vol.97, No.1, 365, Apr. 2021. (Keyword) cytokinesis / 筋萎縮症(遺伝学,病理学,実験的) / 骨格筋(病理学) / 腫瘍壊死因子アルファ / 核内受容体NR2C2(拮抗物質・阻害物質) / マウス / animal
78.	Ranko Kimura, Kiyoe Kurahashi, Minae Hosoki, 辻誠司郎, 三井由加里, Sumiko Yoshida, 明比祐子, Itsuro Endo, Seiji Fukumoto and Masahiro Abe : 繰り返す脆弱性骨折を契機に発見されたクッシング症候群の一例, 第262回徳島医学会学術集会, Mar. 2021.
79.	Minae Hosoki, Sumiko Yoshida, 平岡栞名, Kohsuke Miyataka, 辻誠士郎, Tomoyo Hara, 三井由加里, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : 持続血糖モニタリングシステムを使用した遠隔診療が有効であった高齢1型糖尿病の2症例, 第32回日本老年医学会四国地方会, Feb. 2021.
80.	Chihiro Yoshimoto, Sonoka Aibara, Teruyuki Nagai, Wako Matsuda, 大西幸代, Tomoyo Hara, 中村信元, Kumiko Kagawa, Hirokazu Miki, Masahiro Abe, Akiko Sakurai, Mai Kanai and Itsuro Endo : 血液悪性腫瘍化学療法入院中の骨格筋量の減少ビタミンD充足との関連, 第44回徳島県医学検査学会, Dec. 2020.
81.	Sonoka Aibara, Teruyuki Nagai, Wako Matsuda, Chihiro Yoshimoto, 大西幸代, Tomoyo Hara, Mai Kanai, Itsuro Endo, Hirokazu Miki and Akiko Sakurai : 多発性骨髄腫に対するゾレドロン酸の治療経験, 第44回徳島県医学検査学会, Dec. 2020.
82.	Teruyuki Nagai, Chihiro Yoshimoto, Wako Matsuda, Sonoka Aibara, 大西幸代, Tomoyo Hara, Kiyoe Kurahashi, Masahiro Abe, Mai Kanai and Itsuro Endo : 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44回徳島県医学検査学会, Dec. 2020.
83.	Wako Matsuda, Sonoka Aibara, Teruyuki Nagai, Chihiro Yoshimoto, 金島慶太, 大西幸代, Tomoyo Hara, Akiko Sakurai, Mai Kanai and Itsuro Endo : 原発性骨粗鬆症におけるビタミンD充足の検討, 第44回徳島県医学検査学会, Dec. 2020.
84.	金山涼加, Kiyoe Kurahashi, 明比祐子, Koichi Okamoto, Shingen Nakamura, Sumiko Yoshida, Itsuro Endo, Tetsuji Takayama and Masahiro Abe : 潰瘍性大腸炎とバセドウ病の治療中に汎血球減少を契機に自己免疫性胃炎が判明した一例, 第123回日本内科学会四国地方会, Nov. 2020.
85.	Minae Hosoki, Furi Endo, 三井由加里, 平岡栞名, Kohsuke Miyataka, 辻誠士郎, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo and Masahiro Abe : 推奨量のヒドロコルチゾン補充で症状が改善しなかった中枢性副腎不全の一例, 第123回日本内科学会四国地方会, Nov. 2020.
86.	辻誠士郎, Sumiko Yoshida, Furi Endo, 平岡栞名, Minae Hosoki, Kohsuke Miyataka, 三井由加里, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Masahiro Abe and Seiji Fukumoto : 副腎皮質癌と舌癌を合併しがんゲノム検査を施行した一例, 第30回臨床内分泌代謝Update, Nov. 2020.
87.	Kohsuke Miyataka, Kiyoe Kurahashi, Sumiko Yoshida, 平岡栞名, Minae Hosoki, Furi Endo, 辻誠士郎, 三井由加里, 明比祐子, Itsuro Endo, Masahiro Abe and Seiji Fukumoto : glioblastomaを発症した神経線維腫症1型の1例, 第30回臨床内分泌代謝Update, Nov. 2020.
88.	Minae Hosoki, 三井由加里, 平岡栞名, Kohsuke Miyataka, 辻誠士郎, Tomoyo Hara, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : 顕性Cushing症候群を示し片側副腎切除を施行したBMAHの一例, 第30回臨床内分泌代謝update, Nov. 2020.
89.	平岡栞名, 三井由加里, 細木美苗, 宮高紘輔, 辻誠士朗, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Akio Kuroda, Masahiro Abe and Munehide Matsuhisa : 原田病，重症筋無力症を合併した1型糖尿病の1例, 日本糖尿病学会中国四国地方会第58総会, Oct. 2020.
90.	辻誠士朗, Kiyoe Kurahashi, 平岡栞名, 細木美苗, 宮高紘輔, 三井由加里, Sumiko Yoshida, Akio Kuroda, Itsuro Endo, Masahiro Abe and Munehide Matsuhisa : びまん性膵腫大を契機に膵癌再発と診断したGAD抗体陽性の糖尿病の一例, 日本糖尿病学会中国四国地方会第58総会, Oct. 2020.
91.	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.
92.	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.
93.	Sumiko Yoshida, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Seiji Fukumoto, Masahiro Abe and Munehide Matsuhisa : 血糖管理入院でのテストステロン値の変化の検討, 第63回日本糖尿病学会年次学術集会, Oct. 2020.
94.	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.
95.	Kiyoe Kurahashi, 村井純平, 堀太貴, Ryohei Sumitani, Takeshi Harada, Shingen Nakamura, Mai Kanai, Akiko Sakurai, 原倫世, 桝田志保, Sumiko Yoshida, Itsuro Endo, 松本俊夫, Masahiro Abe and Seiji Fukumoto : 高1,25(OH)2D血症による高Ca血症を来したホジキンリンパ腫の一例, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 150, Oct. 2020. (Keyword) Calcitriol Dacarbazine(治療的利用) Doxorubicin(治療的利用) Hodgkin病(合併症,病理学,薬物療法) Vinblastine(治療的利用) *高カルシウム血症(病因,病理学,薬物療法) 免疫組織化学 Brentuximab Vedotin(治療的利用) ヒト高齢者(65~79) 男
96.	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
97.	Kohsuke Miyataka, Kiyoe Kurahashi, Sumiko Yoshida, 平岡栞名, Minae Hosoki, Furi Endo, 辻誠士郎, 三井由加里, 明比祐子 and Itsuro Endo : 血中IgG4濃度が高値であった甲状腺眼症の一例, 第20回日本内分泌学会四国支部学術集会, Sep. 2020.
98.	Tomoyo Hara, Sumiko Yoshida, 平岡栞名, Minae Hosoki, Kohsuke Miyataka, Furi Endo, 辻誠士郎, 三井由加里, Kiyoe Kurahashi and Itsuro Endo : 当院での高張食塩水負荷試験実施例における新旧中枢性尿崩症診断基準の比較, 第20回日本内分泌学会四国支部学術集会, Sep. 2020.
99.	川原綾香, Kiyoe Kurahashi, 工藤千晶, 鎌田基夢, Shinsuke Katoh, Yukiko Tomioka, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由加里, Sumiko Yoshida, Ken-ichi Aihara, Itsuro Endo, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 歩行不能だったが，多職種の高度な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例, 第261回徳島医学会学術集会, Aug. 2020.
100.	平岡栞名, 三井由加里, Hirokazu Miki, Seidai Satou, Momoyo Azuma, 遠藤ふうり, 宮髙紘輔, 辻誠士郎, 桝田志保, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 発熱・全身リンパ節腫脹で発症し，リンパ節生検で診断しえた結核性リンパ節炎の一例, 第261回徳島医学会学術集会, Aug. 2020.
101.	Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : NAFLD病態指標血漿Heparin Cofactor IIの連関, 第52回日本動脈硬化学会総会・学術集会, Aug. 2020.
102.	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, Vol.96, No.1, 251, Jul. 2020.
103.	Sumiko Yoshida, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 桝田志保, 三井由香里, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa, Masahiro Abe and Seiji Fukumoto : 糖尿病教育入院でのテストステロン値の変化の検討, 第93回日本内分泌学会学術総会, Vol.96, No.1, 287, Jul. 2020.
104.	Tomoyo Hara, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Ken-ichi Aihara : NAFLD病態指標Fib4-indexと血漿Heparin Cofactor Ⅱの連関, 第52回日本動脈硬化学会総会・学術集会, Jul. 2020. (Keyword) NAFLD / Heparin Cofactor Ⅱ
105.	村井純平, 堀太貴, 川田知代, Ryohei Sumitani, 宇高憲吾, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Masahiro Abe, Hirokazu Miki, 桝田志保, Itsuro Endo and Seiji Fukumoto : 高ビタミンD血症による高Ca血症を来したホジキンリンパ腫の一例, Shikoku Acta Medica, Vol.76, No.1-2, 124, Apr. 2020. (Keyword) Calcitriol(毒性・副作用,血液) / Hodgkin病(合併症,薬物療法) / Vitamin D(毒性・副作用,血液) / 高カルシウム血症(化学的誘発) / 腫瘍多剤併用療法 / ヒト / 高齢者(65~79) / 男
106.	桝田志保, Sumiko Yoshida, 工藤千晶, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由加里, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : 診断に時間を要したバセドウ病による甲状腺クリーゼの一例, 第31回日本老年医学会四国地方会, Feb. 2020.
107.	川原綾香, Kiyoe Kurahashi, 工藤千晶, 鎌田基夢, 加藤真介, 富岡有紀子, 辻本賀美, Saya Yasui, Furi Endo, Shiho Masuda, 三井由加里, Sumiko Yoshida, Ken-ichi Aihara, Itsuro Endo, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 歩行不能だったが，多職種の密な連携と患者特性に配慮したケアにより自宅生活可能となった高度肥満症の一例, 第260回徳島医学会学術集会大塚講堂, Feb. 2020.
108.	黒田大智, 水本健斗, Akiko Sakurai, Mai Kanai, 大西幸代, 松岡飛翔 and Itsuro Endo : 鉄剤投与によるFGF23関連低リン血症モデル作成の試み, 第43回徳島県医学検査学会, Dec. 2019.
109.	菊池結愛, 坂井ちか, Akiko Sakurai, Mai Kanai, 大西幸代, Masahiro Abe and Itsuro Endo : 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43回徳島県医学検査学会, Dec. 2019.
110.	水本健斗, 菊池結愛, Kiyoe Kurahashi, Akiko Sakurai, Mai Kanai, 大西幸代 and Itsuro Endo : カルシウム感知受容体活性型変異における耐糖能異常, 第43回徳島県医学検査学会, Dec. 2019.
111.	坂井ちか, 菊池結愛, 黒田大智, Akiko Sakurai, Mai Kanai, 大西幸代 and Itsuro Endo : 副腎皮質機能低下症・不全症のカットオフ値設定の試み, 第43回徳島県医学検査学会, Dec. 2019.
112.	三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, 白神敦久 and Munehide Matsuhisa : SGLT2阻害薬による正常血糖糖尿病ケトアシドーシスの1例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
113.	Kiyoe Kurahashi, 工藤千晶, 鎌田基夢, Shinsuke Katoh, Yoshiko Suzuki, 秋月佐代, Yukiko Tomioka, Sumiko Yoshida, 明比祐子, Itsuro Endo and Munehide Matsuhisa : 療養環境整備に苦慮した，歩行不能の高度肥満症の一例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
114.	Kiyoe Kurahashi, 工藤千晶, 鎌田基夢, Shinsuke Katoh, Yoshiko Suzuki, 秋月佐代, Yukiko Tomioka, Sumiko Yoshida, 明比祐子, Itsuro Endo and 松久宗英 : 療養環境整備に苦慮した，歩行不能の高度肥満症の一例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
115.	三井由加里, Akio Kuroda, Masashi Ishizu, 桝田志保, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Munehide Matsuhisa : 頻回インスリン注射療法下の1型糖尿病患者における基礎インスリン比率の検討, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
116.	桝田志保, Sumiko Yoshida, 安井沙耶, 辻本賀美, 工藤千晶, Furi Endo, 三井由加里, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo and Munehide Matsuhisa : 肥満外科手術後早期に基礎インスリン必要量が減少した高度肥満1型用尿病の1例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
117.	Furi Endo, Sumiko Yoshida, 工藤千晶, 辻本賀美, 安井沙耶, 桝田志保, 三井由加里, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo and Munehide Matsuhisa : 免疫チェックポイント阻害薬関連1型糖尿病の5例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
118.	安井沙耶, 桝田志保, 辻本賀美, 工藤千晶, Furi Endo, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, Itsuro Endo and Munehide Matsuhisa : 基礎インスリン適正化とスクエアボーラス導入で血糖管理が改善した1型糖尿病の1例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
119.	三井由加里, Akio Kuroda, Masashi Ishizu, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Munehide Matsuhisa : 頻回インスリン注射療法下の1型糖尿病患者における基礎インスリン比率の検討, 第19回日本先進糖尿病治療研究会・第17回1型糖尿病研究会, Nov. 2019.
120.	山口純代, 岩城真帆, 清水郁子, 稲垣太造, 湊将典, Hiroyuki Ono, Sayo Ueda, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Kojiro Nagai, Masuda shiho, Itsuro Endo and Hideharu Abe : 透析導入期に急性高Ca血症を生じた一例, 第49回日本腎臓学会西部学術大会, Oct. 2019.
121.	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.
122.	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.
123.	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.
124.	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.
125.	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.
126.	辻本賀美, 三井由加里, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : 勤務時間の影響で副腎皮質機能異常が疑われた2例, 日本内分泌学会第19回四国支部学術集会, Sep. 2019.
127.	工藤千晶, 枡田志保, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe, 新谷保実 and Seiji Fukumoto : 両側副腎偶発腫瘍で発見された123I-MIBGシンチ陰性の褐色細胞腫の一例, 日本内分泌学会第19回四国支部学術集会, Sep. 2019.
128.	安井沙耶, 桝田志保, Sumiko Yoshida, 辻本賀美, 工藤千晶, 遠藤ふうり, 三井由加里, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Munehide Matsuhisa, Masahiro Abe and Seiji Fukumoto : 成長ホルモン分泌不全症と甲状腺機能低下症を呈した小児がん経験者の一例, 第259回徳島医学会学術集会(令和元年度夏期), Aug. 2019.
129.	Tomoyo Hara, 遠藤ふうり, 桝田志保, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo and Ken-ichi Aihara : 原発性アルドステロン症におけるエプレレノンの血管機能への影響, 第51回日本動脈硬化学会総会・学術集会, Jul. 2019.
130.	宮高絋輔, Sumiko Yoshida, Furi Endo, 枡田志保, 三井由加里, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Seiji Fukumoto, Makoto Funaki, Yoshihiro Matsudate, Hiroshi Nokihara, Yasuhiko Nishioka, Masahiro Abe and Munehide Matsuhisa : 免疫チェックポイント阻害薬投与後に1型糖尿病を発症した2例, 第62回日本糖尿病学会年次学術集会, May 2019.
131.	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, Vol.95, No.1, 422, May 2019.
132.	Kohsuke Miyataka, Furi Endo, 三井由加里, 枡田志保, Kiyoe Kurahashi, Sumiko Yoshida, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Seiji Fukumoto, Hiroshi Nokihara, Yasuhiko Nishioka, Masahiro Abe and Munehide Matsuhisa : 抗PD-1抗体投与後に1型糖尿病を発症した1例, 第258回徳島医学会学術集会ポスターセッション, Feb. 2019.
133.	木村優里, 高橋寛典, 松島滉海, Akiko Sakurai, Mai Kanai and Itsuro Endo : TAK1阻害による炎症性サイトカイン誘導性サルコペ二ア改善の可能性, 第42回徳島県医学検査学会, Dec. 2018.
134.	Hiromi Matsushima, Yuri Kimura, 高橋寛典, Akiko Sakurai, Mai Kanai, Takeshi Kondo, 桝田志保, Tomoteru Kishimoto and Itsuro Endo : hCG, FSH製剤の併用によりパートナーの妊娠，健常児正常出産が確認された低ゴナドトロピン性男背性性腺機能低下症の2例, 第42回徳島県医学検査学会, Dec. 2018.
135.	Sumiko Yoshida, 原倫世, 山口佑樹, Takeshi Kondo, 遠藤ふうり, 筒井康継, 桝田志保, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe, Kohhei Nakajima and Seiji Fukumoto : 急速に腫瘍が増大し悪性転化が疑われたCushing病の1例, 第28回臨床内分泌代謝Update, Nov. 2018.
136.	Tomoyo Hara, Sumiko Yoshida, 細井美希, 遠藤ふうり, 筒井康継, 桝田志保, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Kohhei Nakajima, Yoshimi Bando, Masahiro Abe and Seiji Fukumoto : 脳内，副鼻腔，下垂体に炎症を認めステロイドが著効した1例, 第22回日本臨床内分泌病理学会学術総会, Oct. 2018.
137.	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.
138.	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.
139.	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.
140.	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.
141.	Kiyoe Kurahashi, Itsuro Endo, Takeshi Kondo, 遠藤ふうり, 原倫世, 桝田志保, Sumiko Yoshida, 明比祐子, Yoshimi Bando, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : ソマトスタチンアナログ製剤にて著明な縮小がみられたGH産生マクロアデノーマの1例, 第22回日本臨床内分泌病理学会, Sep. 2018.
142.	Kiyoe Kurahashi, Furi Endo, 桝田志保, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Seiji Fukumoto, Itsuro Endo and Munehide Matsuhisa : 足趾上腕血圧比定値を契機に末梢動脈疾患を診断しえた，重症下肢軟部組織感染症を繰り返す2型糖尿病の一例, 第3回日本下肢救済・足病学会中国四国地方会学術集会, Sep. 2018.
143.	桝田志保, Itsuro Endo, 遠藤ふうり, 原倫世, 筒井康継, Kiyoe Kurahashi, Sumiko Yoshida, Tomoteru Kishimoto, Ken-ichi Aihara and Seiji Fukumoto : 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2例, 第18回日本内分泌学会四国支部学術集会, Sep. 2018.
144.	中村昌史, Tomoyo Hara, Kiyoe Kurahashi, 遠藤ふうり, 筒井康継, 桝田志保, Sumiko Yoshida, 明比祐子, Itsuro Endo and Seiji Fukumoto : 股関節痛と歩行困難を契機に診断したCushing症候群の一例, 第18回日本内分泌学会四国支部学術集会, Sep. 2018.
145.	Ken-ichi Aihara, Sumiko Yoshida, Furi Endo, 筒井康継, Tomoyo Hara, 桝田志保, Kiyoe Kurahashi, Toshiki Otoda, Tomoyuki Yuasa, Itsuro Endo, Kana Morimoto, Akio Kuroda, 明比祐子, Makoto Funaki, Munehide Matsuhisa, Seiji Fukumoto and Masahiro Abe : 原発性アルドステロン症におけるミネラルコルチコイド受容体拮抗薬の血管機能への影響, 第18回日本内分泌学会四国支部学術集会, Sep. 2018.
146.	Hiroyasu Mori, Michiko Araki, Akio Kuroda, Masashi Ishizu, Yuichi Takashi, Satoshi Taniguchi, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Motoyuki Tamaki, 明比祐子 and Munehide Matsuhisa : 1型糖尿病患者の血清IGF-1とサルコペニア合併に関する横断的検証, 第18回日本内分泌学会四国支部学術集会, Sep. 2018.
147.	山上紘規, Sumiko Yoshida, 遠藤ふうり, 原倫世, 筒井康継, 桝田志保, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Yusuke Osaki, Ryuji Kaji, Yuichi Takashi, Masahiro Abe and Seiji Fukumoto : 壊死性ミオパチーを合併したX連鎖性低リン血症性くる病・骨軟化症の一例, 第18回日本内分泌学会四国支部学術集会, Sep. 2018.
148.	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.
149.	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.
150.	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.
151.	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.
152.	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.
153.	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.
154.	Sumiko Yoshida, 原倫世, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Munehide Matsuhisa : 高齢者における糖尿病教育入院中の体組成の変化, 第60回日本老年医学会学術集会, Jun. 2018.
155.	Akio Kuroda, Misuzu Yamada, 冨永ゆかり, 鈴木麗子, Motoyuki Tamaki, 明比祐子, Yuichi Takashi, Masashi Ishizu, 古賀大輔, Issei Imoto, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe, Kevin Ferreri and Munehide Matsuhisa : 膵β細胞特異的PCRによる膵β細胞死の検出, 第61回日本糖尿病学会年次学術集会, May 2018.
156.	Sumiko Yoshida, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Seiji Fukumoto, Masahiro Abe and Munehide Matsuhisa : 糖尿病教育入院における筋肉量の変化, 第61回日本糖尿病学会年次学術集会, May 2018.
157.	山上紘規, Sumiko Yoshida, 原倫世, 細井美希, 山口佑樹, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Seiji Fukumoto, Masahiro Abe, Yoshihiro Matsudate and Munehide Matsuhisa : 免疫チェックポイント阻害薬投与後に甲状腺機能異常と劇症1型糖尿病を発症した1例, 第61回日本糖尿病学会年次学術集会, May 2018.
158.	Ken-ichi Aihara, 上元良子, 石川カズ江, Kana Morimoto, 桝田志保, Hiroki Yamagami, Yuki Yamaguchi, Tomoyo Hara, 細井美希, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa, Hiroyuki Azuma and Masahiro Abe : 生活習慣病患者の尿中酸化ストレス指標における糖尿病および薬物療法の影響, 第61回日本糖尿病学会年次学術集会, May 2018.
159.	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.
160.	Sumiko Yoshida, 原倫世, 細井美希, 山上紘規, 山口佑樹, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Seiji Fukumoto, Daisuke Hamada, Munehide Matsuhisa and Masahiro Abe : 待機的高リスク整形外科手術における血糖管理の効果, 第91回日本内分泌学会学術総会, Apr. 2018.
161.	Tomoyo Hara, 桝田志保, Sumiko Yoshida, 細井美希, 山上紘規, 山口佑樹, Kiyoe Kurahashi, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : 急性合併症を来した高齢1型糖尿病の2症例, 第29回日本老年医学会四国地方会, Feb. 2018.
162.	岡諭紀, Mai Kanai, Akiko Sakurai and Itsuro Endo : 免疫チェックポイント阻害薬で中枢性副腎不全を来した2例, 第41回徳島県医学検査学会, Dec. 2017.
163.	野原圭一郎, 岡諭紀, 藤田幸那, Mai Kanai, Akiko Sakurai and Itsuro Endo : デノスマブによる対糖能改善, 第41回徳島県医学検査学会, Dec. 2017.
164.	Tomoyo Hara, Kiyoe Kurahashi, Kana Morimoto, 細井美希, Hiroki Yamagami, 山口佑樹, 桝田志保, Sumiko Yoshida, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa, Yoshimi Bando and Seiji Fukumoto : オクトレオチドが有効であったGH-TSH同時産生下垂体腺腫の一例, 第27回臨床内分泌代謝Update, Nov. 2017.
165.	大黒由加里, 白神敦久 and Itsuro Endo : 含糖酸化鉄投与により FGF-23関連低リン血症を呈した1例, 第27回臨床内分泌代謝Update抄録集, Nov. 2017.
166.	桝田志保, 明比祐子, Sumiko Yoshida, Hiroki Yamagami, Yuki Yamaguchi, 細井美希, Tomoyo Hara, Kiyoe Kurahashi, Itsuro Endo, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki and 福本誠ニ : 123I-MIBGシンチグラフィ陽性の副腎皮質腺腫の一例, 第27回臨床内分泌代謝Update抄録集, Nov. 2017.
167.	細井美希, Kana Morimoto, Takeshi Kondo, Hiroki Yamagami, Yuki Yamaguchi, Tomoyo Hara, 桝田志保, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, 明比祐子, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa and 福本誠ニ : 多発性骨髄腫治療を契機にプランマー病と判明した一例, 第27回臨床内分泌代謝Update抄録集, Nov. 2017.
168.	Yuki Yamaguchi, Sumiko Yoshida, Tomoyo Hara, 細井美希, Hiroki Yamagami, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, 福本誠ニ, Masahiro Abe, Hideya Kashihara, Kouzou Yoshikawa and Munehide Matsuhisa : 高度肥満症に対するスリーブ状胃切除術の長期の耐糖能異常改善効果の検討, 日本糖尿病学会中国四国地方会第55回総会抄録集, Nov. 2017.
169.	Naoto Kunikata, Sumiko Yoshida, Tomoyo Hara, 細井美希, Hiroki Yamagami, Yuki Yamaguchi, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, 福本誠ニ, Masahiro Abe, Daisuke Hamada and Munehide Matsuhisa : 待機的整形外科手術の術後経過における糖尿病の影響, 日本糖尿病学会中国四国地方会第55回総会抄録集, Nov. 2017.
170.	細井美希, Kiyoe Kurahashi, Tomoyo Hara, Yuki Yamaguchi, Hiroki Yamagami, 桝田志保, Sumiko Yoshida, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, 福本誠ニ and Munehide Matsuhisa : 低血糖脳症をきたしたACTH単独欠損症合併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.
171.	山上紘規, Kiyoe Kurahashi, 原倫世, 細井美希, 山口佑樹, 桝田志保, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara and Seiji Fukumoto : 副腎クリーゼと急性膵炎を発症した21‐水酸化酵素欠損症の1例, 第117回日本内科学会四国地方会, Nov. 2017.
172.	Hiroyasu Mori, Mami Ohishi, 鈴木麗子, Akio Kuroda, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 2型糖尿病患者における末梢神経障害の合併が骨格筋力の質的低下に及ぼす影響, 第32回日本糖尿病合併症学会, Oct. 2017.
173.	原倫世, Sumiko Yoshida, 山上紘規, 山口佑樹, 細井美希, 桝田志保, Kiyoe Kurahashi, Itsuro Endo, 明比祐子, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki and Seiji Fukumoto : Frequent syncope and marked blood pressure fluctuation due to antiparkinson drugs: A case report, 2017年10月20日-22日ひめぎんホール, Oct. 2017.
174.	Tomoyo Hara, Sumiko Yoshida, 山上紘規, 山口佑樹, 細井美希, 桝田志保, Kiyoe Kurahashi, Itsuro Endo, 明比祐子, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki and Seiji Fukumoto : 抗パーキンソン病薬により頻回な失神と著明な血圧変動をきたした一例, 第40回日本高血圧学会総会, Oct. 2017.
175.	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.
176.	山上紘規, Kiyoe Kurahashi, 山口佑樹, 細井美希, 原倫世, 桝田志保, Sumiko Yoshida, Itsuro Endo, 明比祐子, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki and Seiji Fukumoto : バセドウ病とTSH産生下垂体腺腫の合併の一例, 第60回日本甲状腺学会学術集会, Oct. 2017.
177.	細井美希, Sumiko Yoshida, 山上紘規, 山口佑樹, 原倫世, 桝田志保, Kiyoe Kurahashi, Itsuro Endo, 明比祐子, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki and Seiji Fukumoto : 無セルロプラスミン血症に合併した甲状腺乳頭癌の一例, 第60回日本甲状腺学会学術集会, Oct. 2017.
178.	桝田志保, Kiyoe Kurahashi, Takeshi Kondo, 細井美希, Yuki Yamaguchi, Tomoyo Hara, Hiroki Yamagami, Sumiko Yoshida, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki and 福本誠ニ : デノスマブ投与により術後の血清Ca/P値を容易に管理しえた巨大異所性副甲状腺腺腫の一例, 第17回日本内分泌学会四国支部学術集会抄録集, Sep. 2017.
179.	Tomoyo Hara, Sumiko Yoshida, Yuki Yamaguchi, 細井美希, Hiroki Yamagami, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki, 福本誠ニ and Masahiro Abe : 当院での免疫チェックポイント阻害薬による下垂体機能低下症の5例, 第17回日本内分泌学会四国支部学術集会抄録集, Sep. 2017.
180.	山口佑樹, Sumiko Yoshida, 細井美希, 山上紘規, 原倫世, 桝田志保, Kiyoe Kurahashi, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Munehide Matsuhisa, Makoto Funaki, Seiji Fukumoto and Hiromitsu Takizawa : 当院での免疫チェックポインント阻害薬による内分泌異常の発生と有害事象対策, 第255回徳島医学会学術集会(平成29年度夏期), Aug. 2017.
181.	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.
182.	Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : 骨格筋のアンドロゲン受容体と耐糖能異常, 第35回内分泌代謝学サマーセミナー, Jul. 2017.
183.	Kana Morimoto, 桝田志保, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Sumiko Yoshida, Tomoyuki Yuasa, Akio Kuroda, Itsuro Endo, Seiji Fukumoto, Munehide Matsuhisa, Masahiro Abe, Hiroyuki Azuma and Ken-ichi Aihara : 生活習慣病患者における血管内皮機能制御に関わる臨床指標の検討, 第49回日本動脈硬化学会総会・学術集会, Jul. 2017.
184.	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.
185.	西山美月, Kiyoe Kurahashi, 桝田志保, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, 小松まち子, Seiji Fukumoto and Masahiro Abe : 維持透析中に管理困難な高Ca血症を契機に診断されたサルコイドーシスの一例, 第116回日本内科学会四国地方会, May 2017.
186.	Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Kondo, Kana Morimoto, Motoyuki Tamaki, Tomoyuki Yuasa, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, 福本誠ニ and Munehide Matsuhisa : 糖尿病教育入院での酸化ストレスマーカーの変化の検討, 第60回日本糖尿病学会年次学術集会抄録集, May 2017.
187.	Motoyuki Tamaki, Akio Kuroda, Kiyoe Kurahashi, Ken-ichi Aihara, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, 山口普史, 白神敦久 and Munehide Matsuhisa : 課程用電気筋刺激装置(EMS)の10週間継続使用は運動障害を有する2型糖尿病患者の血糖コントロールを改善する, 第60回日本糖尿病学会年次学術集会抄録集, May 2017.
188.	Kana Morimoto, 桝田志保, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Sumiko Yoshida, Tomoyuki Yuasa, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, 福本誠ニ, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : 糖尿病患者における自律神経機能をアルブミン尿の相互関連および各病態に影響を及ぼす因子解析, 第60回日本糖尿病学会年次学術集会, May 2017.
189.	Michiko Araki, Hiroyasu Mori, Akio Kuroda, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Hiroshi Sakaue, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 1型糖尿病患者における血清IGF-1とサルコペニア罹患との関連, 第60回日本糖尿病学会年次学術集会, May 2017.
190.	Hiroyasu Mori, Akio Kuroda, Michiko Araki, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 2型糖尿病患者における皮下AGE蓄積が筋機能低下に及ぼす影響, 第60回日本糖尿病学会年次学術集会抄録集, May 2017.
191.	Sumiko Yoshida, Akio Kuroda, Minoru Irahara, Kiyoe Kurahashi, Takeshi Kondo, Itsuro Endo, Ken-ichi Aihara and Munehide Matsuhisa : 加重型妊娠高血圧腎症を来し集学的治療で分娩に至った糖尿病腎症の2症例, 第6回臨床高血圧フォーラム, May 2017.
192.	Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Kondo, Itsuro Endo, Tomoyuki Yuasa, Seiji Fukumoto and Masahiro Abe : 骨格筋におけるアンドロゲン受容体の耐糖能への影響, 第90回日本内分泌学会学術総会, Apr. 2017.
193.	Kana Morimoto, Yuka Takahashi, Saori Yamashita, 上元良子, 石川カズ江, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Akio Kuroda, Itsuro Endo, Tomoyuki Yuasa, Munehide Matsuhisa, 東博之, Masahiro Abe and Ken-ichi Aihara : 生活習慣病患者の血管内皮機能に関わる因子の臨床的検討, 第90回日本内分泌学会学術集会抄録集, Apr. 2017.
194.	Hiroyasu Mori, Akio Kuroda, Michiko Araki, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 2型糖尿病患者におけるサルコペニアのリスク因子解析, 第51回日本成人病学会学術集会, Jan. 2017.
195.	桝田志保, Sumiko Yoshida, Kiyoe Kurahashi, Takeshi Kondo, Itsuro Endo, Masahiro Abe, Akio Kuroda, Munehide Matsuhisa, Ken-ichi Aihara and Seiji Fukumoto : メーグルコシダーゼ阻害薬による腸管気腫症の一例, 第115回日本内科学会四国地方会, Nov. 2016.
196.	Tomoyo Hara, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Akio Kuroda, Munehide Matsuhisa, Ken-ichi Aihara and Seiji Fukumoto : イピリムマブ投与後に続発性副腎不全を発症した一例, 第115回日本内科学会四国地方会, Nov. 2016.
197.	上田浩之, Itsuro Endo, Takeshi Kondo, Kiyoe Kurahashi, Sumiko Yoshida, Masahiro Abe, Akio Kuroda, Munehide Matsuhisa, Ken-ichi Aihara and Seiji Fukumoto : デノスマブによる耐糖能改善, 第115回日本内科学会四国地方会, Nov. 2016.
198.	Takeshi Kondo, Itsuro Endo, 明比祐子, Kiyoe Kurahashi, Motoyuki Tamaki, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Masahiro Abe and Seiji Fukumoto : 免疫チェックポイント阻害剤で中枢性副腎不全を来した2例, 第26回臨床内分泌代謝Update, Nov. 2016.
199.	岡本恵暢, Sumiko Yoshida, Kiyoe Kurahashi, Takeshi Kondo, Kana Morimoto, Motoyuki Tamaki, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Munehide Matsuhisa and Seiji Fukumoto : IGF-2産生神経内分泌癌による重症低血糖の一例, 第26回臨床内分泌代謝Update, Nov. 2016.
200.	Sumiko Yoshida, Kiyoe Kurahashi, Takeshi Kondo, Kana Morimoto, Motoyuki Tamaki, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki, Munehide Matsuhisa and Seiji Fukumoto : 当院のニボルマブおよびイピリムマブ投与21例の内分泌異常の検討, 第26回臨床内分泌代謝Update, Nov. 2016.
201.	山下沙織, Sumiko Yoshida, 高橋優花, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Kondo, Kana Morimoto, Motoyuki Tamaki, Tomoyuki Yuasa, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 糖尿病教育入院における酸化ストレス減少に影響を及ぼす因子の検討, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
202.	Michiko Araki, Hiroyasu Mori, Akio Kuroda, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Hiroshi Sakaue, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 1型糖尿病患者の血清IGF-1がサルコペニア罹患に及ぼす影響, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
203.	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.
204.	Hiroyasu Mori, Akio Kuroda, Michiko Araki, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 2型糖尿病患者におけるAGE蓄積とサルコペニアとの関連の検討, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
205.	荒瀬美晴, Takeshi Kondo, Akio Kuroda, Kiyoe Kurahashi, Motoyuki Tamaki, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Seiji Fukumoto, Masahiro Abe and Munehide Matsuhisa : 術前後で持続血糖モニター(CGM)を比較したアドレナリン優位褐色細胞腫の二例, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
206.	上田浩之, Takeshi Kondo, Akio Kuroda, Kiyoe Kurahashi, Motoyuki Tamaki, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Seiji Fukumoto, Masahiro Abe and Munehide Matsuhisa : 基礎インスリンが不要であった膵性糖尿病の一例, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
207.	Kana Morimoto, 桝田志保, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Sumiko Yoshida, Tomoyuki Yuasa, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : 糖尿病患者における心電図R-R間隔変動係数に影響を及ぼす因子の検討, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
208.	Michiko Araki, Hiroyasu Mori, Akio Kuroda, 鈴木麗子, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, 明比祐子, Hiroshi Sakaue, Kiyoe Kurahashi, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : 1型糖尿病患者の血清IGF-1がサルコペニア罹患に及ぼす影響, 第14回1型糖尿病研究会, Nov. 2016.
209.	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.
210.	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.
211.	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.
212.	高橋優花, 山下沙織, Sumiko Yoshida, 桝田志保, Kana Morimoto, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Akio Kuroda, Tomoyuki Yuasa, Itsuro Endo, Munehide Matsuhisa, Seiji Fukumoto, Hiroyuki Azuma, Masahiro Abe and Ken-ichi Aihara : 生活習慣病患者における血管内皮機能正常群および低下群の臨床指標に関する検討, 第16回日本内分泌学会四国支部学術集会, Sep. 2016.
213.	山上紘規, Kiyoe Kurahashi, Kana Morimoto, Takeshi Kondo, Itsuro Endo, 明比祐子, Sumiko Yoshida, Akio Kuroda, Ken-ichi Aihara, Munehide Matsuhisa, Seiji Fukumoto and Masahiro Abe : バセドウ病を合併したTSH産生下垂体腺腫の一例, 第16回日本内分泌学会四国支部学術集会, Sep. 2016.
214.	遠藤ふうり, Kiyoe Kurahashi, Kana Morimoto, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Akio Kuroda, 明比祐子, Makoto Funaki, Munehide Matsuhisa, Seiji Fukumoto and Masahiro Abe : 日和見感染を合併したACTH依存性Cushing症候群の1例, 第253回徳島医学会学術集会(平成28年度夏期), Jul. 2016.
215.	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.
216.	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.
217.	Kiyoe Kurahashi, Itsuro Endo, Nakamura Mayuko, Ohnishi Yukiyo, Takeshi Kondo, Aizawa Shinichi, Seiji Fukumoto and Masahiro Abe : カルシウム感知受容体活性型変異による耐糖能異常, 第34回日本骨代謝学会学術総会, Jul. 2016.
218.	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.
219.	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.
220.	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.
221.	Takeshi Kondo and Itsuro Endo : 多発性骨髄腫と骨・内分泌異常, 第41回日本骨髄腫学会学術総会, May 2016.
222.	Shusuke Yagi, 西條良仁, 高川由利子, Masashi Akaike, Masataka Sata, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo and Ken-ichi Aihara : 左副腎に腫瘤を認めた両側性特発性アルドステロン症の1例, 日本内科学会第114回四国地方会, May 2016.
223.	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.
224.	Sumiko Yoshida, Ken-ichi Aihara, Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, Itsuro Endo, 明比祐子, Makoto Funaki, Seiji Fukumoto and Munehide Matsuhisa : 当院検診受診者における筋肉量がメタボリックパラメーターに及ぼす影響の検討, 第59回日本糖尿病学会年次学術集会, May 2016.
225.	Kana Morimoto, Ken-ichi Aihara, Sumiko Yoshida, Kiyoe Kurahashi, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 減塩による2型糖尿病入院症例の降圧予測指標, 第59回日本糖尿病学会年次学術集会, May 2016.
226.	Sumiko Yoshida, Ken-ichi Aihara, Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, Itsuro Endo, 明比祐子, Makoto Funaki, Seiji Fukumoto and Munehide Matsuhisa : 当院検診受診者における筋肉量が高血圧に及ぼす影響の検討, 第5回臨床高血圧フォーラム, May 2016.
227.	Kana Morimoto, Ken-ichi Aihara, Sumiko Yoshida, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : 血糖管理入院症例における減塩降圧効果と関連する因子および降圧薬に関する検討, 第5回臨床高血圧フォーラム, May 2016.
228.	Kana Morimoto, Ken-ichi Aihara, Sumiko Yoshida, Kiyoe Kurahashi, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : 2型糖尿病患者の塩分制限による降圧効果を規定する因子の検討, 第89回日本内分泌学会学術総会, Apr. 2016.
229.	Ken-ichi Aihara, Sumiko Yoshida, Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : 心筋リモデリングおよび頸動脈硬化症におけるアンジオテンシンII受容体拮抗薬の効果検証, 第89回日本内分泌学会学術総会, Apr. 2016.
230.	山上紘規, Kiyoe Kurahashi, 森本佳奈, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Akio Kuroda, 明比祐子, Makoto Funaki, Munehide Matsuhisa, Seiji Fukumoto and Masahiro Abe : インターフェロンβ治療中に糖尿病ケトアシドーシスを契機とし，急性発症1A型糖尿病と診断された一例, 第252回徳島医学会学術集会長井記念ホール, Feb. 2016.
231.	森本佳奈, Ken-ichi Aihara, Sumiko Yoshida, Kiyoe Kurahashi, Motoyuki Tamaki, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : 2型糖尿病患者における血糖指標と減塩がもたらす血圧低下との連関, 第252回徳島医学会学術集会長井記念ホール, Feb. 2016.
232.	林亜紀, Takeshi Kondo, Itsuro Endo, Kiyoe Kurahashi, Sumiko Yoshida, Seiji Fukumoto, Ken-ichi Aihara and Masahiro Abe : オクトレオチドLARで画像上，下垂体腺腫が消失した先端巨大症の一例, 第113回日本内科学会四国地方会, Dec. 2015.
233.	森本佳奈, Takeshi Kondo, Itsuro Endo, 倉橋清衛, Motoyuki Tamaki, Sumiko Yoshida, Akio Kuroda, Munehide Matsuhisa, Seiji Fukumoto, Ken-ichi Aihara and Masahiro Abe : 著明な低カルシウム血症を来した胃癌の骨転移の一例, 第25回臨床内分泌Update, Nov. 2015.
234.	小山広士, Takeshi Kondo, 森本佳奈, Itsuro Endo, 倉橋清衛, Motoyuki Tamaki, Sumiko Yoshida, Akio Kuroda, Munehide Matsuhisa, Seiji Fukumoto, Ken-ichi Aihara and Masahiro Abe : ACTH，コルチゾール基礎値正常のACTH単独欠損症の一例, 第25回臨床内分泌Update, Nov. 2015.
235.	Takeshi Kondo, Itsuro Endo, 森本佳奈, 倉橋清衛, Motoyuki Tamaki, Sumiko Yoshida, Akio Kuroda, Munehide Matsuhisa, Seiji Fukumoto, Ken-ichi Aihara and Masahiro Abe : テタニーで来院し，Gitelman症候群を疑った一例, 第25回臨床内分泌Update, Nov. 2015.
236.	Ken-ichi Aihara, Sumiko Yoshida, Kana Morimoto, Kiyoe Kurahashi, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 2型糖尿病患者の左室形態および機能における強化インスリン療法の効果, 日本糖尿病学会第53回中国四国地方会, Oct. 2015.
237.	岡田祐輝, Takeshi Kondo, 森本佳奈, Kiyoe Kurahashi, Motoyuki Tamaki, Sumiko Yoshida, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Seiji Fukumoto, Ken-ichi Aihara and Masahiro Abe : 高CPR血症からグリメピリド誤内服を診断し得た遷延性低血糖の一例, 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.
238.	Ken-ichi Aihara, Sumiko Yoshida, 森本佳奈, Kiyoe Kurahashi, Takeshi Kondo, Motoyuki Tamaki, Akio Kuroda, 明比祐子, Itsuro Endo, Makoto Funaki, Seiji Fukumoto, Munehide Matsuhisa and Masahiro Abe : 2型糖尿病患者の左室形態および機能における強化インスリン療法の効果, 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.
239.	林亜紀, Sumiko Yoshida, Akio Kuroda, 七篠あつ子, Minoru Irahara, 鶴尾美穂, 森本佳奈, 倉橋清衛, Takeshi Kondo, Motoyuki Tamaki, 明比祐子, Itsuro Endo, Makoto Funaki, Munehide Matsuhisa, Seiji Fukumoto, Ken-ichi Aihara and Masahiro Abe : 分娩前に10g/日以上の蛋白尿を合併し，出産に至った糖尿病腎症の1例, 日本糖尿病学会中国四国地方会第53回総会, Oct. 2015.
240.	Satoshi Taniguchi, Akio Kuroda, Motoyuki Tamaki, Hwa In, 森本佳奈, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Munehide Matsuhisa : CGM iPRO2と人工膵臓STG-55との測定グルコース濃度の比較, 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.
241.	Hisami Okumura, 和田宵湖, 新井田裕樹, Hideya Kashihara, Masaaki Nishi, Kouzou Yoshikawa, 森本佳奈, 倉橋清衛, Takeshi Kondo, Sumiko Yoshida, Motoyuki Tamaki, Akio Kuroda, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Mitsuo Shimada and Munehide Matsuhisa : 本院の腹腔鏡下袖状胃切除術後1年で異なった経過を示した2症例の報告, 第53回糖尿病学会中四国大会, Oct. 2015.
242.	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.
243.	森本佳奈, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Motoyuki Tamaki, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : Significance of glycemic markers for sodium restriction-induced blood pressure reduction in hospitalized patients with type 2 diabetes, 第38日本高血圧学会総会, Oct. 2015.
244.	Ken-ichi Aihara, Sumiko Yoshida, 森本佳奈, 倉橋清衛, Motoyuki Tamaki, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : Evaluation for long-term efficacy of angiotensin II receptor blocker-based antihypertensive therapy on cardiac remodeling and carotid atherosclerosis, 第38日本高血圧学会総会, Oct. 2015.
245.	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.
246.	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.
247.	森本佳奈, Takeshi Kondo, Itsuro Endo, Kiyoe Kurahashi, Motoyuki Tamaki, Sumiko Yoshida, Akio Kuroda, Munehide Matsuhisa, Seiji Fukumoto, Ken-ichi Aihara and Masahiro Abe : 診断まで長時間を要したACTH分泌低下症の一例, 第15回日本内分泌学会四国支部学術集会高知大学, Sep. 2015.
248.	加藤正樹, 森本佳奈, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Motoyuki Tamaki, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa, Seiji Fukumoto and Masahiro Abe : 2型糖尿病患者の減塩療法による血圧低下に関連する因子の解析, 第15回日本内分泌学会四国支部学術集会, Sep. 2015.
249.	森本佳奈, Ken-ichi Aihara, Sumiko Yoshida, 倉橋清衛, Motoyuki Tamaki, Takeshi Kondo, Akio Kuroda, Itsuro Endo, Munehide Matsuhisa and Masahiro Abe : 2型糖尿病における血糖指標と減塩がもたらす血圧低下との連関, 第251回徳島医学会学術集会ポスター, Aug. 2015.
250.	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.
251.	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.
252.	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.
253.	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.
254.	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.
255.	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.
256.	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.
257.	Itsuro Endo : 糖尿病と骨折リスク, 第58回日本糖尿病学会年次学術集会, May 2015.
258.	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.
259.	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.
260.	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.
261.	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.
262.	Itsuro Endo : 代謝性骨疾患治療の新たな標的因子としてのRANKL, 第88回日本内分泌学会, Apr. 2015.
263.	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.
264.	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.
265.	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.
266.	Itsuro Endo : 低リン血症への実践的アプローチ, 第24回臨床内分泌Up-date, Nov. 2014.
267.	Itsuro Endo : 低リン血症への実践的アプローチ, 第24回臨床内分泌Update, Nov. 2014.
268.	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.
269.	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.
270.	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.
271.	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.
272.	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.
273.	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.
274.	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.
275.	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.
276.	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.
277.	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.
278.	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.
279.	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.
280.	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.
281.	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.
282.	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.
283.	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.
284.	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.
285.	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.
286.	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.
287.	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.
288.	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.
289.	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.
290.	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.
291.	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.
292.	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.
293.	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.
294.	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.
295.	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.
296.	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.
297.	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.
298.	Dong Bingzi, Takeshi Kondo, Itsuro Endo, Yukiyo Ohnishi, Omatsu Takashi, Shin-ichi Aizawa and Hiroshi Sakaue : Interleukin-11 regulates osteoblast and adipocyte differentiation from mesenchymal stem cells, 2nd joint meeting of the international Bone and Mineral Society and the Japanese Society for Bone Mineral Rsearch, May 2013.
299.	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.
300.	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.
301.	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.
302.	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.
303.	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.
304.	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.
305.	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.
306.	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.
307.	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.
308.	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.
309.	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.
310.	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.
311.	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.
312.	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.
313.	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.
314.	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, Vol.88, No.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
315.	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.
316.	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.
317.	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.
318.	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.
319.	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.
320.	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.
321.	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
322.	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.
323.	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.
324.	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.
325.	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.
326.	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.
327.	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.
328.	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.
329.	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.
330.	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.
331.	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.
332.	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.
333.	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.
334.	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
335.	Itsuro Endo : 骨粗鬆症治療の最前線, 吾川郡医師会学術講演会, Mar. 2012.
336.	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.
337.	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.
338.	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.
339.	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.
340.	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.
341.	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.
342.	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.
343.	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.
344.	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.
345.	Itsuro Endo : 骨粗鬆症治療の最前線, 徳島県薬剤師会講演会, Nov. 2011.
346.	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
347.	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
348.	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.
349.	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.
350.	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.
351.	Itsuro Endo : 動脈石灰化の基礎と臨床, 川島病院病診連携の会, Aug. 2011.
352.	Itsuro Endo : 骨粗鬆症にならんために, 名西郡町民健康講座, Jul. 2011.
353.	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
354.	Itsuro Endo : 内科疾患としての骨粗鬆症に挑む, 徳島県健康寿命講座, Jun. 2011.
355.	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.
356.	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.
357.	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.
358.	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.
359.	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.
360.	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.
361.	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
362.	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.
363.	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.
364.	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.
365.	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.
366.	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.
367.	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.
368.	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.
369.	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.
370.	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.
371.	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.
372.	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, Vol.86, No.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
373.	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.
374.	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.
375.	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.
376.	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.
377.	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.
378.	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.
379.	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.
380.	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.
381.	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
382.	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.
383.	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.
384.	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.
385.	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.
386.	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)
387.	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.
388.	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, Vol.85, No.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
389.	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, Vol.85, No.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
390.	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, Vol.85, No.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
391.	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, Vol.98, No.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
392.	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, Vol.98, No.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
393.	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.
394.	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.
395.	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.
396.	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.
397.	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.
398.	Kumiko Kagawa, Ken-ichiro Yata, 田中修, Shingen Nakamura, Hirokazu Miki, Kyoko Takeuchi, Masahiro Abe, Shuji Ozaki, Sumiko Yoshida and Itsuro Endo : 心筋への広範な直接浸潤を来したNK/T cell lymphoma 鼻型の一例, 第48回に本血液学会中国四国地方会, Mar. 2009.
399.	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.
400.	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
401.	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.
402.	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.
403.	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.
404.	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
405.	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
406.	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.
407.	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.
408.	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, Vol.84, No.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
409.	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, Vol.84, No.1, 222, May 2008. (Keyword) 脂質異常症左心室機能ヒト成人(19~44) 男女
410.	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, Vol.83, No.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
411.	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.
412.	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.
413.	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, Vol.83, No.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
414.	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, Vol.83, No.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
415.	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, Vol.83, No.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
416.	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, Vol.83, No.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
417.	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, Vol.83, No.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
418.	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.
419.	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.
420.	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, Vol.63, No.1, 645, Mar. 1999. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1574231876839482624 (CiNii: 1574231876839482624)
421.	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 and 重清俊雄 : 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, Japanese Circulation Journal, Vol.63, No.Suppl.I, 645, 1999. (Keyword) Heparin Cofactor II(欠損・欠乏) 動脈硬化症(先天性) 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.
2.	Itsuro Endo : 不動性骨粗鬆症, ビスホスホネートエビデンスブック, Oct. 2013.
3.	Takeshi Kondo and Itsuro Endo : テリパラチドの投与は連日皮下注製剤で2年間，週1回皮下注製剤で18ヶ月が上限とされていますが，この範囲なら何回かに分けて投与してもいいですか, ファーマナビゲーターPTH編, 278-281, 2013.
4.	Itsuro Endo : PTH 1-34は低骨代謝回転型に効果が期待できるのでしょうか?, ファーマナビゲーターPTH編, 256-259, 2013.
5.	Itsuro Endo : 間欠投与と持続投与による作用の違い, ファーマナビゲーターPTH編, 90-95, 2013.
6.	Itsuro Endo : 活性型ビタミンD3, 副甲状腺・骨代謝疾患診療マニュアル, 132-133, 2013.
7.	Takeshi Kondo and Itsuro Endo : 副甲状腺関連疾患, 副甲状腺・骨代謝疾患診療マニュアル, 26-29, 2013.

Et cetera, Workshop:

1.	遠藤ふうり, Sumiko Yoshida, 辻本賀美, 工藤千晶, 安井沙耶, 桝田志保, 三井由香里, Kiyoe Kurahashi, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : ソマトスタチンアナログ治療中に胆嚢癌を認めた先端巨大症の1例, 第29回臨床内分泌代謝Update in Kochi, Nov. 2019.
2.	工藤千晶, Kiyoe Kurahashi, 辻本賀美, 安井沙耶, 遠藤ふうり, 三井由香里, 桝田志保, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : ニボルマブ投与により3系統の内分泌障害を発症した2例, 第29回臨床内分泌代謝Update in Kochi, Nov. 2019.
3.	辻本賀美, 三井由香里, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : 免疫関連有害事象の末ロイド治療中ACTH分泌低下症を認めた1例, 第29回臨床内分泌代謝Update in Kochi, Nov. 2019.
4.	Yukari Mitsui, 辻本賀美, 工藤千晶, 安井沙耶, 遠藤ふうり, 桝田志保, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : 治療拒否により甲状腺クリーゼを繰り返したバセドウ病の1例, 第29回臨床内分泌代謝Update in Kochi, Nov. 2019.
5.	Kiyoe Kurahashi, 青山万里子, Hiromitsu Takizawa, 遠藤ふうり, 三井由香里, 桝田志保, Sumiko Yoshida, 明比祐子, Itsuro Endo, Ken-ichi Aihara, Masahiro Abe and Seiji Fukumoto : 薬物治療に抵抗性で，日和見感染も合併したバセドウ病の一例, 第29回臨床内分泌代謝Update in Kochi, Nov. 2019.
6.	松田宙也, 遠藤ふうり, 三井由加里, 桝田志保, Kiyoe Kurahashi, Sumiko Yoshida, 明比祐子, Itsuro Endo and Seiji Fukumoto : 症状発現から診断までに半年を要したACTH単独欠損症の一例, 第258回徳島医学会学術集会, Feb. 2019.
7.	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.
8.	Hiroyasu Mori, Akio Kuroda, Michiko Araki, Reiko Suzuki, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, Yuko Akehi, Hiroshi Sakaue, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa : Advanced glycation end-products are a risk for muscle weakness in patients with type2 diabetes., American Diabetes Association 78th Scientific Sessions, Jun. 2017.
9.	Itsuro Endo : 乳癌の支持療法におけるデノスマブ製剤の位置づけ, 第5回東名古屋乳癌化学療法研究会, Nov. 2014.
10.	Itsuro Endo : 骨粗鬆症治療における最近の話題, 骨粗鬆症治療Web講演会, Jul. 2014.
11.	Itsuro Endo : 骨粗鬆症のビスホスホネート治療, Orthopedics Seminar, Mar. 2014.
12.	Itsuro Endo, Kumiko Kagawa, Hirokazu Miki, 高橋真美子 and Masahiro Abe : B細胞リンパ腫を合併した先端巨大症の一例, 第3回四国GH/IGF1フォーラム, Feb. 2014.
13.	Itsuro Endo : 骨粗鬆症の病態と治療, 愛媛県病院薬剤師会中予支部講演会, Sep. 2013.
14.	Itsuro Endo : 糖尿病の病態と治療, 協和発酵キリン勉強会, Jul. 2013.
15.	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.
16.	Itsuro Endo : 糖尿病治療, ノバルティスファーマ社内研修会, May 2013.
17.	Itsuro Endo : 骨粗鬆症の病態と治療, 骨粗鬆症治療MR研修, Apr. 2013.
18.	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.
19.	Itsuro Endo : ビスホスホネートの特性, 徳島県病院薬剤師会理事会研修会, Dec. 2012.
20.	Itsuro Endo : 生活習慣病・ステロイド過剰に伴う骨粗鬆症の病態と治療, 伊予市医師会学術講演会, Dec. 2012.
21.	Itsuro Endo : 生活習慣病・ステロイド過剰に伴う骨粗鬆症の病態と治療, 美馬市医師会学術講演会, Dec. 2012.
22.	Itsuro Endo : 生活習慣病・ステロイド過剰に伴う骨粗鬆症の病態と治療, 阿波市臨床研究会, Nov. 2012.
23.	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.
24.	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.
25.	Itsuro Endo : 生活習慣病・ステロイド過剰に伴う骨粗鬆症の病態と治療, 新居浜市医師学術講演会, Sep. 2012.
26.	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.
27.	Itsuro Endo : 骨粗鬆症治療の最前線, 吾川郡医師学術講演会医, Mar. 2012.
28.	Itsuro Endo : 骨粗鬆症治療の最前線, 徳島内分泌研究会, Feb. 2012.
29.	Itsuro Endo : 骨粗鬆症治療, アステラス製薬社内勉強会, Jan. 2012.
30.	Itsuro Endo : 骨粗鬆症治療の最前線, ノバルティスファーマ社内勉強会, Nov. 2011.
31.	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.
32.	Itsuro Endo : 内科疾患と骨粗鬆症, 実地医家のための骨粗鬆症を考える会, Oct. 2011.
33.	Itsuro Endo : 副甲状腺ホルモンの基礎と臨床, 旭化成ファーマ社内研修会, Sep. 2011.
34.	Itsuro Endo : フェブリクの使用経験, 徳島内分泌研究会, Aug. 2011.
35.	Itsuro Endo : 先端巨大症に対するサンドスタチン治療, ノバルティスファーマ社内勉強会, Apr. 2011.
36.	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.
37.	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.
38.	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.
39.	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.
40.	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.
41.	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.

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)

骨細胞保護によるがんの骨転移新規治療戦略の開発 (Project/Area Number: 23K27791 )
加齢性サルコペニアへの炎症性サイトカインの関与とTAK1阻害による治療法の開発 (Project/Area Number: 21K07339 )
Elucidation of molecular mechanism of the regulation of skeletal homeostasis, and development of new therapeutic approaches against skeletal disorders (Project/Area Number: 25293215 )
Mechanisms of bone destruction and drug resistance in myeloma: a novel therapeutic strategy targeting a myeloma-bone marrow interaction (Project/Area Number: 23591390 )
Pathophysiological roles of heparin cofactor II in cardiac remodeling and insulin resistance (Project/Area Number: 21591140 )
Relationships among skeletal, adipose and vasclar regulatory system, and elucidation of pathogensis caused by disturbances of these systems (Project/Area Number: 20249050 )
Search by Researcher Number (10432759)

Professor : Endo, Itsuro

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