start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=バソヒビン2を標的としたペプチドワクチンは糖尿病性腎症に対して予防的効果を持つ
kn-title=Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NAKASHIMAYuri
en-aut-sei=NAKASHIMA
en-aut-mei=Yuri
kn-aut-name=中島有理
kn-aut-sei=中島
kn-aut-mei=有理
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=3
article-no=
start-page=157
end-page=166
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Continuous Stimulation with Glycolaldehyde-derived Advanced Glycation End Product Reduces Aggrecan and COL2A1 Production via RAGE in Human OUMS-27 Chondrosarcoma Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Chondrocytes are responsible for the production of extracellular matrix (ECM) components such as collagen type II alpha-1 (COL2A1) and aggrecan, which are loosely distributed in articular cartilage. Chondrocyte dysfunction has been implicated in the pathogenesis of rheumatic diseases such as osteoarthritis (OA) and rheumatoid arthritis (RA). With age, advanced glycation end products (AGEs) accumulate in all tissues and body fluids, including cartilage and synovial fluid, causing and accelerating pathological changes associated with chronic diseases such as OA. Glycolaldehyde-derived AGE (AGE3), which is toxic to a variety of cell types, have a stronger effect on cartilage compared with other AGEs. To understand the long-term effects of AGE3 on cartilage, we stimulated a human chondrosarcoma cell line (OUMS-27), which exhibits a chondrocytic phenotype, with 10 μg/ml AGE3 for 4 weeks. As a result, the expressions of COL2A1 and aggrecan were significantly downregulated in the OUMS-27 cells without inducing cell death, but the expressions of proteases that play an important role in cartilage destruction were not affected. Inhibition of the receptor for advanced glycation end products (RAGE) suppressed the AGE3-induced reduction in cartilage component production, suggesting the involvement of RAGE in the action of AGE3.
en-copyright=
kn-copyright=

en-aut-name=HatipogluOmer Faruk
en-aut-sei=Hatipoglu
en-aut-mei=Omer Faruk
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishinakaTakashi
en-aut-sei=Nishinaka
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YaykasliKursat Oguz
en-aut-sei=Yaykasli
en-aut-mei=Kursat Oguz
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriShuji
en-aut-sei=Mori
en-aut-mei=Shuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WatanabeMasahiro
en-aut-sei=Watanabe
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ToyomuraTakao
en-aut-sei=Toyomura
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakahashiHideo
en-aut-sei=Takahashi
en-aut-mei=Hideo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WakeHidenori
en-aut-sei=Wake
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=

affil-num=2
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen
kn-affil=

affil-num=4
en-affil=Department of Pharmacology, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=5
en-affil=Department of Pharmacology, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=6
en-affil=Department of Pharmacology, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=7
en-affil=Department of Translational Research & Dug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=

affil-num=10
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=
en-keyword=advanced glycation end product
kn-keyword=advanced glycation end product
en-keyword=aging
kn-keyword=aging
en-keyword=cartilage
kn-keyword=cartilage
en-keyword=collagen
kn-keyword=collagen
en-keyword=aggrecan
kn-keyword=aggrecan
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=1
article-no=
start-page=38
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250124
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exacerbation of diabetes due to F. Nucleatum LPS-induced SGLT2 overexpression in the renal proximal tubular epithelial cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Diabetes treatments by the control of sodium-glucose cotransporter 2 (SGLT2) is commonly conducted while there are still uncertainties about the mechanisms for the SGLT2 overexpression in kidneys with diabetes. Previously, we have reported that glomeruli and proximal tubules with diabetic nephropathy express toll-like receptor TLR2/4, and that the TLR ligand lipopolysaccharide (LPS) of periodontal pathogens have caused nephropathy in diabetic model mice. Recently, many researchers suggested that the periodontal pathogenic bacteria Fusobacterium (F.) nucleatum has the TLR4-associated strong activator of the colorectal inflammation and cancer. The present study aimed to investigate the possibility of F. nucleatum as an exacerbation factor of diabetes through the renal SGLT2 induction.<br>
Methods The induction of the SGLT2 by F. nucleatum LPS (Fn-LPS) were investigated in the streptozotocin-induced diabetic mouse renal tissue and cultured renal proximal epithelial cells. The changes of blood glucose levels and survival curves in diabetic mice with Fn-LPS were analyzed. The Fn-LPS-induced SGLT2 production in the diabetic mouse renal tissue and in the cultured proximal epithelial cells was examined by ELISA, quantitative RT-PCR, and immunohistochemical analysis.<br>
Results The SGLT2 expression in the cultured mouse tubular epithelial cells was significantly increased by TNF- or co-culture with Fn-LPS-supplemented J774.1 cells. The period to reach diabetic condition was significantly shorter in Fn-LPS-administered diabetic mice than in diabetic mice. All Fn-LPS-administered-diabetic mice reached humane endpoints during the healthy period of all of the mice administered Fn-LPS only. The promotion of the SGLT2 expression at the inner lumen of proximal tubules were stronger in the Fn-LPS-administered-diabetic mice than in diabetic mice. The renal tissue SGLT2 mRNA amounts and the number of renal proximal tubules with overexpressed SGLT2 in the lumen were more in the Fn-LPS-administered-diabetic mice than in diabetic mice.<br>
Conclusions This study suggests that F. nucleatum causes the promotion of diabetes through the overexpression of SGLT2 in proximal tubules under the diabetic condition. Periodontitis with F. nucleatum may be a diabetic exacerbating factor.
en-copyright=
kn-copyright=

en-aut-name=SekiAiko
en-aut-sei=Seki
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KajiwaraKoichiro
en-aut-sei=Kajiwara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TeramachiJumpei
en-aut-sei=Teramachi
en-aut-mei=Jumpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EgusaMasahiko
en-aut-sei=Egusa
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyawakiTakuya
en-aut-sei=Miyawaki
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SawaYoshihiko
en-aut-sei=Sawa
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=

affil-num=3
en-affil=Department of Oral Function & Anatomy, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Dental Anesthesiology & Special Care Dentistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Dental Anesthesiology & Special Care Dentistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Oral Function & Anatomy, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=F. Nucleatum
kn-keyword=F. Nucleatum
en-keyword=Diabetic exacerbation
kn-keyword=Diabetic exacerbation
en-keyword=Diabetic nephropathy
kn-keyword=Diabetic nephropathy
en-keyword=SGLT2
kn-keyword=SGLT2
END

start-ver=1.4
cd-journal=joma
no-vol=326
cd-vols=
no-issue=6
article-no=
start-page=F1054
end-page=F1065
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240530
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diabetic nephropathy remains the leading cause of end-stage kidney disease in many countries, and additional therapeutic targets are needed to prevent its development and progression. Some angiogenic factors are involved in the pathogenesis of diabetic nephropathy. Vasohibin-2 (VASH2) is a novel proangiogenic factor, and our previous study showed that glomerular damage is inhibited in diabetic Vash2 homozygous knockout mice. Therefore, we established a VASH2-targeting peptide vaccine as a tool for anti-VASH2 therapy in diabetic nephropathy. In this study, the preventive effects of the VASH2-targeting peptide vaccine against glomerular injury were examined in a streptozotocin (STZ)-induced diabetic mouse model. The mice were subcutaneously injected with the vaccine at two doses 2 wk apart and then intraperitoneally injected with 50 mg/kg STZ for 5 consecutive days. Glomerular injury was evaluated 20 wk after the first vaccination. Treatment with the VASH2-targeting peptide vaccine successfully induced circulating anti-VASH2 antibody without inflammation in major organs. Although the vaccination did not affect blood glucose levels, it significantly prevented hyperglycemia-induced increases in urinary albumin excretion and glomerular volume. The vaccination did not affect increased VASH2 expression but significantly inhibited renal angiopoietin-2 (Angpt2) expression in the diabetic mice. Furthermore, it significantly prevented glomerular macrophage infiltration. The preventive effects of vaccination on glomerular injury were also confirmed in db/db mice. Taken together, the results of this study suggest that the VASH2-targeting peptide vaccine may prevent diabetic glomerular injury in mice by inhibiting Angpt2-mediated microinflammation.
en-copyright=
kn-copyright=

en-aut-name=NakashimaYuri
en-aut-sei=Nakashima
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MifuneTomoyo
en-aut-sei=Mifune
en-aut-mei=Tomoyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakadoiTakato
en-aut-sei=Nakadoi
en-aut-mei=Takato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HayashiHiroki
en-aut-sei=Hayashi
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakagamiHironori
en-aut-sei=Nakagami
en-aut-mei=Hironori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatoYasufumi
en-aut-sei=Sato
en-aut-mei=Yasufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=New Industry Creation Hatchery Center, Tohoku University
kn-affil=

affil-num=8
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=albuminuria
kn-keyword=albuminuria
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=macrophages
kn-keyword=macrophages
en-keyword=peptide vaccine
kn-keyword=peptide vaccine
en-keyword=vasohibin-2
kn-keyword=vasohibin-2
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=3
article-no=
start-page=e004237
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202405
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Plasma angiotensin-converting enzyme 2 (ACE2) is a marker for renal outcome of diabetic kidney disease (DKD) (U-CARE study 3)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction ACE cleaves angiotensin I (Ang I) to angiotensin II (Ang II) inducing vasoconstriction via Ang II type 1 (AT1) receptor, while ACE2 cleaves Ang II to Ang (1-7) causing vasodilatation by acting on the Mas receptor. In diabetic kidney disease (DKD), it is still unclear whether plasma or urine ACE2 levels predict renal outcomes or not.<br>
Research design and methods Among 777 participants with diabetes enrolled in the Urinary biomarker for Continuous And Rapid progression of diabetic nEphropathy study, the 296 patients followed up for 9 years were investigated. Plasma and urinary ACE2 levels were measured by the ELISA. The primary end point was a composite of a decrease of estimated glomerular filtration rate (eGFR) by at least 30% from baseline or initiation of hemodialysis or peritoneal dialysis. The secondary end points were a 30% increase or a 30% decrease in albumin-to-creatinine ratio from baseline to 1 year.<br>
Results The cumulative incidence of the renal composite outcome was significantly higher in group 1 with lowest tertile of plasma ACE2 (p=0.040). Group 2 with middle and highest tertile was associated with better renal outcomes in the crude Cox regression model adjusted by age and sex (HR 0.56, 95% CI 0.31 to 0.99, p=0.047). Plasma ACE2 levels demonstrated a significant association with 30% decrease in ACR (OR 1.46, 95% CI 1.044 to 2.035, p=0.027) after adjusting for age, sex, systolic blood pressure, hemoglobin A1c, and eGFR.<br>
Conclusions Higher baseline plasma ACE2 levels in DKD were protective for development and progression of albuminuria and associated with fewer renal end points, suggesting plasma ACE2 may be used as a prognosis marker of DKD.Trial registration number UMIN000011525.
en-copyright=
kn-copyright=

en-aut-name=UenoAsami
en-aut-sei=Ueno
en-aut-mei=Asami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OnishiYasuhiro
en-aut-sei=Onishi
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiseKoki
en-aut-sei=Mise
en-aut-mei=Koki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamaguchiSatoshi
en-aut-sei=Yamaguchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KannoAyaka
en-aut-sei=Kanno
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NojimaIchiro
en-aut-sei=Nojima
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HiguchiChigusa
en-aut-sei=Higuchi
en-aut-mei=Chigusa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiyamotoSatoshi
en-aut-sei=Miyamoto
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HidaKazuyuki
en-aut-sei=Hida
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=WatanabeMayu
en-aut-sei=Watanabe
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=NakatoTatsuaki
en-aut-sei=Nakato
en-aut-mei=Tatsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=ToneAtsuhito
en-aut-sei=Tone
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=MatsuokaTakashi
en-aut-sei=Matsuoka
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=KameiShinji
en-aut-sei=Kamei
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=MurakamiKazutoshi
en-aut-sei=Murakami
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ShimizuIkki
en-aut-sei=Shimizu
en-aut-mei=Ikki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=MiyashitaKatsuhito
en-aut-sei=Miyashita
en-aut-mei=Katsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=AndoShinichiro
en-aut-sei=Ando
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=NunoueTomokazu
en-aut-sei=Nunoue
en-aut-mei=Tomokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

affil-num=1
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Diabetology and Metabolism, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=14
en-affil=Department of Diabetology and Metabolism, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=15
en-affil=Department of Diabetology and Metabolism, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=16
en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=17
en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=18
en-affil=Okayama Saiseikai General Hospital
kn-affil=

affil-num=19
en-affil=Department of Diabetic Medicine, Kurashiki Central Hospital
kn-affil=

affil-num=20
en-affil=Department of Diabetic Medicine, Kurashiki Central Hospital
kn-affil=

affil-num=21
en-affil=Department of Diabetic Medicine, Kurashiki Central Hospital
kn-affil=

affil-num=22
en-affil=Sakakibara Heart Institute of Okayama
kn-affil=

affil-num=23
en-affil=Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=24
en-affil=Okayama City General Medical Center
kn-affil=

affil-num=25
en-affil=Nunoue Clinic
kn-affil=

affil-num=26
en-affil=Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=2
article-no=
start-page=182
end-page=194
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibition of Amino Acids Influx into Proximal Tubular Cells Improves Lysosome Function in Diabetes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Inhibition of glucose influx into proximal tubular cells (PTCs) by sodium–glucose cotransporter 2 inhibitors revealed prominent therapeutic effects on diabetic kidney disease. Collectrin (CLTRN) serves as a chaperone for the trafficking of neutral amino acid (AA) transporters in the apical membranes of PTCs. We investigated the beneficial effects of reduced influx of AAs into PTCs in diabetes and obesity model of Cltrn−/y mice.<br>
Methods Cltrn+/y and Cltrn−/y mice at age 5 weeks were assigned to standard diet and streptozotocin and high-fat diet (STZ-HFD)–treated groups.<br>
Results At age 22–23 weeks, body weight and HbA1c levels significantly increased in STZ-HFD-Cltrn+/y compared with standard diet-Cltrn+/y; however, they were not altered in STZ-HFD-Cltrn−/y compared with STZ-HFD-Cltrn+/y. At age 20 weeks, urinary albumin creatinine ratio was significantly reduced in STZ-HFD-Cltrn−/y compared with STZ-HFD-Cltrn+/y. Under the treatments with STZ and HFD, the Cltrn gene deficiency caused significant increase in urinary concentration of AAs such as Gln, His, Gly, Thr, Tyr, Val, Trp, Phe, Ile, Leu, and Pro. In PTCs in STZ-HFD-Cltrn+/y, the enlarged lysosomes with diameter of 10 μm or more were associated with reduced autolysosomes, and the formation of giant lysosomes was prominently suppressed in STZ-HFD-Cltrn−/y. Phospho-mTOR and inactive form of phospho-transcription factor EB were reduced in STZ-HFD-Cltrn−/y compared with STZ-HFD-Cltrn+/y.<br>
Conclusions The reduction of AAs influx into PTCs inactivated mTOR, activated transcription factor EB, improved lysosome function, and ameliorated vacuolar formation of PTCs in STZ-HFD-Cltrn−/y mice.
en-copyright=
kn-copyright=

en-aut-name=KanoYuzuki
en-aut-sei=Kano
en-aut-mei=Yuzuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamaguchiSatoshi
en-aut-sei=Yamaguchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiseKoki
en-aut-sei=Mise
en-aut-mei=Koki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawakitaChieko
en-aut-sei=Kawakita
en-aut-mei=Chieko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OnishiYasuhiro
en-aut-sei=Onishi
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KurookaNaoko
en-aut-sei=Kurooka
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SugawaraRyosuke
en-aut-sei=Sugawara
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AlbuayjanHaya Hamed Hassan
en-aut-sei=Albuayjan
en-aut-mei=Haya Hamed Hassan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=diabetes mellitus
kn-keyword=diabetes mellitus
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=metabolism
kn-keyword=metabolism
en-keyword=obesity
kn-keyword=obesity
en-keyword=tubular epithelium
kn-keyword=tubular epithelium
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=19
article-no=
start-page=3038
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of Semaphorin 3A in Kidney Development and Diseases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Kidney diseases are worldwide public health problems affecting millions of people. However, there are still limited therapeutic options against kidney diseases. Semaphorin 3A (SEMA3A) is a secreted and membrane-associated protein, which regulates diverse functions, including immune regulation, cell survival, migration and angiogenesis, thus involving in the several pathogeneses of diseases, including eyes and neurons, as well as kidneys. SEMA3A is expressed in podocytes and tubular cells in the normal adult kidney, and recent evidence has revealed that excess SEMA3A expression and the subsequent signaling pathway aggravate kidney injury in a variety of kidney diseases, including nephrotic syndrome, diabetic nephropathy, acute kidney injury, and chronic kidney disease. In addition, several reports have demonstrated that the inhibition of SEMA3A ameliorated kidney injury via a reduction in cell apoptosis, fibrosis and inflammation; thus, SEMA3A may be a potential therapeutic target for kidney diseases. In this review article, we summarized the current knowledge regarding the role of SEMA3A in kidney pathophysiology and their potential use in kidney diseases.
en-copyright=
kn-copyright=

en-aut-name=SangYizhen
en-aut-sei=Sang
en-aut-mei=Yizhen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsujiKenji
en-aut-sei=Tsuji
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakanohHiroyuki
en-aut-sei=Nakanoh
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukushimaKazuhiko
en-aut-sei=Fukushima
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KitamuraShinji
en-aut-sei=Kitamura
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=semaphorin 3A
kn-keyword=semaphorin 3A
en-keyword=neuropilin-1
kn-keyword=neuropilin-1
en-keyword=podocyte
kn-keyword=podocyte
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=acute kidney injury
kn-keyword=acute kidney injury
en-keyword=chronic kidney injury
kn-keyword=chronic kidney injury
en-keyword=lupus nephritis
kn-keyword=lupus nephritis
en-keyword=fibrosis
kn-keyword=fibrosis
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=inflammation
kn-keyword=inflammation
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=10
article-no=
start-page=1148
end-page=1156
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230713
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 in hypertriglyceridemia and diabetes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In diabetes, the impairment of insulin secretion and insulin resistance contribute to hypertriglyceridemia, as the enzymatic activity of lipoprotein lipase (LPL) depends on insulin action. The transport of LPL to endothelial cells and its enzymatic activity are maintained by the formation of lipolytic complex depending on the multiple positive (glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 [GPIHBP1], apolipoprotein C-II [APOC2], APOA5, heparan sulfate proteoglycan [HSPG], lipase maturation factor 1 [LFM1] and sel-1 suppressor of lin-12-like [SEL1L]) and negative regulators (APOC1, APOC3, angiopoietin-like proteins [ANGPTL]3, ANGPTL4 and ANGPTL8). Among the regulators, GPIHBP1 is a crucial molecule for the translocation of LPL from parenchymal cells to the luminal surface of capillary endothelial cells, and maintenance of lipolytic activity; that is, hydrolyzation of triglyceride into free fatty acids and monoglyceride, and conversion from chylomicron to chylomicron remnant in the exogenous pathway and from very low-density lipoprotein to low-density lipoprotein in the endogenous pathway. The null mutation of GPIHBP1 causes severe hypertriglyceridemia and pancreatitis, and GPIGBP1 autoantibody syndrome also causes severe hypertriglyceridemia and recurrent episodes of acute pancreatitis. In patients with type 2 diabetes, the elevated serum triglyceride levels negatively correlate with circulating LPL levels, and positively with circulating APOC1, APOC3, ANGPTL3, ANGPTL4 and ANGPTL8 levels. In contrast, circulating GPIHBP1 levels are not altered in type 2 diabetes patients with higher serum triglyceride levels, whereas they are elevated in type 2 diabetes patients with diabetic retinopathy and nephropathy. The circulating regulators of lipolytic complex might be new biomarkers for lipid and glucose metabolism, and diabetic vascular complications.
en-copyright=
kn-copyright=

en-aut-name=KurookaNaoko
en-aut-sei=Kurooka
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Dibaetes
kn-keyword=Dibaetes
en-keyword=GPIHBP1
kn-keyword=GPIHBP1
en-keyword=Lipoprotein lipase
kn-keyword=Lipoprotein lipase
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=3
article-no=
start-page=243
end-page=254
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Brown Adipose Tissue PPARγ Is Required for the Insulin-Sensitizing Action of Thiazolidinediones
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Brown adipose tissue (BAT) plays a critical role in metabolic homeostasis. BAT dysfunction is associated with the development of obesity through an imbalance between energy expenditure and energy intake. The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) is the master regulator of adipogenesis. However, the roles of PPARγ and thiazolidinediones (TZDs) in the regulation of BAT metabolism remain unclear. TZDs, which are selective PPARγ activators, improve systemic insulin resistance in animals and humans. In the present study, we generated brown adipocyte-specific PPARγ-deficient mice (BATγKO) to examine the in vivo roles of PPARγ and TZDs in BAT metabolism. In electron microscopic examinations, brown adipocyte-specific PPARγ deletion promoted severe whitening of brown fat and morphological alteration of mitochondria. Brown adipocyte-specific PPARγ deletion also reduced mRNA expression of BAT-selective genes. Although there was no difference in energy expenditure between control and BATγKO mice in calorimetry, norepinephrine-induced thermogenesis was impaired in BATγKO mice. Moreover, pioglitazone treatment improved diet-induced insulin resistance in the control mice but not in the BATγKO mice. These findings suggest that BAT PPARγ is necessary for the maintenance of brown adipocyte function and for the insulin-sensitizing action of TZDs.
en-copyright=
kn-copyright=

en-aut-name=ShibataYusuke
en-aut-sei=Shibata
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=PPARγ
kn-keyword=PPARγ
en-keyword=brown adipose tissue
kn-keyword=brown adipose tissue
en-keyword=thiazolidinediones
kn-keyword=thiazolidinediones
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=6
article-no=
start-page=723
end-page=730
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Serum miR-377 Can Be Used as a Diagnostic Marker for Acute Coronary Syndrome and Can Regulate Proinflammatory Factors and Endothelial Injury Markers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The diagnostic value of microRNA-377 (miR-377) in patients with acute coronary syndrome (ACS) and explored miR-377’s potential mechanisms. We performed an qRT-PCR to assess serum miR-377 levels in ACS patients and coronary artery ligation rat models. The diagnostic value of miR-377 was evaluated by determining the ROC curve. An ELISA assay was conducted to detect the model rat endothelial damage markers von Willebrand factor (vWF) and heart-type fatty acid binding protein (H-FABP), and proinflammatory cytokines TNF-α, IL-6, and IL-1β. The serum miR-377 level was elevated in the ACS patients and significantly increased in the ACS rats. MiR-377 has a high diagnostic value in ACS patients, with a 0.844 ROC, 76.47% specificity, and 87.10% sensitivity. MiR-377 was positively correlated with the expressions of vWF, H-FABP, cTnI, TNF-α, IL-6, and IL-1β. In ACS rats, reducing the expression of miR-377 significantly inhibited the increases in vWF, H-FABP, TNF-α, IL-6, and IL-1β. An elevated miR-377 level can be used as a diagnostic marker in patients with ACS. A reduction of miR-377 may alleviate ACS by improving myocardial damage such as endothelial injury and the inflammatory response.
en-copyright=
kn-copyright=

en-aut-name=ZhangQuan
en-aut-sei=Zhang
en-aut-mei=Quan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YangLixia
en-aut-sei=Yang
en-aut-mei=Lixia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WanGuozhen
en-aut-sei=Wan
en-aut-mei=Guozhen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZhangXiaoqiang
en-aut-sei=Zhang
en-aut-mei=Xiaoqiang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangYing
en-aut-sei=Wang
en-aut-mei=Ying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ZhaoGuannan
en-aut-sei=Zhao
en-aut-mei=Guannan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Affiliated Hospital of Gansu Medical College
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Affiliated Hospital of Gansu Medical College
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Affiliated Hospital of Gansu Medical College
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Affiliated Hospital of Gansu Medical College
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Affiliated Hospital of Gansu Medical College
kn-affil=

affil-num=6
en-affil=Department of Dermatological, Pingliang Traditional Chinese Medicine Hospital
kn-affil=
en-keyword=microRNA-377
kn-keyword=microRNA-377
en-keyword=acute coronary syndrome
kn-keyword=acute coronary syndrome
en-keyword=diagnosis
kn-keyword=diagnosis
en-keyword=endothelial injury
kn-keyword=endothelial injury
en-keyword=inflammatory
kn-keyword=inflammatory
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=5
article-no=
start-page=549
end-page=556
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202110
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Glial Cells as Possible Targets of Neuroprotection through Neurotrophic and Antioxidative Molecules in the Central and Enteric Nervous Systems in Parkinson’s Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide. The loss of nigrostriatal dopaminergic neurons produces its characteristic motor symptoms, but PD patients also have non-motor symptoms such as constipation and orthostatic hypotension. The pathological hallmark of PD is the presence of α-synuclein-containing Lewy bodies and neurites in the brain. However, the PD pathology is observed in not only the central nervous system (CNS) but also in parts of the peripheral nervous system such as the enteric nervous system (ENS). Since constipation is a typical prodromal non-motor symptom in PD, often preceding motor symptoms by 10-20 years, it has been hypothesized that PD pathology propagates from the ENS to the CNS via the vagal nerve. Discovery of pharmacological and other methods to halt this progression of neurodegeneration in PD has the potential to improve millions of lives. Astrocytes protect neurons in the CNS by secretion of neurotrophic and antioxidative factors. Similarly, astrocyte-like enteric glial cells (EGCs) are known to secrete neuroprotective factors in the ENS. In this article, we summarize the neuroprotective function of astrocytes and EGCs and discuss therapeutic strategies for the prevention of neurodegeneration in PD targeting neurotrophic and antioxidative molecules in glial cells.
en-copyright=
kn-copyright=

en-aut-name=IsookaNami
en-aut-sei=Isooka
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Parkinson’s disease
kn-keyword=Parkinson’s disease
en-keyword=astrocyte
kn-keyword=astrocyte
en-keyword=enteric glial cell
kn-keyword=enteric glial cell
en-keyword=neurotrophic factor
kn-keyword=neurotrophic factor
en-keyword=antioxidative molecule
kn-keyword=antioxidative molecule
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=1
article-no=
start-page=287
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210823
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Overexpression of SGLT2 in the kidney of a P. gingivalis LPS-induced diabetic nephropathy mouse model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The overexpression of sodium-glucose cotransporter 2 (SGLT2) in diabetic kidneys has been reported. It has also been established that the diabetic glomerular endothelium expresses the toll-like receptors TLR2 and TLR4. The present study aims to examine the renal SGLT2 induction by the TLR2/4 ligand Porphyromonas (P.) gingivalis lipopolysaccharide (Pg-LPS) in mouse diabetic nephropathy. <br>
Methods: Immunohistochemical study and tissue RT-PCR analyses were performed on mouse kidneys in streptozotocin (STZ)-induced diabetic ICR mice (STZ-ICR), in healthy ICR mice administered Pg-LPS (LPS-ICR), and in diabetic ICR mouse kidneys with Pg-LPS-induced nephropathy (LPS-STZ). <br>
Results: In the quantitative analysis of blood sugar levels, the mean time to reach 600 mg/dl was shorter in the LPS-STZ than in the STZ-ICR kidneys. The rise in blood glucose levels was significantly steeper in the LPS-STZ than in the STZ-ICR kidneys. According to these data the LPS-STZ model suggests a marked glucose intolerance. The expression of SGLT2 was significantly stronger in the whole of the renal parenchyma of the LPS-STZ than in the LPS-ICR or in the STZ-ICR. The expression of SGLT2 was observed both in the renal tubules and around the renal tubules, and in the glomeruli of the LPS-STZ kidneys. In the analysis by tissue real-time PCR and cell ELISA, the expression of the SGLT2 gene and protein was significantly stronger in the LPS-STZ than in the LPS-ICR or in the STZ-ICR. There were no differences in the renal SGLT2 production in the LPS-ICR and the STZ-ICR kidneys. <br>
Conclusions: Abnormally high renal expression of SGLT2 occurs in diabetic kidneys with P. gingivalis LPS. Periodontitis may be an exacerbating factor in diabetic nephropathy as well as in diabetes.
en-copyright=
kn-copyright=

en-aut-name=KajiwaraKoichiro
en-aut-sei=Kajiwara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SawaYoshihiko
en-aut-sei=Sawa
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=

affil-num=2
en-affil=Department of Oral Function & Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=P. gingivalis
kn-keyword=P. gingivalis
en-keyword=LPS
kn-keyword=LPS
en-keyword=Diabetic nephropathy
kn-keyword=Diabetic nephropathy
en-keyword=SGLT2
kn-keyword=SGLT2
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=2
article-no=
start-page=169
end-page=175
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Effects of Low-Dose-Rate γ-irradiation on Forced Swim Test-Induced Immobility and Oxidative Stress in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The forced swim test (FST) induces immobility in mice. Low-dose (high-dose-rate) X-irradiation inhibits FSTinduced immobility in mice due to its antioxidative function. We evaluated the effects of low-dose γ-irradiation at a low-dose-rate on the FST-induced depletion of antioxidants in mouse organs. Mice received whole-body low-dose-rate (0.6 or 3.0 mGy/h) of low-dose γ-irradiation for 1 week, followed by daily FSTs (5 days). The immobility rate on day 2 compared to day 1 was significantly lower in the 3.0 mGy/h irradiated mice than in sham irradiated mice. The FST significantly decreased the catalase (CAT) activity and total glutathione (t-GSH) content in the brain and kidney, respectively. The superoxide dismutase (SOD) activity and t-GSH content in the liver of the 3.0 mGy/h irradiated mice were significantly lower than those of the non-FST-treated mice. The CAT activity in the lungs of mice exposed to 3.0 mGy/h γ-irradiation was higher than that of non-FST treated mice and mice treated with FST. However, no significant differences were observed in the levels of these antioxidant markers between the sham and irradiated groups except for the CAT activity in lungs. These findings suggest that the effects of low-dose-rate and low-dose γ-irradiation on FST are highly organ-dependent.
en-copyright=
kn-copyright=

en-aut-name=NakadaTetsuya
en-aut-sei=Nakada
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KataokaTakahiro
en-aut-sei=Kataoka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NomuraTakaharu
en-aut-sei=Nomura
en-aut-mei=Takaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShutoHina
en-aut-sei=Shuto
en-aut-mei=Hina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YanoJunki
en-aut-sei=Yano
en-aut-mei=Junki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaoeShota
en-aut-sei=Naoe
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HanamotoKatsumi
en-aut-sei=Hanamoto
en-aut-mei=Katsumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamaokaKiyonori
en-aut-sei=Yamaoka
en-aut-mei=Kiyonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Central Research Institute of Electric Power Industry
kn-affil=

affil-num=4
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=
en-keyword=low-dose-rate γ-irradiation
kn-keyword=low-dose-rate γ-irradiation
en-keyword=forced swim test
kn-keyword=forced swim test
en-keyword=antioxidant
kn-keyword=antioxidant
en-keyword=oxidative stress
kn-keyword=oxidative stress
END

start-ver=1.4
cd-journal=joma
no-vol=46
cd-vols=
no-issue=9
article-no=
start-page=1773
end-page=1786
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190530
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The next era of renal radionuclide imaging: novel PET radiotracers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although single-photon-emitting radiotracers have long been the standard for renal functional molecular imaging, recent years have seen the development of positron emission tomography (PET) agents for this application. We provide an overview of renal radionuclide PET radiotracers, in particular focusing on novel 18F-labelled and 68Ga-labelled agents. Several reported PET imaging probes allow assessment of glomerular filtration rate, such as [68Ga]ethylenediaminetetraacetic acid ([68Ga]EDTA), [68Ga]IRDye800-tilmanocept and 2-deoxy-2-[18F]fluorosorbitol ([18F]FDS)). The diagnostic performance of [68Ga]EDTA has already been demonstrated in a clinical trial. [68Ga]IRDye800-tilmanocept shows receptor-mediated binding to glomerular mesangial cells, which in turn may allow the monitoring of progression of diabetic nephropathy. [18F]FDS shows excellent kidney extraction and excretion in rats and, as has been shown in the first study in humans. Further, due to its simple one-step radiosynthesis via the most frequently used PET radiotracer 2-deoxy-2-[18F]fluoro-d-glucose, [18F]FDS could be available at nearly every PET centre. A new PET radiotracer has also been introduced for the effective assessment of plasma flow in the kidneys: Re(CO)3-N-([18F]fluoroethyl)iminodiacetic acid (Re(CO)3([18F]FEDA)). This compound demonstrates similar pharmacokinetic properties to its 99mTc-labelled analogue [99mTc](CO)3(FEDA). Thus, if there is a shortage of molybdenum-99, Re(CO)3([18F]FEDA would allow direct comparison with previous studies with 99mTc. The PET radiotracers for renal imaging reviewed here allow thorough evaluation of kidney function, with the tremendous advantage of precise anatomical coregistration with simultaneously acquired CT images and rapid three-dimensional imaging capability.
en-copyright=
kn-copyright=

en-aut-name=WernerRudolf A.
en-aut-sei=Werner
en-aut-mei=Rudolf A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ChenXinyu
en-aut-sei=Chen
en-aut-mei=Xinyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LapaConstantin
en-aut-sei=Lapa
en-aut-mei=Constantin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoshinoKazuhiro
en-aut-sei=Koshino
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=RoweSteven P.
en-aut-sei=Rowe
en-aut-mei=Steven P.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=PomperMartin G.
en-aut-sei=Pomper
en-aut-mei=Martin G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=JavadiMehrbod S.
en-aut-sei=Javadi
en-aut-mei=Mehrbod S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HiguchiTakahiro
en-aut-sei=Higuchi
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Nuclear Medicine/Comprehensive Heart Failure Center, University of Wuerzburg
kn-affil=

affil-num=2
en-affil=Department of Nuclear Medicine/Comprehensive Heart Failure Center, University of Wuerzburg
kn-affil=

affil-num=3
en-affil=Department of Nuclear Medicine/Comprehensive Heart Failure Center, University of Wuerzburg
kn-affil=

affil-num=4
en-affil=Department of Biomedical Imaging, National Cardiovascular and Cerebral Center
kn-affil=

affil-num=5
en-affil=Division of Nuclear Medicine and Molecular Imaging, The Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
kn-affil=

affil-num=6
en-affil=
kn-affil=

affil-num=7
en-affil=Division of Nuclear Medicine and Molecular Imaging, The Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
kn-affil=

affil-num=8
en-affil=Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School
kn-affil=
en-keyword=Kidney
kn-keyword=Kidney
en-keyword=Positron emission tomography
kn-keyword=Positron emission tomography
en-keyword=PET
kn-keyword=PET
en-keyword=[18F]Fluorodeoxysorbitol
kn-keyword=[18F]Fluorodeoxysorbitol
en-keyword=GFR
kn-keyword=GFR
en-keyword=ERPF
kn-keyword=ERPF
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=1
article-no=
start-page=103
end-page=107
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202102
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Marked Hypertriglyceridemia in a Patient with type 2 Diabetes Receiving SGLT2 Inhibitors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 43-year-old male with type 2 diabetes, under treatment with 5 mg/day of dapagliflozin, was referred to our hospital with upper left abdominal pain and marked hypertriglyceridemia (triglycerides [TGs], 5,960 mg/dl). He was also on a low-carbohydrate diet that promoted ketosis under sodium glucose cotransporter 2 (SGLT2) inhibitor administration. Polyacrylamide gel electrophoresis revealed a remarkable increase in very-low-den-sity lipoprotein, a TG-rich lipoprotein particle synthesized in the liver using free fatty acids derived from adi-pose tissue. Although SGLT2 inhibitors generally improve the lipid profile, under certain conditions such as a low-carbohydrate diet, they may adversely exacerbate the lipid profile via ketosis.
en-copyright=
kn-copyright=

en-aut-name=SenooMayumi
en-aut-sei=Senoo
en-aut-mei=Mayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ToneAtsuhito
en-aut-sei=Tone
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImaiYusuke
en-aut-sei=Imai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeSatoko
en-aut-sei=Watanabe
en-aut-mei=Satoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KanetoMitsuhiro
en-aut-sei=Kaneto
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShimomuraYasuyuki
en-aut-sei=Shimomura
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakatouTatsuaki
en-aut-sei=Nakatou
en-aut-mei=Tatsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=2
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=4
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=5
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=6
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=7
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=8
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=
en-keyword=sodium glucose cotransporter 2 inhibitor
kn-keyword=sodium glucose cotransporter 2 inhibitor
en-keyword=dyslipidemia
kn-keyword=dyslipidemia
en-keyword=hypertriglyceridemia
kn-keyword=hypertriglyceridemia
en-keyword=type 2 diabetes mellitus
kn-keyword=type 2 diabetes mellitus
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=1
article-no=
start-page=3
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immunohistochemical study for the expression of leukocyte adhesion molecules, and FGF23 and ACE2 in P. gingivalis LPS-induced diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective</br>
The present study aims to examine the expression of leukocyte adhesion molecules and renal metabolic factors in diabetic mouse kidneys with periodontal pathogen Pg-LPS-induced nephropathy.</br>
Background</br>
We recently reported that the glomerular endothelium expresses toll-like receptor (TLR)2 and TLR4 in diabetic environments and TLR2/4 ligand Porphyromonas (P.) gingivalis lipopolysaccharides (Pg-LPS) induce nephropathy in diabetic mice. It is thought that Pg-LPS promotes the chronic inflammation with the overexpression of leukocyte adhesion molecules and renal-specific metabolic enzymes by the recognition of Pg-LPS via TLR in the diabetic kidneys. There have been no reports of the effects of periodontopathic bacteria on the expression of leukocyte adhesion molecules and the accumulation of physiologically active substances in the kidney.</br>
Methods</br>
The immunohistochemical investigation was performed on diabetic mouse kidney with Pg-LPS-induced nephropathy with glomerulosclerosis in glomeruli.</br>
Results</br>
There were no vessels which expressed vascular cell adhesion molecule-1 (VCAM-1), E-selectin, or fibroblast growth factor (FGF) 23 in streptozotocin (STZ)-induced diabetic ICR mice (STZ-ICR), or in healthy ICR mice administered Pg-LPS (LPS-ICR). However, in diabetic ICR mouse kidneys with Pg-LPS-induced nephropathy (LPS-STZ) the expression of VCAM-1 and the accumulation of FGF23 were observed in renal tubules and glomeruli, and the expression of E-selectin was observed in renal parenchyma and glomeruli. The angiotensin-converting enzyme 2 (ACE2) was detected in the proximal tubules but not in other regions of ICR, STZ-ICR, or LPS-ICR. In LPS-STZ ACE2 was detected both in renal tubules as well as in glomeruli. The Mac-1 and podoplanin-positive cells increased in the renal parenchyma with diabetic condition and there was the distribution of a large number of Mac-1-positive cells in LPS-STZ.</br>
Conclusions</br>
The Pg-LPS may induce diabetic renal inflammation such as glomerulosclerosis and tubulitis with infiltration of Mac-1/podoplanin positive macrophages via glomerular overexpression of VCAM-1 and E-selectin, resulting in accumulation of both ACE2 and FGF23 which were unmetabolized with the inflammation-induced kidney damage under the diabetic condition. Periodontitis may be a critical factor in the progress of nephropathy in diabetic patients.
en-copyright=
kn-copyright=

en-aut-name=KajiwaraKoichiro
en-aut-sei=Kajiwara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SawaYoshihiko
en-aut-sei=Sawa
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujitaTakahiro
en-aut-sei=Fujita
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TamaokiSachio
en-aut-sei=Tamaoki
en-aut-mei=Sachio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=

affil-num=2
en-affil=Department of Oral Function & Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=

affil-num=4
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=
en-keyword=P. gingivalis
kn-keyword=P. gingivalis
en-keyword=LPS
kn-keyword=LPS
en-keyword=Diabetic nephropathy
kn-keyword=Diabetic nephropathy
en-keyword=VCAM-1
kn-keyword=VCAM-1
en-keyword=E-selectin
kn-keyword=E-selectin
en-keyword=ACE2
kn-keyword=ACE2
en-keyword=FGF23
kn-keyword=FGF23
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=2
article-no=
start-page=325
end-page=332
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200517
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prevalence of albuminuria and renal dysfunction, and related clinical factors in Japanese patients with diabetes: The Japan Diabetes Complication and its Prevention prospective study 5
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims/Introduction</br>
To clarify the prevalence of albuminuria and renal dysfunction, and related factors in Japanese patients with diabetes, we analyzed the baseline data of the Japan Diabetes Complication and its Prevention prospective study.</br>
Materials and Methods</br>
We used the data of 355 patients with type 1 diabetes and 5,194 patients with type 2 diabetes to evaluate the prevalence of albuminuria and renal dysfunction, and related factors. A binomial logistic regression analysis was used to investigate independent contributing factors for estimated glomerular filtration rate <60 mL/min/1.73 m2 or albuminuria. </br>
Results</br>
The prevalence of microalbuminuria and macroalbuminuria was 15.2% (54/355) and 3.1% (11/355) in type 1 diabetes patients, and 25.0% (1,298/5,194) and 5.1% (265/5,194) in type 2 diabetes patients, respectively. The proportion of renal dysfunction (estimated glomerular filtration rate <60 mL/min/1.73 m2) was 9.9% (35/355) in type 1 diabetes patients, and 15.3% (797/5,194) in type 2 diabetes patients. The proportion of patients with renal dysfunction with normoalbuminuria was 7.3% (26/355) for type 1 diabetes patients, and 9.0% (467/5,194) for type 2 diabetes patients. The factors related to albuminuria in type 2 diabetes patients were glycated hemoglobin, hypertension, age, duration of diabetes, body mass index and estimated glomerular filtration rate. In contrast, factors to related renal dysfunction were age, duration of diabetes, dyslipidemia, hypertension, body mass index, male sex and albuminuria. </br>
Conclusions</br>
We showed the recent prevalence of albuminuria and renal dysfunction, and related factors in Japanese type 1 and type 2 diabetes patients using the baseline data of the Japan Diabetes Complication and its Prevention prospective study. The current results suggest that renal disease in patients with type 2 diabetes is heterogeneous, and different mechanisms might be involved in albuminuria and deterioration of renal function.
en-copyright=
kn-copyright=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KoderaRyo
en-aut-sei=Kodera
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UtsunomiyaKazunori
en-aut-sei=Utsunomiya
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoyaDaisuke
en-aut-sei=Koya
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishimuraRimei
en-aut-sei=Nishimura
en-aut-mei=Rimei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyamotoSatoshi
en-aut-sei=Miyamoto
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TajimaNaoko
en-aut-sei=Tajima
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=the JDCP study group
en-aut-sei=the JDCP study group
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=The Japan Diabetes Society
kn-affil=

affil-num=3
en-affil=The Japan Diabetes Society
kn-affil=

affil-num=4
en-affil=The Japan Diabetes Society
kn-affil=

affil-num=5
en-affil=The Japan Diabetes Society
kn-affil=

affil-num=6
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=The Japan Diabetes Society
kn-affil=

affil-num=8
en-affil=
kn-affil=
en-keyword=Diabetic nephropathy
kn-keyword=Diabetic nephropathy
en-keyword=Diabetic kidney disease
kn-keyword=Diabetic kidney disease
en-keyword=Japan Diabetes Complication and its Prevention study
kn-keyword=Japan Diabetes Complication and its Prevention study
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=2
article-no=
start-page=207
end-page=216
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200808
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Randomized trial of an intensified, multifactorial intervention in patients with advanced‐stage diabetic kidney disease: Diabetic Nephropathy Remission and Regression Team Trial in Japan (DNETT‐Japan)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims/Introduction</br>
We evaluated the efficacy of multifactorial intensive treatment (IT) on renal outcomes in patients with type 2 diabetes and advanced‐stage diabetic kidney disease (DKD).</br>
Materials and Methods</br>
The Diabetic Nephropathy Remission and Regression Team Trial in Japan (DNETT‐Japan) is a multicenter, open‐label, randomized controlled trial with a 5‐year follow‐up period. We randomly assigned 164 patients with advanced‐stage diabetic kidney disease (urinary albumin‐to‐creatinine ratio ≥300 mg/g creatinine, serum creatinine level 1.2–2.5 mg/dL in men and 1.0–2.5 mg/dL in women) to receive either IT or conventional treatment. The primary composite outcome was end‐stage kidney failure, doubling of serum creatinine or death from any cause, which was assessed in the intention‐to‐treat population.</br>
Results</br>
The IT tended to reduce the risk of primary end‐points as compared with conventional treatment, but the difference between treatment groups did not reach the statistically significant level (hazard ratio 0.69, 95% confidence interval 0.43–1.11; P = 0.13). Meanwhile, the decrease in serum low‐density lipoprotein cholesterol level and the use of statin were significantly associated with the decrease in primary outcome (hazard ratio 1.14; 95% confidence interval 1.05–1.23, P < 0.001 and hazard ratio 0.53, 95% confidence interval 0.28–0.998, P < 0.05, respectively). The incidence of adverse events was not different between treatment groups.</br>
Conclusions</br>
The risk of kidney events tended to decrease by IT, although it was not statistically significant. Lipid control using statin was associated with a lower risk of adverse kidney events. Further follow‐up study might show the effect of IT in patients with advanced diabetic kidney disease.
en-copyright=
kn-copyright=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HanedaMasakazu
en-aut-sei=Haneda
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NinomiyaToshiharu
en-aut-sei=Ninomiya
en-aut-mei=Toshiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoyaDaisuke
en-aut-sei=Koya
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuzukiYoshiki
en-aut-sei=Suzuki
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SuzukiDaisuke
en-aut-sei=Suzuki
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IshidaHitoshi
en-aut-sei=Ishida
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AkaiHiroaki
en-aut-sei=Akai
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TominoYasuhiko
en-aut-sei=Tomino
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=UzuTakashi
en-aut-sei=Uzu
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NishimuraMotonobu
en-aut-sei=Nishimura
en-aut-mei=Motonobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MaedaShiro
en-aut-sei=Maeda
en-aut-mei=Shiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MiyamotoSatoshi
en-aut-sei=Miyamoto
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=the Diabetic Nephropathy Remission and Regression Team Trial in Japan (DNETT‐Japan) collaborative group
en-aut-sei=the Diabetic Nephropathy Remission and Regression Team Trial in Japan (DNETT‐Japan) collaborative group
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Division of Metabolism and Biosystemic Science, Department of Medicine, Asahikawa Medical University
kn-affil=

affil-num=3
en-affil=Department of Epidemiology and Public Health, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=4
en-affil=Department of Diabetology & Endocrinology, Kanazawa Medical University
kn-affil=

affil-num=5
en-affil=Health Administration Center, Niigata University
kn-affil=

affil-num=6
en-affil=Suzuki Diabetes Clinic
kn-affil=

affil-num=7
en-affil=Research Center for Health Care, Nagahama City Hospital
kn-affil=

affil-num=8
en-affil=Division of Metabolism and Diabetes, Tohoku Medical and Pharmaceutical University
kn-affil=

affil-num=9
en-affil=Division of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine
kn-affil=

affil-num=10
en-affil=Division of Nephrology, Department of Medicine, Nippon Life Hospital
kn-affil=

affil-num=11
en-affil=Department of Diabetes and Endocrinology, National Hospital Organization Chiba‐East National Hospital
kn-affil=

affil-num=12
en-affil=Department of Advanced Genomic and Laboratory Medicine, Graduate School of Medicine, University of the Ryukyus
kn-affil=

affil-num=13
en-affil=Okayama Diabetes and Neurology Clinic
kn-affil=

affil-num=14
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=15
en-affil=Okayama University
kn-affil=

affil-num=16
en-affil=
kn-affil=
en-keyword=Diabetic kidney disease
kn-keyword=Diabetic kidney disease
en-keyword=Diabetic nephropathy
kn-keyword=Diabetic nephropathy
en-keyword=Diabetic Nephropathy Remission and Regression Team Trial in Japan
kn-keyword=Diabetic Nephropathy Remission and Regression Team Trial in Japan
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=7
article-no=
start-page=466
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200709
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Deep Learning Could Diagnose Diabetic Nephropathy with Renal Pathological Immunofluorescent Images
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Artificial Intelligence (AI) imaging diagnosis is developing, making enormous steps forward in medical fields. Regarding diabetic nephropathy (DN), medical doctors diagnose them with clinical course, clinical laboratory data and renal pathology, mainly evaluate with light microscopy images rather than immunofluorescent images because there are no characteristic findings in immunofluorescent images for DN diagnosis. Here, we examined the possibility of whether AI could diagnose DN from immunofluorescent images. We collected renal immunofluorescent images from 885 renal biopsy patients in our hospital, and we created a dataset that contains six types of immunofluorescent images of IgG, IgA, IgM, C3, C1q and Fibrinogen for each patient. Using the dataset, 39 programs worked without errors (Area under the curve (AUC): 0.93). Five programs diagnosed DN completely with immunofluorescent images (AUC: 1.00). By analyzing with Local interpretable model-agnostic explanations (Lime), the AI focused on the peripheral lesion of DN glomeruli. On the other hand, the nephrologist diagnostic ratio (AUC: 0.75833) was slightly inferior to AI diagnosis. These findings suggest that DN could be diagnosed only by immunofluorescent images by deep learning. AI could diagnose DN and identify classified unknown parts with the immunofluorescent images that nephrologists usually do not use for DN diagnosis.
en-copyright=
kn-copyright=

en-aut-name=KitamuraShinji
en-aut-sei=Kitamura
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiKensaku
en-aut-sei=Takahashi
en-aut-mei=Kensaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SangYizhen
en-aut-sei=Sang
en-aut-mei=Yizhen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukushimaKazuhiko
en-aut-sei=Fukushima
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsujiKenji
en-aut-sei=Tsuji
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=immunofluorescent image
kn-keyword=immunofluorescent image
en-keyword=renal pathology
kn-keyword=renal pathology
en-keyword=artificial intelligence
kn-keyword=artificial intelligence
en-keyword=deep learning
kn-keyword=deep learning
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20181227
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=血管新生促進因子vasohibin-2欠損は, 糖尿病性腎症マウスモデルにおける糸球体変化を改善させる
kn-title=Deletion of pro-angiogenic factor vasohibin-2 ameliorates glomerular alterations in a mouse diabetic nephropathy model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MasudaKana
en-aut-sei=Masuda
en-aut-mei=Kana
kn-aut-name=益田加奈
kn-aut-sei=益田
kn-aut-mei=加奈
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20180323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=IgA腎症に対する扁桃摘出後ステロイドパルス療法時におけるステロイド糖尿病発症を検討したレトロスペクティブコホート研究
kn-title=A retrospective observational study of glucocorticoid-induced diabetes mellitus with IgA nephropathy treated with tonsillectomy plus methylprednisolone pulse therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MiyawakiYoshia
en-aut-sei=Miyawaki
en-aut-mei=Yoshia
kn-aut-name=宮脇義亜
kn-aut-sei=宮脇
kn-aut-mei=義亜
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=9
article-no=
start-page=e107934
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exacerbation of diabetic renal alterations in mice lacking vasohibin-1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Vasohibin-1 (VASH1) is a unique endogenous inhibitor of angiogenesis that is induced in endothelial cells by pro-angiogenic factors. We previously reported renoprotective effect of adenoviral delivery of VASH1 in diabetic nephropathy model, and herein investigated the potential protective role of endogenous VASH1 by using VASH1-deficient mice. Streptozotocin-induced type 1 diabetic VASH1 heterozygous knockout mice (VASH1(+/-)) or wild-type diabetic mice were sacrificed 16 weeks after inducing diabetes. In the diabetic VASH1(+/-) mice, albuminuria were significantly exacerbated compared with the diabetic wild-type littermates, in association with the dysregulated distribution of glomerular slit diaphragm related proteins, nephrin and ZO-1, glomerular basement membrane thickening and reduction of slit diaphragm density. Glomerular monocyte/macrophage infiltration and glomerular nuclear translocation of phosphorylated NF-κB p65 were significantly exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates, accompanied by the augmentation of VEGF-A, M1 macrophage-derived MCP-1 and phosphorylation of IκBα, and the decrease of angiopoietin-1/2 ratio and M2 macrophage-derived Arginase-1. The glomerular CD31(+) endothelial area was also increased in the diabetic VASH1(+/-) mice compared with the diabetic-wild type littermates. Furthermore, the renal and glomerular hypertrophy, glomerular accumulation of mesangial matrix and type IV collagen and activation of renal TGF-β1/Smad3 signaling, a key mediator of renal fibrosis, were exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates. In conditionally immortalized mouse podocytes cultured under high glucose condition, transfection of VASH1 small interfering RNA (siRNA) resulted in the reduction of nephrin, angiopoietin-1 and ZO-1, and the augmentation of VEGF-A compared with control siRNA. These results suggest that endogenous VASH1 may regulate the development of diabetic renal alterations, partly via direct effects on podocytes, and thus, a strategy to recover VASH1 might potentially lead to the development of a novel therapeutic approach for diabetic nephropathy.
en-copyright=
kn-copyright=

en-aut-name=HinamotoNorikazu
en-aut-sei=Hinamoto
en-aut-mei=Norikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaeshimaYohei
en-aut-sei=Maeshima
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamasakiHiroko
en-aut-sei=Yamasaki
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NasuTatsuyo
en-aut-sei=Nasu
en-aut-mei=Tatsuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaitoDaisuke
en-aut-sei=Saito
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WatataniHiroyuki
en-aut-sei=Watatani
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UjikeHaruyo
en-aut-sei=Ujike
en-aut-mei=Haruyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MasudaKana
en-aut-sei=Masuda
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ArataYuka
en-aut-sei=Arata
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SatoYasufumi
en-aut-sei=Sato
en-aut-mei=Yasufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=
kn-affil=

affil-num=12
en-affil=Department of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University
kn-affil=

affil-num=13
en-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=13
end-page=26
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=201601
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Innate immunity in diabetes and diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The innate immune system includes several classes of pattern recognition receptors (PRRs), including membrane-bound Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). These receptors detect pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) in the extracellular and intracellular space. Intracellular NLRs constitute inflammasomes, which activate and release caspase-1, IL-1β, and IL-18 thereby initiating an inflammatory response. Systemic and local low-grade inflammation and release of proinflammatory cytokines are implicated in the development and progression of diabetes mellitus and diabetic nephropathy. TLR2, TLR4, and the NLRP3 inflammasome can induce the production of various proinflammatory cytokines and are critically involved in inflammatory responses in pancreatic islets, and in adipose, liver and kidney tissues. This Review describes how innate immune system-driven inflammatory processes can lead to apoptosis, tissue fibrosis, and organ dysfunction resulting in insulin resistance, impaired insulin secretion, and renal failure. We propose that careful targeting of TLR2, TLR4, and NLRP3 signalling pathways could be beneficial for the treatment of diabetes mellitus and diabetic nephropathy.
en-copyright=
kn-copyright=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20161227
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=SGLT2の阻害は、1型糖尿病マウスにおける高血糖が誘発する酸化ストレスを抑制することにより、糖尿病性腎症を軽減する
kn-title=Inhibition of SGLT2 alleviates diabetic nephropathy by suppressing high glucose-induced oxidative stress in type 1 diabetic mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HatanakaTakashi
en-aut-sei=Hatanaka
en-aut-mei=Takashi
kn-aut-name=畑中崇志
kn-aut-sei=畑中
kn-aut-mei=崇志
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=3
article-no=
start-page=e92647
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140525
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pemt deficiency ameliorates endoplasmic reticulum stress in diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Phosphatidylethanolamine N-methyltransferase (Pemt) catalyzes the methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) mainly in the liver. Under an obese state, the upregulation of Pemt induces endoplasmic reticulum (ER) stress by increasing the PC/PE ratio in the liver. We targeted the Pemt gene in mice to explore the therapeutic impact of Pemt on the progression of diabetic nephropathy and diabetes, which was induced by the injection of streptozotocin (STZ). Although the blood glucose levels were similar in STZ-induced diabetic Pemt+/+ and Pemt−/−mice, the glomerular hypertrophy and albuminuria in Pemt−/− mice were significantly reduced. Pemt deficiency reduced the intraglomerular F4/80-positive macrophages, hydroethidine fluorescence, tubulointerstitial fibrosis and tubular atrophy. The expression of glucose-regulated protein-78 (GRP78) was enriched in the renal tubular cells in STZ-induced diabetic mice, and this was ameliorated by Pemt deficiency. In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt). The number of apoptotic cells in the renal tubules was significantly reduced in Pemt−/− diabetic mice, and shRNA-Pemt upregulated the phosphorylation of Akt and decreased the cleavage of caspase 3 and 7 in mProx24 cells. Taken together, these findings indicate that the inhibition of Pemt activity ameliorates the ER stress associated with diabetic nephropathy in a model of type 1 diabetes and corrects the functions of the three major pathways downstream of ER stress, i.e. oxidative stress, inflammation and apoptosis.
en-copyright=
kn-copyright=

en-aut-name=WatanabeMayu
en-aut-sei=Watanabe
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MurakamiKazutoshi
en-aut-sei=Murakami
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InoueKentaro
en-aut-sei=Inoue
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TeramiTakahiro
en-aut-sei=Terami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HiguchiChigusa
en-aut-sei=Higuchi
en-aut-mei=Chigusa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=WatanabeEijiro
en-aut-sei=Watanabe
en-aut-mei=Eijiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Diabetic Nephropathy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Diabetic Nephropathy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=11
en-affil=
kn-affil=Dainippon Sumitomo Pharma

affil-num=12
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=13
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=1
article-no=
start-page=e85594
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140122
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Nuclear Hormone Receptor Expression in Mouse Kidney and Renal Cell Lines
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nuclear hormone receptors (NHRs) are transcription factors that regulate carbohydrate and lipid metabolism, immune responses, and inflammation. Although several NHRs, including peroxisome proliferator-activated receptor-γ (PPARγ) and PPARα, demonstrate a renoprotective effect in the context of diabetic nephropathy (DN), the expression and role of other NHRs in the kidney are still unrecognized. To investigate potential roles of NHRs in the biology of the kidney, we used quantitative real-time polymerase chain reaction to profile the expression of all 49 members of the mouse NHR superfamily in mouse kidney tissue (C57BL/6 and db/m), and cell lines of mesangial (MES13), podocyte (MPC), proximal tubular epithelial (mProx24) and collecting duct (mIMCD3) origins in both normal and high-glucose conditions. In C57BL/6 mouse kidney cells, hepatocyte nuclear factor 4α, chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) and COUP-TFIII were highly expressed. During hyperglycemia, the expression of the NHR 4A subgroup including neuron-derived clone 77 (Nur77), nuclear receptor-related factor 1, and neuron-derived orphan receptor 1 significantly increased in diabetic C57BL/6 and db/db mice. In renal cell lines, PPARδ was highly expressed in mesangial and proximal tubular epithelial cells, while COUP-TFs were highly expressed in podocytes, proximal tubular epithelial cells, and collecting duct cells. High-glucose conditions increased the expression of Nur77 in mesangial and collecting duct cells, and liver x receptor α in podocytes. These data demonstrate NHR expression in mouse kidney cells and cultured renal cell lines and suggest potential therapeutic targets in the kidney for the treatment of DN.
en-copyright=
kn-copyright=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TeramiNaoto
en-aut-sei=Terami
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HatanakaTakashi
en-aut-sei=Hatanaka
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TachibanaHiromi
en-aut-sei=Tachibana
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Sato HoriguchiChikage
en-aut-sei=Sato Horiguchi
en-aut-mei=Chikage
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishiiNaoko
en-aut-sei=Nishii
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Diabetic Nephropathy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Diabetic Nephropathy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=
article-no=
start-page=21721
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160217
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Insufficiency of phosphatidylethanolamine N-methyltransferase is risk for lean non-alcoholic steatohepatitis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=　Although obesity is undoubtedly major risk for non-alcoholic steatohepatitis (NASH), the presence of lean NASH patients with normal body mass index has been recognized. Here, we report that the insufficiency of phosphatidylethanolamine N-methyltransferase (PEMT) is a risk for the lean NASH. The Pemt−/− mice fed high fat-high sucrose (HFHS) diet were protected from diet-induced obesity and diabetes, while they demonstrated prominent steatohepatitis and developed multiple liver tumors. Pemt exerted inhibitory effects on p53-driven transcription by forming the complex with clathrin heavy chain and p53, and Pemt−/− mice fed HFHS diet demonstrated prominent apoptosis of hepatocytes. Furthermore, hypermethylation and suppressed mRNA expression of F-box protein 31 and hepatocyte nuclear factor 4α resulted in the prominent activation of cyclin D1. PEMT mRNA expression in liver tissues of NASH patients was significantly lower than those with simple steatosis and we postulated the distinct clinical entity of lean NASH with insufficiency of PEMT activities.
en-copyright=
kn-copyright=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuyamaMakoto
en-aut-sei=Matsuyama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamaguchiSatoshi
en-aut-sei=Yamaguchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MurakamiKazutoshi
en-aut-sei=Murakami
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=WadaNozomu
en-aut-sei=Wada
en-aut-mei=Nozomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YasunakaTetsuya
en-aut-sei=Yasunaka
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IkedaFusao
en-aut-sei=Ikeda
en-aut-mei=Fusao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakakiAkinobu
en-aut-sei=Takaki
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=WatanabeEijiro
en-aut-sei=Watanabe
en-aut-mei=Eijiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Shigei Medical Research Institute

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Diabetic Nephropathy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=11
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=12
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=13
en-affil=
kn-affil=Dainippon Sumitomo Pharma

affil-num=14
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=2
article-no=
start-page=111
end-page=115
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Peritoneal dialysis update
kn-title=腹膜透析Update
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=杉山斉
kn-aut-sei=杉山
kn-aut-mei=斉
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科
en-keyword=持続携行式腹膜透析（CAPD）
kn-keyword=持続携行式腹膜透析（CAPD）
en-keyword=自動腹膜透析（APD）
kn-keyword=自動腹膜透析（APD）
en-keyword=SMAP法
kn-keyword=SMAP法
en-keyword=尿素Kt/V
kn-keyword=尿素Kt/V
en-keyword=腹膜平衡試験（peritoneal equilibration test:PET）
kn-keyword=腹膜平衡試験（peritoneal equilibration test:PET）
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Pemt欠損は糖尿病性腎症における小胞体ストレスを緩和する
kn-title=Pemt Deficiency Ameliorates Endoplasmic Reticulum Stress in Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=WatanabeMayu
en-aut-sei=Watanabe
en-aut-mei=Mayu
kn-aut-name=渡邉真由
kn-aut-sei=渡邉
kn-aut-mei=真由
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=SGLT2阻害薬ダパグリフロジン長期投与によるdb/dbマウスの糖代謝および糖尿病性腎症の改善効果
kn-title=Long-Term Treatment with the Sodium Glucose Cotransporter 2 Inhibitor, Dapagliflozin, Ameliorates Glucose Homeostasis and Diabetic Nephropathy in db/db Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TeramiNaoto
en-aut-sei=Terami
en-aut-mei=Naoto
kn-aut-name=寺見直人
kn-aut-sei=寺見
kn-aut-mei=直人
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院
END

start-ver=1.4
cd-journal=joma
no-vol=69
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=15
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ONO-1301, a Sustained-Release Prostacyclin Analog, Ameliorates the Renal Alterations in a Mouse Type 2 Diabetes Model Possibly Through Its Protective Effects on Mesangial Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diabetic nephropathy is the most common pathological disorder predisposing patients to end-stage renal disease. Considering the increasing prevalence of type 2 diabetes mellitus worldwide, novel therapeutic approaches are urgently needed. ONO-1301 is a novel sustained-release prostacyclin analog that inhibits thromboxane A2 synthase. Here we examined the therapeutic effects of the intermittent administration of slow-release ONO-1301 (SR-ONO) on diabetic nephropathy in obese type 2 diabetes mice, as well as its direct effects on mesangial cells. The subcutaneous injection of SR-ONO (3mg/kg) every 3 wks did not affect the obesity or hyperglycemia in the db/db obese mice used as a model of type 2 diabetes, but it significantly ameliorated their albuminuria, glomerular hypertrophy, glomerular accumulation of type IV collagen, and monocyte/macrophage infiltration, and also the increase of TGF-β1, α-smooth muscle actin (α-SMA) and MCP-1 compared to vehicle treatment. In cultured mouse mesangial cells, ONO-1301 concentration-dependently suppressed the increases in TGF-β, type IV collagen, α-SMA, MCP-1 and fibronectin induced by high ambient glucose, at least partly through prostacyclin (PGI2) receptor-mediated signaling. Taken together, these results suggest the potential therapeutic efficacy of the intermittent administration of SR-ONO against type 2 diabetic nephropathy, possibly through protective effects on mesangial cells.
en-copyright=
kn-copyright=

en-aut-name=WatataniHiroyuki
en-aut-sei=Watatani
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamasakiHiroko
en-aut-sei=Yamasaki
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaeshimaYohei
en-aut-sei=Maeshima
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NasuTatsuyo
en-aut-sei=Nasu
en-aut-mei=Tatsuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HinamotoNorikazu
en-aut-sei=Hinamoto
en-aut-mei=Norikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UjikeHaruyo
en-aut-sei=Ujike
en-aut-mei=Haruyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakaiYoshiki
en-aut-sei=Sakai
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=ONO Pharmaceutical Co., Ltd.

affil-num=9
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=prostacyclin
kn-keyword=prostacyclin
en-keyword=ONO-1301
kn-keyword=ONO-1301
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=TGF-β1
kn-keyword=TGF-β1
en-keyword=diabetes mellitus
kn-keyword=diabetes mellitus
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=
article-no=
start-page=233
end-page=240
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20131022
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Urinary angiotensinogen is a marker for tubular injuries in patients with type 2 diabetes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: Urinary angiotensinogen has been reported as a marker for the activation of intrarenal renin–angiotensin system (RAS) in various kidney diseases. To investigate the importance of urinary angiotensinogen in diabetic nephropathy, we compared the urinary levels of angiotensinogen, albumin, and α1-microglobulin.
Materials and methods: Japanese patients with type 2 diabetes at various stages of nephropathy (n=85) were enrolled, and we measured albumin/creatinine ratio (ACR) and urinary excretion of angiotensinogen and α1-microglobulin. We also compared the clinical data of the patients treated with or without angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors (RAS inhibitors [+], n=51; RAS inhibitors [−], n=34).
Results: Urinary angiotensinogen levels positively correlated with ACR (r =0.367, P=3.84×10-4) and urinary α1-microglobulin (r=0.734, P=1.32 × 10-15), while they negatively correlated with estimated glomerular filtration ratio (eGFR) (r=−0.350, P=1.02 × 10-3) and high-density lipoprotein cholesterol (r=−0.216, P=0.049). Multiple regression analysis was carried out to predict urinary angiotensinogen levels by employing eGFR, ACR, and urinary α1-microglobulin as independent variables; only urinary α1-microglobulin entered the regression equation at a significant level. Although ACR was higher in the RAS inhibitors (+) group, urinary α1-microglobulin and angiotensinogen did not show significant increase in the RAS inhibitors (+) group.
Conclusion: Urinary angiotensinogen is well correlated with urinary α1-microglobulin and reflected the tubular injuries which may be associated with the intrarenal RAS activation in patients with type 2 diabetes.
en-copyright=
kn-copyright=

en-aut-name=TeramiTakahiro
en-aut-sei=Terami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InoueKentaro
en-aut-sei=Inoue
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurakamiKazutoshi
en-aut-sei=Murakami
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Medicine and Clinical Science,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=urinary biomarkers
kn-keyword=urinary biomarkers
en-keyword=renin–angiotensin system
kn-keyword=renin–angiotensin system
en-keyword=angiotensinogen
kn-keyword=angiotensinogen
en-keyword=α1-microglobulin
kn-keyword=α1-microglobulin
en-keyword=albumin
kn-keyword=albumin
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=10
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20131015
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Urinary Fetuin-A Is a Novel Marker for Diabetic Nephropathy in Type 2 Diabetes Identified by Lectin Microarray
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We analyzed the urine samples of patients with type 2 diabetes at various stages of diabetic nephropathy by lectin microarray to identify a biomarker to predict the progression of diabetic nephropathy. Japanese patients with type 2 diabetes at various stages of nephropathy were enrolled and we performed lectin microarray analyses (n = 17) and measured urinary excretion of fetuin-A (n = 85). The increased signals of urine samples were observed in Sia alpha 2-6Gal/GalNAc-binding lectins (SNA, SSA, TJA-I) during the progression of diabetic nephropathy. We next isolated sialylated glycoproteins by using SSA-lectin affinity chromatography and identified fetuin-A by liquid chromatography-tandem mass spectrometer. Urinary excretion of fetuin-A significantly increased during the progression of albuminuria (A1, 0.40 +/- 0.43; A2, 0.60 +/- 0.53; A3 1.57 +/- 1.13 ng/gCr; p = 7.29x10(-8)) and of GFR stages (G1, 0.39 +/- 0.39; G2, 0.49 +/- 0.45; G3, 1.25 +/- 1.18; G4, 1.34 +/- 0.80 ng/gCr; p = 3.89x10(-4)). Multivariate logistic regression analysis was employed to assess fetuin-A as a risk for diabetic nephropathy with microalbuminuria or GFR<60 mL/min. Fetuin-A is demonstrated as a risk factor for both microalbuminuria and reduction of GFR in diabetic nephropathy with the odds ratio of 4.721 (1.881-11.844) and 3.739 (1.785-7.841), respectively. Collectively, the glycan profiling analysis is useful method to identify the urine biomarkers and fetuin-A is a candidate to predict the progression of diabetic nephropathy.
en-copyright=
kn-copyright=

en-aut-name=InoueKentaro
en-aut-sei=Inoue
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MurakamiKazutoshi
en-aut-sei=Murakami
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TeramiTakahiro
en-aut-sei=Terami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ToneAtsuhito
en-aut-sei=Tone
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IsedaIzumi
en-aut-sei=Iseda
en-aut-mei=Izumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HidaKazuyuki
en-aut-sei=Hida
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamadaMasao
en-aut-sei=Yamada
en-aut-mei=Masao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OgawaTomohisa
en-aut-sei=Ogawa
en-aut-mei=Tomohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=10
en-affil=
kn-affil=Natl Hosp Org, Okayama Med Ctr, Dept Diabet & Metab

affil-num=11
en-affil=
kn-affil=Natl Hosp Org, Okayama Med Ctr, Dept Diabet & Metab

affil-num=12
en-affil=
kn-affil=Natl Hosp Org, Okayama Med Ctr, Dept Diabet & Metab

affil-num=13
en-affil=
kn-affil=GlycoTechnica Ltd

affil-num=14
en-affil=
kn-affil=GP BioSci Co Ltd

affil-num=15
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=レクチンマイクロアレイ解析により同定した糖尿病性腎症の新規尿中マーカーFetuin-Aの検討
kn-title=Urinary Fetuin-A Is a Novel Marker for Diabetic Nephropathy in Type 2 Diabetes Identified by Lection Microarray
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=InoueKentaro
en-aut-sei=Inoue
en-aut-mei=Kentaro
kn-aut-name=井上謙太郎
kn-aut-sei=井上
kn-aut-mei=謙太郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=4
article-no=
start-page=235
end-page=241
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Factors Associated with Remission and/or Regression of Microalbuminuria in Type 2 Diabetes Mellitus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of this study was to clarify the factors associated with the remission and/or regression of microalbuminuria in Japanese patients with type 2 diabetes mellitus. We retrospectively analyzed the data of 130 patients with type 2 diabetes mellitus with microalbuminuria for 2-6 years (3.39±1.31 years). Remission was defined as improving from microalbuminuria to normoalbuminuria using the albumin/creatinine ratio (ACR), and regression of microalbuminuria was defined as a decrease in ACR of 50% or more from baseline. Progression of microalbuminuria was defined as progressing from microalbuminuria to overt proteinuria during the follow-up period. Among 130 patients with type 2 diabetes mellitus with microalbuminuria, 57 and 13 patients were defined as having remission and regression, respectively, while 26 patients progressed to overt proteinuria. Sex (female), higher HDL cholesterol and lower HbA1c were determinant factors associated with remission/regression of microalbuminuria by logistic regression analysis. Lower systolic blood pressure (SBP) was also correlated with remission/regression, but not at a significant level. These results suggest that proper control of blood glucose, BP and lipid profiles may be associated with remission and/or regression of type 2 diabetes mellitus with microalbuminuria in clinical practice.
en-copyright=
kn-copyright=

en-aut-name=OnoTetsuichiro
en-aut-sei=Ono
en-aut-mei=Tetsuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ObikaMikako
en-aut-sei=Obika
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyatakeNobuyuki
en-aut-sei=Miyatake
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KoderaRyo
en-aut-sei=Kodera
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HirotaDaisyo
en-aut-sei=Hirota
en-aut-mei=Daisyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KataokaHitomi
en-aut-sei=Kataoka
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Center for Graduate Medical Education, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Hygiene, Faculty of Medicine, Kagawa University

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Diabetic Nephropathy, Okayama University

affil-num=10
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=microalbuminuria
kn-keyword=microalbuminuria
en-keyword=type 2 diabetes mellitus
kn-keyword=type 2 diabetes mellitus
en-keyword=remission
kn-keyword=remission
en-keyword=regression
kn-keyword=regression
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=メタロチオネインの欠損はストレプトゾトシン誘発糖尿病マウスの糖尿病性腎症を増悪する
kn-title=Metallothionein deficiency exacerbates diabetic nephropathy in streptozotocin-induced diabetic mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TachibanaHiromi
en-aut-sei=Tachibana
en-aut-mei=Hiromi
kn-aut-name=橘洋美
kn-aut-sei=橘
kn-aut-mei=洋美
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Cholecystokinin plays a novel protective role in diabetic kidney through anti-inflammatory actions on macrophages
kn-title=糖尿病の腎臓においてcholecystokininはマクロファージに対する抗炎症作用を介した新規の保護効果を発揮する
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MiyamotoSatoshi
en-aut-sei=Miyamoto
en-aut-mei=Satoshi
kn-aut-name=宮本聡
kn-aut-sei=宮本
kn-aut-mei=聡
aut-affil-num=1
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=四方賢一
kn-aut-sei=四方
kn-aut-mei=賢一
aut-affil-num=2
ORCID=

en-aut-name=MiyasakaKyoko
en-aut-sei=Miyasaka
en-aut-mei=Kyoko
kn-aut-name=宮坂京子
kn-aut-sei=宮坂
kn-aut-mei=京子
aut-affil-num=3
ORCID=

en-aut-name=OkadaShinichi
en-aut-sei=Okada
en-aut-mei=Shinichi
kn-aut-name=岡田震一
kn-aut-sei=岡田
kn-aut-mei=震一
aut-affil-num=4
ORCID=

en-aut-name=SasakiMotofumi
en-aut-sei=Sasaki
en-aut-mei=Motofumi
kn-aut-name=佐々木基史
kn-aut-sei=佐々木
kn-aut-mei=基史
aut-affil-num=5
ORCID=

en-aut-name=KoderaRyo
en-aut-sei=Kodera
en-aut-mei=Ryo
kn-aut-name=小寺亮
kn-aut-sei=小寺
kn-aut-mei=亮
aut-affil-num=6
ORCID=

en-aut-name=HirotaDaisho
en-aut-sei=Hirota
en-aut-mei=Daisho
kn-aut-name=廣田大昌
kn-aut-sei=廣田
kn-aut-mei=大昌
aut-affil-num=7
ORCID=

en-aut-name=KajitaniNobuo
en-aut-sei=Kajitani
en-aut-mei=Nobuo
kn-aut-name=梶谷展生
kn-aut-sei=梶谷
kn-aut-mei=展生
aut-affil-num=8
ORCID=

en-aut-name=TakatsukaTetsuharu
en-aut-sei=Takatsuka
en-aut-mei=Tetsuharu
kn-aut-name=高塚哲全
kn-aut-sei=高塚
kn-aut-mei=哲全
aut-affil-num=9
ORCID=

en-aut-name=Kataoka UsuiHitomi
en-aut-sei=Kataoka Usui
en-aut-mei=Hitomi
kn-aut-name=片岡仁美
kn-aut-sei=片岡
kn-aut-mei=仁美
aut-affil-num=10
ORCID=

en-aut-name=NishishitaShingo
en-aut-sei=Nishishita
en-aut-mei=Shingo
kn-aut-name=西下伸吾
kn-aut-sei=西下
kn-aut-mei=伸吾
aut-affil-num=11
ORCID=

en-aut-name=Horiguchi SatoChikage
en-aut-sei=Horiguchi Sato
en-aut-mei=Chikage
kn-aut-name=堀口千景
kn-aut-sei=堀口
kn-aut-mei=千景
aut-affil-num=12
ORCID=

en-aut-name=FunakoshiAkihiro
en-aut-sei=Funakoshi
en-aut-mei=Akihiro
kn-aut-name=船越顕博
kn-aut-sei=船越
kn-aut-mei=顕博
aut-affil-num=13
ORCID=

en-aut-name=NishimoriHisakazu
en-aut-sei=Nishimori
en-aut-mei=Hisakazu
kn-aut-name=西森久和
kn-aut-sei=西森
kn-aut-mei=久和
aut-affil-num=14
ORCID=

en-aut-name=UchidaHaruhito Adam
en-aut-sei=Uchida
en-aut-mei=Haruhito Adam
kn-aut-name=内田治仁
kn-aut-sei=内田
kn-aut-mei=治仁
aut-affil-num=15
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=小川大輔
kn-aut-sei=小川
kn-aut-mei=大輔
aut-affil-num=16
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=17
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=東京家政大学　栄養学科

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=10
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=11
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=12
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=13
en-affil=
kn-affil=国立病院機構九州がんセンター　消化器肝胆膵内科

affil-num=14
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学

affil-num=15
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=16
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=17
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=cholecystokinin
kn-keyword=cholecystokinin
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=抗炎症作用
kn-keyword=抗炎症作用
en-keyword=腎保護効果
kn-keyword=腎保護効果
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130122
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Serum galectin-9 levels are elevated in the patients with type 2 diabetes and chronic kidney disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Galectin-9 (Gal-9) induces apoptosis in activated T helper 1 (T(H)1) cells as a ligand for T cell immunoglobulin mucin-3 (Tim-3). Gal-9 also inhibits the G1 phase cell cycle arrest and hypertrophy in db/db mice, the hallmark of early diabetic nephropathy, by reversing the high glucose-induced up-regulation of cyclin dependent kinase inhibitors such as p27(Kip1) and p21(Cip1). 

Methods: We investigated the serum levels of Gal-9 in the patients with type 2 diabetes and various stages of chronic kidney disease (CKD) (n = 182). 

Results: Serum Gal-9 levels in the patients with type 2 diabetes were 131.9 +/- 105.4 pg/ml and Log(10)Gal-9 levels significantly and positively correlated with age (r = 0.227, p = 0.002), creatinine (r = 0.175, p = 0.018), urea nitrogen (r = 0.162, p = 0.028) and osmotic pressure (r = 0.187, p = 0.014) and negatively correlated with estimated glomerular filtration rate (eGFR) (r = -0.188, p = 0.011). Log(10)Gal-9 levels increased along with the progression of GFR categories of G1 to G4, and they were statistically significant by Jonckheere-Terpstra test (p = 0.012). Log(10)Gal-9 levels remained similar levels in albuminuria stages of A1 to A3. 

Conclusion: The elevation of serum Gal-9 in the patients with type 2 diabetes is closely linked to GFR and they may be related to the alteration of the immune response and inflammation of the patients with type 2 diabetes and CKD.
en-copyright=
kn-copyright=

en-aut-name=KuroseYuko
en-aut-sei=Kurose
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KanzakiMotoko
en-aut-sei=Kanzaki
en-aut-mei=Motoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MurakamiKazutoshi
en-aut-sei=Murakami
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=InoueKentaro
en-aut-sei=Inoue
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TeramiTakahiro
en-aut-sei=Terami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WatanabeMayu
en-aut-sei=Watanabe
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HiguchiChigusa
en-aut-sei=Higuchi
en-aut-mei=Chigusa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MiyatakeNobuyuki
en-aut-sei=Miyatake
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=11
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=12
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=13
en-affil=
kn-affil=Kagawa Univ, Fac Med, Dept Hyg

affil-num=14
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci
en-keyword=Type 2 diabetes
kn-keyword=Type 2 diabetes
en-keyword=Glomerular filtration
kn-keyword=Glomerular filtration
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Kidney disease
kn-keyword=Kidney disease
en-keyword=Nephropathy
kn-keyword=Nephropathy
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=5
article-no=
start-page=739
end-page=748
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201210
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phenotypic change of macrophages in the progression of diabetic nephropathy; sialoadhesin-positive activated macrophages are increased in diabetic kidney
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Inflammatory process is involved in pathogenesis of diabetic nephropathy, although the activation and phenotypic change of macrophages in diabetic kidney has remained unclear. Sialoadhesin is a macrophage adhesion molecule containing 17 extracellular immunoglobulin-like domains, and is an I-type lectin which binds to sialic acid ligands expressed on hematopoietic cells. The aim of this study is to clarify the activation and phenotypic change of macrophages in the progression of diabetic nephropathy. 

We examined the expression of surface markers for pan-macrophages, resident macrophages, sialoadhesin, major histocompatibility complex class II and alpha-smooth muscle actin in the glomeruli of diabetic rats using immunohistochemistry at 0, 1, 4, 12, and 24 weeks after induction of diabetes by streptozotocin. Expression of type IV collagen and the change of mesangial matrix area were also measured. The mechanism for up-regulated expression of sialoadhesin on macrophages was evaluated in vitro. 

The number of macrophages was increased in diabetic glomeruli at 1 month after induction of diabetes and the increased number was maintained until 6 months. On the other hand, sialoadhesin-positive macrophages were increased during the late stage of diabetes concomitantly with the increase of alpha-smooth muscle actin-positive mesangial cells, mesangial matrix area and type IV collagen. Gene expression of sialoadhesin was induced by stimulation with interleukin (IL)-1 beta and tumor necrosis factor-alpha but not with IL-4, transforming growth factor-beta and high glucose in cultured human macrophages. 

The present findings suggest that sialoadhesin-positive macrophages may contribute to the progression of diabetic nephropathy.
en-copyright=
kn-copyright=

en-aut-name=NagaseRyo
en-aut-sei=Nagase
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KajitaniNobuo
en-aut-sei=Kajitani
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KoderaRyo
en-aut-sei=Kodera
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkadaShinichi
en-aut-sei=Okada
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KidoYuichi
en-aut-sei=Kido
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=7
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糖尿病性腎症の進展におけるマクロファージのフェノタイプ変化；シアロアドヘジン陽性活性化マクロファージは糖尿病性腎症で増加する
kn-title=Phenotypic change of macrophages in the progression of diabetic nephropathy; sialoadhesin-positive activated macrophages are increased in diabetic kidney
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NagaseRyo
en-aut-sei=Nagase
en-aut-mei=Ryo
kn-aut-name=永瀬亮
kn-aut-sei=永瀬
kn-aut-mei=亮
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=125
cd-vols=
no-issue=2
article-no=
start-page=97
end-page=102
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Anti‒high mobility group box-1 antibody therapy for traumatic brain injury
kn-title=外傷性脳傷害に対する抗HMGB-1抗体治療
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OkumaYu
en-aut-sei=Okuma
en-aut-mei=Yu
kn-aut-name=大熊佑
kn-aut-sei=大熊
kn-aut-mei=佑
aut-affil-num=1
ORCID=

en-aut-name=LiuKeyue
en-aut-sei=Liu
en-aut-mei=Keyue
kn-aut-name=劉克約
kn-aut-sei=劉
kn-aut-mei=克約
aut-affil-num=2
ORCID=

en-aut-name=WakeHidenori
en-aut-sei=Wake
en-aut-mei=Hidenori
kn-aut-name=和気秀徳
kn-aut-sei=和気
kn-aut-mei=秀徳
aut-affil-num=3
ORCID=

en-aut-name=HarumaJun
en-aut-sei=Haruma
en-aut-mei=Jun
kn-aut-name=春間純
kn-aut-sei=春間
kn-aut-mei=純
aut-affil-num=4
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=吉野正
kn-aut-sei=吉野
kn-aut-mei=正
aut-affil-num=5
ORCID=

en-aut-name=OhtsukaAiji
en-aut-sei=Ohtsuka
en-aut-mei=Aiji
kn-aut-name=大塚愛二
kn-aut-sei=大塚
kn-aut-mei=愛二
aut-affil-num=6
ORCID=

en-aut-name=TakahashiHideo
en-aut-sei=Takahashi
en-aut-mei=Hideo
kn-aut-name=高橋英夫
kn-aut-sei=高橋
kn-aut-mei=英夫
aut-affil-num=7
ORCID=

en-aut-name=MoriShuji
en-aut-sei=Mori
en-aut-mei=Shuji
kn-aut-name=森秀治
kn-aut-sei=森
kn-aut-mei=秀治
aut-affil-num=8
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=西堀正洋
kn-aut-sei=西堀
kn-aut-mei=正洋
aut-affil-num=9
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=伊達勲
kn-aut-sei=伊達
kn-aut-mei=勲
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 脳神経外科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 薬理学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 薬理学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 脳神経外科学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理）

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 人体構成学

affil-num=7
en-affil=
kn-affil=近畿大学医学部 薬理学

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 就実大学薬学部

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科薬理学

affil-num=10
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 脳神経外科学
en-keyword=HMGB-1
kn-keyword=HMGB-1
en-keyword=traumatic brain injury （頭部外傷）
kn-keyword=traumatic brain injury （頭部外傷）
en-keyword=secondary injury （二次的損傷）
kn-keyword=secondary injury （二次的損傷）
en-keyword=blood brain barrier （血液脳関門）
kn-keyword=blood brain barrier （血液脳関門）
END

start-ver=1.4
cd-journal=joma
no-vol=67
cd-vols=
no-issue=3
article-no=
start-page=129
end-page=134
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cell Cycle Abnormality in Metabolic Syndrome and Nuclear Receptors as an Emerging Therapeutic Target
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In recent years, many researchers have emphasized the importance of metabolic syndrome based on its increasing prevalence and its adverse prognosis due to associated chronic vascular complications. Upstream of a cluster of metabolic and vascular disorders is the accumulation of visceral adipose tissue, which plays a central role in the pathophysiology. In the accumulation of adipose tissues, cell cycle regulation is tightly linked to cellular processes such as proliferation, hypertrophy and apoptosis. In addition, various cell cycle abnormalities have also been observed in other tissues, such as kidneys and the cardiovascular system, and they are critically involved in the progression of disease. Here, we discuss cell cycle abnormalities in metabolic syndrome in various tissues. Furthermore, we describe the role of nuclear receptors in cell growth and survival, and glucose and lipid metabolism in the whole body. Therapeutic strategies for modulating various cell cycles in metabolic disorders by targeting nuclear receptors may overcome obesity and its chronic vascular complications in the future.
en-copyright=
kn-copyright=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=nuclear receptor
kn-keyword=nuclear receptor
en-keyword=cell cycle
kn-keyword=cell cycle
en-keyword=metabolic syndrome
kn-keyword=metabolic syndrome
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
END

start-ver=1.4
cd-journal=joma
no-vol=61
cd-vols=
no-issue=11
article-no=
start-page=2823
end-page=2832
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201211
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vaspin Is an Adipokine Ameliorating ER Stress in Obesity as a Ligand for Cell-Surface GRP78/MTJ-1 Complex
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It is unknown whether adipokines derived from adipose tissues modulate endoplasmic reticulum (ER) stress induced in obesity. Here, we show that visceral adipose tissue-derived serine protease inhibitor (vaspin) binds to cell-surface 78-kDa glucose-regulated protein (GRP78), which is recruited from ER to plasma membrane under ER stress. Vaspin transgenic mice were protected from diet-induced obesity, glucose intolerance, and hepatic steatosis, while vaspin-deficient mice developed glucose intolerance associated with upregulation of ER stress markers. With tandem affinity tag purification using HepG2 cells, we identified GRP78 as an interacting molecule. The complex formation of vaspin, GRP78, and murine tumor cell DnaJ-like protein 1 (MTJ-1) (DnaJ homolog, subfamily C, member 1) on plasma membrane was confirmed by cell-surface labeling with biotin and immunoprecipitation in liver tissues and H-4-II-E-C3 cells. The addition of recombinant human vaspin in the cultured H-4-II-E-C3 cells also increased the phosphorylation of Akt and AMP-activated protein kinase (AMPK) in a dose-dependent manner, and anti-GRP78 antibodies completely abrogated the vaspin-induced upregulation of pAkt and pAMPK Vaspin is a novel ligand for cell-surface GRP78/MTJ-1 complex, and its subsequent signals exert beneficial effects on ER stress-induced metabolic dysfunctions. Diabetes 61:2823-2832, 2012
en-copyright=
kn-copyright=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IsedaIzumi
en-aut-sei=Iseda
en-aut-mei=Izumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HigashioKanji
en-aut-sei=Higashio
en-aut-mei=Kanji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MurakamiKazutoshi
en-aut-sei=Murakami
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KanzakiMotoko
en-aut-sei=Kanzaki
en-aut-mei=Motoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=InoueKentaro
en-aut-sei=Inoue
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TeramiTakahiro
en-aut-sei=Terami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HidaKazuyuki
en-aut-sei=Hida
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HoriguchiChikage Sato
en-aut-sei=Horiguchi
en-aut-mei=Chikage Sato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MatsukiYasushi
en-aut-sei=Matsuki
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=HiramatsuRyuji
en-aut-sei=Hiramatsu
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=YagitaHideo
en-aut-sei=Yagita
en-aut-mei=Hideo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=KakutaShigeru
en-aut-sei=Kakuta
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=IwakuraYoichiro
en-aut-sei=Iwakura
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Metabolome Pharmaceut Inc

affil-num=6
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=7
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=9
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=10
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=11
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci, Okayama

affil-num=12
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=13
en-affil=
kn-affil=Okayama Univ, Dept Diabet Nephropathy, Grad Sch Med Dent & Pharmaceut Sci

affil-num=14
en-affil=
kn-affil=Okayama Univ, Dept Diabet Nephropathy, Grad Sch Med Dent & Pharmaceut Sci

affil-num=15
en-affil=
kn-affil=Dainippon Sumitomo Pharma, Genom Sci Labs

affil-num=16
en-affil=
kn-affil=Dainippon Sumitomo Pharma, Genom Sci Labs

affil-num=17
en-affil=
kn-affil=Juntendo Univ, Sch Med, Dept Immunol

affil-num=18
en-affil=
kn-affil=Univ Tokyo, Inst Med Sci, Ctr Expt Med & Syst Biol

affil-num=19
en-affil=
kn-affil=Univ Tokyo, Inst Med Sci, Ctr Expt Med & Syst Biol

affil-num=20
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci
END

start-ver=1.4
cd-journal=joma
no-vol=125
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=3
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Activation of peroxisome proliferator-activated receptor &delta; inhibits streptozotocin-induced diabetic nephropathy through anti-inflammatory mechanisms in mice
kn-title=ペルオキシゾーム増殖因子活性化受容体&delta;の活性化はストレプトゾトシン誘発糖尿病マウスにおいて抗炎症効果により糖尿病性腎症の進展を抑制する
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MatsushitaYuichi
en-aut-sei=Matsushita
en-aut-mei=Yuichi
kn-aut-name=松下裕一
kn-aut-sei=松下
kn-aut-mei=裕一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=核内受容体
kn-keyword=核内受容体
en-keyword=PPAR&delta;
kn-keyword=PPAR&delta;
en-keyword=MCP-1
kn-keyword=MCP-1
en-keyword=Bcl-6
kn-keyword=Bcl-6
END

start-ver=1.4
cd-journal=joma
no-vol=124
cd-vols=
no-issue=2
article-no=
start-page=97
end-page=100
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=RXR antagonism induces G0/G1 cell cycle arrest and ameliorates obesity by up-regulating p53-p21<sup>Cip1</sup> pathway in adipocytes
kn-title=RXR阻害によるp53-p21<sup>Cip1</sup>経路の活性化およびG0/G1細胞周期停止を介した抗肥満作用
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=中司敦子
kn-aut-sei=中司
kn-aut-mei=敦子
aut-affil-num=1
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=和田淳
kn-aut-sei=和田
kn-aut-mei=淳
aut-affil-num=2
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=RXR
kn-keyword=RXR
en-keyword=cell cycle
kn-keyword=cell cycle
en-keyword=obesity
kn-keyword=obesity
en-keyword=p53
kn-keyword=p53
en-keyword=p21<sup>Cip1</sup>
kn-keyword=p21<sup>Cip1</sup>
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=4
article-no=
start-page=353
end-page=364
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=1990
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Study on the change of glomerular antigenicity in various renal diseases with anti-human renal monoclonal antibodies
kn-title=抗ヒト腎モノクローナノレ抗体を用いた疾患腎における抗原性の変化の検討 第1編
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We produced 22 different kinds of monoclonal antibody (Mab) by immunizing mice with human GBM antigens. In these Mabs, Mab-G1 to G5 recognized only GBM in the glomerulas, Mab-E1 and E2 recognized only glomerular epithelial cells, and Mab-M1 to M4 recognized mainly mesangium. The reactions of these Mabs with known GBM antigens such as type IV collagen, fibronectin and laminin were negative by immunoblotting. Using Mab-G1, Mab-E1 and Mab-M1, changes in the antigenicity of antigens recognized by Mabs were examined on kidney sections from the patients with various renal diseases by the indirect immunofluorescence test. When Mab-G1 recognizing GBM was used, there was no particular change of anti-genicity in minimal change nephrotic syndrome (MCNS) and IgA nephropathy (IgA), whereas in membranous nephropathy (MN) thickened GBM was found to maintain anti-genicity and the region of deposits was observed as negative punched-out region. In type I and III of membranoproliferative glomerulonephritis (MPGN), GBM was observed only outside of subendothlial deposits without showing double contour. In type II MPGN, GBM showed a double linear pattern and antigenicity of GBM in regions of dense deposits was not detected. When Mab-E1 recognizing glomerular epithelial cells was used, there was no change of antigenicity in the renal diseases. Further, in crescentic glomerulone-phritis, the region of the cellular crescents was not stained, When Mab-M1 recognizing mesangium was used, extensive staining was observed in the increased mesangium in IgA, MPGN, and diabetic nephropathy. We feel that it is of significance in elucidating the pathogenesis of renal diseases to study the changes of glomerular antigenicity in diseased kidneys by using anti-human renal monoclonal antibodies.
en-copyright=
kn-copyright=

en-aut-name=MinoYasuaki
en-aut-sei=Mino
en-aut-mei=Yasuaki
kn-aut-name=味埜泰明
kn-aut-sei=味埜
kn-aut-mei=泰明
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学第三内科
en-keyword=monoclonal antibody
kn-keyword=monoclonal antibody
en-keyword=human kidney antigen
kn-keyword=human kidney antigen
en-keyword=GBM
kn-keyword=GBM
en-keyword=mesangium
kn-keyword=mesangium
en-keyword=glomerular epithelial cell
kn-keyword=glomerular epithelial cell
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20111231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糸球体血管内皮細胞における糖尿病状態でのICAM-1の発現とMAPK経路の関係
kn-title=Involvement of MAPKs in ICAM-1 Expression in Glomerular Endothelial Cells in Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=WatanabeNaomi
en-aut-sei=Watanabe
en-aut-mei=Naomi
kn-aut-name=渡邊直美
kn-aut-sei=渡邊
kn-aut-mei=直美
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=ペルオキシゾーム増殖因子活性化受容体δの活性化はストレプトゾトシン誘発糖尿病マウスにおいて抗炎症効果により糖尿病性腎症の進展を抑制する
kn-title=Activation of Peroxisome Proliferator-Activated Receptor δ Inhibits Streptozotocin-Induced Diabetic Nephropathy Through Anti-Inflammatory Mechanisms in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MatsushitaYuichi
en-aut-sei=Matsushita
en-aut-mei=Yuichi
kn-aut-name=松下裕一
kn-aut-sei=松下
kn-aut-mei=裕一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=123
cd-vols=
no-issue=3
article-no=
start-page=197
end-page=206
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20111201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A new paradigm for the treatment of lifestyle-related diseases : Microinflammation as a novel therapeutic target
kn-title=生活習慣病治療のパラダイムシフト―慢性炎症を標的とした治療戦略―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=四方賢一
kn-aut-sei=四方
kn-aut-mei=賢一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　新医療研究開発センター
en-keyword=生活習慣病
kn-keyword=生活習慣病
en-keyword=メタボリック症候群
kn-keyword=メタボリック症候群
en-keyword=糖尿病
kn-keyword=糖尿病
en-keyword=炎症
kn-keyword=炎症
en-keyword=心血管疾患
kn-keyword=心血管疾患
END

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=4
article-no=
start-page=247
end-page=257
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=201108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Involvement of MAPKs in ICAM-1 Expression in Glomerular Endothelial Cells in Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Inflammatory processes are involved in the pathogenesis of diabetic nephropathy. The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK) pathways for induction of intercellular adhesion molecule-1 (ICAM-1) expression in glomerular endothelial cells under diabetic conditions. We examined the expression of ICAM-1 in the kidneys of experimental diabetic rats. Human glomerular endothelial cells (GE cells) were exposed to normal glucose concentration, high glucose concentration (HG), or high mannitol concentration (HM), and then the expression of the ICAM-1 protein and the phosphorylation of the 3 subfamilies of mitogen-activated protein kinase (MAPK) were determined using Western blot analysis. Next, to evaluate the involvement of MAPKs in HG- or HM-induced ICAM-1 expression, we preincubated GE cells with the inhibitors for ERK, p38 or JNK 1h prior to the application of glucose or mannitol. Expression of ICAM-1 was increased in the glomeruli of diabetic rats. Both HG and HM induced ICAM-1 expression and phosphorylation of ERK1/2, p38 and JNK in GE cells. Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK. We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions.
en-copyright=
kn-copyright=

en-aut-name=WatanabeNaomi
en-aut-sei=Watanabe
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShikataYasushi
en-aut-sei=Shikata
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SaraiKei
en-aut-sei=Sarai
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OmoriKazuyoshi
en-aut-sei=Omori
en-aut-mei=Kazuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KoderaRyo
en-aut-sei=Kodera
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatoChikage
en-aut-sei=Sato
en-aut-mei=Chikage
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Diabetic Nephropathy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=ICAM-1
kn-keyword=ICAM-1
en-keyword=ERK
kn-keyword=ERK
en-keyword=p38 MAPK
kn-keyword=p38 MAPK
en-keyword=JNK
kn-keyword=JNK
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糖尿病性腎症腹膜透析患者においてイコデキストリン透析液は体液管理を改善することにより治療継続率を増加させる：無作為比較対照試験
kn-title=Icodextrin Increases Technique Survival Rate in Peritoneal Dialysis Patients with Diabetic Nephropathy by Improving Body Fluid Management: A Randomized Controlled Trial
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TakatoriYuji
en-aut-sei=Takatori
en-aut-mei=Yuji
kn-aut-name=髙取優二
kn-aut-sei=髙取
kn-aut-mei=優二
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Microinflammationは日本人2型糖尿病患者における腎症及び動脈硬化症の共通の危険因子である
kn-title=Microinflammation is a common risk factor for progression of nephropathy and atherosclerosis in Japanese patients with type 2 diabetes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KajitaniNobuo
en-aut-sei=Kajitani
en-aut-mei=Nobuo
kn-aut-name=梶谷展生
kn-aut-sei=梶谷
kn-aut-mei=展生
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=2
article-no=
start-page=81
end-page=89
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=201104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Macrophage Is a Key Factor in Renal Injuries Caused by Glomerular Hyperfiltration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glomerular hyperfiltration is a common pathway leading to glomerulosclerosis in various kinds of kidney diseases. The 5/6 renal ablation is an established experimental animal model for glomerular hyperfiltration. On the other hand, low-grade inflammation is also a common mechanism for the progression of kidney diseases including diabetic nephropathy and atherosclerosis. Here we analyzed the gene expression profile in the remnant kidney tissues of 5/6 nephrectomized mice using a DNA microarray system and compared it with that of sham-operated control mice. The 5/6 nephrectomized mice showed glomerular hypertrophy and an increase in the extracellular matrix in the glomeruli. DNA microarray analysis indicated the up-regulated expression of various kinds of genes related to the inflammatory process in remnant kidneys. We confirmed the up-regulated expression of platelet factor-4, and monocyte chemoattractant protein-1, 2, and 5 in remnant kidneys by RT-PCR. The current results suggest that the inflammatory process is involved in the progression of glomerulosclerosis and is a common pathway of the pathogenesis of kidney disease.
en-copyright=
kn-copyright=

en-aut-name=SasakiMotofumi
en-aut-sei=Sasaki
en-aut-mei=Motofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkadaShinichi
en-aut-sei=Okada
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyamotoSatoshi
en-aut-sei=Miyamoto
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishishitaShingo
en-aut-sei=Nishishita
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Usui KataokaHitomi
en-aut-sei=Usui Kataoka
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatoChikage
en-aut-sei=Sato
en-aut-mei=Chikage
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=kidney
kn-keyword=kidney
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=chemokine
kn-keyword=chemokine
END

start-ver=1.4
cd-journal=joma
no-vol=123
cd-vols=
no-issue=1
article-no=
start-page=19
end-page=25
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Vasohibin-1, a negative feedback regulator of angiogenesis, ameliorates renal alterations in a mouse model of diabetic nephropathy
kn-title=血管新生negative feedback制御因子Vasohibin-1によるマウス糖尿病性腎症進展制御効果の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NasuTatsuyo
en-aut-sei=Nasu
en-aut-mei=Tatsuyo
kn-aut-name=那須達世
kn-aut-sei=那須
kn-aut-mei=達世
aut-affil-num=1
ORCID=

en-aut-name=MaeshimaYohei
en-aut-sei=Maeshima
en-aut-mei=Yohei
kn-aut-name=前島洋平
kn-aut-sei=前島
kn-aut-mei=洋平
aut-affil-num=2
ORCID=

en-aut-name=KinomuraMasaru
en-aut-sei=Kinomura
en-aut-mei=Masaru
kn-aut-name=木野村賢
kn-aut-sei=木野村
kn-aut-mei=賢
aut-affil-num=3
ORCID=

en-aut-name=Hirokoshi-KawaharaKumiko
en-aut-sei=Hirokoshi-Kawahara
en-aut-mei=Kumiko
kn-aut-name=川原（広越）久美子
kn-aut-sei=川原（広越）
kn-aut-mei=久美子
aut-affil-num=4
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=田邊克幸
kn-aut-sei=田邊
kn-aut-mei=克幸
aut-affil-num=5
ORCID=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=杉山斉
kn-aut-sei=杉山
kn-aut-mei=斉
aut-affil-num=6
ORCID=

en-aut-name=SonodaHikaru
en-aut-sei=Sonoda
en-aut-mei=Hikaru
kn-aut-name=園田光
kn-aut-sei=園田
kn-aut-mei=光
aut-affil-num=7
ORCID=

en-aut-name=SatoYasufumi
en-aut-sei=Sato
en-aut-mei=Yasufumi
kn-aut-name=佐藤靖史
kn-aut-sei=佐藤
kn-aut-mei=靖史
aut-affil-num=8
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=7
en-affil=
kn-affil=塩野義製薬

affil-num=8
en-affil=
kn-affil=東北大学加齢医学研究所　腫瘍循環研究分野

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=血管新生
kn-keyword=血管新生
en-keyword=vasohibin-1
kn-keyword=vasohibin-1
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=6
article-no=
start-page=407
end-page=410
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=201012
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Sarcoidosis-associated hepatocellular carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sarcoidosis is a systemic granulomatous inflammation of unknown etiology, and seems to involve the liver parenchyma in most cases. However, sarcoidosis-associated hepatocellular carcinoma is rare. We report here a case in which a hepatocellular carcinoma occurred within the liver, which was probably involved as a result of systemic sarcoidosis. A 57-year-old Japanese man had been followed up for 2 years because of diabetic nephropathy and sarcoidosis. On admission for pneumonia, imaging studies revealed an unexpected hepatic tumor. Histology revealed a hepatocellular carcinoma accompanied by T-lymphocytic infiltration and marked granulomatous inflammation, which was surrounding some tumor nodules. The background liver parenchyma exhibited a moderate degree of fibrosis with granulomatous inflammation. The patient had no other apparent liver disease such as viral hepatitis, steatohepatitis, or primary biliary cirrhosis. Therefore, in the present case, sarcoidosis may be considered the probable background etiology for hepatocarcinogenesis.
en-copyright=
kn-copyright=

en-aut-name=OgataSho
en-aut-sei=Ogata
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HorioTakuya
en-aut-sei=Horio
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SugiuraYoshiaki
en-aut-sei=Sugiura
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShimazakiHideyuki
en-aut-sei=Shimazaki
en-aut-mei=Hideyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaitoHiroki
en-aut-sei=Saito
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AikoSatoshi
en-aut-sei=Aiko
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakanishiKuniaki
en-aut-sei=Nakanishi
en-aut-mei=Kuniaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawaiToshiaki
en-aut-sei=Kawai
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Pathology and Laboratory Medicine, National Defense Medical College

affil-num=2
en-affil=
kn-affil=Department of Surgery II, National Defense Medical College

affil-num=3
en-affil=
kn-affil=Department of Surgery, International University of Health and Welfare Mita Hospital

affil-num=4
en-affil=
kn-affil=Department of Laboratory Medicine, National Defense Medical College

affil-num=5
en-affil=
kn-affil=Department of Surgery II, National Defense Medical College

affil-num=6
en-affil=
kn-affil=Department of Surgery II, National Defense Medical College

affil-num=7
en-affil=
kn-affil=Department of Pathology and Laboratory Medicine, National Defense Medical College

affil-num=8
en-affil=
kn-affil=Department of Pathology and Laboratory Medicine, National Defense Medical College
en-keyword=granuloma
kn-keyword=granuloma
en-keyword=hepatocellular carcinoma
kn-keyword=hepatocellular carcinoma
en-keyword=lymphocytic infiltration
kn-keyword=lymphocytic infiltration
en-keyword=sarcoidosis
kn-keyword=sarcoidosis
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=1
article-no=
start-page=39
end-page=47
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=201002
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Influencing Factors for Dietary Behaviors of Patients with Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The aim of this study was to clarify the factors influencing the dietary behavior of patients with diabetic nephropathy. One hundred twenty-two patients with type 2 diabetes were recruited from the outpatients of Okayama University Hospital in Okayama, Japan. We performed a cross-sectional study using a questionnaire including 206 items among 18 categories as follows:background factors, coping behavior (coping scale), degree of uncertainty in illness (uncertainty scale), and dietary behavior. The data were analyzed by correlation analysis, t-test, one-way analysis of variance, Pearson correlation analysis, and multiple regression analysis. We found that those patients with microalbuminuria alone tended to recognize more mild about their kidney status than those with macroalbuminuria and chronic renal failure. We also found that common factors influencing the dietary behavior of diabetic patients with and without nephropathy are as follows:1. coping with the problem (beta0.342, p0.01);2. anxiety about prognosis (beta0.344, p0.01);3. sex (beta0.234, p0.05);4. uncertainty regarding treatment (beta0.377, p0.01);5. negative coping (beta0.354, p0.01);and 6. employment status (beta0.367, p0.01). Coping and uncertainty in illness had a significant relation to positive support and lack of support. To maintain appropriate dietary behavior in diabetic patients, medical staff need to determine what the social supports are important for the patient, and also to ensure good communication among healthcare personnel as well as positive support for patients and families.</p>
en-copyright=
kn-copyright=

en-aut-name=SumiyoshiKazuko
en-aut-sei=Sumiyoshi
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawataChieko
en-aut-sei=Kawata
en-aut-mei=Chieko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Clinical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmceutical Sciences

affil-num=2
en-affil=
kn-affil=Mejiro Unibersity Graduate School of Nursing

affil-num=3
en-affil=
kn-affil=Department of Medicine and Clinical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Medicine and Clinical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmceutical Sciences
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=dietary behavior
kn-keyword=dietary behavior
en-keyword=coping
kn-keyword=coping
en-keyword=uncertainty in illness
kn-keyword=uncertainty in illness
en-keyword=social support
kn-keyword=social support
END

start-ver=1.4
cd-journal=joma
no-vol=46
cd-vols=
no-issue=3
article-no=
start-page=165
end-page=168
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Significance of urinary albumin index in the urine collected arbitrarily in the morning.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>To evaluate urinary albumin index (UAI), the relationship between albumin excretion rate (AER) in the urine stored for 24 h and UAI in the urine collected arbitrarily on the morning of the same day was studied in 123 inpatients. The patients were admitted to our hospital from September 1, 1988 to August 31, 1989, consisting of 67 non-insulin dependent diabetics (Group 1), 40 patients with collagen disease (Group 2), and 16 patients with primary renal disease (Group 3). The relationship between log(e) AER and log(e)UAI was plotted on a graph. Pearson's rank correlation coefficients of Groups 1-3, Group 1, Group 2, and Group 3 were as follows: r = 0.725, r = 0.691, r = 0.855, and r = 0.611, respectively. The formula obtained by using Pearson's rank correlation coefficients to estimate log(e)AER from log(e)UAI in 123 cases of Groups 1-3, 67 cases of Group 1, 40 cases of Group 2, and 16 cases of Group 3 were: log(e)AER/log(e)UAI = 0.815, log(e)AER/log(e)UAI = 0.860, log(e)AER/log(e)UAI = 0.830, log(e)AER/log(e) = 0.722, respectively. In the present study, log(e)UAI was found to correlate well with log(e)AER. As AER is generally accepted to be the most reliable index to know the stage of albuminuria, UAI is considered to be clinically useful.</p>

en-copyright=
kn-copyright=

en-aut-name=OkadaSoji
en-aut-sei=Okada
en-aut-mei=Soji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanokuchiSo
en-aut-sei=Tanokuchi
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IchikiKen
en-aut-sei=Ichiki
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshiiKeita
en-aut-sei=Ishii
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HamadaHiroshi
en-aut-sei=Hamada
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtaZensuke
en-aut-sei=Ota
en-aut-mei=Zensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama University 

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University 
en-keyword=albumin excretion rate
kn-keyword=albumin excretion rate
en-keyword=urinary albumin index
kn-keyword=urinary albumin index
en-keyword=morning urine
kn-keyword=morning urine
en-keyword=non-insulin dependent diabetes
kn-keyword=non-insulin dependent diabetes
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
END

start-ver=1.4
cd-journal=joma
no-vol=56
cd-vols=
no-issue=5
article-no=
start-page=237
end-page=243
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=200210
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Diabetic gastroparesis in association with autonomic neuropathy and microvasculopathy.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Gastroparesis is a frequent and sometimes life-threatening complication of diabetes mellitus. Autonomic neuropathy seems to be one of the most important mechanisms underlying this entity, together with the other probable pathologies. The present study was performed in order to identify an alternative to gastric scintigraphy as a screening test. The gastric emptying times of 60 subjects (Group 1: 20 insulin-dependent patients, Group 2: 20 non-insulin-dependent diabetes mellitus patients, and Group 3: 20 healthy volunteers) were monitored by gastric scintigraphy. Perception thresholds for cold, heat, and vibration were tested by a quantitative sensory test, and QTc dispersions were calculated from standard electrocardiography recordings. In addition, fasting blood glucose, hemoglobin A1c and urine beta2-microglobulin and microalbumin concentrations were determined for the patient groups. Funduscopic examination was performed by an independent ophthalmologist. Gastroparesis was determined in both patient groups, regardless of fasting blood glucose and hemoglobin A1c concentrations. A strong correlation was observed between nephropathy, retinopathy, and cardiac autonomic denervation (QTc) and gastroparesis. In conclusion, retinal and renal microvasculopathy parameters and cardiac autonomic function tests may be useful for screening diabetic patients for gastroparesis.</p>

en-copyright=
kn-copyright=

en-aut-name=KockarM. Cem
en-aut-sei=Kockar
en-aut-mei=M. Cem
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KayahanI. Kaan
en-aut-sei=Kayahan
en-aut-mei=I. Kaan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=BavbekNuket
en-aut-sei=Bavbek
en-aut-mei=Nuket
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Fatih University, Turkey

affil-num=2
en-affil=
kn-affil=Guven Hospital

affil-num=3
en-affil=
kn-affil=Fatih University 
en-keyword=diabetic gastroparesis
kn-keyword=diabetic gastroparesis
en-keyword=microvasculopathy
kn-keyword=microvasculopathy
en-keyword=autonomic neuropathy
kn-keyword=autonomic neuropathy
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=4
article-no=
start-page=267
end-page=272
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ultrastructural changes of the glomerular basement membrane in diabetic nephropathy revealed by newly devised tissue negative staining method.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>In order to clarify the mechanism of proteinuria in diabetic nephropathy, ultrastructural changes of the glomerular basement membrane (GBM) in patients with diabetic nephropathy were examined by electron microscopy using our newly devised &#34;tissue negative staining method&#34;. The normal human GBM showed a fine meshwork structure consisting of fibrils forming the small pores. The diameter of these pores was slightly smaller than that of human albumin molecules. The GBM in patients with diabetic nephropathy showed irregular thickening. At higher magnification, hitherto unknown cavities and tunnel structures, which were not seen in normal controls, were observed in the thickened GBM. In some portions, these cavities presented a honeycomb-like appearance. The diameters of the cavities and tunnels were far larger than the dimensions of albumin molecules. These enlarged structures are believed to allow serum protein molecules to pass through the GBM from the capillary lumen to the urinary space. These results suggest that the cause of massive proteinuria in diabetic nephropathy is the disruption of the size barrier of the GBM.</p>
en-copyright=
kn-copyright=

en-aut-name=OtaKosuke
en-aut-sei=Ota
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtaZensuke
en-aut-sei=Ota
en-aut-mei=Zensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univerisity

affil-num=4
en-affil=
kn-affil=Okayama Uniiversity
en-keyword=glomerular basement membrane
kn-keyword=glomerular basement membrane
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=tissue negative staining
kn-keyword=tissue negative staining
en-keyword=nephrotic syndrome
kn-keyword=nephrotic syndrome
en-keyword=ultrastructure
kn-keyword=ultrastructure
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=3
article-no=
start-page=137
end-page=142
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Changes in Plasma Concentrations of Vitronectin in Patients with Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>To investigate the role of vitronectin in the progression of diabetic nephropathy, plasma concentrations of vitronectin were measured by enzyme-linked immunosorbent assay in patients with diabetes mellitus and compared with normal control subjects. In diabetic patients with normoalbuminuria and microalbuminuria, plasma concentrations of vitronectin were significantly higher than those of control subjects. Plasma concentrations of vitronectin in diabetic patients with chronic renal failure were significantly lower than those with normal renal function. There was a significant positive correlation between plasma concentration of vitronectin and blood platelet counts. In the early stage of diabetic nephropathy, vitronectin may be increased caused by synthesis from activated platelets. With progression of diabetic nephropathy, plasma vitronectin may be decreased because of accumulation in sclerotic glomeruli and arteriosclerotic lesions. In conclusion, the plasma concentration of vitronectin appears to be an important marker for the progression of diabetic nephropathy.</p>
en-copyright=
kn-copyright=

en-aut-name=MoriokaShigeru
en-aut-sei=Morioka
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtaZensuke
en-aut-sei=Ota
en-aut-mei=Zensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univeristy

affil-num=4
en-affil=
kn-affil=Okayama  University
en-keyword=vitronectin(S-protein)
kn-keyword=vitronectin(S-protein)
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=hypertension
kn-keyword=hypertension
en-keyword=chronic renal failure
kn-keyword=chronic renal failure
en-keyword=enzyme-linked immunosorbent assay (ELISA)
kn-keyword=enzyme-linked immunosorbent assay (ELISA)
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=4
article-no=
start-page=309
end-page=318
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1978
dt-pub=197808
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lipoatrophic diabetes. Report of a case
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The female patient initially showed the acquired type of total lipoatrophy at about 8 years of age. At 12 years of age, the onset of diabetes mellitus was speculated from advanced pyodermia and dedentition. At 29 years of age, glucosuria was found, and she developed proteinuria, ascites, and pretibial edema. The physical examination revealed: hepatosplenomegaly, complete absence of subcutanous fat, cutaneous xanthomas, and emaciated facies with pronounced zygomatic arches. Diabetic retinopathy was revealed in the ophthalmological examination, and nephropathy was evident in renal biopsy specimens. She also had peripheral diabetic neuropathy. No adipose tissue was found in the mesenterium under peritoneoscopy. The hepatic biopsy specimen revealed advanced portal liver cirrhosis. Laboratory findings included: hyperlipidemia, elevation of BMR without evidence of hyperthyroidism, impaired renal function, and undetected anti-insulin antibodies and anti-insulin antibodies. Endocrinological examinations revealed normal value, except for an impaired hGH response in the arginine test. C-peptide immunoreactivity was high. Her condition was fairly well controlled by 140 units of insulin injection daily.</p>

en-copyright=
kn-copyright=

en-aut-name=SaraiTetsuo
en-aut-sei=Sarai
en-aut-mei=Tetsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawanishiKoichi
en-aut-sei=Kawanishi
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SaitoYoshihito
en-aut-sei=Saito
en-aut-mei=Yoshihito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AoiKatsuyuki
en-aut-sei=Aoi
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishinaYoshiaki
en-aut-sei=Nishina
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OfujiTadashi
en-aut-sei=Ofuji
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University
en-keyword=lipoatrophic diabetes
kn-keyword=lipoatrophic diabetes
en-keyword=diabetic triopathy
kn-keyword=diabetic triopathy
en-keyword=hepatosplenomegaly
kn-keyword=hepatosplenomegaly
en-keyword=anti-insulin receptor antibodies
kn-keyword=anti-insulin receptor antibodies
en-keyword=CPR
kn-keyword=CPR
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=3
article-no=
start-page=201
end-page=205
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=200606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Disappearance of diabetic macular hard exudates after hemodialysis introduction.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>We report herein the disappearance of macular hard exudates after the introduction of hemodialysis in diabetic patients. A 62-year-old woman and a 52-year-old man with diabetes mellitus showed hard exudates in the macula of the left eyes. Both patients had previously undergone panretinal photocoagulation in both eyes. During the follow-up, hemodialysis was introduced for deteriorating chronic renal failure caused by diabetic nephropathy. Half a year later, macular hard exudates in the left eyes disappeared dramatically in both patients, but the visual acuity remained the same. No additional laser treatment was done during the observation period. Hemodialysis is considered to have accelerated the resolution of macular hard exudates in both patients. The deposition of macular hard exudates in diabetic patients is due in part to concurrent poor renal function.</p>
en-copyright=
kn-copyright=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University
en-keyword=hemodialysis
kn-keyword=hemodialysis
en-keyword=diabetic retinopathy
kn-keyword=diabetic retinopathy
en-keyword=hard exudates
kn-keyword=hard exudates
en-keyword=macular edema
kn-keyword=macular edema
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=3
article-no=
start-page=153
end-page=159
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=199506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Increased urinary excretion of non-albumin antigen detected with YO-2, a novel monoclonal antibody, in diabetic patients.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Monoclonal antibodies were raised against urine proteins from diabetic patients. An antibody, YO-2, stained three protein bands with apparent molecular weights of 66, 49, and 36 kDa. These bands were not reactive with an anti-human albumin antibody. The urine levels of YO-2-reactive antigen in the normal control were 0.97 +/- 0.37 U/g-Cr (units per gram of urine creatinine) (mean +/- SD). Those of the normo-, micro-, and macroalbuminuric diabetic patients, respectively, were 1.38 +/- 1.36, 2.87 +/- 2.07, and 3.92 +/- 3.33 U/g-Cr. They were significantly higher in the micro- and macroalbuminuric patients. The urine levels of YO-2-reactive antigen had no significant correlation with the urine albumin levels and hemoglobin A1c. We concluded that; a) monoclonal antibody YO-2 recognized a non-albumin urine antigen increasingly excreted in diabetic patients with nephropathy, b) recent glycemic control of diabetes would not significantly affect the urinary excretion rate of YO-2-reactive antigen, and c) the excretion rate and probably the mechanism of YO-2-reactive protein differed from those of albumin. The urine levels of YO-2-reactive antigen could be a clinical marker of diabetic nephropathy.</p>

en-copyright=
kn-copyright=

en-aut-name=YoneiTaiji
en-aut-sei=Yonei
en-aut-mei=Taiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WataraiShinobu
en-aut-sei=Watarai
en-aut-mei=Shinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkadaYoshio
en-aut-sei=Okada
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YasudaTatsuji
en-aut-sei=Yasuda
en-aut-mei=Tatsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsujiTakao
en-aut-sei=Tsuji
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University 

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=diabetes
kn-keyword=diabetes
en-keyword=nephropathy
kn-keyword=nephropathy
en-keyword=monoclonal antibody
kn-keyword=monoclonal antibody
en-keyword=microalbuminuria
kn-keyword=microalbuminuria
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糖尿病性腎症患者の食事療法に影響を与える要因
kn-title=Influencing Factors for Dietary behaviors of Patients with Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SumiyoshiKazuko
en-aut-sei=Sumiyoshi
en-aut-mei=Kazuko
kn-aut-name=住吉和子
kn-aut-sei=住吉
kn-aut-mei=和子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=1
article-no=
start-page=27
end-page=31
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Aldosterone breakthrough caused by chronic blockage of angiotensin II type 1 receptors in human adrenocortical cells: Possible involvement of bone morphogenetic protein-6 actions
kn-title=副腎皮質細胞におけるアルドステロンブレイクスルー現象とBMP-6の関与
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OtaniHiroyuki
en-aut-sei=Otani
en-aut-mei=Hiroyuki
kn-aut-name=大谷寛之
kn-aut-sei=大谷
kn-aut-mei=寛之
aut-affil-num=1
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=大塚文男
kn-aut-sei=大塚
kn-aut-mei=文男
aut-affil-num=2
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=アルドステロンブレイクスルー
kn-keyword=アルドステロンブレイクスルー
en-keyword=BMP-6
kn-keyword=BMP-6
en-keyword=MAPK
kn-keyword=MAPK
en-keyword=副腎皮質細胞
kn-keyword=副腎皮質細胞
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20091231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=血管新生negative feedback制御因子Vasohibin-1によるマウス糖尿病性腎症進展制御効果の検討
kn-title=Vasohibin-1, a negative feedback regulator of angiogenesis, ameliorates renal alterations in a mouse model of diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NasuTatsuyo
en-aut-sei=Nasu
en-aut-mei=Tatsuyo
kn-aut-name=那須達世
kn-aut-sei=那須
kn-aut-mei=達世
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=96
cd-vols=
no-issue=1-2
article-no=
start-page=109
end-page=125
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1984
dt-pub=19840228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on β-Glucuronidase and N-Acetyl-β-Glucosaminidase activities in polymorphonuclrar leukocytes and serum Part I. Studies on diabetic patients
kn-title=多核白血球および血清におけるβ-Glucuronidase, N-Acetyl-β-Glucosaminidase活性に関する研究 第1編 糖尿病患者について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=β-Glucuronidase (β-G) and N-acetyl-β-glucosaminidase (NAG) activities were investigated in diabetic patients. Serum β-G activity, NAG activity, total cholesterol (TC), triglyceride (TG) and atherogenic index (A.I.) were significantly higher in diabetics than in controls. In diabetics, there were significantly positive correlations between serum β-G activity and fasting blood glucose level, TC, TG and A.I., and between serum NAG activity and fasting blood glucose level, TC and TG. Serum β-G and NAG activities were significantly higher in diabetics with hyperlipidemia than in diabetics without hyperlipidemia. The elevation of serum β-G and NAG activities in diabetics might be due to metabolic abnormalities accompanying hyperglycemia and hyperlipidemia. Serum NAG activity was significantly higher in diabetics with nephropathy than in those without nephropathy. β-G activity of polymorphonuclear leukocytes (PMN) in poorly controlled diabetics was significantly lower than PMN-β-G activity in controls and fairly controlled diabetics. Degradation of mucopolysaccaride and glycoprotein might be impaired in poorly controlled diabetics, and this impairment might explain glycoprotein-deposition in diabetic microangiopathy and impaired bacteriocidal activity in diabetic leukocytes. PMN-β-G activity was significantly higher in diabetics with severe diabetic retinopathy (ScottⅢ-V) than in those with mild diabetic retinopathy (Scott I-Ⅱ). This data suggests that high PMN-β-G activity contributes to the establishment of diabetic microangiopathy.
en-copyright=
kn-copyright=

en-aut-name=IshidaMakoto
en-aut-sei=Ishida
en-aut-mei=Makoto
kn-aut-name=石田誠
kn-aut-sei=石田
kn-aut-mei=誠
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第2内科教室
en-keyword=多核白血球
kn-keyword=多核白血球
en-keyword=β-Glucuronidase
kn-keyword=β-Glucuronidase
en-keyword=N-Acetyl-β-Glucosaminidase,
kn-keyword=N-Acetyl-β-Glucosaminidase,
en-keyword=糖尿病
kn-keyword=糖尿病
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=5-6
article-no=
start-page=601
end-page=608
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Renal hemodynamics in improvement of diabetic nephropathy in stage Ⅲ and Ⅳ
kn-title=Ⅲ, Ⅳ期糖尿病性腎症の改善における腎血行動態に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diabetic nephropathy is characterized by specific morphological changes and impairment of renal hemodynamics. To determine whether diabetic nephripathy could be improved by improvement of renal hemodynamics, 80μg/day of prostaglandin E(1) (PGE(1)) was administered daily for 4 weeks to 19 non-insulin-dependent diabetic inpatients with overt proteinuria. In 6 patients who initialy had daily urinary protein (UP) values above 3.5g/day, the UP value was sinificantly reduced by PGE(1) administration (p<0.05). However, in 6 patients who initially had UP values above 200mg/day and below 3.5g/day, the UP value was unchanged. In the former group, creatinine clearance was significantly reduced during PGE(1) administration (p<0.05), but was restored after termination of PGE1 adminstration (ns). Serum creatinine, serum total protein and serum albumin values were unchanged by PGE(1) administration in both groups. One petient who had a UP level above 200mg/day showed marked improvement on his renogram during PGE(1) administration and in 7 patiests who had UP values below 200mg/day, the ratio of plasma renin activity 120 minutes after furosemide injection in an upright posture to that of basal condition (PRA120/0) was significantly reduced. These findings inducate that PGE(1) increased renal blood flow, and suggest that improvement of renal hemodynamics is an important method of therapy for diabetic nephropathy with overt proteinuria.
en-copyright=
kn-copyright=

en-aut-name=IchikiKen
en-aut-sei=Ichiki
en-aut-mei=Ken
kn-aut-name=市木研
kn-aut-sei=市木
kn-aut-mei=研
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第三内科学教室
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=蛋白尿
kn-keyword=蛋白尿
en-keyword=腎血行動態
kn-keyword=腎血行動態
en-keyword=プロスタグランディンE(1)
kn-keyword=プロスタグランディンE(1)
en-keyword=糸球体過剰濾過
kn-keyword=糸球体過剰濾過
END

start-ver=1.4
cd-journal=joma
no-vol=120
cd-vols=
no-issue=3
article-no=
start-page=337
end-page=341
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20081201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Clinical practice guidelines and recommendations for diabetic nephropathy, anemia and medication in chronic kidney disease
kn-title=慢性腎臓病の治療 (糖尿病腎症，貧血管理，薬物治療の注意点など）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MorinagaHiroshi
en-aut-sei=Morinaga
en-aut-mei=Hiroshi
kn-aut-name=森永裕士
kn-aut-sei=森永
kn-aut-mei=裕士
aut-affil-num=1
ORCID=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=杉山斉
kn-aut-sei=杉山
kn-aut-mei=斉
aut-affil-num=2
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　慢性腎臓病対策腎不全治療学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
END

start-ver=1.4
cd-journal=joma
no-vol=107
cd-vols=
no-issue=9-10
article-no=
start-page=195
end-page=204
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=19951031
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Expression of β(1) integrin and fibronectin in the glomeruli in patients with glomerulonephritis
kn-title=糸球体腎炎におけるβ(1)インテグリンの発現の変化の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Integrins are a family of adhesion molecules which mediate adhesion and interaction between cells and extracellular matrix. The renal glomerulus is composed of cellular components and extracellular matrix. To clarify the role of integrins in the progression of glomer-ulonephritis, we examined the expression of β(1) integrin and fibronectin, which is a ligand of β(1) integrin, in the glomeruli in patients with IgA nephropathy and membranous nephropathy by an indirect immunofluorescence study and immunoelectron microscopic study using specific antibodies. β(1) integrin was expressed on the surface of mesangial cells, glomerular epithelial cells, endothelial cells and Bowman's capsullar epithelial cells in normal control glomeruli. The expression of β(1) integrin and fibronectin was increased in the mesangial area in patients with IgA nephropathy showing mesangial proliferation and mesangial matrix increase. β(1) integrin may play an important role in the construction of the glomerulus and also in the deposition of immunecomplex, proliferation of mesangial cells, and increase in extracellular matrix in IgA nephropathy.
en-copyright=
kn-copyright=

en-aut-name=KashitaniTadatoshi
en-aut-sei=Kashitani
en-aut-mei=Tadatoshi
kn-aut-name=柏谷忠俊
kn-aut-sei=柏谷
kn-aut-mei=忠俊
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第三内科学教室
en-keyword=β(1)インテグリン
kn-keyword=β(1)インテグリン
en-keyword=フィブロネクチン
kn-keyword=フィブロネクチン
en-keyword=lgA腎症
kn-keyword=lgA腎症
en-keyword=膜性腎症
kn-keyword=膜性腎症
END

start-ver=1.4
cd-journal=joma
no-vol=117
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=15
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20050520
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=糖尿病性腎症の発症・進展における炎症機転の関与
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=岡田震一
kn-aut-sei=岡田
kn-aut-mei=震一
aut-affil-num=1
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=四方賢一
kn-aut-sei=四方
kn-aut-mei=賢一
aut-affil-num=2
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯学総合研究科腎･免疫･内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯学総合研究科腎･免疫･内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯学総合研究科腎･免疫･内分泌代謝内科学
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=マクロファージ
kn-keyword=マクロファージ
en-keyword=ICAM-１
kn-keyword=ICAM-１
en-keyword=炎症
kn-keyword=炎症
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=血清総アディポネクチン濃度および高分子量アディポネクチン濃度は糖尿病網膜症と糖尿病腎症の重症度と関連する
kn-title=Serum total and high molecular weight adiponectin levels are correlated with the severity of diabetic retinopathy and nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KatouKenichi
en-aut-sei=Katou
en-aut-mei=Kenichi
kn-aut-name=加藤健一
kn-aut-sei=加藤
kn-aut-mei=健一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=120
cd-vols=
no-issue=2
article-no=
start-page=215
end-page=218
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Introduction to chronic kidney disease treatment : Anti-hypertensive and dietary treatment
kn-title=慢性腎臓病の治療総論 (降圧療法，食事療法を含めて)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=InoueTatsuyuki
en-aut-sei=Inoue
en-aut-mei=Tatsuyuki
kn-aut-name=井上達之
kn-aut-sei=井上
kn-aut-mei=達之
aut-affil-num=1
ORCID=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=杉山斉
kn-aut-sei=杉山
kn-aut-mei=斉
aut-affil-num=2
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 腎･免疫･内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 慢性腎臓病対策腎不全治療学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 腎･免疫･内分泌代謝内科学
END

start-ver=1.4
cd-journal=joma
no-vol=120
cd-vols=
no-issue=2
article-no=
start-page=143
end-page=147
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Macrophage scavenger receptor-A--deficient mice are resistant to diabetic nephropathy through amelioration of microinflammation
kn-title=マクロファージスカベンジャー受容体（SR-A）は炎症を制御することにより糖尿病性腎症を抑制する
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KataokaHitomi
en-aut-sei=Kataoka
en-aut-mei=Hitomi
kn-aut-name=片岡仁美
kn-aut-sei=片岡
kn-aut-mei=仁美
aut-affil-num=1
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=四方賢一
kn-aut-sei=四方
kn-aut-mei=賢一
aut-affil-num=2
ORCID=

en-aut-name=SasakiMotofumi
en-aut-sei=Sasaki
en-aut-mei=Motofumi
kn-aut-name=佐々木基史
kn-aut-sei=佐々木
kn-aut-mei=基史
aut-affil-num=3
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医療教育統合開発センター; 岡山大学大学院医歯薬学総合研究科　腎･免疫･内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎･免疫･内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎･免疫･内分泌代謝内科学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎･免疫･内分泌代謝内科学
en-keyword=マクロファージスカベンジャー受容体
kn-keyword=マクロファージスカベンジャー受容体
en-keyword=SR-A
kn-keyword=SR-A
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=炎症
kn-keyword=炎症
en-keyword=マクロファージ
kn-keyword=マクロファージ
END

start-ver=1.4
cd-journal=joma
no-vol=119
cd-vols=
no-issue=3
article-no=
start-page=311
end-page=313
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Control of blood pressure in diabetic patients
kn-title=糖尿病患者における血圧管理
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SasakiMotofumi
en-aut-sei=Sasaki
en-aut-mei=Motofumi
kn-aut-name=佐々木基史
kn-aut-sei=佐々木
kn-aut-mei=基史
aut-affil-num=1
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=四方賢一
kn-aut-sei=四方
kn-aut-mei=賢一
aut-affil-num=2
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 腎・免疫・内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 腎・免疫・内分泌代謝内科学
END

start-ver=1.4
cd-journal=joma
no-vol=119
cd-vols=
no-issue=2
article-no=
start-page=191
end-page=194
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070903
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Management of dyslipidemia in diabetic patients
kn-title=糖尿病患者における脂質管理
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KataokaHitomi
en-aut-sei=Kataoka
en-aut-mei=Hitomi
kn-aut-name=片岡仁美
kn-aut-sei=片岡
kn-aut-mei=仁美
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医療教育統合開発センター
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糖尿病性腎症の早期においてTGF-β/Smadシグナル伝達系はAT1a受容体非依存性に増強している
kn-title=Enhanced TGF-β/Smad signaling in the early stage of diabetic nephropathy is independent of AT1a receptor
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OkazakiYuko
en-aut-sei=Okazaki
en-aut-mei=Yuko
kn-aut-name=岡﨑祐子
kn-aut-sei=岡﨑
kn-aut-mei=祐子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=119
cd-vols=
no-issue=1
article-no=
start-page=7
end-page=10
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=腎臓再生へ向けた成体腎臓幹／前駆細胞様細胞を用いた再生医療の可能性
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KitamuraShinji
en-aut-sei=Kitamura
en-aut-mei=Shinji
kn-aut-name=喜多村真治
kn-aut-sei=喜多村
kn-aut-mei=真治
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=傷害尿細管
kn-keyword=傷害尿細管
en-keyword=腎臓再生
kn-keyword=腎臓再生
en-keyword=幹/前駆細胞
kn-keyword=幹/前駆細胞
en-keyword=細胞治療
kn-keyword=細胞治療
END

start-ver=1.4
cd-journal=joma
no-vol=61
cd-vols=
no-issue=
article-no=
start-page=79
end-page=88
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199009
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Diabetic complications in the advanced stage of chronic pancreatitis.
kn-title=膵性糖尿病の合併症
en-subtitle=
kn-subtitle=
en-abstract=Exocrine dysfunction (maldigestion) and endocrine dysfunction (diabetes) are malll clinical features in the advanced stage of chronic pancreatitis. Diabetic complications were previously considered to be infrequent
in diabetes secondary to chronic pancreatitis (pancreatic diabetes). However, the recent improvement in life expectancy and closer observation of the clinical course of patients with chronic pancreatitis have revealed that diabetic complications are not infrequent in pancreatic diabetes as compared with primary diabetes mellitus and that diabetes is one of the most important prognostic factors in chronic pancreatitis. We, therefore, reviewed
recent articles on the topics before beginning a national survey of diabetic complications in patients with pancreatic diabetes. It has been suggested that : (1) diabetic microangiopathy (retinopathy, nephropathy and peripheral neuropathy) is almost as frequent in secondary diabetes as in primary diabetes, although the severity is less in secodary diabetes : (2) peripheral neuropathy
is frequent in alcoholic chronic pancreatitis : (3)macroangiopathy (myocardial infarction, cerebral thrombosis, atherosclerosis) is less frequent in pancreatic diabetes. We also discussed various factors which may precipitate the diabetic complications.
kn-abstract=慢性膵炎が進行すると膵内外分泌不全に対する治療が主体となる。かつては膵疾患に由来する糖尿病（膵性糖尿病）においては糖尿病性合併症の発症が少ないとされていたが，慢性膵炎の長期経過観察例の増加とともにその頻度が一次性糖尿病にくらべて必ずしも低くないことが指摘されるようになった。そこで今回，厚生省難治性膵疾患調査研究班「慢性膵炎の新しい治療法の開発」小委員会の研究活動の一環として膵性糖尿病の治療法を再検討することになったのを機会に，その手始めに野性糖尿病の合併症に関する従来の報告を整理した。その結果，一次性糖尿病の場合にくらべて，細小血管症（網膜症，腎症，神経障害）はほぼ同程度であるが軽症例が多いこと，大血管症（心筋梗塞，脳硬塞，動脈硬化症）は少ないことが示唆された。そのほか，膵性糖尿病の合併症の発症に関与すると考えられる諸因子についても概説した。
en-copyright=
kn-copyright=

en-aut-name=OchiKoji
en-aut-sei=Ochi
en-aut-mei=Koji
kn-aut-name=越智浩二
kn-aut-sei=越智
kn-aut-mei=浩二
aut-affil-num=1
ORCID=

en-aut-name=TachibanaHideo
en-aut-sei=Tachibana
en-aut-mei=Hideo
kn-aut-name=立花英夫
kn-aut-sei=立花
kn-aut-mei=英夫
aut-affil-num=2
ORCID=

en-aut-name=MatsumotoShuji
en-aut-sei=Matsumoto
en-aut-mei=Shuji
kn-aut-name=松本秀次
kn-aut-sei=松本
kn-aut-mei=秀次
aut-affil-num=3
ORCID=

en-aut-name=SenoToshinobu
en-aut-sei=Seno
en-aut-mei=Toshinobu
kn-aut-name=妹尾敏伸
kn-aut-sei=妹尾
kn-aut-mei=敏伸
aut-affil-num=4
ORCID=

en-aut-name=TanakaJuntaro
en-aut-sei=Tanaka
en-aut-mei=Juntaro
kn-aut-name=田中淳太郎
kn-aut-sei=田中
kn-aut-mei=淳太郎
aut-affil-num=5
ORCID=

en-aut-name=HaradaHideo
en-aut-sei=Harada
en-aut-mei=Hideo
kn-aut-name=原田英雄
kn-aut-sei=原田
kn-aut-mei=英雄
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属環境病態研究施設成人病学分野

affil-num=2
en-affil=
kn-affil=岡山大学医学部附属環境病態研究施設成人病学分野

affil-num=3
en-affil=
kn-affil=岡山大学医学部附属環境病態研究施設成人病学分野

affil-num=4
en-affil=
kn-affil=岡山大学医学部附属環境病態研究施設成人病学分野

affil-num=5
en-affil=
kn-affil=岡山大学医学部附属環境病態研究施設成人病学分野

affil-num=6
en-affil=
kn-affil=岡山大学医学部附属環境病態研究施設成人病学分野
en-keyword=膵性糖尿病 (Pancreatic diabetes)
kn-keyword=膵性糖尿病 (Pancreatic diabetes)
en-keyword=慢性膵炎 (Chronic pancreatitis)
kn-keyword=慢性膵炎 (Chronic pancreatitis)
en-keyword=合併症 (Complications)
kn-keyword=合併症 (Complications)
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=チアゾリジン誘導体は細胞周期依存性メカニズムにより糖尿病性腎症を改善する
kn-title=Thiazolidinediones Ameliorate Diabetic Nephropathy via Cell Cycle-Dependent Mechanisms
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OkadaTatsuo
en-aut-sei=Okada
en-aut-mei=Tatsuo
kn-aut-name=岡田達夫
kn-aut-sei=岡田
kn-aut-mei=達夫
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=血清Interleukin-18濃度は２型糖尿病患者の腎症と動脈硬化症に関係がある
kn-title=Serum Interleukin-18 Levels Are Associated With Nephropathy and Atherosclerosis in Japanese Patients With field name="type" 2 Diabetes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakamuraAkihiko
en-aut-sei=Nakamura
en-aut-mei=Akihiko
kn-aut-name=中村明彦
kn-aut-sei=中村
kn-aut-mei=明彦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20061231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=血管新生阻害因子Tumstatin peptideは早期糖尿病性腎症における糸球体肥大を抑制する
kn-title=Tumstatin Peptide, an Inhibitor of Angiogenesis, Prevents Glomerular Hypertrophy in the Early Stage of Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YamamotoYoshihiko
en-aut-sei=Yamamoto
en-aut-mei=Yoshihiko
kn-aut-name=山本佳彦
kn-aut-sei=山本
kn-aut-mei=佳彦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1998
dt-pub=19980325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糖尿病性腎症患者の腎臓におけるセレクチンの発現増加
kn-title=Increased Expression of Selectins in Kidneys of Patients with Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=平田教至
kn-aut-sei=平田
kn-aut-mei=教至
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=19930331
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=新たに考案した Tissue negative staining 法にて観察した糖尿病性腎症糸球体基底膜超微形態の変化
kn-title=Ultrastructural Changes of the Glomerular Basement Membrane in Diabetic Nephropathy Revealed by Newly Devised Tissue Negative Staining Method
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=太田康介
kn-aut-sei=太田
kn-aut-mei=康介
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1996
dt-pub=19960630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=腎機能傷害患者における心筋トロポニンT測定に関する検討)第1編血液透析患者における心筋トロポニンT測定に関する検討) 第2編(糖尿病性腎疾患者における心筋トロポニンT測定に関する検討
kn-title=Myocardial troponin T levels in patients with renal dysfunction 第1編 A comparative study of myocardial troponin T levels in patients undergoing hemodialysis 第'2編 Myocardial troponin T levels in patients with diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=赤木正彦
kn-aut-sei=赤木
kn-aut-mei=正彦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1996
dt-pub=19960325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糖尿病性腎症患者における血漿中ビトロネクチン濃度の変化
kn-title=Changes in Plasma Concentration of Vitronectin in Patients with Diabetic Nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=森岡茂
kn-aut-sei=森岡
kn-aut-mei=茂
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=19880630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=実験的腎障害における糸球体基底膜の微細構造に関する研究 第1編 アミノヌクレオシドネフローゼにおける糸球体基底膜の微細構造の変化 第2編 糖尿病性腎症における糸球体基底膜の微細構造の変化
kn-title=第1編 (Ultrastructural Changes of the Glomerular Basement Membrane in Aminonucleoside Nephrosis) 第2編 (Ultrastructural Changes of the Glomerular Basement Membrane in Diabetic Nephropathy)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=高谷泰正
kn-aut-sei=高谷
kn-aut-mei=泰正
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2003
dt-pub=20030325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=HMG-CoA還元酵素阻害薬の多面的作用による糖尿病性腎症抑制効果
kn-title=HMG-CoA reductase inhibitor ameliorates diabetic nephropathy by its pleiotropic effects in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=臼井仁美
kn-aut-sei=臼井
kn-aut-mei=仁美
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END