Tokushima University / Educator and Researcher Directory --- Yuasa, Tomoyuki

Field of Study

○	Medicine

Subject of Study

○	Shedding of Insulin receptor extra cellular domain in diabetes Mellitus (soluble insulin receptor, insulin resistance, diabetes)

Book / Paper

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.	Taiki Hori, Taro Shimizu, Hidenori ANDO, Naoto Okada, Hiroki Yamagami, Saya Yasui, Minae Hosoki, Akihiro Tojima, Toshiki Otoda, Tomoyuki Yuasa, Ken-ichi Aihara, Makoto Takishita, Sumiko Yoshida, Masahiro Abe, Tatsuhiro Ishida and Shingen Nakamura : Humoral immune response against SARS-CoV-2 and polyethylene glycol elicited by anti-SARS-CoV-2 mRNA vaccine, and effect of pre-existing anti-polyethylene glycol antibody in patients with hematological and autoimmune diseases., Heliyon, Vol.10, No.10, e31489, 2024. (Summary) The effects of vaccination are modified by hematological and autoimmune diseases and/or treatment. Anti-SARS-CoV-2 mRNA vaccine contains polyethylene glycol (PEG), it is largely unknown whether PEG influences the effects of vaccination or induces a humoral response. This study examined whether anti-PEG antibodies before vaccination (pre-existing) influenced the acquisition of SARS-CoV-2 antibodies and evaluated the relationship between the development of anti-SARS-CoV-2 antibodies and anti-PEG antibodies after SARS-CoV-2 vaccination in hematological and autoimmune diseases. Anti-SARS-CoV-2 antibody IgG, anti-PEG IgG, and IgM titers were evaluated in patients with hematological and autoimmune diseases after the second dose of BNT162B2. Anti-PEG IgG and IgM titers were also measured before vaccination to examine changes after vaccination and the relationship with vaccine efficacy. In patients with hematological (n = 182) and autoimmune diseases (n = 96), anti-SARS-CoV-2 and anti-PEG antibody titers were evaluated after a median of 33 days from 2nd vaccination. The median anti-SARS-CoV-2 antibody titers were 1901 AU/mL and 3832 AU/mL in patients with hematological and autoimmune disease, respectively. Multiple regression analysis showed that age and days from 2nd vaccination were negatively associated with anti-SARS-CoV-2 antibody titers. Anti-CD20 antibody treatment was negatively correlated with anti-SARS-CoV-2 antibody titers in hematological disease, and C-reactive protein (CRP) was positively correlated with anti-SARS-CoV-2 antibody titers in autoimmune disease. Baseline anti-PEG antibody titers were significantly higher in patients with autoimmune disease but were not correlated with anti-SARS-CoV-2 antibody titers. Patients with increased anti-PEG IgG acquired higher anti-SARS-CoV-2 antibody titers in patients with autoimmune disease. Anti-SARS-CoV-2 antibody acquisition was suboptimal in patients with hematological disease, but both anti-SARS-CoV-2 antibody and anti-PEG IgG were acquired in patients with autoimmune disease, reflecting robust humoral immune response. Pre-existing anti-PEG antibody titers did not affect anti-SARS-CoV-2 antibody acquisition. (Tokushima University Institutional Repository) ● Metadata: 119625 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.heliyon.2024.e31489 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38813140 ● Search Scopus @ Elsevier (PMID): 38813140 ● Search Scopus @ Elsevier (DOI): 10.1016/j.heliyon.2024.e31489 (Tokushima University Institutional Repository: 119625, DOI: 10.1016/j.heliyon.2024.e31489, PubMed: 38813140)
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.	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): 1870302167614368000 ● Summary page in Scopus @ Elsevier: 2-s2.0-85178346619 (Tokushima University Institutional Repository: 119108, DOI: 10.3390/biomedicines11113020, PubMed: 38002020, CiNii: 1870302167614368000, Elsevier: Scopus)
5.	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): 1870583643033891840 ● Summary page in Scopus @ Elsevier: 2-s2.0-85178271509 (Tokushima University Institutional Repository: 119107, DOI: 10.3390/metabo13111129, PubMed: 37999225, CiNii: 1870583643033891840, Elsevier: Scopus)
6.	Toshiki Otoda, Akiko Sekine, Ryoko Uemoto, Seijiro Tsuji, Tomoyo Hara, Motoyuki Tamaki, Tomoyuki Yuasa, Toshiaki Tamaki, Munehide Matsuhisa and Ken-ichi Aihara : Albuminuria and Serum Tumor Necrosis Factor Receptor Levels in Patients with Type 2 Diabetes on SGLT2 Inhibitors: A Prospective Study., Diabetes Therapy, Vol.15, No.1, 127-143, 2023. (Summary) UMIN000031947. (Tokushima University Institutional Repository) ● Metadata: 119109 (Link to Publication Site) ● Publication site (DOI): 10.1007/s13300-023-01488-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37883001 ● CiNii @ National Institute of Informatics (CRID): 1872272493157884672 ● Summary page in Scopus @ Elsevier: 2-s2.0-85174952372 (Tokushima University Institutional Repository: 119109, DOI: 10.1007/s13300-023-01488-0, PubMed: 37883001, CiNii: 1872272493157884672, Elsevier: Scopus)
7.	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)
8.	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)
9.	Taiki Hori, Saya Yasui, Minae Hosoki, Hiroki Yamagami, Toshiki Otoda, Tomoyuki Yuasa, Kenichi Aihara, Makoto Takishita, Akihiko Yokohama, Mitusharu Ueda, Masahiro Abe and Shingen Nakamura : Systemic amyloidosis associated with non-IgM type paraprotein with lymphoplasmacytic lymphoma, International Journal of Myeloma, Vol.13, No.2, 7-12, 2023. (Tokushima University Institutional Repository) ● Metadata: 118610 (Link to Publication Site) ● Publication site (DOI): 10.57352/ijm.13.2_7 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.13.2_7 (Tokushima University Institutional Repository: 118610, DOI: 10.57352/ijm.13.2_7)
10.	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)
11.	Tomoyuki Yuasa, Yasunori Takata, Nanako Aki, Kotaro Kunimi, Miki Satoh, Mari Nii, Yoshihiko Izumi, Toshiki Otoda, Seiichi Hashida, Haruhiko Osawa and Ken-ichi Aihara : Insulin receptor cleavage induced by estrogen impairs insulin signaling., BMJ Open Diabetes Research & Care, Vol.9, No.2, 2021. (Summary) Soluble insulin receptor (sIR), which is the ectodomain of insulin receptor (IR), is present in human plasma. Plasma sIR levels are positively correlated with blood glucose levels and negatively correlated with insulin sensitivity. An in vitro model of IR cleavage shows that extracellular calpain 2 directly cleaves IR, which generates sIR, and sequential cleavage of the IR subunit by -secretase impairs insulin signaling in a glucose concentration-dependent manner. Nevertheless, sIR levels vary among subjects with normal glucose levels. We examined sIR levels of pregnant women throughout gestation. Using an in vitro model, we also investigated the molecular mechanisms of IR cleavage induced by estradiol. In pregnant women, sIR levels were positively correlated with estrogen levels and significantly increased at late pregnancy independent of glucose levels. Using an in vitro model, estrogen elicited IR cleavage and impaired cellular insulin signaling. Estradiol-induced IR cleavage was inhibited by targeting of calpain 2 and -secretase. Estrogen exerted these biological effects via G protein-coupled estrogen receptor, and its selective ligand upregulated calpain 2 expression and promoted exosome secretion, which significantly increased extracellular calpain 2. Simultaneous stimulation of estrogen and high glucose levels had a synergic effect on IR cleavage. Metformin prevented calpain 2 release in exosomes and restored insulin signaling impaired by estrogen. Estradiol-induced IR cleavage causes cellular insulin resistance, and its molecular mechanisms are shared with those by high glucose levels. sIR levels at late pregnancy are significantly elevated along with estrogen levels. Therefore, estradiol-induced IR cleavage is preserved in pregnant women and could be part of the etiology of insulin resistance in gestational diabetes mellitus and overt diabetes during pregnancy. (Keyword) Diabetes, Gestational / Estrogens / Female / Humans / Insulin / Insulin Resistance / Pregnancy / soluble insulin receptor (Tokushima University Institutional Repository) ● Metadata: 118344 (Link to Publication Site) ● Publication site (DOI): 10.1136/bmjdrc-2021-002467 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34969688 ● Search Scopus @ Elsevier (PMID): 34969688 ● Search Scopus @ Elsevier (DOI): 10.1136/bmjdrc-2021-002467 (Tokushima University Institutional Repository: 118344, DOI: 10.1136/bmjdrc-2021-002467, PubMed: 34969688)
12.	Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda, Yasumasa Ikeda, Itsuro Endo, Soichi Honda, Katsuhiko Yoshimoto, Akira Kondo, Toshiaki Tamaki, Toshio Matsumoto, Munehide Matsuhisa, Masahiro Abe and Ken-ichi Aihara : Plasma Heparin Cofactor II Activity Is Inversely Associated with Albuminuria and Its Annual Deterioration in Patients with Diabetes., Journal of Diabetes Investigation, 2021. (Summary) The plasma HCII activity was inversely and specifically associated with glomerular injury in patients with diabetes. The results suggest that HCII can serve as a novel predictive factor for early-stage DKD development, as represented by albuminuria. (Tokushima University Institutional Repository) ● Metadata: 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)
13.	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)
14.	Tomoyuki Yuasa, Kikuko Amo-Shiinoki, Shuhei Ishikura, Mitsuyoshi Takahara, Takaaki Matsuoka, Hideaki Kaneto, Akio Kuroda, Munehide Matsuhisa and Seiichi Hashida : Sequential cleavage of insulin receptor by calpain 2 and -secretase impairs insulin signalling., Diabetologia, Vol.59, No.12, 2711-2721, 2016. (Summary) Sequential cleavage of IR by calpain 2 and -secretase may contribute to insulin signalling in cells and its inhibition may be partly responsible for the glucose-lowering effects of metformin. Thus, IR cleavage may offer a new mechanism for the aetiology of insulin resistance. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00125-016-4102-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27695899 ● Summary page in Scopus @ Elsevier: 2-s2.0-84989201840 (DOI: 10.1007/s00125-016-4102-5, PubMed: 27695899, Elsevier: Scopus)
15.	Tomoyuki Yuasa, Kikuko Amo, Shuhei Ishikura, Hisao Nagaya, Keiji Uchiyama, Seiichi Hashida and Yousuke Ebina : Development of in vitro model of insulin receptor cleavage induced by high glucose in HepG2 cells., Biochemical and Biophysical Research Communications, Vol.445, No.1, 236-243, 2014. (Summary) Soluble insulin receptor (sIR), the ectodomain of IR, has been detected in human plasma, and its concentration parallels that of blood glucose in patients with diabetes. IR has a pivotal role in glucose homeostasis and diabetes development; therefore, cleavage of IR promoted by hyperglycemia is involved in insulin resistance and glucose toxicity. To elucidate the physiology of sIR, we developed an in vitro model mimicking the changes in sIR levels in plasma from patients with diabetes. Among four human cell lines that expressed IR, spontaneous cleavage of IR occurred only in HepG2 cells. The molecular characteristics of sIR derived from HepG2 cells were similar to those of sIR detected in human plasma. The concentration of sIR in the medium did not differ between basal and high-glucose conditions in the initial 24-h period, but increasing the duration of pre-stimulation (>48 h) led to a significant increase in sIR levels in cells exposed to high glucose. Additionally, glucose-dependent increment of sIR was reversible in this model. These results are consistent with the observation of plasma sIR in patients with diabetes. Using this model, O-linked N-acetylglucosamine modification was determined to be involved in high-glucose-induced IR cleavage. A calcium-dependent protease was shown to cleave IR extracellularly. These findings show that this in vitro model could be useful for determining the molecular mechanism underlying IR cleavage. (Keyword) soluble insulin receptor / Insulin resistance / shedding / O-GlcNAc / Calcium dependent protease / Diabetes / Hep G2 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2014.01.187 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24508798 ● Summary page in Scopus @ Elsevier: 2-s2.0-84896697427 (DOI: 10.1016/j.bbrc.2014.01.187, PubMed: 24508798, Elsevier: Scopus)
16.	Tomoyuki Yuasa, Keiji Uchiyama, OGURA Yuko, Masafumi Kimura, TESHIGAWARA Kiyoshi, Toshio Hosaka, TANAKA Yoshinori, Toshiyuki Obata, SANO Hiroyuki, Kazuhiro Kishi and Yousuke Ebina : The Rab GTPase-Activating Protein AS160 as a Common Regulator of Insulin- and Gαq-Mediated Intracellular GLUT4 Vesicle Distribution, Endocrine Journal, Vol.56, No.3, 345-359, 2009. (Summary) Akt substrate of 160kDa (AS160) is a Rab GTPase activating protein (GAP) and was recently identified as a component of the insulin signaling pathway of glucose transporter type 4 (GLUT4) translocation. We and others, previously reported that the activation of Galphaq protein-coupled receptors (GalphaqPCRs) also stimulated GLUT4 translocation and glucose uptake in several cell lines. Here, we report that the activation of GalphaqPCRs also promoted phosphorylation of AS160 by the 5'-AMP activated protein kinase (AMPK). The suppression of AS160 phosphorylation by the siRNA mediated AMPKalpha1 subunit knockdown promoted GLUT4 vesicle retention in intracellular compartments. This suppression did not affect the ratio of non-induced cell surface GLUT4 to Galphaq-induced it. Rat 3Y1 cells lacking AS160 did not show insulin-induced GLUT4 translocation. The cells stably expressing GLUT4 revealed GLUT4 vesicles that were mainly localized in the perinuclear region and less frequently on the cell surface. After expression of exogenous AS160, GLUT4 on the cell surface decreased and GLUT4 vesicles were redistributed throughout the cytoplasm. Although PMA-induced or sodium fluoride-induced GLUT4 translocation was significantly increased in these cells, insulin did not affect GLUT4 translocation. These results suggest that AS160 is a common regulator of insulin- and GalphaqPCR activation-mediated GLUT4 distribution in the cells. (Keyword) 3T3-L1 Cells / AMP-Activated Protein Kinases / Animals / CHO Cells / Cricetinae / Cricetulus / GTP-Binding Protein alpha Subunits, Gq-G11 / GTPase-Activating Proteins / Glucose Transporter Type 4 / Humans / Insulin / Mice / Rats (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.K08E-216 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19139597 ● Search Scopus @ Elsevier (PMID): 19139597 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.K08E-216 (DOI: 10.1507/endocrj.K08E-216, PubMed: 19139597)
17.	L. Kyle Hoehn, Cordula Hohnen-Behrens, Anna Cederberg, E. Lindsay Wu, Nigel Turner, Tomoyuki Yuasa, Yousuke Ebina and E. David James : IRS1-Independent Defects Define Major Nodes of Insulin Resistance, Cell Metabolism, Vol.7, No.5, 421-433, 2008. (Summary) Insulin resistance is a common disorder caused by a wide variety of physiological insults, some of which include poor diet, inflammation, anti-inflammatory steroids, hyperinsulinemia, and dyslipidemia. The common link between these diverse insults and insulin resistance is widely considered to involve impaired insulin signaling, particularly at the level of the insulin receptor substrate (IRS). To test this model, we utilized a heterologous system involving the platelet-derived growth factor (PDGF) pathway that recapitulates many aspects of insulin action independently of IRS. We comprehensively analyzed six models of insulin resistance in three experimental systems and consistently observed defects in both insulin and PDGF action despite a range of insult-specific defects within the IRS-Akt nexus. These findings indicate that while insulin resistance is associated with multiple deficiencies, the most deleterious defects and the origin of insulin resistance occur independently of IRS. (Keyword) Adaptor Proteins, Signal Transducing / Adipocytes / Animals / Cells, Cultured / Glucose Tolerance Test / Glucose Transporter Type 4 / Hyperinsulinism / Hypoglycemic Agents / Immunoblotting / Inflammation / Insulin / Insulin Receptor Substrate Proteins / Insulin Resistance / Male / Mice / Mice, Inbred C57BL / Mice, Transgenic / Myoblasts / Oxidative Stress / Palmitates / Phosphatidylinositol 3-Kinases / Platelet-Derived Growth Factor / Protein Transport / Proto-Oncogene Proteins c-akt / Rats / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cmet.2008.04.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18460333 ● Search Scopus @ Elsevier (PMID): 18460333 ● Search Scopus @ Elsevier (DOI): 10.1016/j.cmet.2008.04.005 (DOI: 10.1016/j.cmet.2008.04.005, PubMed: 18460333)
18.	Toshiyuki Obata, Ichiro Yokota, Kazuhiro Yokoyama, Eiji Okamoto, Yoshiko Kanezaki, Yoshinori Tanaka, Hiroshi Maegawa, Kiyoshi Teshigawara, Fumiko Hirota, Tomoyuki Yuasa, Kazuhiro Kishi, Atsushi Hattori, Seiichi Hashida, Kazuhiko Masuda, Mitsuru Matsumoto, Toshio Matsumoto, Atsunori Kashiwagi and Yousuke Ebina : Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes mellitus., Diabetes, Vol.56, No.8, 2028-2035, 2007. (Summary) Insulin binds to the alpha-subunit of the insulin receptor (IRalpha) and subsequently exerts its effects in the cells. The soluble ectodomains of several receptors have been found to circulate in the plasma. Therefore, we hypothesized that soluble human insulin receptor (hIR) ectodomain (alpha-subunit and a part of beta-subunit) may exist in the plasma of diabetic patients. We identified soluble hIR ectodomain in human plasma by a two-step purification followed by immunoblotting and gel-filtration chromatography. Furthermore, we established an hIRalpha-specific enzyme-linked immunosorbent assay and measured the plasma IRalpha levels in patients with diabetes. We also investigated this phenomenon in streptozotocin-induced diabetic hIR transgenic mice. Soluble hIRalpha, but not intact hIRbeta or whole hIR, exists in human plasma. The plasma IRalpha levels were significantly higher in type 1 (2.00 +/- 0.60 ng/ml; n = 53) and type 2 (2.26 +/- 0.80; n = 473) diabetic patients than in control subjects (1.59 +/- 0.40 ng/ml; n = 123 (P < 0.001 vs. control). Plasma IRalpha level was positively correlated with blood glucose level, and 10-20% of the insulin in plasma bound to hIRalpha. In the in vivo experiments using diabetic hIR transgenic mice, hyperglycemia was confirmed to increase the plasma hIRalpha level and the half-life estimated to be approximately 6 h. We propose that the increased soluble IR ectodomain level appears to be a more rapid glycemic marker than A1C or glycoalbumin. (Keyword) Animals / Diabetes Mellitus / Diabetes Mellitus, Experimental / Diabetes Mellitus, Type 1 / Diabetes Mellitus, Type 2 / Enzyme-Linked Immunosorbent Assay / Humans / Mice / Mice, Transgenic / Receptor, Insulin / Solubility / Streptozocin (Link to Publication Site) ● Publication site (DOI): 10.2337/db07-0394 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17563065 ● Search Scopus @ Elsevier (PMID): 17563065 ● Search Scopus @ Elsevier (DOI): 10.2337/db07-0394 (DOI: 10.2337/db07-0394, PubMed: 17563065)
19.	Kazuhiro Kishi, Kazuaki Mawatari, K Sakai-Wakamatsu, Tomoyuki Yuasa, M Wang, M Ogura-Sawa, Yutaka Nakaya, S Hatakeyama and Yousuke Ebina : APS-mediated Ubiquitination of the Insulin Receptor Enhances its Internalization but does not Induce its Degradation., Endocrine Journal, Vol.54, No.1, 77-88, 2007. (Summary) APS, a tyrosine kinase adaptor protein with pleckstrin homology and Src homology 2 domains, is rapidly and strongly tyrosine-phosphorylated by insulin receptor kinase upon insulin stimulation. We have previously shown that APS knockout mice have increased insulin sensitivity, and that this enhancement is possibly due to increased insulin-response on adipose tissues. However, the function of APS in insulin signaling has so far been controversial. Here, we report that APS enhanced ligand-dependent multi-ubiquitination of the insulin receptor (IR) in CHO cells overexpressing the IR. APS-mediated ubiquitination of the IR induced enhancement of the IR internalization, but did not affect the IR degradation. This finding shows one of the pleiotropic functions of APS in insulin signaling. (Keyword) Adaptor Proteins, Signal Transducing / Animals / CHO Cells / Cricetinae / Cricetulus / Humans / Insulin / Mice / Protein Processing, Post-Translational / Protein Transport / Receptor, Insulin / Signal Transduction / Transfection / Ubiquitin (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.K06-056 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17102568 ● Search Scopus @ Elsevier (PMID): 17102568 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.K06-056 (DOI: 10.1507/endocrj.K06-056, PubMed: 17102568)
20.	Tomoyuki Yuasa, Rei Kakuhata, Kazuhiro Kishi, Toshiyuki Obata, Yasuo Shinohara, Yoshimi Bando, Keisuke Izumi, Fumiko Kajiura, Mitsuru Matsumoto and Yousuke Ebina : Platelet-derived growth factor stimulates glucose transport in skeletal muscles of transgenic mice specifically expressing PDGF receptor in the muscle, but does not affect blood glucose levels, Diabetes, Vol.53, No.11, 2776-2786, 2004. (Summary) Insulin stimulates the disposal of blood glucose into skeletal muscle and adipose tissues by the translocation of GLUT4 from intracellular pools to the plasma membrane, and consequently the concentration of blood glucose levels decreases rapidly in vivo. Phosphatidylinositol (PI) 3-kinase and Akt play a pivotal role in the stimulation of glucose transport by insulin, but detailed mechanisms are unknown. We and others reported that not only insulin but also platelet-derived growth factor (PDGF) and epidermal growth factor facilitate glucose uptake through GLUT4 translocation by activation of PI 3-kinase and Akt in cultured cells. However, opposite results were also reported. We generated transgenic mice that specifically express the PDGF receptor in skeletal muscle. In these mice, PDGF stimulated glucose transport into skeletal muscle in vitro and in vivo. Thus, PDGF apparently shares with insulin some of the signaling molecules needed for the stimulation of glucose transport. The degree of glucose uptake in vivo reached approximately 60% of that by insulin injection in skeletal muscle, but blood glucose levels were not decreased by PDGF in these mice. Therefore, PDGF-induced disposal of blood glucose into skeletal muscle is insufficient for rapid decrease of blood glucose levels. (Keyword) Animals / Biological Transport / Blood Glucose / Glucose / Heart / Insulin / Mice / Mice, Transgenic / Muscle, Skeletal / Platelet-Derived Growth Factor / Receptor, Platelet-Derived Growth Factor beta / Recombinant Proteins / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.2337/diabetes.53.11.2776 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15504957 ● Search Scopus @ Elsevier (PMID): 15504957 ● Search Scopus @ Elsevier (DOI): 10.2337/diabetes.53.11.2776 (DOI: 10.2337/diabetes.53.11.2776, PubMed: 15504957)
21.	Yoshiko Kanezaki, Toshiyuki Obata, Rie Matsushima, Asako Minami, Tomoyuki Yuasa, Kazuhiro Kishi, Yoshimi Bando, Hisanori Uehara, Keisuke Izumi, Tasuku Mitani, Mitsuru Matsumoto, Yukari Takeshita, Yutaka Nakaya, Toshio Matsumoto and Yousuke Ebina : KATP Channel Knockout Mice Crossbred with Transgenic Mice Expressing a Dominant-Negative Form of Human Insulin Receptor have Glucose Intolerance but not Diabetes, Endocrine Journal, Vol.51, No.2, 133-144, 2004. (Summary) Impaired insulin secretion and insulin resistance are thought to be two major causes of type 2 diabetes mellitus. There are two kinds of diabetic model mice: one is a K(ATP) channel knockout (Kir6.2KO) mouse which is defective in glucose-induced insulin secretion, and the other is a transgenic mouse expressing the tyrosine kinase-deficient (dominant-negative form of) human insulin receptor (hIR(KM)TG), and which has insulin resistance in muscle and fat. However, all of these mice have no evidence of overt diabetes. To determine if the double mutant Kir6.2KO/hIR(KM)TG mice would have diabetes, we generated mutant mice by crossbreeding, which would show both impaired glucose-induced insulin secretion and insulin resistance in muscle and fat. We report here that: 1) blood glucose levels of randomly fed and 6 h fasted double mutant (Kir6.2KO/hIR(KM)TG) mice were comparable with those of wild type mice; 2) in intraperitoneal glucose tolerance test (ipGTT), Kir6.2KO/hIR(KM)TG mice had an impaired glucose tolerance; and 3) during ipGTT, insulin secretion was not induced in either Kir6.2KO/hIR(KM)TG or Kir6.2KO mice, while the hIR(KM)TG mice showed a more prolonged insulin secretion than did wild type mice; 4) hyperinsulinemic euglycemic clamp test revealed that Kir6.2KO, Kir6.2KO/hIR(KM)TG and hIR(KM)TG mice, showed decreased whole-body glucose disposal compared with wild type mice; 5) Kir6.2KO, but not Kir6.2KO/hIR(KM)TG mice had some obesity and hyperleptinemia compared with wild type mice. Thus, the defects in glucose-induced insulin secretion (Kir6.2KO) and an insulin resistance in muscle and fat (hIR(KM)TG) were not sufficient to lead to overt diabetes. (Keyword) Adipose Tissue / Animals / Blood Glucose / Enzyme Activation / Epididymis / Fasting / Genes, Dominant / Genotype / Glucose / Glucose Clamp Technique / Glucose Intolerance / Glucose Tolerance Test / Humans / Insulin / Leptin / Liver / Male / Mice / Mice, Knockout / Mice, Transgenic / Organ Size / Postprandial Period / Potassium Channels, Inwardly Rectifying / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Receptor, Insulin (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.51.133 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15118262 ● Search Scopus @ Elsevier (PMID): 15118262 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.51.133 (DOI: 10.1507/endocrj.51.133, PubMed: 15118262)
22.	Kazuhiro Kishi, Tomoyuki Yuasa, Asako Minami, Mizuki Yamada, Akifumi Hagi, Hideki Hayashi, Bruce E. Kemp, Lee A. Witters and Yousuke Ebina : AMP-Activated protein kinase is activated by the stimulations of G(q)-coupled receptors., Biochemical and Biophysical Research Communications, Vol.276, No.1, 16-22, 2000. (Summary) The AMP-activated protein kinase (AMPK) functions as a metabolic sensor that monitors cellular AMP and ATP levels. Platelet-activating factor (PAF) activates endogeneous AMPKalpha1 in Chinese hamster ovary cells expressing the PAF receptor coupled with both G(i) and G(q), but its activity was not inhibited after treatment with islet-activating protein. Norepinephrine and bradykinin also activated AMPKalpha1 in cells expressing the G(q)-coupled alpha(1b)-adrenergic receptor and bradykinin receptor, respectively. Stimulations of the G(i)-coupled alpha(2A)-adrenergic receptor, fMet-Leu-Phe receptor, prostaglandin EP3alpha receptor, and G(s)-coupled beta(2)-adrenergic receptor did not activate AMPKalpha1. AMPKalpha1 thus is activated specifically by stimulation of G(q)-coupled receptors. G(q)-coupled receptors transmit the signal for GLUT4 translocation and glucose uptake through an insulin-independent pathway. However, direct activation of AMPKalpha1 with treatment of 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside did not trigger GLUT4 translocation nor stimulate glucose uptake in our cells. Thus, activation of AMPKalpha1 via G(q) is not sufficient to trigger GLUT4 translocation or stimulate glucose uptake. (Keyword) AMP-Activated Protein Kinases / Animals / Biological Transport / CHO Cells / Cricetinae / Enzyme Activation / GTP-Binding Protein alpha Subunits, Gq-G11 / Glucose / Glucose Transporter Type 4 / Heterotrimeric GTP-Binding Proteins / Monosaccharide Transport Proteins / Multienzyme Complexes / Muscle Proteins / Protein-Serine-Threonine Kinases / Receptors, Adrenergic, alpha-1 / Receptors, Bradykinin / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1006/bbrc.2000.3417 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11006075 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034675354 (DOI: 10.1006/bbrc.2000.3417, PubMed: 11006075, Elsevier: Scopus)
23.	Satoshi Noda, Kazuhiro Kishi, Tomoyuki Yuasa, Hideki Hayashi, Tetuso Ohnishi, Ikuko Miyata, Hiromu Nishitani and Yousuke Ebina : Overexpression of wild-type Akt1 promoted insulin-stimulated p70S6 kinase (p70S6K) activity and affected GSK3 beta regulation, but did not promote insulin-stimulated GLUT4 translocation or glucose transport in L6 myotubes., The Journal of Medical Investigation : JMI, Vol.47, No.1-2, 47-55, 2000. (Summary) We have developed a simple, direct and sensitive method to detect GLUT4 on the cell surface. Using this system, we found that PI3-kinase plays a key role in the signaling pathway of insulin-stimulated GLUT4 translocation. One of the down stream effectors of PI3-kinase is serine-threonine kinase Akt (protein kinase B, RAK-PK), but the involvement of Akt in insulin-stimulated GLUT4 translocation is controversial. To investigate whether Akt1 regulates insulin-stimulated GLUT4 translocation and glucose uptake in L6 myotubes, we established L6 myotubes stably expressing c-myc epitope-tagged GLUT4 (GLUT4myc) and mouse wild type (WT) Akt1. We found that overexpression of WT Akt1 promoted insulin-stimulated p70S6 kinase (p70S6K) activity and increased the basal activity of GSK3 beta, but did not promote insulin-stimulated GLUT4 translocation or glucose uptake. These data supported the result that Akt is not a main signaling molecule to transmit the signal of insulin-stimulated GLUT4 translocation or glucose uptake from insulin-activated PI3-kinase. (Keyword) Amino Acid Sequence / Animals / Biological Transport / Calcium-Calmodulin-Dependent Protein Kinases / Cell Line / Glucose / Glucose Transporter Type 4 / Glycogen Synthase Kinase 3 / Insulin / Mice / Molecular Sequence Data / Monosaccharide Transport Proteins / Muscle Proteins / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Rats / Recombinant Fusion Proteins / Ribosomal Protein S6 Kinases (Tokushima University Institutional Repository) ● Metadata: 25669 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10740979 ● Search Scopus @ Elsevier (PMID): 10740979 (Tokushima University Institutional Repository: 25669, PubMed: 10740979)

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.	Seijiro Tsuji, Kensuke Mori, Yosuke Kaneko, Saki Kawata, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : Association between serum dehydroepiandrosterone sulfate levels and annual eGFR changes in people with type 2 diabetes, IDF-WPR Congress 2023/15th Scientific Meeting of AASD, 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.	Ken-ichi Aihara, Yamagami Hiroki, Yasui Saya, Hosoki Minae, Hori Taiki, Shingen Nakamura, Toshiki Otoda and Tomoyuki Yuasa : Clinical Significance of Dehydroepiandrosterone Sulfate in Carotid Atherosclerosis and Nonalcoholic Fatty Liver Disease, ESMED Congress 2021, Nov. 2021.
10.	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.
11.	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.
12.	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
13.	Ken-ichi Aihara, Uemoto Ryoko, Ishikawa Kazue, Kana Morimoto, Kiyoe Kurahashi, Sumiko Yoshida, Tomoyuki Yuasa and Masahiro Abe : Heparin cofactor II, a serine protease inhibitor, is associated with albuminuria in humans and mice., International Conference on Diabetes and Its Complications 2017, Baltimore, Nov. 2017. (Keyword) heparin cofactor II / albuminuria
14.	Kana Morimoto, Takahashi Yuka, Yamashita Saori, Kazue Ishikawa, Uemoto Ryoko, Sumiko Yoshida, Tomoyuki Yuasa and Ken-ichi Aihara : Evaluation of Endothelial Function-associated Clinical Parameters and Whole Blood PCR Array Analysis in Patients with Lifestyle-related Diseases, 19th International Vascular Biology Meeting. Boston. USA, Nov. 2016.
15.	TAKATA YASUNORI, KAWAMURA RYOICHI, ONUMA HIROSI, Tomoyuki Yuasa and OSAWA HARUHIKO : Circulating Soluble Insulin Receptor Is Associated with Cardiac Dysfunction in Type 2 Diabetic Subjects, American Diabetes Association 74th scientific sessions, SAN FRANCISCO,CA, Jun. 2014. (Keyword) soluble insulin receptor
16.	Tomoyuki Yuasa, Hisao Nagaya, Seiichi Hashida, Umehara Asako, Ichiro Yokota, Toshiyuki Obata and Yousuke Ebina : Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes., XI INTERNATIONAL SYMPOSIUM ON INSULIN RECEPTORS AND INSULIN ACTION, Naples, Oct. 2010.

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.	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.
3.	三宅南帆, 辻誠士郎, 河田沙紀, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者の推定食塩摂取量と糖尿病性腎臓病指標の連関解析, 第67回日本糖尿病学会年次学術集会, May 2024.
4.	MIYATAKA Kosuke, KANEKO Yohsuke, Yuki Yamaguchi, Tomoyo Hara, Sumiko Yoshida, 辻誠士郎, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者におけるRed blood cell Distribution Width (RDW)と糖尿病性腎臓病バイオマーカーとの関連解析, 第67回日本糖尿病学会年次学術集会, May 2024.
5.	KANEKO Yohsuke, Kensuke Mori, Minae Hosoki, HORI Taiki, 辻誠士郎, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura and Ken-ichi Aihara : 2型糖尿病患者の年間HbA1c変動と肝線維化指標の連関解析, 第67回日本糖尿病学会年次学術集会, May 2024.
6.	辻誠士郎, 河田沙紀, KANEKO Yohsuke, Kensuke Mori, Minae Hosoki, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者におけるdehydroepiandrosterone sulfate(DHEAS)と尿中アルブミン，尿中L型脂肪酸結合蛋白(L-FABP)との関連, 第67回日本糖尿病学会年次学術集会, May 2024.
7.	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.
8.	金子遥祐, 河田沙紀, 森建介, 細木美苗, 堀太貴, 辻誠士郎, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura and Ken-ichi Aihara : 赤血球のmean corpuscular volumeと代謝異常関連脂肪肝疾患の連関解析, Folia endocrinologica Japonica, Vol.100, No.1, 339, May 2024.
9.	Ken-ichi Aihara, 三宅南帆, 辻誠士郎, 河田沙紀, Shingen Nakamura, Toshiki Otoda and Tomoyuki Yuasa : 2型糖尿病患者の糖尿病性腎臓病における推定食塩摂取量の意義, Folia endocrinologica Japonica, Vol.100, No.1, 348, May 2024.
10.	辻誠士郎, 河田沙紀, 村井純平, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura, 滝下誠 and Ken-ichi Aihara : 2型糖尿病患者における年間腎機能変化とdehydroepiandrosterone sulfate(DHEAS)の連関解析, 第121回日本内科学会総会・講演会, Apr. 2024.
11.	KANEKO Yohsuke, Kensuke Mori, HORI Taiki, Minae Hosoki, 辻誠士郎, 河田沙紀, Toshiki Otoda, Tomoyuki Yuasa, Shingen Nakamura and Ken-ichi Aihara : 代謝異常関連脂肪肝疾患におけるmean corpuscular volumeの意義, 第121回日本内科学会総会・講演会, Apr. 2024.
12.	三宅南帆, 辻誠士郎, 河田沙紀, Ken-ichi Aihara, Shingen Nakamura, Toshiki Otoda and Tomoyuki Yuasa : 2型糖尿病患者における推定塩分摂取量に関わる臨床因子の探索, Shikoku Acta Medica, Vol.79, No.5-6, 283-284, Mar. 2024.
13.	三宅南帆, 辻誠士郎, 河田沙紀, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者の推定塩分摂取量に関わる臨床因子解析, 日本糖尿病学会中国四国地方会第61回総会, Oct. 2023.
14.	辻誠士郎, 河田沙紀, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 当院糖尿病患者における高血圧治療の現況, 日本糖尿病学会中国四国地方会第61回総会, Oct. 2023.
15.	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.
16.	堀太貴, 金子遥祐, 細木美苗, 森建介, 村井純平, Toshiki Otoda, Tomoyuki Yuasa, Ken-ichi Aihara, 滝下誠 and Shingen Nakamura : 生活習慣病患者におけるヘモグロビン値と関連因子の検討, 日本血液学会学術集会, 689, Oct. 2023. (Keyword) Hemoglobins 生活習慣病(診断,予後) ヒト中年(45∼64) 高齢者(65∼79) 男女
17.	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.
18.	Kensuke Mori, Yohsuke Kaneko, 辻誠士郎, 河田沙紀, 三宅南帆, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2 型糖尿病患者の年間収縮期血圧変動に関連する臨床因子の解析, 第45回日本高血圧学会総会, Sep. 2023.
19.	三宅南帆, 辻誠士郎, 河田沙紀, Tomoyo Hara, Hiroki Yamagami, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2 型糖尿病患者における推定塩分摂取量に関連する臨床因子の検討, 第45回日本高血圧学会総会, Sep. 2023.
20.	三宅南帆, 辻誠士郎, 河田沙紀, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者における推定塩分摂取量に関わる臨床因子の探索, 第267回徳島医学会, Aug. 2023.
21.	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.
22.	河田沙紀, Yohsuke Kaneko, Kensuke Mori, 辻誠士郎, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 運動習慣及び体組成が2型糖尿病患者受診時HbA1cに及ぼす影響の解析, 第96回日本内分泌学会学術総会, Jun. 2023.
23.	Kensuke Mori, Yohsuke Kaneko, 辻誠士郎, 河田沙紀, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者における糖尿病治療薬の年間収縮期血圧変動への影響, 第96回日本内分泌学会学術集会, Jun. 2023.
24.	辻誠士郎, Kensuke Mori, Yohsuke Kaneko, 河田沙紀, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者における年間腎機能変化とdehydroepiandrosterone sulfate(DHEAS)の連関解析, 第96回日本内分泌学会学術総会, Jun. 2023.
25.	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.
26.	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.
27.	Kensuke Mori, 河田沙紀, Yohsuke Kaneko, 辻誠士郎, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者の年間収縮期血圧変動における糖尿病治療薬の影響, 第66回日本糖尿病学会年次学術集会, May 2023.
28.	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.
29.	Yohsuke Kaneko, 河田沙紀, Kensuke Mori, 辻誠士郎, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者の年間HbA1c変動における糖尿病治療薬の影響, 第66回日本糖尿病学会年次学術集会, May 2023.
30.	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.
31.	辻誠士郎, Kensuke Mori, Yohsuke Kaneko, 河田沙紀, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者のeGFR slopeにおけるdehydroepiandrosterone sulfate(DHEAS)の意義, 第66回日本糖尿病学会年次学術集会, May 2023.
32.	河田沙紀, Yohsuke Kaneko, Kensuke Mori, 辻誠士郎, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 2型糖尿病患者の受診時HbA1cにおける運動習慣及び体組成の影響, 第66回日本糖尿病学会年次学術集会, May 2023.
33.	Yohsuke Kaneko, 河田沙紀, Kensuke Mori, 辻誠士郎, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, 井上善雄 and Ken-ichi Aihara : 多発腹腔内リンパ節腫脹を契機に診断に至ったPSA正常進行前立腺癌の一例, 第266回徳島医学会学術集会, Feb. 2023.
34.	Kensuke Mori, 河田沙紀, Yohsuke Kaneko, Akihiro Tani, 辻誠士郎, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 高齢2型糖尿病患者におけるGNRIスコアと骨格筋異常病態の検討, 第266回徳島医学会学術集会, Feb. 2023.
35.	河田沙紀, Yohsuke Kaneko, Kensuke Mori, Akihiro Tani, 辻誠士郎, Tomoyuki Yuasa, Toshiki Otoda, Shingen Nakamura, Naoki Toda and Ken-ichi Aihara : 集学的治療にて救命し得た未治療糖尿病合併咽後膿瘍の1例, 第266回徳島医学会学術集会, Feb. 2023.
36.	森建介, 河田沙紀, 金子遥祐, 谷彰浩, 辻誠士郎, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 2型糖尿病患者の骨格筋異常におけるGNRIスコアの意義, 日本糖尿病学会中国四国地方会第60回総会, Nov. 2022.
37.	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.
38.	河田沙紀, 金子遥祐, 森建介, 谷彰浩, 辻誠士郎, Tomoyuki Yuasa, Toshiki Otoda, Naoki Toda and Ken-ichi Aihara : 咽後膿瘍を発症した未治療糖尿病の1例, 日本糖尿病学会中国四国地方会第60回総会, Nov. 2022.
39.	Yohsuke Kaneko, 河田沙紀, Kensuke Mori, 辻誠士郎, Tomoyuki Yuasa, Toshiki Otoda, 井上善雄 and Ken-ichi Aihara : 多発肺転移・腹腔内リンパ節腫脹を契機に診断に至ったPSA陰性の進行前立腺癌の一例, 日本内分泌学会第22回四国支部学術集会, Sep. 2022.
40.	細木美苗, Hiroki Yamagami, 安井沙耶, HORI Taiki, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 当院10年間における死亡患者の年齢・死因および併存合併症における糖尿病と治療薬剤の影響, 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.
41.	米田健一, 金子遥祐, 河田沙紀, 森建介, 谷彰浩, 辻誠士郎, Tomoyuki Yuasa, Toshiki Otoda, Shingen Nakamura and Ken-ichi Aihara : SGLT2阻害薬内服中のシックデイ対応困難が契機となり，糖尿病性ケトアシドーシスを認めた認知症高齢2型糖尿病の1例, 第265回徳島医学会学術集会, Jul. 2022.
42.	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.
43.	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.
44.	Toshiki Otoda, Tomoyuki Yuasa, 関根明子, 上元良子, Hiroyasu Mori, Tomoyo Hara, Motoyuki Tamaki, Toshiaki Tamaki, Munehide Matsuhisa and Ken-ichi Aihara : SGLT2 阻害薬投与による蛋白尿減少および炎症抑制効果の検討, 第 65 回日本糖尿病学会年次学術集会, May 2022.
45.	山上紘規, 細木美苗, HORI Taiki, 安井沙耶, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : Skin Autofluorescenceの糖尿病性腎臓病における臨床的意義の解析, 第65回日本糖尿病学会年次学術集会, May 2022.
46.	細木美苗, 山上紘規, 安井沙耶, HORI Taiki, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 当院10年間における死亡患者の年齢・死因および併存合併症における糖尿病と治療薬剤の影響, 第65回日本糖尿病学会年次学術集会, May 2022.
47.	Toshiki Otoda, Tomoyuki Yuasa, 関根明子, 上元良子, Hiroyasu Mori, Tomoyo Hara, Motoyuki Tamaki, Toshiaki Tamaki, Munehide Matsuhisa and Ken-ichi Aihara : SGLT2阻害薬投与による蛋白尿減少および炎症抑制効果の検討, 第65回日本糖尿病学会年次学術集会, May 2022.
48.	Toshiki Otoda, Tomoyuki Yuasa, 関根明子, 上元良子, Hiroyasu Mori, Motoyuki Tamaki, Toshiaki Tamaki, Munehide Matsuhisa and Ken-ichi Aihara : SGLT2阻害薬の投与が蛋白尿減少効果をもたらす要因の検討, 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.
49.	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.
50.	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
51.	細木美苗, 山上紘規, 安井沙耶, HORI Taiki, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 当院死亡患者の年齢・死因および併存合併症における糖尿病の影響, 第59回日本糖尿病学会中国四国地方会, Oct. 2021.
52.	細木美苗, 山上紘規, 安井沙耶, HORI Taiki, Shingen Nakamura, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 糖尿病の有無からみた当院死亡患者の年齢・死因および併存合併症に関する検討, 第21回日本内分泌学会四国支部学術集会, Sep. 2021.
53.	Yohsuke Kaneko, Saya Yasui, Hiroki Yamagami, Taiki Hori, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 糖尿病患者における歩行速度規定臨床因子の解析, 第64回日本糖尿病学会年次学術集会, May 2021.
54.	Ken-ichi Aihara, Taiki Hori, Hiroki Yamagami, Saya Yasui, Yohsuke Kaneko, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Masahiro Abe : 生体電気インピーダンス法による細胞外水分比および位相角と糖尿病患者における血中HbおよびHtレベルの連関解析, 第64回日本糖尿病学会年次学術集会, May 2021.
55.	Hiroki Yamagami, Saya Yasui, Yohsuke Kaneko, Taiki Hori, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 糖尿病患者におけるDehydroepiandrosterone sulfate (DHEAS)の糖尿病性腎臓病進展および高血圧症罹患における意義, 第64回日本糖尿病学会年次学術集会, May 2021.
56.	Saya Yasui, Hiroki Yamagami, Yohsuke Kaneko, Taiki Hori, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 糖尿病患者における非アルコール性脂肪肝疾患および骨格筋異常症におけるDehydroepiandrosterone sulfate (DHEAS)の意義, 第64回日本糖尿病学会年次学術集会, May 2021.
57.	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.
58.	金子遥祐, Tomoyuki Yuasa, Takeshi Soeki, Toshiki Otoda, Tatsuya Taniguchi, Ken-ichi Aihara, 安井沙耶, 堀太貴, 山上紘規 and Shingen Nakamura : 糖尿病患者における歩行速度規定臨床因子の解析, Journal of the The Japan Diabetes Society, Vol.64, No.Suppl.1, III-133-4, May 2021.
59.	山上紘規, 安井沙耶, 金子遥祐, 堀太貴, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 糖尿病患者におけるDehydroepiandrosterone sulfate(DHEAS)の糖尿病性腎臓病進展および高血圧症罹患における意義, Journal of the The Japan Diabetes Society, Vol.64, No.Suppl.1, P-35-6, May 2021.
60.	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.
61.	Taiki Hori, Hiroki Yamagami, Saya Yasui, Yohsuke Kaneko, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki, Masahiro Abe and Ken-ichi Aihara : 生体電気インピーダンス法による細胞外水分比および位相角は糖尿病患者の血中HbおよびHtレベルを規定する, 第94回日本内分泌学会学術総会, Apr. 2021.
62.	Hiroki Yamagami, Saya Yasui, Yohsuke Kaneko, Taiki Hori, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : Dehydroepiandrosterone sulfate (DHEAS)高値は糖尿病性腎臓病進展および高血圧症罹患のリスクとなる, 第94回日本内分泌学会学術総会, Apr. 2021.
63.	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.
64.	Yohsuke Kaneko, Saya Yasui, Hiroki Yamagami, Taiki Hori, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 生活習慣病患者の歩行速度は骨格筋量よりも筋力が規定する, 第94回日本内分泌学会学術総会, Apr. 2021.
65.	金子遥祐, 安井沙耶, 山上紘規, 堀太貴, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 生活習慣病患者の歩行速度は骨格筋量よりも筋力が規定する, Folia endocrinologica Japonica, Vol.97, No.1, 366, Apr. 2021. (Keyword) 筋骨格系生理学的現象骨格筋身体組成筋力生活習慣病(診断) 歩行速度 *筋量ヒト男女
66.	山上紘規, 金子遥祐, 安井沙耶, 堀太貴, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : Dehydroepiandrosterone sulfate(DHEAS)高値は糖尿病性腎臓病進展および高血圧症罹患のリスクとなる, Folia endocrinologica Japonica, Vol.97, No.1, 340, Apr. 2021. (Keyword) 高血圧(病因,診断) 糖尿病性腎症(病因,診断) *Dehydroepiandrosterone Sulfate(血液) ヒト男女
67.	安井沙耶, 山上紘規, 金子遥祐, 堀太貴, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : Dehydroepiandrosterone sulfate(DHEAS)は生活習慣病患者における非アルコール性脂肪肝疾患およびダイナペニアの発症抑制因子である, Folia endocrinologica Japonica, Vol.97, No.1, 287, Apr. 2021. (Keyword) Dehydroepiandrosterone Sulfate(血液) 生活習慣病(診断,病因,合併症) *肝疾患-非アルコール性脂肪性(診断,病因,合併症) ヒト男女
68.	安井沙耶, 山上紘規, 金子遥祐, 堀太貴, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 当院生活習慣病患者における骨格筋量に影響を与える因子の検討, Folia endocrinologica Japonica, Vol.96, No.3, 822, Jan. 2021. (Keyword) 筋骨格系生理学的現象 / 骨格筋 / 身体組成 / 生活習慣病(診断) / 筋量 / ヒト / 中年(45~64) / 高齢者(65~79) / 男 / 女
69.	山上紘規, 安井沙耶, 金子遥祐, 堀太貴, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 当院生活習慣病患者における握力と歩行速度に影響を与える因子の検討, Folia endocrinologica Japonica, Vol.96, No.3, 822, Jan. 2021. (Keyword) 加齢 / 握力 / 生活習慣病(診断) / 歩行速度 / 中年(45~64) / 高齢者(65~79) / 男 / 女
70.	Yohsuke Kaneko, Saya Yasui, Taiki Hori, Hiroki Yamagami, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : インスリングラルギンU300とデュラグルチドの併用からインスリンデグルデク・リラグルチド配合製剤への変更後に著明な血糖コントロールの改善を見た1例, 第20回日本内分泌学会四国支部学術集会, Sep. 2020.
71.	Hiroki Yamagami, Saya Yasui, Yohsuke Kaneko, Taiki Hori, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 当院生活習慣病患者における握力と歩行速度に影響を与える因子の検討, 第20回日本内分泌学会四国支部学術集会, Sep. 2020.
72.	Saya Yasui, Hiroki Yamagami, Yohsuke Kaneko, Taiki Hori, Shingen Nakamura, Tatsuya Taniguchi, Toshiki Otoda, Tomoyuki Yuasa, Takeshi Soeki and Ken-ichi Aihara : 当院生活習慣病患者における骨格筋量に影響を与える因子の検討, 第20回日本内分泌学会四国支部学術集会, Sep. 2020.
73.	Tomoyo Hara, 坂根容子, 仁木裕子, 中野美恵子, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 糖尿病性腎症重症化予防外来受診患者の1年後腎機能評価, 第117回日本内科学会総会, Aug. 2020.
74.	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.
75.	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
76.	Tomoyo Hara, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : エンパグリフロジンの糖尿病性腎臓病に対する効果の検討, 第93回日本内分泌学会学術総会, Jun. 2020.
77.	Toshiki Otoda, 上元良子, 関根明子, Tomoyuki Yuasa and Ken-ichi Aihara : 血清suPAR値の糖尿病性腎臓病進展予測マーカーとしての有用性, 第62回日本糖尿病学会年次学術集会, May 2020.
78.	Tomoyo Hara, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : SGLT2阻害薬の糖尿病性腎臓病に対する効果の検討, 第63回日本糖尿病学会年次学術集会, May 2020.
79.	Tomoyo Hara, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 減塩指導中の糖尿病患者におけるeGFR年間変化量の因子解析, 日本糖尿病学中国四国地方会第57回総会, Dec. 2019.
80.	Tomoyuki Yuasa, 鶴尾美穂, 岸潤, Akio Kuroda, 寺澤敏秀 and Munehide Matsuhisa : ANCA関連血管炎にステロイドを投与し血糖コントロールが改善した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.
81.	毛利咲恵, 鶴尾美穂, 坂東佐知子, 添木武, 松本直也, Tomoyuki Yuasa, Akio Kuroda, Masataka Sata, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 発熱，高血糖，低K血症を契機に一時的にBrugada型心電図を呈した糖尿病の1例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
82.	奥村慈子, 鶴尾美穂, Tomoyuki Yuasa, 瀬尾浩二, 木内美瑞穂, 金川泰彦, Akio Kuroda, 松本俊夫, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 急激にせん妄状態が悪化した高齢2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.
83.	上野裕子, 鶴尾美穂, Tomoyuki Yuasa, Akio Kuroda, 木内美瑞穂, 西正晴, Saya Yasui, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 高齢者糖尿病患者に対するLCDEと徳島市糖尿病サポーター(TCDS)の連携した取り組み, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
84.	Tomoyo Hara, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : SPIDDM様の経過をたどったIA-2抗体単独陽性の中年発症1型糖尿病の1例, 第57回日本糖尿病学会中四国地方会, Dec. 2019.
85.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 木内美瑞穂, 安井沙耶, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : TIR(Time-In-Range)とHbA1cとの関連∼HbA1cと組み合わせる血糖管理方法∼, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
86.	森岡隆子, Akio Kuroda, 鶴尾美穂, 堀筋冨士子, 秋田賢子, 松本幸恵, Tomoyuki Yuasa, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 予測低血糖自動注入停止型インスリンポンプが有効だった高齢1型糖尿病例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
87.	斎村玉緒, Akio Kuroda, 鶴尾美穂, 福井健壮, 掘貫理恵, 藤原敏孝, Tomoyuki Yuasa, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : 脳悪性リンパ腫を発症した2がた糖尿病の1例, 日本糖尿病学会中国四国地方会第57回総会, Dec. 2019.
88.	Tomoyo Hara, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 原発性アルドステロン症患者に対するエプレレノン投与後血管機能の年間変化, 第42回日本高血圧学会総会, Oct. 2019.
89.	Tomoyo Hara, Toshiki Otoda, Tomoyuki Yuasa, Sumiko Yoshida and Ken-ichi Aihara : 生活習慣病患者における血管内皮機能の増悪群と改善群間における年間臨床指標に関する検討, 第19会日本内分泌学会四国支部学術集会, Sep. 2019.
90.	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.
91.	中野美恵子, 坂根容子, 仁木裕子, 山田多喜子, Tomoyo Hara, Toshiki Otoda, Tomoyuki Yuasa and Ken-ichi Aihara : 当院での糖尿病性腎症重症化予防の取り組み, 2. 第62回日本糖尿病学会年次学術集会, May 2019.
92.	Tomoyuki Yuasa, 安藝菜奈子, Koutaro Kunimi, Miki Satou, 新居真里, 和泉佳彦, Yasunori Takata, Toshiki Otoda, 大澤春彦, Seiichi Hashida and Ken-ichi Aihara : インスリン受容体切断が妊娠期に果たすインスリン作用調節機構の可能性, 第62回日本糖尿病学会年次学術集会, May 2019.
93.	Tomoyo Hara, 上元良子, 関根明子, Toshiki Otoda, Tomoyuki Yuasa, Sumiko Yoshida and Ken-ichi Aihara : 糖尿病性腎症における血漿ヘパリンコファクターⅡ活性の臨床的意義, 第62回日本糖尿病学会年次学術集会, May 2019.
94.	Tomoyo Hara, 上元良子, 関根明子, Toshiki Otoda, Tomoyuki Yuasa, Sumiko Yoshida and Ken-ichi Aihara : 糖尿病性腎症における血漿ヘパリンコファクターII活性の臨床的意義, 第62回日本糖尿病学会年次学術集会, May 2019.
95.	秋田賢子, 鶴尾美穂, 森岡隆子, 堀筋冨士子, 上野裕子, 斎村玉緒, 藤島周子, 奥村慈子, 松本幸恵, 福井健壮, 堀貫理恵, 森久志, 細川智也, 野上貴盛, 森上雄三, 橋本章聖, Tomoyuki Yuasa, Akio Kuroda, 寺澤敏秀 and Munehide Matsuhisa : 糖尿病教育入院時の療養指導カードの使用についてのスタッフの評価, 日本糖尿病学会中国四国地方会第56回総会, Oct. 2018.
96.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, Mizuho Kinouchi, Kimiko Sogabe, 加部一行, 瀬尾浩二, Masaharu Nishi, Naoya Matsumoto, Yasuhiko Kanagawa, Masahiro Abe, Toshio Matsumoto, 寺澤敏秀 and Munehide Matsuhisa : リブレ使用糖尿病患者の検討, 日本糖尿病学会中国四国地方会第56回総会, Oct. 2018.
97.	Toshiki Otoda, 上元良子, 関根明子, Tomoyuki Yuasa and Ken-ichi Aihara : 糖尿病性腎臓病における血清suPAR の臨床的意義に関する検討, 本糖尿病学会中国四国地方会第56回総会, Oct. 2018.
98.	Toshiki Otoda, Motoyuki Tamaki, Yuichi Takashi, Kana Morimoto, Tomoyuki Yuasa, Munehide Matsuhisa, Hiroyuki Azuma and Ken-ichi Aihara : 肥満合併2型糖尿病患者におけるSGLT2阻害薬の短期的臨床効果に関する検討, 第39回日本肥満学会, Oct. 2018.
99.	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.
100.	Toshiki Otoda, Motoyuki Tamaki, Yuichi Takashi, Kana Morimoto, Tomoyuki Yuasa, Munehide Matsuhisa, Hiroyuki Azuma and Ken-ichi Aihara : SGLT2阻害薬の糖代謝および各種代謝指標への短期的効果に関する検討, 第61回日本糖尿病学会年次学術集会, May 2018.
101.	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.
102.	Toshiki Otoda, Kana Morimoto, Tomoyuki Yuasa, Motoyuki Tamaki, Hiroyuki Azuma and Ken-ichi Aihara : SGLT2 阻害薬の短期臨床的効果に関する検討, 日本糖尿病学会中国四国地方会第55回総会, Nov. 2017. (Keyword) diabetes mellitus / therapy
103.	斎村玉緒, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 加部一行, Mizuho Kinouchi, Sumiko Yoshida, Hiroki Yamagami, Takeshi Kondo, 西正晴, 松本直也, Toshio Matsumoto, Masahiro Abe, 寺澤敏秀 and Munehide Matsuhisa : フラッシュグルコースモニタリングシステムにより施設入所可能となった高齢1型糖尿病の一例, 日本糖尿病学会中国四国地方会第55回総会抄録集, Nov. 2017.
104.	鶴尾美穂, Toshio Matsumoto, Akio Kuroda, Tomoyuki Yuasa, 加部一行, Takeshi Kondo, Mizuho Kinouchi, 井野口卓, Hiroki Yamagami, 松本直也, 西正晴, 寺澤敏秀, Masahiro Abe and Munehide Matsuhisa : SLADHを発症した高齢1型糖尿病の一例, 日本糖尿病学会中国四国地方会第55回総会抄録集, Nov. 2017.
105.	Ken-ichi Aihara, Kana Morimoto, 上元良子, 石川カズ江, Toshiki Otoda, Sumiko Yoshida, Tomoyuki Yuasa and Hiroyuki Azuma : 生活習慣病患者における血管内皮機能の1年変化に影響を与える臨床指標の検討, 第50回日本動脈硬化学会総会・学術集会, Jul. 2017.
106.	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.
107.	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.
108.	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.
109.	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.
110.	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.
111.	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.
112.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, Takeshi Kondo, Mizuho Kinouchi, Naoko Matsui, 細井恵美子, Masahiro Abe, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : γグロブリン療養後に一過性のGAD抗体価上昇がみられた糖尿病の一例, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
113.	斎村玉緒, 鶴尾美穂, Akio Kuroda, Takeshi Kondo, Tomoyuki Yuasa, Mizuho Kinouchi, Masahiro Abe, Toshio Matsumoto, 寺澤敏秀 and Munehide Matsuhisa : インスリンポンプの院内検定の試み, 日本糖尿病学会中国四国地方会第54回総会, Nov. 2016.
114.	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.
115.	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.
116.	橋本晶慶, 鶴尾美穂, 秋田賢子, 森岡隆子, Akio Kuroda, Tomoyuki Yuasa, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Masahiro Abe, Munehide Matsuhisa and 寺澤敏秀 : 糖尿病教室のスタッフ間の相互評価による改善効果, 第59回日本糖尿病学会年次学術集会, May 2016.
117.	鶴尾美穂, Akio Kuroda, Takeshi Kondo, Tomoyuki Yuasa, Mizuho Kinouchi, Masahiro Abe, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : Sensor Angmented Pump(SAP)療法が有効であった高齢1型糖尿病の1例, 第53回日本糖尿病学会中国四国地方会, Oct. 2015.
118.	森岡隆子, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT2阻害薬が著効したprader, 第53回日本糖尿病学会中国四国地方会米子コンベンションセンター, Oct. 2015.
119.	後藤廣平, 鶴尾美穂, Akio Kuroda, 伊澤真弓, Mizuho Kinouchi, Takeshi Kondo, Tomoyuki Yuasa, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT2阻害薬の強化インスリン療法への併用効果の検討, 第58回日本糖尿病学会年次学術集会口演, May 2015.
120.	浅井廣平, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 伊澤真弓, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT阻害薬の臨床効果の検討, 日本糖尿病学会中国四国地方会第52回総会, Oct. 2014.
121.	鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 松本直也, Takeshi Kondo, Mizuho Kinouchi, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : SGLT2阻害薬が著効したPrader Willi syndrome 合併糖尿病の1例, 日本糖尿病学会中国四国地方会第52回総会, Oct. 2014.
122.	高田康徳, 秋田拓磨, 長尾優, 川村良一, 大村裕, Tomoyuki Yuasa and 大澤春彦 : -, 第57回日本糖尿病学会年次学術集会, May 2014.
123.	松本幸恵, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 秋田賢子, Mizuho Kinouchi, Takeshi Kondo, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 糖尿病患者の考える指示エネルギー量，指示主食量の調査とその介入, 第57回日本糖尿病学会年次学術集会口演, May 2014.
124.	松本幸恵, 鶴尾美穂, Akio Kuroda, Tomoyuki Yuasa, 秋田賢子, Mizuho Kinouchi, Takeshi Kondo, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 糖尿病患者の考える指示エネルギー量，指示主食量の調査とその介入, 第57回日本糖尿病学会年次学術集会, May 2014.
125.	鶴尾美穂, 白神敦久, Munehide Matsuhisa, 福島泰江, 新谷保実, 小松まち子, 藤中雄一, 天満仁, Akio Kuroda, 安芸菜奈子, 大島康志, 金崎淑子, Tomoyuki Yuasa, 近藤絵里, 阿部多賀子, 加藤修司, 伊藤祐司, 倉橋清衛, 三浦眞司, 野間喜彦, 島健二 and 川島周 : -, 第57回日本糖尿病学会年次学術集会, May 2014.
126.	鶴尾美穂, 白神敦久, 松久宗英, 福島泰江, 新谷保実, 小松まち子, 藤中雄一, 天満仁, 黒田暁生, 安芸菜奈子, 大島康志, 金崎淑子, Tomoyuki Yuasa, 近藤絵里, 阿部多賀子, 加藤修司, 伊藤祐司, 倉橋清衛, 三浦眞司, 野間喜彦, 島健二 and 川島周 : -, 第57回日本糖尿病学会年次学術集会, May 2014.
127.	松本幸恵, Akio Kuroda, 秋田賢子, 鶴尾美穂, Mizuho Kinouchi, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 主食の摂取状況調査, 日本糖尿病学会中国四国地方会第51回総会, Nov. 2013.
128.	藤島周子, 森岡隆子, 高田妙子, 岩谷沙紀, 斎村玉緒, 秋田賢子, 松本幸恵, Takeshi Kondo, Sumiko Yoshida, Tomoyuki Yuasa, 鶴尾美穂, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 当院の参加型糖尿病教室の取り組み, 第56回日本糖尿病学会年次学術集会, May 2013.
129.	伊澤真弓, Akio Kuroda, 上野裕子, 堀筋富士子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : インスリン注入器に関する患者の意識調査, 第56回日本糖尿病学会年次学術集会, May 2013.
130.	鶴尾美穂, Akio Kuroda, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Toshio Matsumoto, Munehide Matsuhisa and 寺澤敏秀 : インスリン治療患者に対するチーム医療で行う段階的糖尿病療養指導の試み, 第56回日本糖尿病学会年次学術集会, May 2013.
131.	Tomoyuki Yuasa, Munehide Matsuhisa, 橋田誠一 and Yousuke Ebina : 可溶性インスリン受容体が担うインスリン抵抗性の可能性, 第56回日本糖尿病学会年次学術集会特別シンポジウム3, May 2013.
132.	奥村滋子, Akio Kuroda, 片田英子, 澤井敏子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 運転中の低血糖についての意識調査, 第56回日本糖尿病学会年次学術集会, May 2013.
133.	伊澤真弓, Akio Kuroda, 上野裕子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : インスリン注入器に関する患者の意識調査, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
134.	奥村滋子, Akio Kuroda, 片田英子, 鶴尾美穂, Sumiko Yoshida, Takeshi Kondo, Tomoyuki Yuasa, 松本直也, 笠松哲司, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : 運転中の低血糖についての意識調査, 日本糖尿病学会中国四国地方会第50回総会, Nov. 2012.
135.	鶴尾美穂, 寺澤敏秀, 木戸里佳, Sumiko Yoshida, Tomoyuki Yuasa, Takeshi Kondo, 笠松哲司, 近藤絵里, Mizuho Kinouchi, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and Masashi Akaike : 粥状動脈硬化病変を呈した高Lp(a)血症合併糖尿病の姉妹例, 第55回日本糖尿病学会年次学術集会, May 2012.
136.	上野裕子, 堀筋富士子, 森岡隆子, 鶴尾美穂, Tomoyuki Yuasa, 木戸里佳, Sumiko Yoshida, Mizuho Kinouchi, Takeshi Kondo, 近藤絵里, 笠松哲司, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : サイトローテーションシート(SLS)を使用したインスリン自己注射の指導, 第55回日本糖尿病学会年次学術集会, May 2012.
137.	秋田賢子, 鶴尾美穂, 木戸里佳, Sumiko Yoshida, 近藤絵里, Mizuho Kinouchi, Takeshi Kondo, 笠松哲司, Tomoyuki Yuasa, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺澤敏秀 : カーボカウントを導入した高齢1型糖尿病の3例, 第55回日本糖尿病学会年次学術集会, May 2012.
138.	Tomoyuki Yuasa : 新規糖尿病関連分子可溶性インスリン受容体の基礎と臨床, 第57回日本臨床検査医学会中国・四国支部総会，第152回日本臨床化学会中国支部例会・総会，第22回日本臨床化学会四国支部例会・総会，第8回合同地方会, Feb. 2012.
139.	Tomoyuki Yuasa, 鶴尾美穂, 藤中雄一, 木戸里佳, Sumiko Yoshida, 木内美瑞穂, 瀬尾浩二, 松久宗英, 松本俊夫 and 寺澤敏秀 : 遺伝性球状赤血球症による続発性ヘモクロマトーシスを起因とする糖尿病の一例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
140.	木戸里佳, 鶴尾美穂, Akio Kuroda, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司, Toshio Matsumoto, Munehide Matsuhisa and 寺沢敏秀 : カーボカウント併用CS11療法が有効であった高齢発症1型糖尿病症例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
141.	堀筋富士子, 森岡隆子, 片田英子, 鶴尾美穂, 木戸里佳, Tomoyuki Yuasa, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺沢敏秀 : サイトローテーションシート(SLS)を使用したインスリン自己注射の指導, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
142.	秋田賢子, 木戸里佳, 鶴尾美穂, Sumiko Yoshida, Mizuho Kinouchi, Tomoyuki Yuasa, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and 寺沢敏秀 : カーボカウントを導入した高齢1型糖尿病の3例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
143.	鶴尾美穂, 寺沢敏秀, 木戸里佳, Tomoyuki Yuasa, Sumiko Yoshida, 笠松哲司, Akio Kuroda, Munehide Matsuhisa, Toshio Matsumoto and Masashi Akaike : 粥状動脈硬化病変を呈した糖尿病合併高Lp(a)血症の姉妹例, 日本糖尿病学会中国四国地方会第49回総会, Nov. 2011.
144.	木戸里佳, Mizuho Kinouchi, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司, Toshio Matsumoto, Munehide Matsuhisa, 鶴尾美穂 and 寺沢敏秀 : カーボカウント併用CSⅡ療法が用効であった高齢発症1型糖尿病の2症例, 第54回日本糖尿病学会年次学術集会, May 2011.
145.	森岡隆子, 上野裕子, 堀筋富士子, 澤井敏子, 藤島周子, 奥村滋子, 伊澤真弓, 片田英子, 秋田賢子, 木戸里佳, Sumiko Yoshida, Mizuho Kinouchi, 笠松哲司, Tomoyuki Yuasa, 鶴尾美穂, 寺沢敏秀, Munehide Matsuhisa and Toshio Matsumoto : インスリン治療を行っている高齢糖尿病患者の療養指導について, 第54回日本糖尿病学会年次学術集会, May 2011.
146.	本島寛之, Tomoyuki Yuasa, 堤厚之, 井形元維, 近藤龍也, 河島淳司, 松村剛, 福永麻希子, 前田貴子, 川崎修二, 花谷聡子, 石井規夫, 下田誠也, Noboru Furukawa, 水流添覚, 西川武志, Yousuke Ebina and 荒木栄一 : 短期血糖コントロール指標としての血中可用性インスリン受容体 -ステロイドによる糖代謝悪化を検出できるのか-, 第54回日本糖尿病学会年次学術集会, Vol.54, No.sup1, S119, May 2011.
147.	木戸里佳, Mizuho Kinouchi, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司, 寺澤敏秀 and 鶴尾美穂 : CSIIとカーボカウントにより良好な血糖コントロールを得られた1型糖尿病症例, 第48回日本糖尿病学会中国四国地方会総会, Oct. 2010.
148.	高田妙子, 岩谷沙紀, 伊澤真, 片田英子, 藤島周子, 澤井敏子, 森岡隆子, 堀筋富士子, 上野裕子, 奥村滋子, 秋田賢子, 小賀野桃子, 木戸里佳, Tomoyuki Yuasa, 笠松哲司, 三原正朋, Sumiko Yoshida, Mizuho Kinouchi, 高木純子, 瀬尾浩二, 鶴尾美穂 and 寺澤敏秀 : 糖尿病教育入院による心理状態の変化について(PAIDを用いた教育入院前後の意識調査), 第53回日本糖尿病学会学術総会, May 2010.
149.	高田浩史, 井上眞理, 池田幸雄, 石橋綾子, 公文義雄, Tomoyuki Yuasa, Yousuke Ebina and 寺田典生 : 2型糖尿病患者における血中インスリン受容体αサブユニット濃度の検討, 第53回日本糖尿病学会年次学術集会, May 2010.
150.	本島寛之, Tomoyuki Yuasa, 西川武志, 下田誠也, 近藤龍也, 河島淳司, 松村剛, 後藤理英子, 大久保美那, 前田貴子, 武田佳代, 山城武司, 川崎修二, 堤厚之, 石井規夫, 久木留大介, Noboru Furukawa, 水流添覚, 宮村信博, Yousuke Ebina and Seiichi Hashida : 短期血糖コントロール指標としての血中可溶性インスリン受容体αサブユニットの有用性, 第53回日本糖尿病学会年次学術集会, May 2010.
151.	秋田賢子, 小賀野桃子, 寺澤敏秀, 木戸里佳, 笠松哲司, 鶴尾美穂 and Tomoyuki Yuasa : 療養指導困難な糖尿病患者に対する栄養指導, 第13回日本病態栄養学会年次学術集会, Jan. 2010.
152.	木戸里佳, Yuichi Fujinaka, 寺澤敏秀, Mizuho Kinouchi, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司, Toshio Matsumoto and 鶴尾美穂 : インスリン治療中に副腎不全および粘液水腫を合併し，意識障害を伴う低血糖を繰り返した一例, 第101回日本内科学会四国地方会, Nov. 2009.
153.	木戸里佳, 三原正朋, 寺澤敏秀, Mizuho Kinouchi, Sumiko Yoshida, Tomoyuki Yuasa, 瀬尾浩二, 笠松哲司 and 鶴尾美穂 : 当院でCSIIを導入した1型糖尿病の4症例についての臨床的検討, 第47回日本糖尿病学会中国四国地方会, Nov. 2009.
154.	本島寛之, 河島淳司, 下田誠也, 前田貴子, 大久保美那, 西川武志, 宮村信博, 荒木栄一, Tomoyuki Yuasa and Yousuke Ebina : 血中インスリン受容体αサブユニットは血糖コントロールを反映する, 第287回日本内科学会九州地方会例会, Nov. 2009.
155.	本島寛之, Tomoyuki Yuasa, 河島淳司, 下田誠也, 前田貴子, 久木留大介, 大久保美那, 榊田光倫, Yousuke Ebina, 西川武志 and 荒木栄一 : 可溶性インスリン受容体αサブユニットは血糖値および血糖指標と相関する, 第47回日本糖尿病学会九州地方会, Oct. 2009.
156.	鶴尾美穂, 寺澤敏秀, 三原正明, Tomoyuki Yuasa, 江尻純子, 笠松哲司, 瀬尾浩二, Mizuho Kinouchi, 工藤美千代, Sumiko Yoshida and Masashi Akaike : 著名な高Lp(a)血症を合併した糖尿病患者における血管障害の検討, 第52回日本糖尿病学会年次学術集会, May 2009.
157.	笠松哲司, 三原正明, 寺澤敏秀, Tomoyuki Yuasa, 江尻淳子, Mizuho Kinouchi, Sumiko Yoshida and 鶴尾美穂 : 糖尿病患者における骨密度の検討, 第52回日本糖尿病学会年次学術集会, May 2009.
158.	Tomoyuki Yuasa, Toshiyuki Obata, Ichiro Yokota, Eiji Okamoto, Yoshiko Kanezaki, Hiroshi Maegawa, Fumiko Hirota, Kazuhiro Kishi, Seiichi Hashida, Hisao Nagaya, Ogura Yuko, Masuda Kazuhiko, Mitsuru Matsumoto, Toshio Matsumoto, Atsunori Kashiwagi and Yousuke Ebina : Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes., International Symposium on Diabetes - Kickoff of Hannover-Tokushima Research Communiation, Mar. 2009.

Et cetera, Workshop:

1.	Tomoyuki Yuasa, Toshiyuki Obata, Ichiro Yokota, 岡本英治, Hisao Nagaya, Seiichi Hashida, 前川聡, Atsunori kasiwagi, Mitsuru Matsumoto, Toshio Matsumoto, Kazuhiro Kishi and Yousuke Ebina : 可溶性インスリン受容体細胞外ドメイン(sIRα)は高血糖に相関して血中濃度が高まる, 第7回 1型糖尿病研究会, Nov. 2009.
2.	Tomoyuki Yuasa, Seiji Yano, Yasuhiko Nishioka, Yoshiaki Kubo, Masayuki Takahashi, Hiroyoshi Nakatsuji, Hisao Nagaya, Hiro-omi Kanayama, Seiji Arase, Saburo Sone and Yousuke Ebina : Soluble insulin receptor ectodomain in the plasma is a possible broad-spectrum tumor marker, 第68回日本癌学会学術総会記事, 450, Oct. 2009.
3.	Tomoyuki Yuasa, Toshiyuki Obata, Seiji Yano, 岡本英治, Yasuhiko Nishioka, Yoshiaki Kubo, Masayuki Takahashi, Hiroyoshi Nakatsuji, Hisao Nagaya, Hiro-omi Kanayama, Seiji Arase, Saburo Sone and Yousuke Ebina : Soluble insulin receptor ectodomain level was elevated in the plasma of cancer patients, 第29回日本分子腫瘍マーカー研究会プログラム, 70-71, Sep. 2009.
4.	本島寛之, 西川武志, Tomoyuki Yuasa, 河島淳司, 後藤理英子, 小野薫, 花谷聡子, 木下博之, 川崎修二, 堤厚之, 児島協, 松村剛, 近藤龍也, 宮村信博, Yousuke Ebina and 荒木栄一 : 血中インスリン受容体αサブユニット量は血糖コントロール指標となりうるか?, 第52回日本糖尿病学会年次学術集会, Vol.52, No.1, S-294, May 2009.
5.	Tomoyuki Yuasa, 鶴尾美穂, 工藤美千代, 三原正朋, 江尻純子, 瀬尾浩二 and 寺澤敏秀 : メトホルミン投与により高乳酸血症とケトーシスを併発した2型糖尿病の一例, 日本糖尿病学会中国四国地方会第46回総会, Nov. 2008.
6.	Tomoyuki Yuasa, Toshiyuki Obata, Ichiro Yokota, Eiji Okamoto, Yoshiko Kanezaki, Hiroshi Maegawa, Fumiko Hirota, Kazuhiro Kishi, Seiichi Hashida, Hisao Nagaya, Ogura Yuko, Masuda Kazuhiko, Mitsuru Matsumoto, Toshio Matsumoto, Atsunori Kashiwagi and Yousuke Ebina : Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes., The 1st Insulin Resistance in Metabolic Disease Forum, Aug. 2008.

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

糖尿病とインスリン抵抗性疾患群を横断するインスリン受容体切断機構の解明 (Project/Area Number: 22K08656 )
Clarification of common mechanism in diabetes-related diseases by insulin receptor cleavage (Project/Area Number: 19K09027 )
Pathological mechanism of sequential cleavage model of insulin receptor (Project/Area Number: 15K09391 )
The study of molecular mechanism of insulin receptor cleavage (Project/Area Number: 24790317 )
Is insulin inactivated by the binding with serum soluble insulin receptor(sIR)? (Project/Area Number: 23659156 )
The study of the insulin receptor cleavage and its clinical significance (Project/Area Number: 22790317 )
Molecular mechanisms of Insulin signal transduction and diabetes mellitus (Project/Area Number: 20390095 )
Molecular mechanisms of insulin signal transduction and diabetes mellitus (Project/Area Number: 18390104 )
インスリン受容体細胞内ドメインは転写因子となりうるのか? (Project/Area Number: 17659085 )
Soluble insulin receptor ectodomain is elevated in the plasma of patients with diabetes (Project/Area Number: 17590269 )
Molecular mechanisms of insulin signal transduction and diabetes mellitus (Project/Area Number: 16390097 )
APSノックアウトマウスは肥満によるインスリン抵抗性を回避できる (Project/Area Number: 16046215 )
ヒト血清中に可溶性インスリンレセプターは存在するか? (Project/Area Number: 15659079 )
Elucidation of the molecular mechanisms of insulin transduction using APS knockout mice (Project/Area Number: 15590249 )
Crystallization and structural analysis of the human insulin receptor (Project/Area Number: 15570099 )
Molecular mechanisms of insulin signal transduction and diabetes mellitus (Project/Area Number: 14370045 )
PDGF投与により血糖値が下がるマウスを作れるか? (Project/Area Number: 13877018 )
New cDNAs and proteins phosphorylated by insulin using proteome analysis (Project/Area Number: 13680691 )
Molecular mechanisms of glucose uptake by insulin-independent pathway (Project/Area Number: 13670144 )
Development of a drug for diabetes using human genome information (Project/Area Number: 13557011 )
II型糖尿病の遺伝要因のゲノム的解析と分子病態の解明 (Project/Area Number: 13204065 )
Molecular mechanisms of insulin signal transduction and diabetas mellitus (Project/Area Number: 12470027 )
II型糖尿病の遺伝要因のゲノム的解析と分子病態の解明 (Project/Area Number: 12204082 )
肝臓におけるインスリン作用不全がII型糖尿病発症の真の原因か? (Project/Area Number: 11877028 )
インスリンシグナル伝達転換マウスの作製 (Project/Area Number: 10878097 )
Development of a simple screening system for the discovery of a new drug for diabetes (Project/Area Number: 10557019 )
Molecular mechanisms of insulin signal transduction and diabetes mellitus (Project/Area Number: 10470032 )
インスリン受容体とその作用メカニズムの解析 (Project/Area Number: 10169246 )
Search by Researcher Number (50304556)

Designated Associate Professor : Yuasa, Tomoyuki

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