2021/12/17 更新

写真a

シカタ ケンイチ
四方 賢一
SHIKATA Kenichi
所属
岡山大学病院 教授
職名
教授
外部リンク

学位

  • 医学博士

研究キーワード

  • Nephrology

  • Diabetology

  • 腎臓病学

  • 糖尿病学

研究分野

  • ライフサイエンス / 免疫学

  • ライフサイエンス / 腎臓内科学

  • ライフサイエンス / 代謝、内分泌学  / 糖尿病学

学歴

  • 岡山大学    

    - 1992年

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    国名: 日本国

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  • 岡山大学   Graduate School, Division of Medicine  

    - 1992年

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  • 岡山大学   Medical School   Faculty of Medicine

    - 1985年

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    国名: 日本国

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  • 岡山大学   Faculty of Medicine  

    - 1985年

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経歴

  • - 岡山大学岡山大学病院 教授

    2010年

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  • - Professor,University Hospital of Medicine and Dentistry,Okayama University

    2010年

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委員歴

  • 岡山県糖尿病協会   会長  

    2021年   

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    団体区分:自治体

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  • 腎臓学会   学術評議員  

    2021年   

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    団体区分:学協会

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  • 糖尿病学会   評議員  

    2021年   

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    団体区分:学協会

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  • 糖尿病合併症学会   理事  

    2021年   

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    団体区分:学協会

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  • 内科学会中国支部   評議員  

    2021年   

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    団体区分:学協会

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  • 糖尿病性腎症研究会   世話人  

    2021年   

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    団体区分:学協会

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  • 病態栄養学会 NST実施委員会   委員  

    2021年   

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    団体区分:学協会

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  • 糖尿病療養指導士認定機構編集委員会   委員長  

    2021年   

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    団体区分:学協会

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  • 糖尿病肥満動物学会   評議員  

    2021年   

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    団体区分:学協会

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  • 病態栄養学会   代議員・評議員  

    2021年   

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    団体区分:学協会

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  • 岡山県医師会糖尿病対策推進会議   委員  

    2021年   

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    団体区分:自治体

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  • 岡山県糖尿病対策専門部会   会長  

    2021年   

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    団体区分:自治体

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▼全件表示

 

論文

  • Long-term safety and efficacy of alogliptin, a DPP-4 inhibitor, in patients with type 2 diabetes: a 3-year prospective, controlled, observational study (J-BRAND Registry). 国際誌

    Kohjiro Ueki, Yukio Tanizawa, Jiro Nakamura, Yuichiro Yamada, Nobuya Inagaki, Hirotaka Watada, Iichiro Shimomura, Rimei Nishimura, Hideaki Miyoshi, Atsuko Abiko, Hideki Katagiri, Michio Hayashi, Akira Shimada, Keiko Naruse, Shimpei Fujimoto, Masazumi Fujiwara, Kenichi Shikata, Yosuke Okada, Eiichi Araki, Tsutomu Yamazaki, Takashi Kadowaki

    BMJ open diabetes research & care   9 ( 1 )   2021年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    INTRODUCTION: Given an increasing use of dipeptidyl peptidase-4 (DPP-4) inhibitors to treat patients with type 2 diabetes mellitus in the real-world setting, we conducted a prospective observational study (Japan-based Clinical Research Network for Diabetes Registry: J-BRAND Registry) to elucidate the safety and efficacy profile of long-term usage of alogliptin. RESEARCH DESIGN AND METHODS: We registered 5969 patients from April 2012 through September 2014, who started receiving alogliptin (group A) or other classes of oral hypoglycemic agents (OHAs; group B), and were followed for 3 years at 239 sites nationwide. Safety was the primary outcome. Symptomatic hypoglycemia, pancreatitis, skin disorders of non-extrinsic origin, severe infections, and cancer were collected as major adverse events (AEs). Efficacy assessment was the secondary outcome and included changes in hemoglobin A1c (HbA1c), fasting blood glucose, fasting insulin and urinary albumin. RESULTS: Of the registered, 5150 (group A: 3395 and group B: 1755) and 5096 (3358 and 1738) were included for safety and efficacy analysis, respectively. Group A patients mostly (>90%) continued to use alogliptin. In group B, biguanides were the primary agents, while DPP-4 inhibitors were added in up to ~36% of patients. The overall incidence of AEs was similar between the two groups (42.7% vs 42.2%). Kaplan-Meier analysis revealed the incidence of cancer was significantly higher in group A than in group B (7.4% vs 4.8%, p=0.040), while no significant incidence difference was observed in the individual cancer. Multivariate Cox regression analysis revealed that the imbalanced patient distribution (more elderly patients in group A than in group B), but not alogliptin usage per se, contributed to cancer development. The incidence of other major AE categories was with no between-group difference. Between-group difference was not detected, either, in the incidence of microvascular and macrovascular complications. HbA1c and fasting glucose decreased significantly at the 0.5-year visit and nearly plateaued thereafter in both groups. CONCLUSIONS: Alogliptin as a representative of DPP-4 inhibitors was safe and durably efficacious when used alone or with other OHAs for patients with type 2 diabetes in the real world setting.

    DOI: 10.1136/bmjdrc-2020-001787

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  • Novel Urinary Glycan Biomarkers Predict Cardiovascular Events in Patients With Type 2 Diabetes: A Multicenter Prospective Study With 5-Year Follow Up (U-CARE Study 2). 国際誌

    Koki Mise, Mariko Imamura, Satoshi Yamaguchi, Mayu Watanabe, Chigusa Higuchi, Akihiro Katayama, Satoshi Miyamoto, Haruhito A Uchida, Atsuko Nakatsuka, Jun Eguchi, Kazuyuki Hida, Tatsuaki Nakato, Atsuhito Tone, Sanae Teshigawara, Takashi Matsuoka, Shinji Kamei, Kazutoshi Murakami, Ikki Shimizu, Katsuhiro Miyashita, Shinichiro Ando, Tomokazu Nunoue, Michihiro Yoshida, Masao Yamada, Kenichi Shikata, Jun Wada

    Frontiers in cardiovascular medicine   8   668059 - 668059   2021年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Background: Although various biomarkers predict cardiovascular event (CVE) in patients with diabetes, the relationship of urinary glycan profile with CVE in patients with diabetes remains unclear. Methods: Among 680 patients with type 2 diabetes, we examined the baseline urinary glycan signals binding to 45 lectins with different specificities. Primary outcome was defined as CVE including cardiovascular disease, stroke, and peripheral arterial disease. Results: During approximately a 5-year follow-up period, 62 patients reached the endpoint. Cox proportional hazards analysis revealed that urinary glycan signals binding to two lectins were significantly associated with the outcome after adjustment for known indicators of CVE and for false discovery rate, as well as increased model fitness. Hazard ratios for these lectins (+1 SD for the glycan index) were UDA (recognizing glycan: mixture of Man5 to Man9): 1.78 (95% CI: 1.24-2.55, P = 0.002) and Calsepa [High-Man (Man2-6)]: 1.56 (1.19-2.04, P = 0.001). Common glycan binding to these lectins was high-mannose type of N-glycans. Moreover, adding glycan index for UDA to a model including known confounders improved the outcome prediction [Difference of Harrel's C-index: 0.028 (95% CI: 0.001-0.055, P = 0.044), net reclassification improvement at 5-year risk increased by 0.368 (0.045-0.692, P = 0.026), and the Akaike information criterion and Bayesian information criterion decreased from 725.7 to 716.5, and 761.8 to 757.2, respectively]. Conclusion: The urinary excretion of high-mannose glycan may be a valuable biomarker for improving prediction of CVE in patients with type 2 diabetes, and provides the rationale to explore the mechanism underlying abnormal N-glycosylation occurring in patients with diabetes at higher risk of CVE. Trial Registration: This study was registered with the University Hospital Medical Information Network on June 26, 2012 (Clinical trial number: UMIN000011525, URL: https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000013482).

    DOI: 10.3389/fcvm.2021.668059

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  • Esaxerenone (CS-3150) in Patients with Type 2 Diabetes and Microalbuminuria (ESAX-DN)

    Sadayoshi Ito, Naoki Kashihara, Kenichi Shikata, Masaomi Nangaku, Takashi Wada, Yasuyuki Okuda, Tomoko Sawanobori

    Clinical Journal of the American Society of Nephrology   15 ( 12 )   1715 - 1727   2020年12月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:American Society of Nephrology (ASN)  

    <sec><title>Background and objectives</title>Diabetic kidney disease is an important complication of type 2 diabetes. In a phase 2b study, adding esaxerenone to renin-angiotensin system inhibitors dose dependently reduced the urinary albumin-to-creatinine ratio in patients with type 2 diabetes and microalbuminuria. This 52-week phase 3 study further investigated the effects of esaxerenone on the urinary albumin-to-creatinine ratio in this patient group.

    </sec><sec><title>Design, setting, participants, &amp; measurements</title>In this multicenter, randomized, double-blind study, patients with type 2 diabetes and a urinary albumin-to-creatinine ratio of 45 to &lt;300 mg/g creatinine treated with renin-angiotensin system inhibitors were randomized to esaxerenone or placebo for 52 weeks (<italic>n</italic>=455). Esaxerenone was initiated at 1.25 mg/d and titrated to 2.5 mg/d on the basis of serum potassium monitoring. The primary endpoint was the proportion of patients achieving urinary albumin-to-creatinine ratio remission (&lt;30 mg/g creatinine and ≥30% reduction from baseline on two consecutive occasions).

    </sec><sec><title>Results</title>Overall, 49 (22%) and nine (4%) patients in the esaxerenone and placebo groups, respectively, achieved urinary albumin-to-creatinine ratio remission (absolute difference 18%; 95% confidence interval, 12% to 25%; <italic>P&lt;</italic>0.001). The percent change in urinary albumin-to-creatinine ratio from baseline to end of treatment was significantly higher with esaxerenone versus placebo (−58% versus 8%; geometric least-squares mean ratio to placebo 0.38, 95% confidence interval, 0.33 to 0.44). There was a significant improvement with esaxerenone versus placebo in time to first remission (hazard ratio, 5.13; 95% confidence interval, 3.27 to 8.04) and time to first transition to urinary albumin-to-creatinine ratio ≥300 mg/g creatinine (hazard ratio, 0.23; 95% confidence interval, 0.11 to 0.48). More patients had a serum potassium level ≥6.0 or ≥5.5 mEq/L on two consecutive measurements in the esaxerenone group (20 [9%]) versus placebo (5 [2%]); these events were asymptomatic and resolved after dosage reduction or treatment discontinuation.

    </sec><sec><title>Conclusions</title>Adding esaxerenone to existing renin-angiotensin system inhibitor therapy in patients with type 2 diabetes and microalbuminuria increased the likelihood of albuminuria returning to normal levels, and reduced progression of albuminuria to higher levels.

    </sec>

    DOI: 10.2215/cjn.06870520

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  • Dysfunction of CD8 + PD-1 + T cells in type 2 diabetes caused by the impairment of metabolism-immune axis. 国際誌

    Ichiro Nojima, Shingo Eikawa, Nahoko Tomonobu, Yoshiko Hada, Nobuo Kajitani, Sanae Teshigawara, Satoshi Miyamoto, Atsuhito Tone, Haruhito A Uchida, Atsuko Nakatsuka, Jun Eguchi, Kenichi Shikata, Heiichiro Udono, Jun Wada

    Scientific reports   10 ( 1 )   14928 - 14928   2020年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The metabolic changes and dysfunction in CD8 + T cells may be involved in tumor progression and susceptibility to virus infection in type 2 diabetes (T2D). In C57BL/6JJcl mice fed with high fat-high sucrose chow (HFS), multifunctionality of CD8 + splenic and tumor-infiltrating lymphocytes (TILs) was impaired and associated with enhanced tumor growth, which were inhibited by metformin. In CD8 + splenic T cells from the HFS mice, glycolysis/basal respiration ratio was significantly reduced and reversed by metformin. In the patients with T2D (DM), multifunctionality of circulating CD8 + PD-1 + T cells stimulated with PMA/ionomycin as well as with HLA-A*24:02 CMV peptide was dampened, while metformin recovered multifunctionality. Both glycolysis and basal respiration were reduced in DM, and glycolysis was increased by metformin. The disturbance of the link between metabolism and immune function in CD8 + PD-1 + T cells in T2D was proved by recovery of antigen-specific and non-specific cytokine production via metformin-mediated increase in glycolytic activity.

    DOI: 10.1038/s41598-020-71946-3

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  • 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).

    Shikata K, Haneda M, Ninomiya T, Koya D, Suzuki Y, Suzuki D, Ishida H, Akai H, Tomino Y, Uzu T, Nishimura M, Maeda S, Ogawa D, Miyamoto S, Makino H

    J Diabetes Investig.   2020年6月

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    記述言語:英語  

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  • The hypoglycemia-prevention effect of sensor-augmented pump therapy with predictive low glucose management in Japanese patients with type 1 diabetes mellitus: a short-term study

    Akihiro Katayama, Atsuhito Tone, Mayu Watanabe, Sanae Teshigawara, Satoshi Miyamoto, Jun Eguchi, Atsuko Nakatsuka, Kenichi Shikata, Jun Wada

    Diabetology International   11 ( 2 )   97 - 104   2020年4月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science and Business Media LLC  

    DOI: 10.1007/s13340-019-00408-7

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    その他リンク: http://link.springer.com/article/10.1007/s13340-019-00408-7/fulltext.html

  • 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 査読

    Shikata K, Kodera R, Utsunomiya K, Koya D, Nishimura R, Miyamoto S, Tajima N, JDCP study group.

    J Diabetes Investig   11 ( 2 )   325 - 332   2019年9月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Efficacy and Safety of Esaxerenone (CS-3150) for the Treatment of Type 2 Diabetes with Microalbuminuria: A Randomized, Double-Blind, Placebo-Controlled, Phase II Trial 査読

    Ito S, Shikata K, Nangaku M, Okuda Y, Sawanobori T.

    Clin J Am Soc Nephrol .   14 ( 8 )   1161 - 1172   2019年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • インスリンポンプ療法からSAP療法への治療変更効果に関する後ろ向き観察研究 査読

    山口 哲志(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), 利根 淳仁, 勅使川原 早苗, 渡邊 真由, 片山 晶博, 宮本 聡, 江口 潤, 中司 敦子, 樋口 千草, 小川 大輔, 四方 賢一, 和田 淳

    糖尿病   62 ( 5 )   315 - 321   2019年5月

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

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  • The clinical efficacy of angiotensin II type1 receptor blockers on inflammatory markers in patients with hypertension: a multicenter randomized-controlled trial; MUSCAT-3 study. 国際誌

    Ryoko Umebayashi, Haruhito A Uchida, Yuka Okuyama, Yuki Kakio, Yoshihisa Hanayama, Kenichi Shikata, Jun Wada

    Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals   24 ( 3 )   255 - 261   2019年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Purpose: The purpose of present study was to evaluate the clinical efficacy of irbesartan on the anti-inflammatory and anti-oxidative stress effect in patients with hypertension compared to other ARBs. Further, we assessed the effect of the ARBs on kidney function and urinary albumin excretion. Methods: Eighty-five outpatients with hypertension who took an ARB except irbesartan more than 3 months were assigned into two groups, one continued the same ARB and the other switched the ARB to irbesartan for 6 months. Results: Although blood pressures were equally controlled (continue group: 148 ± 2/79 ± 2 mmHg to 131 ± 2/74 ± 2 mmHg; switch group: 152 ± 2/81 ± 2 mmHg to 132 ± 2/74 ± 2 mmHg; p < 0.001 each), the inflammatory markers (hsCRP, PTX3, MCP-1) and oxidative stress marker (MDA-LDL) did not change after 6 months in both groups. Urinary albumin excretion was significantly reduced only in the switch group without renal function deterioration (switch group 292.4 ± 857.9 mg/gCr to 250.6 ± 906.5 mg/gCr, p = 0.012). Conclusion: These results provide knowledge of the characteristics of irbesartan, suggesting appropriate choice of ARBs in the treatment for hypertension should be considered.

    DOI: 10.1080/1354750X.2018.1548033

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  • 2型糖尿病患者における尿中糖鎖排泄量と腎・心血管イベントおよび総死亡との関連の検討 査読

    今村 麻理子, 三瀬 広記, 中塔 辰明, 清水 一紀, 安藤 晋一郎, 松岡 孝, 宮下 雄博, 肥田 和之, 江口 潤, 中司 敦子, 四方 賢一, 和田 淳

    糖尿病   62 ( 2 )   113 - 113   2019年2月

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    記述言語:日本語   出版者・発行元:(一社)日本糖尿病学会  

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  • Renal expression of trefoil factor 3 mRNA in association with tubulointerstitial fibrosis in IgA nephropathy. 査読

    Tanaka K, Sugiyama H, Yamanari T, Mise K, Morinaga H, Kitagawa M, Onishi A, Ogawa-Akiyama A, Tanabe K, Eguchi J, Ohmoto Y, Shikata K, Wada J

    Nephrology (Carlton, Vic.)   23 ( 9 )   855 - 862   2018年9月

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    記述言語:英語  

    DOI: 10.1111/nep.13444

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  • Identification of Novel Urinary Biomarkers for Predicting Renal Prognosis in Patients With Type 2 Diabetes by Glycan Profiling in a Multicenter Prospective Cohort Study: U-CARE Study 1. 査読

    Mise K, Imamura M, Yamaguchi S, Teshigawara S, Tone A, Uchida HA, Eguchi J, Nakatsuka A, Ogawa D, Yoshida M, Yamada M, Shikata K, Wada J

    Diabetes care   41 ( 8 )   1765 - 1775   2018年8月

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    記述言語:英語  

    DOI: 10.2337/dc18-0030

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  • Development of a novel estimation method for hemoglobin A1c using glycated albumin in type 2 diabetes mellitus patients with end-stage renal disease.

    Nakamura A, Kodera R, Sakamoto N, Ujike H, Wada J, Shikata K, Makino H.

    Diabetol Int   9 ( 3 )   179 - 188   2018年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1007/s13340-018-0342-6

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  • Urine Trefoil Factors as Prognostic Biomarkers in Chronic Kidney Disease. 査読

    Yamanari T, Sugiyama H, Tanaka K, Morinaga H, Kitagawa M, Onishi A, Ogawa-Akiyama A, Kano Y, Mise K, Ohmoto Y, Shikata K, Wada J

    BioMed research international   2018   3024698 - 3024698   2018年

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    記述言語:英語  

    DOI: 10.1155/2018/3024698

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  • Erythromycin ameliorates renal injury via anti-inflammatory effects in experimental diabetic rats. 査読

    A.Tone, K.Shikata, M.Sasaki, S.Ohga,K.Yozai, S.Nishishita, H.Usui, R.Nagase, D.Ogawa, S.Okada, Y.Shikata, J.Wada, H.Makino

    Diabetologia   48 ( 11 )   2402 - 2411   2005年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1007/s00125-005-1945-6

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  • HMG-CoA reductase inhibitor ameliorates diabetic nephropathy by its pleiotropic effects in rats. 査読

    Usui H, Shikata K, Matsuda M, Okada S, Ogawa D, Yamashita T, Hida K, Satoh M, Wada J, Makino H

    Nephrol Dial Transplant   18 ( 2 )   265 - 272   2003年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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書籍等出版物

  • 糖尿病性腎臓病の病態と治療

    宮本聡, 四方賢一( 担当: 共著)

    中外医学社  2021年4月 

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    担当ページ:89-94   記述言語:日本語

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  • 糖尿病療養指導ガイドブック2019

    四方賢一( 担当: 共著)

    メディカルレビュー社  2020年5月 

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    記述言語:日本語

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  • 糖尿病診療ガイドライン

    ( 担当: 共著)

    南江堂  2019年10月 

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    記述言語:日本語

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  • 糖尿病専門医研修指導ガイドブック

    ( 担当: 共著)

    診断と治療社  2019年9月 

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    記述言語:日本語

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  • 【エビデンスに基づく新しい腎臓病診療】CKD患者の合併症管理 糖尿病診療ガイドライン2016

    ( 担当: 共著)

    最新医学社  2018年12月 

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    記述言語:日本語

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  • エビデンスに基づくCKD診療ガイドライン2018

    ( 担当: 共著)

    日本腎臓学会  2018年12月 

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    記述言語:日本語

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  • 糖尿病性腎臓病の診かた、考えかた

    利根淳仁、四方賢一( 担当: 共著 ,  範囲: 糖尿病治療薬の選択.)

    中外医学社  2018年6月 

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    担当ページ:183-190   記述言語:日本語

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  • 糖尿病療養指導ガイドブック2018

    ( 担当: 共著)

    メディカルレビュー社  2018年5月 

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    記述言語:日本語

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  • 糖尿病の療養指導Q&A

    利根淳仁、四方賢一( 担当: 共著 ,  範囲: 糖尿病性腎症病期分類の改訂とCKD重要度分類について.)

    医歯薬出版  2018年5月 

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    担当ページ:123-125   記述言語:日本語

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  • 透析患者診療に役立つ診断と重症度判定

    四方賢一( 担当: 共著)

    日本メディカルセンター  2016年6月 

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    記述言語:日本語

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  • 糖尿病腎症

    ( 担当: 共著)

    南江堂  2016年6月 

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    記述言語:日本語

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  • 糖尿病診療ガイドライン2016

    四方賢一( 担当: 共著)

    2016年6月 

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  • インクレチン関連薬の腎保護効果

    ( 担当: 共著)

    中外医学社  2016年1月 

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    記述言語:日本語

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  • 糖尿病専門医研修ガイドブック改訂第6版

    ( 担当: 共著)

    日本糖尿病学会  2015年12月 

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    記述言語:日本語

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  • CKDステージG3b-5診療ガイドライン2015

    ( 担当: 共著)

    東京医学社  2015年10月 

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    記述言語:日本語

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  • 糖尿病研修ノート改訂第2版

    小寺亮、四方賢一( 担当: 共著 ,  範囲: 尿糖、尿蛋白、尿中アルブミン、その他の尿パラメーター、尿沈渣.)

    診断と治療社  2014年 

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    担当ページ:237-241   記述言語:日本語

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  • わかる! 糖尿病の病態・治療・ケア

    ( 担当: 共著)

    メディカ  2013年9月 

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    記述言語:日本語

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  • エビデンスに基づくCKD診療ガイドライン2013

    ( 担当: 共著)

    日本腎臓学会  2013年7月 

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    担当ページ:585-860   記述言語:日本語

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  • AnnualReview腎臓

    ( 担当: 共著)

    中外医学社  2013年1月 

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    記述言語:日本語

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  • Annual Review腎臓 全身性疾患と腎障害 糖尿病性腎症における核内受容体の役割

    ( 担当: 共著)

    中外医学社  2013年1月 

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    記述言語:日本語

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  • 腎疾患・透析 最新の治療2005?2007

    四方賢一( 範囲: 糖尿病性腎症)

    南江堂  2005年4月 

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    担当ページ:145-147  

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  • AGEs研究の最前線?糖化蛋白関連疾患研究の現状?

    臼井仁美、四方賢一、槇野博史( 範囲: AGEsと糖尿病腎症)

    メディカルレビュー社  2004年4月 

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    担当ページ:p99?p108  

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▼全件表示

MISC

  • DKD変革期の診断 血糖コントロールの指標と腎機能

    四方 賢一

    腎と透析   84 ( 2 )   212 - 214   2018年

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  • 治療の実際 糖尿病性腎症の診断と治療 新たな展開

    四方 賢一

    臨床と研究   95 ( 1 )   135 - 139   2018年

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    記述言語:日本語  

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  • The glucose-lowering efficacy of sitagliptin in obese japanese patients with type 2 diabetes

    Ryo Kodera,Kenichi Shikata*,Akihiko Nakamura,Satoru Okazaki,Ryo Nagase,Tatsuaki Nakatou,Shigeru Haisa,Kazuyuki Hida,Katsuhiro Miyashita,Hirofumi Makino

    Internal Medicine, Japanese Journal of Medicine, Internal medicine (Tokyo, Japan)   56 ( 6 )   605 - 613   2017年

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  • 【臓器炎症からみた糖尿病および糖尿病性合併症】 慢性炎症と糖尿病腎症.

    宮本聡, 四方賢一, 和田淳

    糖尿病診療マスター   15 ( 10 )   856 - 861   2017年

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  • 岡山県健診受診者の慢性腎臓病(CKD)認知度 2015年度.

    内田治仁, 杉山斉, 宮崎雅史, 和田淳, 四方賢一, 柏原直樹, 槇野博史

    岡山医学会雑誌   129 ( 2 )   101 - 105   2017年

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    記述言語:日本語  

    DOI: 10.4044/joma.129.101

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  • 糖尿病患者の「治療に伴うストレス認知尺度」の開発.

    住吉和子, 川田智恵子, 岡本辰夫, 大橋睦子, 實金栄, 高林範子, 太湯好子, 金外淑, 和田淳, 四方賢一, 中嶋和夫

    岡山医学会雑誌   129 ( 2 )   93 - 99   2017年

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    記述言語:日本語  

    DOI: 10.4044/joma.129.93

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  • 【糖尿病治療の個別化-個々の症例にベストな治療とは】 合併症のある糖尿病患者の診療 透析導入直前,透析導入後の糖尿病患者の管理.

    四方賢一

    内科   119 ( 1 )   89 - 93   2017年

  • 【糖尿病治療の個別化-個々の症例にベストな治療とは】 合併症のある糖尿病患者の診療 透析導入直前,透析導入後の糖尿病患者の管理.

    四方賢一

    カレントテラピー   35 ( 1 )   72 - 77   2017年

  • 【心に残る楽しい糖尿病教室・教育】 糖尿病教育の標準化と組織化 岡山県の取り組み.

    利根淳仁, 四方賢一

    DM Ensemble   6 ( 1 )   21 - 24   2017年

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  • 糖尿病性腎症の治療 現状と展望.

    四方賢一

    Diabetes Journal: 糖尿病と代謝   45 ( 1 )   1 - 6   2017年

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  • Renoprotective effects of incretin-based drugs

    Ryo Kodera,Kenichi Shikata*

    Journal of Diabetes Investigation   7 ( 1 )   29 - 31   2016年1月

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    担当区分:筆頭著者   記述言語:英語  

    DOI: 10.1111/jdi.12380

    Web of Science

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  • インクレチン関連薬の腎保護効果.

    小寺亮, 四方賢一

    Annual Review腎臓2016   149 - 155   2016年

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  • 糖尿病性腎症の原因と発症機序.

    小寺亮, 四方賢一

    Jmedmook   42   18 - 23   2016年

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    記述言語:日本語  

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  • SAP導入により基礎インスリン補充の不足が判明し、その増量により血糖コントロールの改善を得た2症例.

    利根淳仁, 四方賢一, 和田淳

    日本先進糖尿病治療研究会雑誌   12   12 - 16   2016年

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    記述言語:日本語  

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  • The management of diabetic patients on hemodialysis or peritoneal dialysis

    Masaru Kinomura, Hitoshi Sugiyama, Kenichi Shikata

    Nippon rinsho. Japanese journal of clinical medicine, Nihon rinsho. Japanese journal of clinical medicine   74   212 - 216   2016年

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    担当区分:筆頭著者   記述言語:英語  

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  • 糖尿病透析患者の管理.XI.糖尿病合併症の病態・診断・治療、2.慢性合併症 (2)糖尿病腎症.新時代の臨床糖尿病学(下).

    木野村 賢, 杉山 斉, 四方賢一

    日本臨床   74 ( 2 )   212 - 216   2016年

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  • 【糖尿病診療のスキルアップ】 糖尿病腎症(腎不全期まで)の治療管理について

    利根 淳仁, 四方 賢一

    月刊糖尿病   7 ( 4 )   37 - 43   2015年

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  • 一週一話:糖尿病腎症に対するインクレチン関連薬の可能性

    小寺亮, 四方賢一

    週刊日本医事新報   4761   51 - 51   2015年

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  • チーム医療の実践とその効果

    利根淳仁, 四方賢一

    月刊糖尿病   7 ( 12 )   48 - 53   2015年

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  • 岡山県糖尿病医科・歯科連携で用いられる「歯周病セルフチェック票」の妥当性についての検討

    天田雅文, 利根淳仁, 角南次郎, 大森一弘, 松尾敬子, 出原陽子, 原本麻代, 伊勢田泉, 内田治仁, 四方賢一, 高柴正悟, 肥田和之, 和田淳

    Diabetes Frontier   26 ( 4 )   512 - 517   2015年

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    記述言語:日本語  

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  • 基礎インスリン比率の適正化はインスリンポンプ療法における1,5-AG値の改善に寄与する -インスリンポンプ療法と血糖変動-

    利根淳仁, 四方賢一, 和田淳

    日本先進糖尿病治療研究会雑誌   11   1 - 4   2015年

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    記述言語:日本語  

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  • 岡山県内統一糖尿病地域連携クリティカルパスの意義と医療連携促進による機能分化についての検討

    利根淳仁, 肥田和之, 大森信彦, 中塔辰明, 四方賢一, 和田 淳

    日本医療マネジメント学会雑誌   16 ( 3 )   134 - 140   2015年

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    記述言語:日本語  

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  • 糖尿病合併CKDステージG4,5の降圧療法では、RA系阻害薬は有用か?

    小寺亮, 四方賢一

    厚生労働科学研究委託事業   25 - 34   2015年

     詳細を見る

    記述言語:日本語  

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  • 【新人スタッフのあやふや知識を確実にする 図解でわかる!糖尿病の病態生理とケア】 徹底解説 糖尿病合併症の病態とケア 糖尿病腎症の病態とケア

    四方 賢一

    糖尿病ケア   12 ( 4 )   342 - 345   2015年

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  • Factors associated with remission and/or regression of microalbuminuria in type 2 diabetes mellitus.

    Ono T, Shikata K, Obika M, Miyatake N, Kodera R, Hirota D, Wada J, Kataoka H, Ogawa D, Makino H

    Acta Med Okayama   68 ( 4 )   235 - 241   2014年8月

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    記述言語:英語  

    Web of Science

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  • Lifestyle modification is associated with improving estimated glomerular filtration rate (eGFR) and proteinuria in Japanese with proteinuria.

    Miyatake N, Shikata K, Makino H, Numata T

    Acta Med Okayama   68 ( 1 )   43 - 46   2014年2月

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    記述言語:英語  

    Web of Science

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  • Dipeptidyl peptidase-4 inhibitor ameliorates early renal injury through its anti-inflammatory action in a rat model of type 1 diabetes.

    Kodera R, Shikata K, Takatsuka T, Oda K, Miyamoto S, Kajitani N, Hirota D, Ono T, Usui HK, Makino H

    Biochem Biophys Res Commun   443 ( 3 )   828 - 833   2014年1月

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  • 降圧薬

    小比賀美香子, 四方賢一

    糖尿病診療マスター   12 ( 4 )   420 - 423   2014年

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  • 糖尿病治療薬Q&A-最新のSGLT-2阻害薬を含め賢く使い分ける-】 SGLT-2阻害薬の有効性について教えてください

    小野哲一郎, 四方賢一

    治療   96 ( 6 )   996 - 997   2014年

     詳細を見る

  • コンサルテーション 糖尿病性腎症患者の症例報告(解説)

    四方賢一

    Diabetes Update   3 ( 3 )   140 - 145   2014年

     詳細を見る

  • 糖尿病の療養指導Q&A 糖尿病性腎症病期分類の改訂とCKD重症度分類(Q&A)

    利根淳仁, 四方賢一

    プラクティス (0289-4947)31巻4号 Page515-517(2014.07)   31 ( 4 )   515 - 517   2014年

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  • 糖尿病の療養指導Q&A 糖尿病性腎症病期分類の改訂とCKD重症度分類.

    利根淳仁, 四方賢一

    プラクティス   31 ( 4 )   515 - 517   2014年

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  • 【糖尿病診療におけるチーム医療はどうあるべきか】 個別の目的に応じたチーム医療の現状とその効果 腎症予防におけるチーム医療

    四方賢一

    月刊糖尿病   6 ( 1 )   88 - 92   2014年

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  • チーム医療で糖尿病性腎症の進展を防ぐ.

    利根淳仁, 四方賢一

    Diabetes Frontier   25 ( 6 )   699 - 703   2014年

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  • インクレチン関連薬の腎保護効果.

    四方賢一, 小寺亮

    血管医学   15 ( 4 )   377 - 384   2014年

     詳細を見る

  • 生理機能検査からみえる糖尿病合併症 糖尿病性腎症.

    小寺亮, 四方賢一

    臨床検査   58 ( 6 )   717 - 722   2014年

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  • 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(解説)

    宮本 聡, 四方 賢一, 宮坂 京子, 岡田 震一, 佐々木 基史, 小寺 亮, 廣田 大昌, 梶谷 展生, 高塚 哲全, 片岡 仁美, 西下 伸吾, 堀口 千景, 船越 顕博, 西森 久和, 内田 治仁, 小川 大輔, 槇野 博史

    岡山医学会雑誌   121 ( 1 )   1 - 6   2014年

  • 【生理機能検査からみえる糖尿病合併症】 糖尿病性腎症

    小寺亮, 四方賢一

    臨床検査   58 ( 6 )   707 - 722   2014年

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  • 【糖尿病診療2014】 糖尿病の合併症・併発疾患 糖尿病透析予防

    四方賢一

    診断と治療   102 ( 9 )   1347 - 1352   2014年

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  • 【糖尿病「前熟考期」の壁-あなたはどうして平気でいられるの?】 熟考期へのアドバイス 練達医師のワザを伝授 治療をためらう人へ 降圧薬

    小比賀 美香子, 四方 賢一

    糖尿病診療マスター   12 ( 4 )   420 - 423   2014年

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  • Combination therapy with an angiotensin-converting-enzyme inhibitor and an angiotensin II receptor antagonist ameliorates microinflammation and oxidative stress in patients with diabetic nephropathy.

    Nakamura A, Shikata K, Nakatou T, kitamura T, Kajitani N, Ogawa D, Makino H

    Journal of Diabetes lnvestigation   4 ( 2 )   195 - 201   2013年3月

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    記述言語:英語  

    DOI: 10.1111/jdi.12004

    Scopus

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  • Microinflammation in the pathogenesis of diabetic nephropathy.

    J Diabetes Inves   2013年

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    記述言語:英語  

    DOI: 10.1111/jdi.12004

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  • Decreasing serum uric acid levels are associated with improving estimated glomerular filtration rate(eGFR) in Japanese women.

    Miyatake N, Shikata K, Makino H, Numata T

    Open Journal of Epidemiology   3 ( 2 )   40 - 43   2013年

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    記述言語:英語  

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  • インクレチンと心血管障害 インクレチン関連薬と腎保護作用.

    小寺 亮, 四方 賢一

    Angiology Frontier   12 ( 1 )   45 - 50   2013年

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  • 糖尿病性腎症における核内受容体の役割.

    小川大輔, 四方賢一

    Annual Review 腎臓   241 - 246   2013年

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  • 糖尿病治療薬と一緒に使われる薬のキホン 高血圧の薬

    Diet Exersize Medicine   2   12 - 13   2013年

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  • 糖尿病腎症の治療.

    小寺 亮, 四方 賢一

    科学的根拠に基づく糖尿病診療ガイドライン2013   97 - 113   2013年

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  • Decreasing abdominal circumference is associated with improving estimated glomerular Filtration Rate(eGFR)with Lifestyle Modification in Japanese Men: A Pilot Study.

    Miyatake N, Shikata K, MakinoH, Numata T

    Acta Med Okayama   65 ( 6 )   363 - 367   2011年12月

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  • Involvement of MAPKs in ICAM-1 expression in glomerular endothelial cells in diabetic nephropathy.

    Watanabe N, Shikata K, Shikata Y, Sarai K, Omori K, Kodera R, Sato C, Wada J, Makino H

    Acta Med Okayama   65 ( 4 )   247 - 257   2011年8月

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  • The relation between estimated glomerular filtration rate and proteinuria in Okayama Prefecture, Japan.

    Miyatake N, Shikata K, Makino H, Numata T.

    Environ Health Prev Med.   16 ( 3 )   191 - 195   2011年5月

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  • The macrophage is a key factor in renal injuries caused by glomerular hyperfiltration.

    Sasaki M, Shikata K, Okada S, Miyamoto S, Nishishita S, Kataoka HU, Sato C, Wada J, Ogawa D, Makino H.

    Acta Med Okayama   65 ( 2 )   81 - 89   2011年4月

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    記述言語:英語  

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  • Intercellular adhesion molecule-1 plays a critical role in glomerulosclerosis after subtotal nephrectomy

    Yuichi Kido, Daisuke Ogawa, Kenichi Shikata, Motofumi Sasaki, Ryo Nagase, Shinichi Okada, Hitomi Usui Kataoka, Jun Wada, Hirofumi Makino

    CLINICAL AND EXPERIMENTAL NEPHROLOGY   15 ( 2 )   212 - 219   2011年4月

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    記述言語:英語   出版者・発行元:SPRINGER  

    Hyperfiltration in the glomeruli have been considered to be an important cause of glomerular injury; however, the role of intercellular adhesion molecule (ICAM)-1 in the pathogenesis of glomerulosclerosis is not known.
    To elucidate the effects of ICAM-1 depletion on hyperfiltration-induced glomerular disorder, we used subtotally nephrectomized ICAM-1(+/+) and ICAM-1(-/-) mice. We evaluated macrophage infiltration, mesangial matrix expansion, transforming growth factor (TGF)-beta and type IV collagen accumulation in glomeruli.
    Macrophage infiltration into the glomeruli and mesangial matrix expansion coincident with increased expression of both ICAM-1 and TGF-beta, and accumulation of type IV collagen were ameliorated in subtotally nephrectomized ICAM-1(-/-) mice compared to ICAM-1(+/+) mice. ICAM-1 depletion significantly reduced hyperfiltration-induced glomerular injury after renal ablation.
    Our present findings suggest that glomerular hyperfiltration is the leading cause of glomerulosclerosis, and it is mediated, at least in part, by ICAM-1 expression and macrophage infiltration.

    DOI: 10.1007/s10157-010-0388-7

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  • Glucagon-like peptide-1 receptor agonist ameliorates renal injury through its anti-inflammatory action without lowering blood glucose level in a rat model of type 1 diabetes.

    Diabetologia   54 ( 4 )   965 - 978   2011年4月

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  • Emphysematous cystitis in a Patient with type 2 diabetes mellitus.

    Toyota N, Ogawa D, Ishii K, Hirata K, Wada J, Shikata K, Makino H

    Acta Med Okayama   65 ( 2 )   129 - 133   2011年4月

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    記述言語:英語  

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  • Intercellular adhesion molecule-1 plays a critical role in glomerulosclerosis after subtotal nephrectomy.

    Clin Exp Nephrol   15 ( 2 )   212 - 219   2011年4月

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  • Activation of peroxisome proliferator-activated receptor delta inhibits streptozotocin-induced diabetic nephropathy through anti-inflammatory mechanisms in mice.

    Matsushita Y, Ogawa D, Wada J, Yamamoto N, Shikata K, Sato C, Tachibana H, Toyota N, Makino H

    Diabetes.   60 ( 3 )   960 - 968   2011年3月

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  • Renoprotective effects of clarithromycin via reduction of urinary MCP-1 levels in type 2 diabetic patients

    Tone A, Shikata K, Nakagawa K, Hashimoto M, Makino H.

    Clin Exp Nephrol   15 ( 1 )   79 - 85   2011年2月

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  • P-selectin glycoprotein ligand-1 deficiency is protective against obesity-related insulin resistance.

    Sato C, Shikata K, Hirota D, Sasaki M, Nishishita S, Miyamoto S, Kodera R, Ogawa D, Tone A, Kataoka HU, Wada J, Kajitani N, Makino H.

    Diabetes   60 ( 1 )   189 - 199   2011年1月

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  • 糖尿病性腎症とCKD―新たな展開と治療法の選択―.

    月刊糖尿病   3 ( 7 )   69 - 77   2011年

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  • 糖尿病性腎症―病態の解明と最新治療戦略―糖尿病性腎症の最新治療戦略.

    医学のあゆみ   239 ( 9 )   851 - 856   2011年

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  • Decreasing serum uric acid levels might be associated with improving estimated glomerular filtration rate(eGFR) in Japanese men.

    Miyatake N, Shikata K, Makino H, Numata T

    Health.   3 ( 8 )   498 - 503   2011年

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    記述言語:英語  

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  • The relation between estimated glomerular filtration rate(eGFR)and consumption in the japanese.

    Miyatake N, Shikata K, Makino H, Numata T

    Health.   3 ( 9 )   549 - 552   2011年

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    記述言語:英語  

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  • High glucose increases metallothioneine xpression in renal proximal tubular epithelial cells.

    Ogawa D, Asanuma M, Miyazaki I, Tachibana H, Wada J, Sogawa N, Sugaya T, Kitamura S, Maeshima Y, Shikata K, Makino H

    Exp Diabetes Res.   534872 - 534872   2011年

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  • Comparison of muscle strength between subjects with and without proteinuria.

    Miyatake N, Shikata K, Makino H, Numata T

    Health.   3 ( 11 )   698 - 702   2011年

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    記述言語:英語  

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  • 特集:糖尿病性腎症の克服を目指して―Microinflammation―.

    メディカル・ビューポイント   32   32011 - 32011   2011年

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  • 糖尿病性腎症の発症と進展におけるMicroinflammationの役割.

    日本腎臓学会誌   53 ( 7 )   1021 - 1026   2011年

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  • 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―.

    岡山医学会雑誌   123   197 - 206   2011年

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  • Insufficient control of morning home blood pressure in Japanese patients with hypertension associated with diabetes mellitus.

    Uchida H, Nakamura Y, Norii H, Kaihara M, Hanayama Y, Sada K, Wada J, Shikata K, Makino H

    Journal of Diabetes Investigation   1 ( 6 )   266 - 272   2010年12月

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  • Decreasing systolic blood pressure is associated with improving estimated glomerular filtration rate (eGFR) with lifestyle modification in Japanese healthy women.

    Miyatake N, Shikata K, Makino H, Numata T.

    Acta Med Okayama   64 ( 5 )   339 - 343   2010年10月

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  • Relationship between estimated glomerular filtration rate(eGFR)and metabolic syndrome in japanese.

    Miyatake N, Shikata K, Makino H, Numata T

    Acta Medica Okayama   64 ( 3 )   203 - 208   2010年6月

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    記述言語:英語  

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  • Comparison of insulin detemir and insulin glargine on glycemic variability in patients with type 1 and type 2 diabetes.

    Tone A, Iseda I, Higuchi C, Tsukamoto K, Katayama A, Matsushita Y, Hida K, Wada J, Shikata K

    Exp Clin Endocrinol Diabetes   118 ( 5 )   320 - 324   2010年5月

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  • Microinflammation is a common risk factor for progression of nephropathy and atherosclerosis in japanese patients with type 2 diabetes.

    Kajitani N, Shikata K, Nakamura A, Nakatou T, Hiramatsu M, Makino H

    Diabetes Research and Clinical Practice   88 ( 2 )   171 - 176   2010年5月

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  • Diabetic nephropathy remission and regression team trial in japan (DNETT-JAPAN): rationale and study design.

    Shikata K, Haneda M, Koya D, Suzuki Y, Tomino Y, Yamada K, Maeda S, Kawakami N, Uzu T, Nishimura M, Sato C, Ogawa D, Makino H

    Diabetes Research and Clinical Practice   87 ( 2 )   228 - 232   2010年2月

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    担当区分:筆頭著者   記述言語:英語  

    DOI: 10.1016/j.diabres.2009.09.025

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  • Influencing factors for dietary behaviors of Patients with Diabetic Nephropathy.

    Sumiyoshi K, Kawata C, Shikata K, Makino H

    Acta Med Okayama   64 ( 1 )   39 - 47   2010年2月

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  • 糖尿病性腎症の成因とmicroinflammation~イルベサルタン(アバプロR)の坑炎症作用への期待~.

    四方賢一

    アバプロR発売2周年記念講演会Power&Protectionの証明   6 - 6   2010年

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  • 腎症の寛解は可能か? -最近のエビデンスより-.

    廣田大昌, 四方賢一

    糖尿病診療マスター   8 ( 4 )   403 - 406   2010年

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  • 糖尿病合併高血圧治療を考える―その実態と腎保護を見据えた治療戦略―.

    四方賢一, 松岡 孝, 中村一分, 津村弘人

    大日本住友製薬   2 - 7   2010年

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  • これからの糖尿病治療を考える―DPP-4阻害薬を中心にー.

    四方賢一, 稲垣暢也, 加来浩平, 谷澤幸生, 山根公則

    万有製薬株式会社   1 - 4   2010年

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  • Relation between the estimated glomerular filtration rate and pulse wave velocity in japanese.

    Miyatake N, Shikata K, Makino H, Numata T

    Intern Med   49 ( 14 )   1315 - 1320   2010年

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  • 1型糖尿病の家族歴を有し、GAD抗体陰性かつIA-2抗体陽性を呈した中年発症1型糖尿病の1例.

    浅野美智子, 利根淳仁, 片山晶博, 古城真秀子, 樋口千草, 塚本啓子, 伊勢田 泉, 肥田和之, 上江洲篤郎, 四方賢一

    糖尿病   53 ( 3 )   174 - 179   2010年

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    記述言語:日本語  

    DOI: 10.11213/tonyobyo.53.174

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  • 新しい時代の糖尿病薬~インクレチン製剤への期待~.

    四方賢一

    山県郡医師会会報   8   46 - 47   2010年

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  • 4.腎不全期.

    四方賢一

    糖尿病 最新の治療   172 - 173   2010年

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  • 白血球機能低下.

    宮本 聡, 四方賢一

    臨床検査   54 ( 9 )   1035 - 1039   2010年

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  • Ⅱ.糖尿病性腎症 糖尿病性腎症の病理.

    小寺 亮, 四方賢一

    糖尿病性細小血管症(第2版)-発症・進展制御の最前線―   68 ( 9 )   370 - 374   2010年

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  • 慢性合併症の臨床2(腎症)1.腎症の成因.

    四方賢一, 槇野博史

    糖尿病学の進歩2010   262 - 266   2010年

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  • 糖尿病性細小血管症の発症・進展の分子メカニズムMicroinflammationの関与.

    梶谷展生, 四方賢一

    糖尿病性細小血管症(第2版)—発症・進展制御の最前線—   68 ( 9 )   61 - 64   2010年

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  • DPP-4阻害薬の登場で薬物療法はどう変わるか.

    小寺 亮, 四方賢一

    薬事   52 ( 3 )   345 - 349   2010年

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  • 脂質異常症・セミナー実地診療で遭遇する問題点の対応 腎疾患患者に合併する脂質異常症―管理の意義と方法―.

    宮本 聡, 四方賢一

    Medical Practice   27 ( 3 )   465 - 468   2010年

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  • チーム医療で一人ひとりの患者に合ったトータルケアを実践 岡山大学病院.

    四方賢一

    DM Frontline   1 - 2   2010年

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  • 糖尿病性腎症治療薬開発の動向.

    小寺 亮, 四方賢一

    細胞   42 ( 4 )   13 - 16   2010年

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  • 糖尿病におけるCKDの成因と治療.

    廣田大昌, 四方賢一

    プラクティス   27 ( 3 )   272 - 280   2010年

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  • 腎症の病期に応じた対応のポイント.

    四方賢一

    対糖尿病合併症のイノベーション 成因から管理、治療まで 糖尿病UP・DATE賢島セミナー26   26   196 - 203   2010年

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  • Long-term effect of modification of dietary protein intake on the progression of diabetic nephropathy: a randomised controlled trial.

    Koya D, Haneda M, Inomata S, Suzuki Y, Suzuki D, Makino H, Shikata K, Murakami Y, Tomino Y, Yamada K, Araki SI, Kashiwagi A, Kikkawa R; Low-Protein Diet Study Group.

    Diabetologia   52 ( 10 )   2037 - 2045   2009年10月

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  • Endothelial barrier protection by FTY720 under hyperglycemic condition: involvement of focal adhesion kinase, small GTPases, and adherens junction proteins.

    Sarai K, Shikata K, Shikata Y, Omori K, Watanabe N, Sasaki M, Nishishita S, Wada J, Goda N ,Kataoka N, Makino H

    Am J Physiol Cell physiol   297 ( 4 )   C945 - C954   2009年10月

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  • Long-term effect of modification of dietary protein intake on the progression of diabetic nephropathy: a randomised controlled trial

    D. Koya, M. Haneda, S. Inomata, Y. Suzuki, D. Suzuki, H. Makino, K. Shikata, Y. Murakami, Y. Tomino, K. Yamada, S. I. Araki, A. Kashiwagi, R. Kikkawa

    DIABETOLOGIA   52 ( 10 )   2037 - 2045   2009年10月

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    記述言語:英語   出版者・発行元:SPRINGER  

    There is currently insufficient evidence to recommend a low-protein diet for type 2 diabetic patients with diabetic nephropathy. We assessed whether a low-protein diet could prevent the progression of diabetic nephropathy.
    This was a multi-site parallel randomised controlled trial for prevention of diabetic nephropathy progression among 112 Japanese type 2 diabetic patients with overt nephropathy. It was conducted in Japan from 1 December 1997 to 30 April 2006. The participants were randomly assigned using a central computer-generated schedule to either low-protein diet (0.8 g kg(-1) day(-1)) and normal-protein diet (1.2 g kg(-1) day(-1)), and were followed for 5 years. The participants and investigators were not blinded to the assignment. The primary outcomes were the annual change in estimated GFR and creatinine clearance, the incidence of doubling of serum creatinine and the time to doubling of baseline serum creatinine.
    The study was completed by 47 (84%) of 56 participants in the low-protein diet group and 41 (73%) of 56 participants in the normal-diet group. During the study period, the difference in mean annual change in estimated GFR between the low-protein diet and the normal-protein diet groups was -0.3 ml min(-1) 1.73 m(-2) (95% CI -3.9, 4.4; p = 0.93). The difference in mean annual change in creatinine clearance between the low-protein diet and the normal-protein diet groups was -0.006 ml s(-1) 1.73 m(-2) (95% CI -0.089, 0.112; p = 0.80). A doubling of serum creatinine was reached in 16 patients of the low-protein group (34.0%), compared with 15 in the normal-protein group (36.6%), the difference between groups being -2.6% (95% CI -22.6, 17.5; p = 0.80). The time to doubling of serum creatinine was similar in both groups (p = 0.66).
    It is extremely difficult to get patients to follow a long-term low-protein diet. Although in the low-protein group overall protein intake was slightly (but not significantly) lower, it did not confer renoprotection.
    Clinical trial registration: ClinicalTrials.gov NCT00448526
    Funding: Research grant from the Ministry of Health, Labour and Welfare of Japan.

    DOI: 10.1007/s00125-009-1467-8

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  • Advanced glycation end products subspecies-selectively induce adhesion molecule expression and cytokine production in human peripheral blood mononuclear cells.

    Takahashi HK, Mori S, Wake H, Liu K, Yoshino T, Ohashi K, Tanaka N, Shikata K, Makino H, Nishibori M.

    Journal of Pharmacological Experimental Therary.   330 ( 1 )   89 - 98   2009年7月

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  • Enhanced interaction between focal adhesion and adherens junction proteins: involvement in sphingosine 1-phosphate-induced endothelial barrier enhancement.

    Sun X, Shikata Y, Wang L, Ohmori K, Watanabe N, Wada J, Shikata K, Birukov KG, Makino H, Jacobson JR, Dudek SM, Garcia JG

    Microvasc Res   77 ( 3 )   304 - 313   2009年5月

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  • 合併症や併発疾患を伴う糖尿病の薬物治療.

    梶谷展生, 四方賢一

    内分泌・糖尿病科   29 ( 4 )   296 - 302   2009年

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  • 糖尿病性腎症の成因としてのmicroinflammation.

    四方賢一, 宮本聡

    月刊糖尿病   1 ( 5 )   43 - 49   2009年

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  • 維持輸液、経腸栄養のインスリン使用の実際.

    佐藤千景, 四方賢一, 槇野博史

    総合臨床「今すぐに役立つ輸液ガイドブック」   58   1032 - 1038   2009年

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  • 糖尿病性腎症の理解と予防.

    梶谷展生, 宮本 聡, 小寺 亮, 四方賢一, 槇野博史

    外来看護最前線 生活習慣病&外来がん看護   14 ( 4 )   32 - 43   2009年

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  • 腎臓専門医での診断とかかりつけ医への逆紹介の要点 4.糖尿病腎症の確定診断はどのように行うのですか?.

    小寺 亮, 四方賢一, 槇野博史

    かかりつけ医と専門医のためのCKD診療ガイド   73 - 77   2009年

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  • 糖尿病が引き起こす細小血管症 ③糖尿病性腎症.

    小寺 亮, 四方賢一, 槇野博史

    からだの科学   ( 261 )   88 - 93   2009年

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  • 糖尿病性腎症.

    小寺亮, 四方賢一

    炎症と免疫   17 ( 6 )   714 - 718   2009年

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  • A case of hypoglycemic brittle diabetes with peripheral edema successfully managed by conversion from insulin lispro to insulin aspart.

    Tone A, Shikata K, Nakagawa K, Hashimoto M, Makino H.

    Diabetes Res Clin Pract.   81 ( 3 )   e15 - e16   2008年9月

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    記述言語:英語   掲載種別:速報,短報,研究ノート等(学術雑誌)  

    DOI: 10.1016/j.diabres.2008.06.013

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  • 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―平成19年度岡山医学会賞(結城賞)受賞論文―.

    片岡仁美, 四方賢一, 佐々木基史, 槇野博史

    岡山医学会雑誌   120   143 - 147   2008年

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  • 糖尿病性腎症の治療におけるMicroinflammation制御の意義.

    四方賢一

    BioClinica   23   52 - 56   2008年

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  • 血管合併症を予防するための糖尿病治療―産業医のための糖尿病管理の指針―.

    四方賢一

    山口県 内科医会誌   ( 8 )   6 - 7   2008年

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  • Pros & Cons 糖尿病性腎症と慢性腎臓病.

    四方賢一

    糖尿病診療マスター   4   378 - 385   2008年

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  • 脂質異常症―基本を踏まえた実践,腎疾患・CKD.

    四方賢一

    内科   103   96 - 99   2008年

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  • 腎症の予防と治療.

    四方賢一

    地域保健   7   48 - 51   2008年

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  • 糖尿病性腎症.

    四方賢一, 槇野博史

    腎と透析   64   945 - 950   2008年

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  • 糖尿病腎症に対するチーム医療と集約的治療の重要性.

    四方賢一

    糖尿病診療マスター   6 ( 4 )   378 - 384   2008年

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  • 糖尿病・妊娠糖尿病合併妊娠.

    四方賢一

    産科と婦人科   101 - 108   2008年

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  • 高齢糖尿病患者の夜間血圧とアルブミン尿.

    小寺 亮, 四方賢一, 槇野博史

    血圧   15 ( 9 )   740 - 741   2008年

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  • 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―平成19年度岡山医学会賞(結城賞)受賞論文―.

    片岡仁美, 四方賢一, 佐々木基史, 槇野博史

    岡山医学会雑誌   120   143 - 147   2008年

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  • Edaravone mimics sphingosine-1-phosphte-induced endothelial barrier enhancement in human microvascular endothelial cells.

    Omori K, Sarai K, Sikata Y, Watanabe N, Wada J, Goda N, Kataoka N, Sikata K, Makino H

    Am J Physiol Cell Physiol   293 ( 5 )   C1523 - C1531   2007年11月

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  • Urinary PGDS levels are associated with vascular injury in type 2 diabetes patients.

    Yoshikawa R , Wada J , Seiki K , Matsuoka T , Miyamato S , Takahashi K , Ota S , Taniai K , Hida K , Yamakado M , Shikata K , Uehara Y , Makino H

    Diabetes Research and Clinical Practice   76 ( 3 )   358 - 367   2007年6月

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  • The association of C-reactive protein with an oxidative metabolite of LDL and its Implication in atherosclerosis.

    Tabuchi.M, Inoue K, Usui-Kataoka H, Kabata H, Kobayashi.K, Teramoto M, Takasugi K, Shikata K, Yamamura M, Ando K, Nishida K, Kasahara J, Kume N, 他

    Journal of Lipid Reserch   48 ( 4 )   768 - 781   2007年4月

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  • Thiazolidinedione ameliorates renal injury in experimental diabetic rats through anti-inflammatory effects mediated by inhibition of NF-kappaB activation.

    Ohga S, Shikata K, Yozai K, Okada S, Ogawa D, Usui H, Wada J, Shikata Y, Makino H

    Am J Physiol Renal Physiol   292 ( 4 )   F1141 - F1150   2007年4月

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  • Changes of gene expression profiles in macrophages stimulated by angiotensin II Angiotensin II induces MCP-2 through AT1-receptor.

    Tone A, Shikata K, Ogawa D, Sasaki S, Nagase R, Sasaki M, Yozai K, Usui Kataoka H, Okada S, Wada J, Shikata Y, Makino H

    J Renin Angiotensin Aldosterone Syst   8 ( 1 )   45 - 50   2007年3月

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  • Macrophage scavenger receptor-a-deficient mice are resistant against diabetic nephropathy through amelioration of microinflammation.

    Usui HK, Shikata K, Sasaki M, Okada S, Matsuda M, Shikata Y, Ogawa D, Kido Y, Nagase R, Yozai R, Ohga S, Tone A, Wada J, Takeya M, Horiuchi S, Kodama T, Makino H

    Diabetes   56 ( 2 )   363 - 372   2007年2月

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  • <国内外のCKDに対するエビデンス> 糖尿病性腎症 -日本の研究からー

    四方賢一, 槇野博史

    内科   100 ( 1 )   2007年

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  • 糖尿病性腎症の成因と新しい治療戦略 生活習慣病による血管疾患の治療戦略

    四方賢一

    Medical View Point   28 ( 3 )   10   2007年

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  • DNETT-Japan

    槇野博史, 四方賢一

    医学のあゆみ   220 ( 13 )   2007年

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  • 糖尿病における血糖管理

    利根淳仁, 四方賢一, 槇野博史

    岡山県医学会雑誌   119   75 - 77   2007年

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  • 糖尿病腎症のremissionをめざした新たな治療戦略

    四方賢一

    内分泌・糖尿病科   24 ( 6 )   2007年

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  • 糖尿病性腎症の成因としてのMicroinflammation

    四方賢一

    日本腎臓学会誌   49 ( 5 )   2007年

  • 注意すべきCKD:糖尿病性腎症

    宮本 聡, 四方賢一, 槇野博史

    医学のあゆみ   222 ( 10 )   2007年

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  • 糖尿病性微小血管障害におけるedaravoneの血管内皮保護作用についての検討

    更井 啓, 四方泰史, 大森一慶, 渡辺直美, 和田 淳, 四方賢一, 槇野博史

    Phrma Medica   25 ( 6 )   2007年

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  • 基礎講座 糖尿病モデル動物 Ⅱ腎症モデル

    佐々木基史, 四方賢一, 槇野博史

    Diabetes Frontier   18 ( 5 )   2007年

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  • Ⅱ腎症モデル.

    佐々木基史, 四方賢一, 槇野博史

    Diabetes Frontier   18 ( 5 )   531 - 534   2007年

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  • Thiazolidinediones Ameliorate Diabetic Nephropathy via Cell Cycle-Dependent Mechanisms.

    Okada T, Wada J, Hida K, Eguchi J, Hashimoto I, Baba M, Yasuhara A, Shikata K, Makino H

    Diabetes   55 ( 6 )   1666 - 1677   2006年6月

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  • Elevated serum monocyte chemoattractant protein-4 and chronic inflammation in overweight subjects.

    Hashimoto I, Wada J, Hida A, Bada M, Miyake N, Eguchi J, Shikata K, Makino H

    Obesity   14 ( 5 )   799 - 811   2006年5月

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  • Therapeutic approach for diabetic nephropathy using gene delivery of translocase of inner mitochondrial membrane 44 by reducing mitochondrial superoxide production.

    Zhang Y, Wada J, Hashimoto I, Eguchi J, Yasuhara A, Yashpal S. Kanwar, Shikata K, Makino H

    J Am Soc Nephrol   17 ( 4 )   1090 - 1101   2006年4月

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  • 糖尿病性腎症の成因におけるMicroinflammationと腎症の寛解を目指した集約的治療

    四方賢一

    心血管障害とその予防 動脈硬化予防   5,3,39-45   2006年

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    月刊カレントテラピー   24,11,29-32   2006年

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    槇野博史, 四方賢一

    最新医学   2006年

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    四方賢一, 槇野博史

    Diabetes Frontier   2006年

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    総合臨牀   2006年

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    産婦人科の実際   55,8,1211-1214   2006年

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    糖尿病の病理 病理と臨床   24,7,720-726   2006年

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  • Serum Interleukin-18 levels are associated with nephropathy and atherosclerosis in patients with type 2 Diabetes.

    A.Nakamura, K.Shikata, M.Hiramatsu, T.Nakatou, T.Kitamura, J.Wada, T.Itoshima, H.Makino

    Diabetes Care   28 ( 12 )   2890 - 2895   2005年12月

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  • Methotrexate prevents renal injury in experimental diabetic rats via anti-inflammatory actions.

    K.Yozai, K.Shikata, M.Sasaki, A.Tone, S.Ohga, H.Usui, S.Okada, J.Wada, R.Nagase, D.Ogawa, Y.Shikata, H.Makino

    J Am Soc Nephrol   16 ( 11 )   3326 - 3338   2005年11月

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  • Galectin-9 inhibits glomerular hypertrophy in db/db diabetic mice via cell cycle-dependent mechanisms.

    M.Baba, J.Wada, J.Eguchi, I.Hashimoto, T.Okada, A.Yasuhara, K.Shikata, YS Kanwar, H.Makino

    J Am Soc Nephrol   16 ( 11 )   3222 - 3234   2005年11月

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  • Gene delivery of tim44 reduces mitochndrial superoxide production and ameliorates neointimal proliferation of injured carotid artery in diabetic rats.

    T.Matsuoka, J.Wada, I.Hashimoto, Y.Zhang, J.Eguchi, N.Ogawa, K.Shikata,Y.S.Kanwar, H.Makino

    Diabetes   54 ( 10 )   2882 - 2890   2005年10月

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  • Clinical features of non-diabetic renal diseases in patients with type 2 diabetes.

    A.Tone, K.Shikata, M.Matsuda, H.Usui, S.Okada, D.Ogawa, J.Wada, H.Makino

    Diabetes Research and Clinical Practice   69 ( 3 )   237 - 242   2005年9月

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  • Visceral adipose tissue-derived serine protease inhibitor: A unique insulin-sensitizing adipocytokine in obesity.

    K.Hida, J.Wada, J.Eguchi, H.Zhang, M.Baba, A.Seida, I.Hashimoto, T.Okada, A.Yasuhara, A.Nakatsuka, K.Shikata, S.Hourai, J.Futami, E.Watanabe, Y.Matsuki, R.Hiramatsu, S.Akagi, H.Makino, Y.S.Kanwar

    Proc Natl Acad Sci U S A   102 ( 30 )   10610 - 10615   2005年7月

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  • Identification of adipocyte adhesion molecule(ACAM),a novel CTX gene family, implicated in adipocyte maturation and development of obesity.

    J.Eguchi, J.Wada, K.Hida, H.Zhang, T.Matsuoka, M.Baba, I.Hashimoto, K.Shikata, N.Ogawa, H.Makino.

    Biochem.J   387   343 - 353   2005年4月

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  • 血糖コントロール

    西下伸吾, 四方賢一, 槇野博史

    日本臨牀   63,6,384-388   2005年

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    大賀佐起子, 四方賢一, 槇野博史

    ファーマナビゲータ 糖尿病編   1,1,300-303   2005年

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    Medicament News   1822,16-18   2005年

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    腎と透析   50,537-541   2005年

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    日本臨牀   63,155-159   2005年

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  • 糖尿病性腎症の発症メカニズム-RASおよびマクロファージの機能-

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    Angiotensin Research   2,1,20-26   2005年

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  • 糖尿病性腎症の成因における内皮細胞障害

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    内分泌・糖尿病科   20,3,209-213   2005年

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  • Sulfated hyaluronic acid, a potential selectin inhibitor, ameliorates experimentally induced crescentic glomeruonephritis.

    D.Ogawa, K.Shikata, M.Matsuda, K.Akima, M.Iwahashi, S.Okada, Y.Tsuchiyama, Y.Shikata, J.Wada, H.Makino

    Nephron Exp Nephrol   99 ( 1 )   E26 - E32   2005年

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  • Erythromycin ameliorates renal injury via anti-inflammatory effects in experimental diabetic rats.

    A.Tone, K.Shikata, M.Sasaki, S.Ohga,K.Yozai, S.Nishishita, H.Usui, R.Nagase, D.Ogawa, S.Okada, Y.Shikata, J.Wada, H.Makino

    Diabetologia   2005年

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  • Long-term Results of Tonsillectomy as a Treatment for IgA Nephropathy

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    Acta Oto-laryngologica   124   38 - 42   2004年12月

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  • The role of adrenomedullin and receptors in glomerlar hyperfiltration in streptozotocine-induced diabetic rats.

    K Hiragushi, J Wada, J Eguchi, T Matsuoka, A Yasuhara, I Hashimoto, T Yamashita, K Hida, Y Nakamura, K Shikata, N Minamino, K Kangawa, H Makino

    Kidney International   65 ( 2 )   540 - 550   2004年2月

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  • グルココルチコイドによる高血糖にナテグリニドが奏効した1症例

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    協和企画   2004年

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  • 糖尿病性腎疾患の治療-エビデンスと展望

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    医学のあゆみ   209,1,54-59   2004年

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  • Ⅱ進行性腎障害の治療と進歩5.糖尿病腎症

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    日本内科学会雑誌   93,5   2004年

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  • 糖尿病性腎症の成因と炎症関連分子―新しい治療ターゲットの検索―

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    腎と透析   56,240-241   2004年

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  • Serum bFGF levels are reduced in Japanese overweight men and restored by a 6-month exercise education.

    Seida A, Wada J, Kunitomi M, Tsuchiyama Y, Miyatake N, Fujii N, Kira S, Takahashi K, Shikata K, Makino H

    Int J Obes Relat Metab Disord   27 ( 11 )   1325 - 1331   2003年11月

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  • Intercellular adhesion molecule-1-deficient mice are resistant against renal injury after induction of diabetes.

    Okada S, Shikata K, Matsuda M, Ogawa D, Usui H, Kido Y, Nagase R, Wada J, Shikata Y, Makino H

    Diabetes   52 ( 10 )   2586 - 2593   2003年10月

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  • Pelvic lymphocyst infection associated with maternally inherited diabetes mellitus.

    Ogawa D, Shikata K, Matsuda M, Wada J, Uchida H, Asada M,Makino H

    Diabetes Research and Clinical Practice   61 ( 2 )   137 - 141   2003年8月

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  • Successful treatment of necrotizing fasciitis associated with diabetic nephropathy.

    Ogawa D, Shikata K, Wada J, Matsuda M, Makino H

    Diabetes Research and Clinical Practise   60 ( 3 )   213 - 216   2003年6月

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  • IgA腎症扁摘例の10年予後

    赤木博文, 福島邦博, 小坂道也, 服部謙志, 土井 彰, 西崎和則, 松田充浩, 四方賢一, 槇野博史

    口咽科   2003年

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  • 糖尿病治療に関連した感染症

    利根淳仁, 四方賢一, 槇野博史

    Diabetes Frontier   14,732-734   2003年

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  • エビデンスに基づいた糖尿病性腎症の治療――レニン・アンジオテンシン系の抑制の重要性――

    岡田震一, 四方賢一, 槇野博史

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    内科   91,119-123   2003年

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    糖尿病合併症   17,128-132   2003年

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  • HMG-CoA reductase inhibitor ameliorates diabetic nephropathy by its pleiotropic effects in rats.

    Usui H, Shikata K, Matsuda M, Okada S, Ogawa D, Yamashita T, Hida K, Satoh M, Wada J, Makino H

    Nephrol Dial Transplant   2003年

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  • Protective Effect of a Novel and Selective Inhibitor of Inducible Nitric Oxide Synthase on Experimental Crescentic Glomerulonephritis in WKY Rats

    D.Ogawa, K.Shikata, M.Matsuda, S.Okada, H.Usui, J.Wada, N.Taniguchi, H.Makino

    Nephrol Dial Transplant   17 ( 12 )   2117 - 2121   2002年12月

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    記述言語:英語  

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  • Therapeutic Effect of Sulphated Hyaluronic Acid, A Potential Selectin- Blocking Agent, on Experimental Progressive Mesangial Proliferative Glomerulonephritis

    M.Matsuda, K.Shikata, F.Shimizu, Y.Suzuki, M.Miyasaka, H.Kawahi, H.Kawashima J.Wada, H.Sugimoto, Y.Shikata, D.Ogawa, S.Tojo, K.Akima, H.Makino

    Journal of Pathology   198 ( 3 )   407 - 414   2002年11月

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  • A Case of Congenital Generalized Lipodystrophy with Lipoatrophic Diabetes Developing Anti- Insulin Antibodies

    H.Usui, K.Shikata, J.Wada, T.Sugimoto, J.Yamana, T.Oishi, M.Matsuda, M.Yoneda, I.Koshima, H.Makino

    Diabetic Medicine   19 ( 9 )   794 - 795   2002年9月

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    記述言語:英語   掲載種別:速報,短報,研究ノート等(学術雑誌)  

    DOI: 10.1046/j.1464-5491.2002.00657_3.x

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  • Beraprost Sodium, Prostacyclin Analogue, Attenuates Glomerular Hyperfiltration and Glomerular Macrophage Infiltration by Modulating ecNOS Expression in Diabetic Rats.

    T.Yamashita, K.Shikata, M.Matsuda, S.Okada, D.Ogawa, H.Sugimoto, J.Wada, H.Makino

    Diabetes Res Clin Pract   57 ( 3 )   149 - 161   2002年9月

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  • Preventive Effect of Sulphated Colominic Acid on P-Selectin ?Dependent Infiltration of Macrophages in Experimentally Induced Crescentic Glomerulonephritis

    D.Ogawa, K.Shikata, M.Matsuda, S.Okada, J.Wada, S.Yamaguchi1), Y.Suzuki2), M.Miyasaka3), S.Tojo4), H.Makino

    Clin Exp Immunol   129 ( 1 )   43 - 53   2002年7月

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  • Relationship between Reduced Serum IGF-I Levels and Accumulation of Visceral Fat in Japanese Men

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    International Journal of Obesity   26 ( 3 )   361 - 369   2002年3月

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  • Angiocentric Immunoproliferative Lesions of the Lung Associated with Diffuse Renal Involvement

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  • Cyanotic Congenital Heart Disease Associated with Glomerulomegaly and Focal Segmental Glomerulosclerosis: Remission of Nephritic Syndrome with Angiotensin Converting enzyme Inhibitor

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    Nephrol Dial Transplant   17 ( 1 )   144 - 147   2002年1月

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  • 糸球体内皮細胞のすべて 接着分子の発現機構と役割

    四方賢一, 松田充浩, 槇野博史

    腎と透析   52(5),570-574   2002年

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    糖尿病   45(10),711-713   2002年

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    今月の治療   10(8),28-33   2002年

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    臨床と研究   79(1),62-67   2002年

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    臨床医   28(9),1948-1951   2002年

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    PRACTICE プラクティス   19(3),243-246   2002年

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    PRACTICE プラクティス   19(2),129-131   2002年

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  • Ⅵ.腎・泌尿器疾患編 8.糖尿病性腎症

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  • Changes in Urinary and Serum Concentrations of Macrophage-Colony Stimulating Factor (M-CSF) in Patients with Renal Diseases

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    Clinical and Experimental Nephrology   6 ( 2 )   91 - 98   2002年

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    記述言語:英語  

    DOI: 10.1007/s101570200015

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  • .特集:糖尿病性腎症の管理と治療―その包括的対策を考える Ⅱ-2糖尿病性腎症の発症・進展機序

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    progress in Medicine   22(11),2608-2614   2002年

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  • 著明な高血糖と早期時低血糖を繰り返した、抗インスリン抗体陽性糖尿病の1例

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  • Nitric Oxide System is Involved in Glomerular Hyperfiltration in Japanese Normo- and Micro-Albuminuric Patients with Type 2 Diabetes

    Hiragushi K, Sugimoto H, *Shikata K, Yamashita T, Miyatake N, Shikata Y, Wada J, Kumagai I, Fukushima M and Makino H

    Diabetes Res Clin Pract   53 ( 3 )   149 - 159   2001年9月

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  • The Effect of Antimicrobial Periodontal Treatment on Circulating Tumor Necrosis Factor- Alpha and Glycated Hemoglobin Level in Patients with Type 2 Diabetes

    Iwamoto Y, Nishimura F, Nakagawa M, Sugimoto H, *Shikata K, Makino H, Fukuda T, Tsuji T, Iwamoto M and Murayama Y

    J Periodontol   72 ( 6 )   774 - 778   2001年6月

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  • Ultrastructure of Glomerular Basement Membrane in Active Heymann Nephritis Rats Revealed by Tissue-Negative Staining Method

    Hayashi Y, Hironaka K, *Shikata K, Ogawa S, Ota K,Wada J, Kamata K, Ota Z and Makino H

    Am J Nephrol   21 ( 3 )   249 - 255   2001年5月

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  • Collectrin, a Collecting Duct-Specific Transmembrane Glycoprotein, Is a Novel Homologue of ACE2 and Is Developmentally Regulated in Embryonic Kidneys

    Zhang H, Wada J, Hida K, Tsuchiyama Y, Hiragushi K, *Shikata K, Wang H, Lin S, Kanwar YS and Makino H

    J Biol Chem   276 ( 20 )   17132 - 17139   2001年5月

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  • Human Fibroblasts Ubiquitously Express Glutamic Acid Decarboxylase 65(GAD65): Possible Effects of Connective Tissue Inflammation on GAD Antibody Titer

    Kono T, Nishimura F, Sugimoto H, *Shikata K, Makino H and .Murayama Y

    J Periodontol   72 ( 5 )   598 - 604   2001年5月

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  • Gene Expression Profile in Strepotozotocin-Induced Diabetic Mice Kidneys Undergoing Glomerulosclerosis

    Wada J, Zhang H, Tsuchiyama Y, Hiragushi K, Hida K, *Shikata K, Kanwar YS and.Makino H

    Kidney Int   59 ( 4 )   1363 - 1373   2001年4月

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  • 特集:糖尿病合併症とEBM 腎症の病態と治療のEBM

    小川大輔, 四方賢一, 槇野博史

    COMPLICATION-糖尿病と血管   6,1,51-59   2001年

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  • OLETFラット内臓脂肪組織に発現する遺伝子の同定

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    肥満研究   7,1,54-56   2001年

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    糖尿病性腎症   2001年

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    からだの科学増刊 糖尿病2001   ,145-150   2001年

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  • 疾患による浮腫の病態と治療法 糖尿病性腎症

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    臨床医   27,10,2347-2351   2001年

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    日本内科学会雑誌   90,2,350-358   2001年

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  • 糖尿病性腎症のすべて 前期から早期、顕性期、腎不全期への進展にかかわる因子(総論)

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    腎と透析(増刊号)   51,317-322   2001年

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  • 病態生理に基づく2型糖尿病の治療 腎症の進展過程と治療手順

    宮武伸行, 四方賢一, 槇野博史

    Pharma Medica   19,6,71-77   2001年

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  • 糖尿病性腎症の分子メカニズム

    槇野博史, 四方賢一, 和田 淳, 山_康司

    内分泌・糖尿病科   12,2,198-206   2001年

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  • 糸球体腎炎に対する抗接着分子療法の可能性

    四方賢一, 槇野博史

    医学のあゆみ(別冊)   ,94-103   2001年

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  • Clinical evaluation of muscle strength in 20-79-years-old obese Japanese

    Nobuyuki Miyatake, Masafumi Fujii, Hidetaka Nishikawa, Jun Wada, Kenichi Shikata, Hirofumi Makino, Ikuro Kimura

    Diabetes Research and Clinical Practice   48 ( 1 )   15 - 21   2000年4月

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    記述言語:英語  

    It is well known that obesity is closely related to non-insulin- dependent diabetes mellitus, hyperlipidemia, hypertension and cardiovascular disease, and the insulin resistance associated with obesity is supposed to play a central role for the development of these diseases. Thus, effective prevention and treatment of obesity need to be explored. In 357 obese (body mass index ≥ 26.4) subjects, aged 20-79 years, grip and leg strength were determined and compared with age- and sex-matched 1683 nonobese control subjects. Age-dependent alteration of body composition, evaluated by waist- hip ratio and the relative fat mass volume, was also compared. Finally, the relationship between the number of risk factors related to atherosclerosis and muscle strength was evaluated. Grip and leg strength in obese subjects were obviously stronger than controls under the age of 60 in both sexes. However, in the subjects over 60 years old, muscle strength was similar between obese subjects and controls. Weight bearing index (WBI) (leg strength (kg)/body weight (kg)) in obese subjects was remarkably lower than that in controls in all generations. In obese subjects, the waist-hip ratio and relative percentage of fat increased with aging, and obese subjects with multiple risk factors had higher waist-hip ratio and a tendency for lower muscle strength. Reduced WBI was considered to be a fundamental feature of obese subjects, and obese subjects increased fat composition with aging, which may be linked with low muscle strength. Thus, we need to design the most effective protocols to maximize and maintain quantitative and qualitative properties of muscle. (C) 2000 Elsevier Science Ireland Ltd.

    DOI: 10.1016/S0168-8227(99)00132-1

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  • Signaling transduction pathway of angiotensin II in human mesangial cells: Mediation of focal adhesion and GTPase activating proteins

    Yasushi Shikata, Kenichi Shikata, Mitsuhiro Matsuda, Hikaru Sugimoto, Jun Wada, Hirofumi Makino

    Biochemical and Biophysical Research Communications   257 ( 1 )   234 - 238   1999年4月

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    記述言語:英語   出版者・発行元:Academic Press Inc.  

    Human mesangial cells (HMCs) respond to angiotensin II stimulation, which modulates their physiological activities, i.e., contraction and proliferation. It has been revealed that focal adhesion kinase (FAK) and paxillin participate in the angiotensin II-mediated signaling and cytoskeletal rearrangements at focal adhesion. We investigated the influences of cell adhesion upon angiotensin II effects in HMCs. In adherent cells, both FAK and paxillin were tyrosine phosphorylated by angiotensin II, while the cell detachment completely inhibited the tyrosine phosphorylation of paxillin. Activation of p44/42 mitogen-activated protein (MAP) kinase by angiotensin II was accentuated in suspended cells. Moreover, p190, a member of Rho GTPase activating protein (GAP), and RasGAP were coprecipitated with paxillin in adherent cells and angiotensin II stimulation reduced the formation of paxillin-p190 and paxillin-RasGAP complexes. These results suggest that the formation of focal adhesion complexes accelerated by accumulation of mesangial matrices may inhibit the proliferation of HMCs by modulating MAP kinase activity and be related to mesangial cell depletion.

    DOI: 10.1006/bbrc.1999.0441

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  • Screening for genes up-regulated in 5/6 nephrectomized mouse kidney

    Hong Zhang, Jun Wada, Yashpal S. Kanwar, Yoshinori Tsuchiyama, Keita Hiragushi, Kazuyuki Hida, Kenichi Shikata, Hirofumi Makino

    Kidney International   56 ( 2 )   549 - 558   1999年

     詳細を見る

    記述言語:英語   出版者・発行元:Blackwell Publishing Inc.  

    Background. In diabetic and nondiabetic renal diseases, glomerular hyperfiltration is believed to play a central role in the subsequent progression of glomerulosclerosis and interstitial renal scarring. To identify genes involved in the process of hyperfiltration and hypertrophy, a polymerase chain reaction (PCR)-based subtraction method, that is, representational difference analysis of cDNA (cDNA-RDA), was employed. Methods. Ten-week-old ICR mice were 5/6 nephrectomized and sham operated. After two weeks, mRNAs were isolated from control and remnant kidneys and were subjected to the cDNA-RDA procedure. Results. We identified 10 known and 9 novel genes. Among 19 clones, 12 clones (8 known and 4 novel) showed 1.5- to 6-fold up-regulation by Northern blot analyses. The remaining seven clones were rarely expressed genes and were barely detected by Northern blot analyses, and their up-regulated expression was confirmed by Southern blot analysis using the PCR-amplified representative amplicons. The known genes included kidney androgen-regulated protein, major urinary protein, lysozyme M, metalloproteinase-3 tissue inhibitor, chaperonin 10, cytochrome oxidase I, ε-sarcoglycan, ribosomal protein S3a, G-proteinγ10 subunit, and splicing factor 9G8. All of the isolated known genes have not been reported to be up- regulated in the nephrectomized mouse kidney and suggest the possible role of androgen action, mitochondrial functions, matrix metabolism, cell-matrix interactions, and intracellular signaling events in the initiation of the progressive renal injury of the remnant kidney. Furthermore, cDNA-RDA facilitates the discovery of novel genes, including two kidney-specific genes. Conclusions. The isolated known and novel genes may be involved in the pathobiological process of initial hyperfiltration and hypertrophy of remnant kidney.

    DOI: 10.1046/j.1523-1755.1999.00561.x

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  • Advanced glycation end products-cytokine-nitric oxide sequence pathway in the development of diabetic nephropathy: Aminoguanidine ameliorates the overexpression of tumour necrosis factor-α and inducible nitric oxide synthase in diabetic rat glomeruli

    H. Sugimoto, K. Shikata, J. Wada, S. Horiuchi, H. Makino

    Diabetologia   42 ( 7 )   878 - 886   1999年

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    記述言語:英語  

    Aims/hypothesis. Advanced glycation end products are believed to contribute to diabetic microvascular complications by inducing glomerular damage but their role has not been fully clarified. In this study, we explain their central role in the induction of inducible nitric oxide synthase and production of nitric oxide (NO) in streptozotocin-induced diabetic rat glomeruli. Methods. Localization of carboxymethyllysine, which is one of the chemical components of advanced glycation end products, glomerular expression of inducible nitric oxide synthase and urinary excretion and glomerular production of NO2-/NO3- were examined at 0, 26, 51, and 52 weeks after the induction of diabetes. Therapeutic effects of aminoguanidine were also examined. Results. Carboxymethyllysine was detected in the mesangial area in glomeruli and it progressively accumulated during 52 weeks of observation. Immunohistochemistry and hybridization studies in situ showed that the number of inducible nitric oxide synthase-positive cells was notably increased in diabetic rat glomeruli at 52 weeks. Further, this augmented expression paralleled intraglomerular expression of TNF-α and NO2-/NO3- in diabetic rat glomeruli. Treatment with aminoguanidine reduced the expression of TNF- α, inducible nitric oxide synthase and intraglomerular NO2-/NO3- production. It also ameliorated proteinuria in diabetic rats. Conclusion/interpretation. This study showed that carboxymethyllysine possibly enhances the expression of inducible nitric oxide synthase by stimulating the expression of TNF-α in diabetic rat glomeruli. The carboxymethyllysine-cytokine-NO sequence pathway could be one of the major mechanisms in the development of diabetic nephropathy.

    DOI: 10.1007/s001250051241

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  • L-selectin and its ligands mediate infiltration of mononuclear cells into kidney interstitium after ureteric obstruction

    Kenichi Shikata, Yasuo Suzuki, Jun Wada, Kyoji Hirata, Mitsuhiro Matsuda, Hiroto Kawashima, Takashi Suzuki, Masako Iizuka, Hirofumi Makino, Masayuki Miyasaka

    Journal of Pathology   188 ( 1 )   93 - 99   1999年

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    記述言語:英語  

    It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the kidney interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the interstitium and peritubular capillary walls, where infiltration of monocytes and CD8+ T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin- sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the kidney following ureteric obstruction.

    DOI: 10.1002/(SICI)1096-9896(199905)188:1<93::AID-PATH305>3.0.CO;2-#

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  • L-selectin and its ligands mediate infiltration of mononuclear cells into kidney interstitium after ureteric obstruction

    Kenichi Shikata, Yasuo Suzuki, Jun Wada, Kyoji Hirata, Mitsuhiro Matsuda, Hiroto Kawashima, Takashi Suzuki, Masako Iizuka, Hirofumi Makino, Masayuki Miyasaka

    Journal of Pathology   188 ( 1 )   93 - 99   1999年

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    記述言語:英語  

    It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the kidney interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the interstitium and peritubular capillary walls, where infiltration of monocytes and CD8+ T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin- sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the kidney following ureteric obstruction.

    DOI: 10.1002/(SICI)1096-9896(199905)188:1<93::AID-PATH305>3.0.CO;2-#

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  • Screening for genes up-regulated in 5/6 nephrectomized mouse kidney

    Hong Zhang, Jun Wada, Yashpal S. Kanwar, Yoshinori Tsuchiyama, Keita Hiragushi, Kazuyuki Hida, Kenichi Shikata, Hirofumi Makino

    Kidney International   56 ( 2 )   549 - 558   1999年

     詳細を見る

    記述言語:英語   出版者・発行元:Blackwell Publishing Inc.  

    Background. In diabetic and nondiabetic renal diseases, glomerular hyperfiltration is believed to play a central role in the subsequent progression of glomerulosclerosis and interstitial renal scarring. To identify genes involved in the process of hyperfiltration and hypertrophy, a polymerase chain reaction (PCR)-based subtraction method, that is, representational difference analysis of cDNA (cDNA-RDA), was employed. Methods. Ten-week-old ICR mice were 5/6 nephrectomized and sham operated. After two weeks, mRNAs were isolated from control and remnant kidneys and were subjected to the cDNA-RDA procedure. Results. We identified 10 known and 9 novel genes. Among 19 clones, 12 clones (8 known and 4 novel) showed 1.5- to 6-fold up-regulation by Northern blot analyses. The remaining seven clones were rarely expressed genes and were barely detected by Northern blot analyses, and their up-regulated expression was confirmed by Southern blot analysis using the PCR-amplified representative amplicons. The known genes included kidney androgen-regulated protein, major urinary protein, lysozyme M, metalloproteinase-3 tissue inhibitor, chaperonin 10, cytochrome oxidase I, ε-sarcoglycan, ribosomal protein S3a, G-proteinγ10 subunit, and splicing factor 9G8. All of the isolated known genes have not been reported to be up- regulated in the nephrectomized mouse kidney and suggest the possible role of androgen action, mitochondrial functions, matrix metabolism, cell-matrix interactions, and intracellular signaling events in the initiation of the progressive renal injury of the remnant kidney. Furthermore, cDNA-RDA facilitates the discovery of novel genes, including two kidney-specific genes. Conclusions. The isolated known and novel genes may be involved in the pathobiological process of initial hyperfiltration and hypertrophy of remnant kidney.

    DOI: 10.1046/j.1523-1755.1999.00561.x

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  • Accumulation of N(ε)-(carboxymethyl)lysine and changes in glomerular extracellular matrix components in Otsuka Long-Evans Tokushima Fatty rat: A model of spontaneous NIDDM

    Masahiko Kushiro, Kenichi Shikata, Hikaru Sugimoto, Kazuyoshi Ikeda, Seikoh Horiuchi, Hirofumi Makino

    Nephron   79 ( 4 )   458 - 468   1998年

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    記述言語:英語  

    Increases in extracellular matrix (ECM) and changes in its components have been documented in the glomeruli of diabetic nephropathy. Advanced glycation end products formed by glycoxidation have been shown to induce the synthesis of ECM components and transforming growth factor beta (TGF-β), suggesting that advanced glycation end products may be involved in the etiology of imbalance of ECM components in diabetic glomerulosclerosis. The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an inbred strain that spontaneously develops non-insulin-dependent diabetes mellitus which progresses to diabetic glomerulosclerosis. N(ε)-(carboxymethyl)lysine (CML) is known to be formed by glycoxidation. To clarify the involvement of glycoxidation in diabetic nephropathy, we examined the localization of CML, ECM components, and TGF-β1 in the glomeruli of OLETF rats. The amounts of α3(IV) collagen, type VI collagen, and fibronectin were significantly increased in the glomeruli of OLETF rats, whereas the heparan sulfate proteoglycan levels were decreased. After 6 months of age, CML levels were significantly increased in the mesangial area of the glomeruli in these animals. The overexpression of TGF-β1 preceded the increase in glomerular ECM components. The present study demonstrated that the accumulation of CML precedes the changes of glomerular ECM components in the glomeruli during the course of diabetic nephropathy, suggesting that glycoxidation may be one of the major causes of diabetic glomerulosclerosis.

    DOI: 10.1159/000045093

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  • Increased expression of selectins in kidneys of patients with diabetic nephropathy

    K. Hirata, K. Shikata, M. Matsuda, K. Akiyama, H. Sugimoto, M. Kushiro, H. Makino

    Diabetologia   41 ( 2 )   185 - 192   1998年

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    記述言語:英語   出版者・発行元:Springer Verlag  

    In diabetic nephropathy leukocytes, mainly composed of monocytes/macrophages, which accumulate in the glomeruli and the interstitium, play an important part in the progression of glomerulosclerosis. The infiltration of leukocytes into inflammatory tissues or atherosclerotic lesions is mediated by adhesion molecules, which are expressed on the vascular endothelial cells, although little is known about the mechanism of leukocyte infiltration into diabetic renal tissues. P- and E-selectin are leukocyte adhesion molecules, which are expressed on the vascular endothelial cells and promote the adhesion of leukocytes to the endothelium. We investigated the expression of P-and E-selectin in the kidney tissue of patients with diabetic nephropathy and compared it with that of patients with other glomerular diseases (minimal change nephrotic syndrome, membranous nephropathy, IgA nephropathy, mesangioproliferative glomerulone- phritis, and lupus nephritis). Expression of P- and E-selectin were both significantly increased in the glomeruli and the interstitium of patients with diabetic nephropathy as compared with those with other glomerular diseases. P- and E-selectin were both expressed along the glomerular capillaries and the peritubular capillaries in the interstitium. Neither P- nor E-selectin were correlated with the number of infiltrated leukocytes in the glomeruli, however, interestingly the E-selectin expression on peritubular capillaries was correlated with the number of infiltrated CD14 positive cells in the interstitium. These results suggest that E-selectin may play a key role in leukocyte infiltration into the renal interstitium in patients with diabetic nephropathy.

    DOI: 10.1007/s001250050888

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  • Soluble p-selectin is released from activated platelets in vivo during hemodialysis

    Kenji Kawabata

    Nephron   78 ( 2 )   148 - 155   1998年

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    記述言語:英語  

    During hemodialysis, platelets are activated across a dialyzer. Soluble P-selectin (sP-selectin) is a form of P-selectin which is a glycoprotein relocated from secretory granules to the surfaces of platelets and endothelial cells after these cells have been physiologically activated. To investigate whether sP-selectin is useful as a marker of platelet activation during hemodialysis, we measured the plasma concentration of sP-selectin by enzyme-linked immunosorbent assay in 6 patients hemodialyzed in our institute using regenerated cellulose (RC) membranes and thereafter polysulfone membranes. Concomitantly, we also measured the plasma concentration of platelet factor 4 and β-thromboglobulin which are released from a-granules of activated platelets. During hemodialysis with RC membranes, the β-thromboglobulin level was significantly increased 15 min (p &lt
    0.05) and the sP-selectin level 15 (p &lt
    0.05) and 180 min (p &lt
    0.05) after initiation of dialysis on the venous side as compared with the arterial side of the hemodialyzer. During hemodialysis with polysulfone membranes, no significant variation in plasma β-thromboglobulin and sP-selectin levels was detected. The platelet factor 4 level increased more significantly across a dialyzer 180 min after initiation of dialysis with RC than with polysulfone membranes (p &lt
    0.01). The changes in plasma platelet factor 4 and β-thromboglobulin levels demonstrated that platelets are more activated during hemodialysis with RC than with polysulfone membranes. The changes in plasma sP-selectin levels during hemodialysis with RC confirm that the release of P-selectin purely from activated platelets was detected by enzyme-linked immunosorbent assay. sP-selectin may be a marker of platelet activation during hemodialysis.

    DOI: 10.1159/000044903

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  • Therapeutic effects of prostacyclin analog on crescentic glomerulonephritis of rat

    Masahiko Kushiro, Kenichi Shikata, Hikaru Sugimoto, Yasushi Shikata, Nobuyuki Miyatake, Jun Wada, Masayuki Miyasaka, Hirofumi Makino

    Kidney International   53 ( 5 )   1314 - 1320   1998年

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    記述言語:英語   出版者・発行元:Nature Publishing Group  

    Prostacyclin (PGI2) is known to have a relaxative action on vascular smooth muscle, an inhibitory action against platelet activation and neutrophil function. Previous studies showed the preventive effects of PGI2 on lupus nephritis and Thy-1 nephritis, although the mechanism has not been clarified. Glomerular endothelial expression of intercellular adhesion molecule-1 (ICAM-1) is up-regulated in experimental and human glomerular diseases, and is known to facilitate leukocyte infiltration into the glomeruli, which ultimately induces the various glomerular injuries. In the present study, we evaluated the therapeutic effects of PGI2 on a rat model for crescentic glomerulonephritis and investigated its putative mechanism in relation to ICAM-1-mediated leukocyte recruitment. Wistar-Kyoto (WKY) rats were injected with nephrotoxic serum and received continuous intraperitoneal infusion of PGI2. PGI2 dramatically decreased proteinuria (123.0 ± 18.8 vs. 31.6 ± 4.5), crescent formation and deposition of fibrinogen in the glomeruli, while the deposition of rabbit IgG, rat IgG and rat C3 along the capillary walls was not changed. Furthermore, intraglomerular expression of ICAM-1 and infiltration of macrophages were significantly suppressed by administration with PGI2. In contrast, influx of CD4 or CD8 positive cells was not altered. The present results suggest that PGI2 shows the preventive effects on experimental crescentic glomerulonephritis by inhibiting intraglomerular coagulation and ICAM-1-mediated macrophage-glomerular endothelial cell adhesive pathway.

    DOI: 10.1046/j.1523-1755.1998.00881.x

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  • Increased expression of selectins in kidneys of patients with diabetic nephropathy

    K. Hirata, K. Shikata, M. Matsuda, K. Akiyama, H. Sugimoto, M. Kushiro, H. Makino

    Diabetologia   41 ( 2 )   185 - 192   1998年

     詳細を見る

    記述言語:英語   出版者・発行元:Springer Verlag  

    In diabetic nephropathy leukocytes, mainly composed of monocytes/macrophages, which accumulate in the glomeruli and the interstitium, play an important part in the progression of glomerulosclerosis. The infiltration of leukocytes into inflammatory tissues or atherosclerotic lesions is mediated by adhesion molecules, which are expressed on the vascular endothelial cells, although little is known about the mechanism of leukocyte infiltration into diabetic renal tissues. P- and E-selectin are leukocyte adhesion molecules, which are expressed on the vascular endothelial cells and promote the adhesion of leukocytes to the endothelium. We investigated the expression of P-and E-selectin in the kidney tissue of patients with diabetic nephropathy and compared it with that of patients with other glomerular diseases (minimal change nephrotic syndrome, membranous nephropathy, IgA nephropathy, mesangioproliferative glomerulone- phritis, and lupus nephritis). Expression of P- and E-selectin were both significantly increased in the glomeruli and the interstitium of patients with diabetic nephropathy as compared with those with other glomerular diseases. P- and E-selectin were both expressed along the glomerular capillaries and the peritubular capillaries in the interstitium. Neither P- nor E-selectin were correlated with the number of infiltrated leukocytes in the glomeruli, however, interestingly the E-selectin expression on peritubular capillaries was correlated with the number of infiltrated CD14 positive cells in the interstitium. These results suggest that E-selectin may play a key role in leukocyte infiltration into the renal interstitium in patients with diabetic nephropathy.

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  • Therapeutic effects of prostacyclin analog on crescentic glomerulonephritis of rat

    Masahiko Kushiro, Kenichi Shikata, Hikaru Sugimoto, Yasushi Shikata, Nobuyuki Miyatake, Jun Wada, Masayuki Miyasaka, Hirofumi Makino

    Kidney International   53 ( 5 )   1314 - 1320   1998年

     詳細を見る

    記述言語:英語   出版者・発行元:Nature Publishing Group  

    Prostacyclin (PGI2) is known to have a relaxative action on vascular smooth muscle, an inhibitory action against platelet activation and neutrophil function. Previous studies showed the preventive effects of PGI2 on lupus nephritis and Thy-1 nephritis, although the mechanism has not been clarified. Glomerular endothelial expression of intercellular adhesion molecule-1 (ICAM-1) is up-regulated in experimental and human glomerular diseases, and is known to facilitate leukocyte infiltration into the glomeruli, which ultimately induces the various glomerular injuries. In the present study, we evaluated the therapeutic effects of PGI2 on a rat model for crescentic glomerulonephritis and investigated its putative mechanism in relation to ICAM-1-mediated leukocyte recruitment. Wistar-Kyoto (WKY) rats were injected with nephrotoxic serum and received continuous intraperitoneal infusion of PGI2. PGI2 dramatically decreased proteinuria (123.0 ± 18.8 vs. 31.6 ± 4.5), crescent formation and deposition of fibrinogen in the glomeruli, while the deposition of rabbit IgG, rat IgG and rat C3 along the capillary walls was not changed. Furthermore, intraglomerular expression of ICAM-1 and infiltration of macrophages were significantly suppressed by administration with PGI2. In contrast, influx of CD4 or CD8 positive cells was not altered. The present results suggest that PGI2 shows the preventive effects on experimental crescentic glomerulonephritis by inhibiting intraglomerular coagulation and ICAM-1-mediated macrophage-glomerular endothelial cell adhesive pathway.

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  • Intercellular adhesion molecule 1 mediates mononuclear cell infiltration into rat glomeruli after renal ablation

    Nobuyuki Miyatake, Kenichi Shikata, Hikaru Sugimoto, Masahiko Kushiro, Yasushi Shikata, Saeko Ogawa, Yoshiko Hayashi, Masayuki Miyasaka, Hirofumi Makino

    Nephron   79 ( 1 )   91 - 98   1998年

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    記述言語:英語  

    Mononuclear cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. Intercellular adhesion molecule 1 (ICAM-1) is expressed on the vascular endothelium and mediates the infiltration of leukocytes into the site of inflammation. Although the expression of ICAM-1 can be induced by the stimulation of inflammatory cytokine, ICAM-1 expression can also be induced by such nonimmune mechanisms as shear stress. Glomerular hyperfiltration is a major mechanism that contributes to the progression of the glomerular sclerosis that results from the loss of functioning nephrons. In the present study, we examined the role of ICAM-1 for mononuclear cell infiltration in the glomeruli of the five-sixth nephrectomized rat as a model of glomerular hyperfiltration. The fluorescence intensity score of the staining for ICAM-1 in the glomeruli of the five-sixth nephrectomized rats was significantly increased as compared with that in the control (sham-operated) rats at 1 week (1.51 ± 0.15 vs. 0.61 ± 0.13, p &lt
    0.01) and 2 weeks (1.31 ± 0.17 vs. 0.51 ± 0.09
    p &lt
    0.01). The number of leukocytes present in the glomeruli was significantly increased in the five-sixth nephrectomized rats compared with control (sham-operated) rats at 1 week (3.44 ± 0.16 vs. 0.99 ± 0.081 p &lt
    0.01) and 2 weeks (3.14 ± 0.14 vs. 0.89 ± 0.07
    p &lt
    0.01). Leukocytes mainly consisted of macrophages in the five-sixth nephrectomized rats at 1 week (2.39 ± 0.19) and 2 weeks (1.46 ± 0.11). Anti-ICAM-1 monoclonal antibody effectively prevented the infiltration of macrophages into the glomerular following nephrectomy. These results indicate that glomerular hyperfiltration may be involved in the induction of the expression of ICAM-1 and the infiltration of macrophages into the renal glomeruli following glomerular injury.

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  • Intercellular adhesion molecule 1 mediates mononuclear cell infiltration into rat glomeruli after renal ablation

    Nobuyuki Miyatake, Kenichi Shikata, Hikaru Sugimoto, Masahiko Kushiro, Yasushi Shikata, Saeko Ogawa, Yoshiko Hayashi, Masayuki Miyasaka, Hirofumi Makino

    Nephron   79 ( 1 )   91 - 98   1998年

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    記述言語:英語  

    Mononuclear cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. Intercellular adhesion molecule 1 (ICAM-1) is expressed on the vascular endothelium and mediates the infiltration of leukocytes into the site of inflammation. Although the expression of ICAM-1 can be induced by the stimulation of inflammatory cytokine, ICAM-1 expression can also be induced by such nonimmune mechanisms as shear stress. Glomerular hyperfiltration is a major mechanism that contributes to the progression of the glomerular sclerosis that results from the loss of functioning nephrons. In the present study, we examined the role of ICAM-1 for mononuclear cell infiltration in the glomeruli of the five-sixth nephrectomized rat as a model of glomerular hyperfiltration. The fluorescence intensity score of the staining for ICAM-1 in the glomeruli of the five-sixth nephrectomized rats was significantly increased as compared with that in the control (sham-operated) rats at 1 week (1.51 ± 0.15 vs. 0.61 ± 0.13, p &lt
    0.01) and 2 weeks (1.31 ± 0.17 vs. 0.51 ± 0.09
    p &lt
    0.01). The number of leukocytes present in the glomeruli was significantly increased in the five-sixth nephrectomized rats compared with control (sham-operated) rats at 1 week (3.44 ± 0.16 vs. 0.99 ± 0.081 p &lt
    0.01) and 2 weeks (3.14 ± 0.14 vs. 0.89 ± 0.07
    p &lt
    0.01). Leukocytes mainly consisted of macrophages in the five-sixth nephrectomized rats at 1 week (2.39 ± 0.19) and 2 weeks (1.46 ± 0.11). Anti-ICAM-1 monoclonal antibody effectively prevented the infiltration of macrophages into the glomerular following nephrectomy. These results indicate that glomerular hyperfiltration may be involved in the induction of the expression of ICAM-1 and the infiltration of macrophages into the renal glomeruli following glomerular injury.

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  • Accumulation of N(ε)-(carboxymethyl)lysine and changes in glomerular extracellular matrix components in Otsuka Long-Evans Tokushima Fatty rat: A model of spontaneous NIDDM

    Masahiko Kushiro, Kenichi Shikata, Hikaru Sugimoto, Kazuyoshi Ikeda, Seikoh Horiuchi, Hirofumi Makino

    Nephron   79 ( 4 )   458 - 468   1998年

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    記述言語:英語  

    Increases in extracellular matrix (ECM) and changes in its components have been documented in the glomeruli of diabetic nephropathy. Advanced glycation end products formed by glycoxidation have been shown to induce the synthesis of ECM components and transforming growth factor beta (TGF-β), suggesting that advanced glycation end products may be involved in the etiology of imbalance of ECM components in diabetic glomerulosclerosis. The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an inbred strain that spontaneously develops non-insulin-dependent diabetes mellitus which progresses to diabetic glomerulosclerosis. N(ε)-(carboxymethyl)lysine (CML) is known to be formed by glycoxidation. To clarify the involvement of glycoxidation in diabetic nephropathy, we examined the localization of CML, ECM components, and TGF-β1 in the glomeruli of OLETF rats. The amounts of α3(IV) collagen, type VI collagen, and fibronectin were significantly increased in the glomeruli of OLETF rats, whereas the heparan sulfate proteoglycan levels were decreased. After 6 months of age, CML levels were significantly increased in the mesangial area of the glomeruli in these animals. The overexpression of TGF-β1 preceded the increase in glomerular ECM components. The present study demonstrated that the accumulation of CML precedes the changes of glomerular ECM components in the glomeruli during the course of diabetic nephropathy, suggesting that glycoxidation may be one of the major causes of diabetic glomerulosclerosis.

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  • Ultrastructural change of the glomerular basement membrane in rats with Heymann nephritis revealed by ultrahigh resolution scanning electron microscopy

    Kazue Hironaka, Hirofumi Makino, Tsuneto Onbe, Yasushi Yamasaki, Kenichi Shikata, Koju Kamata, Zensuke Ota

    Journal of Pathology   179 ( 1 )   112 - 120   1996年

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    記述言語:英語   出版者・発行元:John Wiley and Sons Ltd  

    To assess the relationship between the glomerular injury induced by immune complex deposition and proteinuria, ultrastructural changes of the glomerular basement membrane (GBM) were investigated in Heymann nephritis. Active Heymann nephritis was induced in rats by injecting them with tubular brush border antigen, known as Fx1A, emulsified in complete Freund's adjuvant (CFA). Measurement of urinary protein excretion and histological examinations were carried out for up to 15 weeks after immunization. Proteinuria developed in rats within 10 weeks of immunization and coincided with the development of subepithelial deposits with minimal spike-like basement membrane protrusion. Acellular glomeruli were prepared by detergent treatment and were subjected to tannic acid-osmium conductive staining prior to examination with an ultrahigh resolution scanning electron microscope (HSEM). HSEM of the acellular GBM prepared from control rats injected with CFA alone revealed a meshwork structure, with pores of about 9 nm in diameter. Proteinuric rats immunized with Fx1A showed a loosened meshwork structure, with pores of about 15 nm in the acellular GBM adjacent to the deposits. The newly formed GBM overlying the deposit consisted of a meshwork structure associated with unorganized thin fibrils. Ultrastructural changes were never seen in GBM devoid of deposits. These findings indicate that subepithelial deposits are closely involved in the development of proteinuria by injuring the size selectivity of the GBM.

    DOI: 10.1002/(SICI)1096-9896(199605)179:1<112::AID-PATH542>3.0.CO;2-Q

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  • Ultrastructural change of the glomerular basement membrane in rats with Heymann nephritis revealed by ultrahigh resolution scanning electron microscopy

    Kazue Hironaka, Hirofumi Makino, Tsuneto Onbe, Yasushi Yamasaki, Kenichi Shikata, Koju Kamata, Zensuke Ota

    Journal of Pathology   179 ( 1 )   112 - 120   1996年

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    記述言語:英語   出版者・発行元:John Wiley and Sons Ltd  

    To assess the relationship between the glomerular injury induced by immune complex deposition and proteinuria, ultrastructural changes of the glomerular basement membrane (GBM) were investigated in Heymann nephritis. Active Heymann nephritis was induced in rats by injecting them with tubular brush border antigen, known as Fx1A, emulsified in complete Freund's adjuvant (CFA). Measurement of urinary protein excretion and histological examinations were carried out for up to 15 weeks after immunization. Proteinuria developed in rats within 10 weeks of immunization and coincided with the development of subepithelial deposits with minimal spike-like basement membrane protrusion. Acellular glomeruli were prepared by detergent treatment and were subjected to tannic acid-osmium conductive staining prior to examination with an ultrahigh resolution scanning electron microscope (HSEM). HSEM of the acellular GBM prepared from control rats injected with CFA alone revealed a meshwork structure, with pores of about 9 nm in diameter. Proteinuric rats immunized with Fx1A showed a loosened meshwork structure, with pores of about 15 nm in the acellular GBM adjacent to the deposits. The newly formed GBM overlying the deposit consisted of a meshwork structure associated with unorganized thin fibrils. Ultrastructural changes were never seen in GBM devoid of deposits. These findings indicate that subepithelial deposits are closely involved in the development of proteinuria by injuring the size selectivity of the GBM.

    DOI: 10.1002/(SICI)1096-9896(199605)179:1<112::AID-PATH542>3.0.CO;2-Q

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  • A comparative study of myocardial troponin T levels in patients undergoing hemodialysis

    Masahiko Akagi, Yoshio Nagake, Hirofumi Makino, Kenichi Shikata, Zensuke Ota

    The Japanese Journal of Nephrology   37 ( 11 )   639 - 643   1995年

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    記述言語:英語  

    This study included 25 patients receiving hemodialysis (HD) but in whom diabetes mellitus was not the primary disease (HD-non DM group), 25 patients receiving hemodialysis with diabetes mellitus as the primary disease (HD-DM group), and 50 patients with diabetes mellitus who had not yet been treated with hemodialysis (DM group). The following markers of myocardial injury were measured in these patients: troponin T (TnT), creatine kinase (CK), myoglobin (Mb), and myosin light chain-1 (MLC-1). No significant correlation was found between myocardial TnT and Cr in any study group. The Mb and MLC-1 values in patients receiving HD were markedly higher than normal regardless of the primary disease involvement, while myocardial TnT was found to be only slightly abnormal. These results suggest that myocardial TnT may be a more useful marker of myocardial injury in HD patients than the markers in current use. In the present investigation, myocardial TnT was the only marker that was higher in the HD-DM group than in the HD-non DM group. This suggests the possibility that the HD-DM group included more patients with arteriosclerotic lesions, such as myocardial injury. © 1995, Japanese Society of Nephrology. All rights reserved.

    DOI: 10.14842/jpnjnephrol1959.37.639

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  • Changes in soluble ICAM-1 level during hemodialysis

    Kenji Kawabata, Yoshio Nagake, Kenichi Shikata, Hirofumi Makino, Zensuke Ota

    The Japanese Journal of Nephrology   37 ( 11 )   632 - 638   1995年

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    記述言語:英語  

    Intercellular adhesion molecule-1 (ICAM-1) is expressed on the surface of various types of cells, including lymphocytes, monocytes and vascular endothelial cells. Recently, ICAM-1 was reported to be shed from the cell membranes and released into circulation. The soluble ICAM-1 (sICAM-1) level has been reported to be increased in patients with certain inflammatory diseases. It is well known that the functions of leukocytes including neutrophils, lymphocytes and monocytes are impaired in patients with chronic hemodialysis. In this study, we evaluated the effect of hemodialysis (HD) on the lymphocytes and monocytes by periodically measuring the serum concentration of sICAM-1 during HD. Pre-HD sICAM-1 levels in chronic hemodialysis patients were significantly increased as compared with healthy subjects. Two hundred and forty minutes after the start of HD, sICAM-1 levels were significantly higher than the pre-HD levels. The sICAM-1 levels at the venous side of the dialyzer were significantly increased compared with the levels at the arterial side. There was no significant difference between the sICAM-1 levels of the patients under hemodialysis with the regenerated cellulose membrane and those with the polymethylmethacrylate membrane. These results suggest that ICAM-1 is shed from the surface of mononuclear cells (lymphocytes and monocytes) and released into circulation stimulated by hemodialysis membranes. Chronic hemodialysis may impair the function of mononuclear cells by inducing the shedding of ICAM-1. © 1995, Japanese Society of Nephrology. All rights reserved.

    DOI: 10.14842/jpnjnephrol1959.37.632

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  • Changes in soluble ICAM-1 level during hemodialysis

    Kenji Kawabata, Yoshio Nagake, Kenichi Shikata, Hirofumi Makino, Zensuke Ota

    The Japanese Journal of Nephrology   37 ( 11 )   632 - 638   1995年

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    記述言語:英語  

    Intercellular adhesion molecule-1 (ICAM-1) is expressed on the surface of various types of cells, including lymphocytes, monocytes and vascular endothelial cells. Recently, ICAM-1 was reported to be shed from the cell membranes and released into circulation. The soluble ICAM-1 (sICAM-1) level has been reported to be increased in patients with certain inflammatory diseases. It is well known that the functions of leukocytes including neutrophils, lymphocytes and monocytes are impaired in patients with chronic hemodialysis. In this study, we evaluated the effect of hemodialysis (HD) on the lymphocytes and monocytes by periodically measuring the serum concentration of sICAM-1 during HD. Pre-HD sICAM-1 levels in chronic hemodialysis patients were significantly increased as compared with healthy subjects. Two hundred and forty minutes after the start of HD, sICAM-1 levels were significantly higher than the pre-HD levels. The sICAM-1 levels at the venous side of the dialyzer were significantly increased compared with the levels at the arterial side. There was no significant difference between the sICAM-1 levels of the patients under hemodialysis with the regenerated cellulose membrane and those with the polymethylmethacrylate membrane. These results suggest that ICAM-1 is shed from the surface of mononuclear cells (lymphocytes and monocytes) and released into circulation stimulated by hemodialysis membranes. Chronic hemodialysis may impair the function of mononuclear cells by inducing the shedding of ICAM-1. © 1995, Japanese Society of Nephrology. All rights reserved.

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  • Activation of complement during hemodialysis

    Yoshio Nagake, Tetsuki Amano, Jun Wada, Hikaru Sugimoto, Kenji Kawabata, Kenichi Shikata, Hirofumi Makino, Zensuke Ota

    Japanese Journal of Clinical Immunology   18 ( 2 )   138 - 145   1995年

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    In hemodialysis using 3 types of dialysis membrane materials [regenerated cellulose (RC), cellulose triacetate (CTA), and polysulfone (PS)], activation of the complement, reduction of white blood cells, and variation of vitronectin (VN) were observed. RC membrane caused a significant reduction of white blood cells and elevations of Bb and soluble membrane attack complex (S-MAC), indicating a strong activation of the alternative complement pathway. Especially, the increase of S-MAC persisted for a long time during hemodialysis. Because reduction of VN was transient, it was assumed that the S-MAC escaping removal by VN receptors might have persisted in the circulation. These findings suggested that S-MAC would become useful as an index for evaluating biocompatibility of various artificial organs including dialysis membranes. © 1995, The Japan Society for Clinical Immunology. All rights reserved.

    DOI: 10.2177/jsci.18.138

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  • Activation of complement during hemodialysis

    Yoshio Nagake, Tetsuki Amano, Jun Wada, Hikaru Sugimoto, Kenji Kawabata, Kenichi Shikata, Hirofumi Makino, Zensuke Ota

    Japanese Journal of Clinical Immunology   18 ( 2 )   138 - 145   1995年

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    記述言語:英語  

    In hemodialysis using 3 types of dialysis membrane materials [regenerated cellulose (RC), cellulose triacetate (CTA), and polysulfone (PS)], activation of the complement, reduction of white blood cells, and variation of vitronectin (VN) were observed. RC membrane caused a significant reduction of white blood cells and elevations of Bb and soluble membrane attack complex (S-MAC), indicating a strong activation of the alternative complement pathway. Especially, the increase of S-MAC persisted for a long time during hemodialysis. Because reduction of VN was transient, it was assumed that the S-MAC escaping removal by VN receptors might have persisted in the circulation. These findings suggested that S-MAC would become useful as an index for evaluating biocompatibility of various artificial organs including dialysis membranes. © 1995, The Japan Society for Clinical Immunology. All rights reserved.

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  • Localization of advanced glycation endproducts in the kidney of experimental diabetic rats

    Kenichi Shikata, Hirofumi Makino, Hikaru Sugimoto, Masahiko Kushiro, Kosuke Ota, Kenji Akiyama, Norie Araki, Seikoh Horiuchi, Zensuke Ota

    Journal of Diabetes and Its Complications   9 ( 4 )   269 - 271   1995年

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    記述言語:英語  

    Advanced glycation endproducts (AGE) have been proposed as a major mediator in the development of various diabetic complications. In order to evaluate the involvement of AGE in the development of diabetic nephropathy, we examined the localization of AGE in the kidney of the streptozotocin-induced diabetic rats immunohistochemically using a monoclonal antibody directed to AGE. In the diabetic rats, glomerular hypertrophy, thickening of the glomerular basement membrane, and expansion of mesangial matrix were observed. AGE was detected in expanded mesangial area and glomerular basement membrane in the kidneys of diabetic rats. The present results suggest that AGE may participate in the development of diabetic nephropathy. © 1995.

    DOI: 10.1016/1056-8727(95)80019-B

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  • Transition of Morphologic Features in Lupus Nephritis: Does Steroid Therapy Accelerate Glomerulosclerosis?

    Hirofumi Makino, Yasushi Yamasaki, Kenichi Shikata, Naoki Kashihara, Hitoshi Sugiyama, Toshio Ogura, Zensuke Ota

    Internal Medicine   34 ( 10 )   982 - 987   1995年

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    記述言語:英語  

    We retrospectively evaluated the morphologic change of 28 Follow up biopsies from 24 cases of lupus nephritis according to the classification of the World Health Organization and determined the activity index (AI) and the chronicity index (CI). In the cases with biopsies repeated within 6 months, the AI decreased significantly from 6.7±1.3 to 3.5±0.8, while the CI showed no significant change. In cases which were rebiopsied after longer intervals, AI increased significantly from 3.2±0.7 to 7.5±1.2
    the CI did not change significantly. When AI and CI changes in the cases biopsied again beyond 6 months were compared with respect to therapy, AI showed no significant difference in the methylprednisolone pulse therapy group but was significantly increased in the oral steroid therapy group. The CI tended to be increased in both groups, but not significantly. Steroid pulse therapy was effective in improving active lesions with a high AI. Steroid therapy for lupus nephritis prevented short-term progression of glomerulosclerosis and did not accelerate glomerulosclerosis. © 1995, The Japanese Society of Internal Medicine. All rights reserved.

    DOI: 10.2169/internalmedicine.34.982

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  • A comparative study of myocardial troponin T levels in patients undergoing hemodialysis

    Masahiko Akagi, Yoshio Nagake, Hirofumi Makino, Kenichi Shikata, Zensuke Ota

    The Japanese Journal of Nephrology   37 ( 11 )   639 - 643   1995年

     詳細を見る

    記述言語:英語  

    This study included 25 patients receiving hemodialysis (HD) but in whom diabetes mellitus was not the primary disease (HD-non DM group), 25 patients receiving hemodialysis with diabetes mellitus as the primary disease (HD-DM group), and 50 patients with diabetes mellitus who had not yet been treated with hemodialysis (DM group). The following markers of myocardial injury were measured in these patients: troponin T (TnT), creatine kinase (CK), myoglobin (Mb), and myosin light chain-1 (MLC-1). No significant correlation was found between myocardial TnT and Cr in any study group. The Mb and MLC-1 values in patients receiving HD were markedly higher than normal regardless of the primary disease involvement, while myocardial TnT was found to be only slightly abnormal. These results suggest that myocardial TnT may be a more useful marker of myocardial injury in HD patients than the markers in current use. In the present investigation, myocardial TnT was the only marker that was higher in the HD-DM group than in the HD-non DM group. This suggests the possibility that the HD-DM group included more patients with arteriosclerotic lesions, such as myocardial injury. © 1995, Japanese Society of Nephrology. All rights reserved.

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  • Clinical Significance of Necrosis in Lupus Nephritis

    Hirofumi Makino, Yoshikazu Hayashi, Yasushi Yamasaki, Kenichi Shikata, Naoki Kashihara, Zensuke Ota

    Internal Medicine   33 ( 8 )   461 - 465   1994年

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    記述言語:英語  

    The significance of necrosis (karyorrhexis), among the most characteristic findings in lupus nephritis, was evaluated by studying the correlation between the existence of necrosis in renal biopsy specimens and laboratory findings. The subjects were 54 patients with diffuse proliferative lupus nephritis and 6 patients with focal proliferative lupus nephritis selected from 143 patients with lupus nephritis. We also compared the clinical course of oral prednisolone and intravenous methylprednisolone pulse therapies after steroid administration. Compared with the non-necrosis group, the necrosis group had significantly lower CH50 levels and more proteinuria. Patients with necrosis were effectively treated with repeated pulse therapy judging by immunological activity and the decrease in proteinuria at an early stage, but responded poorly to oral steroid therapy. As the presence of necrosis in cases of lupus nephritis means high immunological activity of the lesion and there is responsiveness to a large dose of steroids, extensive immunosuppressive therapy including methylprednisolone pulse therapy should be applied to these patients. © 1994 The Japanese Society of Internal Medicine. All rights reserved.

    DOI: 10.2169/internalmedicine.33.461

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  • Localization of Fibril/Microfibril and Basement Membrane Collagens in Diabetic Glomerulosclerosis in Type 2 Diabetes

    H. Makino, K. Shikata, J. Wieslander, J. Wada, N. Kashihara, K. Yoshioka, Z. Ota

    Diabetic Medicine   11 ( 3 )   304 - 311   1994年

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    記述言語:英語  

    Collagen is one of the major components of the extracellular matrices of the kidney. Basement membrane collagen, type IV collagen, is the major component in normal glomeruli. Fibril and interstitial collagen such as type III collagen, type V collagen, and type VI collagen are minor components of glomerular extracellular matrices and are localized mainly in the interstitium. Diabetic glomerulosclerosis is characterized by the expansion of the glomerular mesangial matrix as well as by thickening of the glomerular basement membrane. In order to clarify the roles of these various types of collagen in the development of diabetic glomerulosclerosis, immunohistochemical studies were perfomed in kidney specimens from patients with Type 2 diabetes. Early glomerulosclerosis is characterized by expansion of mesangial matrix with basement membrane collagen. However, in later stages glomerulosclerosis is characterized by an increase in the minor collagen components, such as type V and type VI collagen or collagens not normally present, such as type III collagen. Mesangial cells are known to synthesize all these types of collagen. In diabetes, phenotypic change in mesangial cells might produce excess amounts of fibril and interstitial collagen such as type III, type V, and type VI collagen, thus, leading to glomerulosclerosis. 1994 Diabetes UK

    DOI: 10.1111/j.1464-5491.1994.tb00276.x

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  • Localization of Fibril/Microfibril and Basement Membrane Collagens in Diabetic Glomerulosclerosis in Type 2 Diabetes

    H. Makino, K. Shikata, J. Wieslander, J. Wada, N. Kashihara, K. Yoshioka, Z. Ota

    Diabetic Medicine   11 ( 3 )   304 - 311   1994年

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    記述言語:英語  

    Collagen is one of the major components of the extracellular matrices of the kidney. Basement membrane collagen, type IV collagen, is the major component in normal glomeruli. Fibril and interstitial collagen such as type III collagen, type V collagen, and type VI collagen are minor components of glomerular extracellular matrices and are localized mainly in the interstitium. Diabetic glomerulosclerosis is characterized by the expansion of the glomerular mesangial matrix as well as by thickening of the glomerular basement membrane. In order to clarify the roles of these various types of collagen in the development of diabetic glomerulosclerosis, immunohistochemical studies were perfomed in kidney specimens from patients with Type 2 diabetes. Early glomerulosclerosis is characterized by expansion of mesangial matrix with basement membrane collagen. However, in later stages glomerulosclerosis is characterized by an increase in the minor collagen components, such as type V and type VI collagen or collagens not normally present, such as type III collagen. Mesangial cells are known to synthesize all these types of collagen. In diabetes, phenotypic change in mesangial cells might produce excess amounts of fibril and interstitial collagen such as type III, type V, and type VI collagen, thus, leading to glomerulosclerosis. 1994 Diabetes UK

    DOI: 10.1111/j.1464-5491.1994.tb00276.x

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  • Clinical Significance of Necrosis in Lupus Nephritis

    Hirofumi Makino, Yoshikazu Hayashi, Yasushi Yamasaki, Kenichi Shikata, Naoki Kashihara, Zensuke Ota

    Internal Medicine   33 ( 8 )   461 - 465   1994年

     詳細を見る

    記述言語:英語  

    The significance of necrosis (karyorrhexis), among the most characteristic findings in lupus nephritis, was evaluated by studying the correlation between the existence of necrosis in renal biopsy specimens and laboratory findings. The subjects were 54 patients with diffuse proliferative lupus nephritis and 6 patients with focal proliferative lupus nephritis selected from 143 patients with lupus nephritis. We also compared the clinical course of oral prednisolone and intravenous methylprednisolone pulse therapies after steroid administration. Compared with the non-necrosis group, the necrosis group had significantly lower CH50 levels and more proteinuria. Patients with necrosis were effectively treated with repeated pulse therapy judging by immunological activity and the decrease in proteinuria at an early stage, but responded poorly to oral steroid therapy. As the presence of necrosis in cases of lupus nephritis means high immunological activity of the lesion and there is responsiveness to a large dose of steroids, extensive immunosuppressive therapy including methylprednisolone pulse therapy should be applied to these patients. © 1994 The Japanese Society of Internal Medicine. All rights reserved.

    DOI: 10.2169/internalmedicine.33.461

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  • Effect of heparin and low-molecular-weight heparin on proliferative glomerulonephritis

    Yoshitaka Morita, Hirofumi Makino, Kosuke Ota, Jun Wada, Kenichi Shikata, Naoki Kashihara, Shuji Ikeda, Toshio Ogura, Zensuke Ota

    Japanese Journal of Nephrology   36 ( 7 )   832 - 838   1994年

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    記述言語:英語  

    Effect of heparin and low-molecular-weight heparin (LMWH) were evaluated on 15 patients with proliferative glomerulonephritis with various degrees of sclerosing legion. Five cases were subcutaneously administered with 7000 to 11000 units of heparin for 4 weeks. Ten cases were administered with 60 unit/kg of LMWH by drip infusion for 4 weeks. Eleven cases were treated with prednisolone and all cases were treated with anti-platelet agent as well. Urinary protein excretion reduced from 3. 0±1. 8 to 1. 8±0. 6g/day in the heparin-treated group and from 2. 4±1. 9 to 1. 8±1. 4g/day in the LMWH-treated group, respectively. There were no remarkable changes in the renal functions of both groups. In one case, both heparin and LMWH brought about reduction of proteinuria. Therefore, LMWH reduced urinary protein excretion by the same mechanism as heparin. The LMWH has an advantage over heparin in that the former has less risk of causing bleeding. We conclude that heparin and LMWH reduce proteinuria in some patients with proliferative glomerulonephritis. The LMWH is beneficial in the treatment of proliferative glomerulonephritis with a sclerosing lesion. © 1994, Japanese Society of Nephrology. All rights reserved.

    DOI: 10.14842/jpnjnephrol1959.36.832

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  • Effect of heparin and low-molecular-weight heparin on proliferative glomerulonephritis

    Yoshitaka Morita, Hirofumi Makino, Kosuke Ota, Jun Wada, Kenichi Shikata, Naoki Kashihara, Shuji Ikeda, Toshio Ogura, Zensuke Ota

    Japanese Journal of Nephrology   36 ( 7 )   832 - 838   1994年

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    記述言語:英語  

    Effect of heparin and low-molecular-weight heparin (LMWH) were evaluated on 15 patients with proliferative glomerulonephritis with various degrees of sclerosing legion. Five cases were subcutaneously administered with 7000 to 11000 units of heparin for 4 weeks. Ten cases were administered with 60 unit/kg of LMWH by drip infusion for 4 weeks. Eleven cases were treated with prednisolone and all cases were treated with anti-platelet agent as well. Urinary protein excretion reduced from 3. 0±1. 8 to 1. 8±0. 6g/day in the heparin-treated group and from 2. 4±1. 9 to 1. 8±1. 4g/day in the LMWH-treated group, respectively. There were no remarkable changes in the renal functions of both groups. In one case, both heparin and LMWH brought about reduction of proteinuria. Therefore, LMWH reduced urinary protein excretion by the same mechanism as heparin. The LMWH has an advantage over heparin in that the former has less risk of causing bleeding. We conclude that heparin and LMWH reduce proteinuria in some patients with proliferative glomerulonephritis. The LMWH is beneficial in the treatment of proliferative glomerulonephritis with a sclerosing lesion. © 1994, Japanese Society of Nephrology. All rights reserved.

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  • High resolution three-dimensional meshwork structure of the glomerular basement membrane

    Kenichi Shikata, Hirofumi Making, Zensuke Ota

    The Japanese Journal of Nephrology   34 ( 4 )   379 - 385   1992年

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    記述言語:英語  

    To investigate the ultrastructure of the glomerular basement membrane (GBM), rat GBM was treated with sodium dodecyl sulfate and 2-mercaptoethanol and observed under an electron microscope employing ultrathin sectioning and rotary shadowing methods. Further, thick sections of the treated GBM were examined by high voltage transmission electron microscopy. A fine three-dimensional meshwork structure was clearly observed through the entire thickness of the GBM treated with sodium dodecyl sulfate and 2-mercaptoethanol by conventional transmission electron microscopy and high voltage transmission electron microscopy. The diameter of the fibrils forming the meshwork structure was about 3 nm and the dimensions of the pores present in the meshwork were 3 to 4 nm. The rotary shadowing technique revealed fine fibrils disentangled from the GBM that were bound together, and corresponded morphologically type IV collagen molecules. The present findings suggested that the GBM has a fine three-dimensional meshwork structure through its entire thickness which is composed mainly of type IV collagen and may function as a size barrier in the renal glomerulus. © 1992, Japanese Society of Nephrology. All rights reserved.

    DOI: 10.14842/jpnjnephrol1959.34.379

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  • High resolution three-dimensional meshwork structure of the glomerular basement membrane

    Kenichi Shikata, Hirofumi Making, Zensuke Ota

    The Japanese Journal of Nephrology   34 ( 4 )   379 - 385   1992年

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    記述言語:英語  

    To investigate the ultrastructure of the glomerular basement membrane (GBM), rat GBM was treated with sodium dodecyl sulfate and 2-mercaptoethanol and observed under an electron microscope employing ultrathin sectioning and rotary shadowing methods. Further, thick sections of the treated GBM were examined by high voltage transmission electron microscopy. A fine three-dimensional meshwork structure was clearly observed through the entire thickness of the GBM treated with sodium dodecyl sulfate and 2-mercaptoethanol by conventional transmission electron microscopy and high voltage transmission electron microscopy. The diameter of the fibrils forming the meshwork structure was about 3 nm and the dimensions of the pores present in the meshwork were 3 to 4 nm. The rotary shadowing technique revealed fine fibrils disentangled from the GBM that were bound together, and corresponded morphologically type IV collagen molecules. The present findings suggested that the GBM has a fine three-dimensional meshwork structure through its entire thickness which is composed mainly of type IV collagen and may function as a size barrier in the renal glomerulus. © 1992, Japanese Society of Nephrology. All rights reserved.

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▼全件表示

受賞

  • 日本糖尿病合併症学会Young Investigator Award

    1999年  

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    受賞国:日本国

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  • 第1回シンポジウム糖尿病研究会会賞

    1997年  

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    受賞国:日本国

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共同研究・競争的資金等の研究

  • Function of Cell Adhesion Molecule in Glomerulonephirtis

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    資金種別:競争的資金

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  • Etiology and Therapy of Diabetic Nephropathy

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    資金種別:競争的資金

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  • Therapeutic Strategies for Renal Diseases

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    資金種別:競争的資金

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  • 腎疾患における細胞接着分子の機能

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    資金種別:競争的資金

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  • 糖尿病性腎症の成因と治療

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    資金種別:競争的資金

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  • 糖尿病性腎症をはじめとする糖尿病血管合併症の成因と診断・治療に関する研究

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    資金種別:競争的資金

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  • 腎疾患に対する治療法の開発

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    資金種別:競争的資金

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▼全件表示

 

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  • インスリン発見100年 新聞・雑誌

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