Affiliation |
Hospital Geriatrics |
Graduating School 【 display / non-display 】
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-1997.03
Akita University Faculty of Medicine Graduated
Graduate School 【 display / non-display 】
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-2003.09
Akita University Graduate School,Division of Medicine Doctor's Course Completed
Campus Career 【 display / non-display 】
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2018.04-Now
Akita University Hospital Geriatrics Lecturer
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2015.04-2018.03
Akita University School of Medicine School of Medicine Specially-appointed Assistant Professor
Thesis for a degree 【 display / non-display 】
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Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy.
Morii T, Fujita H, Narita T, Shimotomai T, Fujishima H, Yoshioka N, Imai H, Kakei M, Ito S.
Journal of Diabetes and its Complications 17 11 - 15 2003.09
Domestic Co-author
Research Achievements 【 display / non-display 】
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Activation of GLP 1 receptor signalling alleviates cellular stresses and improves beta cell function in a mouse model of Wolfram syndrome.
Kondo M, Tanabe K, Shiinoki A K, Hatanaka M, Morii T, Takahashi H, Seino S, Yamada Y, Tanizawa Y.
Diabetologia 2018.10 [Refereed]
Research paper (journal) Domestic Co-author
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Stromal cell derived factor 1 is upregulated by dipeptidyl peptidase 4 inhibition and has protective roles in progressive diabetic nephropathy.
Takashima S, Fujita H, Fujishima H, Sato T, Shimizu T, Morii T , Tsukiyama K, Narita T, Takahashi T, Drucker DJ, Seino Y, Yamada.
Kidney Int 2016.10 [Refereed]
Research paper (journal) Domestic Co-author
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TCF1 links GIPR signaling to control of beta cell survival.
Campbell J, Dr. Ussher JR, Mulvihill EE, Baggio LL, Kolic J, Cao X, Liu Y, Lamont B, Morii T, Streutker C, Tamarina N, Philipson L, MacDonald P, Wrana J, Drucker DJ.
Nature Med 2016.01 [Refereed]
Research paper (journal) Domestic Co-author
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The protective roles of GLP-1R signaling in diabetic nephropathy: possible mechanism and therapeutic potential.
Fujita H, Morii T, Fujishima H, Sato T, Shimizu T, Hosoba M, Tsukiyama K, Narita T, Takahashi T, Drucker DJ, Seino Y, Yamada Y.
Kidney Int 2014.03 [Refereed]
Research paper (journal) Domestic Co-author
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SOD1, but not SOD3, deficiency accelerates diabetic renal injury in C57BL/6-Ins2(Akita) diabetic mice.
Fujita H, Fujishima H, Takahashi K, Sato T, Shimizu T, Morii T, Shimizu T, Shirasawa T, Qi Z, Breyer MD, Harris RC, Yamada Y, Takahashi T.
Metabolism 2012.12 [Refereed]
Research paper (journal) Domestic Co-author
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Recurrent nocturnal hypoglycemic hemiplegia: a case report and review of the literature
Toyama Hanako, Takahashi Kazuyuki, Shimizu Tatsunori, Otaka Izumi, Abe Sakiko, Kato Shunsuke, Ando Sayaka, Sato Takehiro, Morii Tsukasa, Fujita Hiroki, Waki Hironori
Endocrine Journal ( 一般社団法人 日本内分泌学会 ) advpub ( 0 ) 409 - 416 2024
<p>A 67-year-old man with type 1 diabetes, Cronkhite-Canada syndrome, and membranous nephropathy who received insulin therapy was admitted to our hospital with right hemiplegia and dysarthria. Brain magnetic resonance imaging revealed a lesion with a high diffusion-weighted imaging signal and low apparent diffusion coefficient signal in the posterior limb of the left internal capsule. He was hypoglycemic with a blood glucose level of 56 mg/dL (3.1 mmol/L). Following glucose administration, the patient’s symptoms resolved within several hours. The patient experienced similar transient hypoglycemic hemiplegia at midnight, three times within 10 days. In a literature review of 170 cases of hypoglycemic hemiplegia, 26 cases of recurrent hemiplegia were investigated. Recurrent hypoglycemic hemiplegia occurs more frequently on the right side than on the left side, and most recurrences occur within approximately a week, almost exclusively at midnight and in the early morning. We speculate that hypoglycemia-associated autonomic failure may be involved in the nocturnal recurrence of episodes. In our patient, depleted endogenous insulin secretion and lipodystrophy at the injection site, may have acted as additional factors, leading to severe hypoglycemia despite the absence of apparent autonomic neuropathy. Clinically, it is important to recognize hypoglycemia as a cause of hemiplegia to avoid unnecessary intervention and to maintain an appropriate blood glucose level at midnight and early in the morning to prevent recurrent hypoglycemic hemiplegia.</p>
◆Original paper【 display / non-display 】
◆Other【 display / non-display 】
Grant-in-Aid for Scientific Research 【 display / non-display 】
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Grant-in-Aid for Scientific Research(C)
Project Year: 2019.04 - 2023.03