Updated on 2024/02/01

写真a

 
SHIKATA Kenichi
 
Organization
Okayama University Hospital Professor
Position
Professor
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Degree

  • 医学博士

Research Interests

  • Nephrology

  • Diabetology

  • 腎臓病学

  • 糖尿病学

Research Areas

  • Life Science / Immunology

  • Life Science / Nephrology

  • Life Science / Metabolism and endocrinology  / 糖尿病学

Education

  • Okayama University   医学研究科   内科学

    - 1992

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    Country: Japan

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  • Okayama University    

    - 1992

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  • Okayama University    

    - 1985

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  • Okayama University   医学部   医学科

    - 1985

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    Country: Japan

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Research History

  • - 岡山大学岡山大学病院 教授

    2010

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

    2010

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Committee Memberships

  • 日本糖尿病療養指導士認定機構   監事  

    2022   

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  • 岡山県医師会糖尿病対策推進会議   委員  

    2021   

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    Committee type:Municipal

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  • 岡山県糖尿病対策専門部会   会長  

    2021   

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    Committee type:Municipal

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  • 岡山県糖尿病協会   会長  

    2021   

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    Committee type:Municipal

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  • 病態栄養学会   代議員・評議員  

    2021   

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    Committee type:Academic society

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  • 腎臓学会   学術評議員  

    2021   

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    Committee type:Academic society

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  • 糖尿病学会   評議員  

    2021   

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    Committee type:Academic society

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  • 糖尿病合併症学会   理事  

    2021   

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    Committee type:Academic society

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  • 内科学会中国支部   評議員  

    2021   

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    Committee type:Academic society

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  • 糖尿病性腎症研究会   世話人  

    2021   

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    Committee type:Academic society

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  • 病態栄養学会 NST実施委員会   委員  

    2021   

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    Committee type:Academic society

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  • 糖尿病肥満動物学会   評議員  

    2021   

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    Committee type:Academic society

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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   

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    Committee type:Academic society

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Papers

  • 糖尿病性腎症の診断・治療の進歩と岡山県における重症化予防への取り組み

    四方 賢一

    日本糖尿病教育・看護学会誌   27 ( 特別号 )   65 - 65   2023.8

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    Language:Japanese   Publisher:(一社)日本糖尿病教育・看護学会  

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  • チーム医療と多職種連携 糖尿病性腎症重症化予防のためのチーム医療と多職種連携

    四方 賢一

    糖尿病合併症   37 ( 2 )   190 - 193   2023.7

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    Language:Japanese   Publisher:(一社)日本糖尿病合併症学会  

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  • 糖尿病性腎臓病の成因における炎症の役割の解明と新規治療薬の開発

    四方 賢一

    糖尿病合併症   37 ( 1 )   7 - 13   2023.6

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    Language:Japanese   Publisher:(一社)日本糖尿病合併症学会  

    糖尿病性腎症はわが国における末期腎不全の最大の原因疾患であり,その対策が急務である。糖尿病性腎症の発症・進展にはさまざまなメカニズムが関与しているが,炎症(microinflammation)はその1つである。糖尿病性腎症の腎組織には,ICAM-1などの細胞接着分子やMCP-1などのケモカインの発現が亢進しており,ICAM-1KOマウスでは,糖尿病誘発後の腎障害が抑制される。糖尿病患者では,血中および尿中のサイトカイン,ケモカイン,細胞接着分子の濃度が上昇しており,アルブミン尿と相関している。抗炎症作用を持つ薬剤を糖尿病モデル動物に投与すると腎障害が抑制される。さらに,最近,NLRP3インフラマソームが糖尿病性腎症の病態に関与していることが明らかとなり,糖尿病性腎症の新規治療ターゲットとなる可能性がある。Microinflammationは糖尿病性血管合併症の発症に共通のメカニズムであり,有望な治療ターゲットであると考えられる。(著者抄録)

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  • Suramin prevents the development of diabetic kidney disease by inhibiting NLRP3 inflammasome activation in KK-Ay mice.

    Kaori Oda, Satoshi Miyamoto, Ryo Kodera, Jun Wada, Kenichi Shikata

    Journal of diabetes investigation   14 ( 2 )   205 - 220   2023.2

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    Language:English   Publishing type:Research paper (scientific journal)  

    AIMS/INTRODUCTION: Nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasomes produce IL-18 upon being activated by various stimuli via the P2 receptors. Previously, we showed that serum and urine IL-18 levels are positively associated with albuminuria in patients with type 2 diabetes, indicating the involvement of inflammasome activation in the pathogenesis of diabetic kidney disease (DKD). In the present study, we investigated whether the administration of suramin, a nonselective antagonist of the P2 receptors, protects diabetic KK.Cg-Ay /TaJcl (KK-Ay) mice against DKD progression. MATERIALS AND METHODS: Suramin or saline was administered i.p. to KK-Ay and C57BL/6J mice once every 2 weeks for a period of 8 weeks. Mouse mesangial cells (MMCs) were stimulated with ATP in the presence or absence of suramin. RESULTS: Suramin treatment significantly suppressed the increase in the urinary albumin-to-creatinine ratio, glomerular hypertrophy, mesangial matrix expansion, and glomerular fibrosis in KK-Ay mice. Suramin also suppressed the upregulation of NLRP3 inflammasome-related genes and proteins in the renal cortex of KK-Ay mice. P2X4 and P2X7 receptors were significantly upregulated in the isolated glomeruli of KK-Ay mice and mainly distributed in the glomerular mesangial cells of KK-Ay mice. Although neither ATP nor suramin affected NLRP3 expression in MMCs, suramin inhibited ATP-induced NLRP3 complex formation and the downstream expression of caspase-1 and IL-18 in MMCs. CONCLUSIONS: These results suggest that the NLRP3 inflammasome is activated in a diabetic kidney and that inhibition of the NLRP3 inflammasome with suramin protects against the progression of early stage DKD.

    DOI: 10.1111/jdi.13930

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  • Effect of Patient-Participation Continuous Nutritional Counseling in Gastric Cancer Patients who Underwent Gastrectomy. International journal

    Nobuo Takata, Satoru Kikuchi, Shinji Kuroda, Shunsuke Tanabe, Naoaki Maeda, Kazuhiro Noma, Ayako Takahashi, Yuzo Umeda, Kenichi Shikata, Kazuhide Ozaki, Toshiyoshi Fujiwara

    Annals of surgical oncology   30 ( 2 )   1110 - 1118   2023.2

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    BACKGROUND: Body weight loss (BWL) and skeletal muscle loss (SML) are inevitable after gastrectomy for gastric cancer (GC) and can decrease patients' quality of life (QOL) and survival. OBJECTIVE: The aim of this retrospective study was to evaluate the effect of perioperative and post-discharge patient participation in continuous nutritional counseling (CNC) on post-gastrectomy BWL and SML. METHODS: Ninety-three patients with GC who underwent curative gastrectomy between March 2018 and July 2019 were analyzed. Patients received either pre-discharge nutritional counseling alone (control group, n = 49) or patient-participation CNC (CNC group, n = 44) after gastrectomy. Differences between percentage BWL (%BWL), percentage SML (%SML), and nutrition-related blood parameters between the preoperative values and those at 12 months after surgery were compared between the groups. RESULTS: Compared with the control group, %BWL was significantly lower in the CNC group at 1 month (-6.2 ± 2.5% vs. -7.9 ± 3.3%, p = 0.005), 6 months (-7.8 ± 6.6% vs. -12.3 ± 6.4%, p = 0.001) and 12 months (-7.9 ± 7.6% vs. -13.2 ± 8.2%, p = 0.002), and %SML was significantly lower in the CNC group at 12 months (-5.3 ± 10.3% vs. -12.8 ± 12%, p = 0.002). Regarding nutrition-related blood parameters, change in total cholesterol was significantly lower in the CNC group than the control group at 12 months after surgery (p = 0.02). Multivariate analysis identified no CNC as an independent risk factor for severe BWL (p = 0.001) and SML (p = 0.006) at 12 months after surgery. CONCLUSIONS: Following gastrectomy, patient-participation CNC prevented postoperative BWL and SML after surgery. These results support the induction of such a CNC program in these patients.

    DOI: 10.1245/s10434-022-12572-3

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  • The renoprotective effect of esaxerenone independent of blood pressure lowering: a post hoc mediation analysis of the ESAX-DN trial. International journal

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

    Hypertension research : official journal of the Japanese Society of Hypertension   46 ( 2 )   437 - 444   2023.2

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    Angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) are recommended as first-line drugs for hypertension with diabetic nephropathy owing to their renoprotective effect; however, their effect beyond lowering blood pressure (BP) has not been confirmed. Recent studies have shown that aldosterone plays a key role in causing renal injury; therefore, it is likely that mineralocorticoid receptor (MR) blockers inhibit aldosterone-induced renal damage in different ways from ACE inhibitors and ARBs. Therefore, we investigated the mechanism of the effect of an MR blocker on reducing the urinary albumin-to-creatinine ratio (UACR) using data from a randomized, double-blind, placebo-controlled phase 3 study (ESAX-DN) of a new nonsteroidal MR blocker, esaxerenone. This post hoc analysis used a novel statistical method to quantitatively estimate the effect of esaxerenone on UACR reduction mediated, or not mediated, by changes in systolic BP (SBP) and/or estimated glomerular filtration rate (eGFR). The proportion of the mediated effect by SBP changes to the total effect on UACR reduction was 9.8-10.7%; the UACR was reduced to 0.903-0.911 times the baseline at the end of treatment through the SBP-related pathway and to 0.422-0.426 times the baseline through the non-SBP-related pathway. Even considering both SBP and eGFR simultaneously, the proportion of the mediated effect was 21.9-28.1%. These results confirm that esaxerenone has a direct UACR-lowering effect independent of BP lowering and that its magnitude is much larger than that of the BP-dependent effect. Thus, esaxerenone could be a UACR-reducing treatment option for patients with diabetic nephropathy.

    DOI: 10.1038/s41440-022-01008-w

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  • Edaravone Attenuated Angiotensin II-Induced Atherosclerosis and Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Mice. International journal

    Haruhito A Uchida, Tetsuharu Takatsuka, Yoshiko Hada, Ryoko Umebayashi, Hidemi Takeuchi, Kenichi Shikata, Venkateswaran Subramanian, Alan Daugherty, Jun Wada

    Biomolecules   12 ( 8 )   2022.8

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    BACKGROUND: The aim of the study was to define whether edaravone, a free-radical scavenger, influenced angiotensin II (AngII)-induced atherosclerosis and abdominal aortic aneurysms (AAAs) formation. METHODS: Male apolipoprotein E-deficient mice (8-12 weeks old) were fed with a normal diet for 5 weeks. Either edaravone (10 mg/kg/day) or vehicle was injected intraperitoneally for 5 weeks. After 1 week of injections, mice were infused subcutaneously with either AngII (1000 ng/kg/min, n = 16-17 per group) or saline (n = 5 per group) by osmotic minipumps for 4 weeks. RESULTS: AngII increased systolic blood pressure equivalently in mice administered with either edaravone or saline. Edaravone had no effect on plasma total cholesterol concentrations and body weights. AngII infusion significantly increased ex vivo maximal diameters of abdominal aortas and en face atherosclerosis but was significantly attenuated by edaravone administration. Edaravone also reduced the incidence of AngII-induced AAAs. In addition, edaravone diminished AngII-induced aortic MMP-2 activation. Quantitative RT-PCR revealed that edaravone ameliorated mRNA abundance of aortic MCP-1 and IL-1β. Immunostaining demonstrated that edaravone attenuated oxidative stress and macrophage accumulation in the aorta. Furthermore, edaravone administration suppressed thioglycolate-induced mice peritoneal macrophages (MPMs) accumulation and mRNA abundance of MCP-1 in MPMs in male apolipoprotein E-deficient mice. In vitro, edaravone reduced LPS-induced mRNA abundance of MCP-1 in MPMs. CONCLUSIONS: Edaravone attenuated AngII-induced AAAs and atherosclerosis in male apolipoprotein E-deficient mice via anti-oxidative action and anti-inflammatory effect.

    DOI: 10.3390/biom12081117

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  • Rationale, design and baseline characteristics of the effect of canagliflozin in patients with type 2 diabetes and microalbuminuria in the Japanese population: The CANPIONE study. International journal

    Satoshi Miyamoto, Hiddo J L Heerspink, Dick de Zeeuw, Masao Toyoda, Daisuke Suzuki, Takashi Hatanaka, Tohru Nakamura, Shinji Kamei, Satoshi Murao, Kazuyuki Hida, Shinichiro Ando, Hiroaki Akai, Yasushi Takahashi, Daisuke Koya, Munehiro Kitada, Hisashi Sugano, Tomokazu Nunoue, Akihiko Nakamura, Motofumi Sasaki, Tatsuaki Nakatou, Kei Fujimoto, Daiji Kawanami, Takashi Wada, Nobuyuki Miyatake, Michihiro Yoshida, Kenichi Shikata

    Diabetes, obesity & metabolism   24 ( 8 )   1429 - 1438   2022.8

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    AIM: To evaluate the effect of canagliflozin, a sodium-glucose co-transporter-2 (SGLT2) inhibitor, on albuminuria and the decline of estimated glomerular filtration rate (eGFR) in participants with type 2 diabetes and microalbuminuria. METHODS: The CANPIONE study is a multicentre, randomized, parallel-group and open-labelled study consisting of a unique 24-week preintervention period, during which the rate of eGFR decline before intervention is estimated, followed by a 52-week intervention and a 4-week washout period. Participants with a geometric mean urinary albumin-to-creatinine ratio (UACR) of 50 and higher and less than 300 mg/g in two consecutive first-morning voids at two different time points, and an eGFR of 45 ml/min/1.73m2 or higher, are randomly assigned to receive canagliflozin 100 mg daily or to continue guideline-recommended treatment, except for SGLT2 inhibitors. The first primary outcome is the change in UACR, and the second primary outcome is the change in eGFR slope. RESULTS: A total of 258 participants were screened and 98 were randomized at 21 sites in Japan from August 2018 to May 2021. The mean baseline age was 61.4 years and 25.8% were female. The mean HbA1c was 7.9%, mean eGFR was 74.1 ml/min/1.73m2 and median UACR was 104.2 mg/g. CONCLUSIONS: The CANPIONE study will determine whether the SGLT2 inhibitor canagliflozin can reduce albuminuria and slow eGFR decline in participants with type 2 diabetes and microalbuminuria.

    DOI: 10.1111/dom.14731

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  • Reduction in the magnitude of serum potassium elevation in combination therapy with esaxerenone (CS-3150) and sodium-glucose cotransporter 2 inhibitor in patients with diabetic kidney disease: Subanalysis of two phase III studies.

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

    Journal of diabetes investigation   13 ( 7 )   1190 - 1202   2022.7

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    AIMS/INTRODUCTION: We evaluated the effect of co-administration of esaxerenone and a sodium-glucose cotransporter 2 (SGLT2) inhibitor on the magnitude of serum potassium elevation in Japanese patients with diabetic kidney disease. MATERIALS AND METHODS: We carried out a prespecified subanalysis of data from two phase III studies: a multicenter, randomized, double-blind, placebo-controlled trial in patients with type 2 diabetes and microalbuminuria (J308); and a multicenter, single-arm, open-label trial in patients with type 2 diabetes and macroalbuminuria (J309). Changes in serum potassium levels during the studies and other measures were evaluated according to SGLT2 inhibitor use. RESULTS: In both studies, time-course changes in serum potassium levels, and incidence rates of serum potassium elevation were lower in patients with co-administration of SGLT2 inhibitor in both the placebo and esaxerenone groups than those without the inhibitor. In contrast, time-course changes and mean percentage changes from baseline in urinary albumin-to-creatinine ratio, the proportion of patients with albuminuria remission and time-course changes in blood pressure did not change with or without SGLT2 inhibitor, whereas the albumin-to-creatinine ratio and blood pressure were reduced with esaxerenone. The blood glucose-lowering effect of SGLT2 inhibitor was not affected by esaxerenone. CONCLUSIONS: In Japanese patients with type 2 diabetes and albuminuria treated with esaxerenone, concomitant use of SGLT2 inhibitor reduced the magnitude of serum potassium elevation without any change of its antihypertensive and albuminuria-suppressing effects. Co-administration of esaxerenone and SGLT2 inhibitor might be a beneficial treatment option for patients with diabetic kidney disease.

    DOI: 10.1111/jdi.13778

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  • Impact of Amino Acids Nutrition Following Gastrectomy in Gastric Cancer Patients. International journal

    Satoru Kikuchi, Nobuo Takata, Shinji Kuroda, Hibiki Umeda, Shunsuke Tanabe, Naoaki Maeda, Kosei Takagi, Kazuhiro Noma, Yuko Hasegawa, Kumiko Nawachi, Shunsuke Kagawa, Yuzo Umeda, Kenichi Shikata, Toshiyoshi Fujiwara

    Anticancer research   42 ( 7 )   3637 - 3643   2022.7

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    BACKGROUND/AIM: Postoperative body weight loss (BWL) and skeletal muscle loss (SML) after gastrectomy are associated with a decline in quality of life and worse longterm prognosis in gastric cancer (GC) patients. This study aimed to evaluate the efficacy of amino acids nutrition on BWL and SML in the early period following gastrectomy. PATIENTS AND METHODS: The parameters of body composition were measured by bioelectrical impedance analysis in the patients undergoing radical gastrectomy for GC and analyzed retrospectively. Patients received either peripheral parenteral nutrition (PPN) of 4.3% glucose fluid with regular diet (control group, n=43) or PPN of 7.5% glucose fluid containing amino acids plus oral nutritional supplement (ONS) rich in protein with regular diet (amino acids group, n=40) following gastrectomy. The percentages of BWL and SML from preoperative values to those at 7 days and 1 month after surgery were compared between the two groups. RESULTS: The %BWL and %SML at 7 days after surgery were significantly lower in the amino acids group than those in the control group (%BWL, -2.4±1.7% vs. -4.2±1.8%; p<0.0001, %SML, -4.1±3.8 vs. -6.5±3.8; p=0.006). Moreover, the %BWL at 1 month after surgery was significantly lower in the amino acids group compared to that in the control group (- 4.6±2.9% vs. -6.1±2.6%; p=0.01); however, the %SML was similar between the two groups. The hematological nutritional parameters were similar between the two groups. CONCLUSION: Amino acids nutrition by PPN and ONS following gastrectomy prevented postoperative BWL and SML in the early period after surgery in GC patients.

    DOI: 10.21873/anticanres.15852

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  • Dietary intake and physical activity in Japanese patients with type 2 diabetes: the Japan Diabetes Complication and its Prevention prospective study (JDCP study 8)

    Chika Horikawa, Kinsuke Tsuda, Yoshiharu Oshida, Jo Satoh, Yasuaki Hayashino, Naoko Tajima, Rimei Nishimura, Hirohito Sone, Daisuke Koya, Kenichi Shikata, Shigehiko Kitano, Yukihiro Sato, Hidetoshi Yamashita, Satoshi Kato, Jiro Nakamura, Masayuki Baba, Hitoshi Shimano, Yoshimitsu Yamasaki, Naruhito Yoshioka, Satoshi Sasaki, Jo Sato, Hirohito Sone, Kazuo Izumi, Hideki Origasa, Kouji Inagaki, Fusanori Nishimura, Hidetoshi Noguchi, Naruhito Yoshioka, Jo Sato, Jiro Nakamura, Nobuya Inagaki, Yukio Tanizawa, Eiichi Araki, Eiichi Araki, Kazuo Izumi, Nobuya Inagaki, Kohjiro Ueki, Hirohito Sone, Yukio Tanizawa Rimei Nishimura, Mitsuhiko Noda, Yasuhiko Iwamoto, Masato Kasuga, Kishio Nanjo, Masakazu Haneda, Nigishi Hotta, Masato Kasuga, Yasuhiro Iso, Hiroshi Kiyohara, Masakazu Haneda, Toshimasa Yamauchi, Tsutomu Yamazaki, Eiichi Araki, Jiro Nakamura, Yasuhiro Iso, Hiroshi Kiyohara, Toshimasa Yamauchi, Tsutomu Yamazak

    Diabetology International   13 ( 2 )   344 - 357   2022.4

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    Medical nutrition therapy and exercise therapy are the cornerstones of treatment for patients with type 2 diabetes; however, there has not been a nationwide study on the actual dietary intake and physical activity status of patients since the 2000s. We aimed to clarify this in Japanese patients with type 2 diabetes using data from the Japan Diabetes Complication and its Prevention prospective (JDCP), a nationwide study launched in 2007. A total of 1992 patients with type 2 diabetes, aged 40–75 years, completed either the Brief-type, self-administered Diet History Questionnaire (1643 patients) or International Physical Activity Questionnaire (1834 patients), and their data were analyzed in this study. Mean daily energy intake for all participants was 1686.8 kcal/day, and the mean proportions of carbohydrate, protein, and fat comprising total energy intake were 60.2, 16.2, and 23.6%, respectively. The patients in this study had similar energy and nutrient intake status to patients in the 1996 Japan Diabetes Complications Study; however, Japanese patients still had higher carbohydrate and lower fat consumption than patients with diabetes in Western countries. The physical activity questionnaire reported that 31.0% of patients did not have exercise habits; this was particularly noticeable in female patients and patients under the age of 65. BMI increased from 22.7 to 24.1 kg/m2 in men and 23.2 to 24.8 kg/m2 in women from 1996 to 2007, respectively. Further research is required to investigate how dietary intake and physical activity associates with the risk of developing complications in type 2 diabetes patients.

    DOI: 10.1007/s13340-022-00575-0

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  • Circulating GPIHBP1 levels and microvascular complications in patients with type 2 diabetes: A cross-sectional study. International journal

    Naoko Kurooka, Jun Eguchi, Kazutoshi Murakami, Shinji Kamei, Toru Kikutsuji, Sakiko Sasaki, Akiho Seki, Satoshi Yamaguchi, Ichiro Nojima, Mayu Watanabe, Chigusa Higuchi, Akihiro Katayama, Haruhito A Uchida, Atsuko Nakatsuka, Kenichi Shikata, Jun Wada

    Journal of clinical lipidology   16 ( 2 )   237 - 245   2022.1

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    BACKGROUND: Glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 (GPIHBP1) plays a crucial role in lipolytic processing. Previous studies have shown that GPIHBP1 mutations cause severe hypertriglyceridemia and that serum GPIHBP1 levels are marginally higher in patients with coronary heart disease; however, the role of GPIHBP1 in type 2 diabetes mellitus (T2DM) remains unknown. OBJECTIVE: We investigated the association between circulating GPIHBP1 levels and the prevalence of microvascular complications in T2DM. METHODS: A total of 237 subjects with T2DM and 235 non-diabetic control subjects were enrolled in this study. Their serum GPIHBP1 levels were evaluated using ELISA assays. RESULTS: Circulating GPIHBP1 levels were higher in patients with T2DM (952.7 pg/mL [761.3-1234.6], p < 0.0001) than in non-diabetic subjects (700.6 [570.8-829.6]), but did not differ in T2DM patients with or without hypertriglyceridemia. Serum GPIHBP1 levels were significantly higher in patients with T2DM with diabetic retinopathy (DR), diabetic nephropathy (DN), and microvascular complications than in those without these complications. Multivariable logistic regression and receiver operating characteristic (ROC) curve analyses revealed that the presence of microvascular complications, but not macrovascular complications, was independently associated with serum GPIHBP1 levels, which could predict the presence of diabetic microvascular complications. CONCLUSIONS: Elevated GPIHBP1 levels are associated with microvascular complications in T2DM and may help to predict their progression.

    DOI: 10.1016/j.jacl.2022.01.006

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  • The Association of Postprandial Triglyceride Variability with Renal Dysfunction and Microalbuminuria in Patients with Type 2 Diabetic Mellitus: A Retrospective and Observational Study. International journal

    Natsumi Matsuoka-Uchiyama, Haruhito A Uchida, Shugo Okamoto, Yasuhiro Onishi, Katsuyoshi Katayama, Mariko Tsuchida-Nishiwaki, Hidemi Takeuchi, Rika Takemoto, Yoshiko Hada, Ryoko Umebayashi, Naoko Kurooka, Kenji Tsuji, Jun Eguchi, Hirofumi Nakajima, Kenichi Shikata, Jun Wada

    Journal of diabetes research   2022   3157841 - 3157841   2022

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    OBJECTIVE: We examined whether or not day-to-day variations in lipid profiles, especially triglyceride (TG) variability, were associated with the exacerbation of diabetic kidney disease. METHODS: We conducted a retrospective and observational study. First, 527 patients with type 2 diabetes mellitus (DM) who had had their estimated glomerular filtration rate (eGFR) checked every 6 months since 2012 for over 5 years were registered. Variability in postprandial TG was determined using the standard deviation (SD), SD adjusted (Adj-SD) for the number of measurements, and maximum minus minimum difference (MMD) during the first three years of follow-up. The endpoint was a ≥40% decline from baseline in the eGFR, initiation of dialysis or death. Next, 181 patients who had no micro- or macroalbuminuria in February 2013 were selected from among the 527 patients for an analysis. The endpoint was the incidence of microalbuminuria, initiation of dialysis, or death. RESULTS: Among the 527 participants, 110 reached a ≥40% decline from baseline in the eGFR or death. The renal survival was lower in the higher-SD, higher-Adj-SD, and higher-MMD groups than in the lower-SD, lower-Adj-SD, and lower-MMD groups, respectively (log-rank test p = 0.0073, 0.0059, and 0.0195, respectively). A lower SD, lower Adj-SD, and lower MMD were significantly associated with the renal survival in the adjusted model (hazard ratio, 1.62, 1.66, 1.59; 95% confidence intervals, 1.05-2.53, 1.08-2.58, 1.04-2.47, respectively). Next, among 181 participants, 108 developed microalbuminuria or death. The nonincidence of microalbuminuria was lower in the higher-SD, higher-Adj-SD, and higher-MMD groups than in the lower-SD, lower-Adj-SD, and lower-MMD groups, respectively (log-rank test p = 0.0241, 0.0352, and 0.0474, respectively). CONCLUSIONS: Postprandial TG variability is a novel risk factor for eGFR decline and the incidence of microalbuminuria in patients with type 2 DM.

    DOI: 10.1155/2022/3157841

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  • 周術期管理における多職種チーム医療 管理栄養士による患者教育プロトコールの胃癌術後体重減少、サルコペニア抑制効果

    今井 祥子, 菊地 覚次, 高田 暢夫, 黒田 新士, 田辺 俊介, 前田 直見, 西崎 正彦, 野間 和広, 香川 俊輔, 楳田 祐三, 縄稚 久美子, 高橋 絢子, 長谷川 祐子, 四方 賢一, 藤原 俊義

    日本癌治療学会学術集会抄録集   59回   WS7 - 6   2021.10

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  • Efficacy and safety of esaxerenone (CS-3150) in Japanese patients with type 2 diabetes and macroalbuminuria: a multicenter, single-arm, open-label phase III study.

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

    Clinical and experimental nephrology   25 ( 10 )   1070 - 1078   2021.10

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    BACKGROUND: Esaxerenone has potential renoprotective effects and reduces the urinary albumin-to-creatinine ratio (UACR) in patients with diabetic kidney disease and overt nephropathy. We investigated the efficacy and safety of esaxerenone in Japanese patients with type 2 diabetes (T2D) and macroalbuminuria (UACR ≥ 300 mg/g creatinine). METHODS: We conducted a multicenter, single-arm, open-label phase III study in 56 patients with T2D and UACR ≥ 300 mg/g creatinine with estimated glomerular filtration rate (eGFR) ≥ 30 mL/min/1.73 m2 and treated with a renin-angiotensin system inhibitor. Patients received esaxerenone for 28 weeks at 1.25 mg/day initially with titration to 2.5 mg/day based on serum potassium (K+) monitoring. Efficacy was evaluated as the change in UACR from baseline to week 28. Safety endpoints included adverse events (AEs), incidence of serum K+ increase, and change in eGFR from baseline. RESULTS: UACR decreased by 54.6% (95% CI 46.9%, 61.3%) on average from baseline (544.1 mg/g creatinine) to the end of treatment (246.8 mg/g creatinine); 51.8% of patients showed improvement to early nephropathy. AE incidence was 69.6%. Three patients (5.4%) had serum K+ levels ≥ 6.0 mEq/L or ≥ 5.5 mEq/L on two consecutive occasions. Hyperkalemia in two patients was transient and resolved during the treatment period. One patient discontinued following two consecutive serum K+ values ≥ 5.5 mEq/L. The maximum change from baseline in eGFR was - 8.3 mL/min/1.73 m2 at week 24. CONCLUSIONS: Esaxerenone reduced UACR in Japanese patients with T2D and UACR ≥ 300 mg/g creatinine; more than half experienced a transition from UACR ≥ 300 mg/g creatinine to UACR < 300 mg/g creatinine. CLINICAL TRIAL REGISTRATION: JapicCTI-173696.

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  • 糖尿病性腎臓病の克服を目指して DKDの最近のトレンド

    荒木 信一, 四方 賢一, 和田 隆志

    糖尿病合併症   35 ( 1 )   93 - 96   2021.7

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  • Recent evidence in the etiology and treatment for diabetic kidney disease.

    Kenichi Shikata

    Journal of diabetes investigation   12 ( 5 )   694 - 696   2021.5

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    Etiology and therapeutic targets of diabetic nephropathy.

    DOI: 10.1111/jdi.13433

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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).

    Kenichi Shikata, Masakazu Haneda, Toshiharu Ninomiya, Daisuke Koya, Yoshiki Suzuki, Daisuke Suzuki, Hitoshi Ishida, Hiroaki Akai, Yasuhiko Tomino, Takashi Uzu, Motonobu Nishimura, Shiro Maeda, Daisuke Ogawa, Satoshi Miyamoto, Hirofumi Makino

    Journal of diabetes investigation   12 ( 2 )   207 - 216   2021.2

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    AIMS/INTRODUCTION: We evaluated the efficacy of multifactorial intensive treatment (IT) on renal outcomes in patients with type 2 diabetes and advanced-stage diabetic kidney disease (DKD). MATERIALS AND METHODS: The Diabetic Nephropathy Remission and Regression Team Trial in Japan (DNETT-Japan) is a multicenter, open-label, randomized controlled trial with a 5-year follow-up period. We randomly assigned 164 patients with advanced-stage diabetic kidney disease (urinary albumin-to-creatinine ratio ≥300 mg/g creatinine, serum creatinine level 1.2-2.5 mg/dL in men and 1.0-2.5 mg/dL in women) to receive either IT or conventional treatment. The primary composite outcome was end-stage kidney failure, doubling of serum creatinine or death from any cause, which was assessed in the intention-to-treat population. RESULTS: The IT tended to reduce the risk of primary end-points as compared with conventional treatment, but the difference between treatment groups did not reach the statistically significant level (hazard ratio 0.69, 95% confidence interval 0.43-1.11; P = 0.13). Meanwhile, the decrease in serum low-density lipoprotein cholesterol level and the use of statin were significantly associated with the decrease in primary outcome (hazard ratio 1.14; 95% confidence interval 1.05-1.23, P < 0.001 and hazard ratio 0.53, 95% confidence interval 0.28-0.998, P < 0.05, respectively). The incidence of adverse events was not different between treatment groups. CONCLUSIONS: The risk of kidney events tended to decrease by IT, although it was not statistically significant. Lipid control using statin was associated with a lower risk of adverse kidney events. Further follow-up study might show the effect of IT in patients with advanced diabetic kidney disease.

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  • 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). International journal

    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 )   2021.1

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    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). International journal

    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

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    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): Phase 3 Randomized Controlled Clinical Trial. International journal

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

    Clinical journal of the American Society of Nephrology : CJASN   15 ( 12 )   1715 - 1727   2020.12

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    <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.

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    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. International journal

    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   2020.9

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    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.

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  • 2型糖尿病に対するメトホルミンの抗腫瘍効果

    野島 一郎, 榮川 伸吾, 梶谷 展生, 勅使川原 早苗, 宮本 聡, 利根 淳仁, 内田 治仁, 中司 敦子, 江口 潤, 四方 賢一, 鵜殿 平一郎, 和田 淳

    糖尿病   63 ( Suppl.1 )   S - 111   2020.8

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  • 当院におけるTime-In-Range(TIR)とHbA1cとの関連についての検討

    片山 晶博, 野島 一郎, 樋口 千草, 渡邉 真由, 宮本 聡, 中司 敦子, 江口 潤, 四方 賢一, 和田 淳

    糖尿病   63 ( Suppl.1 )   S - 220   2020.8

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  • 糖尿病性腎臓病のトピックス 糖尿病性腎臓病の新規治療標的の探索 炎症を標的とした治療戦略

    宮本 聡, 四方 賢一

    糖尿病合併症   34 ( 2 )   295 - 297   2020.7

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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.   2020.6

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  • 【症例で学ぶ!腎泌尿器診療ガイドラインの使い方】(第2章)代表的腎疾患 糖尿病性腎臓病(DKD) 保存期

    宮本 聡, 木野村 賢, 四方 賢一

    腎と透析   88 ( 増刊 )   60 - 64   2020.6

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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   2020.4

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    AIMS/INTRODUCTION: The predictive low glucose management (PLGM) system was introduced in March 2018 in Japan. Although there are some reports demonstrating the benefit of PLGM in preventing hypoglycemia, no data are currently available in Japanese patients with type 1 diabetes mellitus (T1DM). The aim of the present study is to evaluate the effect of PLGM with sensor-augmented pump therapy in the prevention of hypoglycemia in Japanese patients. MATERIALS AND METHODS: We included 16 patients with T1DM who used the MiniMed®640G system after switching from the MiniMed®620G system. We retrospectively analysed the data of the continuous glucose monitoring system in 1 month after switching to MiniMed®640G. RESULTS: The area under the curve (AUC) of hypoglycemia of < 70 mg/dL was lowered from 0.42 ± 0.43 mg/dL day to 0.18 ± 0.18 mg/dL day (P = 0.012). Correspondingly, the duration of severe hypoglycemia (< 54 mg/dL) was reduced significantly from 15.3 ± 21.7 min/day to 4.8 ± 6.9 min/day (P = 0.019). The duration of hypoglycemia was reduced, but the reduction was not significant. Regarding the AUC for hyperglycemia > 180 mg/dL and the duration of hyperglycemia did not change. With the PLGM function, 79.3% of the predicted hypoglycemic events were avoided. CONCLUSIONS: The hypoglycemia avoidance rate was comparable to those in previous reports. In addition, we demonstrated that PLGM can markedly suppress severe hypoglycemia without deteriorating glycemic control in Japanese T1DM patients. It is necessary to further investigate the effective use of the PLGM feature such as establishing a lower limit and the timing of resumption.

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  • 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.

    Kenichi Shikata, Ryo Kodera, Kazunori Utsunomiya, Daisuke Koya, Rimei Nishimura, Satoshi Miyamoto, Naoko Tajima

    Journal of diabetes investigation   11 ( 2 )   325 - 332   2020.3

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    AIMS/INTRODUCTION: To clarify the prevalence of albuminuria and renal dysfunction, and related factors in Japanese patients with diabetes, we analyzed the baseline data of the Japan Diabetes Complication and its Prevention prospective study. MATERIALS AND METHODS: We used the data of 355 patients with type 1 diabetes and 5,194 patients with type 2 diabetes to evaluate the prevalence of albuminuria and renal dysfunction, and related factors. A binomial logistic regression analysis was used to investigate independent contributing factors for estimated glomerular filtration rate <60 mL/min/1.73 m2 or albuminuria. RESULTS: The prevalence of microalbuminuria and macroalbuminuria was 15.2% (54/355) and 3.1% (11/355) in type 1 diabetes patients, and 25.0% (1,298/5,194) and 5.1% (265/5,194) in type 2 diabetes patients, respectively. The proportion of renal dysfunction (estimated glomerular filtration rate <60 mL/min/1.73 m2 ) was 9.9% (35/355) in type 1 diabetes patients, and 15.3% (797/5,194) in type 2 diabetes patients. The proportion of patients with renal dysfunction with normoalbuminuria was 7.3% (26/355) for type 1 diabetes patients, and 9.0% (467/5,194) for type 2 diabetes patients. The factors related to albuminuria in type 2 diabetes patients were glycated hemoglobin, hypertension, age, duration of diabetes, body mass index and estimated glomerular filtration rate. In contrast, factors to related renal dysfunction were age, duration of diabetes, dyslipidemia, hypertension, body mass index, male sex and albuminuria. CONCLUSIONS: We showed the recent prevalence of albuminuria and renal dysfunction, and related factors in Japanese type 1 and type 2 diabetes patients using the baseline data of the Japan Diabetes Complication and its Prevention prospective study. The current results suggest that renal disease in patients with type 2 diabetes is heterogeneous, and different mechanisms might be involved in albuminuria and deterioration of renal function.

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  • 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 Reviewed

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

    J Diabetes Investig   11 ( 2 )   325 - 332   2019.9

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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. Reviewed International journal

    Sadayoshi Ito, Kenichi Shikata, Masaomi Nangaku, Yasuyuki Okuda, Tomoko Sawanobori

    Clinical journal of the American Society of Nephrology : CJASN   14 ( 8 )   1161 - 1172   2019.8

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    BACKGROUND AND OBJECTIVES: The progression of kidney disease in some patients with type 2 diabetes mellitus may not be adequately suppressed by renin-angiotensin system inhibitors. Esaxerenone (CS-3150) is a nonsteroidal mineralocorticoid receptor blocker that has shown kidney protective effects in preclinical studies, and it is a potential add-on therapy to treat diabetic kidney disease. This phase 2 study evaluated the efficacy and safety of esaxerenone in Japanese patients with type 2 diabetes mellitus and microalbuminuria. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This multicenter, randomized, double-blind, placebo-controlled trial enrolled 365 hypertensive or normotensive patients with type 2 diabetes mellitus and microalbuminuria (urinary albumin-to-creatinine ratio ≥45 to <300 mg/g creatinine) treated with renin-angiotensin system inhibitor who had eGFR≥30 ml/min per 1.73 m2. Participants were randomized to receive 0.625, 1.25, 2.5, or 5 mg/d esaxerenone or placebo for 12 weeks. The primary end point was the change in urinary albumin-to-creatinine ratio from baseline to week 12 (with last observation carried forward). RESULTS: Esaxerenone treatment at 1.25, 2.5, and 5 mg/d significantly reduced urinary albumin-to-creatinine ratio by the end of treatment (38%, 50%, and 56%, respectively) compared with placebo (7%; all P<0.001). The urinary albumin-to-creatinine ratio remission rate (defined as urinary albumin-to-creatinine ratio <30 mg/g creatinine at the end of treatment and ≥30% decrease from baseline) was 21% in the 2.5- and 5-mg/d groups versus 3% for placebo (both P<0.05). Adverse events occurred slightly more frequently with esaxerenone versus placebo, but the frequencies of drug-related adverse events and discontinuation rates were similar in the placebo and the 0.625-, 1.25-, and 2.5-mg/d groups. Drug-related adverse events and treatment discontinuations were marginally higher in the 5-mg/d group. The most common drug-related adverse event was hyperkalemia, which was dose proportional. CONCLUSIONS: Adding esaxerenone at 1.25, 2.5, and 5 mg/d for 12 weeks to an ongoing renin-angiotensin system inhibitor significantly reduces urinary albumin-to-creatinine ratio in patients with type 2 diabetes mellitus and microalbuminuria.

    DOI: 10.2215/CJN.14751218

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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 Reviewed

    山口 哲志, 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   2019.5

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    本研究はSAP導入後の効果を検討するため、CSIIからSAPに変更後1年以上経過した1型糖尿病22症例を解析した後ろ向き観察研究である。HbA1cはSAP前と比較して6ヵ月(6M)では不変、12Mで有意に低下した(各々7.6±0.7%、7.4±0.9%、7.1±0.9%)。6Mの時点でHbA1c0.1%以上低下した群を6M低下群、変化なし又は0.1%以上上昇した群を6M不変・上昇群と定義したところ、6M不変・上昇群で0MのHbA1cが有意に低値で、重回帰分析では基礎インスリン比率の変化(6M)がHbA1c変化量(6M)の有意な決定因子として採用され、負の相関を示した。また、6M不変・上昇群では0MのSMBGで低血糖頻度が有意に高く、1Mで有意に低下した。臨床的にSMBGでの低血糖が多い症例ではSAP導入後にHbA1c上昇を呈す事もあり、注意を要する。(著者抄録)

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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. International journal

    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   2019.5

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    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 Reviewed

    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   2019.2

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  • 「エビデンスに基づくCKD診療ガイドライン2018」の要点(Essential points from Evidence-based Clinical Practice Guidelines for Chronic Kidney Disease 2018) Reviewed

    Okada Hirokazu, Yasuda Yoshinari, Kashihara Naoki, Asahi Koichi, Ito Takafumi, Kaname Shinya, Kanda Eiichiro, Kanno Yoshihiko, Shikata Kenichi, Shibagaki Yugo, Tsuchiya Ken, Tsuruya Kazuhiko, Nagata Daisuke, Narita Ichiei, Nangaku Masaomi, Hattori Motoshi, Hamano Takayuki, Fujimoto Shouichi, Moriyama Toshiki, Yamagata Kunihiro, Yamamoto Ryohei, Wakasugi Minako, Ashida Akira, Usui Joichi, Kawamura Kazuko, Kitamura Kenichiro, Konta Tsuneo, Suzuki Yusuke, Tsuruoka Shuichi, Nishio Saori, Fujii Naohiko, Fujii Hideki, Wada Takehiko, Yokoyama Hitoshi, Aoki Katsunori, Akiyama Daiichiro, Araki Shin-ichi, Arima Hisatomi, Ishikawa Eiji, Ishikura Kenji, Ishizuka Kiyonobu, Ishimoto Takuji, Ishimoto Yu, Iseki Kunitoshi, Itabashi Mitsuyo, Ichioka Satoko, Ichikawa Kazunobu, Ichikawa Daisuke, Inoue Shuji, Imai Toshimi, Imamura Hideaki, Iwata Yasunori, Iwazu Yoshitaka, Usui Toshiaki, Uchida Keiko, Egawa Masahiro, Ohara Shinichiro, Omori Norio, Okada Rieko, Okuda Yusuke, Ozeki Takaya, Obata Yoko, Kai Hirayasu, Kato Noritoshi, Kanasaki Keizo, Kaneko Yoshikatsu, Kabasawa Hideyuki, Kawaguchi Takehiko, Kawasaki Yukihiko, Kawashima Keisuke, Kawano Haruna, Kikuchi Kan, Kihara Masao, Kimura Yoshiki, Kurita Noriaki, Koike Kentaro, Koizumi Masahiro, Kojima Chiari, Goto Shunsuke, Konomoto Takao, Kohagura Kentaro, Komatsu Hiroyuki, Komaba Hirotaka, Saito Chie, Sakai Yukinao, Sakaguchi Yusuke, Satonaka Hiroshi, Jimi Kanako, Shimizu Akihiro, Shimizu Sayaka, Shirai Sayuri, Shinzawa Maki, Sugiyama Kazuhiro, Suzuki Tomo, Suzuki Hitoshi, Suyama Kazuhide, Segawa Hiroyoshi, Takahashi Kazuya, Tanaka Kenichi, Tanaka Tetsuhiro, Tsunoda Ryoya, Tsuruta Yuki, Nakakura Hyogo, Nagasawa Yasuyuki, Nakanishi Koichi, Nagahama Masahiko, Nakaya Izaya, Nanami Masayoshi, Niihata Kakuya, Nishi Shinichi, Nishiwaki Hiroki, Hasegawa Shoko, Hasegawa Midori, Hanada Ken, Hayashi Hiroki, Harada Ryoko, Hishida Manabu, Hirano Daishi, Hirahashi Junichi, Hirama Akio, Hirayama Kouichi, Fukagawa Masafumi, Fukuda Akihiro, Fujii Yoshiyuki, Fujisaki Kiichiro, Furuya Fumihiko, Hoshino Junichi, Hosojima Michihiro, Honda Kenjiro, Masuda Takahiro, Matsui Kosuke, Matsukuma Yuta, Matsumura Hideki, Mii Akiko, Miura Kenichiro, Mitobe Michihiro, Miyasato Yoshikazu, Miyamoto Satoshi, Miwa Saori, Yazawa Masahiko, Yata Yusuke, Yamamoto Yoshihiro, Watanabe Kimio, Japanese Society of Nephrology, Committee of Evidence-based Practice Guideline for the Treatment of CKD 2018, Evidence-based Practice Guideline for the Treatment of CKD Production Group(Work group)

    Clinical and Experimental Nephrology   23 ( 1 )   1 - 15   2019.1

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

    Keiko Tanaka, Hitoshi Sugiyama, Toshio Yamanari, Koki Mise, Hiroshi Morinaga, Masashi Kitagawa, Akifumi Onishi, Ayu Ogawa-Akiyama, Katsuyuki Tanabe, Jun Eguchi, Yasukazu Ohmoto, Kenichi Shikata, Jun Wada

    Nephrology (Carlton, Vic.)   23 ( 9 )   855 - 862   2018.9

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    AIM: Trefoil factor 3 (TFF3) is a small peptide that is involved in mucosal protection. TFF3 is widely expressed in multiple tissues including kidney tissue. Previous studies have reported that the levels of urinary TFF3 are significantly increased in patients with chronic kidney disease. The aim of this study is to detect the TFF3 mRNA in kidney and elucidate the relationship between renal TFF3 mRNA and tubulointerstitial fibrosis in IgA nephropathy (IgAN). METHODS: We investigated the renal mRNA expression of TFF3 by real-time PCR analysis in biopsy specimens from patients with IgAN, other glomerulonephritis (OGN) and minor glomerular abnormalities (MGA). We also determined the renal localization of TFF3 and the levels of urinary TFF3 by immunostaining and ELISA, respectively. RESULTS: The renal TFF3 mRNA expression was significantly associated with the urinary TFF3 secretion and the tubulointerstitial fibrosis score in the IgAN group alone. Immunostaining of the renal specimen of IgAN patients revealed that TFF3 is located in the renal tubular epithelial cells. The locations were almost the same as those that showed uromodulin positivity; specifically, the thick ascending limb (TAL) of the loop of Henle and the early portion of the distal tubule. The urinary TFF3 levels were positively correlated with the levels of urinary biomarkers of tubulointerstitial injury in such patients. CONCLUSION: Renal TFF3 mRNA is associated with renal tubulointerstitial fibrosis in IgAN patients. The TFF3 located in the renal tubular epithelial cells may play a role in the progression of tubulointerstitial fibrosis in IgAN patients.

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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. Reviewed International journal

    Koki Mise, Mariko Imamura, Satoshi Yamaguchi, Sanae Teshigawara, Atsuhito Tone, Haruhito A Uchida, Jun Eguchi, Atsuko Nakatsuka, Daisuke Ogawa, Michihiro Yoshida, Masao Yamada, Kenichi Shikata, Jun Wada

    Diabetes care   41 ( 8 )   1765 - 1775   2018.8

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    OBJECTIVE: Because quantifying glycans with complex structures is technically challenging, little is known about the association of glycosylation profiles with the renal prognosis in diabetic kidney disease (DKD). RESEARCH DESIGN AND METHODS: In 675 patients with type 2 diabetes, we assessed the baseline urinary glycan signals binding to 45 lectins with different specificities. The end point was a decrease of estimated glomerular filtration rate (eGFR) by ≥30% from baseline or dialysis for end-stage renal disease. RESULTS: During a median follow-up of 4.0 years, 63 patients reached the end point. Cox proportional hazards analysis revealed that urinary levels of glycans binding to six lectins were significantly associated with the outcome after adjustment for known indicators of DKD, although these urinary glycans, except that for DBA, were highly correlated with baseline albuminuria and eGFR. Hazard ratios for these lectins were (+1 SD for the glycan index) as follows: SNA (recognizing glycan Siaα2-6Gal/GalNAc), 1.42 (95% CI 1.14-1.76); RCA120 (Galβ4GlcNAc), 1.28 (1.01-1.64); DBA (GalNAcα3GalNAc), 0.80 (0.64-0.997); ABA (Galβ3GalNAc), 1.29 (1.02-1.64); Jacalin (Galβ3GalNAc), 1.30 (1.02-1.67); and ACA (Galβ3GalNAc), 1.32 (1.04-1.67). Adding these glycan indexes to a model containing known indicators of progression improved prediction of the outcome (net reclassification improvement increased by 0.51 [0.22-0.80], relative integrated discrimination improvement increased by 0.18 [0.01-0.35], and the Akaike information criterion decreased from 296 to 287). CONCLUSIONS: The urinary glycan profile identified in this study may be useful for predicting renal prognosis in patients with type 2 diabetes. Additional investigation of glycosylation changes and urinary glycan excretion in DKD is needed.

    DOI: 10.2337/dc18-0030

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    Other Link: https://syndication.highwire.org/content/doi/10.2337/dc18-0030

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

    Akihiko Nakamura, Ryo Kodera, Noriko Sakamoto, Haruyo Ujike, Jun Wada, Kenichi Shikata, Hirofumi Makino

    Diabetology international   9 ( 3 )   179 - 188   2018.7

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    Aim: We developed a novel estimation method for hemoglobin A1c (HbA1c) in type 2 diabetes (T2D) patients with end-stage renal disease (ESRD). This method is based on the glycated albumin (GA) level. Methods: Of the 788 Japanese patients with T2D included in this study, 545 had normal renal function (NRF group) and 243 had ESRD. Oral glucose tolerance tests (OGTTs) were performed in 80 subjects. The variables GA, body mass index (BMI), hemoglobin (Hb), and estimated glomerular filtration rate (eGFR) were significantly associated with the GA-to-HbA1c ratio and were used to determine the estimated HbA1c (eHbA1c). One method of estimating HbA1c involved dividing GA by the GA-to-HbA1c ratio predicted from the estimated regression equation; the estimated HbA1c obtained in this manner was denoted eHbA1c-1. Results: eHbA1c-1 (%) = GA × [4.688 - 18.833 × GA-1 - 0.015 × BMI - 0.037 × Hb (- 0.002 × eGFR for patients without ESRD)]-1; adjusted R 2 = 0.676 for actual HbA1c. The sensitivity of eHbA1c-1 was better than that of GA for diabetes diagnosis using the 75-g OGTT. There were no differences in the slope of eHbA1c-1 versus GA and the variance of eHbA1c-1 between the ESRD and NRF groups. eHbA1c-1 was not associated with Hb, erythropoiesis-stimulating agent use, or ESRD concomitance. Conclusions: eHbA1c-1 may be a useful parameter for estimating HbA1c in T2D patients with ESRD.

    DOI: 10.1007/s13340-018-0342-6

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  • 2型糖尿病末梢血CD8陽性T細胞における糖代謝異常と免疫疲弊

    野島 一郎, 榮川 伸吾, 樋口 千草, 勅使川原 早苗, 宮本 聡, 利根 淳仁, 中司 敦子, 江口 潤, 小川 大輔, 四方 賢一, 鵜殿 平一郎, 和田 淳

    糖尿病   61 ( 5 )   330 - 330   2018.5

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  • 当院における免疫チェックポイント阻害薬による副作用(耐糖能異常および甲状腺機能異常)の検討

    渡邉 真由, 有木 沙織, 山口 哲志, 樋口 千草, 勅使川原 早苗, 宮本 聡, 利根 淳仁, 中司 敦子, 江口 潤, 四方 賢一, 和田 淳

    糖尿病   61 ( Suppl.1 )   S - 255   2018.4

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  • 2型糖尿病末梢血CD8陽性T細胞における免疫疲弊とメトホルミンの効果

    野島 一郎, 榮川 伸吾, 樋口 千草, 勅使川原 早苗, 宮本 聡, 利根 淳仁, 中司 敦子, 江口 潤, 小川 大輔, 四方 賢一, 鵜殿 平一郎, 和田 淳

    糖尿病   61 ( Suppl.1 )   S - 211   2018.4

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  • Urine Trefoil Factors as Prognostic Biomarkers in Chronic Kidney Disease. Reviewed International journal

    Toshio Yamanari, Hitoshi Sugiyama, Keiko Tanaka, Hiroshi Morinaga, Masashi Kitagawa, Akifumi Onishi, Ayu Ogawa-Akiyama, Yuzuki Kano, Koki Mise, Yasukazu Ohmoto, Kenichi Shikata, Jun Wada

    BioMed research international   2018   3024698 - 3024698   2018

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    Introduction: Trefoil factor family (TFF) peptides are increased in serum and urine in patients with chronic kidney disease (CKD). However, whether the levels of TFF predict the progression of CKD remains to be elucidated. Methods: We determined the TFF levels using peptide-specific ELISA in spot urine samples and performed a prospective cohort study. The association between the levels of urine TFFs and other urine biomarkers as well as the renal prognosis was analyzed in 216 CKD patients (mean age: 53.7 years, 47.7% female, 56.9% with chronic glomerulonephritis, and mean eGFR: 58.5 ml/min/1.73 m2). Results: The urine TFF1 and TFF3 levels significantly increased with the progression of CKD stages, but not the urine TFF2 levels. The TFF1 and TFF3 peptide levels predicted the progression of CKD ≥ stage 3b by ROC analysis (AUC 0.750 and 0.879, resp.); however, TFF3 alone predicted CKD progression in a multivariate logistic regression analysis (odds ratio 3.854, 95% confidence interval 1.316-11.55). The Kaplan-Meier survival curves demonstrated that patients with a higher TFF1 and TFF3 alone, or in combination with macroalbuminuria, had a significantly worse renal prognosis. Conclusion: The data suggested that urine TFF peptides are associated with renal progression and the outcomes in patients with CKD.

    DOI: 10.1155/2018/3024698

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  • 2型糖尿病におけるメトホルミンの免疫機能への影響

    野島 一郎, 榮川 伸吾, 宮本 聡, 勅使川原 早苗, 利根 淳仁, 中司 敦子, 江口 潤, 四方 賢一, 鵜殿 平一郎, 和田 淳

    糖尿病   60 ( Suppl.1 )   S - 259   2017.4

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  • 糖尿病患者の血糖関連因子と認知・情動機能と白質病変

    菱川 望, 佐藤 恒太, 山下 徹, 太田 康之, 和田 淳, 四方 賢一, 槇野 博史, 阿部 康二

    臨床神経学   56 ( Suppl. )   S401 - S401   2016.12

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  • 糖尿病患者における認知機能・情動機能に影響を与える血糖関連因子

    菱川 望, 佐藤 恒太, 山下 徹, 太田 康之, 和田 淳, 四方 賢一, 槇野 博史, 阿部 康二

    日本老年医学会雑誌   53 ( Suppl. )   163 - 164   2016.5

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  • 糖尿病患者の認知機能・情動機能と血糖関連因子

    菱川 望, 佐藤 恒太, 山下 徹, 太田 康之, 和田 淳, 四方 賢一, 槇野 博史, 阿部 康二

    日本認知症ケア学会誌   15 ( 1 )   285 - 285   2016.4

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  • 糖尿病患者における血糖関連因子と認知機能・情動機能

    菱川 望, 佐藤 恒太, 河野 祥一郎, 山下 徹, 出口 健太郎, 太田 康之, 和田 淳, 四方 賢一, 槇野 博史, 阿部 康二

    Dementia Japan   29 ( 3 )   364 - 364   2015.9

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  • 糖尿病患者における認知機能・情動機能

    菱川 望, 山下 徹, 太田 康之, 出口 健太郎, 和田 淳, 四方 賢一, 槇野 博史, 阿部 康二

    日本抗加齢医学会総会プログラム・抄録集   15回   244 - 244   2015.5

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  • アメーバ赤痢を発症したインスリン受容体異常症の1例

    西井 尚子, 和田 淳, 今村 麻理子, 中司 敦子, 片岡 仁美, 小川 大輔, 四方 賢一, 槇野 博史

    糖尿病   58 ( 1 )   69 - 69   2015.1

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  • 糖尿病患者における認知機能・情動機能

    菱川 望, 山下 徹, 出口 健太郎, 太田 康之, 和田 淳, 四方 賢一, 槇野 博史, 阿部 康二

    Anti-aging Science   6 ( 3 )   195 - 195   2014.12

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  • 認知症予防の脳循環代謝 糖尿病患者における血糖関連因子および大脳白質病変の認知機能・情動機能に及ぼす影響

    菱川 望, 山下 徹, 出口 健太郎, 太田 康之, 和田 淳, 四方 賢一, 槇野 博史, 阿部 康二

    脳循環代謝   26 ( 1 )   151 - 151   2014.11

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  • 糖尿病患者における認知機能・情動機能

    菱川 望, 山下 徹, 出口 健太郎, 太田 康之, 和田 淳, 四方 賢一, 槙野 博史, 阿部 康二

    脳循環代謝   26 ( 1 )   157 - 157   2014.11

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  • 2型糖尿病の経過中にBasedow病を発症した1例

    布上 朋和, 江口 潤, 寺見 隆宏, 田中 景子, 平松 澄恵, 小松原 基志, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   57 ( 8 )   654 - 654   2014.8

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  • 糖尿病性腎症の発症・進展におけるmicro RNAの発現変化とその機能解析

    高塚 哲全, 四方 賢一, 小寺 亮, 宮本 聡, 廣田 大昌, 梶谷 展生, 小川 大輔, 和田 淳, 片岡 仁美, 槇野 博史

    糖尿病合併症   27 ( Suppl.1 )   136 - 136   2013.8

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  • 2型糖尿病における腎症の寛解および改善に関与する因子の解析

    小野 哲一郎, 四方 賢一, 小比賀 美香子, 梶谷 展生, 小寺 亮, 廣田 大昌, 村上 和敏, 堀口 千景, 小川 大輔, 和田 淳, 片岡 仁美, 槇野 博史

    糖尿病   56 ( Suppl.1 )   S - 181   2013.4

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  • Case of emphysematous cholecystitis in a patient with type 2 diabetes mellitus associated with schizophrenia. Reviewed

    Ayu Ogawa, Kenichi Shikata, Haruhito Adam Uchida, Susumu Shinoura, Naosuke Yokomichi, Daisuke Ogawa, Chicage Sato-Horiguchi, Takahito Yagi, Jun Wada, Hirofumi Makino

    Journal of diabetes investigation   3 ( 6 )   534 - 5   2012.12

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    Emphysematous cholecystitis is a rare, but life-threatening, form of acute cholecystitis caused by gas-forming organisms in the gallbladder. A 73-year-old male patient with type 2 diabetes mellitus complicated with neuropathy associated with schizophrenia was admitted to Okayama University Hospital, Okayama, Japan, because of a high fever and general malaise. On the fourth hospital day, despite normal liver function tests and little abdominal pain, his abdominal computed tomography showed huge gas formation in the gallbladder lumen along with a dilated gallbladder with a thickened wall, consistent with emphysematous cholecystitis. The patient underwent an emergency open cholecystectomy. Few abdominal symptoms appeared because of the hyposensitivity to pain caused by not only diabetic neuropathy, but also antipsychotic agents the patient was taking for schizophrenia. Emphysematous cholecystitis should be taken into consideration for the differential diagnosis of high fever in diabetic patients with schizophrenia, irrespective of the level of liver function tests and clinical symptoms.

    DOI: 10.1111/j.2040-1124.2012.00232.x

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  • 早期糖尿病性腎症におけるTelmisartanの抗酸化作用の検討

    堀口 千景, 小川 大輔, 橘 洋美, 松下 裕一, 小寺 亮, 廣田 大昌, 梶谷 展生, 片岡 仁美, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病合併症   26 ( Suppl.1 )   128 - 128   2012.10

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  • Phenotypic change of macrophages in the progression of diabetic nephropathy; sialoadhesin-positive activated macrophages are increased in diabetic kidney. Reviewed

    Ryo Nagase, Nobuo Kajitani, Kenichi Shikata, Daisuke Ogawa, Ryo Kodera, Shinichi Okada, Yuichi Kido, Hirofumi Makino

    Clinical and experimental nephrology   16 ( 5 )   739 - 48   2012.10

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    Inflammatory process is involved in pathogenesis of diabetic nephropathy, although the activation and phenotypic change of macrophages in diabetic kidney has remained unclear. Sialoadhesin is a macrophage adhesion molecule containing 17 extracellular immunoglobulin-like domains, and is an I-type lectin which binds to sialic acid ligands expressed on hematopoietic cells. The aim of this study is to clarify the activation and phenotypic change of macrophages in the progression of diabetic nephropathy.
    We examined the expression of surface markers for pan-macrophages, resident macrophages, sialoadhesin, major histocompatibility complex class II and alpha-smooth muscle actin in the glomeruli of diabetic rats using immunohistochemistry at 0, 1, 4, 12, and 24 weeks after induction of diabetes by streptozotocin. Expression of type IV collagen and the change of mesangial matrix area were also measured. The mechanism for up-regulated expression of sialoadhesin on macrophages was evaluated in vitro.
    The number of macrophages was increased in diabetic glomeruli at 1 month after induction of diabetes and the increased number was maintained until 6 months. On the other hand, sialoadhesin-positive macrophages were increased during the late stage of diabetes concomitantly with the increase of alpha-smooth muscle actin-positive mesangial cells, mesangial matrix area and type IV collagen. Gene expression of sialoadhesin was induced by stimulation with interleukin (IL)-1 beta and tumor necrosis factor-alpha but not with IL-4, transforming growth factor-beta and high glucose in cultured human macrophages.
    The present findings suggest that sialoadhesin-positive macrophages may contribute to the progression of diabetic nephropathy.

    DOI: 10.1007/s10157-012-0625-3

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  • 岡山大学病院糖尿病センターにおける医科歯科連携パス運営の課題

    大森 一弘, 高柴 正悟, 四方 賢一, 槇野 博史

    糖尿病合併症   26 ( Suppl.1 )   135 - 135   2012.10

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  • IgG4関連硬化性疾患患者のインスリン分泌能と治療効果についての検討

    片岡 仁美, 佐藤 千景, 平松 万尚, 村上 和敏, 神崎 資子, 水島 孝明, 小比賀 美香子, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   55 ( 6 )   420 - 420   2012.6

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  • 糖尿病性ケトアシドーシスの治療中に意識障害が遷延し、PRESと考えられた1型糖尿病の1例

    谷 和祐, 梶谷 展生, 佐藤 千景, 寺見 直人, 立古 浩雅, 小寺 亮, 小川 大輔, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   55 ( 5 )   370 - 370   2012.5

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  • 2型糖尿病における腎症の発症および進展に関与する因子の解析

    小野 哲一郎, 四方 賢一, 小比賀 美香子, 梶谷 展生, 小寺 亮, 宮本 聡, 廣田 大昌, 村上 和敏, 佐藤 千景, 小川 大輔, 和田 淳, 片岡 仁美, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 333   2012.4

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  • 糖尿病性腎症の発症および病態進展におけるmiR-34aの発現変化とその機能解析

    高塚 哲全, 四方 賢一, 小寺 亮, 宮本 聡, 廣田 大昌, 梶谷 展生, 佐藤 千景, 小川 大輔, 和田 淳, 片岡 仁美, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 86   2012.4

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  • PSGL-1を阻害することにより、肥満マウスにおける内臓脂肪と肝臓の炎症とインスリン抵抗性が抑制される

    廣田 大昌, 四方 賢一, 佐藤 千景, 高塚 哲全, 宮本 聡, 小寺 亮, 梶谷 展生, 小川 大輔, 片岡 仁美, 和田 淳, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 308   2012.4

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  • 1型糖尿病モデルラットにおけるVildagliptinの腎保護効果についての検討

    小寺 亮, 四方 賢一, 高塚 哲全, 宮本 聡, 廣田 大昌, 梶谷 展生, 和田 淳, 小川 大輔, 片岡 仁美, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 88   2012.4

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  • 2型糖尿病患者の腎症に関連する因子の横断的解析

    小比賀 美香子, 四方 賢一, 小野 哲一郎, 梶谷 展生, 小寺 亮, 宮本 聡, 廣田 大昌, 村上 和敏, 佐藤 千景, 小川 大輔, 和田 淳, 片岡 仁美, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 281   2012.4

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  • 糖尿病性腎症の糖鎖プロファイリングの検討

    井上 謙太郎, 和田 淳, 中司 敦子, 江口 潤, 村上 和敏, 神崎 資子, 寺見 隆宏, 勅使川原 早苗, 黒瀬 祐子, 片山 晶博, 樋口 千草, 渡邊 真由, 小川 智央, 山田 雅雄, 四方 賢一, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 281   2012.4

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  • A commentary on the VITAL study: Does vitamin D (receptor activation) protect against nephropathy in type 2 diabetes?

    Shinichi Okada, Kenichi Shikata

    Journal of diabetes investigation   3 ( 1 )   36 - 8   2012.2

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    DOI: 10.1111/j.2040-1124.2011.00161.x

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  • Diabetic Nephropathy and Microinflammation

    KATAOKA H. U, SHIKATA K., MAKINO H.

    Journal of the Japan Diabetes Society   54 ( 7 )   487 - 489   2011.7

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    DOI: 10.11213/tonyobyo.54.487

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  • 重度歯周炎により炎症反応高値・高熱を来した2型糖尿病の1例

    橘 洋美, 和田 淳, 曽我 賢彦, 綿谷 博雪, 神崎 資子, 片山 晶博, 小川 大輔, 佐藤 千景, 四方 賢一, 槇野 博史

    糖尿病   54 ( 6 )   450 - 450   2011.6

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  • 糖尿病性腎症の病態進展に関連するmicroRNAの網羅的解析

    高塚 哲全, 四方 賢一, 小寺 亮, 片岡 仁美, 宮本 聡, 廣田 大昌, 梶谷 展生, 佐藤 千景, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 225   2011.4

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  • [Microinflammation in diabetic nephropathy].

    Daisuke Ogawa, Kenichi Shikata

    Nihon Jinzo Gakkai shi   53 ( 7 )   1021 - 6   2011

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  • [Pathology of diabetic nephropathy].

    Ryo Kodera, Kenichi Shikata

    Nihon rinsho. Japanese journal of clinical medicine   68 Suppl 9   370 - 4   2010.11

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  • [Microinflammation in diabetic microvascular complications].

    Nobuo Kajitani, Kenichi Shikata

    Nihon rinsho. Japanese journal of clinical medicine   68 Suppl 9   61 - 4   2010.11

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  • 腎症における細胞周期異常と核内受容体をターゲットとした治療

    中司 敦子, 和田 淳, 村上 和敏, 神崎 資子, 勅使川原 早苗, 四方 賢一, 槇野 博史

    Diabetes Frontier   21 ( 5 )   626 - 627   2010.10

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  • 糖尿病血管合併症と炎症 糖尿病性腎症の成因と炎症

    稻垣 暢也, 四方 賢一, 片岡 仁美, 梶谷 展生, 槇野 博史

    糖尿病合併症   24 ( 1 )   99 - 102   2010.6

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  • Exendin-4の抗酸化作用と抗炎症作用を介した腎保護効果の解析 1型糖尿病モデルラットを用いた検討

    小寺 亮, 四方 賢一, 片岡 仁美, 高塚 哲全, 佐々木 基史, 宮本 聡, 廣田 大昌, 梶谷 展生, 佐藤 千景, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   53 ( Suppl.1 )   S - 167   2010.4

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  • 糖尿病患者の末梢血液中単球の活性化状態の解析とスタチンによる抗炎症作用のメカニズムの検討

    梶谷 展生, 片岡 仁美, 四方 賢一, 小寺 亮, 宮本 聡, 廣田 大昌, 更井 啓, 佐藤 千景, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   53 ( Suppl.1 )   S - 273   2010.4

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  • 腎症:基礎 1型糖尿病モデルラットにおけるexendin4の抗酸化ストレス、抗炎症作用を介した腎保護効果

    小寺 亮, 片岡 仁美, 四方 賢一, 佐藤 千景, 佐々木 基史, 宮本 聡, 廣田 大昌, 梶谷 展生, 高塚 哲全, 槇野 博史

    糖尿病合併症   23 ( Suppl.1 )   67 - 67   2009.9

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  • 腎症:基礎 Cholecystokininによる糖尿病性腎症の進展抑制効果

    宮本 聡, 四方 賢一, 佐々木 基史, 佐藤 千景, 片岡 仁美, 小寺 亮, 廣田 大昌, 梶谷 展生, 槇野 博史

    糖尿病合併症   23 ( Suppl.1 )   65 - 65   2009.9

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  • 腎症:基礎 糖尿病患者血液中単球の活性化状態解析とスタチンの抗炎症効果の検討

    梶谷 展生, 片岡 仁美, 四方 賢一, 佐々木 基史, 宮本 聡, 小寺 亮, 廣田 大昌, 佐藤 千景, 西下 伸吾, 小川 大輔, 槇野 博史

    糖尿病合併症   23 ( Suppl.1 )   69 - 69   2009.9

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  • 糖尿病血管合併症と炎症 糖尿病性腎症の成因と炎症

    片岡 仁美, 四方 賢一, 梶谷 展生, 槇野 博史

    糖尿病合併症   23 ( Suppl.1 )   51 - 51   2009.9

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  • 1型糖尿病ラットに対するExendin4の抗炎症作用を介した腎保護作用

    小寺 亮, 片岡 仁美, 四方 賢一, 佐々木 基史, 佐藤 千景, 西下 伸吾, 宮本 聡, 廣田 大昌, 梶谷 展生, 小川 大輔, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 301   2009.4

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  • Cholecystokininは抗炎症作用を介し糖尿病性腎症の進展を抑制する

    宮本 聡, 四方 賢一, 佐々木 基史, 西下 伸吾, 佐藤 千景, 片岡 仁美, 小寺 亮, 廣田 大昌, 梶谷 展生, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 301   2009.4

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  • 腎症:基礎 Exendin4は抗炎症作用を介して1型糖尿病ラットの腎障害を改善する

    小寺 亮, 四方 賢一, 片岡 仁美, 佐藤 千景, 佐々木 基史, 西下 伸吾, 宮本 聡, 廣田 大昌, 梶谷 展生, 槇野 博史

    糖尿病合併症   22 ( Suppl.1 )   67 - 67   2008.9

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  • 6. Diagnosis of Diabetic Nephropathy

    Shikata Kenichi

    Nihon Naika Gakkai Kaishi   97 ( 5 )   1028 - 1034   2008.5

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    DOI: 10.2169/naika.97.1028

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  • PSGL-1ノックアウトマウスでは高脂肪食負荷後の内臓脂肪の炎症とインスリン抵抗性が抑制される

    佐藤 千景, 四方 賢一, 廣田 大昌, 佐々木 基史, 西下 伸吾, 宮本 聡, 小寺 亮, 片岡 仁美, 和田 淳, 梶谷 展生, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 109   2008.4

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  • 糖尿病におけるCholecystokinin(CCK)の腎保護作用 CCK受容体欠損マウスでは糖尿病誘発後の腎障害が増悪する

    宮本 聡, 四方 賢一, 佐々木 基史, 岡田 震一, 西下 伸吾, 佐藤 千景, 片岡 仁美, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 297   2008.4

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  • IgG4関連症候群と診断した膵性糖尿病の1例

    小寺 亮, 片岡 仁美, 佐々木 基史, 立古 浩雅, 中村 好男, 四方 賢一, 小出 典男, 越智 浩二, 槇野 博史

    糖尿病   51 ( 1 )   55 - 55   2008.1

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  • 2型糖尿病患者の腎機能の指標としてのシスタチンCの有用性

    丸井 幸之助, 四方 賢一, 片岡 仁美, 和田 淳, 佐藤 千景, 西下 伸吾, 村上 和敏, 槇野 博史

    糖尿病   51 ( 1 )   65 - 65   2008.1

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  • A novel ADP-forming succinyl-CoA synthetase in Thermococcus kodakaraensis structurally related to the archaeal nucleoside diphosphate-forming acetyl-CoA synthetases. International journal

    Kenichi Shikata, Toshiaki Fukui, Haruyuki Atomi, Tadayuki Imanaka

    The Journal of biological chemistry   282 ( 37 )   26963 - 26970   2007.9

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    We have identified and characterized a structurally novel succinyl-CoA synthetase (SCS) from the hyperthermophilic Archaea Thermococcus kodakaraensis. The presence of an SCS completes the metabolic pathway from glutamate to succinate in Thermococcales, which had not been clarified because of the absence of classical SCS homologs on their genomes. The SCS from T. kodakaraensis (SCS(Tk)) is a heteromeric enzyme (alpha(2)beta(2)) encoded by TK1880 (alpha-subunit) and TK0943 (beta-subunit). Although both SCS(Tk) and classical SCSs harbor the five domains present in enzymes of the acyl-CoA synthetase (nucleoside diphosphate-forming) superfamily, the domain order and distribution among subunits in SCS(Tk) (alpha-subunit, domains 1-2-5; beta-subunit, domains 3-4) are distinct from those of classical SCSs (alpha-subunit, domains 1-2; beta-subunit, domains 3-4-5) and instead resemble the acetyl-CoA synthetases from Pyrococcus furiosus (ACSs I(Pf) and II(Pf)). Comparison of the four Thermococcales genomes revealed that each strain harbors five alpha- and two beta-subunit homologs. Sequence similarity suggests that the beta-subunit of SCS(Tk) is also a component of the presumed ACS II from T. kodakaraensis (ACS II(Tk)). We coexpressed the alpha/beta-genes of SCS(Tk) (TK1880/TK0943) and of ACS II(Tk) (TK0139/TK0943). ACS II(Tk) recognizes a broad range of hydrophobic/aromatic acid compounds, as is the case with ACS II(Pf), whereas SCS(Tk) displays a distinct and relatively strict substrate specificity for several acids, including succinate. This indicates that the alpha-subunits are responsible for the distinct substrate specificities of SCS(Tk) and ACS II(Tk).

    DOI: 10.1074/jbc.M702694200

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  • Adipocyte adhesion molecule (ACAM) inhibits adipocyte hypertrophy in obesity

    K. Murakami, J. Wada, A. Nakatsuka, S. Teshigawara, R. Yoshikawa, M. Kanzaki, A. Yasuhara, K. Shikata, H. Makino

    DIABETOLOGIA   50   S57 - S57   2007.9

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  • Vaspin improves insulin sensitivity in obesity

    A. Nakatsuka, J. Wada, K. Murakami, S. Teshigawara, R. Yoshikawa, M. Kanzaki, A. Yasuhara, K. Shikata, H. Makino

    DIABETOLOGIA   50   S56 - S56   2007.9

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  • 腎障害と免疫・凝固異常 糖尿病性腎症の成因とマクロファージ 治療ターゲットとしての炎症

    四方 賢一, 片岡 仁美, 槇野 博史

    日本腎臓学会誌   49 ( 6 )   692 - 692   2007.8

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  • 糖尿病性腎症の寛解を目指した新しい治療 Microinflammationの制御による治療の可能性

    片岡 仁美, 四方 賢一, 槇野 博史

    日本腎臓学会誌   49 ( 3 )   216 - 216   2007.4

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  • [Diabetic nephropathy].

    Motofumi Sasaki, Kenichi Shikata, Hirofumi Makino

    Nihon rinsho. Japanese journal of clinical medicine   Suppl 3   169 - 74   2006.9

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

    Izumi Hashimoto, Jun Wada, Aya Hida, Masako Baba, Nobuyuki Miyatake, Jun Eguchi, Kenichi Shikata, Hirofumi Makino

    Obesity (Silver Spring, Md.)   14 ( 5 )   799 - 811   2006.5

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    OBJECTIVE: Chronic inflammation observed in obesity has been reported to be implicated in the development of atherosclerosis. We screened candidate chemokines that link chronic inflammation and obesity. RESEARCH METHODS AND PROCEDURES: Japanese overweight (n = 39, BMI 28.7 +/- 0.65 kg/m(2)) and normal-weight (n = 24, BMI 22.3 +/- 0.45 kg/m(2)) subjects were enrolled. Using antibody-based protein microarray, spot intensities of monocyte chemoattractant protein (MCP)-4, eotaxin, and eotaxin-2 correlated with anthropometric parameters. We further measured serum concentration of these chemokines and mRNA levels in adipose tissues obtained from volunteers. RESULTS: Serum MCP-4 levels showed positive correlation with BMI (r = 0.318, p = 0.014), waist (r = 0.316, p = 0.018), and waist-to-hip ratio (WHR) (r = 0.264, p = 0.049). Furthermore, MCP-4 correlated with homeostasis model assessment of insulin resistance (r = 0.392, p = 0.002), high-sensitivity C-reactive protein (hsCRP) (r = 0.350, p = 0.006). In step-wise multiple regression analyses, hsCRP independently correlated with MCP-4 levels. The expression of MCP-4 mRNA in visceral adipose tissue positively correlates with BMI. Serum eotaxin levels correlate with BMI (r = 0.262, p = 0.045) and WHR (r = 0.383, p = 0.003). Serum eotaxin-2 levels correlated with BMI (r = 0.464, p < 0.001), waist (r = 0.333, p = 0.017), and WHR (r = 0.278, p = 0.048). However, eotaxin and eotaxin-2 levels did not show significant correlation with hsCRP. DISCUSSION: Serum levels of MCP-4, eotaxin, and eotaxin-2, which belong to CC chemokine family and share CC chemokine receptor 3, correlated with BMI. These chemokines, especially MCP-4, may be critical molecules that link obesity and chronic inflammation.

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

    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   2005.11

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    Aims/hypothesis: Recent studies have shown that the inflammatory process is involved in the pathogenesis of diabetic nephropathy. Fourteen-membered ring macrolides, including erythromycin, have anti-inflammatory, as well as antibacterial effects. The aim of this study was to investigate the renoprotective effects of erythromycin in streptozotocin (STZ)-induced diabetic rats. Methods: STZ-induced diabetic rats were treated orally with erythromycin (5 mg/kg body weight) or vehicle every day for 8 weeks. To evaluate the effect of erythromycin treatment, we measured urinary albumin excretion, and examined the following in the kidney: histological changes, the expression of intercellular adhesion molecule-1 (ICAM-1), macrophage infiltration, and nuclear factor-kappa B (NF-kB) activity. Results: Erythromycin significantly reduced urinary albumin excretion without affecting blood glucose levels and blood pressure. Erythromycin also attenuated glomerular hypertrophy, mesangial expansion, macrophage infiltration and ICAM-1 expression in renal tissues. The expression of the gene encoding TGFB1 (also known as TGF-b1), type IV collagen protein production and NF-kB activity in renal tissues were increased in diabetic rats and reduced by erythromycin treatment. Conclusions/interpretation: Erythromycin prevented renal injuries without changes of blood glucose levels and blood pressure in experimental diabetic rats. These results suggest that the renoprotective effects of erythromycin are based on its anti-inflammatory effect via suppression of NF- activation. Modulation of microinflammation with erythromycin may provide a new approach for diabetic nephropathy.

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  • Forward to the Special Issue

    SHIKATA K.

    Journal of the Japan Diabetes Society   48 ( 9 )   655 - 655   2005.9

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    DOI: 10.11213/tonyobyo.48.655

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  • Inflammatory Mechanism in Pathogenesis of Diabetic Nephropathy

    SHIKATA K.

    Journal of the Japan Diabetes Society   48 ( 9 )   673 - 676   2005.9

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    DOI: 10.11213/tonyobyo.48.673

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    Other Link: http://search.jamas.or.jp/link/ui/2006019533

  • Pathological roles of advanced glycation end product receptors SR-A and CD36. Reviewed International journal

    Seikoh Horiuchi, Yuka Unno, Hitomi Usui, Kenichi Shikata, Kaori Takaki, Wakako Koito, Yu-Ichiro Sakamoto, Ryoji Nagai, Kenji Makino, Akira Sasao, Jun Wada, Hirofumi Makino

    Annals of the New York Academy of Sciences   1043   671 - 5   2005.6

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    The pathological significance of advanced glycation end product (AGE)-modified proteins deposited in several lesions is generally accounted for by their cellular interaction via the AGE receptors and subsequent acceleration of the inflammatory process. In this study, we focused on two AGE receptors-specifically, the role of SR-A in pathogenesis of diabetic nephropathy and the role of CD36 in AGE-induced downregulation of leptin by adipocytes. In terms of SR-A, diabetic wild-type mice exhibited increased urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion, whereas SR-A-knockout mice showed reduced glomerular size and mesangial matrix area. In these diabetic SR-A-knockout mice, the number of macrophages that infiltrated into glomeruli was remarkably reduced (P < 0.05), suggesting that SR-A-dependent glomerular migration of macrophages plays an important role in the pathogenesis of diabetic nephropathy. In terms of CD36, incubation of glycolaldehyde-modified bovine serum albumin (GA-BSA) with 3T3-L1 adipocytes reduced leptin secretion by these cells. The binding of GA-BSA to these cells and subsequent endocytic degradation were effectively inhibited by a neutralizing anti-CD36 antibody. AGE-induced downregulation of leptin was protected by N-acetyl-cysteine, an antioxidant. These results indicate that the interaction of AGE ligands with 3T3-L1 adipocytes via CD36 induces oxidative stress and leads to inhibition of leptin expression by these cells, suggesting a potential link of this phenomenon to exacerbation of the insulin sensitivity in metabolic syndrome.

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  • インスリン抵抗性と肥満を合併したバーター症候群の1例

    村上 和敏, 四方 賢一, 和田 淳, 大塚 文男, 江口 潤, 向井 知之

    糖尿病   48 ( 6 )   464 - 464   2005.6

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  • [Treatment of diabetic nephropathy--control of blood glucose].

    Shingo Nishishita, Kenichi Shikata, Hirofumi Makino

    Nihon rinsho. Japanese journal of clinical medicine   63 Suppl 6   384 - 8   2005.6

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  • [Mechanisms of diabetic nephropathy--endothelial dysfunction].

    Kosuke Yozai, Kenichi Shikata, Hirofumi Makino

    Nihon rinsho. Japanese journal of clinical medicine   63 Suppl 6   341 - 5   2005.6

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  • [Diabetic nephropathy].

    Sakiko Ohga, Kenichi Shikata, Hirofumi Makino

    Nihon rinsho. Japanese journal of clinical medicine   63 Suppl 3   155 - 60   2005.3

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  • Long-term results of tonsillectomy as a treatment for IgA nephropathy. International journal

    Hirofumi Akagi, Michiya Kosaka, Kenshi Hattori, Akira Doi, Kunihiro Fukushima, Mitsuhiro Okano, Shin Kariya, Kazunori Nishizaki, Nobuyoshi Sugiyama, Kenichi Shikata, Hirofumi Makino, Yu Masuda

    Acta oto-laryngologica. Supplementum   ( 555 )   38 - 42   2004.12

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    IgA nephropathy (IgAN) is the most common form of chronic glomerulonephritis with IgA deposits present mainly in the mesangial areas. We performed a 10-year retrospective case-control study of 71 patients with IgAN to evaluate the long-term effects and prognostic factors associated with tonsillectomy. Forty-one patients (19 males and 22 females) underwent tonsillectomy (Group A) and 30 patients (13 males and 17 females) did not (Group B). These patients were followed for more than 10 years after renal biopsy. The average age at initial renal biopsy was 29.78 years in Group A and 33.0 years in Group B. The average follow-up period was 13 years and 3 months in Group A, and 12 years and 7 months in Group B. Glomerular damage demonstrated on renal biopsy was more extensive in Group A than in Group B. Prognosis after 10 years of follow-up was compared between the two groups. The clinical remission rate was 24.4% in Group A and 13.3% in Group B, the stable renal function rate was 82.9% in Group A and 70.0% in Group B, and the renal survival rate was 95.1% in Group A and 73.3% in Group B. The renal survival rate in Group A was significantly higher than that in Group B (p <0.05). Although evaluation of renal pathology based on renal biopsy was useful in predicting the long-term effects of tonsillectomy in IgAN patients, the results of tonsillar provocation tests were not.

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  • 糖尿病性腎症の成因と炎症メカニズム 遺伝子改変動物を用いた検討

    臼井 仁美, 四方 賢一, 岡田 震一, 四方 泰史, 永瀬 亮, 余財 亨介, 大賀 佐起子, 和田 淳, 槇野 博史

    Diabetes Frontier   15 ( 5 )   735 - 735   2004.10

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  • [Nephrotic syndrome due to metabolic disease--special reference to diabetic nephropathy].

    Sakiko Ohga, Kenichi Shikata, Hirofumi Makino

    Nihon rinsho. Japanese journal of clinical medicine   62 ( 10 )   1907 - 13   2004.10

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    Diabetes has become the most common single cause of end stage renal disease. Nephrotic syndrome is often manifested in the progression of diabetic nephropathy. Diabetic nephropathy has several pathways for development, such as glomerular hyperfiltration, upregulation of protein kinase C, advanced glycation end products, activation of polyol pathway, increased oxidative stress and upregulation of growth factors. Intensive control of blood pressure and the use of angiotensin converting enzyme inhibitor or angiotensin receptor blocker can protect the progression of nephropathy with nephrotic syndrome. However further studies are necessary for the clinical guidline in patients with diabetic nephropathy manifesting with nephrotic syndrome.

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  • [Advances in the treatment of progressive renal dysfunction. 5. Diabetic nephropathy].

    Kenichi Shikata, Hirofumi Makino

    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine   93 ( 5 )   928 - 34   2004.5

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  • Cerebroside sulfotransferase deficiency ameliorates L-selectin-dependent monocyte infiltration in the kidney after ureteral obstruction. Reviewed International journal

    Daisuke Ogawa, Kenichi Shikata, Koichi Honke, Shinichi Sato, Mitsuhiro Matsuda, Ryo Nagase, Atsuhito Tone, Shinichi Okada, Hitomi Usui, Jun Wada, Masayuki Miyasaka, Hiroto Kawashima, Yasuo Suzuki, Takashi Suzuki, Naoyuki Taniguchi, Yukie Hirahara, Keiko Tadano-Aritomi, Ineo Ishizuka, Thomas F Tedder, Hirofumi Makino

    The Journal of biological chemistry   279 ( 3 )   2085 - 90   2004.1

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    Mononuclear cells infiltrating the interstitium are involved in renal tubulointerstitial injury. The unilateral ureteral obstruction (UUO) is an established experimental model of renal interstitial inflammation. In our previous study, we postulated that L-selectin on monocytes is involved in their infiltration into the interstitium by UUO and that a sulfated glycolipid, sulfatide, is the physiological L-selectin ligand in the kidney. Here we tested the above hypothesis using sulfatide- and L-selectin-deficient mice. Sulfatide-deficient mice were generated by gene targeting of the cerebroside sulfotransferase (Cst) gene. Although the L-selectin-IgG chimera protein specifically bound to sulfatide fraction in acidic lipids from wild-type kidney, it did not show such binding in fractions of Cst(-/-) mice kidney, indicating that sulfatide is the major L-selectin-binding glycolipid in the kidney. The distribution of L-selectin ligand in wild-type mice changed after UUO; sulfatide was relocated from the distal tubules to the peritubular capillaries where monocytes infiltrate, suggesting that sulfatide relocated to the endothelium after UUO interacted with L-selectin on monocytes. In contrast, L-selectin ligand was not detected in Cst(-/-) mice irrespective of UUO treatment. Compared with wild-type mice, Cst(-/-) mice showed a considerable reduction in the number of monocytes/macrophages that infiltrated the interstitium after UUO. The number of monocytes/macrophages was also reduced to a similar extent in L-selectin(-/-) mice. Our results suggest that sulfatide is a major L-selectin-binding molecule in the kidney and that the interaction between L-selectin and sulfatide plays a critical role in monocyte infiltration into the kidney interstitium.

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  • Collagen XVIII, a basement membrane heparan sulfate proteoglycan, interacts with L-selectin and monocyte chemoattractant protein-1. Reviewed International journal

    Hiroto Kawashima, Norifumi Watanabe, Mayumi Hirose, Xin Sun, Kazuyuki Atarashi, Tetsuya Kimura, Kenichi Shikata, Mitsuhiro Matsuda, Daisuke Ogawa, Ritva Heljasvaara, Marko Rehn, Taina Pihlajaniemi, Masayuki Miyasaka

    The Journal of biological chemistry   278 ( 15 )   13069 - 76   2003.4

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    Leukocyte infiltration during inflammation is mediated by the sequential actions of adhesion molecules and chemokines. By using a rat ureteral obstruction model, we showed previously that L-selectin plays an important role in leukocyte infiltration into the kidney. Here we report the purification, identification, and characterization of an L-selectin-binding heparan sulfate proteoglycan (HSPG) expressed in the rat kidney. Partial amino acid sequencing and Western blotting analyses showed that the L-selectin-binding HSPG is collagen XVIII, a basement membrane HSPG. The binding of L-selectin to isolated collagen XVIII was specifically inhibited by an anti-L-selectin monoclonal antibody, EDTA, treatment of the collagen XVIII with heparitinase or heparin but not by chemically desulfated heparin. A cell binding assay showed that the L-selectin-collagen XVIII interaction mediates cell adhesion. Interestingly, collagen XVIII also interacted with a chemokine, monocyte chemoattractant protein-1, and presented it to a monocytic cell line, THP-1, which enhanced the alpha(4)beta(1) integrin-mediated binding of the THP-1 cells to vascular cell adhesion molecule-1. Thus, collagen XVIII may provide a link between selectin-mediated cell adhesion and chemokine-induced cellular activation and accelerate the progression of leukocyte infiltration in renal inflammation.

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

    Hitomi Usui, Kenichi Shikata, Mitsuhiro Matsuda, Shinichi Okada, Daisuke Ogawa, Tetsuji Yamashita, Kazuyuki Hida, Minoru Satoh, Jun Wada, Hirofumi Makino

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association   18 ( 2 )   265 - 72   2003.2

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    Background. An inflammatory process may be one of the critical factors that contribute to the development of diabetic nephropathy (DN). We reported previously that intercellular adhesion molecule-1 (ICAM-1) is up-regulated and promotes macrophage infiltration in the glomeruli of diabetic rats. 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have recently been emphasized to have anti-inflammatory effects; inhibition of leukocyte adhesion and migration, independent of the cholesterol-lowering effect. The present study was designed to test the hypothesis that statins prevent the development of DN by pleiotropic effects.
    Methods. Streptozotocin-induced diabetic rats were treated with cerivastatin (0.5 mg/kg body weight) or vehicle for 4 weeks. We analysed glomerular macrophage infiltration and ICAM-1 expression. We also evaluated major regulators of ICAM-1, activation of nuclear factor-kappa B (NF-kappaB) using electrophoretic mobility shift assay, and oxidative stress.
    Results. Statin treatment reduced urinary albumin excretion (UAE) (2.96 +/- 0.18 vs 2.38 +/- 0.06; log 10 UAE, P&lt;0.05), glomerular size (12 150 329 vs 9963+/-307 mum(2), P&lt;0.05), and lowered blood pressure, compared with untreated diabetic rats. Immunohistochemistry revealed that macrophage infiltration and ICAM-1 expression in glomeruli were increased in diabetic rats and were inhibited by statin treatment. Renal NF-kappaB activity, urinary excretion and renal deposition of 8-OHdG were increased in diabetic rats, and reduced by statin treatment.
    Conclusion. Statin treatment prevented glomerular injury, independent of the cholesterol-lowering effects. Our findings suggest that the beneficial effect might be mediated by pleiotropic effects including an anti-inflammatory action through a reduction of oxidative stress, NF-kappaB activation, ICAM-1 expression and macrophage infiltration in the early phase of DN.

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  • :A ten-year retrospective case-control study

    Akagi Hirofumi, Fukushima Kunihiro, Kosaka Michiya, Hattori Kenshi, Doi Akira, Nishizaki Kazunori, Matsuda Mitsuhiro, Shikata Kenichi, Makino Hirofumi

    Stomato-pharyngology   15 ( 3 )   335 - 344   2003

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    A retrospective case-control study of 71 patients with IgA nephropathy was performed to evaluate the long-term prognostic effect of tonsillectomy. Forty-one patients (19 males and 22 females) received tonsillectomies (Group A) and 30 patients (13 males and 17 females) did not (Group B). These patients were followed up for more than 10 years after renal biopsy. The average age at the initial renal biopsy was29.78 years old in Group A, and 33.0 years in Group B. The average period from renal biopsy to tonsillectomy in Group A was 15.07 months. The average follow-up period was 13 years and 3 months in Group A, and 12 years and 7 months in Group B. The glomerular injuries proved by renal biopsy were more extensive in Group A than in Group B. Renal prognosis after a 10-year follow-up was compared in these two groups.<BR>The clinical remission rate was 24.4% in Group A and 13.3% in Group B, the stable renal function rate was 82.9% in Group A and 70.0% in Group B, and the renal survival rate was 95.1% in Group A and 73.3% in Group B. The renal survival rate in Group A was significantly higher than that in Group B (P<0.05). Althogh renal pathology based on renal biopsy was useful to predict the long-term effect of tonsillectomy in IgA nephropathy patients, past history of tonsillitis, local findings of palatine tonsil, and results of tonsillar provocation tests were not. Our results show that tonsillectomy for IgA nephropathy is of great value clinically, especially for renal survival after long-term follow-up.

    DOI: 10.14821/stomatopharyngology1989.15.335

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  • Role of macrophages in the pathogenesis of diabetic nephropathy Reviewed

    K Shikata, H Makino

    TYPE-2 DIABETIC NEPHROPATHY IN JAPAN: FROM BENCH TO BEDSIDE   134   46 - 54   2001

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  • 微量アルブミン尿の定義と早期糖尿病性腎症の病態

    平櫛 恵太, 和田 淳, 四方 賢一, 槇野 博史

    内分泌・糖尿病科   11 ( 6 )   606 - 612   2000.12

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  • 糖尿病性腎症成因としての糸球体血行動態の異常 糸球体過剰濾過成因物質としてのNO

    和田 淳, 杉本 光, 四方 賢一, 槇野 博史

    医学のあゆみ   195 ( 2 )   144 - 145   2000.10

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  • 【"糖尿病性腎症" 進展防止を中心に】糖尿病性腎症の進展機序

    槇野 博史, 四方 賢一, 和田 淳

    腎と透析   48 ( 6 )   763 - 770   2000.6

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  • 【腎障害の管理】糖尿病性腎症を合併している透析患者の治療

    土山 芳徳, 長宅 芳男, 和田 淳, 四方 賢一, 槇野 博史

    Heart View   4 ( 6 )   660 - 666   2000.6

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  • 糖尿病 合併症 腎症

    槇野 博史, 和田 淳, 四方 賢一

    Annual Review内分泌,代謝   2000   158 - 166   2000.1

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  • Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats Reviewed

    Tsuchiyama Y, Wada J, Zhang H, Morita Y, Hiragushi K, Hida K, Shikata K, Yamamura M, Kanwar YS, Makino H

    Kidney International   58 ( 5 )   1941 - 1952   2000

  • Identification of genes specifically expressed in the accumulated visceral adipose tissue of OLETF rats Reviewed

    Hida K, Wada J, Zhang H, Hiragushi K, Tsuchiyama Y, Shikata K, Makino H

    Journal of Lipid Research   41 ( 10 )   1615 - 1622   2000

  • Familial interstitial nephritis with progressive renal failure Reviewed

    Zhang H, Wada J, Nanba K, Kunitomi M, Hida K, Nagake Y, Shikata K, Makino H

    American Journal of Kidney Diseases   36 ( 4 )   art. no. - e25   2000

  • 糖尿病 合併症 腎症

    槇野 博史, 和田 淳, 四方 賢一

    Annual Review内分泌,代謝   1999   162 - 172   1999.1

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  • Novel approaches to unravel the genesis of glomerulosclerosis by new methodologies in molecular biology and molecular genetics Reviewed

    Wada J, Shikata K, Makino H

    Nephrology Dialysis Transplantation   14 ( 11 )   2551 - 2553   1999

  • A case of membranous nephropathy associated with psoriasis vulgaris Reviewed

    Yamaji H, Shikata K, Wada J, Hayashi Y, Ikeda S, Makino H

    Nephron   80 ( 1 )   111 - 112   1998

  • Fibrillary glomerulonephritis in a patient with familial sensorineural deafness Reviewed

    H Ichikawa, S Ikeda, M Hashimoto, Y Nagake, K Hironaka, K Shikata, H Makino

    NEPHROLOGY   3 ( 4 )   381 - 384   1997.8

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    A 47-year-old woman was admitted to the hospital for evaluation of proteinuria. Bilateral sensorineural deafness had been diagnosed previously at age 35. She had a positive family history of deafness going back three generations. A renal biopsy showed the presence of highly organized fibrillary deposits in the subendothelial mesangial areas. The microfibrils had a diameter of 11-16 nm, larger than the diameter of amyloid fibrils, and did not have a microtubular appearance. The renal specimen was negative for Congo-red staining. There was no clinical or serologic evidence of paraproteinaemia, cryoglobulinaemia, light-chain disease, or systemic lupus erythematosus. The diagnosis was fibrillary glomerulonephritis. This is the first known case of fibrillary glomerulonephritis in a patient with familial sensorineural deafness.

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  • サイトカインからみた扁桃がIgA腎症に及ぼす影響

    槇野 博史, 四方 賢一, 柏谷 忠俊, 松田 充浩, 赤木 博文, 増田 游

    口腔・咽頭科   9 ( 1 )   16 - 16   1996

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  • A case of non-IgA mesangioproliferative glomerulonephritis with huge paramesangial hemispherical deposits.

    SUGIMOTO HIKARU, MAKING HIROFUMI, WADA JUN, SHIKATA KEN-ICHI, IKEDA SYUJI, OTA ZENSUKE

    Jpn J Nephrol   35 ( 9 )   1091 - 1095   1993

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    A 16-year-old female was admitted to our hospital because of chance proteinuria. On admission, mild proteinuria (0.6g/day) was observed, but microhematuria was not detected during the observation period. All the values of the renal function tests were within the normal range. Her renal biopsy demonstrated a prominent increase in the mesangial area by light microscopy and showed marked paramesangial hemispherical deposits by electron microscopy. Though IgM, IgG, Clq, C3, and fibrinogen were localized in the mesangial region, IgA was not detected by immunofluorescence study. It has been reported that paramesangial hemispherical deposits are strongly indicative of IgA glomerulonephritis. We conclude that this patient is a rare case of non-IgA glomerulonephritis with huge paramesangial hemispher ical deposits.

    DOI: 10.14842/jpnjnephrol1959.35.1091

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  • Serum and Urinary Concentrations of Type IV Collagen in Patients with Renal Diseases.

    HAYASHI Yoshikazu, MAKINO Hirofumi, SHIKATA Kenichi, OTA Zensuke

    RADIOISOTOPES   40 ( 6 )   252 - 255   1991.6

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    We measured serum and urinary concentrations of type IV collagen by radioimmunoassay (RIA) in patients with renal diseases and compared them with normal levels. In diabetics with macroproteinuria or with renal insufficiency, serum and urinary concentrations of type IV collagen were higher than in diabetics without nephropathy or with early renal damage as determined by the presence of microproteinuria. Serum concentrations of type IV collagen in patients with membranous nephropathy (MN) showed a significant increase compared with normal controls. Urinary concentrations of type IV collagen in patients with MN, minimal change nephrotic syndrome at the remission phase and nephrotic phase and IgA nephropathy showed a significant increase compared with normal controls. These increases may indicate that a change in basement membrane metabolism has occurred in these renal diseases.

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  • EFFECT OF DILAZEP DIHYDROCHLORIDE(DZ) THERAPY IN PATIENTS WITH CHRONIC GLOMERULONEPHRITIS Reviewed

    Y NAGAKE, T OGURA, H MAKINO, Y YAMASAKI, K SHIKATA, Z OTA

    NEW THERAPEUTIC STRATEGIES IN NEPHROLOGY   30   66 - 68   1991

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  • Three-dimensional architecture of rat glomerular basement membrane by ultra-high resolution scanning electron microscopy.

    Yamasaki Yasushi, Makino Hirofumi, Hironaka Kazue, Hayashi Yoshikazu, Shikata Kenichi, Ota Zensuke

    Acta Medica Okayama   44 ( 6 )   333 - 335   1990.12

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    DOI: 10.18926/AMO/30431

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  • 糖尿病療養指導ガイドブック2022

    四方賢一( Role: Edit)

    日本糖尿病療養指導士認定機構  2022.5 

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  • 糖尿病療養指導ガイドブック2021

    ( Role: Edit)

    日本糖尿病療養指導士認定機構  2021.5 

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  • 糖尿病性腎臓病の病態と治療

    宮本聡, 四方賢一( Role: Joint author)

    中外医学社  2021.4 

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    Responsible for pages:89-94   Language:Japanese

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  • 糖尿病療養指導ガイドブック2019

    四方賢一( Role: Joint author)

    メディカルレビュー社  2020.5 

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  • 糖尿病療養指導ガイドブック2020

    ( Role: Edit)

    日本糖尿病療養指導士認定機構  2020.5 

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  • 糖尿病診療ガイドライン

    ( Role: Joint author)

    南江堂  2019.10 

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    Language:Japanese

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  • 糖尿病専門医研修指導ガイドブック

    ( Role: Joint author)

    診断と治療社  2019.9 

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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

    ( Role: Joint author)

    最新医学社  2018.12 

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  • エビデンスに基づくCKD診療ガイドライン2018

    ( Role: Joint author)

    日本腎臓学会  2018.12 

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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( Role: Joint author ,  糖尿病治療薬の選択.)

    中外医学社  2018.6 

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    Responsible for pages:183-190   Language:Japanese

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  • 糖尿病療養指導ガイドブック2018

    ( Role: Joint author)

    メディカルレビュー社  2018.5 

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  • 糖尿病の療養指導Q&A

    利根淳仁、四方賢一( Role: Joint author ,  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  2018.5 

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    Responsible for pages:123-125   Language:Japanese

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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( Role: Joint author)

    日本メディカルセンター  2016.6 

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  • 糖尿病腎症

    ( Role: Joint author)

    南江堂  2016.6 

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  • 糖尿病診療ガイドライン2016

    四方賢一( Role: Joint author)

    2016.6 

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  • インクレチン関連薬の腎保護効果

    ( Role: Joint author)

    中外医学社  2016.1 

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  • 糖尿病専門医研修ガイドブック改訂第6版

    ( Role: Joint author)

    日本糖尿病学会  2015.12 

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  • CKDステージG3b-5診療ガイドライン2015

    ( Role: Joint author)

    東京医学社  2015.10 

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  • 糖尿病研修ノート改訂第2版

    小寺亮、四方賢一( Role: Joint author ,  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 

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    Responsible for pages:237-241   Language:Japanese

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  • わかる! 糖尿病の病態・治療・ケア

    ( Role: Joint author)

    メディカ  2013.9 

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  • エビデンスに基づくCKD診療ガイドライン2013

    ( Role: Joint author)

    日本腎臓学会  2013.7 

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    Responsible for pages:585-860   Language:Japanese

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  • AnnualReview腎臓

    ( Role: Joint author)

    中外医学社  2013.1 

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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

    ( Role: Joint author)

    中外医学社  2013.1 

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  • 糖尿病性腎症の治療における新規ターゲット分子の探索 : 炎症メカニズムをターゲットとした治療法の開発

    四方, 賢一

    四方賢一  2008.3 

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    Total pages:48p  

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  • 糖尿病性腎症の発症機構におけるマクロファージの役割の解明と治療への応用 : ICAM-1 KOマウスを用いた新しい治療ターゲット分子の探索

    四方, 賢一

    四方賢一  2006.3 

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    Total pages:83p  

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  • 腎疾患・透析 最新の治療2005?2007

    四方賢一(糖尿病性腎症)

    南江堂  2005.4 

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    Responsible for pages:145-147  

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  • これでわかる糖尿病療養教室 : 患者さんとスタッフのために

    四方, 賢一, 槙野, 博史

    南江堂  2004.6  ( ISBN:4524223886

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    Total pages:xvi, 118p   Language:Japanese

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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(AGEsと糖尿病腎症)

    メディカルレビュー社  2004.4 

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    Responsible for pages:p99?p108  

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  • 糖尿病性腎症の発症機構にマクロファージが果たす役割の解明 : ICAM-1 KO mouseとMacrophage scavenger receptor KO mouseを用いた研究

    四方, 賢一

    四方賢一  2004.3 

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    Total pages:46p  

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  • 腎疾患に対する抗接着分子療法の臨床応用に関する基礎的検討

    四方, 賢一

    四方賢一  2002.3 

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    Total pages:71p  

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  • 腎症(4) NLRP3 inflammasomeの制御を介した糖尿病マウスにおける糖尿病性腎症の発症・進展抑制効果

    小田 香織, 宮本 聡, 和田 淳, 四方 賢一

    糖尿病合併症   37 ( Suppl.1 )   172 - 172   2023.9

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  • 肥満・脂肪細胞・インスリン抵抗性 2型糖尿病,肥満症におけるmicroRNAの機能解析

    和田 淳, 大井 祐貴子, 黒岡 直子, 菅原 亮佑, 宮本 聡, 中司 敦子, 江口 潤, 四方 賢一

    糖尿病合併症   37 ( Suppl.1 )   188 - 188   2023.9

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  • チーム医療・足病変(2) 総社市糖尿病性腎症重症化予防プログラムの取り組みについて(第1報)

    廣澤 裕代, 杉本 太郎, 森下 尚子, 薬師寺 公一, 平川 秀三, 木山 瑛理, 高橋 伸悟, 林 聖子, 四方 賢一

    糖尿病合併症   37 ( Suppl.1 )   187 - 187   2023.9

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  • 微量アルブミン尿期の糖尿病性腎症に対するSGLT2阻害薬の効果とエビデンス

    宮本 聡, Heerspink Hiddo J.L., 四方 賢一

    糖尿病合併症   37 ( Suppl.1 )   90 - 90   2023.9

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  • 糖尿病性腎症の新しい時代を迎えて 研究の歩みと新たなエビデンス

    四方 賢一

    糖尿病合併症   37 ( Suppl.1 )   88 - 88   2023.9

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  • わが国の臨床研究から考える糖尿病合併症の発症・進展予防 進行した糖尿病性腎症に対するチーム医療による集約治療の有効性 DNETT-Japanの結果より

    四方 賢一

    糖尿病合併症   37 ( Suppl.1 )   102 - 102   2023.9

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  • 糖尿病性腎症重症化予防に向けた取組みと展望 岡山県における糖尿病医療連携推進事業と糖尿病性腎症への取組み

    和田 嵩平, 四方 賢一, 加来 浩平

    糖尿病合併症   37 ( Suppl.1 )   95 - 95   2023.9

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  • チーム医療・足病変(2) 当院における糖尿性腎症の進展抑制を目指した取り組み

    長田 麻里, 和田 嵩平, 宮本 聡, 和田 淳, 片山 晶博, 四方 賢一

    糖尿病合併症   37 ( Suppl.1 )   187 - 187   2023.9

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  • 神経障害(2) 糖尿病神経障害におけるミエリン傷害

    片山 勝喜, 内田 治仁, 檜山 武史, 徐 珊珊, 栢野 功政, 松本 真実, 浦久保 秀俊, 大野 伸彦, 宮本 聡, 四方 賢一, 和田 淳

    糖尿病合併症   37 ( Suppl.1 )   149 - 149   2023.9

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  • 大規模臨床試験から紐解く合併症治療の現状と課題 最近の臨床研究に学ぶ糖尿病性腎臓病の現状と課題

    四方 賢一

    日本糖尿病眼学会誌   27   90 - 90   2023.5

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  • 糖尿病性腎臓病の進行を抑制するための包括的アプローチ

    四方 賢一

    糖尿病   66 ( Suppl.1 )   S - 126   2023.4

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  • 岡山県における糖尿病性腎症重症化予防の取組について

    和田 嵩平, 四方 賢一, 加来 浩平

    糖尿病   66 ( Suppl.1 )   S - 317   2023.4

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  • 造血幹細胞移植における急性腸管GVHD発症時の栄養療法 長期絶食後の経口摂取再開と経過について

    庄野 三友紀, 長谷川 祐子, 高橋 絢子, 四方 賢一, 藤井 伸治

    日本病態栄養学会誌   26 ( Suppl. )   S - 43   2023.1

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  • 造血幹細胞移植後肺障害に対する肺移植後の急性拒絶反応で重症化した患者に栄養的アプローチを行った一症例

    三村 智美, 深川 真里, 片山 祥子, 高橋 絢子, 寺本 賀一, 金 聖暎, 田邉 浩代, 大木 晴美, 大森 裕子, 園井 教裕, 山本 昌直, 辻 憲二, 菊地 覚次, 四方 賢一

    日本病態栄養学会誌   26 ( Suppl. )   S - 74   2023.1

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  • 腎症進行予防のためのチーム医療

    中司敦子, 四方賢一, 和田淳

    糖尿病学の進歩   57th   2023

  • 糖尿病性腎症の診断と治療の進歩

    四方賢一

    糖尿病学の進歩   57th   2023

  • 岡山県における糖尿病性腎症重症化予防の取組について

    和田嵩平, 四方賢一, 四方賢一, 加来浩平

    糖尿病(Web)   66 ( Suppl )   2023

  • 糖尿病性腎症の診断・治療の進歩と岡山県における重症化予防への取り組み

    四方賢一

    日本糖尿病教育・看護学会誌(Web)   27   2023

  • 糖尿病性腎臓病の進行を抑制するための包括的アプローチ

    四方賢一

    糖尿病(Web)   66 ( Suppl )   2023

  • 早期栄養介入とNSTによる多職種連携により良好な転帰を得た多発褥瘡患者の1例

    開原 裕子, 深川 真里, 片山 祥子, 長谷川 祐子, 高橋 絢子, 大木 晴美, 山重 達也, 川西 英明, 三浦 太郎, 金 聖暎, 山田 太平, 安井 和也, 菊地 覚次, 田辺 俊介, 四方 賢一

    学会誌JSPEN   4 ( Suppl.2 )   160 - 161   2022.12

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  • 免疫関連有害事象による1型糖尿病を発症した疾患感受性HLA保有2例

    山崎 遥香, 田中 小百合, 四方田 美和子, 田中 賢一郎, 野津 雅和, 守田 美和, 山本 昌弘, 金崎 啓造

    糖尿病   65 ( 11 )   612 - 612   2022.11

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  • 幻聴を契機にインスリン5700単位を自己注射し低血糖が遷延した1型糖尿病の1例

    和田 嵩平, 宮本 聡, 中島 有里, 岡本 修吾, 当真 貴志雄, 野島 一郎, 四方 賢一, 和田 淳

    糖尿病   65 ( 11 )   612 - 612   2022.11

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  • カルニチン補充により低血糖を回避し得た高インスリン血症を有する維持透析患者の1例

    大谷 はづき, 田中 小百合, 中野 里菜, 川北 恵美, 四方田 美和子, 槇野 裕文, 田中 賢一郎, 金沢 一平, 山本 昌弘, 山内 美香, 金崎 啓造

    糖尿病   65 ( 11 )   627 - 627   2022.11

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  • がん治療におけるサルコペニアとフレイルの意義 患者参加型継続的栄養指導による胃癌術後のサルコペニア予防効果

    菊地 覚次, 高田 暢夫, 黒田 新士, 田辺 俊介, 前田 直見, 賀島 肇, 垣内 慶彦, 野間 和広, 香川 俊輔, 高橋 絢子, 楳田 祐三, 四方 賢一, 藤原 俊義

    日本癌治療学会学術集会抄録集   60回   WS19 - 2   2022.10

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  • チーム医療と多職種連携 糖尿病性腎症重症化予防のためのチーム医療と多職種連携

    四方 賢一

    糖尿病合併症   36 ( Suppl.1 )   122 - 122   2022.9

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  • NLRP3 inflammasomeの活性化を抑制することによる糖尿病性腎臓病治療の可能性

    小田 香織, 宮本 聡, 小寺 亮, 和田 淳, 四方 賢一

    糖尿病合併症   36 ( Suppl.1 )   208 - 208   2022.9

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  • 大規模臨床試験から紐解く合併症治療の現状と課題 最近の臨床研究に学ぶ糖尿病性腎臓病の現状と課題

    四方 賢一

    糖尿病合併症   36 ( 2 )   200 - 201   2022.7

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  • 糖尿病性腎症重症化予防の取り組みと成果 おかやまDMネットの取り組みと糖尿病性腎症重症化予防プログラム岡山方式

    和田 嵩平, 四方 賢一, 加来 浩平

    糖尿病合併症   36 ( 1 )   112 - 115   2022.6

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  • 病棟での栄養連携が奏功した中毒性表皮壊死症患者への管理栄養士の関わり

    開原 裕子, 長谷川 祐子, 山重 達也, 石川 真衣, 宮岡 里衣, 加藤 湖月, 大川 恭昌, 藤崎 宣友, 山田 太平, 中尾 篤典, 四方 賢一

    日本病態栄養学会誌   24-25 ( Suppl. )   S - 81   2022.1

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  • COVID-19流行下に造血幹細胞移植後3年経過した患者における体組成を用いた栄養状態の把握

    庄野 三友紀, 長谷川 祐子, 藤井 伸治, 四方 賢一

    日本病態栄養学会誌   24-25 ( Suppl. )   S - 69   2022.1

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  • 幻聴を契機にインスリン5700単位を自己注射し低血糖が遷延した1型糖尿病の1例

    和田嵩平, 宮本聡, 中島有里, 岡本修吾, 当真貴志雄, 野島一郎, 四方賢一, 和田淳

    糖尿病(Web)   65 ( 11 )   2022

  • 治験実施の効率化を目指したCRCとリサーチナース(病棟/外来連携看護師)との取り組み

    竹中稚子, 竹中稚子, 福光江美子, 齋藤まど香, 齋藤まど香, 原山愛, 原山愛, 臂香代子, 竹内真喜子, 昌子美智代, 難波志穂子, 黒田智, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   22nd   2022

  • 免疫関連有害事象による1型糖尿病を発症した疾患感受性HLA保有2例

    山崎遥香, 田中小百合, 四方田美和子, 田中賢一郎, 野津雅和, 守田美和, 山本昌弘, 金崎啓造

    糖尿病(Web)   65 ( 11 )   2022

  • カルニチン補充により低血糖を回避し得た高インスリン血症を有する維持透析患者の1例

    大谷はづき, 田中小百合, 中野里菜, 川北恵美, 四方田美和子, 四方田美和子, 槇野裕文, 田中賢一郎, 田中賢一郎, 金沢一平, 金沢一平, 山本昌弘, 山内美香, 山内美香, 金崎啓造

    糖尿病(Web)   65 ( 11 )   2022

  • 頭頸部・消化器疾患の治療における栄養管理の工夫(外科・内科) 頭頸部癌集学的治療に対する胃瘻を有効に活用した栄養管理確立への道のり

    田辺 俊介, 今井 祥子, 開原 裕子, 長谷川 祐子, 岡野 寛子, 大木 晴美, 三浦 太郎, 金 聖暎, 前田 直見, 菊地 覚次, 野間 和広, 白川 靖博, 四方 賢一, 藤原 俊義

    学会誌JSPEN   3 ( Suppl.1 )   233 - 233   2021.10

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  • 重症感染症を伴った菌状息肉症症例へのNST介入の経験

    今井 祥子, 開原 裕子, 長谷川 祐子, 岡野 寛子, 大木 晴美, 三浦 太郎, 金 聖暎, 森山 裕美, 山本 昌直, 前田 直見, 菊地 覚次, 田辺 俊介, 四方 賢一

    学会誌JSPEN   3 ( Suppl.1 )   574 - 574   2021.10

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  • 日本発!腎領域の最新エビデンス:2020 Update わが国の臨床研究による糖尿病性腎症の新たなエビデンスと集約治療の有効性

    四方 賢一

    日本腎臓学会誌   63 ( 6-W )   815 - 815   2021.9

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  • 糖尿病性腎症重症化予防の取り組みと成果 おかやまDMネットの取り組みと糖尿病性腎症重症化予防プログラム岡山方式

    和田 嵩平, 四方 賢一, 加来 浩平

    糖尿病合併症   35 ( Suppl.1 )   119 - 119   2021.9

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  • 大規模臨床試験から紐解く合併症治療の現状と課題 最近の臨床研究に学ぶ糖尿病性腎臓病の現状と課題

    四方 賢一

    糖尿病合併症   35 ( Suppl.1 )   107 - 107   2021.9

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  • 糖尿病性腎症患者における造影検査のリスクと注意点

    四方 賢一

    日本糖尿病眼学会誌   25   78 - 78   2021.8

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  • 【腎疾患治療薬update】(第1章)腎疾患患者への薬の使い方 糖尿病性腎臓病 スルホニル尿素(SU)薬、ビグアナイド薬、チアゾリジン薬、α-グルコシダーゼ阻害薬

    四方 賢一

    腎と透析   91 ( 増刊 )   114 - 115   2021.8

  • 治験関連文書保管スペースの削減・業務効率化を目的とした治験電磁化手続きシステム「DDworks NX/Trial Site」の導入とその効果

    佐藤 あさ美, 黒田 智, 難波 志穂子, 大江 祐子, 雪吉 歌小里, 門田 真紀子, 四方 賢一

    Clinical Research Professionals   ( 85 )   2 - 9   2021.8

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  • 糖尿病性腎臓病の克服を目指して DKD治療におけるSGLT2阻害薬への期待

    草場 哲郎, 冨田 彩[八木], 尾関 奈津子[奥野], 渡邊 乃梨子[上原], 亀崎 通嗣, 四方 賢一, 和田 隆志

    糖尿病合併症   35 ( 1 )   97 - 100   2021.7

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  • 糖尿病性腎臓病の克服を目指して 残存リスクに挑む 今後期待できる新規治療薬

    南学 正臣, 四方 賢一, 和田 隆志

    糖尿病合併症   35 ( 1 )   104 - 107   2021.7

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  • 糖尿病性腎臓病の克服を目指して 地域での糖尿病重症化予防対策

    酒井 武則, 四方 賢一, 和田 隆志

    糖尿病合併症   35 ( 1 )   108 - 111   2021.7

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  • 糖尿病性腎臓病の克服を目指して DKD治療におけるRAS阻害薬とMR拮抗薬への期待

    西山 成, 四方 賢一, 和田 隆志

    糖尿病合併症   35 ( 1 )   101 - 103   2021.7

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  • がんゲノム医療におけるCRCの取り組みと役割

    宮本 理史, 奥田 浩人, 武田 達明, 難波 志穂子, 黒田 智, 平沢 晃, 千堂 年昭, 四方 賢一

    薬理と治療   49 ( 6 )   826 - 829   2021.6

  • 糖尿病性腎臓病の基礎研究Update 糖尿病性腎臓病と炎症(Diabetic kidney disease and inflammation)

    宮本 聡, 四方 賢一

    糖尿病   64 ( Suppl.1 )   S2 - 1   2021.5

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  • 糖尿病性腎症と糖尿病性腎臓病の新たな展開(日本腎臓学会,日本糖尿病対策推進会議合同シンポジウム) おかやまDMネットの取り組みと糖尿病性腎症重症化予防プログラム岡山方式

    片山 晶博, 和田 嵩平, 四方 賢一, 加来 浩平

    糖尿病   64 ( Suppl.1 )   S16 - 6   2021.5

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  • Diabetic kidney disease and inflammation

    宮本聡, 四方賢一

    糖尿病(Web)   64 ( Suppl )   2021

  • 再生医療等製品の治験製品管理・調製の現状と市販化に向けた課題

    武田達明, 晴田佑介, 河崎陽一, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   21st   2021

  • わが国の臨床研究による糖尿病性腎症の新たなエビデンスと集約治療の有効性

    四方賢一

    日本腎臓学会誌(Web)   63 ( 6-W )   2021

  • 岡山大学病院における治験逸脱管理ワーキンググループの取り組み~「重大かつ予防可能な逸脱」発生防止に向けて~

    三原直子, 三原直子, 脇坂真弓, 脇坂真弓, 難波志穂子, 奥田浩人, 奥田浩人, 東影明人, 東影明人, 今中泰子, 齋藤まど香, 齋藤まど香, 廣江訓子, 黒田智, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   21st   2021

  • 治験依頼者と治験責任医師等への満足度調査を指標とした品質マネジメント活動の取り組み

    妹尾鮎美, 妹尾鮎美, 奥田浩人, 奥田浩人, 羽里美保, 羽里美保, 難波志穂子, 雪吉歌小里, 門田真紀子, 黒田智, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   21st   2021

  • NST介入中にRefeeding症候群を呈した神経性食思不振症の1症例

    内山 慶子, 岡田 健, 開原 裕子, 今井 祥子, 長谷川 祐子, 三宅 裕高, 森山 裕美, 金 聖暎, 日野 隼人, 菊池 覚次, 田辺 俊介, 四方 賢一

    学会誌JSPEN   2 ( Suppl.1 )   1392 - 1392   2020.11

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  • 腎症 Inflammasomeの制御を介したsuraminによる糖尿病性腎症の進展抑制効果

    小田 香織, 宮本 聡, 小寺 亮, 和田 淳, 四方 賢一

    糖尿病合併症   34 ( Suppl.1 )   222 - 222   2020.11

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  • 疾患感受性HLAを有しPembrolizumabの免疫関連有害事象によって発症した1型糖尿病の1例

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    糖尿病   63 ( 9 )   642 - 642   2020.9

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  • アルブミン尿を有する2型糖尿病患者に対するエサキセレノン(ESAX)のアルブミン尿減少効果と安全性の検討

    四方 賢一, 伊藤 貞嘉, 柏原 直樹, 南学 正臣, 和田 隆志, 奥田 恭行, 沢登 智子

    糖尿病   63 ( Suppl.1 )   S - 208   2020.8

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  • 糖尿病性腎症重症化予防への取り組み-現状と課題、そして新たな展開- 糖尿病性腎症の重症化を予防するための糖尿病治療 新たなエビデンスと今後の展望

    四方 賢一

    糖尿病   63 ( Suppl.1 )   S - 17   2020.8

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  • DKDの病態と成因の解明を目指して~新たな進歩~ 糖尿病性腎症に対するインフラマソームの標的化(Targeting inflammasome in diabetic kidney disease)

    宮本 聡, 小田 香織, 四方 賢一

    糖尿病   63 ( Suppl.1 )   S - 91   2020.8

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  • 糖尿病性腎症重症化予防への取り組み-現状と課題、そして新たな展開- おかやまDMネットの取り組みと糖尿病性腎症重症化予防プログラム岡山方式

    片山 晶博, 四方 賢一, 加来 浩平, 岡山県糖尿病医療連携推進事業

    糖尿病   63 ( Suppl.1 )   S - 18   2020.8

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  • 微量アルブミン尿を有する2型糖尿病患者に対するエサキセレノンのアルブミン尿減少効果に関するpost-hoc解析

    伊藤 貞嘉, 柏原 直樹, 四方 賢一, 南学 正臣, 和田 隆志, 奥田 恭行, 沢登 智子

    日本腎臓学会誌   62 ( 4 )   275 - 275   2020.7

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  • ポストSGLT2阻害薬時代の糖尿病性腎臓病の新規治療戦略 糖尿病性腎臓病に対する新規治療薬の開発状況 新たなエビデンス

    四方 賢一

    日本腎臓学会誌   62 ( 4 )   235 - 235   2020.7

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  • アルブミン尿を有する2型糖尿病患者に対するエサキセレノンのアルブミン尿減少効果と安全性の検討

    柏原 直樹, 伊藤 貞嘉, 四方 賢一, 南学 正臣, 和田 隆志, 奥田 恭行, 沢登 智子

    日本腎臓学会誌   62 ( 4 )   277 - 277   2020.7

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  • 【糖尿病性腎臓病-その疾患概念と克服への挑戦-】糖尿病性腎臓病の薬物療法における新たなエビデンス

    四方 賢一

    糖尿病プラクティス   37 ( 3 )   301 - 304   2020.5

  • 下顎切除した血糖コントロール不良の血液透析患者の栄養介入に難渋した一症例

    今井 祥子, 開原 裕子, 高橋 絢子, 長谷川 祐子, 濱中 麻矢, 大木 晴美, 金 聖暎, 日野 隼人, 山本 昌直, 村田 尚道, 縄稚 久美子, 菊地 覚次, 田辺 俊介, 四方 賢一

    日本病態栄養学会誌   23 ( Suppl. )   S - 56   2020.1

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  • 神経疾患患者に対する多職種での関わり

    今井 祥子, 開原 裕子, 長谷川 祐子, 瀬戸山 祐佳, 濱中 麻矢, 金 聖暎, 日野 隼人, 名和 秀起, 田尻 絢子, 山本 昌直, 村田 尚道, 縄稚 久美子, 水口 真実, 菊地 覚次, 田辺 俊介, 宗 淳一, 四方 賢一

    学会誌JSPEN   1 ( Suppl.2 )   59 - 60   2020.1

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  • 当院でのNSTと総合リハビリテーション部との関わり

    森山 裕美, 三宅 裕高, 今井 祥子, 長谷川 祐子, 開原 裕子, 内山 慶子, 濱中 麻矢, 岡野 寛子, 金 聖暎, 日野 隼人, 田尻 絢子, 村田 尚道, 前田 直見, 菊地 覚次, 田辺 俊介, 四方 賢一

    学会誌JSPEN   1 ( Suppl.2 )   103 - 104   2020.1

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  • 2型糖尿病に対するメトホルミンの抗腫瘍効果

    野島一郎, 榮川伸吾, 梶谷展生, 勅使川原早苗, 宮本聡, 利根淳仁, 内田治仁, 中司敦子, 江口潤, 四方賢一, 鵜殿平一郎, 和田淳

    糖尿病(Web)   63 ( Suppl )   2020

  • 当院におけるTime-In-Range(TIR)とHbA1cとの関連についての検討

    片山晶博, 野島一郎, 樋口千草, 渡邉真由, 宮本聡, 中司敦子, 江口潤, 四方賢一, 和田淳

    糖尿病(Web)   63 ( Suppl )   2020

  • 治療ターゲットとしてのインフラマゾーム

    宮本聡, 四方賢一

    日本腎臓学会誌(Web)   62 ( 6 )   2020

  • 糖尿病性腎症の重症化を予防するための糖尿病治療~新たなエビデンスと今後の展望~

    四方賢一

    糖尿病(Web)   63 ( Suppl )   2020

  • アルブミン尿を有する2型糖尿病患者に対するエサキセレノンのアルブミン尿減少効果と安全性の検討

    柏原直樹, 伊藤貞嘉, 四方賢一, 南学正臣, 和田隆志, 奥田恭行, 沢登智子

    日本腎臓学会誌(Web)   62 ( 4 )   2020

  • アルブミン尿を有する2型糖尿病患者に対するエサキセレノン(ESAX)のアルブミン尿減少効果と安全性の検討

    四方賢一, 伊藤貞嘉, 柏原直樹, 南学正臣, 和田隆志, 奥田恭行, 沢登智子

    糖尿病(Web)   63 ( Suppl )   2020

  • おかやまDMネットの取り組みと糖尿病性腎症重症化予防プログラム岡山方式

    片山晶博, 片山晶博, 四方賢一, 四方賢一, 四方賢一, 加来浩平, 加来浩平

    糖尿病(Web)   63 ( Suppl )   2020

  • Targeting inflammasome in diabetic kidney disease

    宮本聡, 小田香織, 四方賢一

    糖尿病(Web)   63 ( Suppl )   2020

  • Web会議を利用したリモートSDV環境整備に向けた取り組み~新型コロナウイルス感染症への医療機関の対応~

    奥田浩人, 奥田浩人, 黒田智, 黒田智, 難波志穂子, 雪吉歌小里, 郷原英夫, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   20th   2020

  • 有事における治験薬配送の手順構築と課題

    晴田佑介, 晴田佑介, 三好弘子, 三好弘子, 河崎陽一, 河崎陽一, 雪吉歌小里, 黒田智, 黒田智, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   20th   2020

  • 微量アルブミン尿を有する2型糖尿病患者に対するエサキセレノンのアルブミン尿減少効果に関するpost-hoc解析

    伊藤貞嘉, 柏原直樹, 四方賢一, 南学正臣, 和田隆志, 奥田恭行, 沢登智子

    日本腎臓学会誌(Web)   62 ( 4 )   2020

  • 糖尿病性腎臓病に対する新規治療薬の開発状況~新たなエビデンス~

    四方賢一

    日本腎臓学会誌(Web)   62 ( 4 )   2020

  • 心腎連関を断ち切るためのチーム医療による集約治療の重要性

    四方賢一

    糖尿病学の進歩   54th   2020

  • The effect of protein sufficiency during early hematopoietic stem cell transplantation on hospital stay and transplantation-related mucosal disorder

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    日本造血細胞移植学会総会プログラム・抄録集   42nd   2020

  • 糖尿病患者の認知・情動機能・血統関連因子と大脳白質病変との関連

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  • 糖尿病性腎臓病の診断と治療~最新のエビデンスと今後の展望~

    四方賢一

    糖尿病学の進歩   54th   2020

  • 嚥下障害を呈した肺癌術後患者が経口摂取可能となるまでのNST・嚥下チームでの関わり

    櫻根 裕子, 今井 祥子, 長谷川 祐子, 田尻 絢子, 村田 尚道, 金 聖暎, 日野 隼人, 名和 秀起, 谷口 恵子, 菊地 覚次, 田辺 俊介, 宗 淳一, 四方 賢一

    学会誌JSPEN   1 ( Suppl. )   1130 - 1130   2019.9

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  • 糖尿病性腎臓病のトピックス 糖尿病性腎臓病の新規治療標的の探索 炎症を標的とした治療戦略

    宮本 聡, 四方 賢一

    糖尿病合併症   33 ( Suppl.1 )   148 - 148   2019.9

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  • 肺移植患者に対する多職種によるNST介入の取り組み

    田辺 俊介, 櫻根 裕子, 今井 祥子, 長谷川 祐子, 金 聖暎, 日野 隼人, 内山 慶子, 三宅 裕高, 森山 裕美, 縄稚 久美子, 水口 真実, 菊地 覚次, 白川 靖博, 四方 賢一, 藤原 俊義

    学会誌JSPEN   1 ( Suppl. )   593 - 593   2019.9

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  • 糖尿病性腎症患者における造影検査のリスクと注意点

    四方 賢一

    糖尿病合併症   33 ( Suppl.1 )   168 - 168   2019.9

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  • 【腎疾患の新規治療薬】GLP-1受容体作動薬

    四方 賢一

    日本腎臓学会誌   61 ( 4 )   472 - 476   2019.5

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  • アログリプチンの安全性・有効性評価のための前向き観察研究 J-BRAND Registry

    植木 浩二郎, 谷澤 幸生, 中村 二郎, 山田 祐一郎, 稲垣 暢也, 綿田 裕孝, 下村 伊一郎, 西村 理明, 三好 秀明, 安孫子 亜津子, 片桐 秀樹, 林 道夫, 島田 朗, 成瀬 桂子, 藤本 新平, 藤原 正純, 四方 賢一, 岡田 洋右, 荒木 栄一, 山崎 力, 門脇 孝

    糖尿病   62 ( Suppl.1 )   S - 303   2019.4

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  • 糖尿病マウスにおけるP2X受容体阻害による腎保護効果

    小田 香織, 宮本 聡, 小寺 亮, 和田 淳, 四方 賢一

    糖尿病   62 ( Suppl.1 )   S - 163   2019.4

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  • 糖尿病薬による多彩な臓器保護作用とそのメカニズム 抗糖尿病薬による器官保護作用の潜在能力と合併症予防のための新しい戦略(Overview: Potential of organ protection by anti-diabetic agents and new strategies for prevention of complications)

    四方 賢一

    糖尿病   62 ( Suppl.1 )   S - 76   2019.4

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  • おかやまDMネットにおける「おかやま糖尿病サポーター」スキルアップの取り組み 糖尿病性腎症重症化予防にむけて

    大橋 睦子, 片山 晶博, 長田 麻里, 四方 賢一, 岡山県糖尿病対策専門会議

    糖尿病   62 ( Suppl.1 )   S - 305   2019.4

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  • SAP療法PLGS(予測低血糖一時停止機能)による低血糖発現抑制効果の検討

    利根 淳仁, 片山 晶博, 渡邊 真由, 勅使川原 早苗, 中塔 辰明, 四方 賢一, 和田 淳

    糖尿病   62 ( 2 )   114 - 114   2019.2

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  • おかやまDMネット サポータースキルアップの取り組み 糖尿病性腎症重症化予防にむけて

    大橋 睦子, 利根 淳仁, 長田 麻里, 四方 賢一

    糖尿病   62 ( 2 )   139 - 139   2019.2

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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

    勅使川原 早苗, 利根 淳仁, 片山 晶博, 渡邊 真由, 四方 賢一, 和田 淳, 中塔 辰明

    糖尿病   62 ( 2 )   114 - 114   2019.2

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  • 「エビデンスに基づくCKD診療ガイドライン2018」の要点(Essential points from Evidence-based Clinical Practice Guidelines for Chronic Kidney Disease 2018) Reviewed

    Okada Hirokazu, Yasuda Yoshinari, Kashihara Naoki, Asahi Koichi, Ito Takafumi, Kaname Shinya, Kanda Eiichiro, Kanno Yoshihiko, Shikata Kenichi, Shibagaki Yugo, Tsuchiya Ken, Tsuruya Kazuhiko, Nagata Daisuke, Narita Ichiei, Nangaku Masaomi, Hattori Motoshi, Hamano Takayuki, Fujimoto Shouichi, Moriyama Toshiki, Yamagata Kunihiro, Yamamoto Ryohei, Wakasugi Minako, Ashida Akira, Usui Joichi, Kawamura Kazuko, Kitamura Kenichiro, Konta Tsuneo, Suzuki Yusuke, Tsuruoka Shuichi, Nishio Saori, Fujii Naohiko, Fujii Hideki, Wada Takehiko, Yokoyama Hitoshi, Aoki Katsunori, Akiyama Daiichiro, Araki Shin-ichi, Arima Hisatomi, Ishikawa Eiji, Ishikura Kenji, Ishizuka Kiyonobu, Ishimoto Takuji, Ishimoto Yu, Iseki Kunitoshi, Itabashi Mitsuyo, Ichioka Satoko, Ichikawa Kazunobu, Ichikawa Daisuke, Inoue Shuji, Imai Toshimi, Imamura Hideaki, Iwata Yasunori, Iwazu Yoshitaka, Usui Toshiaki, Uchida Keiko, Egawa Masahiro, Ohara Shinichiro, Omori Norio, Okada Rieko, Okuda Yusuke, Ozeki Takaya, Obata Yoko, Kai Hirayasu, Kato Noritoshi, Kanasaki Keizo, Kaneko Yoshikatsu, Kabasawa Hideyuki, Kawaguchi Takehiko, Kawasaki Yukihiko, Kawashima Keisuke, Kawano Haruna, Kikuchi Kan, Kihara Masao, Kimura Yoshiki, Kurita Noriaki, Koike Kentaro, Koizumi Masahiro, Kojima Chiari, Goto Shunsuke, Konomoto Takao, Kohagura Kentaro, Komatsu Hiroyuki, Komaba Hirotaka, Saito Chie, Sakai Yukinao, Sakaguchi Yusuke, Satonaka Hiroshi, Jimi Kanako, Shimizu Akihiro, Shimizu Sayaka, Shirai Sayuri, Shinzawa Maki, Sugiyama Kazuhiro, Suzuki Tomo, Suzuki Hitoshi, Suyama Kazuhide, Segawa Hiroyoshi, Takahashi Kazuya, Tanaka Kenichi, Tanaka Tetsuhiro, Tsunoda Ryoya, Tsuruta Yuki, Nakakura Hyogo, Nagasawa Yasuyuki, Nakanishi Koichi, Nagahama Masahiko, Nakaya Izaya, Nanami Masayoshi, Niihata Kakuya, Nishi Shinichi, Nishiwaki Hiroki, Hasegawa Shoko, Hasegawa Midori, Hanada Ken, Hayashi Hiroki, Harada Ryoko, Hishida Manabu, Hirano Daishi, Hirahashi Junichi, Hirama Akio, Hirayama Kouichi, Fukagawa Masafumi, Fukuda Akihiro, Fujii Yoshiyuki, Fujisaki Kiichiro, Furuya Fumihiko, Hoshino Junichi, Hosojima Michihiro, Honda Kenjiro, Masuda Takahiro, Matsui Kosuke, Matsukuma Yuta, Matsumura Hideki, Mii Akiko, Miura Kenichiro, Mitobe Michihiro, Miyasato Yoshikazu, Miyamoto Satoshi, Miwa Saori, Yazawa Masahiko, Yata Yusuke, Yamamoto Yoshihiro, Watanabe Kimio, Japanese Society of Nephrology, Committee of Evidence-based Practice Guideline for the Treatment of CKD 2018, Evidence-based Practice Guideline for the Treatment of CKD Production Group(Work group)

    Clinical and Experimental Nephrology   23 ( 1 )   1 - 15   2019.1

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    DOI: 10.1007/s10157-018-1648-1

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  • 肝疾患患者家族を支援するための家族支援講座に関する実態調査

    中西 智美, 高橋 絢子, 長谷川 祐子, 難波 志穂子, 池田 房雄, 四方 賢一

    日本病態栄養学会誌   22 ( Suppl. )   S - 71   2019.1

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  • 働き方改革!~残業時間削減のために管理職・スタッフ一丸で取り組んだ成果です~

    難波志穂子, 細羽章子, 長井美貴, 林桂一郎, 奥田浩人, 鷲田綾子, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   19th   2019

  • 円滑な治験実施のための業務連携体制の整備~外来における治験病棟看護師による治験業務の実施~

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    CRCと臨床試験のあり方を考える会議プログラム・抄録集   19th   2019

  • おかやまDMネットにおける「おかやま糖尿病サポーター」スキルアップの取り組み~糖尿病性腎症重症化予防にむけて~

    大橋睦子, 片山晶博, 長田麻里, 四方賢一, 四方賢一

    糖尿病(Web)   62 ( Suppl )   2019

  • リスクマネージメントの観点から治験薬投与ルートのマニュアル化を図って

    谷本一水, 山内昭子, 蒔田仁美, 大久保瞳, 石井舞, 木村彩華, 昌子美智代, 難波志穂子, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   19th   2019

  • 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

    勅使川原早苗, 利根淳仁, 片山晶博, 渡邊真由, 四方賢一, 和田淳, 中塔辰明

    糖尿病(Web)   62 ( 2 )   2019

  • SAP療法PLGS(予測低血糖一時停止機能)による低血糖発現抑制効果の検討

    利根淳仁, 片山晶博, 渡邊真由, 勅使川原早苗, 中塔辰明, 四方賢一, 和田淳

    糖尿病(Web)   62 ( 2 )   2019

  • 糖尿病マウスにおけるP2X受容体阻害による腎保護効果

    小田香織, 宮本聡, 小寺亮, 小寺亮, 和田淳, 四方賢一

    糖尿病(Web)   62 ( Suppl )   2019

  • Overview; Potential of organ protection by anti-diabetic agents and new strategies for prevention of complications.

    四方賢一

    糖尿病(Web)   62 ( Suppl )   2019

  • 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

    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(Web)   62 ( 2 )   2019

  • おかやまDMネット:サポータースキルアップの取り組み~糖尿病性腎症重症化予防にむけて~

    大橋睦子, 利根淳仁, 長田麻里, 四方賢一, 四方賢一

    糖尿病(Web)   62 ( 2 )   2019

  • 【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

    四方 賢一

    最新医学   73 ( 12 )   1578 - 1581   2018.12

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    糖尿病性腎症は、糖尿病の重要な合併症であり、我が国における末期腎不全の最大の原因疾患である。日本糖尿病学会による『糖尿病診療ガイドライン2016』では、アルブミン尿測定の意義、腎機能評価の指標、血糖管理、血圧管理、脂質管理の有効性、RAS阻害薬の有用性、食事の食塩制限とたんぱく質制限の有効性、貧血治療の有効性、および他の合併症への腎症の影響について、エビデンスに基づいたステートメントが掲載されている。本稿では、この診療ガイドラインの内容に基づいて、糖尿病腎症の管理について最近のエビデンスを解説した。(著者抄録)

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2018&ichushi_jid=J00516&link_issn=&doc_id=20181207020005&doc_link_id=%2Fap7saisa%2F2018%2F007312%2F006%2F1578-1581%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fap7saisa%2F2018%2F007312%2F006%2F1578-1581%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • エビデンスに基づくCKD診療ガイドライン2018

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    日本腎臓学会誌   60 ( 8 )   1037 - 1193   2018.11

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  • エビデンスに基づくCKD診療ガイドライン2018

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    糖尿病合併症   32 ( Suppl.1 )   243 - 243   2018.10

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  • 【糖尿病】合併症 糖尿病性腎症 早期の診断と進展の抑制のために

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    糖尿病   61 ( 5 )   332 - 332   2018.5

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    四方 賢一

    診断と治療   106 ( 4 )   505 - 509   2018.4

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    <Headline> 1 SGLT2阻害薬は糖尿病性腎症の進展を抑制する可能性がある。2 GLP-1受容体作動薬は糖尿病性腎症の進展を抑制する可能性がある。3 糖尿病性腎症や慢性腎臓病(CKD)を対象としたSGLT2阻害薬の治験が進行中である。(著者抄録)

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    四方 賢一

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    糖尿病(Web)   61 ( 5 )   2018

  • 日本人2型糖尿病患者における腎症の合併率と発症関連因子~JDCP研究データの解析~

    四方賢一, 宇都宮一典, 古家大祐, 小寺亮, 宮本聡, 西村理明, 田嶼尚子

    糖尿病(Web)   61 ( Suppl )   2018

  • 高齢者へのSAP導入において事前のFree Styleリブレの使用が有効だった1例

    有木沙織, 利根淳仁, 利根淳仁, 村川公央, 北村佳久, 四方賢一, 四方賢一, 和田淳, 千堂年昭

    糖尿病(Web)   61 ( 5 )   2018

  • 治験審査委員会委員教育の審査に与える影響に関する調査

    黒田智, 黒田智, 雪吉歌小里, 大江祐子, 山田あさ美, 田中雄太, 田中雄太, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   18th   2018

  • 外注検査キット管理ツールの導入に関する試みについて

    永山理美, 田中雄太, 田中雄太, 山下房子, 鷲田綾子, 大野由貴, 蔵田靖子, 黒田智, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   18th   2018

  • 腎障害進展予防と腎代替療法へのスムーズな移行 CKDステージG3b〜5診療ガイドライン 2017(2015追補版)

    山縣 邦弘, 岡田 浩一, 柏原 直樹, 旭 浩一, 斎藤 知栄, 四方 賢一, 柴垣 有吾, 杉山 斉, 鶴岡 秀一, 鶴屋 和彦, 仲谷 達也, 長田 太助, 西 慎一, 深川 雅史, 横山 仁, 和田 隆志, 荒谷 紗絵, 今澤 俊之, 大野 岩男, 甲斐 平康, 風間 順一郎, 要 伸也, 金子 朋広, 菅野 義彦, 佐藤 博, 佐藤 稔, 常喜 信彦, 鈴木 祐介, 寺脇 博之, 中井 健太郎, 長沼 俊秀, 中山 昌明, 長谷部 直幸, 花房 規男, 馬場園 哲也, 原 章規, 藤井 秀毅, 藤野 貴行, 古市 賢吾, 宮本 聡, 守山 敏樹, 谷澤 雅彦, 安田 宜成, 渡辺 裕輔, 日本腎臓学会, 日本糖尿病学会, 日本高血圧学会, 日本老年医学会, 日本透析医学会, 日本臨床腎移植学会

    日本腎臓学会誌   59 ( 8 )   1093 - 1216   2017.12

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  • 1型糖尿病合併妊娠の妊娠前から分娩後におけるインスリン必要量の変動

    勅使川原 早苗, 利根 淳仁, 天田 雅文, 四方 賢一, 和田 淳

    日本先進糖尿病治療研究会雑誌   13   32 - 32   2017.12

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  • 糖尿病合併症の抑制を目指して 新たな薬剤介入研究の結果から

    宇都宮 一典, 植木 浩二郎, 四方 賢一

    動脈硬化予防   16 ( 4 )   58 - 70   2017.12

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  • 糖尿病/慢性腎疾患 糖尿病と慢性腎臓病

    四方 賢一

    日本歯周病学会会誌   59 ( 秋季特別 )   116 - 116   2017.11

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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   2017.10

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    <POINT>慢性炎症は糖尿病腎症の発症・進展に関与している.近年,慢性炎症のメカニズムにToll-like receptor(TLR)やインフラマソームの関与が示唆されている.(著者抄録)

    DOI: 10.11477/mf.1415200773

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2017&ichushi_jid=J03818&link_issn=&doc_id=20171020200007&doc_link_id=10.11477%2Fmf.1415200773&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1415200773&type=%E5%8C%BB%E6%9B%B8.jp_%E3%82%AA%E3%83%BC%E3%83%AB%E3%82%A2%E3%82%AF%E3%82%BB%E3%82%B9&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

  • 腎症 Inflammasomeの抑制によるsuraminの糖尿病マウスにおける腎保護効果

    小田 香織, 宮本 聡, 小寺 亮, 和田 淳, 四方 賢一

    糖尿病合併症   31 ( Suppl.1 )   252 - 252   2017.10

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  • 多職種で取り組む糖尿病性腎症重症化抑制 多職種協働の重要性 腎症の進展抑制を目指した糖尿病チーム医療

    長田 麻里, 四方 賢一

    日本腎臓学会誌   59 ( 6 )   690 - 690   2017.9

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  • The development of a scale to measure stress recognition during the treatment of diabetes patients

    Sumiyoshi Kazuko, Kawata Chieko, Okamoto Tatsuo, Ohashi Mutsuko, Mikane Sakae, Takabayashi Noriko, Futoyu Yoshiko, Kim Woesook, Wada Jun, Shikata Kenichi, Nakajima Kazuo

    Okayama Igakkai Zasshi (Journal of Okayama Medical Association)   129 ( 2 )   93 - 99   2017.8

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    &emsp;The purpose of this study was to establish a measurement scale for &ldquo;stress recognition in receiving treatment&rdquo; in patients with diabetes. A self-completed questionnaire was distributed to 149 type-2 diabetes outpatients in March-May 2015 after authorization from Okayama Prefectural University and the ethics committee of the hospital. <br/>&emsp;The &ldquo;stress recognition in receiving treatment&rdquo; scale was designed as a second-order factor model consisting of 14 items and the following four factors : the respondent's sense of (1) the burden of being sick, (2) the burden on interpersonal relationships, (3) the burden of treatment, and (4) the burden of medical expenses. <br/>&emsp;Stress recognition in treatment means recognition of being stressed in the burdens related to the illness, interpersonal relationships, treatment and medical expenses.<br/>&emsp;The suitability of the questionnaire data was then evaluated with a structural equation model. The suitability of the factor model to the data satisfied the statistically acceptable standards as Comparative Fit Index (CFI) =0.931, Root Mean Square Error of Approximation (RMSEA) =0.096, Tucker-Lewis Index (TLI) =0.946. <br/>&emsp;As the construct validity was not examined by the scale created in this study or by existing scale, it was verified by using the degrees of mental healthiness and HbA1c that were proved to be associated with the sense of burden.<br/>&emsp;In addition, the construct validity of the questionnaire was supported by a significant correlation between the Japanese version of the WHO-Five Well-being Index (S-WHO-5-J) and the patients' HbA1c levels. The use of this measure is expected to contribute to the early detection of a decline in a diabetic patient's activities of daily living and to the early confirmation of patients' support status.

    DOI: 10.4044/joma.129.93

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    Other Link: http://search.jamas.or.jp/link/ui/2017339769

  • The perception of chronic kidney disease in a general population in Okayama, Japan : 2015

    Uchida Haruhito A., Sugiyama Hitoshi, Miyazaki Masashi, Wada Jun, Shikata Kenichi, Kashihara Naoki, Makino Hirofumi

    Okayama Igakkai Zasshi (Journal of Okayama Medical Association)   129 ( 2 )   101 - 105   2017.8

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    &emsp;Public education programs about chronic kidney disease (CKD) have been performed in Okayama, Japan for the past 10 years. The present study investigated the perception of CKD in a general population in Okayama. In October and November 2015, a questionnaire survey was distributed by 12 medical centers in five medical districts in Okayama prefecture. A total of 7,022 respondents who underwent their physical checkup at these centers answered the questionnaire. In response to a questionnaire item asking about the respondent's familiarity with the term &ldquo;CKD,&rdquo; only 4% of the respondents answered &ldquo;know it well&rdquo; and 10% answered &ldquo;unfamiliar.&rdquo; In contrast, in response to a questionnaire item asking about the respondent's familiarity with &ldquo;chronic kidney disease,&rdquo; 27% answered &ldquo;know it well&rdquo; and 38% answered &ldquo;unfamiliar.&rdquo; The leading avenue by which the respondents learned about CKD/chronic kidney disease was television, followed by newspapers, magazines, and a family doctor or nurse. The leading component which the respondents considered essential for the diagnosis of CKD/chronic kidney disease was proteinuria. A stratified analysis demonstrated a higher recognition of &ldquo;CKD&rdquo; or &ldquo;chronic kidney disease&rdquo; in the medical districts in northern Okayama prefecture compared to southern Okayama prefecture. These results indicated that the awareness of CKD in Okayama prefecture is still inadequate. Many people did not appear to realize that the term &ldquo;CKD&rdquo; represents &ldquo;chronic kidney disease&rdquo;. Further continuous public education efforts are required to enlighten people about CKD/chronic kidney disease.

    DOI: 10.4044/joma.129.101

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    Other Link: http://search.jamas.or.jp/link/ui/2017339770

  • 【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   2017.5

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  • 糖尿病性腎症の診療の進歩 糖尿病性腎症の診断と治療における新たな展開

    四方 賢一

    日本腎臓学会誌   59 ( 3 )   189 - 189   2017.4

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  • SAP療法の治療反応性を予見する患者像の検討

    利根 淳仁, 勅使川原 早苗, 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   60 ( Suppl.1 )   S - 390   2017.4

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  • 新しい病診連携システムの未来、展望、そして夢 地域チーム医療の確立から広域的医療連携体制の構築へ 「おかやまDMネット」の事業展開

    利根 淳仁, 四方 賢一

    糖尿病   60 ( Suppl.1 )   S - 16   2017.4

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  • 微量アルブミン尿を有する2型糖尿病患者に対するESAXERENONE(CS-3150)のアルブミン尿減少作用

    四方 賢一, 伊藤 貞嘉, 南学 正臣, 奥田 恭行, 沢登 智子

    日本腎臓学会誌   59 ( 3 )   293 - 293   2017.4

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  • Suraminはinflammasomeを制御し糖尿病性腎症の進展を抑制する

    小田 香織, 宮本 聡, 小寺 亮, 和田 淳, 四方 賢一

    糖尿病   60 ( Suppl.1 )   S - 260   2017.4

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  • 日本人2型糖尿病患者における腎症の合併率と発症関連因子 JDCP studyにおける解析

    四方 賢一, 宇都宮 一典, 古家 大祐, 小寺 亮, 宮本 聡, 西村 理明, 田嶼 尚子

    糖尿病   60 ( Suppl.1 )   S - 254   2017.4

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  • 糖尿病合併症の成因Up to Date-その発症機序の解明に迫る 「腎症の成因と新たな治療標的」

    四方 賢一

    日本糖尿病眼学会誌   21   62 - 62   2017.4

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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   2017.3

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    糖尿病性腎症はわが国における末期腎不全の最大の原因疾患である。また、アルブミン尿は腎不全のみならず心血管死の危険因子であり、腎症の早期診断と治療は糖尿病患者の生命予後の改善のために重要である。腎症の治療には、血糖と血圧の管理、レニン-アンジオテンシン(RA)系の抑制に加えて、脂質管理、食事療法などに介入する集約的治療が求められる。現在、腎症に対する有効性が確立されている薬剤はACE阻害薬とARBのみであり、腎症に対する新規治療薬の開発が喫緊の課題である。腎症の成因には、高血糖の下流にあるRA系の亢進、糖化反応の亢進によるAGEsの増加、酸化ストレス、細胞内代謝異常、炎症などの複数のメカニズムが関与しており、これらのメカニズムが新規治療薬開発の標的となる。最近、糖尿病治療薬であるSGLT2阻害薬とGLP-1受容体作動薬の腎保護作用が報告され注目を集めている。さらに、現在、エンドセリンA受容体阻害薬、抗酸化薬、抗炎症薬、ミネラルコルチコイド受容体拮抗薬などが腎症の新規治療薬として開発中であり、今後の治験の結果が期待されている。(著者抄録)

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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   2017.1

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    糖尿病腎症はわが国における末期腎不全の最大の原因疾患である.腎不全期においても良好な血糖コントロールが必要であるが,治療にあたっては低血糖に十分注意が必要である.腎不全期,透析期には,薬剤の代謝・排泄を考慮した血糖降下薬の選択が必要となる.腎不全期には,食塩と蛋白質摂取制限が必要であるが,エネルギー不足にならないように注意する.糖尿病合併透析患者は,神経障害や心血管疾患を有している症例が多く,透析による体液量管理を行う際に注意が必要である.(著者抄録)

    DOI: 10.15106/J00974.2017114800

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2017&ichushi_jid=J00974&link_issn=&doc_id=20170116140018&doc_link_id=10.15106%2FJ00974.2017114800&url=https%3A%2F%2Fdoi.org%2F10.15106%2FJ00974.2017114800&type=%E5%8C%BB%E6%9B%B8.jp_%E3%82%AA%E3%83%BC%E3%83%AB%E3%82%A2%E3%82%AF%E3%82%BB%E3%82%B9&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

  • NST介入による肺移植術後患者の投与エネルギー量の検討

    櫻根 裕子, 坂本 八千代, 長谷川 祐子, 三宅 裕高, 森山 裕美, 内山 慶子, 日野 隼人, 名和 秀起, 谷口 恵子, 前田 直見, 田辺 俊介, 宗 淳一, 大藤 剛宏, 三好 新一郎, 四方 賢一

    日本静脈経腸栄養学会雑誌   32 ( Suppl. )   802 - 802   2017.1

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  • 皮膚筋炎治療中に嚥下障害が重症化した患者にNST介入し経口摂取が可能になった1症例

    谷口 恵子, 服部 芳枝, 田辺 俊介, 前田 直見, 櫻根 裕子, 長谷川 祐子, 日野 隼人, 名和 秀起, 内山 慶子, 古西 隆之, 前川 享子, 村田 尚道, 四方 賢一

    日本静脈経腸栄養学会雑誌   32 ( Suppl. )   663 - 663   2017.1

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  • 【糖尿病性腎症の現況と進展阻止対策-生活習慣の修正と薬物療法】治療薬解説 糖尿病性腎症の新しい治療薬

    四方 賢一

    カレントテラピー   35 ( 1 )   72 - 77   2017.1

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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 (Tokyo, Japan)   56 ( 6 )   605 - 613   2017

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    Objective Dipeptidyl peptidase-4 (DPP-4) inhibitors are the most frequently prescribed oral hypoglycemic agents in Japan. Although a relationship between the efficacy of DPP-4 inhibitors and the body mass index (BMI) has been reported, this relationship is controversial. We investigated whether the BMI value affects the glucose-lowering efficacy of sitagliptin in obese Japanese patients with type 2 diabetes.
    Methods One hundred sixty-two outpatients with inadequate glycemic control were divided into four groups based on their baseline BMI values. They were then treated with sitagliptin (a DPP-4 inhibitor) for 3 months and followed-up for 12 months.
    Results Sitagliptin significantly reduced the hemoglobin A1c level (HbA1c: -0.71 +/- 0.55%) after 3 months, and continued to reduce the HbA1c level until 12 months. There was no significant difference in the efficacy of sitagliptin among the four BMI groups. A multiple linear regression analysis indicated that the factors contributing to the change in the HbA1c level were the baseline level of HbA1c and the homeostasis model assessment of beta-cell function (HOMA-beta). In terms of the relationship between the baseline BMI value and the efficacy of sitagliptin treatment, the number of patients who responded to sitagliptin treatment after 3 months was lowest in the group of patients with the highest BMI values. A multiple logistic regression analysis revealed that the baseline HOMA-beta function and HbA1c level and a baseline BMI value of similar to 30 kg/m(2) significantly contributed to the response to sitagliptin treatment.
    Conclusion The results indicated that sitagliptin treatment was effective in controlling glucose metabolism disorder in obese Japanese patients with type 2 diabetes. However, the efficacy of sitagliptin treatment might be attenuated in severely obese patients, such as those with a BMI value of similar to 30 kg/m(2).

    DOI: 10.2169/internalmedicine.56.7428

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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

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

  • 2型糖尿病におけるメトホルミンの免疫機能への影響

    野島一郎, 榮川伸吾, 宮本聡, 勅使川原早苗, 利根淳仁, 中司敦子, 江口潤, 四方賢一, 鵜殿平一郎, 和田淳

    糖尿病(Web)   60 ( Suppl )   2017

  • SAP療法の治療反応性を予見する患者像の検討

    利根淳仁, 勅使川原早苗, 宮本聡, 江口潤, 中司敦子, 樋口千草, 小川大輔, 四方賢一, 四方賢一, 和田淳

    糖尿病(Web)   60 ( Suppl )   2017

  • 地域チーム医療の確立から広域的医療連携体制の構築へ~「おかやまDMネット」の事業展開~

    利根淳仁, 四方賢一

    糖尿病(Web)   60 ( Suppl )   2017

  • 日本人2型糖尿病患者における腎症の合併率と発症関連因子-JDCP studyにおける解析-

    四方賢一, 四方賢一, 宇都宮一典, 古家大祐, 小寺亮, 宮本聡, 西村理明, 田嶼尚子

    糖尿病(Web)   60 ( Suppl )   2017

  • 同種造血幹細胞移植におけるたんぱく質充足率が入院日数に与える影響について

    庄野三友紀, 長谷川祐子, 佐田光, 高橋郁名代, 四方賢一, 西森久和, 藤井伸治, 前田嘉信

    日本造血細胞移植学会総会プログラム・抄録集   40th   2017

  • Suraminはinflammasomeを制御し糖尿病性腎症の進展を抑制する

    小田香織, 宮本聡, 小寺亮, 和田淳, 四方賢一, 四方賢一

    糖尿病(Web)   60 ( Suppl )   2017

  • 重篤な有害事象ならびに24時間以内に報告を必要とする項目に関する調査

    田中雄太, 田中雄太, 黒田智, 黒田智, 山田あさ美, 北村佳久, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   17th   2017

  • 治験薬移動に関する手順書作成の試み

    小沼利光, 小沼利光, 川上英治, 川上英治, 宮本理史, 宮本理史, 田中雄太, 田中雄太, 川端崇義, 川端崇義, 黒田智, 黒田智, 北村佳久, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   17th   2017

  • 糖尿病と慢性腎臓病

    四方賢一

    日本歯周病学会会誌(Web)   59   2017

  • 岡山大学病院における治験病床開設時の取り組み

    草信洋子, 石川貴子, 久山めぐみ, 田中雄太, 三宅薫, 三宅薫, 藤井仁惠, 藤井仁惠, 難波志穂子, 黒田智, 堀田勝幸, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   17th   2017

  • 依頼者貸与心電計の精度管理に関する調査について

    赤澤明日美, 田中雄太, 東影明人, 青江佐佳恵, 黒田智, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   17th   2017

  • 移植患者に対する低菌食の検討について

    長谷川 祐子, 櫻根 裕子, 佐野 優子, 庄野 三友紀, 野口 絢子, 田中 暁美, 林本 加奈枝, 坂本 八千代, 高橋 郁名代, 藤井 伸治, 四方 賢一

    日本病態栄養学会誌   20 ( Suppl. )   S - 125   2016.12

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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 SAPによる基礎インスリン補充の増量

    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   2016.11

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    SAP(Sensor Augmented Pump)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が改善した2症例を経験した。【症例1】70歳代男性。罹病歴14年の1型糖尿病。農作業中に低血糖を頻発するため、基礎インスリン投与量は3.00単位/日に設定。SAP導入後、日中の持続的な高血糖が明らかとなり、基礎インスリン補充の増量(基礎インスリン比率:11%→30%)により血糖改善を得た。【症例2】30歳代女性。罹病歴16年の1型糖尿病。授乳中のため基礎インスリン投与量を3.40単位/日まで減量していたが、低血糖が頻発していた。SAP導入後、暁現象から引き続く午前中の高血糖、午後の高血糖が明らかとなり、基礎インスリン補充を増量し(基礎インスリン比率:12%→22%)、血糖コントロールは改善した。身体活動量の多い例や授乳中など基礎インスリン増量の判断に苦慮する症例において、SAP療法により安全かつ段階的に基礎インスリン投与量の是正を図ることが可能と考えられた。(著者抄録)

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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、その適正化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   44 - 44   2016.11

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  • 糖尿病腎症の治療 食事療法を中心に

    四方 賢一

    糖尿病合併症   30 ( Suppl.1 )   102 - 102   2016.9

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  • 腎症 Mass spectrometry imagingによる糖尿病性腎症におけるAMPKの活性制御因子の探索

    宮本 聡, Cheng-Chih Hsu, Gregory Hamm, Manjula Darshi, Jonathan Stauber, Pieter C. Dorrestein, 四方 賢一, Kumar Sharma

    糖尿病合併症   30 ( Suppl.1 )   228 - 228   2016.9

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  • 糖尿病腎症・心血管病の予防・進展抑制に向けた集学的アプローチ 糖尿病腎症の治療における血糖管理のエビデンスと実際

    四方 賢一

    日本高血圧学会総会プログラム・抄録集   39回   304 - 304   2016.9

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  • 質量分析イメージングを用いた糖尿病性腎症における新規AMPK活性制御因子の探索

    宮本 聡, Hsu Cheng-Chih, Hamm Gregory, Darshi Manjula, Stauber Jonathan, Dorrestein Pieter C., 四方 賢一, Sharma Kumar

    JSBMS Letters   41 ( Suppl. )   46 - 46   2016.8

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  • 糖尿病性腎症の診断と治療の新たな展開 透析を予防するために

    四方 賢一

    ぎふ病薬: 岐阜県病院薬剤師会雑誌   ( 60 )   65 - 65   2016.8

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  • 【糖尿病性腎症の克服を目指して~up to date~】糖尿病性腎症の新規標的分子と今後の治療戦略の開発

    四方 賢一

    Pharma Medica   34 ( 6 )   61 - 64   2016.6

  • 効果的なCKD検査教育入院プログラムを考える 医療としてのCKD教育入院と糖尿病透析予防指導の効果・意義

    和田 淳, 木野村 賢, 田邊 克幸, 森永 裕士, 杉山 斉, 四方 賢一

    日本腎臓学会誌   58 ( 3 )   241 - 241   2016.5

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  • 【新時代の臨床糖尿病学(下)-より良い血糖管理をめざして-】糖尿病合併症の病態・診断・治療 慢性合併症 糖尿病腎症 糖尿病透析患者の管理

    木野村 賢, 杉山 斉, 四方 賢一

    日本臨床   74 ( 増刊2 新時代の臨床糖尿病学(下) )   212 - 216   2016.4

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  • [The management of diabetic patients on hemodialysis or peritoneal dialysis].

    Masaru Kinomura, Hitoshi Sugiyama, Kenichi Shikata

    Nihon rinsho. Japanese journal of clinical medicine   74 Suppl 2   212 - 6   2016.4

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  • 糖尿病腎症の診断と治療

    四方 賢一

    糖尿病   59 ( Suppl.1 )   S - 118   2016.4

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  • 1型糖尿病合併妊娠における基礎インスリン比率に関する検討

    天田 雅文, 利根 淳仁, 勅使川原 早苗, 四方 賢一, 和田 淳

    糖尿病   59 ( Suppl.1 )   S - 199   2016.4

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  • 全県的な糖尿病診療レベル均てん化と広域的チーム医療の確立を目指ざす「おかやまDMネット」の取り組み

    利根 淳仁, 四方 賢一, 岡山県生活習慣病対策推進会議糖尿病対策専門部会

    糖尿病   59 ( Suppl.1 )   S - 394   2016.4

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  • 【あなたも名医!糖尿病性腎症をどう治療する?外来でここまでやろう!】(1章)糖尿病性腎症の基本を押さえておこう! 糖尿病性腎症の原因と発症機序

    小寺 亮, 四方 賢一

    jmed mook   42 ( 42 )   18 - 23   2016.2

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    <ココがポイント!>糖尿病性腎症の成因は、高血糖に由来する代謝性因子と血行動態によるところが大きい。アルブミン尿、蛋白尿などの機能異常は、糸球体の構造学的な変化による濾過排泄の増加と、尿細管における再吸収の低下が関与している。中でもポドサイト(糸球体足細胞)の障害が濾過機能に重要と考えられている。炎症、細胞外基質の増加を特徴とした基底膜の肥厚、メサンギウム基質の増加、尿細管基底膜肥厚、間質の線維化なども腎機能低下につながる。(著者抄録)

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  • SAP導入により基礎インスリン補充が適正化され、血糖コントロールの改善に寄与した2症例

    利根 淳仁, 四方 賢一, 和田 淳

    糖尿病   59 ( 1 )   73 - 73   2016.2

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  • 【元気の出る糖尿病チーム医療-Building and Coordination】糖尿病チーム医療の現状とアウトカム 糖尿病医療連携におけるチーム医療

    利根 淳仁, 四方 賢一

    糖尿病診療マスター   14 ( 2 )   109 - 114   2016.2

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    <POINT>医療連携の深化には「地域チーム医療」が重要である.「明確なビジョンの共有」と「自律性の確立」は,医療連携におけるチーム医療を強化する.(著者抄録)

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  • 【新時代の臨床糖尿病学(上)-より良い血糖管理をめざして-】血糖制御に関わる臓器・関連因子 腎臓

    四方 賢一

    日本臨床   74 ( 増刊1 新時代の臨床糖尿病学(上) )   255 - 257   2016.2

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  • Renoprotective effects of incretin-based drugs: A novel pleiotropic effect of dipeptidyl peptidase-4 inhibitor.

    Ryo Kodera, Kenichi Shikata

    Journal of diabetes investigation   7 ( 1 )   29 - 31   2016.1

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    Renoprotective effects of incretin‐based drug. [Image: see text]

    DOI: 10.1111/jdi.12380

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  • 筋萎縮性側索硬化症(ALS)患者の摂食嚥下障害に対する当院での取り組みの1例

    田中 暁美, 櫻根 裕子, 佐野 優子, 庄野 三友紀, 野口 絢子, 林本 加奈枝, 坂本 八千代, 長谷川 祐子, 前川 享子, 村田 尚道, 四方 賢一

    日本静脈経腸栄養学会雑誌   31 ( 1 )   401 - 401   2016.1

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  • 食道癌術前化学療法から根治術施行後まで多岐に渡るNST介入により低栄養患者への栄養管理が奏功した1例

    庄野 三友紀, 田辺 俊介, 谷口 恵子, 日野 隼人, 名和 秀起, 水口 真実, 内山 慶子, 長谷川 祐子, 白川 靖博, 四方 賢一

    日本静脈経腸栄養学会雑誌   31 ( 1 )   454 - 454   2016.1

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  • 糖尿病腎症の診断と治療

    四方賢一, 四方賢一

    糖尿病(Web)   59 ( Suppl )   2016

  • 全県的な糖尿病診療レベル均てん化と広域的チーム医療の確立を目指ざす「おかやまDMネット」の取り組み

    利根淳仁, 四方賢一

    糖尿病(Web)   59 ( Suppl )   2016

  • SAP導入により基礎インスリン補充が適正化され,血糖コントロールの改善に寄与した2症例

    利根淳仁, 四方賢一, 四方賢一, 和田淳

    糖尿病(Web)   59 ( 1 )   2016

  • 臨床研究品質確保体制整備事業 中央西日本臨床研究コンソーシアム

    四方賢一

    岡山医学会雑誌   128 ( 2 )   2016

  • 1型糖尿病合併妊娠における基礎インスリン比率に関する検討

    天田雅文, 利根淳仁, 勅使川原早苗, 四方賢一, 四方賢一, 和田淳

    糖尿病(Web)   59 ( Suppl )   2016

  • わが国の臨床研究から何を学べば良いか DNETT-Japan

    四方賢一

    糖尿病学の進歩   50th   2016

  • Clinical nephrology C.全身性疾患と腎障害 3.インクレチン関連薬の腎保護効果

    四方賢一, 小寺亮

    Annual Review 腎臓   2016   2016

  • 岡山大学病院におけるCRC等を対象とした英語に関する意識調査及び英語力向上に向けた取り組みについて

    田中雄太, 田中雄太, 長井美貴, 長井美貴, 人部友, 人部友, 細羽章子, 細羽章子, 斎藤まど香, 斎藤まど香, 奥田浩人, 奥田浩人, 難波志穂子, 黒田智, 黒田智, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   16th   2016

  • 企業治験における健康被害補償の内容に関する調査

    三宅薫, 三宅薫, 成本由佳, 成本由佳, 田中雄太, 田中雄太, 上田久美子, 上田久美子, 細羽章子, 細羽章子, 長井美貴, 長井美貴, 藤井仁惠, 藤井仁惠, 黒田智, 黒田智, 千堂年昭, 四方賢一

    CRCと臨床試験のあり方を考える会議プログラム・抄録集   16th   2016

  • Benefit evaluation of the clinical collaborative path for diabetes mellitus used in Okayama Prefecture

    16 ( 3 )   134 - 140   2015.12

  • 【糖尿病腎症の診断と治療Up To Date】治療の実践 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 )   49 - 54   2015.12

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    Other Link: http://search.jamas.or.jp/link/ui/2016057946

  • 小児てんかん患者におけるケトン食療法による食事介入が効を奏した一例

    長谷川 祐子, 櫻根 裕子, 佐野 優子, 庄野 三友紀, 野口 絢子, 田中 暁美, 林本 加奈枝, 坂本 八千代, 柴田 敬, 吉永 治美, 四方 賢一

    日本病態栄養学会誌   19 ( Suppl. )   S - 73   2015.12

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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   2015.11

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    インスリンポンプ療法施行中の1型糖尿病患者において、血糖変動指標である1,5-AG値の改善に寄与する因子について検討した。当院外来でインスリンポンプ療法施行中の1型糖尿病患者21名(全員ボーラスウィザード機能を活用)のうち、HbA1c値による分類ではインスリン投与状況に有意差は認められなかったが、1,5-AG 3.3μg/m(l中央値)以上の群では基礎インスリン比率(%totalbasal insulin dose:%TBD)が有意に低値で(26.0±4.8% vs. 42.5±11.5%,p=0.004)、ボーラス注入の際にポンプに入力した糖質摂取量が有意に高値であった。加えて、同群では年齢と発症年齢が有意に高値であった。また、1,5-AG値は%TBDと有意な負の相関を認め、糖質入力値および発症年齢と有意な正の相関を示した。重回帰分析(ステップワイズ法)では、%TBDが1,5-AG値の決定因子として有意差をもって採用された。インスリンポンプ療法中の1型糖尿病患者における血糖変動の是正のためには、%TBDの適正化が重要である。(著者抄録)

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  • 糖尿病腎症の診断と治療

    四方 賢一

    糖尿病合併症   29 ( Suppl.1 )   83 - 83   2015.11

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  • 【糖尿病は回復するだろうか Part 2-腎障害は寛解するか】組織所見は回復するか

    三瀬 広記, 四方 賢一

    糖尿病診療マスター   13 ( 11 )   873 - 877   2015.11

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    <POINT>尿蛋白/アルブミン尿やeGFRによって推定できない病理所見を呈する症例も存在する.多角的強化治療によって組織学的な寛解も可能であるが,metabolic memoryを踏まえた早期の治療介入が望まれる.(著者抄録)

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  • 糖尿病合併症の成因Up to Date その発症機序の解明に迫る 腎症の成因と新たな治療標的

    四方 賢一

    糖尿病合併症   29 ( Suppl.1 )   107 - 107   2015.11

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  • インスリンポンプ療法における基礎インスリン比率適正化に寄与する因子についての検討

    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   44 - 45   2015.11

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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   2015.8

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    「歯周病セルフチェック票(以下セ票)」の妥当性を検討する目的で、2型糖尿病患者156名を対象に、セ票(全11項目、計21点)に記入後、歯科検診を実施した。検診評価項目として残存歯数、プラークスコア、歯肉炎指数、歯周ポケット深さを用いた。合計点数4点以下(罹患の可能性小)が32名、5〜9点(罹患の可能性大)が66名、10点以上(重度罹患の可能性大)が58名で、歯周ポケットの最大深度および全歯周ポケットに対する4mm以上の歯周ポケット深さが占める割合は、10点以上の群で他の2群より有意に高値を示した。セ票10点以上は、糖尿病患者における歯周病スクリーニングに有用であると考えられた。(著者抄録)

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  • 慢性腎臓病・腎不全診療のトピックス 糖尿病性腎症診療の現状と課題

    四方 賢一

    日本腎臓学会誌   57 ( 6 )   1093 - 1093   2015.8

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  • 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

    日本医事新報   4761 ( 4761 )   51 - 51   2015.7

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  • 【糖尿病と合併症(後篇) 糖尿病合併症】糖尿病慢性合併症の発症メカニズム 慢性炎症

    四方 賢一

    最新医学   70 ( 7月増刊 )   1391 - 1396   2015.7

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    動脈硬化の成因に炎症が関与することは以前から知られていたが,その後,腎症を始めとする糖尿病細小血管障害にも,炎症が関与することが明らかになった.近年注目されているメタボリックシンドロームの成因や心腎連関のメカニズムにも,慢性炎症がかかわっていることが示唆されている.このような慢性炎症は,血管に起る軽微な慢性炎症であることから,microinflammationやlow grade vascular inflammatoinなどと呼ばれているが,最近その成因に,インフラマソームの活性化がかかわることが示唆されている.今後,糖尿病を始めとする生活習慣病に対して,炎症を標的とした新しい治療法の開発が期待される.(著者抄録)

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  • 糖尿病合併症から考える薬物療法 腎症に対する薬物療法

    四方 賢一

    糖尿病合併症   29 ( 1 )   76 - 78   2015.6

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  • 末期腎疾患患者の血糖コントロールの指標に関与する因子の検討

    河口 宏美, 中村 明彦, 小寺 亮, 那須 由美, 中田 淳子, 四方 賢一

    日本透析医学会雑誌   48 ( Suppl.1 )   446 - 446   2015.5

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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   2015.4

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    CiNii Article

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    Other Link: http://search.jamas.or.jp/link/ui/2015174501

  • 【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   2015.4

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    Other Link: http://search.jamas.or.jp/link/ui/2015158036

  • CSII療法施行中の1型糖尿病患者における血糖変動に影響を与える因子と血糖変動指標についての検討

    柴田 祐助, 利根 淳仁, 四方 賢一, 和田 淳

    糖尿病   58 ( Suppl.1 )   S - 368   2015.4

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  • estimate hemoglobin A1cの血糖コントロールの指標としての有用性

    目賀 実千代, 中村 明彦, 河口 宏美, 内田 知沙, 那須 由美, 中田 淳子, 小寺 亮, 四方 賢一

    糖尿病   58 ( Suppl.1 )   S - 454   2015.4

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  • 糖尿病性腎症のメカニズム

    四方 賢一

    日本腎臓学会誌   57 ( 3 )   438 - 438   2015.4

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  • 岡山県糖尿病等生活習慣病医療連携事業

    利根 淳仁, 四方 賢一, 岡山県生活習慣病対策推進会議糖尿病対策専門部会

    糖尿病   58 ( Suppl.1 )   S - 248   2015.4

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  • 糖尿病腎症治療の深化と展望 腎症治療薬開発の現状と課題

    四方 賢一

    糖尿病   58 ( Suppl.1 )   S - 67   2015.4

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  • 糖尿病診断におけるestimate HbA1cの有用性

    中村 明彦, 河口 宏美, 目賀 実千代, 内田 知沙, 那須 由美, 中田 淳子, 小寺 亮, 四方 賢一

    糖尿病   58 ( Suppl.1 )   S - 453   2015.4

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  • 糖尿病患者を透析患者にしない工夫 糖尿病性腎症の診断と治療の最前線

    四方 賢一

    医工学治療   27 ( Suppl. )   65 - 65   2015.3

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  • 糖尿病性腎症悪化予防のための地域共同教育の試み

    住吉 和子, 金 外淑, 松田 佳美, 川田 智恵子, 四方 賢一, 山下 眞宏, 冨岡 加代子

    岡山県立大学保健福祉学部紀要   21   143 - 149   2015.3

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    本研究は、独自の教育システムを持たない医療機関が、将来、地域の中で連携して共同教育を実施するにはいかなる準備が必要であるか探るために、A市とS市にある内科を標榜している医療施設に通院している糖尿病患者を対象に、医療施設の協力を得て、腎症悪化予防のための教室を開催した。教室は3回シリーズで、A市とS市でそれぞれに開催し、参加者はA市9名、S市3名の合計12名であった。教育プログラムは、参加者の体験を共有する集団教育と個別面接を組み合わせて実施した。評価は、教室開始時と終了後3ヵ月のBMI、血圧、HbA1c、終了時の糖尿病問題領域質問票(PAID)と腎症の知識の得点を用いた。HbA1cでは有意な変化は見られなかったが、血圧が190/102mmHgから148/86mmHg、147/91mmHgから120/70mmHgと下降していたことが認められた。腎症教室への積極的な参加が、病気と向き合うきっかけとなり、日常生活での悪化予防の方法の実践に繋がる可能性が示唆された。(著者抄録)

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  • 「岡山県糖尿病等生活習慣病医療連携事業」3年目の課題と今後の展開

    利根 淳仁, 四方 賢一

    糖尿病   58 ( 2 )   139 - 139   2015.2

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  • 脂質異常症を合併した2型糖尿病患者におけるエゼチミブの効果の検討

    畑中 崇志, 小川 大輔, 寺見 直人, 西井 尚子, 佐藤 幹雄, 四方 賢一, 槇野 博史, 和田 淳

    糖尿病   58 ( 2 )   142 - 142   2015.2

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  • インスリンを使用せずインスリン非依存状態を維持しているGAD抗体強陽性高齢者糖尿病の1例

    野島 一郎, 江口 潤, 堀口 千景, 四方 賢一, 和田 淳

    糖尿病   58 ( 1 )   52 - 52   2015.1

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  • 早期糖尿病性腎症におけるバイオマーカーとして尿中TFF(Trefoil factor)の検討

    寺見 直人, 小川 大輔, 畑中 崇志, 山成 俊夫, 杉山 斉, 四方 賢一, 槇野 博史, 和田 淳

    糖尿病   58 ( 1 )   51 - 51   2015.1

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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

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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

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  • Cognitive and affective functions in diabetic patients associated with diabetes-related factors, white matter abnormality and aging

    Hishikawa N, Yamashita T, Deguchi K, Wada J, Shikata K, Makino H, Abe K

    Eur J Neurol.   22 ( 2 )   313 - 321   2015

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  • 当院におけるNST活動における現況と課題

    田辺俊介, 田辺俊介, 長谷川祐子, 庄野三友紀, 岡田恵子, 平健太郎, 名和秀起, 坂本八千代, 白川靖博, 四方賢一, 藤原俊義

    日本静脈経腸栄養学会雑誌   30 ( 5 )   2015

  • 糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 糖尿病性腎症症例のレジストリーの運用 尿検体収集を伴った糖尿病性腎レジストリーの運用

    和田隆志, 安部秀斉, 北村博司, 佐藤博, 柴垣有吾, 鈴木芳樹, 羽田勝計, 槇野博史, 松尾清一, 丸山彰一, 湯澤由紀夫, 荒木信一, 井関邦敏, 岩野正之, 上杉憲子, 上田善彦, 乳原善文, 木村健二郎, 古波蔵健太郎, 古家大祐, 四方賢一, 中村裕之, 中山昌明, 西愼一, 西野友哉, 馬場園哲也, 原茂子, 久野敏, 古市賢吾, 森潔, 守屋達美, 山縣邦弘, 山本格, 横山仁, 横山宏樹, 清水美保

    糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 平成26年度 総括・分担研究報告書   2015

  • CKDとDKD-病因による治療法を学ぶ-透析を予防するための糖尿病チーム医療

    四方賢一, 四方賢一, 利根淳仁

    糖尿病学の進歩   49th   2015

  • 慢性腎不全診療最適化による新規透析導入減少実現のための診療システム構築に関する研究 糖尿病診療連携分科会

    四方賢一, 和田隆志, 小寺亮, 原章規

    慢性腎不全診療最適化による新規透析導入減少実現のための診療システム構築に関する研究 平成26年度 委託業務成果報告書   2015

  • 糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 診療水準向上にむけた重症度評価法の開発

    湯澤由紀夫, 佐藤博, 鈴木芳樹, 北村博司, 荒木信一, 井関邦敏, 岩野正之, 上杉憲子, 上田善彦, 乳原善文, 古波蔵健太郎, 古家大祐, 四方賢一, 中山昌明, 西愼一, 西野友哉, 馬場園哲也, 原茂子, 久野敏, 守屋達美, 山縣邦弘, 横山仁, 横山宏樹

    糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 平成26年度 総括・分担研究報告書   2015

  • 【インクレチン製剤と心血管代謝病】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   2014.12

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    インクレチン関連薬は血糖依存性のインスリン分泌作用のみならず、多臓器にも有益な作用があることが報告されている。腎臓もそのうちのひとつであり、多くがpreclinicalにおける検討であるが、徐々にclinicalにおける検討も集積しつつある。その作用は、尿細管におけるナトリウム再吸収抑制作用、抗酸化・抗炎症作用、抗アポトーシス作用などであるが、近年、線維化の抑制作用についても報告がみられる。インクレチン関連薬に期待される作用機序としては、インクレチンそのものによるものから薬剤の特性によるものなどが想定されている。本稿では糖尿病性腎症のみならず、インクレチン関連薬の腎保護効果の可能性について概説する。(著者抄録)

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  • 【糖尿病とチーム医療】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   2014.12

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  • 統合失調症をもつ妊娠糖尿病患者への他職種での連携支援

    料治 三恵, 佐藤 久恵, 上杉 明子, 箱崎 文香, 吉田 由理, 野口 絢子, 岡本 真由美, 高樽 由美, 大橋 睦子, 高取 佐智子, 坂本 八千代, 江口 潤, 瀬川 友功, 和田 淳, 四方 賢一, 平松 祐司

    糖尿病と妊娠   14 ( 2 )   S - 110   2014.10

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  • エビデンスに基づくネフローゼ症候群診療ガイドライン2014

    松尾 清一, 木村 健二郎, 乳原 善文, 宇都宮 保典, 岡田 浩一, 小畑 陽子, 甲斐 平康, 清元 秀泰, 後藤 眞, 今田 恒夫, 笹冨 佳江, 佐藤 壽伸, 西 慎一, 西野 友哉, 鶴屋 和彦, 古市 賢吾, 星野 純一, 渡辺 裕輔, 石村 栄治, 岩野 正之, 内田 啓子, 遠藤 正之, 奥田 誠也, 柏原 直樹, 片渕 律子, 四方 賢一, 杉山 斉, 鈴木 芳樹, 寺田 典生, 南学 正臣, 平和 伸仁, 御手洗 哲也, 武曾 惠理, 守山 敏樹, 横山 仁, 吉田 篤博, 吉村 吾志夫, 厚生労働科学研究費補助金難治性疾患等克服研究事業(難治性疾患克服研究事業)「進行性腎障害に関する調査研究」, エビデンスに基づくネフローゼ症候群診療ガイドライン2014作成分科会

    日本腎臓学会誌   56 ( 7 )   909 - 1028   2014.10

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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 - 1355   2014.9

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    <Headline>1. 糖尿病性腎症はわが国における最大の透析導入原因疾患である。2. アルブミン尿は腎症の早期診断の指標であると同時に、心血管死の危険因子である。3. 腎症の治療の基本は、血糖、血圧、脂質の管理とRAS系の抑制、食事療法である。4. 腎症の食事療法の基本は食塩とたんぱく質の制限である。5. 2012年より糖尿病透析予防指導管理料の算定が開始された。(著者抄録)

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    Other Link: http://search.jamas.or.jp/link/ui/2015006352

  • 糖尿病合併症から考える薬物療法 腎症に対する薬物療法

    四方 賢一, 小寺 亮

    糖尿病合併症   28 ( Suppl.1 )   82 - 82   2014.9

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

    Tetsuichiro Ono, Kenichi Shikata, Mikako Obika, Nobuyuki Miyatake, Ryo Kodera, Daisyo Hirota, Jun Wada, Hitomi Kataoka, Daisuke Ogawa, Hirofumi Makino

    Acta medica Okayama   68 ( 4 )   235 - 41   2014.8

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    The aim of this study was to clarify the factors associated with the remission and/or regression of microalbuminuria in Japanese patients with type 2 diabetes mellitus. We retrospectively analyzed the data of 130 patients with type 2 diabetes mellitus with microalbuminuria for 2-6 years (3.39 +/- 1.31 years). Remission was defined as improving from microalbuminuria to normoalbuminuria using the albumin/creatinine ratio (ACR), and regression of microalbuminuria was defined as a decrease in ACR of 50% or more from baseline. Progression of microalbuminuria was defined as progressing from microalbuminuria to overt proteinuria during the follow-up period. Among 130 patients with type 2 diabetes mellitus with microalbuminuria, 57 and 13 patients were defined as having remission and regression, respectively, while 26 patients progressed to overt proteinuria. Sex (female), higher HDL cholesterol and lower HbAlc were determinant factors associated with remission/regression of microalbuminuria by logistic regression analysis. Lower systolic blood pressure (SBP) was also correlated with remission/regression, but not at a significant level. These results suggest that proper control of blood glucose, BP and lipid profiles may be associated with remission and/or regression of type 2 diabetes mellitus with microalbuminuria in clinical practice.

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  • 2型糖尿病患者に合併したFisher症候群の1例

    天田 雅文, 和田 淳, 片山 晶博, 江口 潤, 佐藤 恒太, 河野 祥一郎, 出口 健太郎, 四方 賢一, 槇野 博史

    糖尿病   57 ( 8 )   672 - 672   2014.8

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  • 下肢の異常感覚と脱力で発症し糖尿病性筋萎縮症が疑われた1例

    柴田 祐助, 江口 潤, 小松原 基史, 和田 淳, 四方 賢一, 出口 健太郎, 阿部 康二, 槇野 博史

    糖尿病   57 ( 8 )   672 - 672   2014.8

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  • 岡山県糖尿病医療連携推進のための看護研修会の有用性 行政と連動した取り組みを通して

    大橋 睦子, 吉沢 祐子, 廣田 大昌, 長田 麻里, 仲野 真奈美, 四方 賢一, 槇野 博史, 田中 茂人

    糖尿病   57 ( 8 )   659 - 659   2014.8

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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   2014.7

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  • コンサルテーション 糖尿病性腎症患者の症例報告

    四方 賢一

    Diabetes Update   3 ( 3 )   140 - 145   2014.7

  • 【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   2014.6

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    糖尿病性腎症の成因は,高血糖に由来する代謝性因子と血行動態によるところが大きい.細胞外基質の増加を特徴とした基底膜の肥厚,メサンギウム基質の増加,尿細管基底膜肥厚,間質の拡大が認められる.画像検査において糖尿病性腎症では,腎肥大がみられ,他病変による慢性腎不全時の萎縮の程度と比べて軽度である.(著者抄録)

    DOI: 10.11477/mf.1542103925

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2014&ichushi_jid=J01541&link_issn=&doc_id=20140602050009&doc_link_id=10.11477%2Fmf.1542103925&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1542103925&type=%E5%8C%BB%E6%9B%B8.jp_%E3%82%AA%E3%83%BC%E3%83%AB%E3%82%A2%E3%82%AF%E3%82%BB%E3%82%B9&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

  • 【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   2014.6

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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   2014.5

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    DOI: 10.11477/mf.1415101744

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  • 慢性腎臓病の経過において尿中Trefoil Factor 3の変化率はアルブミン尿の変化率と有意相関する

    山成 俊夫, 杉山 斉, 森永 裕士, 大西 章史, 小川 愛由, 北川 正史, 菊本 陽子, 田邊 克幸, 喜多村 真治, 前島 洋平, 小川 大輔, 四方 賢一, 大本 安一, 槇野 博史

    日本腎臓学会誌   56 ( 3 )   347 - 347   2014.5

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  • URINARY TREFOIL FACTOR 3 LEVELS IN ASSOCIATION WITH ALBUMINURIA IN PATIENTS WITH EARLY STAGES OF DIABETIC NEPHROPATHY

    Terami Naoto, Ogawa Daisuke, Tachibana Hiromi, Hatanaka Takashi, Sugiyama Hitoshi, Shikata Kenichi, Makino Hirofumi

    NEPHROLOGY   19   88 - 88   2014.5

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  • A NOVEL BIOMARKER, URINARY TREFOIL FACTOR 3 SIGNIFICANTLY PREDICTS THE RENAL OUTCOMES IN PATIENTS WITH CHRONIC KIDNEY DISEASE

    Yamanari Toshio, Sugiyama Hitoshi, Morinaga Hiroshi, Kitagawa Masashi, Onishi Akifumi, Ogawa Ayu, Kikumoto Yoko, Kitamura Shinji, Maeshima Yohei, Ogawa Daisuke, Shikata Kenichi, Ohmoto Yasukazu, Makino Hirohumi

    NEPHROLOGY   19   73 - 73   2014.5

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  • 早期糖尿病性腎症患者における尿中TFF3(Urinary Trefoil factor3)と尿中アルブミンの関連についての検討

    寺見 直人, 小川 大輔, 山成 俊夫, 杉山 斉, 畑中 崇志, 和田 淳, 四方 賢一, 西井 尚子, 槇野 博史

    日本腎臓学会誌   56 ( 3 )   276 - 276   2014.5

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  • 糖尿病性腎症と炎症 新規治療薬開発への道

    四方 賢一

    日本腎臓学会誌   56 ( 3 )   269 - 269   2014.5

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  • 糖尿病血液透析患者におけるestimated hemoglobin A1cの有用性

    中村 明彦, 河口 宏美, 小寺 亮, 氏家 はる代, 那須 由美, 中田 淳子, 四方 賢一

    日本透析医学会雑誌   47 ( Suppl.1 )   565 - 565   2014.5

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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

    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   126 ( 1 )   1 - 6   2014.4

  • エクソーム解析を行った若年発症糖尿病の1例

    布上 朋和, 江口 潤, 天田 雅文, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   57 ( Suppl.1 )   S - 313   2014.4

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  • 糖尿病腎症第1期および第2期における腎機能低下要因の解析

    小比賀 美香子, 四方 賢一, 小野 哲一郎, 小寺 亮, 江口 潤, 廣田 大昌, 村上 和敏, 中司 敦子, 小川 大輔, 和田 淳, 片岡 仁美, 槇野 博史

    糖尿病   57 ( Suppl.1 )   S - 410   2014.4

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  • ACAM(adipocyte adhesion molecule)/CLMPの一次繊毛機能を介した脂肪細胞分化と肥満症における意義

    村上 和敏, 和田 淳, 佐藤 美和, 江口 潤, 布上 朋和, 片山 晶博, 中司 敦子, 小川 大輔, 四方 賢一, 槇野 博史

    糖尿病   57 ( Suppl.1 )   S - 445   2014.4

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  • 岡山県における糖尿病医療連携推進事業の取り組み

    廣田 大昌, 四方 賢一, 田中 茂人, 加来 浩平, 槇野 博史

    糖尿病   57 ( Suppl.1 )   S - 262   2014.4

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  • 慢性腎臓病を合併する糖尿病患者におけるestimated hemoglobin A1cの有用性

    中村 明彦, 河口 宏美, 小寺 亮, 氏家 はる代, 那須 由美, 中田 淳子, 四方 賢一

    糖尿病   57 ( Suppl.1 )   S - 412   2014.4

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

    Nobuyuki Miyatake, Kenichi Shikata, Hirofumi Makino, Takeyuki Numata

    Acta medica Okayama   68 ( 1 )   43 - 6   2014.2

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    The link between lifestyle modification and changes in both proteinuria and estimated glomerular filtration rates (eGFRs) was evaluated in Japanese subjects with proteinuria who were not taking medications. We used data from 51 men (35.8 +/- 10.0 years) and 74 women (38.0 +/- 11.0 years) with proteinuria at baseline and a 1-year follow up. eGFR was defined by a new equation developed specifically for Japanese subjects. Subjects were given advice for dietary and lifestyle improvement at the initial appointment. At the 1-year follow up, eGFR was increased in both sexes, but not at significant levels. (men: p = 0.7709, women: p = 0.2180). Proteinuria was also improved in many subjects. A decrease hi proteinuria may be associated with improving eGFR in Japanese.

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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. International journal

    Ryo Kodera, Kenichi Shikata, Tetsuharu Takatsuka, Kaori Oda, Satoshi Miyamoto, Nobuo Kajitani, Daisho Hirota, Tetsuichiro Ono, Hitomi Kataoka Usui, Hirofumi Makino

    Biochemical and biophysical research communications   443 ( 3 )   828 - 33   2014.1

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    Introduction: Dipeptidyl peptidase-4 (DPP-4) inhibitors are incretin-based drugs in patients with type 2 diabetes. In our previous study, we showed that glucagon-like peptide-1 (GLP-1) receptor agonist has reno-protective effects through anti-inflammatory action. The mechanism of action of DPP-4 inhibitor is different from that of GLP-1 receptor agonists. It is not obvious whether DPP-4 inhibitor prevents the exacerbation of diabetic nephropathy through anti-inflammatory effects besides lowering blood glucose or not. The purpose of this study is to clarify the reno-protective effects of DPP-4 inhibitor through anti-inflammatory actions in the early diabetic nephropathy.
    Materials and methods: Five-week-old male Sprague-Dawley (SD) rats were divided into three groups; non-diabetes, diabetes and diabetes treated with DPP-4 inhibitor (PKF275-055; 3 mg/kg/day). PKF275-055 was administered orally for 8 weeks.
    Results: PKF275-055 increased the serum active GLP-1 concentration and the production of urinary cyclic AMP. PKF275-055 decreased urinary albumin excretion and ameliorated histological change of diabetic nephropathy. Macrophage infiltration was inhibited, and inflammatory molecules were down-regulated by PKF275-055 in the glomeruli. In addition, nuclear factor-kappa B (NF-kappa B) activity was suppressed in the kidney.
    Conclusions: These results indicate that DPP-4 inhibitor, PKF275-055, have reno-protective effects through anti-inflammatory action in the early stage of diabetic nephropathy. The endogenous biological active GLP-1 might be beneficial on diabetic nephropathy besides lowering blood glucose. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2013.12.049

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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   2014.1

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    Other Link: http://search.jamas.or.jp/link/ui/2014089998

  • 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

  • 【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

  • 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

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  • 糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 尿検体収集を伴った糖尿病性腎症レジストリーの運用

    和田隆志, 安部秀斉, 北村博司, 木村健二郎, 佐藤博, 鈴木芳樹, 羽田勝計, 槇野博史, 松尾清一, 丸山彰一, 湯澤由紀夫, 荒木信一, 井関邦敏, 岩野正之, 上杉憲子, 上田善彦, 乳原善文, 古波蔵健太郎, 古家大祐, 四方賢一, 中村裕之, 中山昌明, 西愼一, 西野友哉, 馬場園哲也, 原茂子, 久野敏, 古市賢吾, 森潔, 守屋達美, 山縣邦弘, 山本格, 横山仁, 横山宏樹

    糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 平成25年度 総括・分担研究報告書   2014

  • 糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究

    湯澤由紀夫, 佐藤博, 鈴木芳樹, 北村博司, 荒木信一, 井関邦敏, 岩野正之, 上杉憲子, 上田善彦, 乳原善文, 古波蔵健太郎, 古家大祐, 四方賢一, 中山昌明, 西愼一, 西野友哉, 馬場園哲也, 原茂子, 久野敏, 守屋達美, 山縣邦弘, 横山仁, 横山宏樹

    糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 平成25年度 総括・分担研究報告書   2014

  • 栄養の数字を伝えるチカラ~Excelを使った栄養設計・提案支援~

    平健太郎, 伊野英男, 名和秀起, 長谷川祐子, 岡田恵子, 田邊俊介, 坂本八千代, 四方賢一

    静脈経腸栄養   29 ( 3 )   2014

  • 食塩摂取量のエビデンスと食塩制限の効果

    四方 賢一, 坂本 八千代, 野口 絢子

    日本病態栄養学会誌   17 ( Suppl. )   S - 18   2013.12

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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

    四方 賢一, 厚田 幸一郎

    DxM: Diet Exercise Medicine   2   12 - 13   2013.11

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  • 肥満で脂肪組織に誘導される膜蛋白Gpnmbの脂肪肝炎抑制効果

    片山 晶博, 和田 淳, 中司 敦子, 江口 潤, 村上 和敏, 勅使川原 早苗, 寺見 隆宏, 樋口 千草, 布上 朋和, 天田 雅文, 四方 賢一, 肥田 和之, 槇野 博史

    肥満研究   19 ( Suppl. )   161 - 161   2013.9

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  • 【どこが違う?どう違う? 図解でくらべる→わかる! 糖尿病の病態・治療・ケア】(第3章)糖尿病合併症~慢性合併症 糖尿病腎症第3期と第4期

    四方 賢一

    糖尿病ケア   ( 2013秋季増刊 )   114 - 119   2013.9

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  • 糖尿病マウス腎および培養腎細胞における核内受容体の発現の検討

    寺見 直人, 小川 大輔, 橘 洋美, 堀口 千景, 江口 潤, 中司 敦子, 畑中 崇史, 小寺 亮, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病合併症   27 ( Suppl.1 )   138 - 138   2013.8

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  • 糖尿病腎症に対する新たな治療戦略 GLP-1の抗炎症作用とインクレチン製剤への期待

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    糖尿病合併症   27 ( 2 )   189 - 193   2013.8

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  • 【エビデンスに基づくCKD診療ガイドライン2013】

    木村 健二郎, 岡田 浩一, 今井 裕一, 田村 功一, 西 慎一, 和田 隆志, 福井 次矢, 松尾 清一, 湯澤 由紀夫, 有村 義宏, 堀江 重郎, 丸山 彰一, 今井 圓裕, 守山 敏樹, 池住 洋平, 石倉 健司, 井関 邦敏, 上田 仁康, 小尾 佳嗣, 大野 岩男, 貝藤 裕史, 香美 祥二, 金崎 啓造, 要 伸也, 川田 典孝, 河原崎 宏雄, 北川 清樹, 北田 宗弘, 小井手 裕一, 古家 大祐, 後藤 俊介, 後藤 眞, 後藤 憲彦, 近藤 秀治, 佐古 まゆみ, 柴垣 有吾, 嶋 英昭, 庄司 哲雄, 新沢 真紀, 鈴木 芳樹, 諏訪部 達也, 坪井 伸夫, 鶴岡 秀一, 徳山 博文, 富田 亮, 長澤 康行, 西尾 妙織, 長谷部 直幸, 花房 規男, 濱 ひとみ, 早川 洋, 原 章規, 深川 雅史, 藤井 直彦, 藤井 秀毅, 藤野 貴行, 古市 賢吾, 丸山 達也, 丸山 之進, 三浦 健一郎, 三浦 直人, 三ツ木 加代, 武藤 智, 望月 俊雄, 森 一越, 谷澤 雅彦, 安田 宜成, 山本 裕康, 山本 陵平, 脇野 修, 鷲田 直輝, 渡辺 裕輔, 原田 浩, 荒木 信一, 伊藤 貞嘉, 上村 治, 臼井 丈一, 内田 俊也, 宇津 貴, 宇都宮 保典, 風間 順一郎, 柏原 直樹, 川村 哲也, 栗山 哲, 小松 康宏, 斉藤 喬雄, 斎藤 知栄, 酒井 謙, 佐田 憲映, 四方 賢一, 杉山 斉, 竹村 司, 土谷 健, 椿原 美治, 成田 一衛, 服部 元史, 花岡 一成, 馬場園 哲也, 樋口 誠, 平野 勉, 星野 純一, 堀尾 勝, 山縣 邦弘, 横山 啓太郎, 横山 仁, 吉川 徳茂, 渡邊 有三, 船橋 徹, 益崎 裕章, エビデンスに基づくCKD診療ガイドライン2013作成委員会, 日本腎臓学会

    日本腎臓学会誌   55 ( 5 )   585 - 860   2013.7

  • 2型糖尿病患者に対するレパグリニドの有効性の検討

    寺見 直人, 橘 洋美, 堀口 千景, 中司 敦子, 江口 潤, 小川 大輔, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   56 ( 5 )   321 - 321   2013.5

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  • 若年性白内障および糖尿病を契機に発見された筋強直性ジストロフィーの1例

    片山 晶博, 水野 智文, 畑中 崇志, 原 孝行, 和田 淳, 江口 潤, 中司 敦子, 小川 大輔, 四方 賢一, 槇野 博史

    糖尿病   56 ( 5 )   339 - 339   2013.5

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  • 【糖尿病性腎症への挑戦】糖尿病性腎症に対する新たな治療戦略 炎症を標的とした治療の試み

    四方 賢一

    糖尿病の最新治療   4 ( 3 )   136 - 141   2013.5

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    糖尿病性腎症の成因には、炎症が関与している。動脈硬化の成因に炎症が関与することは以前から知られており、炎症は糖尿病における大血管障害と細小血管障害に共通の成因であり、心腎連関のメカニズムにも炎症が関与していることが強く示唆される。さらに、最近、メタボリックシンドロームや、NASH、がんなどの成因にも炎症が関与することが明らかになったことから、炎症は生活習慣病に共通した病態であり、新しい治療標的の有力な候補である。糖尿病モデル動物に、抗炎症作用を持つ既存の薬剤(スタチン、ARB、チアゾリジン誘導体、GLP-1受容体作動薬など)を投与すると、血糖非依存的な腎保護効果が得られることから、抗炎症作用を持つ薬剤は糖尿病性腎症に対して有効であることが示唆される。また、DNAマイクロアレイなどを用いた網羅的探索により、糖尿病性腎症の成因に関わる炎症関連分子が明らかにされており、創薬の新しい標的となることが期待される。(著者抄録)

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    Other Link: http://search.jamas.or.jp/link/ui/2013243041

  • 特発性器質化肺炎を合併した1型糖尿病の1例

    橘 洋美, 和田 淳, 小川 大輔, 豊田 智子, 堀口 千景, 寺見 直人, 四方 賢一, 槇野 博史

    糖尿病   56 ( 5 )   338 - 338   2013.5

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  • インクレチン関連薬の長期展望 インクレチン関連薬の腎保護効果

    四方 賢一

    糖尿病   56 ( Suppl.1 )   S - 71   2013.4

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    インクレチン関連薬にはGLP-1受容体作動薬とDPP-4阻害薬が存在する.これらの薬剤は膵臓に対してインスリン分泌を増強する作用をもつことから,糖尿病治療のひとつとして幅広く使用されている.さらに,腎臓も含めた他の臓器に対しても有益な効果が多く報告されており,糖尿病の血管合併症の発症・進展抑制にも期待されている.腎臓における特徴的な作用としてはナトリウム再吸収の抑制であるが,インクレチン関連薬が持つ抗酸化・抗炎症作用,抗アポトーシス作用,線維化抑制作用などは腎障害のみならず,全身の臓器の保護作用として期待される.インクレチン関連薬における腎保護効果については,現状,多くの検討が基礎実験によるものであり,今後,臨床試験によって検証していく必要がある.(著者抄録)

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  • 【インクレチンと血管障害】インクレチン関連薬の腎保護作用

    小寺 亮, 四方 賢一

    Angiology Frontier   12 ( 1 )   45,8 - 50,8   2013.4

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    インクレチン関連薬はグルカゴン様ペプチド(GLP)-1受容体作動薬、ジペプチジルペプチダーゼ(DPP)-4阻害薬に分けられ、血糖降下作用だけではなく、他臓器に対する多面的な効果(膵外作用)も注目されている。腎臓に対する作用もそのうちの1つであり、その作用は尿細管におけるナトリウム再吸収抑制、また近年では抗酸化・抗炎症といった新たな作用が発見されている。腎保護に関しては、血糖降下薬として血糖低下による腎保護効果が期待されるが、さらにナトリウム再吸収抑制作用によるナトリウム利尿が血圧低下につながり、また抗酸化・抗炎症作用による腎保護効果が期待される。(著者抄録)

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  • 全身倦怠感を契機に診断した若年発症糖尿病の1例

    布上 朋和, 江口 潤, 天田 雅文, 渡辺 晴樹, 三好 智子, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   56 ( 4 )   252 - 252   2013.4

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  • 糖尿病マウス腎および高糖濃度刺激下での培養腎細胞における核内受容体の発現解析

    寺見 直人, 小川 大輔, 橘 洋美, 堀口 千景, 小寺 亮, 江口 潤, 中司 敦子, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   56 ( Suppl.1 )   S - 307   2013.4

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  • 糖尿病性腎症の糖鎖プロファイリングによる新規バイオマーカーの同定(U-CARE研究)

    和田 淳, 井上 謙太郎, 中司 敦子, 江口 潤, 村上 和敏, 寺見 隆宏, 勅使川原 早苗, 片山 晶博, 小川 智央, 山田 雅雄, 四方 賢一, 槇野 博史

    日本腎臓学会誌   55 ( 3 )   296 - 296   2013.4

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  • 内臓脂肪蓄積に伴って強発現する膜蛋白Gpnmbの脂肪肝炎抑制効果と可溶性分泌型の関与

    片山 晶博, 和田 淳, 中司 敦子, 江口 潤, 村上 和敏, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 渡邉 真由, 樋口 千草, 肥田 和之, 四方 賢一, 槇野 博史

    糖尿病   56 ( Suppl.1 )   S - 111   2013.4

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  • 糖尿病性腎症の糖鎖プロファイリングの検討

    井上 謙太郎, 和田 淳, 小川 大輔, 中司 敦子, 江口 潤, 村上 和敏, 神崎 資子, 寺見 隆宏, 勅使川原 早苗, 片山 晶博, 小川 智央, 山田 雅雄, 四方 賢一, 槇野 博史

    糖尿病   56 ( Suppl.1 )   S - 365   2013.4

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  • マウス腎および培養腎細胞における核内受容体の発現と高糖濃度刺激による発現変化の検討

    寺見 直人, 小川 大輔, 橘 洋美, 堀口 千景, 小寺 亮, 江口 潤, 中司 敦子, 和田 淳, 四方 賢一, 槇野 博史

    日本腎臓学会誌   55 ( 3 )   379 - 379   2013.4

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  • 糖尿病診療のスキルアップ 糖尿病腎症の治療と管理について

    廣田 大昌, 四方 賢一, 槇野 博史

    糖尿病   56 ( Suppl.1 )   S - 35   2013.4

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  • 尿中Trefoil Factor 3は慢性腎臓病における腎機能予後を予測するバイオマーカーである

    山成 俊夫, 森永 裕士, 杉山 斉, 小川 愛由, 北川 正史, 菊本 陽子, 内田 治仁, 喜多村 真治, 赤木 滋, 前島 洋平, 小川 大輔, 四方 賢一, 大本 安一, 槇野 博史

    日本腎臓学会誌   55 ( 3 )   399 - 399   2013.4

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  • 糖尿病診療の絆(チーム医療の現状と課題) 腎症の進展を予防するための糖尿病チーム医療

    四方 賢一

    糖尿病   56 ( Suppl.1 )   S - 7   2013.4

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  • メタボリック症候群におけるアルブミン尿と炎症及びインスリン抵抗性についての検討

    梶谷 展生, 四方 賢一, 石井 啓太, 平田 教至, 小寺 亮, 廣田 大昌, 和田 淳, 槇野 博史

    糖尿病   56 ( Suppl.1 )   S - 440   2013.4

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  • Microinflammation in the pathogenesis of diabetic nephropathy.

    Kenichi Shikata, Hirofumi Makino

    Journal of diabetes investigation   4 ( 2 )   142 - 9   2013.3

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    Diabetic nephropathy is the leading cause of end-stage renal failure in developed countries. Furthermore, diabetic nephropathy is related to the risk of cardiovascular diseases and an increase in mortality of diabetic patients. Several factors are involved in the development of nephropathy, including glomerular hyperfiltration, oxidative stress, accumulation of advanced glycation end-products, activation of protein kinase C, acceleration of the polyol pathway and over-expression of transforming growth factor-β. Recently, accumulated data have emphasized the critical roles of chronic low-grade inflammation, 'microinflammation', in the pathogenesis of diabetic nephropathy, suggesting that microinflammation is a common mechanism in the development of diabetic vascular complications. Expression of cell adhesion molecules, chemokines and pro-inflammatory cytokines are increased in the renal tissues of diabetic patients and animals. Deficiency of pro-inflammatory molecules results in amelioration of renal injuries after induction of diabetes in mice. Plasma and urinary levels of cytokines, chemokines and cell adhesion molecules, are elevated and correlated with albuminuria. Several kinds of drugs that have anti-inflammatory actions as their pleiotropic effects showed renoprotective effects on diabetic animals. Modulation of the inflammatory process prevents renal insufficiency in diabetic animal models, suggesting that microinflammation is one of the promising therapeutic targets for diabetic nephropathy, as well as for cardiovascular diseases.

    DOI: 10.1111/jdi.12050

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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.

    Akihiko Nakamura, Kenichi Shikata, Tatsuaki Nakatou, Takuya Kitamura, Nobuo Kajitani, Daisuke Ogawa, Hirofumi Makino

    Journal of diabetes investigation   4 ( 2 )   195 - 201   2013.3

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    Aims/Introduction: Recent studies have pointed to the effectiveness of combination therapy with an angiotensin-converting-enzyme inhibitor (ACEI) and an angiotensin receptor blocker (ARB) for diabetic nephropathy. However, some controversy over this combination treatment remains and the mechanisms underlying its renoprotective effects have not been fully clarified. Therefore, we compared the renoprotective effects of imidapril (ACEI) and losartan (ARB) combination therapy with losartan monotherapy in patients with diabetic nephropathy. We also compared the anti-inflammatory and anti-oxidative stress effects of these two treatments. Materials and Methods: A total of 32 Japanese patients with type2 diabetes and nephropathy were enrolled. Patients were randomized to either 100mg/day losartan (n=16) or 50mg/day losartan plus 5mg/day imidapril (n=16). We evaluated clinical parameters, serum concentrations of high-sensitivity C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-18 (IL-18) and monocyte chemotactic protein-1 (MCP-1), and the urinary concentrations of IL-18, MCP-1 and 8-hydroxy-2′-deoxyguanosine (8-OHdG) at 24 and 48weeks after starting treatment. Results: Blood pressure was not significantly different between the two groups. The serum levels of hs-CRP, sICAM-1 and IL-18, as well as urinary excretion of albumin, IL-18 and 8-OHdG decreased significantly in the combination therapy group at 48weeks. The percent decreases in serum IL-18 concentrations and urinary IL-18 and 8-OHdG were significantly greater in the combination therapy group than in the monotherapy group. Conclusions: Combination therapy with an ACEI and an ARB could be beneficial for treating diabetic nephropathy through its anti-inflammatory and anti-oxidative stress effects. © 2012 Asian Association for the Study of Diabetes and Wiley Publishing Asia Pty Ltd.

    DOI: 10.1111/jdi.12004

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  • 化学物質過敏症有訴者に対する匂いによる嗅覚刺激が脳血流変化に及ぼす影響(その2)

    東 賢一, 内山 巖雄, 高野 裕久, 谷川 真理, 東 実千代, 萬羽 郁子, 井上 正雄, 四方田 聡, 吉川 敏一

    日本衛生学雑誌   68 ( Suppl. )   S159 - S159   2013.3

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  • 【糖尿病腎症-透析をいかに防ぐか-】糖尿病腎症患者に対する降圧療法の実際

    廣田 大昌, 四方 賢一

    プラクティス   30 ( 2 )   191 - 197   2013.3

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  • 【糖尿病腎症-透析をいかに防ぐか-】糖尿病腎症の診断と臨床経過

    四方 賢一

    プラクティス   30 ( 2 )   167 - 172   2013.3

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  • Clinical nephrology 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

    小川 大輔, 四方 賢一

    Annual Review腎臓   2013   241 - 246   2013.1

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    核内受容体は糖・脂質代謝のみならず,全身の免疫応答や炎症反応に深く関わることが判明している.種々の核内受容体が同定されているが,中でもペルオキシソーム増殖因子活性化受容体(PPAR)に関する研究が最も進んでいる.PPARには,α,δ,γの三つのサブタイプが存在し,それぞれ異なるリガンドと結合することにより薬理学的作用を発揮する.PPARγやPPARαに対するアゴニストは2型糖尿病や脂質異常症の治療薬としてすでに臨床応用されている.また,ビタミンD受容体(VDR)はカルシウム代謝や骨代謝に関わることが知られており,VDRアゴニストが低カルシウム血症や骨粗鬆症の治療薬として現在使用されている.一方,これらのアゴニストの腎局所に対する効果も報告されており,核内受容体作動薬は糖尿病性腎症を含めた腎疾患に対する治療手段として最近注目を浴びている.本稿では核内受容体,特にPPARとVDRについて,臨床研究および基礎的検討をふまえて概説する.(著者抄録)

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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

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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

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  • 2型糖尿病における腎症の寛解および改善に関与する因子の解析

    小野哲一郎, 四方賢一, 小比賀美香子, 梶谷展生, 小寺亮, 廣田大昌, 村上和敏, 堀口千景, 小川大輔, 和田淳, 片岡仁美, 槇野博史

    糖尿病   56 ( Supplement 1 )   2013

  • 糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究

    湯澤由紀夫, 佐藤博, 鈴木芳樹, 北村博司, 荒木信一, 井関邦敏, 岩野正之, 上杉憲子, 上田善彦, 古家大祐, 四方賢一, 中山昌明, 西愼一, 馬場園哲也, 原茂子, 久野敏, 守屋達美, 山縣邦弘, 横山仁, 横山宏樹

    糖尿病性腎症ならびに腎硬化症の診療水準向上と重症化防止にむけた調査・研究 平成24年度 総括・分担研究報告書   2013

  • 糖尿病性腎症の治療薬に関する臨床的評価方法確立に関する研究 平成24年度

    四方賢一

    糖尿病性腎症の治療薬に関する臨床的評価方法確立に関する研究 平成24年度 総括報告書   2013

  • Liver X Receptor Agonist Ameliorates Diabetic Nephropathy by Inhibiting High Glucose-Induced Osteopontin Expression

    Daisuke Ogawa, Hiromi Tachibana, Jun Wada, Naoto Terami, Chikage Sato-Horiguchi, Kenichi Shikata, Hirofumi Makino

    CIRCULATION   126 ( 21 )   2012.11

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  • 【腎疾患診療の最前線】糖尿病性腎症の病態と新たな治療 核内受容体PPARを中心に

    小川 大輔, 四方 賢一

    医薬ジャーナル   48 ( 11 )   55 - 61   2012.11

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    糖尿病性腎症は、わが国における透析導入原疾患の第1位である。また、単に末期腎不全に至るだけでなく、その進行の過程で脳梗塞や狭心症・心筋梗塞など心血管疾患を引き起こす危険性が高いことが認識されている。早期より血糖・血圧・脂質などを厳格にコントロールする集約的治療が糖尿病性腎症の進行を阻止することが明らかにされているが、進行した症例に対しては現時点で有効な治療法がない。一方、種々の核内受容体が同定されているが、中でもペルオキシソーム増殖因子活性化受容体(PPAR)に関する研究が最も進んでいる。PPARには、α、δ、γの三つのサブタイプが存在し、それぞれ異なるリガンドと結合することにより、薬理学的作用を発揮することが判明している。また、PPARγやPPARαに対するアゴニストが、糖尿病や脂質異常症の治療薬として既に臨床応用されており、糖尿病性腎症に対しても効果のあることが報告されている。本稿では、核内受容体、特にPPARを標的とした糖尿病性腎症治療の可能性について、臨床研究および基礎的検討を踏まえて概説する。(著者抄録)

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  • 【糖尿病性腎症の現況と今後の展望】発症・進展のメカニズムと治療展望 Microinflammationと新規治療薬

    四方 賢一

    Diabetes Frontier   23 ( 5 )   547 - 553   2012.10

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  • 糖尿病性腎症に対するVildagliptin analogの効果の検討

    小寺 亮, 四方 賢一, 高塚 哲全, 宮本 聡, 廣田 大昌, 梶谷 展生, 和田 淳, 小川 大輔, 槇野 博史

    糖尿病合併症   26 ( Suppl.1 )   126 - 126   2012.10

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  • 糖尿病腎症に対する新たな治療戦略 GLP-1の抗炎症作用とインクレチン製剤への期待

    四方 賢一

    糖尿病合併症   26 ( Suppl.1 )   96 - 96   2012.10

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  • 【一緒にみて、考えれば結果が変わる!患者さんとみる糖尿病検査値ガイド】糸球体濾過量(GFR)

    四方 賢一

    糖尿病ケア   9 ( 9 )   846 - 847   2012.9

  • 【一緒にみて、考えれば結果が変わる!患者さんとみる糖尿病検査値ガイド】尿蛋白

    四方 賢一

    糖尿病ケア   9 ( 9 )   844 - 845   2012.9

  • 【高血圧in糖尿病 その対策!!】顕性糖尿病性腎症の降圧治療

    四方 賢一

    糖尿病診療マスター   10 ( 6 )   521 - 524   2012.9

  • 肥満症におけるGpnmbの意義

    片山 晶博, 和田 淳, 中司 敦子, 江口 潤, 村上 和敏, 神崎 資子, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 渡邉 真由, 樋口 千草, 肥田 和之, 四方 賢一, 槇野 博史

    肥満研究   18 ( Suppl. )   156 - 156   2012.9

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  • 糖尿病性腎症と心腎連関

    四方 賢一

    Diabetes Update   1 ( 1 )   45 - 48   2012.8

  • 【糖尿病性腎症への挑戦】腎症の発症と炎症

    小寺 亮, 四方 賢一

    腎と透析   73 ( 2 )   139 - 144   2012.8

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  • 集中治療室での加療を要し、救命し得た劇症1型糖尿病の1例

    沼 哲也, 更井 啓, 大森 一慶, 布上 朋和, 杉山 淳一, 岡原 修司, 四方 賢一

    糖尿病   55 ( 6 )   435 - 435   2012.6

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  • CSIIの導入に際し、CGMSによる血糖プロファイルの解析が有効であった1型糖尿病の1例

    梶谷 展生, 四方 賢一, 小寺 亮, 佐藤 千景, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   55 ( 6 )   435 - 435   2012.6

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  • 2型糖尿病治療中にLP-X、LP-Yの出現を認めた1例

    神崎 資子, 和田 淳, 片山 晶博, 那須 淳一郎, 四方 賢一, 山本 和秀, 槇野 博史

    糖尿病   55 ( 5 )   363 - 363   2012.5

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  • メタボリックシンドロームにおけるGalectin-9の機能解析

    神崎 資子, 和田 淳, 江口 潤, 中司 敦子, 村上 和敏, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 片山 晶博, 四方 賢一, 平島 光臣, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 93   2012.4

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    J-GLOBAL

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  • 慢性腎臓病患者における尿中Trefoil Factor 3は腎機能低下に伴い排泄増加し蛋白尿と相関する

    森永 裕士, 杉山 斉, 小川 愛由, 瀧上 慶一, 北川 正史, 菊本 陽子, 内田 治仁, 喜多村 真治, 赤木 滋, 前島 洋平, 大本 安一, 小川 大輔, 四方 賢一, 槇野 博史

    日本腎臓学会誌   54 ( 3 )   256 - 256   2012.4

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  • グライコーム解析による糖尿病性腎症バイオマーカーの探索

    井上 謙太郎, 和田 淳, 中司 敦子, 江口 潤, 村上 和敏, 神崎 資子, 寺見 隆宏, 黒瀬 祐子, 片山 晶博, 樋口 千草, 渡邉 真由, 小川 智央, 山田 雅雄, 四方 賢一, 槇野 博史

    日本腎臓学会誌   54 ( 3 )   250 - 250   2012.4

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  • 糖尿病性腎症モデルラットにおけるメタロチオネイン(metallothionein)の発現の検討

    橘 洋美, 小川 大輔, 松下 裕一, 佐藤 千景, 和田 淳, 喜多村 真治, 前島 洋平, 四方 賢一, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 331   2012.4

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  • メタボリックシンドロームにおけるGpnmbの意義

    片山 晶博, 和田 淳, 中司 敦子, 江口 潤, 村上 和敏, 神崎 資子, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 渡邉 真由, 樋口 千草, 肥田 和之, 四方 賢一, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 93   2012.4

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  • メタボリック症候群におけるアルブミン尿発症因子の解析

    梶谷 展生, 四方 賢一, 石井 啓太, 平田 教至, 宮武 伸行, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 251   2012.4

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  • 早期糖尿病性腎症におけるTelmisartanの抗酸化作用の検討

    佐藤 千景, 小川 大輔, 松下 裕一, 橘 洋美, 小寺 亮, 廣田 大昌, 宮本 聡, 梶谷 展生, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 87   2012.4

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  • CDEJの展開と深化に向けて 糖尿病性腎症進展予防のためのチーム医療

    四方 賢一, 槇野 博史

    糖尿病   55 ( Suppl.1 )   S - 30   2012.4

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  • 糖尿病性腎症の成因とmicroinflammation 新規治療薬開発に向けた展開

    四方 賢一

    Nephrology Frontier   11 ( 1 )   49 - 51   2012.3

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  • 【糖尿病性腎症治療と腎症治療薬の新しい展望】腎症治療薬の新しい展望 炎症をターゲットとした治療薬

    小寺 亮, 四方 賢一, 槇野 博史

    Medicinal   2 ( 2 )   86 - 94   2012.2

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  • 糖尿病の食事療法(第2回) 糖尿病腎症の食事

    梶谷 展生, 四方 賢一

    月刊糖尿病   4 ( 2 )   110 - 118   2012.2

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  • 化学物質過敏症有訴者に対する匂いによる嗅覚刺激が脳血流変化に及ぼす影響

    東 賢一, 内山 巖雄, 高野 裕久, 谷川 真理, 東 実千代, 萬羽 郁子, 井上 正雄, 四方田 聡, 吉川 敏一

    日本衛生学雑誌   67 ( 2 )   285 - 285   2012.2

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  • 糖尿病性腎症におけるCholecystokininの抗炎症作用のメカニズム

    宮本聡, 四方賢一, 四方賢一, 宮坂京子, 小寺亮, 小寺亮, 廣田大昌, 梶谷展生, 佐藤千景, 佐藤千景, 片岡仁美, 片岡仁美, 小川大輔, 小川大輔, 内田治仁, 西森久和, 槇野博史

    日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集   26th   2012

  • 2型糖尿病における腎症の発症および進展に関与する因子の解析

    小野哲一郎, 四方賢一, 小比賀美香子, 梶谷展生, 小寺亮, 宮本聡, 廣田大昌, 村上和敏, 佐藤千景, 小川大輔, 和田淳, 片岡仁美, 槇野博史

    糖尿病   55 ( Supplement 1 )   2012

  • IgG4関連硬化性疾患患者のインスリン分泌能と治療効果についての検討

    片岡仁美, 佐藤千景, 平松万尚, 村上和敏, 神崎資子, 水島孝明, 小比賀美香子, 和田淳, 四方賢一, 槇野博史

    糖尿病   55 ( 6 )   2012

  • 2型糖尿病患者の腎症に関連する因子の横断的解析

    小比賀美香子, 四方賢一, 小野哲一郎, 梶谷展生, 小寺亮, 宮本聡, 廣田大昌, 村上和敏, 佐藤千景, 小川大輔, 和田淳, 片岡仁美, 槇野博史

    糖尿病   55 ( Supplement 1 )   2012

  • 糖尿病性腎症の治療薬に関する臨床的評価方法確立に関する研究

    四方賢一

    糖尿病性腎症の治療薬に関する臨床的評価方法確立に関する研究 平成23年度 総括・分担研究報告書   2012

  • 糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 糖尿病性腎症の新規治療法の開発 糖尿病性腎症に対するGLP-1受容体作動薬の効果の検討

    四方賢一

    糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 平成21-23年度 総合研究報告書   2012

  • CKDの早期発見・予防・治療標準化・進展阻止に関する調査研究 メタボリック症候群とCKDの関連に関する調査研究

    四方賢一, 梶谷展生, 和田淳, 利根惇仁, 肥田和之, 石井啓太, 平田教至, 宮武伸行, 中村明彦

    CKDの早期発見・予防・治療標準化・進展阻止に関する調査研究 平成23年度 総括・分担研究報告書   2012

  • 糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 糖尿病性腎症症例のレジストリーの運用

    和田隆志, 安部秀斉, 奥田誠也, 草野英二, 古家大祐, 佐藤博亮, 鈴木芳樹, 篁俊成, 羽田勝計, 槇野博史, 湯澤由紀夫, 荒木信一, 井関邦敏, 岩野正之, 四方賢一, 中村裕之, 二宮利治, 馬場園哲也, 原章規, 原茂子, 深水圭, 古市賢吾, 森潔, 守屋達美, 山本格, 横山仁, 横山宏樹

    糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 平成23年度 総括・分担研究報告書   2012

  • 糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 糖尿病性腎症の新規治療法の開発 糖尿病性腎症に対するGLP-1受容体作動薬の効果の検討

    四方賢一

    糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 平成23年度 総括・分担研究報告書   2012

  • Decreasing abdominal circumference is associated with improving estimated glomerular filtration rate (eGFR) with lifestyle modification in Japanese men: a pilot study.

    Nobuyuki Miyatake, Kenichi Shikata, Hirofumi Makino, Takeyuki Numata

    Acta medica Okayama   65 ( 6 )   363 - 7   2011.12

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    The link between changes in a subject's metabolic syndrome components and his estimated glomerular filtration rate (eGFR) was evaluated in healthy Japanese men. We used data from 120 Japanese men (45.5 +/- 8.4 years) with a 1-year follow up. eGFR was defined by a new equation developed for Japan. There were no significant differences in eGFR between men with and without metabolic syndrome components at baseline. Subjects were given advice for dietary and lifestyle improvement. At the 1-year follow up, almost all metabolic syndrome components were significantly improved. However, eGFR was significantly decreased. The changes in eGFR were weakly correlated with abdominal circumference (r = -0.232, p = 0.0106). A decrease in abdominal circumference may be associated with improving eGFR in Japanese men.

    DOI: 10.18926/AMO/47261

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  • A new paradigm for the treatment of lifestyle-related diseases : Microinflammation as a novel therapeutic target

    123 ( 3 )   197 - 206   2011.12

  • 【糖尿病性腎症の成因と病態-新たな展開】Microinflammationの役割

    小川 大輔, 四方 賢一

    日本腎臓学会誌   53 ( 7 )   1021 - 1026   2011.10

  • 糖尿病性腎症の治療における新しい展開 Microinflammationを標的とした治療戦略

    四方 賢一

    日本高血圧学会総会プログラム・抄録集   34回   552 - 552   2011.10

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  • Telmisartan attenuates diabetic nephropathy through anti-oxidative and anti-inflammatory actions via activation of peroxisome proliferator-activated receptor-gamma

    N. Kajitani, K. Shikata, R. Kodera, S. Miyamoto, D. Hirota, C. Sato, J. Wada, D. Ogawa, H. Makino

    DIABETOLOGIA   54   S442 - S443   2011.9

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

    Naomi Watanabe, Kenichi Shikata, Yasushi Shikata, Kei Sarai, Kazuyoshi Omori, Ryo Kodera, Chikage Sato, Jun Wada, Hirofumi Makino

    Acta medica Okayama   65 ( 4 )   247 - 57   2011.8

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    Inflammatory processes are involved in the pathogenesis of diabetic nephropathy. The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK) pathways for induction of intercellular adhesion molecule-1 (ICAM-1) expression in glomerular endothelial cells under diabetic conditions. We examined the expression of ICAM-1 in the kidneys of experimental diabetic rats. Human glomerular endothelial cells (GE cells) were exposed to normal glucose concentration, high glucose concentration (HG), or high mannitol concentration (HM), and then the expression of the ICAM-1 protein and the phosphorylation of the 3 subfamilies of mitogen-activated protein kinase (MAPK) were determined using Western blot analysis. Next, to evaluate the involvement of MAPKs in HG- or HM-induced ICAM-1 expression, we preincubated GE cells with the inhibitors for ERK, p38 or JNK 1h prior to the application of glucose or mannitol. Expression of ICAM-1 was increased in the glomeruli of diabetic rats. Both FIG and HM induced ICAM-1 expression and phosphorylation of ERK1/2, p38 and JINX in GE cells. Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK. We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions.

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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

    小寺 亮, 四方 賢一

    医学のあゆみ   238 ( 9 )   851 - 856   2011.8

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    糖尿病性腎症の治療戦略はさまざまな成因に基づく見解から種々の治療戦略が検討されているが、腎不全を完全に予防できる画期的な治療法がないのが現状である。糖尿病性腎症の患者数は増加し、慢性透析療法導入の最大の原因疾患となっており、その対策が喫緊の課題となっている。本稿では糖尿病性腎症の治療戦略に関する最近の知見を概説する。(著者抄録)

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2011&ichushi_jid=J00060&link_issn=&doc_id=20110826020007&doc_link_id=%2Faa7ayuma%2F2011%2F023809%2F008%2F0851-0856%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faa7ayuma%2F2011%2F023809%2F008%2F0851-0856%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • 【糖尿病性腎症とCKD-新たな展開と治療法の選択-】糖尿病性腎症の治療 血糖コントロール 糖尿病治療薬間に優劣はあるか

    小寺 亮, 四方 賢一, 槇野 博史

    月刊糖尿病   3 ( 7 )   69 - 77   2011.7

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  • Micro-inflammationとしての歯周病 さまざまな疾患領域におけるMicro-inflammation研究の最新動向 糖尿病性腎症

    梶谷 展生, 四方 賢一

    歯界展望   117 ( 6 )   1090 - 1091   2011.6

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  • 糖尿病腎症の新展開 Microinflammationの新たな展開

    四方 賢一, 槇野 博史

    糖尿病合併症   25 ( 1 )   40 - 43   2011.6

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  • 【慢性炎症-多様な疾患の基盤病態 生活習慣病、がん、免疫・神経疾患に至る分子メカニズムと診断・治療への応用】(第2章)慢性炎症と生活習慣病 糖尿病性腎症の成因としての慢性炎症

    廣田 大昌, 四方 賢一, 槇野 博史

    実験医学   29 ( 10 )   1560 - 1565   2011.6

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    糖尿病性腎症の成因として、高血糖から腎障害に至るにはさまざまな経路が存在する。われわれはこれまでに、この経路の中でも、局所の微小炎症(microinflammation)が重要な因子であることを提唱して一連の研究を進め、マクロファージが糖尿病性腎症の進展に関与していることを明らかにしてきた。microinflammationは、動脈硬化やインスリン抵抗性の機序にも関連していることから、microinflammationを制御することがこれからの治療戦略に重要であり、広範囲な分野での今後の検討が望まれる。(著者抄録)

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  • 気腫性膀胱炎を発症した2型糖尿病の一例

    豊田 智子, 石井 啓太, 平田 教至, 小川 大輔, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   54 ( 6 )   450 - 450   2011.6

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  • 少量のインスリンで血糖コントロールが可能であったIA-2抗体強陽性1型糖尿病の1例

    松下 裕一, 四方 賢一, 寺見 隆宏, 梶谷 展生, 佐藤 千景, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   54 ( 6 )   441 - 441   2011.6

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  • 当院における糖尿病教室の取り組み

    高取 佐智子, 高樽 由美, 廣田 大昌, 佐藤 千景, 四方 賢一, 槇野 博史

    糖尿病   54 ( 6 )   454 - 454   2011.6

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

    Nobuyuki Miyatake, Kenichi Shikata, Hirofumi Makino, Takeyuki Numata

    Environmental health and preventive medicine   16 ( 3 )   191 - 5   2011.5

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    Objective We investigated the link between renal function as evaluated by estimated glomerular filtration rate (eGFR) and proteinuria in Okayama Prefecture, Japan. Subjects and methods A total of 11030 Japanese subjects, aged between 20 and 79 years, were recruited in a crosssectional clinical investigation study. eGFR was calculated using serum creatinine, age, and sex. Proteinuria was measured by using urine strip devices. Results Age-related variations in eGFR were noted. Two hundred sixteen men (6.2%) and 316 women (4.2%) were diagnosed with trace positive (±) and 140 men (4.0%) and 130 women (1.7%) were diagnosed with positive (?B) proteinuria. eGFR in subjects with ?B proteinuria was significantly lower than that in subjects without proteinuria, in both sexes. Conclusion The present study indicates that proteinuria might be an important marker in the etiology of lower eGFR in Okayama Prefecture, Japan. © 2010 The Japanese Society for Hygiene.

    DOI: 10.1007/s12199-010-0183-9

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  • 糖尿病性腎症におけるPPARδアゴニストの腎保護効果

    小川 大輔, 松下 裕一, 四方 賢一, 和田 淳, 佐藤 千景, 橘 洋美, 豊田 智子, 槇野 博史

    日本腎臓学会誌   53 ( 3 )   462 - 462   2011.5

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  • メタボリック症候群とCKDの関連に関する調査研究

    四方 賢一, 梶谷 展生, 宮武 伸行, 石井 啓太, 槇野 博史

    日本腎臓学会誌   53 ( 3 )   333 - 333   2011.5

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

    Motofumi Sasaki, Kenichi Shikata, Shinichi Okada, Satoshi Miyamoto, Shingo Nishishita, Hitomi Usui Kataoka, Chikage Sato, Jun Wada, Daisuke Ogawa, Hirofumi Makino

    Acta medica Okayama   65 ( 2 )   81 - 9   2011.4

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    Glomerular hyperfiltration is a common pathway leading to glomerulosclerosis in various kinds of kidney diseases. The 5/6 renal ablation is an established experimental animal model for glomerular hyperfiltration. On the other hand, low-grade inflammation is also a common mechanism for the progression of kidney diseases including diabetic nephropathy and atherosclerosis. Here we analyzed the gene expression profile in the remnant kidney tissues of 5/6 nephrectomized mice using a DNA microarmy system and compared it with that of sham-operated control mice. The 5/6 nephrectomized mice showed glomerular hypertrophy and an increase in the extracellular matrix in the glomeruli. DNA microarray analysis indicated the up-regulated expression of various kinds of genes related to the inflammatory process in remnant kidneys. We confirmed the up-regulated expression of platelet factor-4, and monocyte chemoattractant protein-1, 2, and 5 in remnant kidneys by RT-PCR. The current results; suggest that the inflammatory process is involved in the progression of glomerulosclerosis and is a common pathway of the pathogenesis of kidney disease.

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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 - 9   2011.4

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    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

    R. Kodera, K. Shikata, H. U. Kataoka, T. Takatsuka, S. Miyamoto, M. Sasaki, N. Kajitani, S. Nishishita, K. Sarai, D. Hirota, C. Sato, D. Ogawa, H. Makino

    DIABETOLOGIA   54 ( 4 )   965 - 978   2011.4

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    Glucagon-like peptide-1 (GLP-1) has various extra-pancreatic actions, in addition to its enhancement of insulin secretion from pancreatic beta cells. The GLP-1 receptor is produced in kidney tissue. However, the direct effect of GLP-1 on diabetic nephropathy remains unclear. Here we demonstrate that a GLP-1 receptor agonist, exendin-4, exerts renoprotective effects through its anti-inflammatory action via the GLP-1 receptor without lowering blood glucose.
    We administered exendin-4 at 10 mu g/kg body weight daily for 8 weeks to a streptozotocin-induced rat model of type 1 diabetes and evaluated their urinary albumin excretion, metabolic data, histology and morphometry. We also examined the direct effects of exendin-4 on glomerular endothelial cells and macrophages in vitro.
    Exendin-4 ameliorated albuminuria, glomerular hyperfiltration, glomerular hypertrophy and mesangial matrix expansion in the diabetic rats without changing blood pressure or body weight. Exendin-4 also prevented macrophage infiltration, and decreased protein levels of intercellular adhesion molecule-1 (ICAM-1) and type IV collagen, as well as decreasing oxidative stress and nuclear factor-kappa B activation in kidney tissue. In addition, we found that the GLP-1 receptor was produced on monocytes/macrophages and glomerular endothelial cells. We demonstrated that in vitro exendin-4 acted directly on the GLP-1 receptor, and attenuated release of pro-inflammatory cytokines from macrophages and ICAM-1 production on glomerular endothelial cells.
    These results indicate that GLP-1 receptor agonists may prevent disease progression in the early stage of diabetic nephropathy through direct effects on the GLP-1 receptor in kidney tissue.

    DOI: 10.1007/s00125-010-2028-x

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

    Noriko Toyota, Daisuke Ogawa, Keita Ishii, Kyoji Hirata, Jun Wada, Kenichi Shikata, Hirofumi Makino

    Acta medica Okayama   65 ( 2 )   129 - 33   2011.4

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    A 62-year-old woman with a history of poorly controlled type 2 diabetes mellitus was admitted to our hospital with a 3-week history of mild fever, vomiting, and anorexia. Abdominal computed tomography (CT) showed bilateral hydronephrosis and gas accumulation in the urinary bladder wall and left ureter. Laboratory tests showed leukocytosis and elevated C-reactive protein level. Urine culture showed heavy growth of Escherichia coli. The final diagnosis was emphysematous cystitis. The patient was treated with systemic antibiotics and drainage using a urethral catheter. The clinical and radiographic findings resolved rapidly, and she was discharged from the hospital on day 28. Emphysematous cystitis is a relatively rare urinary tract infection associated with gas formation, and has the potential for a serious outcome if untreated. Early detection by imaging studies such as CT is important in providing prompt treatment and favorable clinical outcome.

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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   2011.4

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    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.

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  • Galectin-9-Tim-3経路を介した1型糖尿病制御

    神崎 資子, 和田 淳, 中司 敦子, 村上 和敏, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 片山 晶博, 四方 賢一, 秋葉 久弥, 八木田 秀雄, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 105   2011.4

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  • メタボリックシンドロームにおけるphosphatidylethanolamine N-methyltransferase(PEMT)の意義

    中司 敦子, 和田 淳, 村上 和敏, 神崎 資子, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 片山 晶博, 四方 賢一, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 316   2011.4

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  • 糖尿病性腎症に重症インフルエンザ感染を併発しペラミビルが奏功した1例

    氏家 はる代, 小川 大輔, 那須 達世, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   54 ( 4 )   315 - 315   2011.4

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  • 運動負荷試験が有用であったミトコンドリア遺伝子異常による糖尿病の一例

    安田 麻衣子, 小野 哲一郎, 小川 愛由, 小川 大輔, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   54 ( 4 )   294 - 294   2011.4

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  • 追加発言 岡山県における取り組み

    四方 賢一, 加来 浩平, 岡崎 悟, 田中 茂人, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 29   2011.4

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  • 気腫性胆嚢炎を発症した統合失調症合併糖尿病の一例

    内田 治仁, 四方 賢一, 小川 愛由, 篠浦 歩, 横道 直佑, 八木 孝仁, 小川 大輔, 佐藤 千景, 和田 淳, 梶谷 展生, 槇野 博史

    糖尿病   54 ( 4 )   316 - 316   2011.4

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  • 新規脂肪細胞膜蛋白Gpnmbの同定

    片山 晶博, 和田 淳, 中司 敦子, 村上 和敏, 神崎 資子, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 肥田 和之, 四方 賢一, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 356   2011.4

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  • TelmisartanはPPAR-γ活性化を介した抗炎症作用により糖尿病性腎症の進展を抑制する

    梶谷 展生, 四方 賢一, 小寺 亮, 宮本 聡, 廣田 大昌, 佐藤 千景, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 127   2011.4

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  • PPARδアゴニストは抗炎症効果により糖尿病性腎症の進展を抑制する

    松下 裕一, 小川 大輔, 橘 洋美, 豊田 智子, 佐藤 千景, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 127   2011.4

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  • 糖尿病性腎症の糖鎖プロファイングの検討

    井上 謙太郎, 和田 淳, 中司 敦子, 村上 和敏, 神崎 資子, 寺見 隆宏, 勅使川原 早苗, 黒瀬 祐子, 片山 晶博, 小川 智央, 山田 雅雄, 四方 賢一, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 225   2011.4

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  • ACAMの脂肪分化とメタボリックシンドロームにおける意義

    村上 和敏, 和田 淳, 中司 敦子, 神崎 資子, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 片山 晶博, 四方 賢一, 槇野 博史

    糖尿病   54 ( Suppl.1 )   S - 132   2011.4

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  • eGFRとメタボリックシンドロームとの関係

    宮武 伸行, 四方 賢一, 槇野 博史, 沼田 健之

    糖尿病   54 ( Suppl.1 )   S - 355   2011.4

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

    Yuichi Matsushita, Daisuke Ogawa, Jun Wada, Noriko Yamamoto, Kenichi Shikata, Chikage Sato, Hiromi Tachibana, Noriko Toyota, Hirofumi Makino

    Diabetes   60 ( 3 )   960 - 8   2011.3

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    OBJECTIVE-Activation of the nuclear hormone receptor peroxisome proliferator-activated receptor (PPAR)-delta has been shown to improve insulin resistance, adiposity, and plasma HDL levels. Several studies have reported that activation of PPAR delta is atheroprotective; however, the role of PPAR delta in renal function remains unclear. Here, we report the renoprotective effects of PPAR delta activation in a model of streptozotocin-induced diabetic nephropathy.
    RESEARCH DESIGN AND METHODS-Eight-week-old male C57BL/6 mice were divided into three groups: 1) nondiabetic control mice, 2) diabetic mice, and,9) diabetic mice treated with the PPAR delta agonist GW0742 (1 mg/kg/day). GW0742 was administered by gavage for 8 weeks after inducing diabetes.
    RESULTS-GW0742 decreased urinary albumin excretion without altering blood glucose levels. Macrophage infiltration, mesangial matrix accumulation, and type IV collagen deposition were substantially attenuated by GW0742. The gene expression of inflammatory mediators in the kidney cortex, such as monocyte chemoattractant protein-1 (MCP-1) and osteopontin (OPN), was also suppressed. In vitro studies demonstrated that PPAR delta activation increased the expression of anti-inflammatory corepressor B-cell lymphoma-6, which subsequently suppressed MCP-1 and OPN expression.
    CONCLUSIONS-These findings uncover a previously unrecognized mechanism for the renoprotective effects of PPAR delta agonists and support the concept that PPAR delta agonists may offer a novel therapeutic approach for the treatment of diabetic nephropathy. Diabetes 60:960-968, 2011

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

    Atsuhito Tone, Kenichi Shikata, Koichi Nakagawa, Masaaki Hashimoto, Hirofumi Makino

    Clinical and experimental nephrology   15 ( 1 )   79 - 85   2011.2

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    Recent studies have shown the involvement of microinflammation in the pathogenesis of diabetic nephropathy. We previously demonstrated that erythromycin, one of the macrolides, ameliorated renal injury via anti-inflammatory effects in experimental diabetic rats. We conducted an open randomized controlled pilot study to investigate the renoprotective effect of clarithromycin for diabetic nephropathy in type 2 diabetic patients manifesting albuminuria.
    Sixteen patients were randomly assigned to the control (n = 8) or the CAM group in which they received 200 mg/day of clarithromycin (n = 8). At the beginning of the study and after 3 months of investigation, the following parameters were assessed: urinary albumin creatinine ratio (ACR), the levels of serum MCP-1, soluble ICAM-1, IL-18, IL-6 and hs-CRP, and the levels of urinary MCP-1 and IL-18.
    The changes in urinary ACR were significantly improved (P = 0.039), and serum creatinine levels showed a decreasing trend (P = 0.053) in the CAM group compared with the control group. Urinary MCP-1 levels were significantly reduced in the clarithromycin-administrated group (P = 0.009). However, there was no significant difference in other proinflammatory markers. A significant positive correlation was obtained between the post-to-pre-urinary ACR and the post-to-pre-urinary MCP-1 ratio(r = 0.526, P = 0.043). In the CAM group, the changes of serum creatinine also showed a significant positive correlation with those of urinary ACR, urinary MCP-1, urinary IL-18 and serum levels of soluble ICAM-1.
    The results from our study suggest that clarithromycin may attenuate the production of renal MCP-1 in type 2 diabetic patients, resulting in amelioration of urinary ACR via anti-inflammatory effects. Modulation of microinflammation with clarithromycin may provide a new approach for diabetic nephropathy.

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

    Chikage Sato, Kenichi Shikata, Daisho Hirota, Motofumi Sasaki, Shingo Nishishita, Satoshi Miyamoto, Ryo Kodera, Daisuke Ogawa, Atsuhito Tone, Hitomi Usui Kataoka, Jun Wada, Nobuo Kajitani, Hirofumi Makino

    Diabetes   60 ( 1 )   189 - 99   2011.1

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    OBJECTIVE An inflammatory process is involved in the mechanism of obesity-related insulin resistance. Recent studies indicate that monocyte chemoattractant protein-1 (MCP-1) is a major chemokine that promotes monocyte infiltration into adipose tissues; however, the adhesion pathway in adipose tissues remains unclear. We aimed to clarify the adhesion molecules that mediate monocyte infiltration into adipose tissue.
    RESEARCH DESIGN AND METHODS We used a DNA microarray to compare the gene expression profiles in epididymal white adipose tissues (eWAT) between db/db mice and C57/BL6 mice each fed a high-fat diet (HFD) or a low-fat diet (LFD). We investigated the change of insulin resistance and inflammation in eWAT in P-selectin glycoprotein ligand-1 (PSGL-1) homozygous knockout (PSGL-1(-/-)) mice compared with wild-type (WT) mice fed HFD.
    RESULTS DNA microarray analysis revealed that PSGL-1, a major ligand for selectins, is upregulated in eWAT from both db/db mice and WT mice fed HFD. Quantitative real-time RT-PCR and immunohistochemistry showed that PSGL-1 is expressed on both endothelial cells and macrophages in eWAT of obese mice. PSGL-1-/- mice fed HFD showed a remarkable reduction of macrophage accumulation and expression of proinflammatory genes, including MCP-1 in eWAT. Moreover, adipocyte hypertrophy, insulin resistance, lipid metabolism, and hepatic fatty change were improved in PSGL-1-/- mice compared with WT mice fed HFD.
    CONCLUSIONS These results indicate that PSGL-1 is a crucial adhesion molecule for the recruitment of monocytes into adipose tissues in obese mice, making it a candidate for a novel therapeutic target for the prevention of obesity-related insulin resistance. Diabetes 60:189-199, 2011

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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

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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

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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

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  • High glucose increases metallothionein expression in renal proximal tubular epithelial cells. International journal

    Daisuke Ogawa, Masato Asanuma, Ikuko Miyazaki, Hiromi Tachibana, Jun Wada, Norio Sogawa, Takeshi Sugaya, Shinji Kitamura, Yohei Maeshima, Kenichi Shikata, Hirofumi Makino

    Experimental diabetes research   2011   534872 - 534872   2011

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    Metallothionein(MT) is an intracellular metal-binding, cysteine-rich protein, and is a potent antioxidant that protects cells and tissues from oxidative stress. Although the major isoforms MT-1 and -2 (MT-1/-2) are highly inducible in many tissues, the distribution and role of MT-1/-2 in diabetic nephropathy are poorly understood. In this study, diabetes was induced in adult male rats by streptozotocin, and renal tissues were stained with antibodies for MT-1/-2. MT-1/-2 expression was also evaluated in mProx24 cells, a mouse renal proximal tubular epithelial cell line, stimulated with high glucose medium and pretreated with the antioxidant vitamin E. MT-1/-2 expression was gradually and dramatically increased, mainly in the proximal tubular epithelial cells and to a lesser extent in the podocytes in diabetic rats, but was hardly observed in control rats. MT-1/-2 expression was also increased by high glucose stimulation in mProx24 cells. Because the induction of MT was suppressed by pretreatment with vitamin E, the expression of MT-1/-2 is induced, at least in part, by high glucose-induced oxidative stress. These observations suggest that MT-1/-2 is induced in renal proximal tubular epithelial cells as an antioxidant to protect the kidney from oxidative stress, and may offer a novel therapeutic target against diabetic nephropathy.

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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

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  • 重度歯周炎により炎症反応高値・高熱を来した2型糖尿病の1例

    橘洋美, 和田淳, 曽我賢彦, 綿谷博雪, 神崎資子, 片山晶博, 小川大輔, 佐藤千景, 四方賢一, 槇野博史

    糖尿病   54 ( 6 )   2011

  • Comparison of ventilator threshold between subjects with and without proteinuria in Japanese.

    Miyatake N, Shikata K, Makino H, Numata T

    Health   3 ( 6 )   394 - 399   2011

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  • 糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 糖尿病性腎症の新規治療法の開発 糖尿病性腎症に対するGLP-1受容体作動薬の効果の検討

    四方賢一

    糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 平成22年度 総括・分担研究報告書   2011

  • 糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 糖尿病性腎症症例のレジストリーの作成

    和田隆志, 安部秀斉, 奥田誠也, 草野英二, 古家大祐, 佐藤博亮, 鈴木芳樹, 篁俊成, 羽田勝計, 槇野博史, 湯澤由紀夫, 荒木信一, 井関邦敏, 岩野正之, 四方賢一, 中村裕之, 二宮利治, 馬場園哲也, 原章規, 原茂子, 深水圭, 古市賢吾, 森潔, 守屋達美, 山本格, 横山仁, 横山宏樹

    糖尿病性腎症の病態解明と新規治療法確立のための評価法の開発 平成22年度 総括・分担研究報告書   2011

  • 糖尿病性腎症合同委員会ジョイントシンポジウム(日本糖尿病学会,日本腎臓学会,日本透析医学会)追加発言:岡山県における取り組み

    四方賢一, 加来浩平, 岡崎悟, 田中茂人, 槇野博史

    糖尿病   54 ( Supplement 1 )   2011

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

    Haruhito A Uchida, Yoshio Nakamura, Hisanao Norii, Masanobu Kaihara, Yoshihisa Hanayama, Ken-Ei Sada, Jun Wada, Kenichi Shikata, Hirofumi Makino

    Journal of diabetes investigation   1 ( 6 )   266 - 72   2010.12

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    Aims/Introduction: The combination of hypertension with diabetes mellitus (DM) has been recognized as a critical risk factor for cardiovascular disease (CVD). We investigated the blood pressure levels in hypertensive patients with DM (HDM patients) compared with those without DM (HnDM patients). Furthermore, we examined the effect of risk factors, including chronic kidney disease (CKD) and stroke, on the management of both office blood pressure (OBP) and morning home blood pressure (MHBP).
    Materials and Methods: OBP and MHBP were evaluated in 1230 essential hypertensive patients in 30 institutions. Among them, 366 (30%) were complicated with DM.
    Results: The ratio of masked hypertensives whose systolic OBP was &lt; 140 mmHg and systolic MHBP was more than 135 mmHg in HDM patients was significantly higher than that in HnDM patients (P &lt; 0.02). HDM patients had significantly lower systolic and diastolic OBP and diastolic MHBP than HnDM patients (P &lt; 0.05, respectively). However, systolic MHBP in HDM patients tended to be higher compared with HnDM patients (P = 0.0623). A stratified analysis showed that HDM patients with CKD or stroke had significantly higher systolic MHBP than others (P &lt; 0.05, respectively). The adjusted odds ratio for morning hypertension defined by a systolic MHBP more than 135 mmHg was significantly higher in the HDM patients with CKD (1.98) compared with HnDM patients without CKD (reference).
    Conclusions: Diabetes, CKD and stroke are risk factors for MHBP. More intensive treatment is needed to achieve the therapeutic goal for systolic MHBP in HDM patients, especially those who are complicated with CKD or stroke. (J Diabetes Invest, doi:10.1111/j.2040-1124.2010.00056.x, 2010).

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  • 炎症と治療 糖尿病性腎症の成因におけるMicroinflammation

    四方 賢一, 槇野 博史

    Diabetes Frontier   21 ( 6 )   735 - 735   2010.12

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  • 糖尿病性腎症の寛解を目指した新しい治療戦略

    四方 賢一

    Diabetes Frontier   21 ( 6 )   748 - 748   2010.12

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  • 【糖尿病性細小血管症(第2版) 発症・進展制御の最前線】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

    日本臨床   68 ( 増刊9 糖尿病性細小血管症 )   61 - 64   2010.11

  • 【糖尿病性細小血管症(第2版) 発症・進展制御の最前線】糖尿病性腎症 糖尿病性腎症の病理

    小寺 亮, 四方 賢一

    日本臨床   68 ( 増刊9 糖尿病性細小血管症 )   370 - 374   2010.11

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

    Nobuyuki Miyatake, Kenichi Shikata, Hirofumi Makino, Takeyuki Numata

    Acta medica Okayama   64 ( 5 )   339 - 43   2010.10

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    The link between changes in a subject's metabolic syndrome components and her estimated glomerular filtration rate (eGFR) was evaluated in healthy Japanese women. We used data for 53 Japanese women (46.0 +/- 10.9 years) with a 1-year follow up. eGFR was defined by a new equation developed for Japan. There were no significant relationships between eGFR and clinical parameters at baseline. Subjects were given advice for dietary and lifestyle improvement. At the 1-year follow up, eGFR was significantly increased. In addition, changes in eGFR were weakly correlated with systolic blood pressure (r = -0.306, p = 0.0260). A decrease in systolic blood pressure may be associated with improving eGFR in Japanese women.

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  • 糖尿病性腎症の進展におけるPPARδアゴニストの有効性の検討

    小川 大輔, 松下 裕一, 四方 賢一, 佐藤 千景, 和田 淳, 槇野 博史

    Diabetes Frontier   21 ( 5 )   618 - 618   2010.10

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  • 糖尿病マウスにおけるPPARδアゴニストの腎保護効果

    松下 裕一, 小川 大輔, 佐藤 千景, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病合併症   24 ( Suppl.1 )   106 - 106   2010.10

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  • 糖尿病腎症の新展開 Microinflammationの新たな展開

    四方 賢一, 槇野 博史

    糖尿病合併症   24 ( Suppl.1 )   50 - 50   2010.10

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  • 慢性合併症の臨床(腎症) 腎症の成因

    四方 賢一, 槇野 博史

    糖尿病学の進歩   ( 44 )   262 - 266   2010.9

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  • 【糖尿病の病態解析】白血球機能低下

    宮本 聡, 四方 賢一

    臨床検査   54 ( 9 )   1035 - 1039   2010.9

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    糖尿病患者では,感染症が発症・重症化しやすく,健常者に比し死亡率も高い.高血糖状態では白血球機能の障害,特に遊走能・走化性,貪食能,殺菌能の低下をきたすことがこれまでに報告されている.血行障害や神経障害なども易感染性に寄与しており,合併症の進行した糖尿病患者では特に留意する必要がある.高血糖により低下した白血球機能は血糖の是正により改善することが報告されており,感染症の発症・増悪を防ぐためには良好な血糖コントロールが必要である.(著者抄録)

    DOI: 10.11477/mf.1542102388

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2010&ichushi_jid=J01541&link_issn=&doc_id=20100907210011&doc_link_id=10.11477%2Fmf.1542102388&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1542102388&type=%E5%8C%BB%E6%9B%B8.jp_%E3%82%AA%E3%83%BC%E3%83%AB%E3%82%A2%E3%82%AF%E3%82%BB%E3%82%B9&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

  • Micro-inflammationと疾患 ペリオドンタルメディシン研究の可能性を探る 糖尿病血管合併症の成因としてのMicroinflammation

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    日本歯周病学会会誌   52 ( 秋季特別 )   57 - 57   2010.9

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  • 【糖尿病合併症とその治療に関するエポックメーキングトピックスの展開】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   2010.7

  • 【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】病期からみた糖尿病合併症対策 腎症の病期に応じた対応のポイント

    四方 賢一

    糖尿病UP-DATE   26 ( 26 )   196 - 203   2010.6

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    糖尿病性腎症には、病期に応じた治療が必要である。腎症の早期において出現し、心血管疾患のリスクファクターとされているアルブミン尿を減少、あるいは陰性化させることにより、腎症の予後改善のみならず、心血管疾患による死亡の抑制につながることが期待できる。(著者抄録)

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

    Nobuyuki Miyatake, Kenichi Shikata, Hirofumi Makino, Takeyuki Numata

    Acta medica Okayama   64 ( 3 )   203 - 8   2010.6

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    We investigated the link between renal function as evaluated by estimated glomerular filtration rate (eGFR) and metabolic syndrome in Japanese. A total of 11,711 Japanese subjects, aged 20-79 years, were recruited in a cross-sectional clinical investigation. From this group, we further investigated the data on 1,576 subjects. eGFR was calculated using serum creatinine (Cr), age and sex. The diagnosis of metabolic syndrome was based on the Japanese criteria. In the first analysis, 288 men (7.8%) and 498 women (6.2%) were diagnosed with reduced eGFR (&lt; 60 ml/min). eGFR was not correlated with anthropometric, body composition parameters in either sex. In the second analysis, in subjects without medications, 132 men (20.8%) and 15 women (1.6%) were diagnosed with metabolic syndrome. eGFR was lower in men with abdominal obesity and in women with hypertension was than in those without. Among Japanese not taking medications, lower eGFR may be a characteristic of men with abdominal obesity and of women with hypertension.

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  • 【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】病期からみた糖尿病合併症対策

    南條 輝志男, 羽田 勝計, 四方 賢一, 高木 均, 中村 二郎

    糖尿病UP-DATE   ( 26 )   222 - 235   2010.6

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  • 糖尿病血管合併症と炎症 高インスリン血症と血管炎症における転写因子の役割

    稻垣 暢也, 四方 賢一, 西尾 善彦, 前川 聡, 柏木 厚典

    糖尿病合併症   24 ( 1 )   83 - 86   2010.6

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  • 糖尿病血管合併症と炎症 日本人2型糖尿病の腫瘍壊死因子(TNF)、インスリン抵抗性、慢性血管合併症の関係について

    稻垣 暢也, 四方 賢一, 谷口 中, 福島 光夫, 中井 義勝, 長坂 昌一郎, 西村 英紀, 野村 慶雄, 黒江 彰, 清野 裕

    糖尿病合併症   24 ( 1 )   79 - 82   2010.6

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  • 糖尿病血管合併症と炎症 網膜症炎症病態におけるレニン-アンジオテンシン系の役割

    稻垣 暢也, 四方 賢一, 石田 晋

    糖尿病合併症   24 ( 1 )   93 - 98   2010.6

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  • 糖尿病血管合併症と炎症 肥満と血管炎症

    稻垣 暢也, 四方 賢一, 真鍋 一郎

    糖尿病合併症   24 ( 1 )   87 - 92   2010.6

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  • 【糖尿病と慢性腎臓病(CKD)】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   2010.5

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

    Nobuo Kajitani, Kenichi Shikata, Akihiko Nakamura, Tatsuaki Nakatou, Makoto Hiramatsu, Hirofumi Makino

    Diabetes research and clinical practice   88 ( 2 )   171 - 6   2010.5

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    Aim: This study aimed to evaluate the change of serum levels of proinflammatory molecules in patients with type 2 diabetes and clarify the involvement of these molecules in diabetic nephropathy and atherosclerosis.
    Methods: Sixty-six Japanese type 2 diabetic patients (T2DM) and 39 healthy control subjects were enrolled. We assessed clinical parameters, urinary albumin excretion rate (AER), brachial-ankle pulse wave velocity (baPWV), intima media thickness (IMT) and serum levels of proinflammatory molecules.
    Results: Serum levels of IL-6, IP-10 and MCP-1 were significantly higher in T2DM than in control subjects. In T2DM, serum levels of high-sensitivity (hs) CRP, IP-10, hsTNF-alpha, VCAM-1 and E-selectin were positively correlated with AER. Serum levels of IP-10, hsTNF-alpha and VCAM-1 were positively correlated with baPWV. Serum levels of hsCRP, IL-6, IP-10 and hSTNF-alpha were positively correlated with IMT. Multiple linear regression analysis revealed that serum levels of hsTNF-alpha were independently associated with AER (beta = 0.235, P = 0.038) and serum levels of IP-10 were independently associated with baPWV (beta = 0.209, P = 0.047) and IMT (beta = 0.303, P = 0.032).
    Conclusion: Our results suggest that low-grade inflammation, microinflammation, may be a common risk factor for diabetic nephropathy and atherosclerosis in Japanese type 2 diabetic patients. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

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  • Comparison of Insulin Detemir and Insulin Glargine on Glycemic Variability in Patients with Type 1 and Type 2 Diabetes

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

    EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES   118 ( 5 )   320 - 324   2010.5

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    Aims: To compare the glycemic variability of insulin detemir and insulin glargine in type 1 and type 2 diabetic patients.
    Methods: 15 type 1 and 14 type 2 diabetic patients receiving intensive insulin therapy with insulin glargine were enrolled. Before and after switching insulin glargine to insulin detemir, we assessed fasting glucose variability using the standard deviation (SD) and the coefficient of variance (CV) of self-monitored fasting blood sugar (FBS) levels.
    Results: The SD and CV values were significantly decreased in type 1 diabetes after switching the therapy, though there was no significant difference in type 2 diabetes. The frequency of hypoglycemia was decreased in type 1 diabetes and there was no change in type 2 diabetes. The changes of the CV value also showed significant positive correlation with fasting serum CPR levels in all patients and total insulin dose in type 1 diabetes. The changes of frequency of hypoglycemia showed significant positive correlation with total and basal insulin dose adjusted for body weight in type 1 diabetes.
    Conclusion: The present study demonstrated lower within-subject variability of insulin detemir compared to insulin glargine, suggesting that the basal insulin replacement with insulin detemir may provide a useful therapeutic strategy for uncontrolled type 1 diabetes with high glucose variability.

    DOI: 10.1055/s-0029-1243230

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  • メタボリック症候群・慢性腎臓病の核内受容体をターゲットとした治療

    中司 敦子, 和田 淳, 影近 弘之, 肥田 和之, 村上 和敏, 神崎 資子, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 小川 大輔, 四方 賢一, 槇野 博史

    日本腎臓学会誌   52 ( 3 )   321 - 321   2010.5

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  • 【インスリン抵抗性】総論 インスリン抵抗性と腎機能障害

    梶谷 展生, 四方 賢一

    ホルモンと臨床   58 ( 5 )   369 - 373   2010.5

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  • 糖尿病性腎症研究の新たな展望 糖尿病性腎症の進展における血管新生関連因子の重要性と治療応用

    前島 洋平, 四方 賢一, 槇野 博史

    日本腎臓学会誌   52 ( 3 )   258 - 258   2010.5

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  • 糖尿病性腎症の進展における核内受容体PPARδの役割の検討

    小川 大輔, 松下 裕一, 四方 賢一, 和田 淳, 佐藤 千景, 槇野 博史

    日本腎臓学会誌   52 ( 3 )   321 - 321   2010.5

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  • ORIENT Studyサブ解析 尿蛋白とイベントの関連に対する検討

    四方 賢一, 伊藤 貞嘉, 羽田 勝計, 今井 圓裕, Chan Juliana CN, 槇野 博史

    日本腎臓学会誌   52 ( 3 )   287 - 287   2010.5

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  • Trends in development of diabetic nephropathy treatment

    The Cell   42 ( 4 )   147 - 150   2010.4

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  • Galectin-9-Tim-3経路を介した1型糖尿病制御

    神崎 資子, 和田 淳, 中司 敦子, 村上 和敏, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 四方 賢一, 秋葉 久弥, 八木田 秀雄, 槇野 博史

    糖尿病   53 ( Suppl.1 )   S - 236   2010.4

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  • ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

    勅使川原 早苗, 和田 淳, 中司 敦子, 村上 和敏, 神崎 資子, 井上 謙太郎, 寺見 隆宏, 松下 裕一, 利根 淳仁, 伊勢田 泉, 肥田 和之, 宮武 伸行, 堀田 紀久子, 四方 賢一, 槇野 博史

    糖尿病   53 ( Suppl.1 )   S - 164   2010.4

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  • P-selectin glycoprotein ligand-1(PSGL-1)を阻害することにより肥満マウスのインスリン抵抗性が改善する

    廣田 大昌, 四方 賢一, 佐藤 千景, 宮本 聡, 小寺 亮, 梶谷 展生, 高塚 哲全, 小川 大輔, 槇野 博史

    糖尿病   53 ( Suppl.1 )   S - 248   2010.4

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  • 糖尿病性腎症におけるPPARδアゴニストの有効性の検討

    松下 裕一, 小川 大輔, 佐藤 千景, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   53 ( Suppl.1 )   S - 167   2010.4

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  • メタボリック症候群・慢性腎臓病の核内受容体をターゲットとした治療

    和田 淳, 中司 敦子, 影近 弘之, 肥田 和之, 村上 和敏, 神崎 資子, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 小川 大輔, 四方 賢一, 槇野 博史

    糖尿病   53 ( Suppl.1 )   S - 251   2010.4

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  • 【脂質異常症 明日からの実地診療に役立つ最新の知識】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   2010.3

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  • A Case of Elderly-Onset Type 1 Diabetes with First-Degree Family History with Negative GAD Antibody and Positive IA-2 Antibody

    ASANO Michiko, TONE Atsuhito, KATAYAMA Akihiro, FURUJO Mahoko, HIGUCHI Chigusa, TSUKAMOTO Keiko, ISEDA Izumi, HIDA Kazuyuki, UESU Tokurou, SHIKATA Kenichi

    Journal of the Japan Diabetes Society   53 ( 3 )   174 - 179   2010.3

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    A 50-year-old man, whose second of two daughters was treated for type 1 diabetes, seen for polyuria and weight loss in August 2008 had been found to have HbA1C of 6.2% in an annual physical cheakup in April 2008. He was hospitalized for markedly elevated HbA1C of 10.3% and plasma glucose of 463 mg/dl detected in a blood test. Laboratory studies showed a urinary CPR concentration of 21.9 &mu;g/day and serum CPR of 0.2 ng/ml before and 0.4 ng/ml 6 minutes after glucagon administration, indicating decreased insulin secretion. Intensive insulin therapy was initiated. Although GAD antibody was negative, IA-2 antibody was positive (9.1 U/ml) , leading to a diagnosis of type 1 diabetes mellitus. HLA typing was DRB1*010101 and 090102, type 1 diabetes-susceptibility gene, identical to the typing of his second daughter. This case of elderly-onset of type 1 diabetes is interesting, manifesting negative GAD antibody and positive IA-2 antibody, especially with a family history of type 1 diabetes.<br>

    DOI: 10.11213/tonyobyo.53.174

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    Other Link: http://search.jamas.or.jp/link/ui/2010173707

  • 【新たなステージへ進む糖尿病診療】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   2010.3

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    Other Link: http://search.jamas.or.jp/link/ui/2010134426

  • Diabetic Nephropathy Remission and Regression Team Trial in Japan (DNETT-Japan): Rationale and study design. International journal

    Kenichi Shikata, Masakazu Haneda, Daisuke Koya, Yoshiki Suzuki, Yasuhiko Tomino, Kenichi Yamada, Shiro Maeda, Norito Kawakami, Takashi Uzu, Motonobu Nishimura, Chikage Sato, Daisuke Ogawa, Hirofumi Makino

    Diabetes research and clinical practice   87 ( 2 )   228 - 32   2010.2

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    The prevalence of end-stage renal disease (ESRD) is uprising in the paralleled with the increase of chronic kidney disease (CKD) patients. Diabetic nephropathy (DN) is the most important underlying disease of CKD and a leading cause of ESRD in Japan. Intensified multifactorial intervention in patients with type 2 diabetes with microalbuminuria slows the progression to nephropathy, and progression of retinopathy and autonomic neuropathy. However, further studies are needed to establish the effect of intensified multifactorial treatment on DN with overt proteinuria. In this trial, doctors and co-medicals collaborate to treat the DN patients to prevent the deterioration of DN by multifactorial intensive therapy. Diabetic Nephropathy Remission and Regression Team Trial in Japan (DNETT-Japan) is an open, randomized controlled trial to evaluate the efficacy of renal protection of multifactorial intensive therapy in type 2 diabetes patients with overt proteinuria (urinary albumin-to-creatinine ratio &gt;= 300 mg/g creatinine). The study has a targeted enrollment of 600 Japanese patients, and divided into two protocols by renal insufficiency (protocol A: serum creatinine: &lt;1.2 mg/dl in male and &lt;1.0 mg/dl in female, and protocol B: serum creatinine: 1.2-2.5 mg/dl in male and 1.0-2.5 mg/dl in female). The patients were allocated standard treatment or intensive multifactorial treatment. Intensive treatment was a step-wise implementation of behavior modification, pharmacological therapy targeting hyperglycaemia, hypertension, dyslipidaemia, and proteinuria. The primary outcome is the proteinuria in protocol A and the composite endpoint of time to the first occurrence of doubling of serum creatinine, ESRD (the need for chronic dialysis, or renal transplantation) or death in protocol B. The follow-up period is 5 years and the study ends in 2014. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

    DOI: 10.1016/j.diabres.2009.09.025

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  • Influencing factors for dietary behaviors of patients with diabetic nephropathy.

    Kazuko Sumiyoshi, Chieko Kawata, Kenichi Shikata, Hirofumi Makino

    Acta medica Okayama   64 ( 1 )   39 - 47   2010.2

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    The aim of this study was to clarify the factors influencing the dietary behavior of patients with diabetic nephropathy. One hundred twenty-two patients with type 2 diabetes were recruited from the outpatients of Okayama University Hospital in Okayama, Japan. We performed a cross-sectional study using a questionnaire including 206 items among 18 categories as follows: background factors, coping behavior (coping scale), degree of uncertainty in illness (uncertainty scale), and dietary behavior. The data were analyzed by correlation analysis, t-test, one-way analysis of variance, Pearson correlation analysis, and multiple regression analysis. We found that those patients with microalbuminuria alone tended to recognize more mild about their kidney status than those with macroalbuminuria and chronic renal failure. We also found that common factors influencing the dietary behavior of diabetic patients with and without nephropathy are as follows: 1. coping with the problem (beta = 03,12, P &lt; 0.01); 2. anxiety about prognosis (beta = -0.344, p &lt; 0.0 1); 3. sex (beta = -0.234, p &lt; 0.05); 4. uncertainty regarding treatment (beta = 0.377, p &lt; 0.01); 5. negative coping (beta = -0.354, p &lt; 0.01); and 6. employment status (beta = 0.367, p &lt; 0.01). Coping and uncertainty in illness had a significant relation to positive support and lack of support. To maintain appropriate dietary behavior in diabetic patients, medical staff need to determine what the social supports are important for the patient, and also to ensure good communication among healthcare personnel as well as positive support for patients and families.

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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

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

    Nobuyuki Miyatake, Kenichi Shikata, Hirofumi Makino, Takeyuki Numata

    Internal medicine (Tokyo, Japan)   49 ( 14 )   1315 - 20   2010

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    Objective We investigated the link between renal function as evaluated by estimated glomerular filtration rate (eGFR) and pulse wave velocity (PWV) in Japanese without medications.
    Methods A total of 1,244 Japanese subjects, aged 20-79 years, were recruited in a cross-sectional clinical investigation study. They received no medications. eGFR was calculated using serum creatinine (Cr), age and sex. Peripheral arterial stiffness was evaluated by brachial-ankle PWV (baPWV).
    Results eGFR and baPWV were significantly correlated with age. eGFR was negatively correlated with baPWV (men: r=-0.308, p&lt;0.0001, women: r=-0.293, p&lt;0.0001). Twenty-six men (5.6%) and 35 women (4.5%) were diagnosed as reduced eGFR (eGFR &lt;60 mL/min/1.73 m(2)). We compared clinical parameters between subjects with reduced eGFR (Group R) and without such reduction (Group N). baPWV in Group R was significantly higher than that in Group N even after adjusting for age. In women, systolic blood pressure in Group R was also significantly higher than that in Group N.
    Conclusion eGFR was closely associated with peripheral arterial stiffness in Japanese.

    DOI: 10.2169/internalmedicine.49.3085

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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

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  • 4.腎不全期.

    四方賢一

    糖尿病 最新の治療   172 - 173   2010

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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

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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

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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

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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

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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

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  • CKDの早期発見・予防・治療標準化・進展阻止に関する調査研究 CKDの早期発見,予防,治療標準化,進展阻止に関する調査研究に関する研究

    四方賢一

    CKDの早期発見・予防・治療標準化・進展阻止に関する調査研究 平成21年度 総括・分担研究報告書   2010

  • P-selectin glycoprotein ligand-1(PSGL-1)ノックアウトマウスを用いた内臓脂肪炎症のメカニズムの解析

    佐藤千景, 四方賢一, 廣田大昌, 宮本聡, 小寺亮, 小川大輔, 梶谷展生, 槇野博史

    日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集   24th   2010

  • ブシラミン内服が誘因となったインスリン自己免疫症候群の1例

    松下 裕一, 和田 淳, 更井 啓, 四方 賢一, 足羽 敦子, 槇野 博史

    糖尿病   52 ( 12 )   984 - 984   2009.12

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  • ミトコンドリア糖尿病患者の組織間におけるミトコンドリア遺伝子3243(A-G)変異率の検討

    松下 由美, 西田 亙, 中西 公王, 藤沢 義人, 能美 幸信, 中村 舞, 高田 康徳, 四方 賢一, 大沼 裕, 牧野 英一, 大澤 春彦

    糖尿病   52 ( 12 )   983 - 983   2009.12

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  • 生体肝移植により血糖コントロールが改善した非代償性肝硬変患者の1例 周術期代謝・栄養学的指標の推移

    長谷川 祐子, 野口 絢子, 田中 暁美, 坂本 八千代, 吉田 龍一, 八木 孝仁, 四方 賢一

    日本病態栄養学会誌   12 ( 5 )   219 - 219   2009.12

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  • 人工関節置換術後にケトアシドーシスを発症し劇症1型糖尿病と診断された1例

    更井 啓, 四方 賢一, 広越 久美子, 大谷 寛之, 松下 裕一, 和田 淳, 安原 章浩, 藤原 一夫, 槇野 博史

    糖尿病   52 ( 12 )   987 - 987   2009.12

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  • 【合併症や併発疾患を伴う糖尿病の薬物治療】腎機能障害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   2009.10

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  • 【糖尿病性腎症 成因解明と寛解をめざした治療戦略】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   2009.10

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

    Kei Sarai, Kenichi Shikata, Yasushi Shikata, Kazuyoshi Omori, Naomi Watanabe, Motofumi Sasaki, Shingo Nishishita, Jun Wada, Noriko Goda, Noriyuki Kataoka, Hirofumi Makino

    American journal of physiology. Cell physiology   297 ( 4 )   C945-54 - C954   2009.10

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    Sarai K, Shikata K, Shikata Y, Omori K, Watanabe N, Sasaki M, Nishishita S, Wada J, Goda N, Kataoka N, Makino H. Endothelial barrier protection by FTY720 under hyperglycemic condition: involvement of focal adhesion kinase, small GTPases, and adherens junction proteins. Am J Physiol Cell Physiol 297: C945-C954, 2009. First published August 5, 2009; doi:10.1152/ajpcell.00606.2008.-Recently, sphingosine 1-phosphate (S1P) has been highlighted as an endothelial barrier-stabilizing mediator. FTY720 is a S1P analog originally developed as a novel immunosuppressant. The phosphorylated form of FTY720 binds to S1P receptors to exert S1P-like biological effects, suggesting endothelial barrier promotion by FTY720. To elucidate whether FTY720 induces signaling events related to endothelial barrier enhancement under hyperglycemic conditions, human microvascular endothelial cells (HMVECs) preincubated with hyperglycemic (30 mM) medium were treated with 100 nM FTY720 for 3 h. Immunofluorescent microscopy and coprecipitation study revealed FTY720-induced focal adhesion kinase (FAK)-associated adherens junction (AJ) assembly at cell-cell contacts coincident with formation of a prominent cortical actin ring. FTY720 also induced transmonolayer electrical resistance (TER) augmentation in HMVEC monolayers in both normoglycemic and hyperglycemic conditions, implying endothelial barrier enhancement. Similar to S1P, site-specific FAK tyrosine phosphorylation analysis revealed FTY720-induced FAK [Y(576)] phosphorylation without phosphorylation of FAK [Y(397)/Y(925)]. Furthermore, FTY720 conditioned the phosphorylation profile of FAK [Y(397)/Y(576)/Y(925)] in hyperglycemic medium to the same pattern observed in normoglycemic medium. FTY720 challenge resulted in small GTPase Rac activation under hyperglycemic conditions, whereas increased Rho activity in hyperglycemic medium was restored to the basal level. Rac protein depletion by small interfering RNA (siRNA) technique completely abolished FTY720-induced FAK [Y(576)] phosphorylation. These findings strongly suggest the barrier protective effect of FTY720 on HMVEC monolayers in hyperglycemic medium via S1P signaling, further implying the possibility of FTY720 as a therapeutic agent of diabetic vascular disorder.

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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   2009.10

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    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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  • 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   2009.10

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    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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  • 免疫抑制薬の臨床応用実践論(第23回) 糖尿病性腎症

    小寺 亮, 四方 賢一

    炎症と免疫   17 ( 6 )   714 - 718   2009.10

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    糖尿病性腎症の進展には血管を主体とした微小な炎症(microinflammation)が関連していることをわれわれは証明してきた。現在、免疫抑制薬が糖尿病性腎症の治療に使用されることはないが、動物モデルでは、スタチンやチアゾリジン誘導体に加えて免疫抑制薬も、抗炎症作用を介して腎症の進展を抑制する。実際の臨床応用までには多くの解決すべき問題があるが、今後、臨床試験を積み重ねることにより、将来的に、免疫抑制薬が糖尿病性腎症の新たな治療薬となる可能性も期待される。(著者抄録)

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  • 肥満・脂肪細胞 抗PSGL-1抗体はdb/dbマウスのインスリン抵抗性を改善する

    廣田 大昌, 四方 賢一, 佐藤 千景, 佐々木 基史, 西下 伸吾, 宮本 聡, 小寺 亮, 梶谷 展生, 小川 大輔, 槇野 博史

    糖尿病合併症   23 ( Suppl.1 )   80 - 80   2009.9

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  • 糖尿病足病変 重症化予防フットケアの実際

    高樽 由美, 四方 賢一, 槇野 博史

    糖尿病合併症   23 ( Suppl.1 )   60 - 60   2009.9

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  • 腎症:遺伝子 糖尿病で3期腎症を合併した人が退院後の食事療法に抱く思い

    前川 ゆかり, 高樽 由美, 藤原 幸恵, 佐々木 可奈, 高取 佐智子, 佐藤 千景, 四方 賢一, 槇野 博史

    糖尿病合併症   23 ( Suppl.1 )   98 - 98   2009.9

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

    Hideo Kohka Takahashi, Shuji Mori, Hidenori Wake, Keyue Liu, Tadashi Yoshino, Katsuhisa Ohashi, Noriaki Tanaka, Kenichi Shikata, Hirofumi Makino, Masahiro Nishibori

    The Journal of pharmacology and experimental therapeutics   330 ( 1 )   89 - 98   2009.7

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    Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to diverse reducing sugars. Accumulation of AGEs induces diabetes complications. Microinflammation is a common major mechanism in the pathogenesis of diabetic vascular complications. Activation of monocytes/macrophages and T cells plays roles in the pathogenesis of atherosclerosis. The activation of T cells requires the enhanced expression of adhesion molecules on monocytes. AGEs activate monocytes by engaging the receptor for AGE (RAGE); however, little is known about the profile of agonist activity of diverse AGE moieties on monocytes. We investigated the effect of four distinct AGE subtypes (AGE-modified bovine serum albumin; AGE-2, AGE-3, AGE-4, and AGE-5) at concentrations ranging from 0.1 to 100 mu g/ml on the expression of intercellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes and its impact on the production of interferon-gamma and tumor necrosis factor-alpha in human peripheral blood mononuclear cells. Among the AGEs examined, AGE-2 and AGE-3 selectively induced adhesion molecule expression and cytokine production. Antagonism experiments using antibodies against adhesion molecules demonstrated that cell-to-cell interaction between monocytes and T/natural killer cells was involved in AGE-2-and AGE-3-induced cytokine production. AGE-2 and AGE-3 up-regulated the expression of RAGE on monocytes. The effects of AGE-2 and AGE-3 were inhibited by nuclear factor-kappa B and p38 mitogen-activated protein kinase inhibitors. These results indicated that AGE-2 and AGE-3 activated monocytes via RAGE, leading to the up-regulation of adhesion molecule expression and cytokine production.

    DOI: 10.1124/jpet.109.150581

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  • 【糖尿病のすべて】糖尿病の合併症 糖尿病がひきおこす細小血管症 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   2009.5

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

    Xiaoguang Sun, Yasushi Shikata, Lichun Wang, Kazuyoshi Ohmori, Naoko Watanabe, Jun Wada, Kenichi Shikata, Konstantin G Birukov, Hirofumi Makino, Jeffrey R Jacobson, Steven M Dudek, Joe G N Garcia

    Microvascular research   77 ( 3 )   304 - 13   2009.5

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    Sphingosine 1-phosphate (S1P) is an important vascular barrier regulatory agonist which enhances the junctional integrity of human lung endothelial cell monolayers. We have now demonstrated that S1P induced cortical actin ring formation and redistribution of focal adhesion kinase (FAK) and paxillin to the cell periphery suggesting the critical role of cell-cell adhesion in endothelial barrier enhancement. Co-immunoprecipitation studies revealed increased association of VE-cadherin with FAK and paxillin in S1P-challenged human pulmonary artery endothelial cell (HPAEC) monolayers. Furthermore, SIP-induced enhancement of VE-cadherin interaction with alpha-catenin and beta-catenin was associated with the increased formation of FAK-beta-catenin protein complexes. Depletion of beta-catenin (siRNA) resulted in loss of S1P-mediated VE-cadherin association with FAK and paxillin rearrangement. Furthermore, transendothelial electrical resistance (an index of barrier function) demonstrated that beta-catenin siRNA significantly attenuated S1P-induced barrier enhancement. These results demonstrate a mechanism of S1P-induced endothelial barrier enhancement via beta-catenin-linked adherens junction and focal adhesion interaction. (C) 2009 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.mvr.2008.12.004

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  • 【生活習慣病看護における看護師の役割】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, 大橋 睦子

    外来看護最前線: 生活習慣病&外来がん看護   14 ( 4 )   32 - 43   2009.4

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  • 【今すぐに役立つ輸液ガイドブック】維持輸液、栄養輸液、経腸栄養 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

    綜合臨床   58 ( 増刊 )   1032 - 1038   2009.4

  • 糖尿病性腎症の糖鎖プロファイリングの検討

    井上 謙太郎, 和田 淳, 中司 敦子, 村上 和敏, 神崎 資子, 寺見 隆宏, 勅使川原 早苗, 黒瀬 祐子, 小川 智央, 山田 雅雄, 四方 賢一, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 220   2009.4

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    J-GLOBAL

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  • Galectin-9-Tim-3経路による1型糖尿病制御

    神崎 資子, 和田 淳, 中司 敦子, 村上 和敏, 勅使川原 早苗, 寺見 隆宏, 井上 謙太郎, 黒瀬 祐子, 四方 賢一, 秋葉 久弥, 八木田 秀雄, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 300   2009.4

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  • 糖尿病性腎症の発症・進展におけるシアロアドヘジン陽性マクロファージの役割の検討

    梶谷 展生, 四方 賢一, 永瀬 亮, 佐々木 基史, 宮本 聡, 小寺 亮, 廣田 大昌, 佐藤 千景, 西下 伸吾, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 302   2009.4

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  • 糖尿病性血管障害におけるedaravoneの腎保護作用についての検討

    更井 啓, 四方 賢一, 四方 泰史, 大森 一慶, 渡邊 直美, 和田 淳, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 302   2009.4

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  • ACAMの脂肪分化とメタボリックシンドロームにおける意義

    村上 和敏, 和田 淳, 中司 敦子, 勅使川原 早苗, 神崎 資子, 吉川 理津子, 寺見 隆宏, 井上 謙太郎, 黒瀬 祐子, 四方 賢一, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 162   2009.4

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  • 糖尿病とCKD 管理の面から チーム医療による集約的治療の意義

    四方 賢一, 佐藤 千景, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 68   2009.4

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  • RXRアンタゴニストによる細胞周期異常制御とメタボリック症候群

    中司 敦子, 和田 淳, 村上 和敏, 神崎 資子, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 黒瀬 祐子, 四方 賢一, 影近 弘之, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 246   2009.4

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  • ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

    勅使川原 早苗, 和田 淳, 中司 敦子, 村上 和敏, 神崎 資子, 肥田 和之, 伊勢田 泉, 利根 淳仁, 松下 裕一, 宮武 伸行, 井上 謙太郎, 寺見 隆宏, 黒瀬 裕子, 四方 賢一, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 245   2009.4

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  • 抗PSGL-1抗体はdb/dbマウスのインスリン抵抗性を改善する

    廣田 大昌, 四方 賢一, 佐藤 千景, 佐々木 基史, 西下 伸吾, 宮本 聡, 小寺 亮, 梶谷 展生, 小川 大輔, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 247   2009.4

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  • 高脂肪食負荷PSGL-1 KOマウスの内臓脂肪および肝臓における炎症性変化とインスリン抵抗性

    佐藤 千景, 四方 賢一, 廣田 大昌, 佐々木 基史, 小川 大輔, 西下 伸吾, 宮本 聡, 小寺 亮, 梶谷 展生, 槇野 博史

    糖尿病   52 ( Suppl.1 )   S - 247   2009.4

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  • 【脂質異常症 基本を踏まえた実践】こんな病態にはどうすべきか? 腎疾患・CKD

    四方 賢一

    内科   103 ( 1 )   96 - 99   2009.1

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    慢性腎臓病(CKD)は、米国において最初に提唱された疾患概念であり、蛋白尿とGFRの低下によって診断される慢性的な腎障害を総称したものである。CKDにおいては、LDLコレステロールと中性脂質の軽度上昇と、HDLコレステロールの低下傾向を認めることが多いが、ネフローゼ症候群をきたした場合には、リポ蛋白合成亢進と代謝低下に伴う著明な高LDLコレステロール血症をきたす。一方、総コレステロール、非HDLコレステロールの上昇とHDLコレステロールの低下がCKD発症の危険因子であることが明らかにされている。CKDにおける脂質管理の目標値に関するエビデンスは少ないが、日本腎臓学会による『CKD診療ガイド』では、LDLコレステロール120mg/dl未満(可能であれば100mg/dl未満)を管理目標値とすることを推奨している。スタチンとフィブラート系薬には、いずれも横紋筋融解症の副作用が報告されているが、腎機能障害時にはとくにフィブラート系薬による横紋筋融解症の危険性が高くなるため、注意が必要である。(著者抄録)

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2009&ichushi_jid=J00974&link_issn=&doc_id=20081225240017&doc_link_id=issn%3D0022-1961%26volume%3D103%26issue%3D1%26spage%3D96&url=http%3A%2F%2Fwww.pieronline.jp%2Fopenurl%3Fissn%3D0022-1961%26volume%3D103%26issue%3D1%26spage%3D96&type=PierOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00005_2.gif

  • Microinflammationをターゲットとした新しい治療戦略

    四方 賢一

    HUMAN SCIENCE   20 ( 1 )   37 - 37   2009.1

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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

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  • 糖尿病性腎症の糖鎖プロファイリングの検討

    井上謙太郎, 和田淳, 中司敦子, 村上和敏, 神崎資子, 寺見隆宏, 勅使川原早苗, 黒瀬祐子, 小川智央, 山田雅雄, 四方賢一, 槇野博史

    糖尿病   52 ( Supplement 1 )   2009

  • Exendin4による抗炎症作用を介した腎保護作用

    小寺亮, 片岡仁美, 四方賢一, 佐藤千景, 佐々木基史, 西下伸吾, 宮本聡, 廣田大昌, 梶谷展生, 槇野博史

    日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集   23rd   2009

  • 高脂肪食負荷PSGL-1 KOマウスの内臓脂肪におけるマクロファージ浸潤とインスリン抵抗性の変化

    佐藤千景, 四方賢一, 廣田大昌, 佐々木基史, 小川大介, 西下伸吾, 宮本聡, 小寺亮, 梶谷展生, 槇野博史

    日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集   23rd   2009

  • 腎症:遺伝子 糖尿病性腎症の糖鎖プロファイリングの検討

    井上謙太郎, 和田淳, 中司敦子, 村上和敏, 神崎資子, 寺見隆宏, 勅使川原早苗, 小川智央, 山田雅雄, 四方賢一, 槇野博史

    糖尿病合併症   23 ( Supplement 1 )   2009

  • 遺伝子改変動物を用いた糖尿病性腎症の成因の解明~Microinflammationを標的とした治療戦略開発の試み~

    四方賢一, 片岡仁美, 佐々木基史, 西下伸吾, 宮本聡, 小寺亮, 廣田大昌, 梶谷展生, 佐藤千景, 槇野博史

    日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集   23rd   2009

  • 生活習慣病に対するチーム・岡大の取り組み

    坂本 八千代, 大橋 睦子, 中内 麻里, 出石 通博, 一村 光子, 堅山 佳美, 四方 賢一

    日本病態栄養学会誌   11 ( 5 )   152 - 152   2008.12

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  • 糖尿病の画像診断 糖尿病性腎症の画像診断 MRあるいはシンチなどでの画像診断が可能であるかどうか

    佐々木 基史, 四方 賢一

    Diabetes Frontier   19 ( 6 )   729 - 731   2008.12

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  • Concept of diabetic nephropathy, classification of disease stage, diagnosis

    Japanese journal of clinical medicine   66 ( 増刊9 新時代の糖尿病学(4) )   230 - 233   2008.11

  • 腎機能評価としてのクレアチニンクリアランス予測式の有用性に関する比較検討

    赤澤 明日美, 岩井 富美恵, 矢尾 和久, 西原 茂樹, 黒田 智, 北川 航平, 田中 靖子, 川上 恭弘, 四方 賢一, 千堂 年昭

    臨床薬理   39 ( Suppl. )   S223 - S223   2008.11

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  • 【新時代の糖尿病学 病因・診断・治療研究の進歩】糖尿病のフォローアップシステム チーム医療 DNETT-Japan

    四方 賢一, 槇野 博史

    日本臨床   66 ( 増刊9 新時代の糖尿病学(4) )   511 - 514   2008.11

  • 【CKD×糖尿病 血糖・血圧コントロールの重要性】「CKD×糖尿病」に必要な管理 血圧

    梶谷 展生, 四方 賢一, 槇野 博史

    薬局   59 ( 12 )   3361 - 3365   2008.11

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  • 【高血圧の治療 エビデンスに基づいたアプローチ】糖尿病性腎症合併高血圧の治療

    梶谷 展生, 四方 賢一, 槇野 博史

    日本医師会雑誌   137 ( 8 )   1663 - 1666   2008.11

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  • 血管新生抑制因子Vasohibin-1による糖尿病腎症進展抑制効果の検討

    那須 達世, 前島 洋平, 木野村 賢, 広越 久美子, 田邊 克幸, 斎藤 大輔, 杉山 斉, 四方 賢一, 園田 光, 佐藤 靖史, 槇野 博史

    Diabetes Frontier   19 ( 5 )   683 - 684   2008.10

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  • 【糖尿病性腎症治療の進歩】糖尿病性腎症治療におけるMicroinflammation制御の意義

    四方 賢一

    BIO Clinica   23 ( 11 )   1025 - 1030   2008.10

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    糖尿病性腎症の腎組織には、動脈硬化巣と同様に、マクロファージを主体とする炎症細胞浸潤、細胞接着分子やケモカインの発現と炎症性サイトカインの増加など、炎症と共通した特徴が認められる。このような血管を主座とする軽微な炎症をmicroinflammationと呼んでいる。Microinflammationは糖尿病血管合併症に共通した重要な進展因子の一つと考えられる。ACE阻害薬、ARB、スタチン製剤やチアゾリジン誘導体などは、本来の血圧、コレステロール、血糖降下作用とは独立して抗炎症作用を持つことが知られており、糖尿病動物において抗炎症作用を介して腎保護効果を示すことが明らかとなっている。糖尿病患者の治療に際して、血糖、血圧、脂質の管理に加えて、microinflammationを制御することにより、合併症の進展をより効果的に抑制できることが期待される。(著者抄録)

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

    Atsuhito Tone, Kenichi Shikata, Koichi Nakagawa, Masaaki Hashimoto, Hirofumi Makino

    Diabetes research and clinical practice   81 ( 3 )   e15-6 - e16   2008.9

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  • ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

    勅使川原 早苗, 和田 淳, 中司 敦子, 村上 和敏, 神崎 資子, 寺見 隆宏, 井上 謙太郎, 肥田 和之, 伊勢田 泉, 利根 淳仁, 松下 裕一, 宮武 伸行, 四方 賢一, 槇野 博史

    肥満研究   14 ( Suppl. )   196 - 196   2008.9

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  • 著明な低体温と乳酸アシドーシスを合併した高齢糖尿病の1例

    木下 智香子, 永瀬 亮, 藤木 茂篤, 四方 賢一

    津山中央病院医学雑誌   22 ( 1 )   89 - 93   2008.9

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    86歳女。患者は意識障害を主訴とした。35年前から糖尿病でインスリン治療を受けていたが、HbA1c 10%以上とコントロール不良であった。今回、嘔吐して倒れ、救急搬送された。所見では血糖高値で、血液ガス分析でAG上昇を伴う代謝性アシドーシスが認められた。そのため、糖尿病性ケトアシドーシス(DKA)を疑い、インスリン持続静注、生理的食塩水の点滴を開始した。しかし、3時間を経てもアシドーシスや血糖の改善を認めず、ICU入室後は食道温が29.8℃であり、保温を開始した。体温の回復とともに血糖値、乳酸値も改善し、血液検査では総ケトン体の上昇を認めたが、DKAにしては高値ではなく、動脈血pH6.93、乳酸値6.6mmol/lと診断基準を満たしていた。ことから本症例は乳酸アシドーシスと診断され、血糖コントロール、脱水の補正、アルカリ化を図り、意識状態は改善した。以上、本症例はコントロール不良な糖尿病であり、腎不全、脱水、肺炎等様々な負荷因子が加わり、乳酸アシドーシスが生じたものと考えられた。

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  • ACAMの脂肪分化とメタボリックシンドロームにおける意義

    村上 和敏, 和田 淳, 中司 敦子, 勅使川原 早苗, 神崎 資子, 寺見 隆宏, 井上 謙太郎, 四方 賢一, 槇野 博史

    肥満研究   14 ( Suppl. )   176 - 176   2008.9

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  • 糖尿病療養指導に必要な知識 インスリン導入に伴う諸問題

    四方 賢一

    糖尿病の療養指導: 糖尿病学の進歩   42回   92 - 94   2008.9

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  • The 2007 Okayama Medical Association Awards: Macrophage scavenger receptor-A: deficient mice are resistant to diabetic nephropathy through amelioration of microinflammation

    120 ( 2 )   143 - 147   2008.8

  • 糖尿病性腎症 病態解明と治療の進歩 Microinflammationをターゲットとした新たな治療戦略の可能性

    佐々木 基史, 四方 賢一, 槙野 博史

    糖尿病合併症   22 ( 2 )   164 - 166   2008.8

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  • 【Pros & Cons 糖尿病腎症と慢性腎臓病(CKD)】多量の蛋白尿あるいは腎機能低下例では早めに腎臓医に管理を依頼すべきである Cons 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   2008.7

  • 【特定健診・保健指導で知っておきたい糖尿病予防・治療の最新知見】腎症の予防と治療

    四方 賢一

    地域保健   39 ( 7 )   48 - 51   2008.7

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  • 糖尿病合併症予防のための患者教育 療養指導、看護、および心理面を含めたアプローチ 糖尿病血管合併症を予防するためのチーム医療 腎症に対する集約的治療の試み

    四方 賢一, 槇野 博史

    糖尿病合併症   22 ( 1 )   59 - 62   2008.7

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  • 【腎機能と画像診断】糖尿病の腎画像診断の考え方

    佐々木 基史, 四方 賢一, 槇野 博史

    成人病と生活習慣病   38 ( 7 )   835 - 837   2008.7

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    糖尿病性腎症の画像所見として腎肥大が認められる。腎肥大の評価方法には、腹部超音波、腹部CTなどの方法があるが、腹部超音波が非侵襲的かつ簡便である。糖尿病性腎症の診断において、画像診断は必須ではないが、腎症診断に参考となる所見を得ることができる。特に腎症以外の腎疾患との鑑別が必要である場合に有用である。主に海外において、糖尿病性腎症をシンチグラムを使って評価する試みがなされている。シンチグラムによる診断を糖尿病患者に行っていくことは現実的ではないが、シンチグラムから得られる情報は、腎症の発症メカニズムの解明や新たな治療戦略開発に有用である可能性がある。(著者抄録)

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2008&ichushi_jid=J03723&link_issn=&doc_id=20080807180014&doc_link_id=%2Faq9seijd%2F2008%2F003807%2F015%2F0835-0837%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faq9seijd%2F2008%2F003807%2F015%2F0835-0837%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • 【糖尿病診療に必要な検査ABC】糖尿病合併症のための検査と評価 糖尿病腎症の検査と評価

    廣田 大昌, 四方 賢一, 槇野 博史

    綜合臨床   57 ( 7 )   1947 - 1951   2008.7

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    糖尿病腎症(以下腎症)は糖尿病の細小血管合併症の一つであり、糖代謝異常により発症・進展し、慢性の経過をたどる。また、1998年に透析導入原因疾患の第1位となって以降は年々増加し続け、2006年には透析導入原因の42.9%を占めている。さらに、透析療法に至った糖尿病患者の5年生存率は約50%ときわめて不良であり、早期に診断し進展を阻止することは、患者の生命やQOL維持への貢献のみならず、糖尿病患者数の増加を考慮すれば医療経済的にも重要な課題である。しかし末期になるまで臨床症状に乏しいため、早期から積極的に検査を行い、発症の診断や病期の評価を続けることが不可欠である。(著者抄録)

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2008&ichushi_jid=J00779&link_issn=&doc_id=20080704190019&doc_link_id=%2Faf2sgrsa%2F2008%2F005707%2F019%2F1947-1951%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faf2sgrsa%2F2008%2F005707%2F019%2F1947-1951%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • 【ネフローゼ症候群 最新の知見】糖尿病性腎症

    四方 賢一, 槇野 博史

    腎と透析   64 ( 6 )   945 - 950   2008.6

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  • 【産婦人科ホルモン療法マニュアル】周産期 糖尿病・妊娠糖尿病合併妊娠

    平松 祐司, 四方 賢一

    産科と婦人科   75 ( Suppl. )   101 - 108   2008.4

  • ヒト血中Vaspin濃度の検討とメタボリックシンドロームにおける意義

    勅使川原 早苗, 和田 淳, 中司 敦子, 村上 和敏, 肥田 和之, 伊勢田 泉, 利根 淳仁, 松下 裕一, 宮武 伸行, 井上 謙太郎, 寺見 隆宏, 四方 賢一, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 308   2008.4

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  • 糖尿病合併症に関する最近の知見 慢性腎臓病(CKD)からみた糖尿病性腎症

    四方 賢一

    分子糖尿病学の進歩: 基礎から臨床まで   2008   138 - 146   2008.4

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  • Galectin-9による1型糖尿病発症抑制の検討

    神崎 資子, 和田 淳, 吉川 理津子, 中司 敦子, 村上 和敏, 安原 章浩, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 四方 賢一, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 211   2008.4

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  • 糖尿病腎症 研究の最前線 糖尿病性腎症の成因とMicroinflammation 新しい治療戦略の開発を目指して

    四方 賢一, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 23   2008.4

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  • 糖尿病におけるアディポネクチンの腎保護効果 アディポネクチン欠損マウスでは糖尿病誘発後の腎障害が増悪する

    西下 伸吾, 四方 賢一, 窪田 直人, 門脇 孝, 佐々木 基史, 宮本 聡, 佐藤 千景, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 297   2008.4

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  • 糖尿病・脂肪肝モデル動物FLSマウスの腎障害:チアゾリジン誘導体とARBの効果

    藤澤 智巳, 下吉 里実, 野嶋 孝次, 浅野 克明, 深井 綾, 新堂 修康, 吉川 由貴, 四方 賢一, 槇野 博史, 池上 博司, 楽木 宏実

    糖尿病   51 ( Suppl.1 )   S - 296   2008.4

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  • Vaspinのメタボリックシンドロームにおける意義

    中司 敦子, 和田 淳, 村上 和敏, 神崎 資子, 安原 章浩, 吉川 理津子, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 四方 賢一, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 307   2008.4

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  • ACAMの脂肪分化とメタボリックシンドロームにおける意義

    村上 和敏, 和田 淳, 中司 敦子, 神崎 資子, 安原 章浩, 吉川 理津子, 勅使川原 早苗, 井上 謙太郎, 寺見 隆宏, 四方 賢一, 槇野 博史

    糖尿病   51 ( Suppl.1 )   S - 306   2008.4

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  • 糖尿病性腎症の診療指針

    槇野 博史, 四方 賢一, 前島 洋平, 古家 大祐, 羽田 勝計

    日本腎臓学会誌   50 ( 3 )   224 - 224   2008.4

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  • 糖尿病 臨床分野での進歩 CKDにおける糖尿病性腎症の意義

    西下 伸吾, 四方 賢一, 槇野 博史

    Annual Review糖尿病・代謝・内分泌   2008   34 - 39   2008.1

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  • ガイドライン 糖尿病患者における血圧管理

    佐々木 基史, 四方 賢一, 槇野 博史

    岡山医学会雑誌   119 ( 3 )   311 - 313   2008.1

  • ウイルス性結膜炎罹患後に発症し、CSIIが有効であった高齢発症1型糖尿病の1例

    廣田 大昌, 佐々木 基史, 四方 賢一, 大森 一慶, 小寺 亮, 和田 淳, 安原 章浩, 槇野 博史, 羽井佐 茂

    糖尿病   51 ( 1 )   58 - 58   2008.1

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  • 著明な低体温と乳酸アシドーシスを合併した高齢糖尿病の1例

    木下 智香子, 永瀬 亮, 四方 賢一

    糖尿病   51 ( 1 )   55 - 55   2008.1

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  • 糖尿病性自律神経障害と鑑別を要したShy-Drager症候群の1例

    安原 章浩, 和田 淳, 四方 賢一, 槇野 博史, 神谷 達司

    糖尿病   51 ( 1 )   59 - 59   2008.1

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  • 一過性の舞踏様運動を呈した緩徐進行1型糖尿病の1例

    田中 由希子, 永瀬 亮, 四方 賢一

    糖尿病   51 ( 1 )   59 - 59   2008.1

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  • 糖尿病血管合併症の成因における炎症の関与

    梶谷 展生, 四方 賢一, 中村 明彦, 北村 卓也, 中塔 辰明, 槇野 博史

    糖尿病   51 ( 1 )   73 - 73   2008.1

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  • 膵性糖尿病の経過中に抗インスリン抗体を伴う低血糖が出現した1例

    大森 一慶, 四方 賢一, 井上 淳子, 和田 淳, 槇野 博史

    糖尿病   51 ( 1 )   62 - 62   2008.1

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  • 糖尿病性舞踏病を発症した多腺性自己免疫症候群3型の1例

    安原 章浩, 和田 淳, 四方 賢一, 槇野 博史, 出口 健太郎

    糖尿病   51 ( 1 )   81 - 81   2008.1

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  • 糖尿病性腎症に膜性増殖性腎炎を併発し、血液透析導入を要した1例

    佐々木 佐起子, 金尾 浩一郎, 笠原 順子, 大田 祥子, 谷合 一陽, 四方 賢一

    糖尿病   51 ( 1 )   74 - 74   2008.1

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  • The 2007 Okayama Medical Association Awards: Macrophage scavenger receptor-A: deficient mice are resistant to diabetic nephropathy through amelioration of microinflammation

    120 ( 2 )   143 - 147   2008

  • 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

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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―.

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    山口県 内科医会誌   ( 8 )   6 - 7   2008

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  • Pros & Cons 糖尿病性腎症と慢性腎臓病.

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    糖尿病診療マスター   4   378 - 385   2008

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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

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  • Edaravone mimics sphingosine-1-phosphate-induced endothelial barrier enhancement in human microvascular endothelial cells. International journal

    Kazuyoshi Omori, Yasushi Shikata, Kei Sarai, Naomi Watanabe, Jun Wada, Noriko Goda, Noriyuki Kataoka, Kenichi Shikata, Hirofumi Makino

    American journal of physiology. Cell physiology   293 ( 5 )   C1523-31 - C1531   2007.11

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    Edaravone is a potent scavenger of hydroxyl radicals and is quite successful in patients with acute cerebral ischemia, and several organ-protective effects have been reported. Treatment of human microvascular endothelial cells with edaravone (1.5 mu M) resulted in the enhancement of transmonolayer electrical resistance coincident with cortical actin enhancement and redistribution of focal adhesion proteins and adherens junction proteins to the cell periphery. Edaravone also induced small GTPase Rac activation and focal adhesion kinase (FAK; Tyr(576)) phosphorylation associated with sphingosine-1-phosphate receptor type 1 (S1P(1)) transactivation. S1P(1) protein depletion by the short interfering RNA technique completely abolished edaravone-induced FAK ( Tyr576) phosphorylation and Rac activation. This is the first report of edaravone-induced endothelial barrier enhancement coincident with focal adhesion remodeling and cytoskeletal rearrangement associated with Rac activation via S1P(1) transactivation. Considering the well-established endothelial barrier-protective effect of S1P, endothelial barrier enhancement as a consequence of S1P(1) transactivation may at least partly be the potent mechanisms for the organ-protective effect of edaravone and is suggestive of edaravone as a therapeutic agent against systemic vascular barrier disorder.

    DOI: 10.1152/ajpcell.00524.2006

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  • 【腎臓病のすべて】腎臓の病気 糖尿病性腎症

    西下 伸吾, 四方 賢一, 槇野 博史

    からだの科学   ( 255 )   32 - 35   2007.11

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  • 臨床試験における安全性評価項目としてのQT/QTc間隔評価方法の検討

    高橋 里沙, 岩井 富美恵, 黒田 智, 西原 茂樹, 矢尾 和久, 北川 航平, 川上 恭弘, 四方 賢一, 千堂 年昭

    臨床薬理   38 ( Suppl. )   S223 - S223   2007.11

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  • 岡山大学NST研修第2回を実施しての報告

    坂本 八千代, 野口 絢子, 内藤 稔, 伊野 英男, 石田 瞭, 出石 通博, 内田 慶子, 大橋 睦子, 住吉 由紀子, 四方 賢一

    日本病態栄養学会誌   10 ( 4 )   569 - 569   2007.11

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  • 基礎講座 糖尿病モデル動物 腎症モデル

    佐々木 基史, 四方 賢一, 槇野 博史

    Diabetes Frontier   18 ( 5 )   531 - 534   2007.10

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  • 糖尿病性腎症の成因におけるMacrophage scavenger receptor Aの役割

    片岡 仁美, 四方 賢一, 佐々木 基史, 岡田 震一, 小川 大輔, 西下 伸吾, 宮本 聡, 佐藤 千景, 槇野 博史

    Diabetes Frontier   18 ( 5 )   587 - 587   2007.10

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  • 【CKD(慢性腎臓病) 日本人の新しいGFR推算式への期待】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 )   795 - 798   2007.9

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    糖尿病性腎症はCKDのなかでも近年増加しつづけている疾患であり、新規透析導入患者の主要原疾患のなかで42%を占め、生命予後も不良である。糖尿病性腎症を可能なかぎり早期に診断しかつ的確な治療を開始するため、最近になって糖尿病性腎症の早期診断基準が改訂され、日常の外来診療においても簡便に診断を行うことが可能となった。糖尿病性腎症の治療は血糖・脂質管理・蛋白摂取制限が主体であり、大規模臨床試験によりエビデンスが集積されてきている。とくに最近になって、進行した病期においても集約的治療によりアルブミン尿・蛋白尿が減少し組織学的な変化も改善しうるとの報告が散見されるようになった。腎症の進展を抑制するばかりではなく、remission(寛解)、regression(退縮)をめざした集約的治療を行うことがこれからの糖尿病性腎症治療に求められる。(著者抄録)

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2007&ichushi_jid=J00060&link_issn=&doc_id=20070906100006&doc_link_id=%2Faa7ayuma%2F2007%2F022210%2F007%2F0795-0798%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faa7ayuma%2F2007%2F022210%2F007%2F0795-0798%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • Edaravone protects from endothelial barrier injuries under diabetic condition

    K. Sarai, Y. Shikata, K. Shikata, K. Ohmori, N. Watanabe, J. Wada, H. Makino

    DIABETOLOGIA   50   S93 - S94   2007.9

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  • 糖尿病性腎症 病態解明と治療の進歩 Microinflammationをターゲットとした新たな治療戦略の可能性

    佐々木 基史, 四方 賢一, 槇野 博史

    糖尿病合併症   21 ( Suppl.1 )   56 - 56   2007.9

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  • 脂肪細胞分化 ACAMトランスジェニックマウスとメタボリック症候群

    村上 和敏, 和田 淳, 中司 敦子, 神崎 資子, 勅使川原 早苗, 四方 賢一, 槇野 博史

    肥満研究   13 ( Suppl. )   157 - 157   2007.9

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  • 【慢性腎臓病 新しい展開】慢性腎臓病を見直す 今、なぜ慢性腎臓病か?

    佐藤 千景, 四方 賢一, 槇野 博史

    カレントテラピー   25 ( 9 )   721 - 724   2007.9

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  • 糖尿病合併症予防のための患者教育 療養指導、看護、および心理面を含めたアプローチ 糖尿病血管合併症を予防するためのチーム医療 腎症に対する集約的治療の試み

    四方 賢一

    糖尿病合併症   21 ( Suppl.1 )   45 - 45   2007.9

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  • Vaspinとメタボリック症候群

    中司 敦子, 和田 淳, 村上 和敏, 神崎 資子, 勅使川原 早苗, 四方 賢一, 槇野 博史

    肥満研究   13 ( Suppl. )   193 - 193   2007.9

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  • 腎症 糖尿病性腎症の成因におけるアディポネクチンの機能 アディポネクチンノックアウトマウスを用いた検討

    西下 伸吾, 四方 賢一, 窪田 直人, 門脇 孝, 佐々木 基史, 宮本 聡, 佐藤 千景, 槇野 博史

    糖尿病合併症   21 ( Suppl.1 )   108 - 108   2007.9

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  • 糖尿病・脂肪肝モデル動物FLSマウスの腎障害 ARBの効果

    下吉 里実, 藤澤 智巳, 池上 博司, 四方 賢一, 槇野 博史, 荻原 俊男

    日本腎臓学会誌   49 ( 6 )   725 - 725   2007.8

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  • 【慢性腎臓病 CKDキャンペーンをめぐる話題】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

    四方 賢一, 槇野 博史

    内科   100 ( 1 )   74 - 78   2007.7

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    わが国では、2型糖尿病の増加に伴って糖尿病性腎症は増加の一途をたどり、透析導入原因疾患の第1位を占めている。最近の疫学研究の結果より、日本人2型糖尿病患者の40%以上がアルブミン尿陽性であると推定される。糖尿病性腎症の治療の基本は、(1)血糖の管理、(2)血圧の管理、(3)レニン-アンジオテンシン系(RA系)の抑制、(4)食事療法(塩分、蛋白質の制限)、(5)禁煙などの生活習慣の改善であり、これらの治療を臨床研究によるエビデンスに基づいて的確に行う必要がある。近年、わが国においても、Kumamoto study,Japan-IDDM,RENAAL study,INNOVATION,SMARTなどの臨床研究により、血糖コントロールと、アンジオテンシン変換酵素(ACE)阻害薬/アンジオテンシンII受容体拮抗薬(ARB)のエビデンスが集積されつつある。最近、早期腎症は厳格な管理により高率に寛解することが明らかとなり、糖尿病性腎症の治療は、従来の進展を遅らせるための治療の時代から、寛解を目指した集約的治療が求められる時代に入った。今後、日本人のエビデンスを積み重ねることにより、わが国における腎症の集約的治療法の確立が期待される。(著者抄録)

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  • [Microinflammation in the pathogenesis of diabetic nephropathy].

    Kenichi Shikata

    Nihon Jinzo Gakkai shi   49 ( 5 )   474 - 480   2007.7

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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 )   635 - 638   2007.6

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

    Ritsuko Yoshikawa, Jun Wada, Kousuke Seiki, Takashi Matsuoka, Satoshi Miyamoto, Kenji Takahashi, Sachiko Ota, Kazuhi Taniai, Kazuyuki Hida, Minoru Yamakado, Kenichi Shikata, Yoshio Uehara, Yoshihiro Urade, Hirofumi Makino

    Diabetes research and clinical practice   76 ( 3 )   358 - 67   2007.6

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    Background: The presence of metabolic syndrome has been shown to be predictors of cardiovascular morbidity and mortality in patients with type 2 diabetes. In a cross-sectional clinical study, we investigated the association of metabolic syndrome with asymptomatic lacunar strokes and cardiovascular disease (CVD) and we compared its significance with urinary protein markers.
    Methods: We studied Japanese type 2 diabetes patients (n = 233, men = 124, women = 109). The diagnosis of metabolic syndrome was made according to WHO and International Diabetes Federation (IDF) criteria. Cardiovascular events were recorded and asymptomatic lacunar lesions were evaluated with magnetic resonance imaging (MRI). We also measured urinary levels of albumin, type IV collagen, beta 2-microglobulin (beta 2MG), N-acetyl-beta-D-glucosaminidase (NAG) and lipocalin-type prostaglandin D synthase (PGDS).
    Results: The prevalence of metabolic syndrome is 31.3% (IDF) and 52% (WHO) in 233 patients and microalbuminuria was present in 62 subjects (26.6%). Metabolic syndrome (WHO) significantly associated with asymptomatic lacunar lesions (p = 0.035, OR = 2.854, CI 1.075-7.579), while metabolic syndrome (IDF) or urinary markers failed to associate with presence of asymptomatic lacunar lesions. The presence of metabolic syndrome or microalbuminuria did not show significant association with CVD; however, the elevation of beta 2MG, NAG and PGDS showed significant association with CVD. By a logistic regression analysis using urinary proteins as independent variables, the presence of higher PGDS excretion independently associated with history of CVD (p = 0.025, OR= 3.847, CI 1.180-12.545).
    Conclusions: In type 2 diabetes patients, the elevation of urinary PGDS secretion closely associated with cardiovascular events and may be a supplemental or additional marker to the criteria of metabolic syndrome. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

    DOI: 10.1016/j.diabres.2006.09.004

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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

    Pharma Medica   25 ( 6 )   194 - 194   2007.6

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  • 【糖尿病の実践的外来治療】糖尿病性腎症の診断と治療

    佐藤 千景, 四方 賢一, 槇野 博史

    Diabetes Frontier   18 ( 3 )   259 - 263   2007.6

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  • Blood glucose management in diabetic patients

    119 ( 1 )   75 - 77   2007.5

  • 十二指腸乳頭部癌術後の増悪を契機に診断されたバセドウ病合併緩徐進行1型糖尿病の1例

    永瀬 亮, 四方 賢一

    糖尿病   50 ( 5 )   355 - 355   2007.5

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  • microinflammationとしての糖尿病性腎症

    槇野 博史, 四方 賢一

    Pharma Medica   25 ( 5 )   195 - 198   2007.5

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  • 蛋白尿出現後に発症したミトコンドリア3243A-G変異糖尿病の1例

    武智 恵, 西田 亙, 岡村 美里, 川村 良一, 高田 康徳, 柱本 満, 大澤 春彦, 牧野 英一, 三好 賢一, 四方 賢一, 藤澤 義人

    糖尿病   50 ( 5 )   339 - 339   2007.5

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  • インスリンアナログへの変更により低血糖発作が改善した抗インスリン抗体陽性糖尿病の1例

    佐藤 千景, 四方 賢一, 渡辺 直美, 丸井 幸之助, 和田 淳, 槇野 博史

    糖尿病   50 ( 5 )   337 - 337   2007.5

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  • 著明な低血糖を伴った悪性血管周皮腫の1例

    村上 和敏, 和田 淳, 神崎 資子, 利根 淳仁, 三宅 剛平, 四方 賢一, 槇野 博史

    糖尿病   50 ( 5 )   342 - 342   2007.5

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  • 横紋筋融解症から急性腎不全を発症した清涼飲料水ケトーシスの1例

    中尾 一志, 利根 淳仁, 三宅 剛平, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   50 ( 5 )   340 - 340   2007.5

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  • バセドウ病ともやもや病を合併し経過中に脳梗塞を発症した1型糖尿病の1例

    更井 啓, 四方 賢一, 大森 一慶, 佐藤 千景, 西下 伸吾, 和田 淳, 鈴木 二郎, 大塚 文男, 槇野 博史, 山本 久美子, 佐々原 渉

    糖尿病   50 ( 5 )   356 - 356   2007.5

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

    Masako Tabuchi, Katsumi Inoue, Hitomi Usui-Kataoka, Kazuko Kobayashi, Misako Teramoto, Koji Takasugi, Kenichi Shikata, Masahiro Yamamura, Kenji Ando, Keiichiro Nishida, Junko Kasahara, Noriaki Kume, Luis R Lopez, Kazuaki Mitsudo, Masakiyo Nobuyoshi, Tatsuji Yasuda, Toru Kita, Hirofumi Makino, Eiji Matsuura

    Journal of lipid research   48 ( 4 )   768 - 81   2007.4

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    C-reactive protein (CRP) is one of the strongest independent predictors of cardiovascular disease. We have previously reported that oxidized LDL (oxLDL) interacts with beta 2-glycoprotein I (beta 2GPI), implicating oxLDL/P2GPI complexes as putative autoantigens in autoimmune-mediated atherosclerotic vascular disease. In this study, we investigated the interaction of CRP with oxLDL/beta 2GPI complexes and its association with atherosclerosis in patients with diabetes mellitus (DM). CRP/oxLDL/R2GPI complexes were predominantly found in sera of DM patients with atherosclerosis. In contrast, noncomplexed CRP isoforms were present in sera of patients with acute/chronic inflammation, i.e., various pyrogenic diseases, rheumatoid arthritis (RA), and DM. Immunohistochemistry staining colocalized CRP and beta 2GPI together with oxLDL in carotid artery plaques but not in synovial tissue from RA patients, strongly suggesting that complex formation occurs during the development of adierosclerosis. Serum levels of CRP correlated with soluble forms of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and oxLDL/beta 2GPI complexes correlated with total cholesterol and hemoglobin Al c. Thus, the generation of CRP/oxLDL/beta 2GPI complexes seems to be associated with arterial inflammation, hyperglycemia, and hypercholesterolemia. CRP/oxLDL/R2GPI complexes can be distinguished from pyrogenic noncomplexed CRP isoforms and may represent a more specific and predictive marker for atherosclerosis.

    DOI: 10.1194/jlr.M600414-JLR200

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

    Sakiko Ohga, Kenichi Shikata, Kosuke Yozai, Shinichi Okada, Daisuke Ogawa, Hitomi Usui, Jun Wada, Yasushi Shikata, Hirofumi Makino

    American journal of physiology. Renal physiology   292 ( 4 )   F1141-50 - F1150   2007.4

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    Thiazolidinedione (TZD), a ligand for peroxisome proliferator-activated receptor-gamma (PPAR-gamma), exerts anti-inflammatory effects independently of the insulin-sensitizing effect. In the present study, we tested the hypothesis that TZD prevents the progression of diabetic nephropathy by modulating the inflammatory process. Five-week-old Sprague-Dawley rats were divided into three groups: 1) nondiabetic control rats (non-DM), 2) diabetic rats (DM), and 3) diabetic rats treated with pioglitazone (DM + pio). Diabetes was induced by injection with streptozotocin (STZ). The DM + pio group received 0.0002% pioglitazone mixed in chow for 8 wk after induction of diabetes. Blood glucose and HbA1c were elevated in diabetic rats but did not change by treatment with pioglitazone. Pioglitazone reduced urinary albumin excretion and glomerular hypertrophy, suppressed the expression of transforming growth factor (TGF)-beta, type IV collagen, and ICAM-1, and infiltration of macrophages in the kidneys of diabetic rats. Furthermore, renal NF-kappa B activity was increased in diabetic rats and reduced by pioglitazone. PPAR-gamma was expressed in glomerular endothelial cells in the diabetic kidney and in cultured glomerular endothelial cells. High-glucose conditions increased the expression of ICAM-1 and the activation of NF-kappa B in cultured glomerular endothelial cells. These changes were reduced by pioglitazone, ciglitazone, and pyrrolidine dithiocarbamate, an inhibitor of NF-kappa B. However, pioglitazone did not show the changes in the presence of PPAR-kappa B antagonist GW9662. Our results suggest that the preventive effects of pioglitazone may be mediated by its anti-inflammatory actions, including inhibition of NF-kappa B activation, ICAM-1 expression, and macrophage infiltration in the diabetic kidney.

    DOI: 10.1152/ajprenal.00288.2005

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  • 慢性腎臓病(CKD)の概念と糖尿病 糖尿病性腎症とチーム医療 DENETT-Japanの取り組み

    槇野 博史, 四方 賢一

    糖尿病   50 ( Suppl.1 )   S - 9   2007.4

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  • Vaspin(visceral adipose tissue-derived serpin)とインスリン抵抗性

    中司 敦子, 和田 淳, 村上 和敏, 勅使川原 早苗, 吉川 理津子, 神崎 資子, 四方 賢一, 槇野 博史

    糖尿病   50 ( Suppl.1 )   S - 166   2007.4

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  • Adipocyte adhesion molecule(ACAM)トランスジェニックマウスとメタボリックシンドローム

    村上 和敏, 和田 淳, 中司 敦子, 勅使川原 早苗, 吉川 理津子, 神崎 資子, 安原 章浩, 四方 賢一, 槇野 博史

    糖尿病   50 ( Suppl.1 )   S - 163   2007.4

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  • 肥満マウスの内臓脂肪における炎症関連遺伝子の発現プロファイルと白血球接着分子の役割に関する検討

    佐藤 千景, 四方 賢一, 利根 淳仁, 佐々木 基史, 佐々木 佐起子, 西下 伸吾, 宮本 聡, 和田 淳, 更井 啓, 槇野 博史

    糖尿病   50 ( Suppl.1 )   S - 220   2007.4

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  • Cholecystokinin(CCK)は抗炎症作用を介して糖尿病腎症の進展を抑制する

    佐々木 基史, 四方 賢一, 宮本 聡, 西下 伸吾, 佐藤 千景, 更井 啓, 利根 淳仁, 舩越 顕博, 宮坂 京子, 和田 淳, 眞野 博史

    糖尿病   50 ( Suppl.1 )   S - 83   2007.4

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  • 糖尿病腎症の寛解を目指した診断と治療

    四方 賢一

    糖尿病   50 ( Suppl.1 )   S - 71   2007.4

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  • FTY720はスフィンゴシン1リン酸(S1P)類似の作用により、高糖濃度下で内皮細胞保護効果を示す

    更井 啓, 四方 泰史, 大森 一慶, 渡邊 直美, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   50 ( Suppl.1 )   S - 112   2007.4

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  • メタボリックシンドロームと尿蛋白異常との関連

    宮武 伸行, 和田 淳, 四方 賢一, 槇野 博史, 沼田 健之

    糖尿病   50 ( Suppl.1 )   S - 107   2007.4

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

    Atsuhito Tone, Kenichi Shikata, Daisuke Ogawa, Sakiko Sasaki, Ryo Nagase, Motofumi Sasaki, Kosuke Yozai, Hitomi Kataoka Usui, Shinichi Okada, Jun Wada, Yasushi Shikata, Hirofumi Makino

    Journal of the renin-angiotensin-aldosterone system : JRAAS   8 ( 1 )   45 - 50   2007.3

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    Introduction. Macrophages play critical roles in the development of atherosclerosis and diabetic nephropathy as well as many inflammatory diseases. Angiotensin II type 1 receptor antagonists (AIIA) are beneficial for the prevention of atherosclerosis and diabetic nephropathy suggesting that angiotensin II (Ang II) promotes the development of these diseases. it has recently been reported that Ang II exerts proinflammatory actions in vivo and in vitro. This study was aimed to clarify the direct effects of Ang II on monocytes/macrophages.
    Materials and methods. PMA-treatedTHP-1 cells, a human monocytic leukaemia cell line, were treated with Ang II (10(-6) mol/L) for 24 hours with or without AIIA (CV11974). We evaluated gene expression profiles of these cells using DNA microarray system and quantified them by real-time RT-PCR.
    Results. DNA microarray revealed that in total 19 genes, including monocyte chemoattractant protein (MCP)-2, were up-regulated by Ang II and down-regulated by AIIA. Real-time RT-PCR showed that up-regulation of MCP-2 with Ang II is blocked by the ARA (CV11974) but not by an AT(2)-receptor antagonist.
    Conclusions. These results suggest that Ang II directly stimulates MCP-2 expression through AT(1)-receptors in activated macrophages. Ang II may contribute to the persistence or amplification of microinflammation in vessel walls, heart and kidney. Vasculoprotective or renoprotective effects of ARA might partly depend on direct anti-inflammatory effects on macrophages.

    DOI: 10.3317/jraas.2007.007

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  • Macrophage scavenger receptor-A - deficient mice are resistant against diabetic nephropathy through amelioration of microinflammation (vol 56, pg 363, 2007)

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

    DIABETES   56 ( 3 )   897 - 897   2007.3

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    DOI: 10.2337/db07-er03

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  • 【メタボリックシンドローム時代の糖尿病研究の最前線】組織的な糖尿病対策のあり方 DNETT-Japan

    四方 賢一, 槇野 博史

    医学のあゆみ   220 ( 13 )   1292 - 1295   2007.3

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    糖尿病性腎症はわが国における慢性透析導入の最大の原因疾患である。糖尿病性腎症はいったん発症すると進行性で非可逆性であると考えられていたが、近年、早期腎症は、血圧、血糖および脂質の厳格な管理により高率にアルブミン尿が減少し、さらにアルブミン尿が陰性化(寛解)することが明らかとなった。しかし、進行した顕性腎症の寛解が可能であるかどうかについては大規模臨床試験によるエビデンスは存在しない。Diabetic Nephropathy Remission and Regression Team Trial(DNETT-Japan)は、顕性腎症を伴う2型糖尿病患者を対象に、医師と糖尿病療養指導士(CDEJ)を中心としたコメディカルスタッフがチーム医療によって強力な治療介入を行う(集約的治療)ことにより、腎症の進展の抑制、さらには寛解が可能であるかどうかを検証する多施設共同無作為化臨床試験である。DNETT-Japanによって顕性腎症に対する集約的治療が確立されることが期待される。(著者抄録)

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2007&ichushi_jid=J00060&link_issn=&doc_id=20070405160051&doc_link_id=%2Faa7ayuma%2F2007%2F022013%2F052%2F1292-1295%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faa7ayuma%2F2007%2F022013%2F052%2F1292-1295%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • 組織的な糖尿病対策の現状 糖尿病腎症の寛解を目指した多施設共同臨床研究 DNETT-Japan

    槇野 博史, 四方 賢一

    糖尿病学の進歩   ( 41 )   256 - 259   2007.3

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  • 2型糖尿病における大血管および細小血管障害に対する各種サイトカインの関連性(頸動脈超音波検査を用いた動脈硬化における炎症メカニズムの評価)

    松本 吉弘, 中村 明彦, 北村 卓也, 中塔 辰明, 四方 賢一, 槙野 博史

    超音波医学   34 ( 2 )   214 - 214   2007.3

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  • 糖尿病腎症の克服をめざして 糖尿病腎症の成因とMicroinflammation

    四方 賢一

    糖尿病学の進歩   ( 41 )   142 - 147   2007.3

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

    Hitomi Kataoka Usui, Kenichi Shikata, Motofumi Sasaki, Shinichi Okada, Mitsuhiro Matsuda, Yasushi Shikata, Daisuke Ogawa, Yuichi Kido, Ryo Nagase, Kosuke Yozai, Sakiko Ohga, Atsuhito Tone, Jun Wada, Motohiro Takeya, Seikoh Horiuchi, Tatsuhiko Kodama, Hirofumi Makino

    Diabetes   56 ( 2 )   363 - 72   2007.2

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    Microinflammation is a common major mechanism in the pathogenesis of diabetic vascular complications, including diabetic nephropathy. Macrophage scavenger receptor-A (SR-A) is a multifunctional receptor expressed on macrophages. This study aimed to determine the role of SR-A in diabetic nephropathy using SR-A-deficient (SR-A(-/-)) mice. Diabetes was induced in SR-A(-/-) and wild-type (SRA(+/+)) mice by streptozotocin injection. Diabetic SR-A(+/+) mice presented characteristic features of diabetic nephropathy: albuminuria, glomerular hypertrophy, mesangial matrix expansion, and overexpression of transforming growth factor-P at 6 months after induction of diabetes. These changes were markedly diminished in diabetic SR-A(-/-) mice, without differences in blood glucose and blood pressure levels. Interestingly, macrophage infiltration in the kidneys was dramatically decreased in diabetic SR-A(-/-) mice compared with diabetic SR-A(+/+) mice. DNA microarray revealed that proinflammatory genes were overexpressed in renal cortex of diabetic SR-A(+/+) mice and suppressed in diabetic SR-A(-/-) mice. Moreover, anti-SR-A antibody blocked the attachment of monocytes to type IV collagen substratum but not to endothelial cells. Our results suggest that SR-A promotes macrophage migration into diabetic kidneys by accelerating the attachment to renal extracellular matrices. SR-A may be a key molecule for the inflammatory process in pathogenesis of diabetic nephropathy and a novel therapeutic target for diabetic vascular complications.

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  • 内臓脂肪組織に由来するセリンプロテアーゼ阻害剤 Vaspinの同定肥満状態でインスリン感受性を高める新規アディポサイトカイン

    肥田 和之, 和田 淳, 江口 潤, Hong Zhang, 馬場 雅子, 清田 綾, 橋本 泉, 岡田 達夫, 安原 章浩, 中司 敦子, 赤木 滋, 四方 賢一, 宝来 真志, 二見 淳一郎, 渡辺 英二郎, 松木 泰, 平松 隆司, 槇野 博史, Kanwar Yashpal S.

    岡山医学会雑誌   118 ( 3 )   215 - 220   2007.1

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    Other Link: http://ousar.lib.okayama-u.ac.jp/13354

  • DNETT-Japan

    槇野博史, 四方賢一

    医学のあゆみ   220 ( 13 )   2007

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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

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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

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  • DNETT-Jpanの取り組み 糖尿病腎症の寛解を目指したチーム医療による集約的治療

    槇野博史, 四方賢一

    週間医学会新聞   ( 2726 )   2007

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  • 糖尿病腎症患者の看護モデル作成の試み

    住吉和子, 川田智惠子, 四方賢一, 槇野博史, 中尾美幸, 大橋睦子, 高取佐知子

    日本糖尿病教育・看護学会誌   11   2007

  • ステロイド糖尿病患者の看護

    綱崎幸恵, 西田保子, 宮村純子, 下宮暁子, 佐々木可菜, 前川ゆかり, 難波孝子, 四方賢一, 槇野博史

    日本糖尿病教育・看護学会誌   11   2007

  • 【腎・尿路疾患の診療指針'06】続発性腎疾患 糖尿病性腎症

    佐藤 千景, 四方 賢一, 槇野 博史

    腎と透析   61 ( 増刊 )   260 - 265   2006.12

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  • 【糖尿病性合併症 新たなる治療戦略の可能性】糖尿病腎症 糖尿病腎症の病態生理

    利根 淳仁, 四方 賢一, 槇野 博史

    カレントテラピー   24 ( 11 )   943 - 946   2006.11

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  • 医師および医学生へ向けたeラーニング用治験教育コンテンツの作成

    黒田 智, 矢尾 和久, 西原 茂樹, 田中 靖子, 藤井 仁恵, 武居 徳子, 永禮 優子, 岩井 富美恵, 佐藤 順子, 川上 恭弘, 四方 賢一, 五味田 裕

    臨床薬理   37 ( Suppl. )   S197 - S197   2006.11

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  • 蛋白制限と腎症 「糖尿病性腎症に対する蛋白制限食の効果」に関する多施設共同介入研究

    古家 大祐, 羽田 勝計, 槇野 博史, 四方 賢一, 吉川 隆一

    日本病態栄養学会誌   9 ( 4 )   412 - 412   2006.11

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  • 【CKD(慢性腎臓病)と動脈硬化予防】心・血管障害とその予防 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, 槇野 博史

    動脈硬化予防   5 ( 3 )   39 - 45   2006.10

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  • 2型糖尿病患者における各種炎症マーカーと血管合併症の関連

    中村 明彦, 四方 賢一, 大賀 佐起子, 利根 淳仁, 平松 信, 糸島 達也, 槇野 博史

    Diabetes Frontier   17 ( 5 )   670 - 670   2006.10

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  • 【内分泌症候群(第2版) その他の内分泌疾患を含めて】糖代謝 糖尿病性合併症 糖尿病性腎症

    佐々木 基史, 四方 賢一, 槇野 博史

    日本臨床   別冊 ( 内分泌症候群III )   169 - 174   2006.9

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  • 腎症-治療の実験的検討 Cholecystokinin(CCK)は抗炎症作用を介して糖尿病性腎症の進展を抑制する

    佐々木 基史, 四方 賢一, 岡田 震一, 西下 伸吾, 佐藤 千景, 城戸 雄一, 宮本 聡, 和田 淳, 宮坂 京子, 舩越 顕博, 松井 利充, 槇野 博史

    糖尿病合併症   20 ( Suppl.1 )   101 - 101   2006.9

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  • 【症例に学ぶ 糖尿病合併妊娠のpitfall】糖尿病ケトアシドーシスの診断と治療

    四方 賢一

    産婦人科の実際   55 ( 8 )   1211 - 1214   2006.8

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  • 【糖尿病性腎症治療の新しい展望】新しい腎症治療薬の展望 炎症を制御する薬剤

    利根 淳仁, 四方 賢一, 槇野 博史

    Diabetes Frontier   17 ( 4 )   497,449 - 502,449   2006.8

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  • 【糖尿病性腎症治療の新しい展望】糖尿病性腎症の治療とそのエビデンス 糖尿病性腎症の寛解とDNETT-Japan

    四方 賢一, 槇野 博史

    Diabetes Frontier   17 ( 4 )   475 - 478   2006.8

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  • 全身性疾患と腎障害up to date 糖尿病性腎症

    利根 淳仁, 四方 賢一, 槇野 博史

    日本腎臓学会誌   48 ( 6 )   473 - 473   2006.8

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  • 【糖尿病の病理】糖尿病合併症の病理 腎合併症

    利根 淳仁, 四方 賢一, 槇野 博史

    病理と臨床   24 ( 7 )   720 - 726   2006.7

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  • Thiazolidinediones ameliorate diabetic nephropathy via cell cycle-dependent mechanisms. International journal

    Tatsuo Okada, Jun Wada, Kazuyuki Hida, Jun Eguchi, Izumi Hashimoto, Masako Baba, Akihiro Yasuhara, Kenichi Shikata, Hirofumi Makino

    Diabetes   55 ( 6 )   1666 - 77   2006.6

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    Thiazolidinediones are ligands for peroxisome proliferator-activated receptor-activated receptor (PPAR)-gamma, widely used as insulin sensitizer in type 2 diabetic patients and implicated in apoptosis, cell proliferation, and cell cycle regulation. Here, the effect of thiazolidinediones on G1-phase cell cycle arrest, the hallmark in diabetic nephropathy, was investigated. Eight-week-old male Otsuka Long-Evans Tokushima fatty rats were treated with pioglitazone (1 mg kg body wt(-1) (.) day(-1)) until 50 weeks of age and compared with insulin treatment. Although similar HbA(1c) levels were observed in both groups, pioglitazone significantly inhibited glomerular hypertrophy and mesangial matrix expansion and reduced urinary albumin excretion compared with the insulin-treated group. In addition, pioglitazone significantly reduced the number of glomerular p27(Kip1)-positive cells. Because prominent expression of PPAR-gamma was observed in podocytes in glomeruli and cultured cells, conditionally immortalized mouse podocyte cells were cultured under 5.5 and 25 mmol/l D-glucose supplemented with pioglitazone. Pioglitazone inhibited cell hypertrophy revealed by [H-3]thymidine and [H-3]proline incorporation, and pioglitazone reversed high glucose-induced G1-phase cell cycle arrest, i.e., an increase in G0/G1 phase and decrease in S and G2 phases. Pioglitazone suppressed high glucose-induced phosphorylation of p44/42 mitogen-activated protein kinase and reduced Bcl-2 and P27(Kip1) protein levels. Besides glucose-lowering action, pioglitazone ameliorates diabetic nephropathy via cell cycle-dependent mechanisms.

    DOI: 10.2337/db05-1285

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

    Izumi Hashimoto, Jun Wada, Aya Hida, Masako Baba, Nobuyuki Miyatake, Jun Eguchi, Kenichi Shikata, Hirofumi Makino

    OBESITY   14 ( 5 )   799 - 811   2006.5

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    Objective: Chronic inflammation observed in obesity has been reported to be implicated in the development of atherosclerosis. We screened candidate chemokines that link chronic inflammation and obesity.
    Research Methods and Procedures: Japanese overweight (n = 39, BMI 28.7 +/- 0.65 kg/m(2)) and normal-weight (n = 24, BMI 22.3 +/- 0.45 kg/m(2)) subjects were enrolled. Using antibody-based protein microarray, spot intensities of monocyte chemoattractant protein (MCP)-4, eotaxin, and eotaxin-2 correlated with anthropometric parameters. We further measured serum concentration of these chemokines and mRNA levels in adipose tissues obtained from volunteers.
    Results: Serum MCP-4 levels showed positive correlation with BMI (r = 0.318, p = 0.014), waist (r = 0.316, p = 0.018), and waist-to-hip ratio (WHR) (r = 0.264, p = 0.049). Furthermore, MCP-4 correlated with homeostasis model assessment of insulin resistance (r = 0.392, p = 0.002), high-sensitivity C-reactive protein (hsCRP) (r = 0.350, p = 0.006). In step-wise multiple regression analyses, hsCRP independently correlated with MCP-4 levels. The expression of MCP-4 mRNA in visceral adipose tissue positively correlates with BMI. Serum eotaxin levels correlate with BMI (r = 0.262, p = 0.045) and WHR (r = 0.383, p = 0.003). Serum eotaxin-2 levels correlated with BMI (r = 0.464, p &lt; 0.001), waist (r = 0.333, p = 0.017), and WHR (r = 0.278, p = 0.048). However, eotaxin and eotaxin-2 levels did not show significant correlation with hsCRP.
    Discussion: Serum levels of MCP-4, eotaxin, and eotaxin-2, which belong to CC chemokine family and share CC chemokine receptor 3, correlated with BMI. These chemokines, especially MCP-4, may be critical molecules that link obesity and chronic inflammation.

    DOI: 10.1038/oby.2006.93

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  • 肝膿瘍から多臓器不全をきたした2型糖尿病の1例

    西下 伸吾, 四方 賢一, 則井 久尚, 渡辺 直美, 余財 亨介, 杉山 斉, 四方 泰史, 和田 淳, 槇野 博史

    糖尿病   49 ( 5 )   387 - 387   2006.5

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  • Clostridium perfringensによる敗血症から血管内溶血をきたした2型糖尿病の1例

    渡辺 直美, 村上 和春, 大谷 彰一郎, 四方 賢一, 槇野 博史

    糖尿病   49 ( 5 )   402 - 402   2006.5

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  • 糖尿病性腎症の発症と進展 腎症はなぜ起こるのか

    四方 賢一

    日本透析医学会雑誌   39 ( Suppl.1 )   616 - 616   2006.5

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  • 【慢性腎臓病総合対策】介入的アプローチ 糖尿病性腎症の寛解をめざしたチーム医療とDNETT-Japan

    槇野 博史, 四方 賢一

    綜合臨床   55 ( 4 )   1266 - 1270   2006.4

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    近年のわが国では,生活習慣の欧米化による糖尿病の増加に伴って糖尿病性腎症患者が増加の一途を辿っている.糖尿病性腎症は慢性的な高血糖によりアルブミン尿,蛋白尿の出現,腎機能低下の過程を経て,最終的には腎不全へと進展し,透析療法や腎移植などの治療を余儀なくされる.日本透析医学会の調査結果によると,1998年以降は糖尿病性腎症が新規透析導入原因疾患の第1位であり,2004年には13,920人と新規透析導入患者の41.3%を占めるに至った.わが国は疫学的なエビデンスが不足しており,正確な数は捉えられていないが,微量アルブミン尿を呈する早期腎症,顕性蛋白尿を認める顕性腎症,腎不全期と糖尿病性腎症の2期から5期まで含めると,糖尿病性腎症はCKDの中で最も多い疾患といえる.2型糖尿病は生活習慣の乱れを基盤にして発症しており,薬物治療のみでは根本的な治療とはいえない.生活習慣の改善のためにはコメディカルも参加したチーム医療が必須となってくる.デンマークのStenoグループが取り組んできた早期腎症と,スコットランドにおける顕性腎症に対する集約的治療の成果を述べ,最後に筆者が厚生労働省の班長としてスタートした顕性腎症に対する寛解をめざしたチーム医療による集約的治療を紹介する(著者抄録)

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

    Yanling Zhang, Jun Wada, Izumi Hashimoto, Jun Eguchi, Akihiro Yasuhara, Yashpal S Kanwar, Kenichi Shikata, Hirofumi Makino

    Journal of the American Society of Nephrology : JASN   17 ( 4 )   1090 - 101   2006.4

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    Hyperglycemia-induced overproduction of mitochondrial reactive oxygen species has emerged as a major player in diabetic vascular complications. Mammalian translocase of inner mitochondrial membrane 44 (TIM44) was identified by upregulation in diabetic mouse kidneys. TIM44 functions as a membrane anchor of mitochondrial heat-shock protein 70 (mtHsp70) to TIM23 complex and is involved in the import of mitochondria-targeted preproteins into mitochondrial matrix. The process is dependent on inner membrane potential and ATP hydrolysis on ATPase domain of mitochondrial heat-shock protein 70. Hemagglutination virus of Japan-envelope vector that carries pcDNA3.1 plasmid that contains the full-length cDNA of TIM44 and control plasmid were injected weekly into the tail vein of uninephrectomized streptozotocin-induced diabetic CD-1 mice. The gene delivery alleviated proteinuria and renal hypertrophy at 8 wk after the injection, inhibited renal cell proliferation and apoptosis, and suppressed superoxide production. In vitro experiments, using human proximal tubular (HK2) cells, revealed that the gene delivery of TIM44 reversed high glucose-induced metabolic and cellular abnormalities such as enhanced reactive oxygen species production, increased ATP contents, alterations in inner membrane potential, increased cell proliferation, and apoptosis. Transfection with siRNA and expressing vector of TIM44 revealed that TIM44 facilitates import of antioxidative enzymes such as superoxide dismutase and glutathione peroxidase into mitochondria. The gene delivery of TIM44 therefore seems to be beneficial for the maintenance of mitochondrial function and is a novel therapeutic approach for diabetic nephropathy.

    DOI: 10.1681/ASN.2005111148

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  • Vaspin(visceral Adipose Tissue-derived Serine Protease Inhibitor)とインスリン抵抗性

    中司 敦子, 和田 淳, 村上 和敏, 肥田 和之, 肥田 綾, 江口 潤, 江口 雅子, 伊勢田 泉, 安原 章浩, 岡田 達夫, 四方 賢一, 槇野 博史

    糖尿病   49 ( Suppl.1 )   S246 - S246   2006.4

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    J-GLOBAL

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  • Adipocyte adhesion molecule(ACAM)のC/EBPβによる発現制御と脂肪分化における役割

    村上 和敏, 和田 淳, 中司 敦子, 肥田 和之, 肥田 綾, 江口 潤, 江口 雅子, 伊勢田 泉, 安原 章浩, 岡田 達夫, 四方 賢一, 槇野 博史

    糖尿病   49 ( Suppl.1 )   S207 - S207   2006.4

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    J-GLOBAL

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  • ヒト血管内皮細胞におけるAngiotensinIIとS1Pのsignaling crosstalk

    大森 一慶, 四方 泰史, 更井 啓, 渡辺 直美, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   49 ( Suppl.1 )   S199 - S199   2006.4

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  • 2型糖尿病患者における炎症性マーカーと血管合併症との関連

    中村 明彦, 四方 賢一, 平松 信, 和田 淳, 四方 泰史, 槇野 博史

    日本腎臓学会誌   48 ( 3 )   249 - 249   2006.4

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  • 糖尿病動物にみられた腎病変:レプチン欠損脂肪肝自然発症マウスにおける検討

    藤澤 智巳, 池上 博司, 四方 賢一, 槇野 博史, 荻原 俊男

    日本腎臓学会誌   48 ( 3 )   191 - 191   2006.4

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  • 糖尿病性腎症の進展におけるCholecystokininとレセプターの役割の検討

    佐々木 基史, 四方 賢一, 岡田 震一, 大賀 佐起子, 西下 伸吾, 利根 淳仁, 余財 亨介, 城戸 雄一, 佐藤 千景, 舩越 顕博, 宮坂 京子, 槇野 博史

    糖尿病   49 ( Suppl.1 )   S158 - S158   2006.4

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  • 糖尿病性腎症の成因と治療 Macroangiopathyとの共通項をめぐって 糖尿病性腎症と動脈硬化の成因におけるMicroinflammation

    四方 賢一, 槇野 博史

    糖尿病   49 ( Suppl.1 )   S13 - S13   2006.4

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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

    糖尿病   49 ( Suppl.1 )   S159 - S159   2006.4

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  • チアゾリジン誘導体は抗炎症作用を介して糖尿病性腎症の進展を抑制する

    大賀 佐起子, 四方 賢一, 余財 亨介, 利根 淳仁, 佐々木 基史, 西下 伸吾, 渡邊 直美, 佐藤 千景, 四方 泰史, 和田 淳, 槇野 博史

    糖尿病   49 ( Suppl.1 )   S158 - S158   2006.4

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  • レプチン欠損脂肪肝自然発症マウス 新しい糖尿病腎症のモデル動物

    藤澤 智巳, 池上 博司, 野嶋 孝次, 能宗 伸輔, 小林 美里, 廣峰 義久, 四方 賢一, 槇野 博史, 荻原 俊男

    糖尿病   49 ( Suppl.1 )   S164 - S164   2006.4

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  • 糖尿病性腎症に対するACE阻害薬・AT1受容体拮抗薬併用療法の抗炎症効果

    中村 明彦, 四方 賢一, 平松 信, 中塔 辰明, 北村 卓也, 梶谷 展生, 和田 淳, 四方 泰史, 糸島 達也, 槇野 博史

    糖尿病   49 ( Suppl.1 )   S255 - S255   2006.4

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  • 【腎・尿路疾患 一般診療から専門診療へ】腎・尿路疾患の診断と治療 疾患各論 糖尿病性腎症

    大賀 佐起子, 四方 賢一, 槇野 博史

    Medicina   43 ( 3 )   444 - 447   2006.3

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  • 日本人肥満者における血中ケモカインのプロテオミクス解析

    和田 淳, 橋本 泉, 肥田 綾, 宮武 伸行, 四方 賢一, 槇野 博史

    日本内科学会雑誌   95 ( Suppl. )   144 - 144   2006.2

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  • 【糖尿病腎症 進展阻止・寛解と発症予防を目指して】治療 厳格な血糖・血圧・脂質コントロールによる集約的治療とDNETT-Japan

    槇野 博史, 四方 賢一

    最新医学   61 ( 1 )   83 - 89   2006.1

  • 糖尿病療養指導でのPOCTによるHbA1c測定の精度

    一村 光子, 住吉 和子, 臼井 真一, 柴倉 美砂子, 唐下 博子, 池田 敏, 四方 賢一

    医学検査   55 ( 1 )   41 - 44   2006.1

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    糖尿病外来診察時に,複数のコ・メディカルスタッフが受診患者と面談しながら直接HbA1cを測定し,同時に測定結果を主治医に報告する療養指導の現場での測定精度について検討した.また,HbA1c測定に高コレステロール血症の影響が疑われるため,HbA1c測定に対するリポタンパク質の影響について検討した.HbA1cの測定は,ラテックス凝集阻止反応を原理とするDCA2000を使用した.HPLC法との相関は,相関係数r=0.976,回帰直線y=0.995x-6.043であった.症例ごとの相関は高コレステロール血症が認められた症例を除き良好であった.LDL,HDLとも添加濃度が増加することによりHbA1c測定値は減少傾向となった.療養指導の場でのDCA2000の使用はランニングコストで問題はあるが,患者と多種コ・メディカル療養指導士の良好なコミュニケーションの場となる可能性が考えられた

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2006&ichushi_jid=J02467&link_issn=&doc_id=20060118460005&doc_link_id=%2Fcg6jjomt%2F2006%2F005501%2F005%2F0041-0044%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcg6jjomt%2F2006%2F005501%2F005%2F0041-0044%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • 糖尿病性腎症の成因と炎症

    四方賢一

    メディカル・ビューポイント   27,5,2   2006

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  • VII. 各論 続発性腎疾患 54. 糖尿病性腎症

    佐藤千景, 四方賢一, 槇野博史

    腎と透析   61   2006

  • 糖尿病性腎症 No.1 糖尿病性腎症の病態と疫学

    西下伸吾, 四方賢一, 槇野博史

    日本医師会雑誌   135 ( 7 )   2006

  • ナイチンゲールの看護論に基づいた糖尿病患者の継続支援

    綱崎幸恵, 西田保子, 宮村純子, 佐々木可菜, 下宮暁子, 橋本美穂, 難波孝子, 四方賢一, 住吉和子

    日本糖尿病教育・看護学会誌   10   2006

  • Mitochondrial protein import machineryと動脈硬化

    和田淳, 橋本泉, 張艶玲, 四方賢一, 槇野博史

    日本糖尿病動物研究会プログラム・講演抄録集   20th   2006

  • 糖尿病性腎症の患者の認識に影響を与える要因

    住吉和子, 川田智恵子, 四方賢一, 槇野博史, 中尾美幸, 大橋睦子, 高取佐智子, 中内麻里

    日本糖尿病教育・看護学会誌   10   2006

  • 糖尿病性腎症の寛解を目指したチーム医療による集約的治療に関する研究 「糖尿病性腎症の寛解を目指したチーム医療による集約的治療」に関する研究(事務局)糖尿病性腎症の予後予測因子としての炎症マーカーに関する研究

    四方賢一

    糖尿病性腎症の寛解を目指したチーム医療による集約的治療に関する研究 平成17年度 総括・分担研究報告書   2006

  • Serum interleukin-18 levels are associated with nephropathy and atherosclerosis in Japanese patients with type 2 diabetes. International journal

    Akihiko Nakamura, Kenichi Shikata, Makoto Hiramatsu, Tatsuaki Nakatou, Takuya Kitamura, Jun Wada, Tatsuya Itoshima, Hirofumi Makino

    Diabetes care   28 ( 12 )   2890 - 5   2005.12

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    OBJECTIVE - interleukin (IL)- 18 is a proinflammatory cytokine secreted from mononuclear cells. Serum concentration of IL-18 is a strong predictor of death in patients with cardiovascular diseases. Recent studies have shown that microinflammation is involved in the pathogenesis of diabetic nephropathy as well as of cardiovascular diseases. This study aimed to test the hypothesis that the serum level of IL-18 is a common predictor of nephropathy and atherosclerosis in patients with type 2 diabetes.
    RESEARCH DESIGN AND METHODS - Eighty-two Japanese patients with type 2 diabetes and 55 age- and sex-matched healthy control subjects were enrolled. Patients With renal dysfunction (creatinine clearance &lt; 1 ml/s) were excluded. We assessed clinical parameters and measured serum and urinary IL-18 levels, serum IL-6 levels, Carotid intima-media thickness (IMT), and brachial-ankle pulse wave velocity (baPWV) in all patients. Further, we evaluated changes of urinary albumin excretion rate (AER) after 6 months in 76 diabetic patients.
    RESULTS - Serum and urinary IL-18 levels were significantly elevated in patients with type 2 diabetes as compared with control subjects (serum IL-18 179 62 vs. 121 - 55 pg/ml, P &lt; 0.001; urinary IL-18 97 - 159 vs. 47 - 54 pg/ml, P = 0.035). Univariate linear regression analysis showed significant positive correlations between serum IL- 18 and AER (r [correlation coefficient] = 0.525, P &lt; 0.001), HbA(1C) (r = 0.242, P = 0.029), high-sensitivity C-reactive protein (hs-CRP) (r = 0.240, P = 0.031), and urinary beta-2 microglobulin (r = 0.235, P = 0.036) Serum IL-18 levels also correlated positively with carotid IMT (r = 0.225, P = 0.042) and baPWV (r = 0.232, P = 0.040). We also found a significant correlation between urinary IL-18 and AER (r = 0.309, P = 0.005). Multivariate linear regression analysis showed that AER (standard correlation coefficients [B] = 0.405, P &lt; 0.001) and hs-CPP (B = 0.207, P = 0.033) were independently associated with serum IL- 18 levels. AER was also independently associated with urinary IL-18 levels (B = 0.295, P = 0.005). Moreover, serum and urinary IL-18 levels correlated positively with AER after 6 months (r = 0.489, P &lt; 0.001 and r = 0.320, P - 0.005) and changes in AER during the follow-up period (r = 0.268, P = 0.018 and r = 0.234, P = 0.042).
    CONCLUSIONS - Serum levels of IL- 18 might be a predictor of progression of diabetic nephropathy as well as cardiovascular diseases.

    DOI: 10.2337/diacare.28.12.2890

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  • 【ネフローゼ症候群のすべて】臨床 治療各論 糖尿病性腎症

    四方 泰史, 中村 明彦, 四方 賢一, 槇野 博史

    腎と透析   59 ( 増刊 )   537 - 541   2005.12

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

    Kosuke Yozai, Kenichi Shikata, Motofumi Sasaki, Atsuhiro Tone, Sakiko Ohga, Hitomi Usui, Shinichi Okada, Jun Wada, Ryo Nagase, Daisuke Ogawa, Yasushi Shikata, Hirofumi Makino

    Journal of the American Society of Nephrology : JASN   16 ( 11 )   3326 - 38   2005.11

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    Recent studies suggested the involvement of inflammatory processes in the pathogenesis of diabetic nephropathy. Methotrexate (MTX), a folic acid antagonist, is widely used for the treatment of inflammatory diseases. Recently, it has been shown that treatment with low-dose MTX reduces the cardiovascular mortality in patients with rheumatoid arthritis, suggesting that MTX has anti-atherosclerotic effects via its anti-inflammatory actions. This study was designed to determine the anti-inflammatory effects of this agent on diabetic nephropathy. Diabetes was induced in Sprague-Dawley rats with streptozotocin, and MTX (0.5 or 1.0 mg/kg) was administered once a week for 8 wk. Treatment with MTX reduced urinary albumin excretion, mesangial matrix expansion, macrophage infiltration, expression of TGF-beta and type IV collagen, and intercellular adhesion molecule-1 in glomeruli. MTX also reduced the high glucose-induced NF-kappa B activation in vitro and in vivo. The results indicate that intermittent administration of MTX prevented renal injuries without changes in blood glucose level and BP in experimental diabetic rats. The protective effects of MTX are suggested to be mediated by its anti-inflammatory actions through inhibition of NF-kappa B activation and consequent reduction of intercellular adhesion molecule-1 expression and macrophage infiltration. The results suggest that anti-inflammatory agents might be beneficial for the treatment of diabetic nephropathy.

    DOI: 10.1681/ASN.2004111011

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

    Masako Baba, Jun Wada, Jun Eguchi, Izumi Hashimoto, Tatsuo Okada, Akihiro Yasuhara, Kenichi Shikata, Yashpal S Kanwar, Hirofumi Makino

    Journal of the American Society of Nephrology : JASN   16 ( 11 )   3222 - 34   2005.11

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    Galectins are beta-galactoside-binding lectins that are involved in various biologic processes, such as apoptosis, cell proliferation, and cell-cycle regulation. Galectin-9 (Gal-9) was identified previously and demonstrated to have apoptotic potential to thymocytes in mice and activated CD8(+) T cells in nephrotoxic serum nephritis model. In this study, the effect of Gal-9 on G1-phase cell-cycle arrest, one of the hallmark pathologic changes in early diabetic nephropathy, was investigated. Eight-week-old male db/db mice received injections of recombinant Gal-9 or vehicle for 8 wk. The injection of Gal-9 into db/db mice significantly inhibited glomerular hypertrophy and mesangial matrix expansion and reduced urinary albumin excretion. Gal-9 reduced glomerular expression of TGF-beta 1 and the number of p27(Kip1)- and p21(Cip1)-positive cells in glomeruli. Double staining with nephrin and type IV collagen revealed that podocytes were mainly positive for p27(kip1). For further confirming the cell-cycle regulation by Gal-9, conditionally immortalized mouse podocyte cells were cultured under 5.5 and 25 MM D-glucose supplemented with Gal-9. Cell-cycle distribution analyses revealed that Gal-9 maintained further progression of cell cycle from the G1 phase. Gal-9 reversed the high-glucose-mediated upregulation of p27(Kip1) and p21(Cip1) and inhibited cell-cycle-dependent hypertrophy, i.e., reduced [H-3]proline incorporation. The data suggest that Gal-9 plays a central role in inducing their successful progression from G1 to G2 phase by suppressing glomerular expression of TGF-beta 1 and inhibition of cyclin-dependent kinase inhibitors. Gal-9 may give an impetus to develop new therapeutic tools targeted toward. diabetic nephropathy.

    DOI: 10.1681/ASN.2004110915

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  • Gene delivery of Tim44 reduces mitochondrial superoxide production and ameliorates neointimal proliferation of injured carotid artery in diabetic rats. International journal

    Takashi Matsuoka, Jun Wada, Izumi Hashimoto, Yanling Zhang, Jun Eguchi, Norio Ogawa, Kenichi Shikata, Yashpal S Kanwar, Hirofumi Makino

    Diabetes   54 ( 10 )   2882 - 90   2005.10

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    Hyperglycemia induces the production of reactive oxygen species (ROS) from mitochondria, which is closely related to diabetic vascular complications. Mammalian translocase of inner mitochondrial membrane (Tim)44 was identified by upregulation in streptozotocin (STZ)-induced diabetic mouse kidneys; Tim44 functions as a membrane anchor of mtHsp70 to TIM23 complex and is involved in the import of preproteins with mitochondria-targeted presequence into mitochondrial matrix. The process is dependent on inner membrane potential (Delta psi) and ATP hydrolysis on ATPase domain of mtHsp70. Here, we show that the gene delivery of Tim44 using pcDNA3.1 vector (pcDNA3.1/TIM44) into the balloon injury model of STZ-induced diabetic rats ameliorated neointinial proliferation. ROS production, inflammatory responses, and cell proliferation in injured carotid artery were diminished by delivery of pcDNA3.1/ TIM44. In vitro experiments using human aortic smooth muscle cells (HASMCs) revealed that the gene delivery of Tim.44 normalized high-glucose-induced enhanced ROS production and increased ATP production, alterations in inner membrane potential, and cell proliferation. Transfection of siRNA and pcDNA3.1/TIM44 using HASMC culture clarified that import of antioxidative enzymes such as superoxide dismutase and glutathione peroxidase was facilitated by Tim44. Tim44 and its related molecules in mitochondrial import machinery complex are novel targets in the therapeutic interventions for diabetes and its vascular complications.

    DOI: 10.2337/diabetes.54.10.2882

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

    Atsuhito Tone, Kenichi Shikata, Mitsuhiro Matsuda, Hitomi Usui, Shinichi Okada, Daisuke Ogawa, Jun Wada, Hirofumi Makino

    Diabetes research and clinical practice   69 ( 3 )   237 - 42   2005.9

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    Although persistent proteinuria is characteristic of diabetic nephropathy (DN), it is important to differentiate non-diabetic renal diseases (NDRD) in diabetic patients with proteinuria. In order to re-evaluate the indications for renal biopsy in the diabetic patients, we retrospectively analyzed the relationship between clinical features and histological diagnosis in 97 Japanese patients with type 2 diabetes manifesting overt proteinuria. Renal biopsy was performed because they were clinically suspected to have NDRD. Patients were divided into three groups according to the histological diagnosis: (1) the DN group (n = 35) had only diabetic lesions, (2) the complicated group (n = 16) had histological changes of NDRD superimposed on DN and (3) the non-DN group (n = 46) had NDRD without diabetic lesions. We evaluated the specificity and sensitivity of four clinical parameters (duration of diabetes, presence or absence of diabetic retinopathy, microscopic hematuria and granular casts as urinary sediments) for the prediction of NDRD. Short duration of diabetes (&lt; 5 years) showed high sensitivity (75%) and specificity (70%). Diabetic retinopathy showed the highest sensitivity (87%) and specificity (93%). The sensitivity and specificity of microscopic hematuria (56 and 58%) and granular casts (68 and 47%) were lower. Our study confirmed that the absence of retinopathy and short duration of diabetes are useful clinical indications for renal biopsy in diabetic patients with overt protemuria. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

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  • 炎症メカニズムは2型糖尿病患者の動脈硬化症および糖尿病腎症に共通した進展因子である

    中村 明彦, 四方 賢一, 平松 信, 中塔 辰明, 北村 卓也, 四方 泰史, 和田 淳, 糸島 達也, 槇野 博史

    糖尿病合併症   19 ( Suppl.1 )   57 - 57   2005.9

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  • 糖尿病合併症発症の分子機構と新たな治療法の開発を目指して 腎症(2)

    四方 賢一

    糖尿病学の進歩   ( 39 )   193 - 195   2005.9

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  • 糖尿病合併症の分子学的アプローチ 糖尿病性腎症の成因と炎症関連分子

    四方 賢一

    糖尿病合併症   19 ( 2 )   123 - 125   2005.8

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

    Kazuyuki Hida, Jun Wada, Jun Eguchi, Hong Zhang, Masako Baba, Aya Seida, Izumi Hashimoto, Tatsuo Okada, Akihiro Yasuhara, Atsuko Nakatsuka, Kenichi Shikata, Shinji Hourai, Junichiro Futami, Eijiro Watanabe, Yasushi Matsuki, Ryuji Hiramatsu, Shigeru Akagi, Hirofumi Makino, Yashpal S Kanwar

    Proceedings of the National Academy of Sciences of the United States of America   102 ( 30 )   10610 - 5   2005.7

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    There is a rapid global rise in obesity, and the link between obesity and diabetes remains somewhat obscure. We identified an adipocytokine, designated as visceral adipose tissue-derived serpin (vaspin), which is a member of serine protease inhibitor family. Vaspin cDNA was isolated by from visceral white adipose tissues (WATs) of Otsuka Long-Evans Tokushima fatty (OLETIF) rat, an animal model of abdominal obesity with type 2 diabetes. Rat, mouse, and human vaspins are made up of 392,394, and 395 amino acids, respectively; exhibit approximate to 40% homology with alpha(1)-antitrypsin; and are related to serine protease inhibitor family. Vaspin was barely detectable in rats at 6 wk and was highly expressed in adipocytes of visceral WATs at 30 wk, the age when obesity, body weight, and insulin levels peak in OLETF rats. The tissue expression of vaspin and its serum levels decrease with worsening of diabetes and body weight loss at 50 wk. The expression and serum levels were normalized with the treatment of insulin or insulin-sensitizing agent, pioglitazone, in OLETF rats. Administration of vaspin to obese CRL:CD-1 (ICR) (ICR) mice fed with high-fat high-sucrose chow improved glucose tolerance and insulin sensitivity reflected by normalized serum glucose levels. It also led to the reversal of altered expression of genes relevant to insulin resistance, e.g., leptin, resistin, TNF alpha, glucose transporter-4, and adiponectin. In DNA chip analyses, vaspin treatment resulted in the reversal of expression in approximate to 50% of the high-fat high-sucrose-induced genes in WATs. These findings indicate that vaspin exerts an insulin-sensitizing effect targeted toward WATs in states of obesity.

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  • 【糖尿病性細小血管症 基礎・臨床のアップデート】糖尿病性腎症 病態生理 内皮機能障害

    余財 亨介, 四方 賢一, 槇野 博史

    日本臨床   63 ( 増刊6 糖尿病性細小血管症 )   341 - 345   2005.6

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  • COLLECTRIN IS A NOVEL TARGET OF HNF-1 IN RENAL COLLECTING DUCT CELLS

    Yanling Zhang, Jun Wada, Akihiro Yasuhara, Jun Eguchi, Izumi Hashimoto, Kazuya Yamagata, Kenichi Shikata, Hirofumi Makino

    NEPHROLOGY   10   A238 - A238   2005.6

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  • CHRONIC INJECTION OF RECOMBINANT GALECTIN-9 INHIBITS THE GLOMERULAR HYPERTROPHY IN DB/DB MICE

    Jun Wada, Masako Baba, Jun Eguchi, Yashpal S. Kanwar, Hirofumi Makino, Kenichi Shikata

    NEPHROLOGY   10   A22 - A22   2005.6

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  • 体重減少が診断の契機となった糖尿病性筋萎縮症の1例

    利根 淳仁, 臼井 仁美, 四方 賢一, 宮本 真和, 浅田 麻紀, 森定 宏之, 増田 浩三, 水島 孝明, 和田 淳, 小出 典男, 槇野 博史

    糖尿病   48 ( 6 )   466 - 466   2005.6

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  • 糖尿病性舞踏病の1例

    余財 亨介, 和田 淳, 四方 賢一, 槇野 博史, 佐藤 正樹, 佐藤 幹雄

    糖尿病   48 ( 6 )   464 - 464   2005.6

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  • 腎膿瘍を合併した2型糖尿病の一例

    大賀 佐起子, 臼井 仁美, 四方 賢一, 森定 宏之, 増田 浩三, 余財 享介, 渡辺 直美, 和田 淳, 水島 孝明, 小出 典男, 槇野 博史

    糖尿病   48 ( 6 )   462 - 462   2005.6

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  • 発症時にケトアシドーシスに伴う意識障害を認めた高齢の劇症1型糖尿病の一例

    佐々木 基史, 内田 治仁, 開原 正展, 佐藤 元, 小坂 恭一, 東 徹, 四方 賢一, 槇野 博史

    糖尿病   48 ( 6 )   471 - 471   2005.6

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  • 糖尿病性腎症の発症・進展における炎症機転の関与

    岡田 震一, 四方 賢一, 槇野 博史

    岡山医学会雑誌   117 ( 1 )   9 - 15   2005.5

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    Other Link: http://ousar.lib.okayama-u.ac.jp/13407

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

    Jun Eguchi, Jun Wada, Kazuyuki Hida, Hong Zhang, Takashi Matsuoka, Masako Baba, Izumi Hashimoto, Kenichi Shikata, Norio Ogawa, Hirofumi Makino

    The Biochemical journal   387 ( Pt 2 )   343 - 53   2005.4

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    Few cell adhesion molecules have been reported to be expressed in mature adipocytes, and the significance of cell adhesion process in adipocyte biology is also unknown. In the present study, we identified ACAM (adipocyte adhesion molecule), a novel homologue of the CTX (cortical thymocyte marker in Xenopus) gene family. ACAM cDNA was isolated during PCR-based cDNA subtraction, and its mRNA was shown to be up-regulated in WATs (white adipose tissues) of OLETF (Otsuka Long-Evans Tokushima fatty) rats, an animal model for Type II diabetes and obesity. ACAM, 372 amino acids in total, has a signal peptide, V-type (variable) and C2-type (constant) Ig domains, a single transmembrane segment and a cytoplasmic tail. The amino acid sequence in rat is highly homologous to mouse (94%) and human (87%). ACAM mRNA was predominantly expressed in WATs in OLETF rats, and increased with the development of obesity until 30 weeks of age, which is when the peak of body mass is reached. Western blot analysis revealed that ACAM protein, approx. 45 kDa, was associated with plasma membrane fractions of mature adipocytes isolated from mesenteric and subdermal adipose deposits of OLETF rats. Up-regulation of ACAM mRNAs in obesity was also shown in WATs of genetically obese db/db mice, diet-induced obese ICR mice and human obese subjects. In primary cultured mouse and human adipocytes, ACAM mRNA expression was progressively up-regulated during differentiation. Several stably transfected Chinese-hamster ovary K1 cell lines were established, and the quantification of ACAM mRNA and cell aggregation assay revealed that the degree of homophilic aggregation correlated well with ACAM mRNA expression. In summary, ACAM may be the critical adhesion molecule in adipocyte differentiation and development of obesity.

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  • 日本人肥満者における血中ケモカインのプロテオミクス解析

    橋本 泉, 和田 淳, 肥田 綾, 馬場 雅子, 宮武 伸行, 江口 潤, 四方 賢一, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S221 - S221   2005.4

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  • 白色脂肪特異的新規膜蛋白Adipocyte adhesion molecule (ACAM)の機能解析

    江口 潤, 和田 淳, 肥田 和之, 馬場 雅子, 中司 敦子, 橋本 泉, 安原 章浩, 岡田 達夫, 四方 賢一, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S137 - S137   2005.4

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  • Interleukin-18は2型糖尿病患者のアルブミン尿に密接な関係がある

    中村 明彦, 四方 賢一, 平松 信, 中塔 辰明, 北村 卓也, 和田 淳, 糸島 達也, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S228 - S228   2005.4

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  • 糖尿病性腎症におけるスフィンゴシン1燐酸(S1P)の血管内皮保護作用についての検討

    大森 一慶, 四方 泰史, 渡辺 直美, 大賀 佐起子, 四方 賢一, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S154 - S154   2005.4

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  • 糖尿病性腎症のremissionを目指して 腎症のremissionを目指した新たな治療戦略

    四方 賢一, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S45 - S45   2005.4

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  • 糖尿病性腎症に対するPioglitazoneの治療効果と作用メカニズムの検討

    岡田 達夫, 和田 淳, 肥田 和之, 江口 潤, 馬場 雅子, 橋本 泉, 安原 章浩, 中司 敦子, 肥田 綾, 吉川 理津子, 四方 賢一, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S155 - S155   2005.4

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  • 糸球体内皮細胞における高糖濃度刺激・高浸透圧刺激によるICAM-1の発現とその細胞内シグナル伝達についての検討

    渡辺 直美, 四方 泰史, 大森 一慶, 大賀 佐起子, 四方 賢一, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S228 - S228   2005.4

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  • 代謝症候群における微量アルブミン尿の意義

    吉川 理津子, 和田 淳, 橋本 泉, 松岡 孝, 高橋 健二, 宮本 聡, 大田 祥子, 谷合 一陽, 肥田 和之, 四方 賢一, 槇野 博史

    糖尿病   48 ( Suppl.2 )   S223 - S223   2005.4

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  • 【糖尿病腎症の発症と進展】糖尿病性腎症の成因における内皮細胞障害

    四方 賢一, 槇野 博史

    内分泌・糖尿病科   20 ( 3 )   209 - 213   2005.3

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  • 【糖尿病薬の効果的な使い方】他疾患の併発や特別な状況における経口薬の使い方 糖尿病腎症

    四方 賢一

    臨床医   31 ( 3 )   341 - 344   2005.3

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  • 【臨床分子内分泌学 心血管内分泌代謝系(下)】レニン-アンジオテンシン系 病態と疾患からみたレニン-アンジオテンシン系 糖尿病性腎症

    大賀 佐起子, 四方 賢一, 槇野 博史

    日本臨床   63 ( 増刊3 臨床分子内分泌学(2) )   155 - 160   2005.3

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  • 【腎臓とRAS】腎臓におけるRASの基礎医学 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

    利根 淳仁, 四方 賢一, 槇野 博史

    Angiotensin Research   2 ( 1 )   20 - 26   2005.1

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    世界的に末期腎不全の主原因である糖尿病性腎症の発症の成因には,レニン・アンジオテンシン系(renin-angiotensin system:RAS)が,その血行動態に対する作用と炎症促進作用を介して深く関与している.一方,RASはケモカインを介してマクロファージの腎組織への浸潤を促進することが明らかとなり,RASとマクロファージの相互作用が最近注目されている.接着分子の増加によって腎組織に浸潤したマクロファージは,種々のサイトカインを産生し,またメサンギウム細胞に直接はたらいて細胞外基質の産生を刺激することにより,糸球体硬化に促進的にはたらく.今後,マクロファージを中心とした炎症メカニズムを制御することが,糖尿病性腎症に対する新しい治療戦略となり得る可能性がある(著者抄録)

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  • Sulfated hyaluronic acid, a potential selectin inhibitor, ameliorates experimentally induced crescentic glomerulonephritis. International journal

    Daisuke Ogawa, Kenichi Shikata, Mitsuhiro Matsuda, Kazuo Akima, Mitsuhiro Iwahashi, Shinichi Okada, Yoshinori Tsuchiyama, Yasushi Shikata, Jun Wada, Hirofumi Makino

    Nephron. Experimental nephrology   99 ( 1 )   e26-32 - E32   2005

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    Background/Aims: Sulfated polysaccharides are known to interfere with the binding of selectins and their ligands. Recently, we demonstrated that sulfated hyaluronic acid (SHA), a synthetic sulfated polysaccharide, showed preventive and therapeutic effects on experimental mesangial proliferative glomerulonephritis. Here we evaluated the protective potential of SHA on crescentic glomerulonephritis, using nephrotoxic serum (NTS) nephritis in Wistar-Kyoto (WKY) rats. Methods: Crescentic glomerulonephritis was induced by injection of NTS in WKY rats. Rats subsequently received intraperitoneal administration of SHA (0.5 or 1.5 mg/kg/day) or non-sulfated hyaluronic acid ( HA) ( 1.5 mg/kg/day) for 14 days. The urinary protein excretion was measured, and expression of selectins, intraglomerular leukocytes and crescent formation were examined by immunohistochemistry. In addition, we examined the urinary protein excretion of SHA ( 1.5 mg/kg/day) administered from day 7 after the induction of crescentic glomerulonephritis. Results: The expression of P-selectin was increased in the glomerulus of crescentic glomerulonephritis. SHA reduced proteinuria, macrophage infiltration, and crescent formation in a dose-dependent manner. Furthermore, administration of SHA ( 1.5 mg/kg/day) from day 7 also reduced the urinary protein excretion on day 14 compared with that in saline and HA group. Conclusion: Our results suggest that SHA inhibits intraglomerular infiltration of macrophages, and prevents progression of experimental crescentic glomerulonephritis. Sulfated polysaccharides might be beneficial for the treatment of crescentic glomerulonephritis. Copyright (C) 2005 S. Karger AG, Basel.

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

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

    DIABETOLOGIA   48   A378 - A378   2005

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    DOI: 10.1007/s00125-005-1945-6

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  • IRMA 2

    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   1,1,296-299   2005

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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

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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

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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

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  • Serum interleukin-18 levels is associated with albuminuria and atherosclerosis in patients with type 2 diabetes

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

    DIABETOLOGIA   48   A376 - A376   2005

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  • 糖尿病腎症患者の食事管理行動に影響を与える要因

    住吉和子, 川田智恵子, 四方賢一, 槙野博史

    日本糖尿病教育・看護学会誌   9   2005

  • II.臨 床 治療各論 糖尿病性腎症

    四方泰史, 中村明彦, 四方賢一, 槙野博史

    腎と透析   59   2005

  • 糖尿病腎症の看護~意識付けへのアプローチ~

    佐々木可菜, 奥道保子, 宮村純子, 笹田雅子, 綱崎幸恵, 下宮暁子, 四方賢一, 槙野博史, 住吉和子

    日本糖尿病教育・看護学会誌   9   2005

  • Long-term results of tonsillectomy as a treatment for IgA nephropathy

    H Akagi, M Kosaka, K Hattori, A Doi, K Fukushima, M Okano, S Kariya, K Nishizaki, N Sugiyama, K Shikata, H Makino, Y Masuda

    ACTA OTO-LARYNGOLOGICA   124   38 - 42   2004.12

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    IgA nephropathy (IgAN) is the most common form Of chronic glomerulonephritis with IgA deposits present mainly in the mesangial areas. We performed a 10-year retrospective case-control study of 71 patients with IgAN to evaluate the long-term effects and prognostic factors associated with tonsillectomy Forty-one patients (19 males and 22 females) Underwent tonsillectomy (Group A) and 30 patients ( 13 males and 17 females) did not (Group B). These patients were followed for more than 10 years after renal biopsy The average age at initial renal biopsy was 29.78 years in Group A and 33.0 years in Group B. The average follow-up period was 13 years and 3 months in Group A, and 12 years and 7 months in Group B. Glomerular damage demonstrated on renal biopsy was more extensive in Group A than in Group B. Prognosis after 10 years of follow-up was compared between the two groups. The clinical remission rate was 24.4% in Group A and 13.3% in Group B. the stable renal function rate was 82.9% in Group A and 70.0% in Group B. and the renal survival rate was 95.1% in Group A and 73.3% in Group B. The renal survival rate in Group A was significantly higher than that in Group B (p &lt;0.05). Although evaluation of renal pathology based on renal biopsy was useful in predicting the long-term effects of tonsillectomy in IgAN patients. the results of tonsillar provocation tests were not.

    DOI: 10.1080/03655230410003332

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  • 抗リン脂質抗体症候群に由来する自己抗体の動脈血栓形成への関与

    小林 和子, 田淵 雅子, 梶原 敏充, 井出 将博, 四方 賢一, 槇野 博史, 保田 立二, 小池 隆夫, 松浦 栄次

    日本免疫学会総会・学術集会記録   34   282 - 282   2004.11

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  • 【産婦人科医が知っておきたい女性内科疾患 外来プライマリ・ケア】腎・尿路(系)の疾患 急性腎不全

    矢野 愛, 中尾 一志, 四方 賢一, 槇野 博史

    産科と婦人科   71 ( 11 )   1706 - 1711   2004.11

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  • 血中酸化LDL・β2-グリコプロテインI・CRP複合体の臨床的意義

    田淵 雅子, 小林 和子, 四方 賢一, 槇野 博史, 小池 隆夫, 保田 立二, 松浦 栄次

    日本免疫学会総会・学術集会記録   34   282 - 282   2004.11

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  • 【ネフローゼ症候群 基礎研究の最新動向と臨床の進歩】二次性ネフローゼ症候群 原因病態別考察 代謝疾患

    大賀 佐起子, 四方 賢一, 槇野 博史

    日本臨床   62 ( 10 )   1907 - 1913   2004.10

  • 新規アディポサイトカインVaspin(visceral adipose tissue specific serpin)の機能解析

    肥田 和之, 和田 淳, 江口 潤, 松岡 孝至, 馬場 雅子, 四方 賢一, 槇野 博史

    肥満研究   10 ( Suppl. )   166 - 166   2004.9

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    J-GLOBAL

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  • 脂肪細胞特異的新規膜蛋白Adipocyte cell adhesion molecule(ACAM)の機能解析

    江口 潤, 和田 淳, 肥田 和之, 馬場 雅子, 松岡 孝至, 四方 賢一, 槇野 博史

    肥満研究   10 ( Suppl. )   171 - 171   2004.9

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  • 糖尿病合併症の分子学的アプローチ 糖尿病腎症の成因と炎症関連分子

    四方 賢一, 槇野 博史

    糖尿病合併症   18 ( Suppl.1 )   45 - 45   2004.9

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  • Erythromycinは抗炎症作用により糖尿病ラットの腎障害を抑制する

    利根 淳仁, 四方 賢一, 佐々木 基史, 大賀 佐起子, 臼井 仁美, 余財 亨介, 岡田 震一, 小川 大輔, 四方 泰史, 和田 淳, 槇野 博史

    糖尿病合併症   18 ( Suppl.1 )   53 - 53   2004.9

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  • Induction of pro-inflammatory genes in the kidney in early phase of diabetic nephropathy

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

    DIABETOLOGIA   47   A394 - A395   2004.8

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  • Methotrexate prevents renal injuries through its anti-inflammatory effects in experimental diabetic rats.

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

    DIABETOLOGIA   47   A397 - A398   2004.8

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  • Thiazolidinedione ameliorates renal injuries through anti-inflammatory actions by inhibition of NF-kappa B activation in experimental diabetic rats

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

    DIABETOLOGIA   47   A398 - A398   2004.8

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  • 【糖尿病の治療と対策】糖尿病合併症の治療 糖尿病性腎症の新しい治療

    佐々木 基史, 四方 賢一, 槇野 博史

    医学と薬学   52 ( 2 )   166 - 173   2004.8

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  • 糖尿病性腎症の発症メカニズムと新しい治療ターゲット 糖尿病性腎症の発症進展メカニズムにおける炎症機序の役割と治療への応用

    臼井 仁美, 四方 賢一, 槇野 博史

    日本腎臓学会誌   46 ( 6 )   495 - 495   2004.8

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  • 【ネフローゼ症候群 発症メカニズムと治療の最前線】二次性ネフローゼ症候群の治療 糖尿病性腎症

    永瀬 亮, 四方 賢一, 槇野 博史

    内科   94 ( 1 )   102 - 106   2004.7

  • 糖尿病の慢性合併症 糖尿病性腎症

    岡田 震一, 四方 賢一, 槇野 博史

    からだの科学 増刊   増刊 ( 糖尿病2005 )   168 - 172   2004.7

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  • 【進行性腎障害 診断と治療の進歩】進行性腎障害の治療の進歩 糖尿病性腎症

    四方 賢一, 槇野 博史

    日本内科学会雑誌   93 ( 5 )   928 - 934   2004.5

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    糖尿病性腎症の治療の基本は血糖と血圧の厳格な管理と食事療法である.ACE阻害薬やアンジオテンシンII受容体拮抗薬によるレニン-アンジオテンシン系の抑制が薬物療法の中心となるが,多くの進展因子を同時に治療する集約的治療が重要である.近年,糖尿病性腎症の成因に基づいた新しい治療薬の開発と,遺伝素因の解明が精力的に行われつつあり,今後の発展が期待される

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2004&ichushi_jid=J01159&link_issn=&doc_id=20040521030010&doc_link_id=1390282681419404032&url=https%3A%2F%2Fcir.nii.ac.jp%2Fcrid%2F1390282681419404032&type=CiNii&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00003_3.gif

  • 【慢性腎不全の病態と治療 CKDからESRDへの進行をいかに阻止するか】糖尿病性腎症の治療 エビデンスと展望

    四方 賢一, 槇野 博史

    医学のあゆみ   209 ( 1 )   54 - 59   2004.4

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    糖尿病性腎症の治療の基本は血糖と血圧の管理と食事療法である.降圧薬のなかではACE阻害薬とアンジオテンシンII受容体拮抗薬(ARB)に関する数多くのエビデンスが集積しており,糖尿病性腎症に対する第一選択薬となっている.蛋白質制限食の効果に関するエビデンスはいまだ不十分であるが,腎不全期には他の腎疾患と同様に蛋白質制限が行われる.糖尿病性腎症の進展を阻止するためには,血糖と血圧のみならず多くの因子を考慮した集約的治療を行う必要がある

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2004&ichushi_jid=J00060&link_issn=&doc_id=20040402210010&doc_link_id=%2Faa7ayuma%2F2004%2F020901%2F011%2F0054-0059%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faa7ayuma%2F2004%2F020901%2F011%2F0054-0059%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • Fournier壊疽の1例

    渡辺 直美, 村上 和春, 村松 友義, 橋本 泉, 江口 潤, 四方 賢一, 槇野 博史

    糖尿病   47 ( 4 )   335 - 335   2004.4

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  • 血糖コントロールにより精神神経症状の改善をみた糖尿病合併MELASの1例

    松岡 孝至, 城戸 雄一, 橋本 泉, 江口 潤, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   47 ( 4 )   326 - 326   2004.4

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  • Macrophage scavenger receptorが糖尿病性腎症におけるマクロファージの浸潤に関与するメカニズム

    臼井 仁美, 四方 賢一, 岡田 震一, 城戸 雄一, 永瀬 亮, 余財 亨介, 大賀 佐起子, 佐々木 基史, 利根 淳仁, 小川 大輔, 和田 淳, 海野 雄加, 堀内 正公, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S175 - S175   2004.4

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  • 糖尿病大血管障害におけるミトコンドリア機能異常の関与

    松岡 孝至, 和田 淳, 江口 潤, 橋本 泉, 清田 綾, 岡田 達夫, 安原 章浩, 中司 敦子, 馬場 雅子, 肥田 和之, 中村 好男, 四方 賢一, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S256 - S256   2004.4

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  • 糖尿病における血管内皮機能障害 糖尿病性腎症の成因における内皮機能障害

    四方 賢一, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S18 - S18   2004.4

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  • 新規膜蛋白Adipocyte adhesion molecule(ACAM)の同定と機能解析

    江口 潤, 和田 淳, 肥田 和之, 岡田 達夫, 安原 章浩, 橋本 泉, 清田 綾, 中司 敦子, 松岡 孝至, 馬場 雅子, 四方 賢一, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S100 - S100   2004.4

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  • 当科で腎生検を施行した糖尿病症例の臨床病理学的検討

    利根 淳仁, 四方 賢一, 臼井 仁美, 松田 充浩, 和田 淳, 岡田 震一, 槇野 博史

    糖尿病   47 ( 4 )   328 - 328   2004.4

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  • AngiotensinII刺激によるマクロファージの遺伝子発現プロファイルの変化

    利根 淳仁, 四方 賢一, 小川 大輔, 岡田 震一, 臼井 仁美, 大賀 佐起子, 佐々木 基史, 和田 淳, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S175 - S175   2004.4

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  • リコンビナントGalectin-9慢性投与はdb/db糖尿病マウスの糸球体肥大を抑制する

    馬場 雅子, 和田 淳, 岡田 達夫, 安原 章浩, 橋本 泉, 清田 綾, 江口 潤, 中司 敦子, 松岡 孝至, 肥田 和之, 四方 賢一, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S175 - S175   2004.4

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  • 糖尿病性腎症に対するPioglitazoneの作用メカニズムの検討

    岡田 達夫, 和田 淳, 肥田 和之, 江口 潤, 橋本 泉, 馬場 雅子, 松岡 孝至, 安原 章浩, 清田 綾, 中司 敦子, 四方 賢一, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S195 - S195   2004.4

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  • 糖尿病誘発後のICAM-1ノックアウトマウスの腎組織における遺伝子発現プロファイルの解析

    岡田 震一, 四方 賢一, 臼井 仁美, 城戸 雄一, 永瀬 亮, 余財 亨介, 大賀 佐起子, 利根 淳仁, 佐々木 基史, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S176 - S176   2004.4

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  • 炎症メカニズムを抑制することによる糖尿病性腎症の進展抑制効果

    余財 亨介, 四方 賢一, 佐々木 基史, 利根 淳仁, 大賀 佐起子, 永瀬 亮, 城戸 雄一, 臼井 仁美, 岡田 震一, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S196 - S196   2004.4

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  • Pioglitazoneは糖尿病ラットの腎臓におけるICAM-1の発現とマクロファージの浸潤を抑制する

    大賀 佐起子, 四方 賢一, 岡田 震一, 小川 大輔, 臼井 仁美, 城戸 雄一, 永瀬 亮, 余財 亨介, 利根 淳仁, 佐々木 基史, 渡邊 直美, 西下 伸吾, 和田 淳, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S196 - S196   2004.4

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  • VASPIN(visceral adipose tissue specific SERPIN)とインスリン抵抗性

    肥田 和之, 和田 淳, 江口 潤, 松岡 孝至, 橋本 泉, 安原 章浩, 中司 敦子, 清田 綾, 岡田 達夫, 馬場 雅子, 四方 賢一, 槇野 博史

    糖尿病   47 ( Suppl.1 )   S252 - S252   2004.4

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  • 5/6腎摘出後のICAM-1ノックアウトマウスの腎組織における遺伝子発現プロファイルの変化

    佐々木 基史, 四方 賢一, 城戸 雄一, 大賀 佐起子, 余財 亨介, 永瀬 亮, 臼井 仁美, 岡田 震一, 小川 大輔, 和田 淳, 槇野 博史

    日本腎臓学会誌   46 ( 3 )   222 - 222   2004.4

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  • 1型糖尿病にバセドウ病を合併した3症例

    西下 伸吾, 四方 賢一, 清田 綾, 渡辺 直美, 岸田 雅之, 大塚 文雄, 余財 亨介, 和田 淳, 槇野 博史

    糖尿病   47 ( 4 )   324 - 324   2004.4

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  • 糖尿病性腎症の発症・進展と遺伝 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探索

    四方 賢一, 槇野 博史

    腎と透析   56 ( 2 )   240 - 244   2004.2

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  • The role of adrenomedullin and receptors in glomerular hyperfiltration in streptozotocin-induced diabetic rats. International journal

    Keita Hiragushi, Jun Wada, Jun Eguchi, Takashi Matsuoka, Akihiro Yasuhara, Izumi Hashimoto, Tetsuji Yamashita, Kazuyuki Hida, Yoshio Nakamura, Kenichi Shikata, Naoto Minamino, Kenji Kangawa, Hirofumi Makino

    Kidney international   65 ( 2 )   540 - 50   2004.2

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    Background. Since adrenomedullin (AM) elicits vasodilatation by binding to specific AM receptors consisted of calcitonin-receptor-like receptor (CRLR)/receptor-activity-modifying protein 2 (RAMP2) or CRLR/receptor-activity-modifying protein 3 (RAMP3) on endothelial cells and stimulating nitric oxide production, AM possibly involves in glomerular capillary dilatation in early phase of diabetic nephropathy.
    Methods. Streptozotocin (STZ)-induced diabetic Sprague-Dawley rats at 4 weeks after the injection were employed for expression studies of AM, RAPM2, and RAMP3. The measurement of AM peptide levels in kidney tissue, plasma, and urine was performed. Human aortic endothelial cells (HAEC) were used to investigate functional link between glucose-induced AM production and nitric oxide release.
    Results. STZ rats showed glomerular hypertrophy and increased urinary NO2- and NO3- excretion. By Northern blot analyses, AM and RAPM2 mRNAs significantly increased in the kidneys of STZ rats, while RAMP3 mRNA was not altered. In STZ rats, AM peptide was actively secreted into urine (1280 +/- 360 fmol/day vs. control 110 +/- 36 fmol/day). AM peptide was mainly detected on cortical and medullary collecting duct cells in control rat kidneys and AM peptide and mRNA were up-regulated on afferent arterioles and glomeruli of STZ rats. RAMP2 expression was detected on afferent arterioles and not in glomeruli in control rats and it was up-regulated on glomerular endothelial cells in STZ rats. In HAEC culture, D-glucose stimulated AM and nitric oxide production and they were suppressed by addition of AM antisense oligodeoxynucleotides.
    Conclusion. Up-regulated expression of AM and RAMP2 in afferent arterioles and glomeruli may be related to selective dilatation of glomerular capillary in acute phase of type 1 diabetes.

    DOI: 10.1111/j.1523-1755.2004.00407.x

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  • 【腎疾患の基礎と臨床の新しい展開】糖尿病性腎症の治療とフォローアップ

    永瀬 亮, 四方 賢一, 槇野 博史

    現代医療   36 ( 2 )   395 - 400   2004.2

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  • 【腎疾患診療とEBM】保存期腎疾患診療のエビデンス 保存期慢性腎不全 糖尿病性腎症

    大賀 佐起子, 四方 賢一, 槇野 博史

    EBMジャーナル   5 ( 2 )   166 - 171   2004.2

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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

    四方賢一, 開原正展, 槇野博史, 松田充浩

    協和企画   2004

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  • Ⅱ進行性腎障害の治療と進歩5.糖尿病腎症

    四方賢一, 槇野博史

    日本内科学会雑誌   93,5 ( 5 )   928 - 934   2004

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    Language:Japanese   Publisher:The Japanese Society of Internal Medicine  

    近年の糖尿病患者の急激な増加に伴って,糖尿病性腎症も増加の一途を辿っている.糖尿病性腎症の治療の基本は血糖と血圧の厳格な管理と食事療法である. ACE阻害薬やアンジオテンシンII受容体拮抗薬によるレニン-アンジオテンシン系の抑制が薬物療法の中心となるが,多くの進展因子を同時に治療する集約的治療が重要である.近年,糖尿病性腎症の成因に基づいた新しい治療薬の開発と,遺伝素因の解明が精力的に行われつつあり,今後の発展が期待される.

    DOI: 10.2169/naika.93.928

    CiNii Article

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  • 糖尿病の慢性合併症-II 糖尿病性腎症

    岡田震一, 四方賢一, 槙野博史

    からだの科学   2004

  • 【糖尿病と感染症】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 ( 6 )   732 - 734   2003.12

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

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

    INTERNATIONAL JOURNAL OF OBESITY   27 ( 11 )   1325 - 1331   2003.11

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    OBJECTIVE: To investigate whether the changes in vascular endothelial growth factor ( VEGF) and basic fibroblast growth factor ( bFGF) concentrations before and after weight reduction in Japanese overweight men are associated with changes in body mass index (BMI), visceral, subcutaneous fat, VO2 and work rate (WR) at ventilatory threshold (VT).
    DESIGN: Cross-sectional and longitudinal clinical intervention study with exercise education.
    SUBJECTS: In total, 30 Japanese overweight men (BMI, 29.0 +/- 2.2 kg/m(2)) and 31 normal- weight men (BMI, 22.5 +/- 1.6 kg/m(2)) at baseline were enrolled: 30 overweight men (BMI, 29.0 +/- 2.2 kg/m(2)) were further enrolled into a 6-month exercise program.
    MEASUREMENTS: Fat distribution evaluated by visceral fat ( V) and subcutaneous fat ( S) areas measured with computed tomography scanning at umbilical levels, angiogenic peptides including VEGF and bFGF, exercise tests at baseline and after 6 months.
    RESULTS: In normal- weight and overweight subjects at baseline, VEGF positively correlated with S area (r = 0.350, P = 0.007) but not with V area. In contrast, bFGF negatively correlated with BMI (r = - 0.619, P&lt;0.001), S (r = - 0.457, P&lt;0.001) and V areas (r = -0.466, P&lt;0.001). By intervention with exercise education, 30 overweight subjects showed reduction in BMI (29.0 +/- 2.2 to 28.0 +/- 2.0, P&lt;0.001), V and S areas, increase in VO2 and WR at VT, increase in bFGF (9.21 +/- 5.82 - 21.2+/-7.04 ng/ ml, P&lt;0.001), and no change in VEGF (1.45 +/- 0.72 - 1.88 +/- 0.52 ng/ml, P = 0.016). The stepwise multiple regression analysis revealed that &UDelta;BMI (&beta; = - 6.052) and &UDelta;VO2 (&beta; = 2.806) were independently related to &UDelta;bFGF (P&lt;0.001) and all other variables including DeltaS area, and DeltaV area, and DeltaWR did not enter the equation at significant levels.
    CONCLUSION: The present study indicated a negative correlation between serum bFGF levels and BMI at baseline as well as an association of DeltaBMI and DeltaVO(2) with DeltabFGF after exercise intervention. The exercise-induced elevation of bFGF may be beneficial in the prevention of the atherosclerosis in overweight subjects.

    DOI: 10.1038/sj.ijo.0802408

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  • 【糖尿病 予防から治療まで】臨床の進歩 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

    医学のあゆみ   207 ( 9 )   797 - 802   2003.11

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    近年の日本透析医学会の統計によれば,1998年以降,慢性血液透析への新規導入患者は慢性糸球体腎炎によるものを上まわって透析導入原因疾患の第一位となっており,腎症の患者数が増加の一途をたどっていることがわかる.腎症を早期に診断し,早期に治療を開始することが多くの患者の予後や生活の質に対してのみならず医療経済的にもますます重要性を増してきている.そこで,近年蓄積されてきた糖尿病性腎症治療におけるエビデンスについて述べた

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

    Shinichi Okada, Kenichi Shikata, Mitsuhiro Matsuda, Daisuke Ogawa, Hitomi Usui, Yuichi Kido, Ryo Nagase, Jun Wada, Yasushi Shikata, Hirofumi Makino

    Diabetes   52 ( 10 )   2586 - 93   2003.10

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    Diabetic nephropathy is a leading cause of end-stage renal failure. Several mechanisms, including activation of protein kinase C, advanced glycation end products, and overexpression. of transforming growth factor (TGF)-beta, are believed to be involved in the pathogenesis of diabetic nephropathy. However, the significance of inflammatory processes in the pathogenesis of diabetic microvascular complications is poorly understood. Accumulation of macrophages and overexpression of leukocyte adhesion molecules and chemokines are prominent in diabetic human kidney tissues. We previously demonstrated that intercellular adhesion molecule (ICAM)-1 mediates macrophage infiltration into the diabetic kidney. In the present study, to investigate the role of ICAM-1 in diabetic nephropathy, we induced diabetes in ICAM-1-deficient (ICAM-1(-/-)) mice and ICAM-1(+/+) mice with streptozotocin and examined the renal pathology over a period of 6 months. The infiltration of macrophages was markedly suppressed in diabetic ICAM-1(-/-) mice compared with that of ICAM-1(+/+) mice. Urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion were significantly lower in diabetic ICAM-1(-/-) mice than in diabetic ICAM-1(+/+) mice. Moreover, expressions of TGF-beta and type IV collagen in glomeruli were also suppressed in diabetic ICAM-1(-/-) mice. These results suggest that ICAM-1 is critically involved in the pathogenesis of diabetic nephropathy.

    DOI: 10.2337/diabetes.52.10.2586

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  • 日本人男性肥満者における血清VEGF,bFGF濃度の検討

    和田 淳, 清田 綾, 宮武 伸行, 藤井 昌史, 四方 賢一, 槇野 博史

    肥満研究   9 ( Suppl. )   112 - 112   2003.10

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  • 白色脂肪特異的新規膜蛋白(OL-16)の機能解析

    江口 潤, 和田 淳, 肥田 和之, 松岡 孝至, 馬場 雅子, 中司 敦子, 橋本 泉, 清田 綾, 安原 章浩, 岡田 達夫, 四方 賢一, 槇野 博史

    肥満研究   9 ( Suppl. )   76 - 76   2003.10

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  • Macrophage scavenger receptor Aは糖尿病性腎症におけるマクロファージの浸潤に関与する

    臼井 仁美, 四方 賢一, 岡田 震一, 城戸 雄一, 永瀬 亮, 余財 亨介, 大賀 佐起子, 佐々木 基史, 利根 淳仁, 和田 淳, 海野 雄加, 堀内 正公, 槇野 博史

    糖尿病合併症   17 ( Suppl.1 )   76 - 76   2003.9

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  • Pelvic lymphocyst infection associated with maternally inherited diabetes mellitus. International journal

    Daisuke Ogawa, Kenichi Shikata, Mitsuhiro Matsuda, Jun Wada, Haruhito Uchida, Maki Asada, Hirofumi Makino

    Diabetes research and clinical practice   61 ( 2 )   137 - 41   2003.8

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    A 45-year-old woman with 20-year history of diabetes mellitus was admitted to our hospital because of high fever and abdominal pain. Radical hysterectomy and bilateral pelvic lymphadenectomy had been performed 4 months before admission for invasive cervical cancer. On admission, elastic hard tumors were palpable in the lower abdomen. Laboratory examination showed positive C-reactive protein (CRP), anemia and renal dysfunction. Computed tomography (CT) revealed several lymphocysts in the pelvis. She was diagnosed with infection of pelvic lymphocysts. Since her mother also had diabetes associated with deafness, we examined mitochondrial DNA in leukocytes and detected an A to G transition at the nucleotide position of 3243 (A3243G mutation). She was diagnosed as maternally inherited diabetes mellitus and deafness (MIDD). Puncture of the cysts followed by administration of antibiotics resulted in marked improvement of symptoms and laboratory findings. This is a rare case of pelvic lymphocyst infection in a patient with a mitochondrial disorder. Although the exact mechanism of infection is not clear, MIDD may represent an unusual risk factor for infection, and further investigation is necessary to assess the influence of mitochondrial dysfunction on the immune system. Pelvic lymphocyst infection should be considered in the differential diagnosis of abdominal pain and fever in patients with MIDD after abdominal surgery. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

    DOI: 10.1016/S0168-8227(03)00120-7

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  • Involvement of inflammatory process in the pathogenesis of diabetic nephropathy

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

    DIABETOLOGIA   46   A341 - A341   2003.8

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  • エビデンスに基づいた糖尿病性腎症の治療

    岡田 震一, 四方 賢一, 槇野 博史

    日本腎臓学会誌   45 ( 6 )   611 - 611   2003.8

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  • HMG-CoA reductase inhibitor ameliorates diabetic nephropathy by its pleiotropic effects in rats (vol 18, pg 265, 2003)

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

    NEPHROLOGY DIALYSIS TRANSPLANTATION   18 ( 7 )   1418 - 1418   2003.7

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    DOI: 10.1093/ndt/gfg337

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  • Successful treatment of necrotizing fasciitis associated with diabetic nephropathy. International journal

    Daisuke Ogawa, Kenichi Shikata, Jun Wada, Mitsuhiro Matsuda, Hirofumi Makino

    Diabetes research and clinical practice   60 ( 3 )   213 - 6   2003.6

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    A 50-year-old woman with a 15-year history of type 2 diabetes mellitus was admitted to our hospital due to high fever and a skin lesion with severe pain, swelling and a sensation of heat in the right thigh. Laboratory examination showed elevated C-reactive protein (CRP), thrombocytopenia, nephrotic syndrome and renal dysfunction. Her blood glucose level had been well controlled. Streptococcus agalactiae was detected in both the skin lesion and blood culture, and pathological examination revealed neutrophil infiltration in the fascia and muscle layer. The patient was diagnosed with necrotizing fasciitis, septic shock and disseminated intravascular coagulation. A combination therapy of antibiotics and suraical debridement resulted in the improvement of symptoms as supported by laboratory findings, and the skin lesion also showed improvement. Although group A streptococcus is well known to be implicated in the pathogenesis of necrotizing fasciitis, only S. agalacticie, belonging to group B streptococcus, was isolated from the tissue and blood cultures in this case. Although this organism is not virulent and rarely causes a necrotizing fasciitis, both the superficial fascial layer and underlying muscle were affected in this case. There have been only a few reports of necrotizing fasciitis due to S. agalactiae in patients with diabetes mellitus. Although the blood glucose level was well controlled in our patient, this disease might be caused by other factors, including diminished sense of touch and pain, abnormality of microcirculation and hypogammaglobulinemia due to nephrotic syndrome. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.

    DOI: 10.1016/S0168-8227(03)00034-2

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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

    口腔・咽頭科   15 ( 3 )   335 - 344   2003.6

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    腎生検施行後,IgA腎症と診断され,扁摘を行った41例(扁摘群),扁摘を行わなかった30例(非扁摘群)を対象に,予後とIgA腎症の適応について検討した.扁摘群は寛解群10例(24.4%),腎機能保持群24例(58.5%),腎機能低下群5例(12.2%),腎不全群2例(4.9%)で,寛解率24.4%,腎機能保持率82.9%,腎生存率95.1%であった.一方,非扁摘群は寛解群4例(13.3%),腎機能保持群8例(56.7%),腎機能低下群1例(3.3%),腎不全群8例(26.7%)で,寛解率13.3%,腎機能保持率70.0%,腎生存率73.3%であった.腎生存率において,扁摘群が統計学的に有意に高率であった.また,腎病理組織障害度による長期予後は,重症群に比較して軽症群の方が有意に良好で,腎病理組織障害度は扁摘の適応の決定に有効であった.これに対し,病歴,扁桃局所所見,扁桃誘発試験は,有用とはいえなかった

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  • 内臓脂肪特異的蛋白VASPIN(visceral adipose tissue specific SERPIN)の肥満における病態生理学的意義

    肥田 和之, 和田 淳, 松岡 孝至, 江口 潤, 馬場 雅子, 清田 綾, 橋本 泉, 四方 賢一, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S259 - S259   2003.4

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  • 白色脂肪特異的新規膜蛋白(OL-16)の同定と発現調節

    江口 潤, 和田 淳, 肥田 和之, 松岡 孝至, 馬場 雅子, 清田 綾, 橋本 泉, 四方 賢一, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S255 - S255   2003.4

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  • 日本人男性肥満者における血清VEGF,bFGF濃度の検討

    清田 綾, 和田 淳, 国富 三絵, 土山 芳徳, 宮武 伸行, 藤井 昌史, 吉良 尚平, 高橋 香代, 四方 賢一, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S257 - S257   2003.4

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  • 糖尿病性腎症におけるマクロファージスカベンジャーレセプター(MSR-A)の関与 MSR-Aノックアウトマウスを用いた検討

    臼井 仁美, 四方 賢一, 佐々木 基史, 利根 淳仁, 大賀 佐起子, 余財 亨介, 城戸 雄一, 永瀬 亮, 岡田 震一, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S225 - S225   2003.4

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  • 糖尿病性腎症の糸球体硬化の成因におけるICAM-1とマクロファージの役割 ICAM-1ノックアウトマウスを用いた検討

    城戸 雄一, 四方 賢一, 岡田 震一, 臼井 仁美, 佐々木 基史, 利根 淳仁, 大賀 佐起子, 余財 亨介, 永瀬 亮, 小川 大輔, 和田 淳, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S224 - S224   2003.4

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  • 糖尿病大血管障害におけるミトコンドリア機能異常の関与

    松岡 孝至, 和田 淳, 江口 潤, 橋本 泉, 清田 綾, 肥田 和之, 中村 好男, 四方 賢一, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S127 - S127   2003.4

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  • 糖尿病性腎症の発症機序の解明とその展望 糖尿病性腎症の成因における炎症メカニズムの関与 新しい治療ターゲットの探索

    四方 賢一, 和田 淳, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S7 - S7   2003.4

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  • 糖尿病性腎症における活性化マクロファージの役割 マクロファージのフェノタイプと活性化状態の経時的変化

    永瀬 亮, 四方 賢一, 小川 大輔, 大賀 佐起子, 余財 亨介, 城戸 雄一, 臼井 仁美, 岡田 震一, 和田 淳, 槇野 博史

    糖尿病   46 ( Suppl.1 )   S223 - S223   2003.4

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  • ピオグリタゾンが奏効した脂肪萎縮性糖尿病の1例

    永瀬 亮, 大賀 佐起子, 山名 二郎, 臼井 仁美, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   46 ( 3 )   290 - 290   2003.3

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  • 反応性マクロファージ活性化症候群を合併したGAD抗体陽性の1型糖尿病の1例

    橋本 泉, 四方 賢一, 城戸 雄一, 江口 潤, 和田 淳, 槇野 博史

    糖尿病   46 ( 3 )   268 - 268   2003.3

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  • ガス壊疽にケトアシドーシスを合併した糖尿病の1例

    清田 綾, 四方 賢一, 城戸 雄一, 馬場 雅子, 和田 淳, 槇野 博史

    糖尿病   46 ( 3 )   287 - 287   2003.3

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  • 十二指腸瘻の造設を要した糖尿病性胃症の1例

    大賀 佐起子, 四方 賢一, 城戸 雄一, 和田 淳, 槇野 博史, 佐藤 千景, 石井 啓太

    糖尿病   46 ( 3 )   269 - 269   2003.3

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  • 悪性腎硬化症を呈した2型糖尿病の1例

    中尾 一志, 市川 晴夫, 田邊 克幸, 矢野 愛, 来山 浩之, 清田 綾, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   46 ( 3 )   289 - 289   2003.3

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  • ネフローゼ症候群に対してLDL吸着療法,シクロスポリンが奏効した糖尿病の1例

    余財 亨介, 四方 賢一, 木原 隆司, 市川 晴夫, 前島 洋平, 和田 淳, 槇野 博史

    糖尿病   46 ( 3 )   289 - 289   2003.3

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  • シベンゾリンにより低血糖を生じた1型糖尿病の1例

    城戸 雄一, 四方 賢一, 馬場 雅子, 橋本 泉, 永瀬 亮, 和田 淳, 槇野 博史, 黒瀬 幸子

    糖尿病   46 ( 3 )   292 - 292   2003.3

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  • 【糖尿病 成因解明と治療法の進歩】糖尿病性腎症 積極的治療による「不可逆」からの回復

    岡田 震一, 四方 賢一, 槇野 博史

    内科   91 ( 1 )   119 - 123   2003.1

  • 【腎疾患 state of arts】病態生理に関する基礎的・臨床的研究の進歩 糸球体腎炎とNF-κB

    臼井 仁美, 四方 賢一, 槇野 博史

    医学のあゆみ   別冊 ( 腎疾患ーstate of arts 2003-2005 )   71 - 74   2003.1

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  • 不稔性を利用した花持ちのよいバーベナの商品化

    鈴木賢一, 宮崎潔, 四方康範, 勝元幸久, 久住高章

    日本原子力研究所JAERI-Conf   2003

  • イオンビーム育種研究の最前線 重イオンビーム照射を利用した花き新品種育種と実用化

    鈴木賢一, 宮崎潔, 四方康範, 勝元幸久, 浦谷宏, 田中隆治, 久住高章, 福井祐子

    放射線と産業   ( 99 )   2003

  • Protective effect of a novel and selective inhibitor of inducible nitric oxide synthase on experimental crescentic glomerulonephritis in WKY rats. International journal

    Daisuke Ogawa, Kenichi Shikata, Mitsuhiro Matsuda, Shinichi Okada, Hitomi Usui, Jun Wada, Naoyuki Taniguchi, Hirofumi Makino

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association   17 ( 12 )   2117 - 21   2002.12

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    Background. Nitric oxide (NO) plays important roles in a variety of pathophysiological processes. It has been reported that inducible NO synthase (iNOS) is upregulated in the glomeruli of patients with glomerulonephritis, although there has been no direct evidence that NO generated by iNOS contributes to the progression of glomerulonephritis. ONO-1714, a novel cyclic amidine analog, is a selective inhibitor of iNOS. To elucidate the role of iNOS in the pathogenesis of experimental crescentic glomerulonephritis, we examined the effect of ONO-1714 given to rats with nephrotoxic serum (NTS) nephritis.
    Methods. We induced NTS nephritis in Wistar-Kyoto (WKY) rats. These rats were given ONO-1714 or physiological saline intraperitoneally for 14 days using an osmotic pump after intraperitoneal injection with NTS.
    Results. Glomerular expression of iNOS and urinary excretion of NO metabolites (nitrite/nitrate) were increased in rats after injection of NTS. As compared with the control group, ONO-1714 significantly reduced proteinuria, crescent formation, glomerular infiltration of macrophages and urinary excretion of nitrite/nitrate.
    Conclusion. The present results suggest that NO radicals generated by iNOS contribute to the progression of experimental crescentic glomerulonephritis in WKY rats. The selective iNOS inhibitor ONO-1714 may be beneficial for the treatment of crescentic glomerulonephritis.

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  • Therapeutic effect of sulphated hyaluronic acid, a potential selectin-blocking agent, on experimental progressive mesangial proliferative glomerulonephritis. International journal

    Mitsuhiro Matsuda, Kenichi Shikata, Fujio Shimizu, Yasuo Suzuki, Masayuki Miyasaka, Hiroshi Kawachi, Hiroto Kawashima, Jun Wada, Hikaru Sugimoto, Yasushi Shikata, Daisuke Ogawa, Shinichiro J Tojo, Kazuo Akima, Hirofumi Makino

    The Journal of pathology   198 ( 3 )   407 - 14   2002.11

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    The initial event in the process of leukocyte infiltration is characterized by leukocyte rolling on the surface of the endothelium, which is mediated by selectins. P- and L-selectin bind to the sulphated sugar chains of their natural ligands, including sulphated glycolipids such as sulphatide. Recently, it has been demonstrated that sulphated glycolipids and sulphated oligosaccharides interfere with selectin binding pathways. This study synthesized sulphated hyaluronic acid (SHA), which is a potential selectin-blocking agent, and examined its therapeutic effect on the experimental progressive mesangial proliferative glomerulonephritis induced by anti-Thy-1 monoclonal antibody (1-22-3 MAb) after unilateral nephrectomy. The selectin-inhibitory effect of SHA in vitro was confirmed. SHA inhibited the binding of P- and L-selectin to sulphatide, which is a glycolipid ligand for P- and L-selectin, at a concentration of 1.5 mug/ml and 100 mug/ml. Immunohistochemical examination showed that P-selectin was up-regulated in the glomeruli in the 1-22-3 MAb nephritis model, while the ligands for L-selectin were not detected in the glomerular tufts. A single administration of SHA ameliorated proteinuria and glomerular leukocyte infiltration in 24 h after the injection of anti-Thy-1 MAb. Anti-P-selectin MAb, but not anti-L-selectin MAb, inhibited proteinuria and glomerular leukocyte infiltration. To examine further the therapeutic effect of SHA on chronic glomerulonephritis, SHA was administered daily from day 3 to day 14 in this model. Proteinuria and glomerular leukocyte infiltration were significantly diminished in SHA-treated rats on day 14. These results suggest that SHA ameliorated rat progressive mesangial proliferative glomerulonephritis by inhibiting P-selectin-dependent leukocyte infiltration in glomeruli. Sulphated oligosaccharides may be beneficial for the therapy of mesangial proliferative glomerulonephritis. Copyright (C) 2002 John Wiley Sons, Ltd.

    DOI: 10.1002/path.1209

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  • 【糖尿病性腎症の管理と治療 その包括的対策を考える】糖尿病性腎症の基礎 糖尿病性腎症の発症・進展機序

    臼井 仁美, 四方 賢一, 槇野 博史

    Progress in Medicine   22 ( 11 )   2608 - 2614   2002.11

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  • Pathophysiology and Management of Diabetic Nephropathy

    SHIKATA K., MAKINO H.

    Journal of the Japan Diabetes Society   45 ( 10 )   711 - 713   2002.10

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  • 【糖尿病のトータルケア】糖尿病の診断 腎症の病態と診断

    四方 賢一, 槇野 博史

    臨床医   28 ( 9 )   1948 - 1951   2002.9

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  • Beraprost sodium, prostacyclin analogue, attenuates glomerular hyperfiltration and glomerular macrophage infiltration by modulating ecNOS expression in diabetic rats. International journal

    Tetsuji Yamashita, Kenichi Shikata, Mitsuhiro Matsuda, Shinichi Okada, Daisuke Ogawa, Hikaru Sugimoto, Jun Wada, Hirofumi Makino

    Diabetes research and clinical practice   57 ( 3 )   149 - 61   2002.9

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    Stable prostacyclin analogue, beraprost sodium (BPS) has recently been reported to attenuate glomerular hyperfiltration in diabetic rats, however, the mechanism has been still unknown. We previously reported that overexpression of endothelial cell nitric oxide synthase (ecNOS) in afferent arterioles and glomeruli induce inappropriate dilatation of afferent arterioles and glomerular hyperfiltration through overproduction of nitric oxide in early stage of diabetic nephropathy. In this study, we tested the hypothesis that BPS ameliorates glomerular hyperfiltration through modulating ecNOS expression in diabetic nephropathy. Furthermore, we examined the effects of BPS on the expression of intercellular adhesion molecule-1 (ICAM-1) and macrophage infiltration in diabetic glomeruli, because glomerular hyperfiltration induces the expression of ICAM-1 resulting in macrophage infiltration. Male Sprague Dawley (SD) rats were administered continuously with BPS for 4 weeks after induction of diabetes by streptozotocin. In diabetic rats, the diameters of afferent arterioles, glomerular volume, creatinine clearance and urinary excretion of albumin and NO2/NO3 were increased as compared with non-diabetic control rats. Treatment with BPS improved these changes. The expression of ecNOS was increased in afferent arterioles and glomeruli in diabetic rats and suppressed by BPS. Prostacyclin receptor was expressed along afferent arterioles. Our results suggest that BPS attenuates glomerular hyperfiltration by modulating ecNOS expression in early stage of diabetic nephropathy. Moreover, BPS may inhibit ICAM-1-dependent infiltration of macrophages in diabetic glomeruli. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

    DOI: 10.1016/S0168-8227(02)00054-2

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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, Koshima, I, H Makino

    DIABETIC MEDICINE   19 ( 9 )   794 - 795   2002.9

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

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  • 糖尿病性腎症 point of no returnをどう考えるか 成因からみた新しい治療の展望

    松田 充浩, 四方 賢一, 槇野 博史

    糖尿病合併症   16 ( Suppl.1 )   54 - 54   2002.9

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  • 糖尿病性大血管障害におけるミトコンドリア機能異常の関与

    松岡 孝至, 和田 淳, 江口 潤, 橋本 泉, 清田 綾, 肥田 和之, 中村 好男, 四方 賢一, 槇野 博史

    糖尿病合併症   16 ( Suppl.1 )   96 - 96   2002.9

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  • 新しい腎疾患マーカーとしての尿中リポカリン型プロスタグランジンD合成酵素(L-PGDS) 尿中L-PGDSの臨床意義について(2)

    清木 興介, 織田 浩司, 椎名 康彦, 土田 貴正, 佐藤 信行, 申 偉秀, 戸塚 康男, 濱野 久美子, 安島 美保, 秋山 義隆, 作家 有実子, 五味 朋子, 池田 寿男, 高木 正雄, 山門 実, 高橋 英孝, 沼部 敦司, 梅村 敏, 平和 伸仁, 池田 弓子, 常田 康夫, 四方 賢一, 和田 淳, 高橋 健二, 谷合 一陽, 尾山 秀樹, 松岡 孝, 江口 豊, 江口 直美, 上原 誉志夫, 槇野 博史, 裏出 良博

    臨床化学   31 ( Suppl.1 )   77a - 77a   2002.9

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  • 新しい腎疾患マーカーとしての尿中リポカリン型プロスタグランジンD合成酵素(L-PGDS) 尿中L-PGDSの臨床意義について(1)

    織田 浩司, 土田 貴正, 清木 興介, 椎名 康彦, 佐藤 信行, 申 偉秀, 戸塚 康男, 濱野 久美子, 安島 美保, 秋山 義隆, 作家 有実子, 五味 朋子, 池田 寿男, 高木 正雄, 山門 実, 高橋 英孝, 沼部 敦司, 梅村 敏, 平和 伸仁, 池田 弓子, 常田 康夫, 四方 賢一, 和田 淳, 高橋 健二, 谷合 一陽, 尾山 秀樹, 松岡 孝, 江口 豊, 江口 直美, 上原 誉志夫, 槇野 博史, 裏出 良博

    臨床化学   31 ( Suppl.1 )   87a - 87a   2002.9

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  • 腎症管理のための指標 何が必要か

    四方 賢一, 和田 淳, 槇野 博史

    日本腎臓学会誌   44 ( 6 )   520 - 520   2002.8

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  • 【身近な腎臓疾患 治療のコツと最新のトピックス】糖尿病性腎症

    小川 大輔, 松田 充浩, 四方 賢一, 槇野 博史

    今月の治療   10 ( 8 )   848 - 853   2002.7

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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 Yamaguchi, Y Suzuki, M Miyasaka, S Tojo, H Makino

    CLINICAL AND EXPERIMENTAL IMMUNOLOGY   129 ( 1 )   43 - 53   2002.7

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    Leucocytes infiltrate into renal tissue and are involved in the pathogenesis of crescentic glomerulonephritis. The initial event in the process of leucocyte infiltration is characterized by selectin-mediated leucocyte rolling on endothelial surface. Role of selectins in pathogenesis of glomerulonephritis has still been controversial. Sulphated glycolipids and sulphated polysaccharides interfere with the binding of P- and L-selectin with carbohydrate ligands on endothelial cells or on leucocytes. Here we evaluated the role of selectins and the preventive effects of sulphated colominic acid (SCA), a synthetic sulphated polysaccharide, on experimental crescentic glomerulonephritis in Wistar-Kyoto (WKY) rats. Crescentic glomerulonephritis was induced by injection of nephrotoxic serum (NTS) in WKY rats. Rats subsequently received intraperitoneal injection of saline, neutralizing or non-neutralizing monoclonal antibody (mAb) to rat P-selectin and L-selectin, SCA (5 or 10mg/kg/day) or nonsulphated colominic acid (CA) (10mg/kg/day) for 2 weeks. Localization of P-, E-selectin, ligands for L-selectin and intraglomerular leucocytes was examined by immunohistochemistry. Gene expression of platelet-derived growth factor (PDGF) B chain in glomeruli was quantified using real-time RT-PCR. P-selectin was highly expressed on glomerular endothelial cells after injection of NTS, whereas E-selectin and L-selectin ligands were not detected. Anti-P-selectin mAb, but not anti-L-selectin mAb, significantly reduced glomerular infiltration of macrophages, crescent formation, and proteinuria. SCA also reduced proteinuria, macrophage infiltration, and crescent formation in a dose-dependent manner. Furthermore, SCA suppressed gene expression of PDGF B chain in glomeruli. Our results indicate that P-selectin partially mediate glomerular infiltration of macrophage in experimental crescentic glomerulonephritis. Moreover, SCA may inhibit intraglomerular infiltration of macrophages by interfering with P-selectin-dependent adhesion pathway, and progression of experimental crescentic glomerulonephritis.

    DOI: 10.1046/j.1365-2249.2002.01875.x

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  • 糖尿病性腎症の成因

    四方 賢一, 槇野 博史

    プラクティス   19 ( 3 )   243 - 246   2002.5

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  • Case Reports : Recurrent Daytime Hyperglycemia and Fasting Hypoglycemia Due to Insulin Antibodies in a Patient with Diabetes Mellitus

    Journal of the Japan Diabetes Society   45 ( 5 )   319 - 323   2002.5

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  • 【検査計画法】腎・泌尿器疾患編 糖尿病性腎症

    松田 充浩, 四方 賢一, 槇野 博史

    綜合臨床   51 ( 増刊 )   1552 - 1556   2002.5

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  • 【糸球体内皮細胞の全て】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   2002.5

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  • 糖尿病性腎症の成因と治療 Update 腎症発症機構におけるマクロファージの役割

    四方 賢一, 槇野 博史

    日本腎臓学会誌   44 ( 3 )   182 - 182   2002.4

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  • スルファチドはL-セレクチンの主要なリガンドとして腎間質への白血球浸潤を誘導する

    小川 大輔, 四方 賢一, 松田 充浩, 岡田 震一, 臼井 仁美, 和田 淳, 槇野 博史

    日本腎臓学会誌   44 ( 3 )   250 - 250   2002.4

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  • 糸球体硬化の成因におけるマクロファージの役割 ICAM-1ノックアウトマウスを用いた検討

    城戸 雄一, 四方 賢一, 大賀 佐起子, 余財 亨介, 永瀬 亮, 臼井 仁美, 岡田 震一, 小川 大輔, 松田 充浩, 和田 淳

    日本腎臓学会誌   44 ( 3 )   207 - 207   2002.4

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  • OLETFラット内臓脂肪組織よりクローニングした白色脂肪特異的膜蛋白(OL-16)の構造解析

    江口 潤, 和田 淳, 肥田 和之, 松岡 孝至, 馬場 雅子, 永瀬 亮, 城戸 雄一, 山下 哲二, 国富 三絵, 清田 綾, 橋本 泉, 四方 賢一, 槇野 博史

    糖尿病   45 ( Suppl.2 )   S222 - S222   2002.4

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  • 腎症の病態と遺伝子研究最前線 遺伝子発現プロファイリングによる腎症の分子機構の解明

    和田 淳, 四方 賢一, 槇野 博史

    糖尿病   45 ( Suppl.2 )   S15 - S15   2002.4

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  • 糖尿病性腎症の腎組織におけるマクロファージのフェノタイプと活性化状態の経時的変化

    永瀬 亮, 四方 賢一, 岸 亮太郎, 小川 大輔, 城戸 雄一, 臼井 仁美, 岡田 震一, 松田 充浩, 和田 淳, 槇野 博史

    糖尿病   45 ( Suppl.2 )   S176 - S176   2002.4

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  • ケトン体による蛋白のAGE化

    永井 竜児, 凌 霞, 高木 香織, 小糸 和歌子, 中野 菜穂子, 海野 雄加, 四方 賢一, 槇野 博史, 堀内 正公

    糖尿病   45 ( Suppl.2 )   S120 - S120   2002.4

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  • 糖尿病性腎症の発症,進展に対するスタチンの抑制効果

    臼井 仁美, 四方 賢一, 大賀 佐起子, 余財 亨介, 城戸 雄一, 永瀬 亮, 岡田 震一, 小川 大輔, 松田 充浩, 和田 淳

    糖尿病   45 ( Suppl.2 )   S178 - S178   2002.4

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  • 糖尿病性腎症におけるマクロファージの役割(第2報) ICAM-1ノックアウトマウスを用いた検討

    岡田 震一, 四方 賢一, 大賀 佐起子, 余財 亨介, 永瀬 亮, 城戸 雄一, 臼井 仁美, 小川 大輔, 松田 充浩, 和田 淳, 槇野 博史

    糖尿病   45 ( Suppl.2 )   S176 - S176   2002.4

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  • OLETFラット内臓脂肪特異的分泌蛋白のvaspin(visceral adipose tissue specific SERPIN)のPioglitazoneによる発現調節

    肥田 和之, 和田 淳, 松岡 孝至, 江口 潤, 馬場 雅子, 山下 哲二, 永瀬 亮, 城戸 雄一, 国富 三絵, 橋本 泉, 清田 綾, 四方 賢一, 槇野 博史

    糖尿病   45 ( Suppl.2 )   S240 - S240   2002.4

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  • 糖尿病性腎症の治療方針

    四方 賢一, 槇野 博史

    プラクティス   19 ( 2 )   129 - 131   2002.3

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  • Angiocentric immunoproliferative lesions of the lung associated with diffuse renal involvement. International journal

    Shinichi Okada, Jun Wada, Tomoko Tsukinoki, Naoko Hirano, Yoichi Watanabe, Kenichi Shikata, Yasushi Yamasaki, Sumie Takase, Tadashi Yoshino, Tadaatsu Akagi, Hirofumi Makino

    American journal of kidney diseases : the official journal of the National Kidney Foundation   39 ( 3 )   E12   2002.3

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    A 62-year-old Japanese man presented with high fever, cough, and sputa. Computed tomography (CT) scan of the chest revealed lung infiltrates with air bronchogram of the right middle lobe and mediastinal lymphadenopathy. Bronchoscopic examination was performed, and Mycobacterium avium complex was detected from bronchoalveolar lavage fluid. Although the administration of clarithromycin and levofloxacin improved the patient's symptoms, the lung infiltrates on chest CT scan gradually worsened. Lung biopsy of segments 4 and 8 by video-assisted thorachoscopy revealed angiocentric and angiodestructive massive lymphoplasmocytic Infiltrations with multinucleated giant cells, which were compatible with grade II angiocentric immunoproliferative lesions. The patient was found to have deterioration of renal function, and glomerular filtration rate was 32.6 mL/min. His kidneys were enlarged and showed prominent and diffuse uptake of gallium-67 citrate. Percutaneous renal biopsy revealed massive infiltration of CD4(+) mononuclear cells, plasma cells, and eosinophils in the interstitium and destruction of normal structure of tubules. Blood vessels were destroyed and replaced by inflammatory cells. The combination chemotherapy achieved a remission, and the patient has remained free of disease at 2 years after onset of the illness. We recommend the imaging of kidneys for diagnosis and following renal biopsy to evaluate the renal involvement of angiocentric immunoproliferative lesions. (C) 2002 by the National Kidney Foundation, Inc.

    DOI: 10.1053/ajkd.2002.31423

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  • Relationship between reduced serum IGF-I levels and accumulation of visceral fat in Japanese men

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

    INTERNATIONAL JOURNAL OF OBESITY   26 ( 3 )   361 - 369   2002.3

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    OBJECTIVE: To investigate whether the changes in IGF-1 concentrations after weight reduction in Japanese overweight men are associated with changes in visceral and subcutaneous fat.
    DESIGN: Cross-sectional and longitudinal clinical intervention study with exercise education.
    SUBJECTS: One-hundred and twelve Japanese overweight men aged 30-59y (body mass index (BMI) 28.4+/-2.5 kg/m(2)) and 33 normal-weight men aged 30-39y (BMI 22.1+/-1.5 kg/m(2)) at baseline. From the participants, 56 randomly selected overweight men (BMI 28.8+/-2.8) were further enrolled into a 1 y exercise program.
    MEASUREMENTS: Fat distribution was evaluated by visceral fat M and subcutaneous fat (S) areas measured with computed tomography scanning at umbilical levels, metabolic parameters and hormones including insulin, leptin and IGF-1 at baseline and after 1 y.
    RESULTS: In 112 overweight subjects at baseline, insulin (10.5+/-5.0 muUl/ml) and leptin (6.4+/-3.7 ng/ml) significantly correlated with both V (r=0.260, P=0.0073; r=0.410, P&lt;0.0001) and S areas (r=0.377, P&lt;0.0001; r=0.613, P&lt;0.0001), respectively. IGF-1 (156.8+/-48.7 muU/ml) significantly and negatively correlated with V area (r= -0.242, P=0.0125)and age (r= - 0.192, P=0.0480). In normal-weight men aged 30-39y (n=33) and age-matched subjects (n=30) selected from the 112 overweight men, the serum IGF-1 further tightly correlated with V area (r= - 0.467, P&lt;0.0001). Visceral fat area and age were independently related to serum IGF-1 levels by multiple regression analysis. By intervention with exercise education, 56 overweight subjects showed an increase in daily steps (6224+/-2781 to 7898+/-4141 steps/day) and reduction of BMI (28.8+/-2.8 to 27.7+/-2.9). DeltaIGF-1 significantly correlated with DeltaV area (r= - 0.432, P = 0.0009) but not with DeltaS area or DeltaBMI.
    CONCLUSION: The present study indicated a negative correlation between IGF-1 levels and visceral fat at baseline as well as an association between the reduction in visceral fat and increase in IGF-1 levels after an exercise intervention.

    DOI: 10.1038/sj/ijo/0801899

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  • 比較的早期より腎性貧血を認めた1型糖尿病の一例

    馬場 雅子, 四方 賢一, 城戸 雄一, 永瀬 亮, 江口 潤, 松田 充浩, 和田 淳, 槇野 博史

    糖尿病   45 ( 2 )   163 - 163   2002.2

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  • 著明なインスリン抵抗性を認めたWerner症候群の一例

    城戸 雄一, 臼井 仁美, 山下 哲二, 松田 充浩, 和田 淳, 四方 賢一, 槇野 博史, 時信 政史

    糖尿病   45 ( 2 )   145 - 145   2002.2

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  • Basedow病で発症し中枢性甲状腺機能低下に移行した1型糖尿病の一例

    永瀬 亮, 臼井 仁美, 松田 充浩, 大石 徹也, 四方 賢一, 槇野 博史, 小倉 俊郎, 三村 由香里, 和田 淳

    糖尿病   45 ( 2 )   162 - 162   2002.2

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  • 【新時代を迎えた糖尿病治療】糖尿病性細小・大血管障害の現状と治療 糖尿病性腎症

    小川 大輔, 四方 賢一, 槇野 博史

    臨牀と研究   79 ( 1 )   62 - 67   2002.1

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  • Cyanotic congenital heart disease associated with glomerulomegaly and focal segmental glomerulosclerosis: remission of nephrotic syndrome with angiotensin converting enzyme inhibitor. International journal

    Kazuyuki Hida, Jun Wada, Hiroko Yamasaki, Yoshio Nagake, Hong Zhang, Hitoshi Sugiyama, Kenichi Shikata, Hirofumi Makino

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association   17 ( 1 )   144 - 7   2002.1

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  • 腎症 糖尿病性腎症の診断

    四方 賢一, 槇野 博史

    プラクティス   19 ( 1 )   10 - 13   2002.1

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  • 糖尿病性腎症の治療方針

    四方賢一, 槇野博史

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

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  • Changes in urinary and serum concentrations of macrophage-colony stimulating factor (M-CSF) in patients with renal diseases

    H. Yamaji, K. Shikata, M. Matsuda, D. Ogawa, Y. Ohmoto, H. Makino

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

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    Background. The infiltration of monocytes/macrophages into renal tissues is a typical feature of progressive renal diseases. Macrophage-colony stimulating factor (M-CSF) is one of the cytokines that are required for the activation of macrophages. It was previously reported that the glomerular expression of M-CSF was increased in patients with mesangial proliferative glomerulonephritis and that the urinary and serum M-CSF concentrations were increased in IgA nephropathy. In this study, we measured the urinary and serum M-CSF concentrations in patients with renal diseases to elucidate the role of M-CSF and macrophages in the progression of renal diseases. Methods. We examined urinary and serum M-CSF concentrations in patients with IgA nephropathy (IgA-N), lupus nephritis (LN), minimal change nephrotic syndrome (MCNS), and membranous nephropathy (MN), and in normal controls. The M-CSF concentrations were compared with the clinical parameters and the histological changes. These concentrations were also compared with the number of glomerular macrophages in the IgA-N group. In addition, the effects of prednisolone therapy on the M-CSF concentrations were examined in the patients with IgA-N. Results. Urinary and serum M-CSF concentrations were increased in the severe IgA-N group, the severe LN group, and the MCNS group (nephrotic) compared with concentrations in the control group. Urinary and serum M-CSF concentrations were correlated with the degree of proteinuria, mesangial proliferation, and the number of glomerular macrophages in IgA-N and LN. In addition, the urinary and serum M-CSF concentrations were decreased with prednisolone therapy in the patients with IgA-N. Conclusions. Urinary and serum M-CSF concentrations were elevated in patients with severe stage of mesangial proliferative glomerulonephritis and were correlated with the amount of urinary protein excretion, mesangial proliferation, and glomerular macrophage infiltration. Urinary and serum M-CSF concentrations may be useful markers with which to assess the extent of glomerular changes in mesangial proliferative glomerulonephritis.

    DOI: 10.1007/s101570200015

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  • 【糖尿病性腎症の全て】糖尿病性腎症の病期,診断,進展因子 糖尿病性腎症の進展因子 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

    松田 充浩, 四方 賢一, 槇野 博史

    腎と透析   51 ( 増刊 )   317 - 322   2001.12

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  • 【浮腫 診療のポイント】疾患による浮腫の病態と治療法 糖尿病性腎症

    松田 充浩, 四方 賢一, 槇野 博史

    臨床医   27 ( 10 )   2347 - 2351   2001.10

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  • 糖尿病性腎症の発症・進展に対するセリバスタチンの抑制効果

    臼井 仁美, 四方 賢一, 松田 充浩, 山下 哲二, 岡田 震一, 小川 大輔, 城戸 雄一, 永瀬 亮, 和田 淳, 槇野 博史

    糖尿病合併症   15 ( Suppl.1 )   90 - 90   2001.10

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  • 糖尿病性腎症の発症機構 ICAM-1ノックアウトマウスを用いた糖尿病性腎症の成因におけるマクロファージの役割の検討

    岡田 震一, 四方 賢一, 松田 充浩, 小川 大輔, 臼井 仁美, 城戸 雄一, 永瀬 亮, 和田 淳, 槇野 博史

    糖尿病合併症   15 ( Suppl.1 )   52 - 52   2001.10

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  • 【糖尿病とサイトカイン】糖尿病性腎症とサイトカイン

    四方 賢一, 槇野 博史

    Diabetes Frontier   12 ( 5 )   616 - 621   2001.10

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  • 糖尿病の慢性合併症 糖尿病性腎症

    岡田 震一, 四方 賢一, 槇野 博史

    からだの科学 増刊   増刊 ( 糖尿病2001 )   145 - 150   2001.9

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  • Nitric oxide system is involved in glomerular hyperfiltration in Japanese normo- and micro-albuminuric patients with type 2 diabetes

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

    DIABETES RESEARCH AND CLINICAL PRACTICE   53 ( 3 )   149 - 159   2001.9

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    Glomerular hyperfiltration plays a pathogenic role in the early stages of diabetic nephropathy. Experimental studies in laboratory animals suggest that nitric oxide (NO) alight be involved in the pathogenesis of glomerular hyperfiltration. We performed a cross-sectional study to determine the relationship between diabetic glomerular hyperfiltration and the NO system. Normoalbuminuric (n=41), microalbuminuric (n=25), and macroalbuminuric(n=16) patients with type 2 diabetes were recruited in this study and compared with age-matched 84 non-diabetic control subjects. Creatinine clearance and urinary NO2-/NO3- excretion (urinary NOx) were measured, and the expression of endothelial cell nitric oxide synthase (ecNOS) was evaluated in human renal tissues. Glomerular hyperfiltration was present in 19 (37.5%) and nine (36.6%) of normoalbuminuric and microalbuminuric type 2 diabetic patients, respectively. The urinary NOx was significantly higher in normoalbuminuric patients compared with normal subjects. Creatinine clearance correlated significantly with urinary NOx in normoalbuminuric and micro albuminuric patients. Immunohistochemical staining intensities for ecNOS were significantly increased in glomerular endothelial cells of microalbuminuric type 2 diabetic patients as compared with the control subjects. These results suggest that NO may contribute to the: pathogenesis of glomerular hyperfiltration in Japanese type 2 diabetic patients. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

    DOI: 10.1016/S0168-8227(01)00260-1

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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   2001.6

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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

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

    JOURNAL OF PERIODONTOLOGY   72 ( 6 )   774 - 778   2001.6

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    Background: Tumor necrosis factor-alpha (TNF-alpha) may play an important role in insulin resistance. In this study, we hypothesized that TNF-alpha produced due to periodontal inflammation synergistically affects insulin resistance as well as TNF-alpha produced from adipose tissues in insulin-resistant type 2 diabetes patients. Therefore, to understand the effects of antimicrobial periodontal therapy on serum TNF-alpha concentration and subsequent metabolic control of diabetes, we examined the periodontal and diabetic status on 13 type-2 diabetes patients.
    Methods: These patients were treated with local minocycline administration in every periodontal pocket around all existing teeth once a week for a month. Before and after treatment, the number of total bacteria in the periodontal pockets and circulating TNF-alpha concentration were measured and the HbA1c value was assessed.
    Results: Antimicrobial therapy significantly reduced the number of microorganisms in periodontal pockets (P &lt;0.01). After treatment, the circulating TNF-alpha level was significantly reduced (P &lt;0.015). The HbA1c value was also reduced significantly (P &lt;0.007). In addition, the 6 patients who were not receiving insulin therapy demonstrated decreased fasting insulin levels (P &lt;0.03), and HOMA-R (P &lt;0.03) indices. The average reductions in circulating TNF-alpha concentration and HbA1c value were 0.49 pg/ml and 0.8%, respectively.
    Conclusion: The results indicate that anti-infectious treatment is effective in improving metabolic control in diabetics, possibly through reduced serum TNF-alpha and improved insulin resistance.

    DOI: 10.1902/jop.2001.72.6.774

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  • Identification of vaspin, visceral adipose tissue specific SERPIN, isolated from OLETF rats

    K Hida, J Wada, T Matsuoka, M Kunitomi, K Shikata, H Makino

    DIABETES   50   A272 - A272   2001.6

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  • 【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   2001.5

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  • Collectrin, a collecting duct-specific transmembrane glycoprotein, is a novel homolog of ACE2 and is developmentally regulated in embryonic kidneys

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

    JOURNAL OF BIOLOGICAL CHEMISTRY   276 ( 20 )   17132 - 17139   2001.5

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    Collectrin, a novel homolog of angiotensin-converting enzyme-related carboxypeptidase (ACE2), was identified during polymerase chain reaction-based cDNA subtraction and up-regulated in 5/6 ablated kidneys at hypertrophic phase. Collectrin, with 222 amino acids, has an apparent signal peptide and a transmembrane domain; the sequence is conserved in mouse, rat, and human and shares 81.9% identity. Human collectrin has 47.8% identity with non-catalytic extracellular, transmembrane, and cytosolic domains of AGES; however, unlike ACE and AGES, collectrin lacks active dipeptidyl carboxypeptidase catalytic domains. The collectrin mRNA transcripts are expressed exclusively in the kidney. In situ hybridization reveals its mRNA expression in renal collecting ducts, and immunohistochemistry shows that it is localized to the luminal surface and cytoplasm of collecting ducts. Immunoprecipitation studies, using [S-35]methionine-labeled renal cortical and inner medullar collecting duct cells, i.e. M-1 and mIMCD-3, indicate that the protein size is similar to 32 kDa. During the development of mouse kidney, mRNA signal is detectable at day 13 of gestation, and the protein product is observed in the ureteric bud branches. Its expression is progressively increased during later stages of the gestation extending into the neonatal periods and then is decreased in adult life. Up-regulated expression of collectrin in the hypertrophic kidneys after renal ablation and restricted spatio-temporal expression during development indicates a possible role(s) in the process of progressive renal failure and renal organogenesis.

    DOI: 10.1074/jbc.M006723200

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  • Human fibroblasts ubiquitously express glutamic acid decarboxylase 65 (GAD 65): Possible effects of connective tissue inflammation on GAD antibody titer

    T Kono, F Nishimura, H Sugimoto, K Sikata, H Makino, Y Murayama

    JOURNAL OF PERIODONTOLOGY   72 ( 5 )   598 - 604   2001.5

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    Background: Type 1 diabetes is caused by a destruction of pancreatic beta cells due to autoimmunity. Autoantibody against glutamic acid decarboxylase (GAD) 65 expressed in pancreatic beta cells is widely used as a predictive marker for pancreatic destruction. In this study, we hypothesized that if certain cells in periodontal tissues could express GAD, then it may influence GAD antibody titer.
    Methods: We used: 1) reverse transcription-polymerase chain reaction (PCR) analysis to detect GAD 65 mRNA in various cells; 2) nucleotide sequencing analysis to confirm that amplified PCR product is the gene encoding GAD; and 3) Western blotting to determine the expression of GAD 65 protein in human gingival fibroblasts. Immunohistochemical staining of GAD 65 protein in normal and inflamed gingiva was performed to examine the potential influence of periodontal inflammation on GAD 65 expression. GAD antibody titer in sera of periodontal patients as well as healthy subjects was measured to determine if periodontal patients could develop autoantibody against GAD 65.
    Results: Cultured human gingival, periodontal, and dermal fibroblasts and mesangial cells expressed GAD mRNA. Nucleotide sequencing analyses confirmed the amplified PCR product as GAD 65. Western immunoblotting analyses and immunohistochemical staining revealed that the GAD 65 protein was expressed in vitro and in vivo. The expression of GAD 65 in inflamed tissue was higher than that in normal tissues. Two of 62 periodontal patients without diabetes showed an increased antibody titer against GAD 65, while none of the systemically healthy subjects showed an increased antibody titer against this antigen.
    Conclusions: We concluded that periodontal inflammation may result in higher levels of GAD and influence GAD antibody titer, and, hence, affect diabetic diagnosis based upon GAD antibody production.

    DOI: 10.1902/jop.2001.72.5.598

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  • Ultrastructure of glomerular basement membrane in active Heymann nephritis rats revealed by tissue-negative staining method

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

    AMERICAN JOURNAL OF NEPHROLOGY   21 ( 3 )   249 - 255   2001.5

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    Recently, we have developed a tissue-negative staining method, and successfully visualized fine meshwork structure of the glomerular basement membrane (GBM). To clarify the mechanism of proteinuria in active Heymann nephritis, we performed tissue-negative staining and investigated the ultrastructural alterations of the GEM. Active Heymann nephritis, the animal model of human membranous nephropathy, was induced in Lewis rats by the injection of proximal tubular brush border antigen, i.e. Fx1A. Urinary protein excretion was measured and histological studies were performed over 15 weeks following the Fx1A injection. Proteinuria developed at 10 weeks after injection (38.2 +/-7.4 mg/day) and progressively increased (160.2 +/- 20.6 mg/day at 15 weeks). Capillary fine deposits of IgG and C3 were seen by immunofluorescence, and subepithelial electron dense deposits (EDD) by transmission electron microscopy (TEM). Using the tissue-negative staining method, regular meshwork structure consisted of fine fibrils and pores (2.5 +/- 0.7 nm in short dimension) was observed in the GEM of control rats. At 10 and 15 weeks after injection, the GEM, directly facing the endothelial side of EDD, contained enlarged pores and nephrotic tunnels. Mean values of the short dimension of enlarged pores were 2.9 +/- 0.5 nm at 10 weeks and 3.1 +/-0.4 nm at 15 weeks, which were significantly larger than that of control rats (p &lt; 0.01). The rest area of the GEM, including newly produced GEM covering the epithelial side of EDD, had no significant difference in size of the pores from control GEM and no tunnels. Although there was no significant difference in the size of enlarged pores between 10 and 15 weeks, the percentage area of GBM with impaired size barrier increased at 15 weeks (51.4&lt;plus/minus&gt;8.1%) compared with 10 weeks (24.0 +/-8.3%) and related to severity of proteinuria. The density of the tunnels also increased at 15 weeks. In conclusion, immune deposits may affect the GBM biosynthesis and induce the defect of size barrier of the GEM, which is responsible for proteinuria in active Heymann nephritis. Copyright (C) 2001 S. Karger AG, Basel.

    DOI: 10.1159/000046257

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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

    和田 淳, 肥田 和之, 四方 賢一, 槇野 博史

    肥満研究   7 ( 1 )   54 - 56   2001.4

  • Gene expression profile in streptozotocin-induced diabetic mice kidneys undergoing glomerulosclerosis

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

    KIDNEY INTERNATIONAL   59 ( 4 )   1363 - 1373   2001.4

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    Background. To elucidate the molecular mechanism of diabetic nephropathy, a high-density DNA filter array was employed to survey the gene expression profile of streptozotocin-induced diabetic CD-1 (ICR) mouse kidneys.
    Methods. Ten-week-old CD-1 male mice were divided into four groups: (1) control, (2) unilaterally nephrectomized (UX) mice, (3) streptozotocin (STZ)-induced diabetic (STZ) mice, and (4) STZ mice with unilateral renal ablation (STZ-UX). Pathological changes were examined at 24 weeks after the induction. The gene expression profile was compared between the control and STZ mice by a Gene Discovery Array (GDA).
    Results. The glomeruli in UX mouse kidney showed prominent glomerular hypertrophy, while the accumulation of mesangial matrix was minimal. Both STZ and STZ + UX mice had significant glomerular hypertrophy and glomerulosclerosis, and the lesions were not enhanced by renal ablation. By comparison between control and STZ mice, 16 clones that increased in expression with the induction of diabetes and 65 clones that decreased in diabetic kidneys were identified. The 37 known genes were related to glucose and lipid metabolism, ion transport, transcription factors, signaling molecules, and extracellular matrix-related molecules. The genes known to be involved in cell differentiation and organogenesis in various tissues (that is, Unc-18 homolog, POU domain transcription factor 2, lunatic fringe gene homolog, fibrous sheath component 1, Sox-17, fibulin 2, and MRJ) were found to be differentially expressed in the early phase of diabetic kidneys.
    Conclusions. Hyperglycemia is a major determinant of glomerulosclerosis in STZ-induced diabetic CD-1 mice, and the altered gene expression in the early phase of diabetic kidney may be critical for the development of diabetic nephropathy.

    DOI: 10.1046/j.1523-1755.2001.0590041363.x

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  • レーザーを応用した根管拡大に関する研究(第一報) 根管壁面形状の比較検討

    四方 二郎, 池田 賢一, 勝呂 尚, 原田 優子, 林 宏徳, 山根 雅仁, 手嶋 健介, 小森 規雄, 明石 俊和

    日本歯科保存学雑誌   44 ( 春季特別 )   101 - 101   2001.4

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  • 半月体形成性腎炎に対する硫酸化コロミン酸の有効性の検討

    小川 大輔, 四方 賢一, 松田 充浩, 岡田 震一, 臼井 仁美, 和田 淳, 槇野 博史, 鈴木 康夫

    日本腎臓学会誌   43 ( 3 )   210 - 210   2001.4

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  • セレクチンによる腎間質への白血球浸潤誘導のメカニズム(第2報)

    松田 充浩, 四方 賢一, 小川 大輔, 岡田 震一, 臼井 仁美, 和田 淳, 槇野 博史

    日本腎臓学会誌   43 ( 3 )   178 - 178   2001.4

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  • 5/6腎臓摘出マウス腎臓よりクローニングされた集合管特異的膜蛋白collectrinの同定と発生腎における発現制御(第4報)

    和田 淳, 張 宏, 土山 芳徳, 平櫛 恵太, 肥田 和之, 四方 賢一, Yashpal Kanwar, 槇野 博史

    日本腎臓学会誌   43 ( 3 )   277 - 277   2001.4

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  • OLETFラット内臓脂肪特異的遺伝子OL-64とその遺伝子産物vaspin(visceral adipose tissue specific SERPIN)の同定(第3報)

    肥田 和之, 和田 淳, 松岡 孝至, 國富 三絵, 江口 潤, 馬場 雅子, 四方 賢一, 槇野 博史

    糖尿病   44 ( Suppl.1 )   S29 - S29   2001.3

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  • OLETFラットにおけるpioglitazone投与及び運動療法の長期効果

    松岡 孝至, 和田 淳, 肥田 和之, 江口 潤, 馬場 雅子, 山下 哲二, 平櫛 恵太, 四方 賢一, 槙野 博文

    糖尿病   44 ( Suppl.1 )   S29 - S29   2001.3

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  • 血中可溶性接着分子濃度と糖尿病血管合併症との関連

    臼井 仁美, 四方 賢一, 松田 充浩, 和田 淳, 岡田 震一, 小川 大輔, 平櫛 恵太, 肥田 和之, 松岡 孝至, 槇野 博史

    糖尿病   44 ( Suppl.1 )   S144 - S144   2001.3

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  • 糖尿病性腎症に紫斑病性腎炎を合併した高齢者の一例

    臼井 仁美, 杉本 太郎, 松岡 孝至, 松田 充浩, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   44 ( 3 )   263 - 263   2001.3

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  • 糖尿病性腎症の成因におけるマクロファージの役割 ICAM-1ノックアウトマウスを用いた検討

    岡田 震一, 四方 賢一, 松田 充浩, 小川 大輔, 臼井 仁美, 山下 哲二, 永瀬 亮, 城戸 雄一, 和田 淳, 槇野 博史

    糖尿病   44 ( Suppl.1 )   S8 - S8   2001.3

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  • 骨盤内リンパ嚢胞感染症を合併したミトコンドリア糖尿病(3243 A-G変異)の1例

    小川 大輔, 四方 賢一, 上野 明子, 岡田 震一, 山下 哲二, 松田 充浩, 和田 淳, 槇野 博史

    糖尿病   44 ( 3 )   281 - 281   2001.3

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  • ストレプトゾトシン(STZ)糖尿病SDラットの糸球体過剰濾過におけるAdrenomedullin(AM)の関与

    平櫛 恵太, 和田 淳, 肥田 和之, 山下 哲二, 杉本 光, 四方 賢一, 槇野 博史, 南野 直人, 寒川 賢治

    糖尿病   44 ( Suppl.1 )   S10 - S10   2001.3

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  • プロスタサイクリン誘導体によるOLETFラットに対する血糖降下を介した腎症進展抑制効果

    山下 哲二, 四方 賢一, 平櫛 恵太, 岡田 震一, 小川 大輔, 肥田 和之, 臼井 仁美, 松田 充浩, 和田 淳, 槇野 博史

    糖尿病   44 ( Suppl.1 )   S145 - S145   2001.3

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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, 山崎 康司

    内分泌・糖尿病科   12 ( 2 )   198 - 206   2001.2

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  • 医学と医療の最前線 糖尿病性腎症の診断と治療

    槇野 博史, 四方 賢一, 和田 淳

    日本内科学会雑誌   90 ( 2 )   350 - 358   2001.2

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    我が国に多い2型糖尿病では腎症を蛋白尿・腎機能の面より5期に病期分類している.糖尿病性腎症は第3期の顕性腎症を過ぎると大多数は進行性であり,慢性腎不全に陥り,予後不良である.従って腎症を早期に診断して,充分な治療を行い腎症が進行しないようにすることが重要である.現在のところ微量アルブミン尿が早期腎症の診断の確立されたマーカーであるが,筆者らの研究が契機となり開発された尿中IV型コラーゲン測定法の臨床応用が可能となり,腎症のより早期の指標となるのではないかと期待されている.一方腎症の治療においては血糖・血圧の厳格なコントールと蛋白制限食が原則である.膵移植後10年で結節性病変が治癒した報告がなされたが,これは我々に血糖コントロールの重要性を再認識させるものである.

    DOI: 10.2169/naika.90.350

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  • 男性肥満者における内臓脂肪蓄積とIGF-1の検討

    和田 淳, 國富 三絵, 土山 芳徳, 肥田 和之, 四方 賢一, 槇野 博史, 高橋 香代, 吉良 尚平, 宮武 信行, 藤井 昌史

    日本内科学会雑誌   90 ( 臨増 )   146 - 146   2001.2

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  • ストレプトゾトシン誘発糖尿病マウスにおいて発現の上昇する新規遺伝子群の同定

    和田 淳, 四方賢一, 槇野博史

    糖尿病性腎症   2001

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  • 重イオンビーム照射による効率的なバーベナ(Verbena hybrida)不稔系統の育成

    鈴木賢一, 四方康範, 阿部知子, 勝元幸久, 吉田茂男, 久住高章

    日本植物細胞分子生物学会大会・シンポジウム講演要旨集   19th   2001

  • 糖尿病性腎症の成因におけるマクロファージの役割 治療への展望

    四方賢一

    Medical Tribune   34 ( 24 )   2001

  • 糖尿病2001 第7章 糖尿病の慢性合併症 II 糖尿病性腎症

    岡田震一, 四方賢一, 槙野博史

    からだの科学   2001

  • 【糖尿病と合併症へのアプローチ】糖尿病合併症への対応の実際 早期腎症への対応

    久代 昌彦, 四方 賢一, 槇野 博史

    Medicina   37 ( 13 )   1973 - 1976   2000.12

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  • 【糖尿病と腎症 その新しい展開】基礎 発症・進展機構 浸潤マクロファージ

    四方 賢一, 槇野 博史

    Diabetes Frontier   11 ( 5 )   677 - 684   2000.10

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  • 【慢性腎疾患 遺伝因子,増悪因子,臓器再生への新たなアプローチ】遺伝子解明へのアプローチ 糖尿病性腎症の遺伝素因

    四方 賢一, 和田 淳, 槇野 博史

    BIO Clinica   15 ( 11 )   833 - 837   2000.10

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  • 【糖尿病の細胞生物学と病態】糖尿病性腎症の細胞生物学と病態 糸球体過剰濾過の成因とNO

    山下 哲二, 四方 賢一, 槇野 博史

    細胞   32 ( 12 )   464 - 466   2000.10

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  • 糖尿病腎不全患者における血清クレアトール値

    長宅 芳男, 福田 真治, 市川 晴夫, 四方 賢一, 川野 克己, 平松 信, 槇野 博史

    日本腎臓学会誌   42 ( 6 )   446 - 446   2000.9

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  • 糖尿病性腎症の発症及び進展に関連する遺伝子へのアプローチ

    四方 賢一, 和田 淳, 槇野 博史

    日本腎臓学会誌   42 ( 6 )   424 - 424   2000.9

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  • ストレプトゾトシン(STZ)糖尿病SDラットの糸球体過剰濾過におけるAdrenomedullin(AM)の関与

    平櫛 恵太, 和田 淳, 山下 哲二, 肥田 和之, 土山 芳徳, 岡田 震一, 小川 大輔, 杉本 光, 四方 賢一, 槇野 博史

    糖尿病合併症   14 ( Suppl.1 )   51 - 51   2000.9

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  • 【蛋白尿・血尿の診療】二次性糸球体疾患の診断と治療 糖尿病性腎症

    四方 賢一, 和田 淳, 槇野 博史

    診断と治療   88 ( 7 )   1161 - 1168   2000.7

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    Other Link: http://search.jamas.or.jp/link/ui/2000274694

  • 糖尿病性腎症とRA等

    四方 賢一, 尾上 佳子, 槇野 博史

    Cardiac Practice   11 ( 3 )   326 - 330   2000.7

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  • 糖尿病性腎症の分子機構 糖尿病性腎症における細胞接着分子の発現とマクロファージ浸潤のメカニズム

    四方 賢一, 杉本 光, 槇野 博史

    糖尿病合併症   14 ( 2 )   111 - 115   2000.7

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  • 【慢性腎不全の治療 保存期から移植まで】保存期腎不全の管理と治療 糖尿病性腎症の治療

    四方 賢一, 槇野 博史

    日本内科学会雑誌   89 ( 7 )   1317 - 1323   2000.7

  • 糖尿病性腎症の腎組織における細胞接着分子の発現機構の解明

    四方 賢一

    糖尿病合併症   14 ( 1 )   31 - 39   2000.6

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  • Identification of genes specifically expressed in the accumulated visceral adipose tissue of OLETF rats

    K Hida, J Wada, H Zhang, K Hiragushi, Y Tsuchiyama, K Shikata, H Makino

    DIABETES   49   A311 - A311   2000.5

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  • The alteration of gene expression profile in streptozotocin-induced diabetic ICR mice kidney revealed by high density DNA array

    J Wada, H Zhang, Y Tsuchiyama, K Hiragushi, K Hida, S Okada, D Ogawa, K Shikata, H Makino

    DIABETES   49   A161 - A161   2000.5

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  • 【処方計画】腎・尿路系疾患 糖尿病性腎症

    四方 賢一, 槇野 博史

    綜合臨床   49 ( 増刊 )   1489 - 1492   2000.5

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  • 【内科治療のグローバルスタンダード】腎疾患 糖尿病性腎症

    宮武 伸行, 四方 賢一, 槇野 博史

    臨床医   26 ( 増刊 )   1179 - 1183   2000.5

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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   2000.4

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    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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  • 【肥満の細胞生物学】OLETFラットの内臓脂肪組織特異的に発現する遺伝子の同定

    和田 淳, 肥田 和之, 張 宏, 四方 賢一, 槇野 博史

    糖尿病   43 ( Suppl.1 )   56 - 56   2000.4

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  • 糖尿病患者の腎組織及び動脈硬化巣における各種AGE構造体の局在

    岡田 震一, 四方 賢一, 松田 充浩, 小川 大輔, 久代 昌彦, 杉本 光, 和田 淳, 槇野 博史, 永井 竜児, 堀内 正公

    糖尿病   43 ( Suppl.1 )   148 - 148   2000.4

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  • 歯周治療は2型糖尿病患者のインスリン抵抗性と血糖値を改善する

    岩本 義博, 西村 英紀, 杉本 光, 四方 賢一, 槇野 博史, 福田 哲也, 辻 孝夫, 岩本 正博, 村山 洋二

    糖尿病   43 ( Suppl.1 )   98 - 98   2000.4

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  • 糖尿病性腎症患者の腎組織におけるMCSFの発現の検討

    松田 充浩, 四方 賢一, 小川 大輔, 岡田 震一, 山下 哲二, 宮武 伸行, 四方 泰史, 和田 淳, 槇野 博史

    糖尿病   43 ( Suppl.1 )   148 - 148   2000.4

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  • 糖尿病ラットの糸球体過剰濾過と蛋白尿に対するベラプロストナトリウムの抑制効果

    山下 哲二, 杉本 光, 四方 賢一, 小川 大輔, 岡田 震一, 平櫛 恵太, 土山 芳徳, 四方 泰史, 和田 淳, 槇野 博史

    糖尿病   43 ( Suppl.1 )   269 - 269   2000.4

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  • ストレプトゾトシン(STZ)糖尿病ICRマウス腎臓の高密度DNAアレイによる遺伝子発現プロファイルの検討

    和田 淳, 土山 芳徳, 張 宏, 平櫛 恵太, 肥田 和之, 國富 三絵, 小川 大輔, 四方 賢一, 槇野 博史

    糖尿病   43 ( Suppl.1 )   172 - 172   2000.4

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  • ストレプトゾトシン(STZ)糖尿病SDラットの糸球体過剰濾過におけるAdrenomedullin(AM)の関与

    平櫛 恵太, 和田 淳, 張 宏, 山下 哲二, 肥田 和之, 土山 芳徳, 杉本 光, 四方 賢一, 寒川 賢治, 槇野 博史

    糖尿病   43 ( Suppl.1 )   171 - 171   2000.4

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  • 男性肥満者における内臓脂肪蓄積とIGF-Iの年代別検討

    國富 三絵, 和田 淳, 高橋 香代, 土山 芳徳, 肥田 和之, 宮武 伸行, 藤井 昌史, 四方 賢一, 吉良 尚平, 槇野 博史

    糖尿病   43 ( Suppl.1 )   182 - 182   2000.4

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  • ストレプトゾトシン(STZ)糖尿病ICRマウス腎臓の糸球体病変の組織学的検討

    土山 芳徳, 和田 淳, 張 宏, 平櫛 恵太, 山下 哲二, 肥田 和之, 岡田 震一, 四方 賢一, 槇野 博史

    糖尿病   43 ( Suppl.1 )   173 - 173   2000.4

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  • 2型糖尿病における糸球体過剰濾過とNOの関連の検討

    平櫛 恵太, 杉本 光, 四方 賢一, 山下 哲二, 土山 芳徳, 和田 淳, 熊谷 功, 福島 正樹, 槇野 博史

    日本腎臓学会誌   42 ( 3 )   227 - 227   2000.4

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  • ストレプトゾトシン(STZ)糖尿病ICRマウス腎臓の高密度DNAアレイによる遺伝子発現プロファイルの検討

    和田 淳, 土山 芳徳, 張 宏, 平櫛 恵太, 肥田 和之, 国富 三絵, 四方 賢一, 槇野 博史

    日本腎臓学会誌   42 ( 3 )   160 - 160   2000.4

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  • ProstaglandinI2 analogueが糖尿病ラットの糸球体過剰濾過を抑制するメカニズムの検討

    山下 哲二, 杉本 光, 四方 賢一, 平櫛 恵太, 久代 昌彦, 四方 泰史, 土山 芳徳, 國富 三絵, 和田 淳, 槇野 博史

    日本腎臓学会誌   42 ( 3 )   240 - 240   2000.4

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  • 血中酸化LDLの測定法の確立とそれを用いた臨床的検討

    笠原 順子, 松浦 栄次, 山崎 康司, 杉山 斉, 丸山 啓輔, 四方 賢一, 小林 和子, 劉 慶平, 保田 立二, 槇野 博史

    日本腎臓学会誌   42 ( 3 )   193 - 193   2000.4

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  • ストレプトゾトシン(STZ)糖尿病ICRマウス腎臓の糸球体病変の組織学的検討

    土山 芳徳, 和田 淳, 張 宏, 平櫛 恵太, 山下 哲二, 肥田 和之, 岡田 震一, 四方 賢一, 槇野 博史

    日本腎臓学会誌   42 ( 3 )   160 - 160   2000.4

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  • セレクチンによる腎組織への白血球浸潤誘導のメカニズム

    松田 充浩, 四方 賢一, 小川 大輔, 岡田 震一, 四方 泰史, 和田 淳, 槇野 博史

    日本腎臓学会誌   42 ( 3 )   213 - 213   2000.4

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  • 半月体形成性腎炎に対するセレクチン阻害剤の有効性の検討

    小川 大輔, 四方 賢一, 岡田 震一, 平櫛 恵太, 土山 芳徳, 四方 泰史, 松田 充浩, 和田 淳, 槇野 博史, 鈴木 康夫

    日本腎臓学会誌   42 ( 3 )   213 - 213   2000.4

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  • 5/6腎摘マウス腎臓からクローニングされた腎特異発現遺伝子NX-17の同定(第3報)

    和田 淳, 張 宏, 土山 芳徳, 平櫛 恵太, 肥田 和之, 小川 大輔, 四方 賢一, 槇野 博史

    日本腎臓学会誌   42 ( 3 )   200 - 200   2000.4

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  • 歯周病は歯肉線維芽細胞由来GAD 65の発現に影響を与える

    河野 隆幸, 西村 英紀, 杉本 光, 四方 賢一, 槇野 博史, 村山 洋二

    糖尿病   43 ( Suppl.1 )   98 - 98   2000.4

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  • 腎疾患の分子医学 腎臓病と接着分子

    四方 賢一, 槇野 博史

    現代医療   32 ( 3 )   735 - 743   2000.3

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    Other Link: http://search.jamas.or.jp/link/ui/2000153358

  • 壊死性筋膜炎,敗血症,DICを合併した糖尿病性腎症の1例

    小川 大輔, 四方 賢一, 上野 明子, 内田 治人, 浅田 麻紀, 岡田 震一, 松田 充浩, 和田 淳, 槇野 博史

    糖尿病   43 ( 3 )   262 - 262   2000.3

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  • 頭蓋咽頭腫術後の尿崩症に糖尿病を続発したKlippel-Trenaunay-Weber syndromeの1例

    岡田 震一, 橋本 泉, 四方 賢一, 岩橋 充啓, 小川 大輔, 肥田 和之, 和田 淳, 槇野 博史, 小倉 俊郎

    糖尿病   43 ( 3 )   254 - 254   2000.3

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  • 家族内に1型糖尿病とSLEを発症したSPIDDMの1例

    肥田 和之, 四方 賢一, 井上 裕子, 小川 大輔, 岡田 震一, 松田 充浩, 和田 淳, 槇野 博史, 服部 輝彦

    糖尿病   43 ( 3 )   260 - 260   2000.3

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  • 合併症の基礎知識 糖尿病性腎症 透析患者の血糖コントロールについて

    土山 芳徳, 長宅 芳男, 和田 淳, 四方 賢一, 槇野 博史

    透析ケア   6 ( 2 )   184 - 189   2000.2

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  • 糖尿病性腎症における糸球体基底膜障害に対するアンギオテンシン変換酵素阻害薬の効果

    四方 賢一, 林 佳子, 小川 さえ子, 松田 充浩, 山下 哲二, 平櫛 恵太, 和田 淳, 槇野 博史, 太田 康介

    日本内科学会雑誌   89 ( 臨増 )   145 - 145   2000.2

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  • 【糖尿病】糖尿病性腎症の病期と治療の実際

    久代 昌彦, 四方 賢一, 槇野 博史

    Medical Practice   17 ( 1 )   69 - 74   2000.1

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  • 糖尿病患者への服薬カウセリングと医療薬学実践教育について

    荒木 博陽, 川崎 博巳, 出石 通博, 二神 幸次郎, 四方 賢一, 和田 淳, 杉本 光, 久代 昌彦, 槇野 博史, 五味田 裕

    病院薬学   26 ( 1 )   17 - 26   2000

  • RA系をめぐる最近の話題 糖尿病性腎症とRA系

    四方賢一, 尾上佳子, 槙野博史

    Cardiac Practice   11 ( 3 )   2000

  • ベラプロストによる糖尿病ラット糸球体へのマクロファージ浸潤抑制効果

    山下 哲二, 四方 賢一, 杉本 光, 平櫛 恵太, 國富 三絵, 土山 芳徳, 四方 泰史, 久代 昌彦, 和田 淳, 槇野 博史

    糖尿病合併症   13 ( Suppl.1 )   88 - 88   1999.10

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  • 糖尿病性腎症における糸球体基底膜障害に対するアンギオテンシン変換酵素阻害薬の効果

    四方 賢一, 尾上 佳子, 小川 さえ子, 太田 康介, 太田 善介, 槇野 博史

    日本臨床電子顕微鏡学会誌   32 ( 増刊 )   S85 - S85   1999.10

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  • 2型糖尿病患者における糸球体過剰濾過と一酸化窒素(NO)の関連の検討

    平櫛 恵太, 杉本 光, 四方 賢一, 山下 哲二, 宮武 伸行, 四方 泰史, 和田 淳, 熊谷 功, 福島 正樹, 槇野 博史

    糖尿病合併症   13 ( Suppl.1 )   90 - 90   1999.10

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  • LDL吸着療法により血液透析から離脱し得た巣状糸球体硬化症(FGS)の1例

    吉永 泰彦, 服部 美佳, 松岡 孝至, 松本 光仁, 平櫛 恵太, 和田 淳, 四方 賢一, 槇野 博史

    日本腎臓学会誌   41 ( 6 )   543 - 543   1999.9

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  • Integrins mediate the inhibitory effect of focal adhesion on angiotensin II-induced p44/42 mitogen-activated protein (MAP) kinase activity in human mesangial cells

    Yasushi Shikata, Kenichi Shikata, Mitsuhiro Matsuda, Keita Hiragushi, Daisuke Ogawa, Hikaru Sugimoto, Jun Wada, Hirofumi Makino

    Biochemical and Biophysical Research Communications   261 ( 3 )   820 - 823   1999.8

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    Previously, we reported that the formation of focal adhesion accelerated by accumulation of extracellular matrices may inhibit the angiotensin II-stimulated proliferation of human mesangial cells (HMCs). The process is regulated by p44/42 MAP kinase activity through the mediation of paxillin and GTPase activating proteins. In this report, we investigated the effect of integrin molecules on the angiotensin II-induced p44/42 MAP kinase activation in non-adherent HMCs. The results demonstrated that incubation of cells with both antibody to integrin β1 chain (K20) and GRGDS peptide induced integrin clustering, paxillin aggregation, and marked suppression of angiotensin II-induced p44/42 MAP kinase activation. On the other hand, incubation of cells with K20 alone induced integrin clustering without paxillin aggregation and the suppressive effect on angiotensin II-stimulated p44/42 MAP kinase activity. Our results strongly suggest the pivotal role of integrins in the inhibitory effect of focal adhesion on p44/42 MAP kinase activity, the checking system against angiotensin II-induced MAP kinase overactivation.

    DOI: 10.1006/bbrc.1999.1080

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  • Integrins mediate the inhibitory effect of focal adhesion on angiotensin II-induced p44/42 mitogen-activated protein (MAP) kinase activity in human mesangial cells

    Yasushi Shikata, Kenichi Shikata, Mitsuhiro Matsuda, Keita Hiragushi, Daisuke Ogawa, Hikaru Sugimoto, Jun Wada, Hirofumi Makino

    Biochemical and Biophysical Research Communications   261 ( 3 )   820 - 823   1999.8

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    Previously, we reported that the formation of focal adhesion accelerated by accumulation of extracellular matrices may inhibit the angiotensin II-stimulated proliferation of human mesangial cells (HMCs). The process is regulated by p44/42 MAP kinase activity through the mediation of paxillin and GTPase activating proteins. In this report, we investigated the effect of integrin molecules on the angiotensin II-induced p44/42 MAP kinase activation in non-adherent HMCs. The results demonstrated that incubation of cells with both antibody to integrin β1 chain (K20) and GRGDS peptide induced integrin clustering, paxillin aggregation, and marked suppression of angiotensin II-induced p44/42 MAP kinase activation. On the other hand, incubation of cells with K20 alone induced integrin clustering without paxillin aggregation and the suppressive effect on angiotensin II-stimulated p44/42 MAP kinase activity. Our results strongly suggest the pivotal role of integrins in the inhibitory effect of focal adhesion on p44/42 MAP kinase activity, the checking system against angiotensin II-induced MAP kinase overactivation.

    DOI: 10.1006/bbrc.1999.1080

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  • 【糖尿病診療(Step:3)合併症をいかにチェックするか】専門医への紹介,他科医との連携

    槇野 博史, 平櫛 恵太, 杉本 光, 四方 賢一

    治療   81 ( 8 )   2095 - 2105   1999.8

  • 【メサンギウム細胞の全て】メサンギウム細胞の増殖誘導因子

    松田 充浩, 四方 賢一, 槇野 博史

    腎と透析   47 ( 2 )   193 - 200   1999.8

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  • 【糸球体腎炎の発症と治療】糸球体腎炎の治療 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   190 ( 1 )   95 - 104   1999.7

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    炎症巣や動脈硬化巣へのマクロファージを中心とする白血球の浸潤は,細胞接着分子によって調節される.様々な疾患において,接着分子の機能を制御することによる治療(抗接着分子療法)が開発されつつある

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=1999&ichushi_jid=J00060&link_issn=&doc_id=19990705020018&doc_link_id=%2Faa7ayuma%2F1999%2F019001%2F019%2F0095-0104%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faa7ayuma%2F1999%2F019001%2F019%2F0095-0104%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • 糖尿病性腎症 overviewと遺伝素因

    四方 賢一, 和田 淳, 槇野 博史

    日本透析医学会雑誌   32 ( Suppl.1 )   571 - 571   1999.6

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  • プロスタグランジンI2誘導体による糖尿病ラット糸球体へのマクロファージ浸潤抑制効果

    山下 哲二, 杉本 光, 平櫛 恵太, 久代 昌彦, 四方 泰史, 土山 芳徳, 國富 三絵, 和田 淳, 四方 賢一, 槇野 博史

    日本腎臓学会誌   41 ( 3 )   327 - 327   1999.5

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  • NODマウスとMus Spretusを用いた連鎖解析による糸球体硬化関連遺伝子座位の同定

    四方 賢一, 槇野 博史, 服部 正和, 土井 俊夫

    日本腎臓学会誌   41 ( 3 )   264 - 264   1999.5

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  • 【糖尿病の生涯】糖尿病性腎症 overviewと遺伝素因

    四方 賢一, 和田 淳, 槇野 博史

    日本腎臓学会誌   41 ( 3 )   210 - 210   1999.5

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  • Representational difference analysis of cDNA(cDNA-RDA)による5/6腎摘マウス腎臓に発現する遺伝子の検索(第2報)

    張 宏, 和田 淳, 土山 芳徳, 平櫛 恵太, 肥田 和之, 四方 賢一, 槇野 博史

    日本腎臓学会誌   41 ( 3 )   267 - 267   1999.5

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  • galectin-9の腎炎抑制効果の検討(第2報)

    土山 芳徳, 和田 淳, 張 宏, 守田 吉孝, 平櫛 恵太, 肥田 和之, 杉本 光, 四方 賢一, 槇野 博史, Kanwar YashpalS.

    日本腎臓学会誌   41 ( 3 )   337 - 337   1999.5

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  • Angiotensin IIの細胞増殖刺激に対する細胞接着斑のGAP蛋白を介した抑制作用の検討

    四方 泰史, 四方 賢一, 松田 充浩, 和田 淳, 杉本 光, 槇野 博史

    日本腎臓学会誌   41 ( 3 )   280 - 280   1999.5

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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   1999.4

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    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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  • ベラプロストナトリウムによる糖尿病ラット糸球体のマクロファージ浸潤抑制効果

    山下 哲二, 杉本 光, 平櫛 恵太, 久代 昌彦, 四方 泰史, 土山 芳徳, 國富 三絵, 和田 淳, 四方 賢一, 槇野 博史

    糖尿病   42 ( Suppl.1 )   S115 - S115   1999.4

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  • 糖尿病性腎症の病態と最新の治療ガイドライン 微量アルブミン尿の定義と早期腎症の病態

    槇野 博史, 四方 賢一, 杉本 光, 谷亀 光則

    糖尿病   42 ( Suppl.1 )   S24 - S24   1999.4

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  • OLETFラットの腎組織障害に対するACE阻害剤イミダプリルの効果

    林 佳子, 四方 賢一, 小川 さえ子, 平櫛 恵太, 宮武 伸行, 四方 泰史, 太田 康介, 杉本 光, 和田 淳, 槇野 博史

    糖尿病   42 ( Suppl.1 )   S115 - S115   1999.4

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  • OLETFラットの内臓脂肪に発現する遺伝子のクローニング

    肥田 和之, 和田 淳, 張 宏, 土山 芳徳, 平櫛 恵太, 杉本 光, 四方 賢一, 槇野 博史

    糖尿病   42 ( Suppl.1 )   S125 - S125   1999.4

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  • 糖尿病ラット腎における内皮細胞型一酸化窒素合成酵素(ecNOS)の糸球体過剰濾過への関与

    杉本 光, 四方 賢一, 久代 昌彦, 林 佳子, 平櫛 恵太, 山下 哲二, 和田 淳, 槇野 博史

    糖尿病   42 ( Suppl.1 )   S139 - S139   1999.4

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  • LDL吸着療法が奏効した巣状糸球体硬化症の1例

    服部 美佳, 松岡 孝至, 吉永 泰彦, 松本 光仁, 平櫛 恵太, 和田 淳, 四方 賢一

    尾道市立市民病院医学雑誌   14 ( 2 )   118 - 122   1999.3

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    50歳女.3年半前に発症した巣状糸球体硬化症による頻回再発性ネフローゼ症候群で,徐々にステロイド抵抗性となり,シクロスポリンを併用した.ステロイド糖尿病,著明な高コレステロール血症を合併するため,インスリン療法,LDL吸着療法を施行した.施行後,ステロイド,シクロスポリンの反応性が改善した.今回,ネフローゼ再燃と,腎機能の増悪で再入院し,2回の血液透析に引き続き,再度LDL吸着療法を施行し,蛋白尿の減少と腎機能の改善を認めた

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  • 著明な高血糖と早朝時低血糖を繰り返した,抗インスリン抗体陽性NIDDMの1例

    山下 哲二, 岡田 震一, 河本 順子, 河本 紀一, 肥田 和之, 国富 三絵, 土山 芳徳, 杉本 光, 和田 淳, 四方 賢一

    糖尿病   42 ( 3 )   232 - 232   1999.3

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  • Relational data baseを用いての糖尿病外来者の管理

    肥田 和之, 和田 淳, 四方 泰史, 尾上 佳子, 佐藤 正樹, 佐藤 幹雄, 杉本 光, 四方 賢一, 槇野 博史

    糖尿病   42 ( 3 )   250 - 250   1999.3

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  • 【臨床糖尿病学】糖尿病性慢性合併症 糖尿病性腎症 発症・進展機序と治療法に関する最近の研究成果

    槇野 博史, 杉本 光, 四方 賢一

    日本臨床   57 ( 3 )   590 - 600   1999.3

  • 進行性腎障害の腎臓に発現する遺伝子の同定

    和田 淳, 張 宏, 土山 芳徳, 平櫛 恵太, 肥田 和之, 四方 賢一, 槇野 博史

    日本内科学会雑誌   88 ( 臨増 )   142 - 142   1999.2

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  • 間質・尿細管 発症進展における接着分子の役割

    四方 賢一, 槇野 博史

    Annual Review腎臓   1999   98 - 107   1999.1

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  • 【糖尿病 病態解明と治療の最前線】糖尿病の合併症とその治療 糖尿病性腎症の形態学的アプローチ 糸球体過剰濾過の発症メカニズム

    槇野 博史, 杉本 光, 四方 賢一

    医学のあゆみ   188 ( 5 )   591 - 596   1999.1

  • 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

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    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

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    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.

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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

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    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

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    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

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    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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  • High-resolution ultrastructural comparison of renal glomerular and tubular basement membranes

    Saeko Ogawa, Zensuke Ota, Kenichi Shikata, Kazue Hironaka, Yoshiko Hayashi, Kosuke Ota, Masahiko Kushiro, Nobuyuki Miyatake, Noboru Kishimoto, Hirofumi Makino

    American Journal of Nephrology   19 ( 6 )   686 - 693   1999

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    Background/Aims: Glomerular basement membranes (GBM) and tubular basement membranes (TBM) consist of a fine meshwork composed mainly of type IV collagen. Each segment of tubules has specialized physiologic functions, and thus we investigated the ultrastructure of various basement membranes in rat kidneys. Methods: Since purifying basement membranes from different tubule segments is technically challenging, we employed tissue negative staining rather than conventional negative staining to compare the ultrastructures of proximal and distal TBM and GBM in normal rats. We also assessed the distribution of extracellular matrix components including type IV collagen, laminin, heparan sulfate proteoglycan, and fibronectin in the basement membranes by immunohistochemistry. Results: TBM and GBM of normal rats showed a fine meshwork structure consisting of fibrils forming small round to oval pores. Short- and long-pore diameters in proximal tubules were 3.3 ± 0.5 and 3.9 ± 0.6 nm, respectively, and in distal tubules 3.5 ± 0.7 and 4.3 ± 0.8 nm, respectively. For GBM the respective diameters were 2.5 ± 0.5 and 3.0 ± 0.5 nm. Immunohistochemical analysis showed no significant difference in distribution of extracellular matrix components between proximal and distal TBM. However, immunofluorescence scores of α1 chain of type IV collagen, fibronectin, and laminin were higher in the TBM than in the GBM. On the other hand, heparan sulfate proteoglycan was higher in the GBM. Conclusion: Ultrastructural differences in renal basement membranes may be related to differences in physiologic function in each segment.

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  • 脛骨超音波伝播速度測定法による糖尿病患者骨強度の検討

    宮武 伸行, 四方 賢一, 高橋 香代, 鈴木 久雄, 和田 淳, 国富 三絵, 山本 晃史, 松枝 睦美, 槇野 博史

    日本骨形態計測学会雑誌   8 ( 3 )   165 - 171   1998.12

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    インスリン非依存型糖尿病では,超音波伝播速度による皮質骨骨強度は正常人と有意差はないが低下傾向を認めた.高齢者程骨強度の低下は軽い傾向を示した

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  • 【分子腎臓病学】腎生理的機能調節系の分子生物学 その他 インテグリン受容体と接着分子

    四方 賢一, 杉本 光, 和田 淳, 槇野 博史

    腎と透析   45 ( 増刊 )   366 - 378   1998.12

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  • 【細胞接着分子研究の最新動向】臨床的研究 病態と接着分子 腎疾患と接着分子

    松田 充浩, 四方 賢一, 和田 淳, 槇野 博史

    医学のあゆみ   187 ( 1 )   77 - 82   1998.10

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    Other Link: http://search.jamas.or.jp/link/ui/1999033906

  • 【接着分子の全て】病態・疾患と接着分子 腎疾患と接着分子

    和田 淳, 四方 賢一, 槇野 博史

    臨床免疫   30 ( Suppl.18 )   269 - 275   1998.10

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  • 腎臓中に見いだされたL-セレクチン結合性アズール陽性物質

    小坂 寛一, 宮本 大誠, 鈴木 隆, 左 一八, 宮坂 昌之, 四方 賢一, 槇野 博史, 鈴木 康夫

    生化学   70 ( 8 )   892 - 892   1998.8

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  • 21世紀へ向けての糖尿病性腎症 進展防止と治療法の開発 アルドース還元酵素阻害剤の糖尿病ラットにおける白血球浸潤抑制効果

    杉本 光, 四方 賢一, 槇野 博史

    日本腎臓学会誌   40 ( 6 )   388 - 388   1998.8

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  • Dynamic analysis on rupture of glomerular basement membranes in glomerulonephritis

    Z Ota, K Ota, S Ota, K Shikata, T Ogura, H Makino, S Okuda

    NEPHRON   79 ( 3 )   345 - 347   1998.7

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  • 【腎間質へのアプローチ】糸球体障害に引き続く間質障害 接着因子

    四方 賢一, 杉本 光, 和田 淳

    腎と透析   45 ( 1 )   79 - 87   1998.7

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  • 【血液浄化膜の生体適合性に関する最近の話題】細胞膜表面蛋白とその可溶性成分からみた血液透析療法の生体適合性

    川端 研治, 山崎 浩子, 西 宏行, 林 恭子, 渡辺 千史, 河本 紀一, 長宅 芳男, 四方 賢一, 槇野 博史

    腎と透析   45 ( 別冊 ハイパフォーマンスメンブレン'98 )   24 - 28   1998.7

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  • 【HDF療法'98】膜の評価 HDFにおける血清AGE値の検討

    福田 真治, 長宅 芳男, 四方 賢一, 川端 研治, 市川 晴夫, 川野 克己, 槇野 博史

    腎と透析   44 ( 別冊 HDF療法'98 )   149 - 152   1998.5

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    HDFによる血清メイラード反応後期生成物(AGE)の除去はHDに比し効率的であり,又,HDFはAGE生成に関して抑制的に働く.したがってHDFは,透析患者の合併症の予防に対して有効であると考えられた

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  • Mechanisms of Development and Progression of Diabetic Nephropathy. Glomerular Hypertrophy in Diabetic Nephropathy.

    Journal of the Japan Diabetes Society   41 ( 1 )   15 - 17   1998.1

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    DOI: 10.11213/tonyobyo1958.41.15

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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

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    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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  • 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

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

    Kenji Kawabata

    Nephron   78 ( 2 )   148 - 155   1998

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    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.

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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

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    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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  • 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

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    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

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    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

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    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

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    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.

    DOI: 10.1159/000044997

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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

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    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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  • 【臓器障害と接着分子】腎疾患と接着分子

    四方 賢一, 杉本 光, 槇野 博史

    BIO Clinica   12 ( 13 )   967 - 972   1997.12

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  • Macrophage colony stimulating factor (M-CSF) is a major mediator for mesangial proliferative glomerulonephritis.

    H Yamaji, K Shikata, M Matsuda, Y Shikata, J Wada, H Sugimoto, H Makino

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   8   A0474 - A0474   1997.9

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  • Focal adhesion kinase (FAK) and paxillin tyrosine phosphorylation by angiotensin II (A II) stimulation in mesangial cells.

    Y Shikata, K Shikata, H Sugimoto, J Wada, H Makino

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   8   A2072 - A2072   1997.9

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  • 臨床上重要な腎臓疾患 糖尿病性腎症

    槇野 博史, 四方 賢一

    Medical Practice   14 ( 8 )   1263 - 1271   1997.8

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  • 【次世代人工腎と在宅医療】血液透析中の血小板活性化に及ぼす透析膜の影響

    川端 研治, 長宅 芳男, 四方 賢一

    腎と透析   43 ( 別冊 ハイパフォーマンスメンブレン97 )   60 - 64   1997.7

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    再生セルロース膜を用いた血液透析では,血小板の活性化が認められた.血小板の活性化に伴い,血管内皮細胞の存在しないdialyzer内で,sP-selectinが放出されていることがELISAで確認できた.sP-selectinは接着活性を保持しており,好中球機能にも影響を与えるとされていることから,生体適合性の指標となり得ると考えられた

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  • 両側腎動脈狭窄と高度の腎組織障害を伴った強直性脊椎炎の一症例

    秋山 賢次, 四方 賢一, 槇野 博史

    綜合臨床   46 ( 7 )   2038 - 2042   1997.7

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    36歳男.蛋白尿,血尿により,尿素窒素31mg/dl血清クレアチニン1.86mg/dl, HLA-B27陽性で,経皮的胃生検の結果,高度の糸球体硬化に加えて尿細管の変性,間質の細胞浸潤と線維化を伴った高度の腎組織障害を認めた

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  • 【次世代人工腎と在宅医療】血液透析患者における血清AGE値の検討

    福田 真治, 長宅 芳男, 四方 賢一

    腎と透析   43 ( 別冊 ハイパフォーマンスメンブレン97 )   172 - 175   1997.7

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    血清advanced glycation end products(AGE)は透析膜間では有意差はなかった.しかし,前期生成物までAGEに変換させて測定したAGE生成能は,高血糖と透析膜の生体適合性が関与していることが示唆された.また,ELISA法による血清AGE値とAGE生成能の測定は,病態解明や生体適合性の評価に有用であると考えられた

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  • 症例から学ぶDiabetes Mellitus 発症早期より糸球体基底膜の著明な肥厚を認めたインスリン依存型糖尿病の1例

    宮武 伸行, 四方 賢一, 丸山 啓輔

    Complication: 糖尿病と血管   2 ( 1 )   5 - 8   1997.5

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  • 糖尿病合併症の成因・病因 細小血管症 腎症の病理・病態生理

    槇野 博史, 杉本 光, 四方 賢一

    Complication: 糖尿病と血管   2 ( 1 )   31 - 44   1997.5

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  • 間質尿細管障害の分子機構(2) 接着分子の役割

    四方 賢一

    日本腎臓学会誌   39 ( 3 )   199 - 199   1997.4

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  • 糖尿病性腎症の成因 最近の話題から

    槇野 博史, 宮武 伸行, 四方 賢一

    臨床栄養   90 ( 5 )   546 - 553   1997.4

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  • 糖尿病性腎症の発症・進展機序

    槇野 博史, 四方 賢一, 杉本 光

    Diabetes Journal: 糖尿病と代謝   25 ( 1 )   1 - 7   1997.3

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  • 糸球体腎炎患者の糸球体におけるM-CSFの発現と尿中M-CSF濃度の検討

    四方 賢一

    日本内科学会雑誌   86 ( 臨増 )   226 - 226   1997.2

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  • サイトカインからみた扁桃がIgA腎症に及ぼす影響

    槇野 博史, 松田 充浩, 四方 賢一

    口腔・咽頭科   9 ( 2 )   261 - 264   1997.2

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    扁桃誘発試験,摘出術前後で血中M-CSF値は変動しなかった.扁桃誘発試験での尿中M-CSF値は3日後をピークに上昇し,IgA腎症患者ではより高値であった.扁桃摘出術では尿中IL-6,M-CSF値は術後2~7日後をピークに上昇し,腎障害が高度な症例でより高値であった.扁桃刺激時に尿中IL-6値,M-CSF値を測定する事により,扁桃のメサンギウム増殖性腎炎に対する影響がある程度推察できた

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=1997&ichushi_jid=J02661&link_issn=&doc_id=19970327230008&doc_link_id=10.14821%2Fstomatopharyngology1989.9.261&url=https%3A%2F%2Fdoi.org%2F10.14821%2Fstomatopharyngology1989.9.261&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_2.gif

  • Study on coagulation and fibrinolytic systems in predialysis patients with chronic renal failure. Comparison between patients with chronic glomerulonephritis and patients with diabetic nephropathy.:—Comparison between patients with chronic glomerulonephritis and patients with diabetic nephropathy—

    NAGAKE Yoshio, MAKINO Hirofumi, YORIOKA Noriaki, NOMURA Shinsuke, OSAWA Gengo, YAMAKIDO Michio, KAWASAKI Hironaka, KATO Yuzuru, MATSUZAKI Masunori, SHIKATA Kenichi, UEMASU Jiro, SOMIYA Hajime, FUJII Zenzo, HAYASHIDA Shigeaki, NASU Takahito, OYABUB Yasuhiko, NITTA Yutaka, KAWANISHI Hideki, USUI Koji, FUJIWARA Kenta, TAKASUGI Norihisa, KANEHARA Koji, HAMAGUCHI Naoki, KUMAGAI Isao, ICHIKAWA Haruo, TAKAHASHI Maki, OMORI Hiroyuki, ARIMOTO Katsuhiko, MINO Yasuaki, KAWABATA Kenji, AKAGI Masahiko, MAEDA Teiryo, OTA Zensuke

    Jpn J Nephrol   39 ( 5 )   474 - 482   1997

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    To clarify the abnormalities of coagulation and fibrinolytic systems in predialysis patients with chronic renal failure, we measured indices of coagulation and fibrinolytic systems in 33 predialysis patients whose creatinine (Cr) levels were over 3.0 mg/dl. We termed twenty-four patients with chronic glomerulonephritis the "CGN group". We also termed nine patients with diabetes mellitus the "DM group". We measured thrombin •antithrombin III complex (TAT), α2 plasmin inhibitor plasmin complex (PIC), D-dimer, protein C, protein S, thrombomodulin (TM), vitronectin, tissue plasminogen activator •plasminogen activator inhibitor-1 complex (tPAI-C) in these two groups. Furthermore, we measured the same indices after 6 months in the CGN group. As a result, the plasma levels of both TAT, PIC, TM/Cr ratio in the DM group were significantly higher than those in the CGN group. In the CGN group, changes in both protein S activities and plasma levels of tPAI-C were reduced significantly after 6 months. In conclusion, the abnormalities of coagulation and fibrinolytic systems in predialysis diabetic patients were stronger than those in predialysis patients with CGN. Furthermore, these abnormalities were worsened after 6 months in predialysis patients with chronic renal failure.

    DOI: 10.14842/jpnjnephrol1959.39.474

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  • Changes in serum concentrations of matrix metalloproteinases, tissue inhibitors of metalloproteinases and type IV collagen in patients with various types of glomerulonephritis

    Kenji Akiyama, Kenichi Shikata, Hikaru Sugimoto, Mitsuhiro Matsuda, Yasushi Shikata, Noboru Fujimoto, Kenichi Obata, Hideki Matsui, Hirofumi Makino

    Research Communications in Molecular Pathology and Pharmacology   95 ( 2 )   115 - 128   1997

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    One of the major causes of glomerular sclerosis which precedes renal failure is an increase in glomerular extracellular matrices (ECMs). Glomerular ECMs which are composed of mesangial matrix and basement membrane play an important role in physical, mechanical and structural functions of the glomerulus. Matrix metalloproteinases (MMPs) are the enzymes which degrade both the collagenous and noncollagenous components of the ECMs. Tissue inhibitors of metalloproteinases (TIMPs) are inhibitors of MMPs. The regulations by MMPs and TIMPs are considered to contribute to maintain homeostasis in the production and degradation of ECMs in the glomeruli. In the glomeruli of patients with glomerulonephritis, the imbalance between production and degradation of ECMs is supposed to cause the increase in ECMs and glomerular sclerosis. In this study, serum concentrations of MMP-1, -2, and -3, TIMP-1 and 2 and type IV collagen were measured in patients with IgA nephropathy, lupus nephritis and membranous nephropathy. In patients with IgA nephropathy and lupus nephritis which are mesangial proliferative glomerulonephritis, the levels of MMP-3 and TIMP-2 were increased. On the other hand, the levels of type IV collagen, MMP-2 and TIMP-1 were increased in patients with membranous nephropathy in which the thickening of basement membrane is characteristic. These differences may be caused by the difference of the pathogenesis of these diseases. The present results suggest that the imbalance between the metabolism of ECMs occurs in patients with glomerulonephritis and contributes to the progression of glomerulonephritis.

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  • Identification of new L - selectin ligand using renal cultivated cell.

    川島博人, 渡辺哲史, 李永韮, 四方賢一, 宮坂昌之

    日本免疫学会総会・学術集会記録   27   1997

  • Analysis of L - selectin legand obtained from rat kidney.

    渡辺哲史, 川島博人, 李永韮, 四方賢一, 宮坂昌之

    日本免疫学会総会・学術集会記録   27   1997

  • Examination of distribution change and roles of L - selectin ligand in rat interstitial nephritis.

    李永韮, 川島博人, 渡辺哲史, 四方賢一, 宮坂昌之

    日本免疫学会総会・学術集会記録   27   1997

  • 糖尿病性腎症のメカニズムと進行防止 糖尿病性腎症における尿細管異常とAGE

    槇野 博史, 久代 昌彦, 四方 賢一

    内分泌・糖尿病科   3 ( 6 )   512 - 518   1996.12

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  • 腎糸球体内皮細胞の微細構造と機能

    太田 善介, 弘中 一江, 四方 賢一

    月刊細胞   28 ( 13 )   519 - 524   1996.11

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  • 糖尿病性腎症の糸球体病変 免疫組織化学及び電顕的検討

    弘中 一江, 四方 賢一, 槇野 博史

    Diabetes Frontier   7 ( 5 )   521 - 526   1996.10

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  • 糖尿病性腎症診断マーカーの用い方,評価の仕方

    槇野 博史, 宮武 伸行, 四方 賢一

    Diabetes Frontier   7 ( 4 )   385 - 389   1996.8

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  • 腎障害を伴う糖尿病の治療

    槇野 博史, 宮武 伸行, 四方 賢一

    Medical Practice   13 ( 6 )   923 - 927   1996.6

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  • 早期糖尿病性腎症の指標としての尿中IV型コラーゲン濃度測定の有用性

    秋山 賢次, 四方 賢一, 槇野 博史

    診断と治療   84 ( 4 )   729 - 732   1996.4

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    著者等の用いたキットでは,尿を濃縮することなくそのままIV型コラーゲン濃度を測定することができた.糖尿病患者では,微量アルブミン尿を認めない腎症前期から,尿中IV型コラーゲン濃度が健常人と比較して高値をとっており,腎症の進行に従って増加していた

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  • 糖尿病性腎症患者の腎組織におけるセレクチンの発現動態の検討

    四方 賢一

    糖尿病   39 ( Suppl.1 )   503 - 503   1996.4

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  • 高脂血症は腎疾患の悪化を促進するか

    槇野 博史, 杉本 光, 四方 賢一

    Medical Practice   13 ( 2 )   249 - 252   1996.2

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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

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    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

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    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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  • What is the best index of glycemic control in patients with diabetes mellitus on hemodialysis?

    Haruo Ichikawa, Yoshio Nagake, Maki Takahashi, Hiroshi Nakazono, Kenji Kawabata, Kenichi Shikata, Hirofumi Makino

    Japanese Journal of Nephrology   38 ( 7 )   305 - 308   1996

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    Since red blood cell survival time is shortened in patients with diabetes mellitus (DM) on hemodialysis (HD), it is unlikely that indices of glycemic control accurately reflect the glycemic state of these individuals. In this study, in order to determine the best index of glycemic control in diabetic patients on HD, we measured HhAlc, 1,5-anhydroglucitol (1,5-AG), fructosamine (Fr) and glycated albumin (GA) in 31 diabetic patients on HD (20 males and 11 females, mean age: 66.9 years), and examined the correlation between each index and predialysis plasma glucose level. Since the mean values of predialysis plasma glucose during the final 2 and 4 weeks before the study were best correlated with HbAlc, this parameter was considered to be the most reliable index of glycemic control in diabetic patients on HD. GA was more closely correlated with mean values of predialysis plasma glucose during the final 2 and 4 weeks, than any other index of glycemic control, followed by HbAlc. In conclusion, HbAlc is considered to be the most reliable index of glycemic control in diabetic patients on HD.

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  • The changes of mac-1 and l-selectin expression on granulocytes and soluble l-selectin level during hemodialysis?

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

    Nephron   73 ( 4 )   573 - 579   1996

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    L-selectin and Mac-1 expressed on leukocytes are critical for leukocyte adhesion to inflamed endothelium. L-selectin is known to be rapidly shed from the cell surface of granulocytes after activation. In the present study the change of expressions of these adhesion molecules on granulocytes were analyzed by flow cytometry, and the serum concentration of shed L-selectin (soluble L-selectin
    sL-selectin) was measured by enzyme-linked immunosorbent assay (ELISA) during hemodialysis in patients treated with regenerated cellulose membranes (RC group) versus polysulfone membranes (PS group). In the RC group, Mac-1 expression on granulocytes increased significantly at 30 min after the initiation of hemodialysis (p &lt
    0.05) compared with predialysis values, coinciding with the nadir of dialysis-induced granulocytopenia. Granulocyte L-selectin expression decreased significantly at 15 min after the initiation of hemodialysis (p &lt
    0.05) and remained decreased through the course of dialysis session, compared with predialysis values. Serum sL-selectin level significantly increased at 15 min after the initiation of hemodialysis (p &lt
    0.05), compared with predialysis values. In the PS group, no significant variation in Mac-1 and L-selectin expression on granulocytes and serum sL-selectin level were detected. This reciprocal change of Mac-1 and L-selectin on granulocyte cell surface was attributed to development of granulocytopenia and subsequent reversal during dialysis with cellulose membranes. In this study, we confirmed the shedding of L-selectin during cellulosic dialysis by ELISA. The increase in sL-selectin, which has potential activity of inhibiting L-selectin-dependent adhesion of granulocyte to endothelium, might be involved in rebound granu-locytosis during dialysis with cellulose membranes and impairment of the granulocyte function in patients on chronic hemodialysis. © 1996 S. Karger AG, Basel.

    DOI: 10.1159/000189143

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  • Ultrastructure and function of the glomerular endothelial cell.

    太田善介, 弘中一江, 四方賢一

    月刊細胞   28 ( 13 )   1996

  • Retrieval of the ligand of L - selectine in a rat kidney.

    渡辺哲史, 川島博人, LI Y-F, 四方賢一, 宮坂昌之

    日本免疫学会総会・学術集会記録   26   1996

  • 腎臓におけるL-セレクチンのリガンドとしてのスルファチドの生理的機能

    四方 賢一

    日本臨床電子顕微鏡学会誌   28 ( 増刊 )   80 - 80   1995.8

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  • 接着分子の基礎と臨床 腎疾患と接着分子

    槇野 博史, 四方 賢一

    医学のあゆみ   174 ( 1 )   71 - 76   1995.7

  • 糖尿病性腎症の進展過程におけるAGEの関与 OLETFラットを用いた検討

    四方 賢一

    糖尿病   38 ( Suppl.1 )   385 - 385   1995.4

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  • 炎症モデルと接着分子(3)腎炎と接着分子

    四方 賢一, 槇野 博史, 平田 教至

    病理と臨床   13 ( 3 )   375 - 381   1995.3

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  • 腎臓におけるL-セレクチンのリガンドとしてのスルファチドの機能と白血球浸潤に対する抑制効果

    四方 賢一

    日本内科学会雑誌   84 ( 臨増 )   105 - 105   1995.2

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  • Ultrastructure of nonenzymatically glycated mesangial matrix in diabetic nephropathy

    Hirofumi Makino, Kenichi Shikata, Kazue Hironaka, Masahiko Kushiro, Yasushi Yamasaki, Hikaru Sugimoto, Zensuke Ota, Norie Araki, Seikoh Horiuchi

    Kidney International   48   527 - 536   1995.1

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    Advanced protein glycation has been proposed as a major factor in the development of diabetic nephropathy. Advanced glycation end products (AGEs) have altered the structure of extracellular matrix component and impaired self association in vitro. To elucidate the role of AGEs in the progression of diabetic nephropathy, the present study was undertaken to localize glomerular AGEs immunohistochemically. Ultrastructural changes of the mesangial matrix were analyzed with high resolution scanning electron microscopy. No glomerular AGEs staining was noted in normal control kidney specimens, or in tissue from glomerulonephritis patients without diabetes mellitus. The mesangium showed a positive AGEs staining in advanced stages of diabetic nephropathy, and the most characteristic finding was the strong AGEs staining in nodular lesions. By high resolution scanning electron microscopy, control and diabetic mesangial matrices revealed a meshwork structure composed of fine fibrils (10 nm in width) and numerous pores (12 to 13 nm in diameter). In the nodular lesions, however, loosening of the meshwork was significant, and the diameter of the pores was enlarged (approximately 24 nm). This study provides the first immunohistochemical evidence that AGEs are localized in diabetic glomeruli, most notably to nodular lesions. Advanced glycation might play a role in the progression of diabetic nephropathy through impairment of the assembly of matrix proteins in vivo.

    DOI: 10.1038/ki.1995.322

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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

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    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

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    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

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    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

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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.

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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

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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.

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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

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    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

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    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

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    Language:English  

    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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  • Escape of red blood cells through gaps in glomerular basement membrane in a patient with mixed connective tissue disease

    Hirofiumi Makino, Isao Kumagai, Kazue Hironaka, Kosuke Ota, Kenichi Shikata, Zensuke Ota

    American Journal of Nephrology   15 ( 2 )   168 - 171   1995

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    Hematuria in patients with glomerulonephritis seems to result from the passage of red blood cells through anatomical gaps in the glomerular basement membrane. However, such morphological evidence has rarely been demonstrated. A patient with mixed connective tissue disease associated with membranous glomerulonephritis is described in whom the renal biopsy specimen showed an escape of red blood cells through a gap in the basement membrane. These findings support the morphological basis of hematuria in glomerulonephritis. © 1995 S. Karger AG, Basel.

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  • The ultrastructural disruption of the glomerular basement membrane in diabetic nephropathy revealed by "tissue negative staining method"

    Kosuke Ota, Zensuke Ota, Kenichi Shikata, Hirofumi Makino

    Journal of Diabetes and Its Complications   9 ( 4 )   285 - 287   1995

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    To clarify the ultrastructural changes of the glomerular basement membrane (GBM) in diabetic nephropathy, the renal tissues of the patients with diabetic nephropathy were examined by electron microscopy using our newly devised "tissue negative staining method." A fine meshwork structure consisting of fibrils forming the small pores are observed in the normal human GBM. The diameter of these pores was slightly smaller than that of human albumin molecules. The GBM in patients with diabetic nephropathy showed irregular thickening. At higher magnification, cavities and tunnel structures, which were not seen in normal controls, were observed in the thickened GBM. As the diameters of the cavities and tunnels were far larger than the dimensions of albumin molecules, these enlarged structures are considered to allow serum protein molecules to pass through the GBM from the capillary lumen to the urinary space. The present results suggest that the cause of massive proteinuria in diabetic nephropathy is the disruption of the size barrier of the GBM. © 1995.

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  • Immunohistological localization of the novel epitope related to type IV collagen in normal and diseased renal tissues

    Kyoji Hirata, Kenichi Shikata, Hirofumi Makino, Toshihiko Hayashi, Zensuke Ota

    The Journal of Pathology   177 ( 4 )   407 - 413   1995

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    Type IV collagen is a major component of the renal glomerular extracellular matrix. A recently characterized monoclonal antibody, JK 132, which was originally produced by immunization with human placental type IV collagen, recognizes a new epitope which is different from α1–α6 chains of type IV collagen. Using immunofluorescence and immunogold electron microscopy, the distribution of the epitope of JK132 has been compared with the distribution of α1, α2, α3 and α4 chains of type IV collagen in normal human kidney and in the renal tissues of patients with various types of glomerulonephritis. In normal human kidney, JK132 reacted with mesangial matrix, Bowman's capsular basement membrane (BCBM), tubular basement membrane, and vessel walls, but did not react with glomerular basement membrane (GBM). This distribution is different from the distribution of α1–α4(IV) chains. In IgA nephropathy and membranoproliferative glomerulonephritis, the staining intensity for JK132 was increased in expanded mesangial matrix. In glomeruli with severe mesangial proliferation, the epitope of JK132 extended to the endothelial side of the GBM. In membranous nephropathy, staining for JK132 was virtually unchanged from normal. This study suggests that the epitope of JK132 increases in amount during the process of mesangial proliferation and could serve as a marker for mesangial matrix expansion in glomerulonephritis. Copyright © 1995 John Wiley &amp
    Sons, Ltd.

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  • Ultrastructure of nonenzymatically glycated mesangial matrix in diabetic nephropathy

    Hirofumi Makino, Kenichi Shikata, Kazue Hironaka, Masahiko Kushiro, Yasushi Yamasaki, Hikaru Sugimoto, Zensuke Ota, Norie Araki, Seikoh Horiuchi

    Kidney International   48 ( 2 )   517 - 526   1995

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    Language:English   Publisher:Nature Publishing Group  

    Advanced protein glycation has been proposed as a major factor in the development of diabetic nephropathy. Advanced glycation end products (AGEs) have altered the structure of extracellular matrix component and impaired self association in vitro. To elucidate the role of AGEs in the progression of diabetic nephropathy, the present study was undertaken to localize glomerular AGEs immunohistochemically. Ultrastructural changes of the mesangial matrix were analyzed with high resolution scanning electron microscopy. No glomerular AGEs staining was noted in normal control kidney specimens, or in tissue from glomerulonephritis patients without diabetes mellitus. The mesangium showed a positive AGEs staining in advanced stages of diabetic nephropathy, and the most characteristic finding was the strong AGEs staining in nodular lesions. By high resolution scanning electron microscopy, control and diabetic mesangial matrices revealed a meshwork structure composed of fine fibrils (10 nm in width) and numerous pores (12 to 13 nm in diameter). In the nodular lesions, however, loosening of the meshwork was significant, and the diameter of the pores was enlarged (approximately 24 nm). This study provides the first immunohistochemical evidence that AGEs are localized in diabetic glomeruli, most notably to nodular lesions. Advanced glycation might play a role in the progression of diabetic nephropathy through impairment of the assembly of matrix proteins in vivo.

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  • Distribution of extracellular matrix receptors in various forms of glomerulonephritis

    Kenichi Shikata, Hirofumi Makino, Shigeru Morioka, Tadatoshi Kashitani, Kyoji Hirata, Zensuke Ota, Jun Wada, Yashpal S. Kanwar

    American Journal of Kidney Diseases   25 ( 5 )   680 - 688   1995

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    Integrins are heterodimeric transmembrane receptor glycoproteins consisting of α and β subunits that mediate adhesion and interactions between cells and extracellular matrix. Such interactions may be perturbed in various pathologic states, resulting in the altered phenotypic expressions of the integrins in affected tissues. To ascertain the alterations in integrins in various renal diseases, their distribution was investigated in different forms of glomerulonephritis by indirect immunofluorescence and immunoelectron microscopy using specific antibodies directed against β1 integrins and integrin αvβ3 (vitronectin receptor). In addition, the distribution of certain extracellular matrix components (ie, fibronectin, vitronectin, and type IV collagen) was examined. Integrin β1 and αvβ3 were highly expressed in proliferating mesangial cells in immunoglobulin A nephropathy, membranoproliferative glomerulonephritis type I and diffuse proliferative lupus nephritis. Their putative ligands (ie, fibronectin, vitronectin, and type IV collagen) also were increased in the expanded mesangial regions. In immunoglobulin A nephropathy, integrin β1 and αvβ3 were seen by immunoelectron microscopy to be localized to the mesangial cell membranes in close proximity to the immune complex deposits
    however, fibronectin and vitronectin immunoreactivities were observed in the mesangial immune complex deposits. Similarly, vitronectin also was detected in the immune complex deposits of other forms of proliferative nephritis, ie, membranoproliferative glomerulonephritis type I and diffuse proliferative lupus nephritis. In diffuse proliferative lupus nephritis, the cellular crescents displayed immunoreactivity toward integrin αvβ3 and vitronectin. In nonimmune complex glomerular disease associated with nephrotic syndrome (ie, minimal change nephrotic syndrome), integrin α3β1, which normally has a linear capillary distribution, was decreased. In immune complex nephritis associated with nephrotic syndrome (ie, membranous nephropathy), integrin α3β1 immunoreactivity was focally disrupted and capillary loops displayed a discontinuous linear distribution. Finally, in membranous nephropathy, immunoreactivity toward vitronectin was accentuated in immune complex deposits. The differential altered distributions of the integrins and of their ligands may be reflective of mesangial cell proliferative activity in certain forms of glomerulonephritis, while in other forms of glomerular diseases, the decreased immunoreactivity of integrin α3β1 may be related to the glomerular capillary wall alterations associated with proteinuric states. © 1995.

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  • Escape of red blood cells through gaps in glomerular basement membrane in a patient with mixed connective tissue disease

    Hirofiumi Makino, Isao Kumagai, Kazue Hironaka, Kosuke Ota, Kenichi Shikata, Zensuke Ota

    American Journal of Nephrology   15 ( 2 )   168 - 171   1995

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    Language:English  

    Hematuria in patients with glomerulonephritis seems to result from the passage of red blood cells through anatomical gaps in the glomerular basement membrane. However, such morphological evidence has rarely been demonstrated. A patient with mixed connective tissue disease associated with membranous glomerulonephritis is described in whom the renal biopsy specimen showed an escape of red blood cells through a gap in the basement membrane. These findings support the morphological basis of hematuria in glomerulonephritis. © 1995 S. Karger AG, Basel.

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  • Binding capacity of sulfatide and sulfation glycolipid to selection and inhibiting action for selectin dependence kidney and pulmonary inflammation.

    鈴木康夫, 飯塚真子, 鈴木隆, 四方賢一, 平田教至, 長谷川明, 木曽真, 宮坂昌之, WARD P A

    脂質生化学研究   37   1995

  • セレクチンファミリーの硫酸化糖鎖に対する結合特異性およびスルファチドによる腎間質へのL-セレクチン依存性白血球浸潤の抑制

    鈴木康夫, 飯塚真子, 宮本大誠, 四方賢一, 平田教至, 太田善介, 長谷川明, 木曽真, 宮坂昌之

    日本薬学会年会要旨集   115th ( Pt 3 )   1995

  • Tissue negative staining法により観察した尿細管基底膜の超微構造

    小川さえ子, 四方賢一, 太田康介, 弘中一江, 林佳子, 槙野博史, 太田善介

    日本電子顕微鏡学会学術講演会発表要旨集   51st   1995

  • 腎炎治療に対する細胞接着分子からのアプローチ

    四方 賢一

    日本腎臓学会誌   36 ( Suppl. )   23 - 23   1994.11

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  • 糸球体腎炎の成因 細胞接着分子

    槇野 博史, 四方 賢一

    腎と透析   37 ( 増刊 )   198 - 203   1994.11

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  • 多臓器不全に進展したサルモネラ敗血症の1例

    松田 充浩, 四方 賢一, 槇野 博史

    内科   74 ( 4 )   764 - 766   1994.10

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  • 糖尿病腎症患者の血漿内ビトロネクチン濃度の変化

    森岡 茂, 槇野 博史, 四方 賢一

    Acta Medica Okayama   48 ( 3 )   137 - 142   1994.6

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    NIDDM患者59例,健常者16例を対象とした。正常蛋白尿,微量蛋白尿を有するDM患者では,健常例よりビトロネクチン(VN)の血漿内濃度は有意に高かった。慢性腎不全を有するDM患者の血漿内VN濃度は腎機能正常の患者より有意に低かった。血漿内VM濃度と血中血小板数との間には有意の正の相関があった。血漿内VN濃度は糖尿病腎症の進展の重要なマーカーである

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=1994&ichushi_jid=J04474&link_issn=&doc_id=19950087570004&doc_link_id=https%3A%2F%2Fousar.lib.okayama-u.ac.jp%2F31126&url=https%3A%2F%2Fousar.lib.okayama-u.ac.jp%2F31126&type=%E5%B2%A1%E5%B1%B1%E5%A4%A7%E5%AD%A6%EF%BC%9A%E5%B2%A1%E5%B1%B1%E5%A4%A7%E5%AD%A6%E5%AD%A6%E8%A1%93%E6%88%90%E6%9E%9C%E3%83%AA%E3%83%9D%E3%82%B8%E3%83%88%E3%83%AA&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F80034_3.gif

  • RGDペプチドの糸球体腎炎治療への応用の可能性 合成環状RGDペプチドを用いた検討

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    日本腎臓学会誌   36 ( 5 )   611 - 611   1994.5

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  • 糖尿病性腎症の進展におけるAdvanced Glycation End Productsの関与

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    糖尿病   37 ( Suppl.1 )   344 - 344   1994.4

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  • 腎生検組織におけるPDGF及びPDGF receptorの遺伝子発現の検討

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    日本内科学会雑誌   83 ( 臨増 )   208 - 208   1994.2

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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

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    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

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    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

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    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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  • 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

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    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.

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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

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    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

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    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

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    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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  • Role of L-selectin in leukocyte recruitment in the kidney.

    平田教至, 四方賢一, 槙野博史, 太田善介, 鈴木隆, 鈴木康夫, 宮坂昌之

    日本免疫学会総会・学術集会記録   24   1994

  • 糸球体疾患と接着因子

    槇野 博史, 四方 賢一

    最新医学   48 ( 9 )   1364 - 1372   1993.9

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  • Ultrastructural Changes of the Glomerular Basement Membrane in Diabetic Nephropathy Revealed by Newly Devised Tissue Negative Staining Method (jointly worked)

    Ota Kosuke, Ota Zensuke, Shikata Kenichi, Makino Hirofumi

    Acta Medica Okayama   47 ( 4 )   267 - 272   1993.8

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    DOI: 10.18926/AMO/31556

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  • Ultrastructural changes of the glomerular basement membrane in diabetic nephropathy revealed by newly devised tissue negative staining method.

    Ota Kosuke, Ota Zensuke, Shikata Kenichi, Makino Hirofumi

    Acta Medica Okayama   47 ( 4 )   267 - 272   1993.8

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    DOI: 10.18926/AMO/31556

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  • 新しく考案された組織陰性染色法より明らかにされた糖尿病性腎症の糸球体基底膜(GBM)の超微構造的変化

    太田 康介, 太田 善介, 四方 賢一

    Acta Medica Okayama   47 ( 4 )   267 - 272   1993.8

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    正常基底膜のメッシュ状の線維による小孔の径はアルブミン分子より小さいが,腎症患者の肥厚したGBMでは高倍率でみると,これまで知られていなかった洞とトンネルが見付かった。そのある部分では洞は蜂の巣様構造になっていた。これらの洞とトンネルの直径は遥かにアルブミン分子より大きく,血清蛋白は基底膜より尿中に容易に排出され,糖尿病性腎症にみられる大量の蛋白尿はこのGBMのサイズ障壁の崩壊によることを示唆した

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=1993&ichushi_jid=J04474&link_issn=&doc_id=19950087520007&doc_link_id=1390853649511127552&url=https%3A%2F%2Fcir.nii.ac.jp%2Fcrid%2F1390853649511127552&type=CiNii&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00003_2.gif

  • 糖尿病性腎症における糸球体基底膜の超微細構造の変化

    四方 賢一

    Connective Tissue   25 ( 1 )   46 - 46   1993.6

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  • 糸球体腎炎における接着分子(第1報)馬杉腎炎におけるICAM-1の経時的発現

    四方 賢一

    日本腎臓学会誌   35 ( 5 )   472 - 472   1993.5

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  • 糖尿病性腎症腎組織におけるビトロネクチンの局在の検討

    四方 賢一

    糖尿病   36 ( Suppl.1 )   296 - 296   1993.4

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  • 糸球体腎炎における接着分子の発現と機能 ICAM-1を中心に

    四方 賢一

    日本内科学会雑誌   82 ( 臨増 )   213 - 213   1993.2

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  • 糖尿病性腎症におけるコラーゲンの異常 特に4型コラーゲン鎖について

    槇野 博史, 原本 俊則, 四方 賢一

    日本糖尿病学会総会記録   ( 35 )   221 - 224   1993.1

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    糖尿病性腎症における糸球体硬化には,基底膜コラーゲンである4型コラーゲンの各鎖のみならず,線維型コラーゲンも関与していると思われた

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  • Study on changes in plasma vitronectin levels during hemodialysis.

    Nagake Yoshio, Wada Jun, Makino Hirofumi, Shikata Kenichi, Kumagai Isao, Awata Toshie, Morioka Shigeru, Ogura Toshio, Ota Zensuke

    Nihon Toseki Igakkai Zasshi   26 ( 9 )   1539 - 1542   1993

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    The plasma vitronectin (VN) levels of patient undergoing hemodialysis are known to below and to become lower as the duration of hemodialysis grows longer. Based on the foregoing, hemodialysis was conducted in the same patient by changing the membrane from regenerated cellulose (RC) to cellulose triacetate (CTA) and then to polysulfone (PS) to determine whether significant changes in plasma VN levels resulted from changing the membrane by measuring levels during hemodialysis. In addition, to assess the effect of heparin on changes in VN levels, changes of the level were compared when heparin and nafamostat mesilate (NM) were used as anticoagulants.<br>Predialysis plasma VN levels were lower than normal with all of the membranes. Significant reductions in VN levels were observed when the RC membrane was used 15 minutes after the start of dialysis, though no significant changes in VN levels were observed when CTA or PS membranes were used. This suggests that the degree of complement activation differs according to the type of membrane used, causing differences in the amount of VN consumed. Concerning the effect of heparin on changes in VN levels, there were no significant differences from when NM was used, irrespective of which membrane was used. Thus, the theory that VN is consumed by binding to heparin was not supported by our study.

    DOI: 10.4009/jsdt1985.26.1539

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  • Tissue Inhibitors of Metalloproteinases (TIMP) in Diabetic Patients

    Yoshikazu Hayashi, Hirofumi Makino, Shigeru Morioka, Kenichi Shikata, Zensuke Ota, Yasuo Nagai

    Journal of the Japan Diabetes Society   36 ( 8 )   661 - 663   1993

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    Tissue inhibitors of metalloproteinases (TIMP) play important regulatory roles in degradation of the extracellular matrix (ECM). We measured serum and urinary concentrations of TIMP in diabetic patients and compared the values obtained with those of normal controls. Serum concentrations of TIMP in diabetic patients were not significantly higher than those of control subjects. However, urinary concentrations of TIMP in diabetic patients with proteinuria and renal insufficiency were significantly higher than those of control subjects. Urinary concentrations of TIMP may be increased in patients with advanced diabetic nephropathy. These results suggest that accumulation of glomerular extracellular matrix in diabetes is partly due to increased secretion of TIMP in renal glomeruli. © 1993, THE JAPAN DIABETES SOCIETY. All rights reserved.

    DOI: 10.11213/tonyobyo1958.36.661

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  • 免疫複合体型およびpauci immune型急速進行性糸球体腎炎の臨床病理学的検討 (共著)

    杉山 斉, 槇野野博史, 和田 淳, 太田康介, 長宅芳男, 森岡 茂, 山崎康司, 四方賢一, 柏原直樹, 池田修二, 小倉俊郎, 太田善介

    日本腎臓学会誌   XXXV ( 6 )   777 - 782   1993

  • Expression of the VLA Family of Integrins in the Renal Glomerulus

    Hirofumi Makino, Kenichi Shikata, Shigeru Morioka, Jun Wada, Zensuke Ota

    the japanese journal of nephrology   35 ( 1 )   19 - 21   1993

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    The expression of glomerular extracellular matrix receptors of the very late antigen (VLA) family was examined in the human renal glomerulus by indirect immunofluorescence studies. β1 subunits of integrin were localized in glomerular epithelial, endothelial and mesangial cells and Bowman's capsule. α 3 integrin was localized dominantly in the glomerular capillary wall and less in the mesangium and Bowman's capsule. α2, α4 and α5 integrins were barely stained in the glomerulus. Our findings indicate that the VLA family of integrins plays an important role in the attachment of glomerular cells to the extracellular matrices. © 1993, Japanese Society of Nephrology. All rights reserved.

    DOI: 10.14842/jpnjnephrol1959.35.19

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  • Expression of the VLA Family of Integrins in the Renal Glomerulus

    Hirofumi Makino, Kenichi Shikata, Shigeru Morioka, Jun Wada, Zensuke Ota

    the japanese journal of nephrology   35 ( 1 )   19 - 21   1993

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    The expression of glomerular extracellular matrix receptors of the very late antigen (VLA) family was examined in the human renal glomerulus by indirect immunofluorescence studies. β1 subunits of integrin were localized in glomerular epithelial, endothelial and mesangial cells and Bowman's capsule. α 3 integrin was localized dominantly in the glomerular capillary wall and less in the mesangium and Bowman's capsule. α2, α4 and α5 integrins were barely stained in the glomerulus. Our findings indicate that the VLA family of integrins plays an important role in the attachment of glomerular cells to the extracellular matrices. © 1993, Japanese Society of Nephrology. All rights reserved.

    DOI: 10.14842/jpnjnephrol1959.35.19

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  • 腎生検で高Ca血症性腎症を確認し得た、原発性副甲状腺機能亢進症の2例(共著)

    柏谷忠俊, 槇野博史, 長宅芳男, 弘中一江, 四方賢一, 小倉俊郎, 太田善介

    日本腎臓学会誌   XXXV ( 10 )   1189 - 1194   1993

  • Tissue Inhibitors of Metalloproteinases (TIMP) in Diabetic Patients

    Yoshikazu Hayashi, Hirofumi Makino, Shigeru Morioka, Kenichi Shikata, Zensuke Ota, Yasuo Nagai

    Journal of the Japan Diabetes Society   36 ( 8 )   661 - 663   1993

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    Tissue inhibitors of metalloproteinases (TIMP) play important regulatory roles in degradation of the extracellular matrix (ECM). We measured serum and urinary concentrations of TIMP in diabetic patients and compared the values obtained with those of normal controls. Serum concentrations of TIMP in diabetic patients were not significantly higher than those of control subjects. However, urinary concentrations of TIMP in diabetic patients with proteinuria and renal insufficiency were significantly higher than those of control subjects. Urinary concentrations of TIMP may be increased in patients with advanced diabetic nephropathy. These results suggest that accumulation of glomerular extracellular matrix in diabetes is partly due to increased secretion of TIMP in renal glomeruli. © 1993, THE JAPAN DIABETES SOCIETY. All rights reserved.

    DOI: 10.11213/tonyobyo1958.36.661

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  • Tissue Inhibitors of Metalloproteinases (TIMP) in Diabetic Patients

    Yoshikazu Hayashi, Hirofumi Makino, Shigeru Morioka, Kenichi Shikata, Zensuke Ota, Yasuo Nagai

    Journal of the Japan Diabetes Society   36 ( 8 )   661 - 663   1993

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    Tissue inhibitors of metalloproteinases (TIMP) play important regulatory roles in degradation of the extracellular matrix (ECM). We measured serum and urinary concentrations of TIMP in diabetic patients and compared the values obtained with those of normal controls. Serum concentrations of TIMP in diabetic patients were not significantly higher than those of control subjects. However, urinary concentrations of TIMP in diabetic patients with proteinuria and renal insufficiency were significantly higher than those of control subjects. Urinary concentrations of TIMP may be increased in patients with advanced diabetic nephropathy. These results suggest that accumulation of glomerular extracellular matrix in diabetes is partly due to increased secretion of TIMP in renal glomeruli. © 1993, THE JAPAN DIABETES SOCIETY. All rights reserved.

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  • ネフローゼ症候群における蛋白尿の機序

    太田 善介, 四方 賢一, 太田 康介

    Acta Medica Okayama   46 ( 6 )   483 - 487   1992.12

  • 炎症性腎疾患と接着分子(共著)

    四方 賢一, 槇野 博史, 太田 善介

    最新医学   47 ( 12 )   46 - 55   1992.12

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  • 糸球体腎炎におけるICAM-1の関与の検討

    四方 賢一

    Connective Tissue   24 ( 1 )   96 - 96   1992.6

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  • 腎炎の進展と細胞外基質 電子顕微鏡的アプローチ

    槇野 博史, 四方 賢一, 太田 善介

    興和医報   35 ( 3 )   8 - 15   1992.3

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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

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    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

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    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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  • Heymann nephritisにおける糸球体基底膜の微細構造の検討

    弘中一江, 牧野博史, 原本俊則, 四方賢一, 池田修二, 太田善介

    日本臨床電子顕微鏡学会総会ならびに学術講演会予稿集   24th   1992

  • 腎糸球体における細胞外マトリックス受容体の局在とその変化

    柏谷忠俊, 槙野博史, 原本俊則, 四方賢一, 池田修二, 太田善介

    日本臨床電子顕微鏡学会総会ならびに学術講演会予稿集   24th   1992

  • Tissue Negative Staining法による糖尿病性腎症糸球体基底膜の超微構造

    太田康介, 四方賢一, 太田善介

    日本臨床電子顕微鏡学会総会ならびに学術講演会予稿集   24th   1992

  • 糸球体腎炎における接着分子の機能

    四方賢一, 槙野博史, 和田淳, 森岡茂, 平田教至, 柏原直樹, 太田善介, 玉谷卓也, 宮坂昌之

    日本臨床電子顕微鏡学会総会ならびに学術講演会予稿集   24th   1992

  • ネフローゼ症候群を合併した慢性リンパ性白血病の1例

    水戸川 剛秀, 西谷 皓次, 四方 賢一

    日本臨床免疫学会会誌   14 ( 6 )   646 - 652   1991.12

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    56歳男.昭和61年蛋白尿を指摘され,昭和63年8月より下肢の浮腫,全身倦怠感,盗汗,レイノー現象が出現した.同年11月急性扁桃腺炎を契機にネフローゼ症候群を発症し抗核抗体陽性,抗DNA抗体高値,低補体価よりループス腎炎の疑いにてプレドニゾロン(PSL) 30 mg/日,dipyridamole 300 mg/日投与され,腎生検ではループス腎炎に類似の組織学的所見を呈していた.経過中に末梢血リンパ球数(10,560/mm3)の増加と膜表面免疫グロブリン保有細胞(IgM, IgD, κ鎖陽性)が80%を占め,モノクローナルなBリンパ球の増殖が認められた.さらに,骨髄穿刺では同じ表面マーカーを有する成熟小リンパ球が50%を占めCLL (stage 0)と診断した.PSLの投与により蛋白尿の消失,末梢血リンパ球数も減少し,良好な経過をたどっている

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=1991&ichushi_jid=J01882&link_issn=&doc_id=19870424670011&doc_link_id=10.2177%2Fjsci.14.646&url=https%3A%2F%2Fdoi.org%2F10.2177%2Fjsci.14.646&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_2.gif

  • 腎糸球体基底膜の網目構造の免疫組織化学的検討

    四方 賢一

    Connective Tissue   23 ( Suppl. )   43 - 43   1991.6

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  • 腎糸球体基底膜分子篩の超微構造

    太田 善介, 槇野 博史, 一安 朗, 四方 賢一

    岡山医学会雑誌   103 ( 3 )   179 - 186   1991.6

  • IgA腎症に対するAzelastine (Azeptin(R))の効果の検討

    四方 賢一, 槇野 博史, 吉永 泰彦

    診断と治療   79 ( 2 )   396 - 400   1991.2

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  • A case of Bartter’s syndrome with severe decalcification of systemic bones and bilateral nephrocalcinosis.

    吉原正彦, 黒田広生, 佐野玲美, 鳥越弘幸, 佐野佳子, 菊地武志, 四方賢一, 高取克彦, 槙野博史

    腎と透析   30 ( 5 )   1991

  • 腎糸球体基底膜超微細構造の電顕的観察

    四方 賢一

    岡山医学会雑誌   102 ( 5~6 )   800 - 801   1990.6

  • 化学的処理による腎糸球体基底膜の立体的網目構造の電子顕微鏡的観察

    四方 賢一

    日本腎臓学会誌   32 ( 5 )   606 - 606   1990.5

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  • 腎糸球体基底膜の超微細構造の電顕的観察のための化学的処理法

    四方 賢一, 一安 朗, 槇野 博史

    医学のあゆみ   152 ( 4 )   249 - 250   1990.1

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  • 腎糸球体超微細構造の観察

    四方賢一, 槙野博史, 太田善介, 有井達夫

    生理学研究所年報   11   1990

  • Diabetic nephropathy associated with IgA nephropathy and review of literature.

    槙野博史, 吉永泰彦, 池田修二, 四方賢一, 熊谷功, 高岡道夫, 太田善介, 高取悦子

    腎と透析   28 ( 4 )   1990

  • HUMAN-LIVER FERRITIN AS A NEW TRACER FOR STUDYING GLOMERULAR-PERMEABILITY

    Z OTA, KUMAGAI, I, K SHIKATA, H MAKINO

    ACTA MEDICA OKAYAMA   43 ( 6 )   363 - 365   1989.12

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  • 糸球体濾過性観察の新たなトレーサーとしてのヒト肝フェリチン

    太田 善介, 熊谷 功, 四方 賢一

    Acta Medica Okayama   43 ( 6 )   363 - 365   1989.12

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    6頭のaminonucleoside nephrosisおよび6頭の対照Sprague-Dawleyラットにヒト肝フェリチンを静脈内投与し,採取した24時間尿中のヒトフェリチンを測定した.その結果,尿中に排泄されたフェリチン量は,aminonucleoside nephrosisラットでは,対照ラットの40倍に達した.また,重合型フェリチンよりもmonomerのフェリチンの方が遥かに多量に検出された.これらの成績から,糸球体基底膜のsize barrierとしての重要な意義が明らかになった

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=1989&ichushi_jid=J04474&link_issn=&doc_id=19870505930008&doc_link_id=https%3A%2F%2Fousar.lib.okayama-u.ac.jp%2F30866&url=https%3A%2F%2Fousar.lib.okayama-u.ac.jp%2F30866&type=%E5%B2%A1%E5%B1%B1%E5%A4%A7%E5%AD%A6%EF%BC%9A%E5%B2%A1%E5%B1%B1%E5%A4%A7%E5%AD%A6%E5%AD%A6%E8%A1%93%E6%88%90%E6%9E%9C%E3%83%AA%E3%83%9D%E3%82%B8%E3%83%88%E3%83%AA&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F80034_3.gif

  • 急速進行性腎炎の経過をとり,糸球体係蹄壁に著明なフィブリノーゲンの沈着を認めたIgA腎症の一例

    四方 賢一, 槇野 博史, 高取 克彦

    綜合臨床   38 ( 12 )   3107 - 3110   1989.12

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  • Elastase,SDS,2-mercaptoethanol処理により明らかにされたGBMの基本的網目構造

    四方 賢一

    日本腎臓学会誌   31 ( 5 )   600 - 600   1989.5

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  • Diabetic Nephropathy associated with membranous nephropathy. Effect of dipyridamole.

    槙野博史, 田野口創, 熊谷功, 四方賢一, 高岡道夫, 太田善介, 美野真悟, ZHU Z L

    腎と透析   27 ( 6 )   1989

  • Secondary amyloidosis associated with overlap syndrome of rheumatoid arthritis, progressive systemic sclerosis and polymyositis.

    熊谷功, 佐々木徹, 高取克彦, 四方賢一, 池田修二, 高岡道夫, 槙野博史, 太田善介

    日本内科学会雑誌   78 ( 9 )   1989

  • 糸球体基底膜に膠原線維を認めた膜性腎炎の一例

    四方 賢一

    日本腎臓学会誌   30 ( 12 )   1497 - 1497   1988.12

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  • 酵素処理により明らかにされた腎糸球体基底膜の基本的網目構造 分子篩構造

    四方 賢一

    結合組織   20 ( 3~4 )   198 - 199   1988.12

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  • 腸管吻合法に関する検討(第2報)食餌性低蛋白症犬における各種吻合法の比較

    四方淳一, 安藤博文, 山川達郎, 石黒敏一, 金子三蔵, 藤田賢一, 田野倉吉則, 手塚新吉, 関谷智, 竹内啓

    日本消化器外科学会雑誌   11 ( 4 )   354 - 354   1978.4

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  • 低蛋白血漿犬の腸管吻合における層別二層吻合法の応用(2)大腸について

    安藤博文, 金子三蔵, 田野倉吉則, 藤田賢一, 石黒敏一, 手塚新吉, 関谷智, 山川達郎, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   85回   71 - 71   1978.4

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  • 低蛋白血漿犬の腸管吻合における層別二層吻合法の応用(1)小腸について

    金子三藏, 安藤博文, 田野倉吉則, 藤田賢一, 石黒敏一, 手塚新吉, 関谷智, 山川達郎, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   85回   70 - 70   1978.4

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  • 腹膜炎における所謂shockfactorsの吸収経路に関する実験的研究(第1報)E.coliの吸収経路について

    小牧文雄, 田野倉吉則, 藤田賢一, 石黒敏一, 手塚進吉, 金子三蔵, 関谷智, 安藤博文, 四方淳一

    日本消化器外科学会雑誌   11 ( 4 )   341 - 341   1978.4

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  • 小腸・大腸の各種吻合法の物理・生化学的検査結果と病理学的裏付

    田野倉吉則, 石黒敏一, 藤田賢一, 金子三蔵, 安藤博文, 手塚新吉, 関谷智, 山川達郎, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   83回   108 - 108   1977.4

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  • 低蛋白血症犬における腸管吻合法に関する実験的研究(2)大腸における各種吻合法の比較検討

    安藤博文, 石黒敏一, 金子三蔵, 藤田賢一, 田野倉吉則, 手塚新吉, 関谷智, 山川達郎, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   82回   186 - 186   1976.10

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  • 低蛋白血症犬における腸管吻合法に関する実験的研究(1)小腸における各種吻合法の比較検討

    石黒敏一, 安藤博文, 金子三蔵, 藤田賢一, 田野倉吉則, 手塚新吉, 関谷智, 山川達郎, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   82回   185 - 185   1976.10

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  • 低蛋白飼料で飼育せるイヌの腸内細菌叢の変動

    藤田賢一, 安藤博文, 石黒敏一, 金子三蔵, 田野倉吉則, 手塚新吉, 山川達郎, 小林国男, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   81回   194 - 194   1976.4

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  • 腸管吻合法に関する検討(第1報)小腸および大腸における各種吻合法の比較

    四方淳一, 山川達郎, 小林国男, 安藤博文, 石黒敏一, 金子三蔵, 藤田賢一, 田野倉吉則, 手塚新吉

    日本外科学会雑誌   77 ( 3 )   265 - 266   1976.3

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  • 低蛋白症犬における腸管吻合法に関する実験的研究(2)大腸における各種吻合法の比較検討

    安藤博文, 田野倉吉則, 石黒敏一, 金子三蔵, 藤田賢一, 手塚新吉, 山川達郎, 小林国男, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   136 - 136   1975.11

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  • 低蛋白症犬における腸管吻合法に関する実験的研究(1)小腸における各種吻合法の比較検討

    田野倉吉則, 安藤博文, 石黒敏一, 金子三蔵, 藤田賢一, 手塚新吉, 山川達郎, 小林国男, 四方淳一, 竹内啓

    日本獣医学会学術集会講演要旨集   136 - 136   1975.11

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  • イヌの実験的絞扼性イレウスの血行動態に及ぼす影響(第I報)静脈還流(VenousReturn)について

    田野倉吉則, 石黒敏一, 手塚新吉, 安藤博文, 金子三蔵, 藤田賢一, 重松史郎, 四方淳一, 竹内啓

    日本獣医学会講演要旨集   79回   99 - 99   1975.4

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  • イヌにおける腸管吻合法に関する実験的研究(II)大腸における各種吻合法の比較検討

    安藤博文, 石黒敏一, 金子三蔵, 藤田賢一, 田野倉吉則, 手塚新吉, 山川達郎, 小林国男, 四方淳一, 竹内啓

    日本獣医学会講演要旨集   79回   97 - 97   1975.4

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  • イヌにおける腸管吻合法に関する実験的研究(I)小腸における各種吻合法の比較検討

    藤田賢一, 安藤博文, 石黒敏一, 金子三蔵, 田野倉吉則, 手塚新吉, 山川達郎, 小林国男, 四方淳一, 竹内啓

    日本獣医学会講演要旨集   79回   97 - 97   1975.4

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  • 低蛋白食,腸管切除,Plasmaphaeresisなどによりつくられた低蛋白犬における血漿蛋白像の変化について

    安藤博文, 金子三蔵, 藤田賢一, 石黒敏一, 永江文博, 小林国男, 山川達郎, 四方淳一, 竹内啓

    日本獣医学会講演要旨集   77回   96 - 96   1974.4

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Awards

  • Expert Investigator Award

    2022.10   Japan Diabetes Complication Society   Role of inflammation in the pathogenesis of diabetic kidney disease and development of new therapeutic drug.

    Kenichi Shikata

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    Award type:International academic award (Japan or overseas)  Country:Japan

    Role of inflammation in the pathogenesis of diabetic kidney disease and development of new therapeutic drug.

  • Expert Investigator Award

    2022   日本糖尿病合併症学会  

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

    1999  

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  • 第1回シンポジウム糖尿病研究会会賞

    1997  

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Research Projects

  • 糖尿病性腎臓病におけるIL-18によるインフラマソーム活性化機構の解明と治療応用

    Grant number:22K08353  2022.04 - 2026.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    宮本 聡, 四方 賢一

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    Grant amount:\4160000 ( Direct expense: \3200000 、 Indirect expense:\960000 )

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  • Quality management of Advanced medical care clinical resarch under Clinical Trial Act for pharmaceutial approval application

    Grant number:20K12715  2020.04 - 2024.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    櫻井 淳, 四方 賢一, 堀田 勝幸, 大野 彩, 加藤 有加

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    Grant amount:\4290000 ( Direct expense: \3300000 、 Indirect expense:\990000 )

    この研究では、先進医療Bとして実施する臨床研究を薬事承認申請に活用するための試験の品質レベルを明らかにする。先進医療Bとして実施されてきた臨床研究(臨床研究法下の「特定臨床研究」に相当)は薬事承認申請の根拠となりうる。しかしながら特定臨床研究の成果を薬事承認申請の根拠資料として活用するための具体的な品質レベルについては未だ明確になされていない。特定臨床研究として実施する先進医療Bの品質レベルが明らかになれば、従来治験が行われていた開発初期の臨床試験(いわゆる探索的試験)を先進医療Bとして実施する可能性が高まり、試験の効率化、低コスト化が図られる。
    2022年度には、特定臨床研究においてRisk-based approach(RBA)を実装するための基本的手順及び標準業務手順書「Risk Based Approachに関する手順書」を確定した。さらに、プロジェクトに自ら治験を実施する者が治験期間を通じ適切なQRM(Quality Risk Management)を実行していくための「品質リスクマネジメントに関する手順書」及び付随する様式として「品質リスクマネジメント計画書(Integrated Quality Management Plan: IQRMP)」、「QTL(Quality Tolerance Limit:品質許容限界)定義書」、「リスク管理表」、「リスクレビュー報告書」等のそれぞれひな形も確定した。さらに、昨今の特定臨床研究の薬事承認申請への利用に関する通知の理解や、QMSの視点でスタッフの教育を行った。
    さらに、本研究を適応する先進医療B2試験の支援を継続して行い、品質リスクマネジメントの実行性を確認した。

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  • Development of the new therapeutic strategy for diabetic nephropathy by modulation of inflammasome.

    Grant number:20K08635  2020.04 - 2023.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    四方 賢一, 宮本 聡

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    Grant amount:\4420000 ( Direct expense: \3400000 、 Indirect expense:\1020000 )

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  • 3次元マルチオミックス解析による糖尿病性腎症の新規治療標的の探索と同定

    Grant number:18K08211  2018.04 - 2022.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    宮本 聡, 四方 賢一

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    Grant amount:\4290000 ( Direct expense: \3300000 、 Indirect expense:\990000 )

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  • Development of new therapeutic strategy by targeting the inflammasome.

    Grant number:17K09698  2017.04 - 2021.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Shikata Kenichi

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    Grant amount:\4680000 ( Direct expense: \3600000 、 Indirect expense:\1080000 )

    The aim of this study is to clarify the role of inflammasome in the pathogenesis of diabetic nephropathy and develop a new therapeutic strategy of diabetic nephropathy by inhibition of inflammasome activation. We demonstrated that inflammasome-related molecules are over expressed in the glomeruli and interstitium of diabetic mice. Suramin inhibited the activation of inflammasome in the kidney of diabetic mice (KK-Ay mice) and renal injuries.From these results. It is suggested that inflammasome in involved in the pathogenesis of diabetic nephropathy and that inhibition of inflammasome activation is beneficial for the therapy of diabetic nephropathy.

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  • Influences of Lifestyles on Health Conditions of Diabetic Patients and of Those Who Are Likely to Get Diabetic

    Grant number:26463317  2014.04 - 2017.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Sumiyoshi Kazuko, SEKI Akiho, SADA Yoshiko

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    Grant amount:\3770000 ( Direct expense: \2900000 、 Indirect expense:\870000 )

    For the purpose of clarifying the causal association between the lifestyles and health conditions of diabetic patients and of those who are likely to get diabetic, we created a model based on the stress recognition theory, and conducted a longitudinal research. Defining the newly created “stress recognition scale upon treatments” as the stressor, and the “lifestyle scale” as the coping, we analyzed the model of lifestyles influencing health conditions by using the structural equation modeling. We used WHO-5J’s mental health and HbA1c value for the evaluation of health conditions. As a result, significant associations were observed between treatment stress and lifestyles, and between lifestyles and mental health conditions. However, no significant association was observed between lifestyles and HbA1c value. In the future, we intend to analyze the causal association between lifestyles and health conditions.

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  • Investigation of the novel therapeutic targets for diabetic nephropathy.

    Grant number:25461224  2013.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Shikata Kenichi, Kodera Ryo

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    Grant amount:\5070000 ( Direct expense: \3900000 、 Indirect expense:\1170000 )

    Chronic low grade inflammation, “microinflammation”, is one of the major mechanisms in the pathogenesis of diabetic nephropathy. The aim of this study is to clarify the role of microinflammation in the pathogenesis of diabetic nephropathy and find the novel therapeutic target for diabetic nephropathy. We investigated the change of expression of micro RNA in the glomeruli of the two types of mouse model using streptozotocin-induced type 1 diabetes and db/db mice. We performed Micro RNA array using RNA from diabetic mice and found several micro RNAs which up-regulated in the glomeruli of both diabetic mouse models. Moreover, these microRNA upregulated in the glomeruli for long period from the early phase of diabetes. One of these microRNA induced up-regulation of TGF-beta and down-regulaton of eNOS and SIRT-1 after transfection in glomerular endothelial cells and mesangial cells. These results suggest that micro RNA might be one of the new therapeutic target for diabetic nephropathy.

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  • New therapeutic approach to diabetic nephropathy by modulating mitochondrial function

    Grant number:18390249  2006 - 2008

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    MAKINO Hirofumi, WADA Jun, SHIKATA Kenichi

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    Grant amount:\17180000 ( Direct expense: \15800000 、 Indirect expense:\1380000 )

    生活習慣の変化により糖尿病患者は増加の一途をたどり、糖尿病性腎症により透析導入となる患者も年々増加している.糖尿病マウスへのtranslocase of inner mitochondrial membrane 44 (Tim44)遺伝子導入によって、糸球体肥大・メサンギウム基質の増加・アルブミン尿の増加が抑制された.Tim44はミトコンドリアへのsuperoxide dismutaseやglutathione dismutaseといった抗酸化酵素をimportしてミトコンドリア由来の活性酸素の産生を抑制することにより治療効果を発揮すると考えられた.

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  • Effects of uncertainty and coping on dietary behaviors in patients with diabetic nephropathy: Development of a model to predict dietary behavior.

    Grant number:17592245  2005 - 2007

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    ICHIMURA Mituko, KAWATA Chieko, SHIKATA Kenichi, NAKAO Miyuki, NAKANISHI Yoshiko

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    Grant amount:\2480000 ( Direct expense: \2300000 、 Indirect expense:\180000 )

    A questionnaire survey was conducted among diabetic outpatients to identify their disease-related coping behaviors, disease complexity, future anxiety and uncertainty, physical symptoms, awareness of kidney status, knowledge of nephropathy, and dietary self-management. Path analysis showed that coping behaviors and uncertainty directly affected dietary management. Based on this finding, an educational program was developed by reviewing these interactions with diabetic patients who had stage II-IV nephropathy.
    A patient with stage II nephropathy was told by Ms attending physician that a test detected micro albuminuria. The patient then worriedly contacted a nurse and told the nurse about Ms test result. The nurse explained the meaning of micro albuminuria and diabetic nephropathy and told the patient that his renal function would recover with proper glycemic control. Since the patient indicated that he would do his best to improve his renal function, the nurse talked to the patient about measures that he could take to improve glycemic control. For the last several years, the patient's HbAlc had been 〓8.0%; by eliminating snacks, his HbAlc improved to around 7%. The patient had kidney failure, and though he knew that he needed to restrict his protein and salt intakes, he failed to do so, and his serum creatinine continued increasing. The patient indicated that he felt anxious about his future and isolated from his family. The nurse explained the patient's condition to his family, and she told the family that the patient was trying to do his best. Afterwards, the family was more helpful towards the patient.
    Based on the above, the following program was designed for diabetics with stage II nephropathy. Since these patients lack symptoms, they are not fully aware that they have nephropathy. However, by mentioning that they have micro albuminuria, nurses can explain how patients can improve their kidney function. For patients who need to restrict their protein intake, nurses provide not only conventional dietary guidance, but they also explain the necessity and effectiveness of protein-restricted diets and ask the family members to support their diabetic relative.

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  • Identification of Interacting Molecules with Collectrin and their roles in Hypertension

    Grant number:17590829  2005 - 2007

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    WADA Jun, MAKINO Hirofumi, SHIKATA Kenichi

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    Grant amount:\3710000 ( Direct expense: \3500000 、 Indirect expense:\210000 )

    Collectrin, a homologue of angiotensin converting enzyme 2 (ACE2), is a type I transmembrane protein and we originally reported its localization to the cytoplasm and apical membrane of collecting duct cells. Collectrin has been reported to be under the transcriptional regulation by HNF-1α which is exclusively expressed in proximal tubules and localized at the luminal side of brush border membranes. In this research project, we found that collectrin is a target of HNF-1β and heavily expressed in the primary cilium of renal collecting duct cells. Collectrin is also localized in the vesicles near the peri-basal body region and binds to γ-actin-myosin II-A, SNARE, and polycystin-2-polaris complexes, and all of these are involved in intracellular and ciliary movement of vesicles and membrane proteins. Treatment of mIMCD3 cells with collectrin siRNA resulted in defective cilium formation, increased cell proliferation and apoptosis, and disappearance of polycystin-2 in the primary cilium. Suppression of collectrin mRNA in metanephric culture resulted in the formation of multiple longitudinal cysts in ureteric bud branches. Taken together the cystic change and formation of defective cilium with the interference in the collectrin functions would suggest that it is necessary for recycling of the primary cilia-specific membrane proteins, the maintenance of the primary cilia and cell polarity of collecting duct cells. The transcriptional hierarchy between HNF-1β and PKD (polycystic kidney disease) genes expressed in the primary cilia of collecting duct cells has been suggested and collectrin is one of such HNF-1β regulated genes.

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  • Novel therapeutic targets for diabetic nephropathy.

    Grant number:17590828  2005 - 2006

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    SHIKATA Kenichi, MAKINO Hirofumi, WADA Jun

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    Grant amount:\3500000 ( Direct expense: \3500000 )

    Diabetic nephropathy is a leading cause of end-stage renal failure. Several mechanisms, including activation of protein kinase C, advanced glycation end products, and overexpression of transforming growth factor (TGF)-beta, are believed to be involved in the pathogenesis of diabetic nephropathy. However, the significance of inflammatory processes in the pathogenesis of diabetic microvascular complications is poorly understood. Accumulation of macrophages and overexpression of leukocyte adhesion molecules and chemokines are prominent in diabetic human kidney tissues. We previously demonstrated that intercellular adhesion molecule (ICAM)-1 mediates macrophage infiltration into the diabetic kidney. To find a novel therapeutic target for diabetic nephropathy, we induced diabetes or 5/6 nepphrectomy in ICAM-1-deficient (ICAM-1(-/-)) mice and ICAM-1(+/+) mice and examined the renal pathology over a period of 6 months. The infiltration of macrophages, albuminuria anc renal tissue injuries were markedly suppressed in diabetic ICAM-1(-/-) mice or 5/6 nephrectomized ICAM-1(-/-) mice compared with ICAM-1(+/+) mice. We investigated the gene expression profiles in the kidneys of these mice using DNA microarray system. Several genes including osteopontin, cholecystokinin (CCK) and scavenger receptor A are up-regulated in the kidneys of diabetic or 5/6 nephretomized ICAM-1(+/+) mice, while the expression levels of these genes were decreased in diabetic or 5/6 nephrectomized ICAM-1(-/-) mice as compared to ICAM-1(+/+) mice. Scavenger receptor A deficient mice revealed diminished albuminuria and renal injuries after induction of dianetes as compared with wild type mice. Renal injuries were ameliorated in CCK-receptor deficient mice after 5/6 nephrectomy as compared with wild type mice. Our results indicate that microinflammation is involved in the pathogenesis of diabetic nephropathy. CCK, scavenger receptor A and osteopontin may be novel therapeutic target for diabetic nephropathy.

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  • "タンパク質"修飾酸化LDLの診断法の確立と動脈硬化における意義に関する研究

    Grant number:16659141  2004 - 2005

    日本学術振興会  科学研究費助成事業  萌芽研究

    松浦 栄次, 四方 賢一, 稲垣 純子

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    Grant amount:\3300000 ( Direct expense: \3300000 )

    酸化ストレスが原因となる生活習慣病が我が国でも増加の一途を辿っている。この状況の中、動脈硬化や冠動脈疾患の早期診断、治療中の経過観察に有益な診断法として、酸化LDLや高感度C-反応性タンパク質(CRP)の測定法が開発されてきた。しかしながら、CRPおよびβ_2-グリコプロテインI(β_2GPI)が酸化LDLと複合体を形成していることが明らかになったため、早期に、これらタンパク質修飾LDLの臨床意義を明らかにし、それらの診断法を確立する必要があると考えた。そこで、平成16年度からの2年間の本萌芽研究で、基礎・臨床分野に跨る解析を体系的に行い、タンパク質修飾酸化LDLの動脈硬化への関わりについて検証すると共に、臨床診断薬としてのELISAによる修飾酸化LDLの測定法を確立することを計画した。
    今年度は、抗β_2GPI抗体、抗CRP抗体などを用いたCRP/β_2GPI修飾酸化LDLのELISA法を確立し、糖尿病、虚血性心疾患、脳血管障害、閉塞性動脈硬化症、慢性腎疾患等の動脈硬化性疾患、および膠原病(特に、SLE、APS)を対象に、古典的な動脈硬化の指標とCRP/β_2GPI修飾酸化LDLとの関連性について検討を行った。CRP/酸化LDL/β_2GPI複合体は、動脈硬化性疾患である糖尿病患者血中、特に、IMTで診断される動脈硬化陽性の患者で特異的に検出された。一方、急性炎症性(熱発性)疾患で、CRP陽性の患者では全く検出されなかった。高感度CRPと高い相関を示すため、冠動脈疾患の危険因子と考えられている高感度CRPの本体が本複合体であると考えられる。動脈硬化を有する患者の頸動脈(動脈硬化巣)にCRP、酸化LDL、β_2GPIの局在が認められたことより、これらの複合体は動脈硬化巣で形成され末梢血流中へ逸脱すると考えられた。

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  • Role of Macrophage in the pathogenesis of diabetic nephropathy and novel therapeutic target.

    Grant number:15590850  2003 - 2004

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    SHIKATA Kenichi, MAKINO Hirofumi

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    Grant amount:\3500000 ( Direct expense: \3500000 )

    Diabetic nephropathy is a leading cause of end-stage renal failure. Several mechanisms, including activation of protein kinase C, advanced glycation end products, and overexpression of transforming growth factor (TGF)-beta, are believed to be involved in the pathogenesis of diabetic nephropathy. However, the significance of inflammatory processes in the pathogenesis of diabetic microvascular complications is poorly understood. Accumulation of macrophages and overexpression of leukocyte adhesion molecules and chemokines are prominent in diabetic human kidney tissues. We previously demonstrated that intercellular adhesion molecule (ICAM)- 1 mediates macrophage infiltration into the diabetic kidney. In the present study, to investigate the role of macrophage in diabetic nephropathy and find a novel therapeutic target, we induced diabetes or 5/6 nepphrectomy in ICAM-1-deficient (ICAM-1(-/-)) mice and ICAM-1(+/+) mice and examined the renal pathology over a period of 6 months. The infiltration of macrophages, albuminuria anc renal tiossue injuries were markedly suppressed in diabetic ICAM-1(-/-) mice or 5/6 nephrectomized ICAM-1(-/-) mice compared with ICAM-1(+/+) mice. We investigated the gene expression profiles in the kidneys of these mice using DNA microarray system. Proinflammatory geses including osteopontin are up-regulated in the kidneys of diabetic or 5/6 nephrectomized ICAM-1(+/+) mice, while the expression levels of these genes were decresased in diabetic or 5/6nephrectomized ICAM-1(-/-) mice as compared to ICAM-1(+/+) mice. These genes might be novel targets for the therapy of diabetic nephropathy.

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  • Identification of Novel ACE2 homologue, collectrin, and its role in renal organogenesis and progressive renal failure.

    Grant number:14571025  2002 - 2004

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    WADA Jun, MAKINO Hirofumi, SHIKATA Kenichi

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    Grant amount:\2800000 ( Direct expense: \2800000 )

    Collectrin, a novel homologue of angiotensin converting enzyme-related carboxypeptidase (ACE2), was identified in 5/6 ablated kidneys at hypertrophic phase (Zhang H et al. J Biol Chem 276(20),17132-17139,2001). By using an animal model of partial nephrectomy, several differentially expressed genes were isolated by the PCR-based cDNA-subtraction method (Zhang H et al. Kidney Int 56(2),549-558,1999). Because one of these genes was kidney-specific and highly localized to the collecting ducts, it was designated as collectrin. The sequence analyses revealed that collectrin with 222 amino acids has an apparent signal peptide and a transmembrane domain (black box in figure shown below) ; the sequence is conserved in mouse, rat and human and shared 81.9% identity. Human collectrin has 47.8% identity with non-catalytic extracellular and cytosolic domains of ACE2 (white box in figure), however, unlike ACE and ACE2, collectrin lacks active dipeptidyl carboxypeptidase catalytic domains. Interestingly, ACE2 and collectrin are located close to each other in the same chromosomal region (Xp22) and whereas ACE is located chromosome 17. The collectrin mRNA transcripts are expressed exclusively in the kidney. In situ hybridization reveals its mRNA expression in renal collecting ducts and immunohistochemistry shows it is localized to the luminal surface and cytoplasm of collecting ducts.

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  • Reactive oxygen species and diabetic nephropathy

    Grant number:14370319  2002 - 2004

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    MAKINO Hirofumi, WADA Jun, SHIKATA Kenichi, NAKAMURA Yoshio

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    Grant amount:\9100000 ( Direct expense: \9100000 )

    Hyperglycemia-induced overproduction of mitochondrial reactive oxygen species (ROS) has emerged as a major player in diabetic vascular complications. Mammalian translocase of inner mitochondrial membrane 44 (Tim44) was identified by up-regulation in diabetic mouse kidneys. Tim44 functions as a membrane anchor of mtHsp70 to TIM23 complex and involves in the import of mitochondria-targeted preproteins into mitochondrial matrix. The process is dependent on inner membrane potential (Δψ) and ATP hydrolysis on ATPase domain of mtHsp70. Hemagglutination virus of Japan (HVJ)-envelope vector carrying pcDNA3.1 plasmid containing the full length cDNA of Tim44 and control plasmid were weekly injected from tail vein into uninephrectomized streptozotocin-induced diabetic CD-1 mice. The gene delivery alleviated proteinuria and renal hypertrophy at 8 weeks after the injection and inhibited renal cell proliferation and apoptosis, and suppressed superoxide production. In vitro experiments, using human proximal tubular (HK2) cells, revealed that the gene delivery of Tim44 reversed high glucose induced metabolic and cellular abnormalities such as, enhanced ROS production, increased ATP contents, alterations in inner membrane potential, increased cell proliferation and apoptosis. Transfection with siRNA and expressing vector of Tim44 revealed that Tim44 facilitates import of anti-oxidative enzymes such as superoxide dismutase (SOD) and glutathione peroxidase into mitochondria. The gene delivery of Tim44 thus seems to be beneficial for the maintenance of mitochondrial function and is a novel therapeutic approach for diabetic nephropathy.

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  • Role of Macrophage in the pathogenesis of diabetic nephropathy revealed by ICAM-1 deficient mice.

    Grant number:13671116  2001 - 2002

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    SHIKATA Kenichi, WADA Jun, MAKINO Hirofumi

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    Grant amount:\3500000 ( Direct expense: \3500000 )

    Diabetic nephropathy is a leading cause of end-stage renal failure. Several mechanisms, including activation of protein kinase C, advanced glycation end products, and overexpression of transforming growth factor (TGF)-beta, are believed to be involved in the pathogenesis of diabetic nephropathy. However, the significance of inflammatory processes in the pathogenesis of diabetic microvascular complications is poorly understood. Accumulation of macrophages and overexpression of leukocyte adhesion molecules and chemokines are prominent in diabetic human kidney tissues. We previously demonstrated that intercellular adhesion molecule (ICAM)-1 mediates macrophage infiltration into the diabetic kidney. In the present study, to investigate the role of macrophage in diabetic nephropathy, we induced diabetes in ICAM-1-deficient (ICAM-1(-/-)) mice and ICAM-1(+/+) mice with streptozotocin and examined the renal pathology over a period of 6 months. The infiltration of macrophages was markedly suppressed in diabetic ICAM-1(-/-) mice compared with that of ICAM-1(+/+) mice. Urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion were significantly lower in diabetic ICAM-1(-/-) mice than in diabetic ICAM-1(+/+) mice. Moreover, expressions of TGF-beta and type IV collagen in glomeruli were also suppressed in diabetic ICAM-1(-/-) mice. Moreover, we investigated the gene expression profiles in the kidneys. of these mice using DNA microarray system. Proinflammatory genes are up-regulated in the kidneys of diabetic ICAM-1(+/+) mice, while the expression levels of these genes were decresased in diabetic ICAM-1(-/-) mice as compared to ICAM-1(+/+) mice. These results suggest that ICAM-1 is critically involved in the pathogenesis of diabetic nephropathy.

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  • A study on the establishment of periodontal treatment for patients with insulin resistant diabetes mellitus.

    Grant number:12470470  2000 - 2001

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    MURAYAMA Yoji, SHIKATA Kenichi, MAKINO Hirofumi, NISHIMURA Fusanori, FUKUDA Tetsuya

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    Grant amount:\14500000 ( Direct expense: \14500000 )

    The number of diabetes increased markedly due possibly to the rapid change of our lifestyle, and to the increase in obese subjects with insulin resistance. Tumor necrosis factor-α (TNF-α) produced from adipocytes in the adipose tissues has been suggested to be affect insulin resistance in obese subjects. Apart from adipocytes, activated macrophages infiltrated in inflammatory lesion also produce large quantity of TNF-α. Based on these backgrounds, we hypothesized that successful periodontal treatment in diabetes patients may result in decrease in circulating TNF-α and subsequent metabolic control of diabetes. The results indicated that anti-microbial periodontal treatment resulted in marked decrease in 1) the number of microorganism in periodontal pockets and 2) circulating TNF-α concentration, and in significant improvement in 3) insulin resistance and 4) subsequent metabolic control.
    We also found that some periodontitis patients exhibited increased anti-GAD antibody which is widely used as a sero-diagnostic marker in patients with type 1 diabetes. Generally, GAD is known to be produced in pancreatic β-cells and some nerve cells. However, we also found that fibroblastic cells including gingival fibroblasts express GAD both at gene and protein level. Thus, we thought that periodontal inflammation which destruct periodontal connective tissues resulted in the release of GAD and in exposure of such GAD to immune cells, led to the production of anti-GAD antibodies. Therefore, it is possible that periodontal inflammation influences sero-diagnosis of type 1 diabetes.
    These results indicate that diabetes not only influence the susceptibility and progression of periodontitis, but periodontal inflammation also influences diabetic status. Thus, it can be concluded that periodontitis is an important complication of diabetes modulating the clinical course and diagnostic procedure of diabetes.

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  • Molecular mechanism of glomerular hyperfiltration in diabetic nephropathy revealed by gene expression profiling.

    Grant number:11470218  1999 - 2001

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    MAKINO Hirofumi, HIDA Kazuyuki, SHIKATA Tenichi, WADA Jun

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    Grant amount:\16500000 ( Direct expense: \16500000 )

    Background. To elucidate molecular mechanism of diabetic nephropathy, high density DNA filter array was employed for the survey of gene expression profile of streptozotocin-induced diabetic CD-1 (ICR) mice kidney.
    Methods. Ten-week-old CD-1 male mice were divided into four groups (1) control, (2) unilaterally nephretomized (UX) mice, (3) STZ-induced diabetic (STZ) mice, and (4) STZ mice with unilateral renal ablation (STZ-UX). The pathological changes were examined at 24 weeks after the induction. The gene expression profile was compared between the control and STZ mice by Gene Discovery Array (GDA).
    Results. The glomeruli in UX mouse kidney showed prominent glomerular hypertrophy, while the accumulation of mesangial matrix was minimal. Both STZ and STZ + UX mice had significant glomerular hypertrophy and glomerulosclerosis and lesions were not enhanced by renal ablation. By comparison between control and STZ mice, 16 clones that increased in expression with the induction of diabetes and 65 clones that decreased in diabetic kidneys were identified. The 37 known genes were related to glucose and lipid metabolism, ion transport, transcription factors, signaling molecules and extracellular matrix-related molecules. The genes known to be involved in cell differentiation and organogenesis in various tissues, i.e. Unc-18 homologue, POU domain transcription factor 2, lunatic fringe gene homolog, fibrous sheath component 1, Sox-17, fibulin 2, and MRJ, were found to be differentially expressed in early phase of diabetic kidneys.
    Conclusions. Hyperglycemia was major determinant of glomerulosclerosis in STZ-induced diabetic CD-1 mice and the altered gene expression in the early phase of diabetic kidney may be critical for the development of diabetic nephropathy.

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  • Application of anti-adhesion molecule therapy for glomerulonephritis -Effects of sulfated oligosaccharides as selectin-blocking agents-

    Grant number:11671036  1999 - 2000

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    SHIKATA Kenichi, HIDA Kazuyuki, WADA Jun

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    Grant amount:\3900000 ( Direct expense: \3900000 )

    Background. Selectins are adhesion molecules which mediate leukocyte infiltration into inflammatory tissues. P- and L-selectin bind to sulfated oligosaccharide chains on the ligand molecules. Synthesized sulfated oligosaccharides, including sulfated hyarulonic acid (SHA) and sulfated colominic acid (SCA), inhibit both P- and L-selectin-dependent adhesion pathways in vitro. We evaluated the preventive effects of SHA and SCA on rat mesangial proliferative glomerulonephritis and rat crescentic glomerulonephritis.
    Methods. Female Wistar rats were injected with anti-Thy-1 antibody after unilateral nephrectomy for a mesangial proliferative glomerulonephritis model. Female WKY rats were injected with nephrotoxic serum for a crescentic glomerulonephritis model. Rats were administered with neutralizing or non-neutralizing monoclonal antibodies to rat P-selectin and L-selectin, SHA, hyarulonic acid, SCA and colominic acid. Localization of P-selectin and macrophages were examined by immunohistochemical methods. Gene expression of PDGF B chain in the glomeruli was quantified using real-time RT-PCR method.
    Results. Increased expression of P-selectin and macrophage infiltration was prominent in the glomeruli in both two models. Proteinuria, crescent formation and glomerular infiltration of macrophages were significantly reduced by anti-P-selectin mAb, but not by anti-L-SL mAb. SHA and SCA reduced proteinuria, macrophage infiltration and crescent formation in dose dependent manner. Gene expression of PDGF B chain was significantly decreased in SHA and SCA treatment groups. In conclusion, SHA and SCA inhibited glomerular macrophage infiltration by blocking P-selectin-dependent adhesion pathway, and prevented disease progression in rat mesangial proliferative glomerulonephritris and rat crescentic glomerulonephritis. We conclude that sulfated oligosaccharides may be beneficial for the treatment of glomerulonephritis.

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  • Application of anti-cell adhesion molecule therapies for renal diseases.

    Grant number:08671287  1996 - 1997

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    MAKINO Hirofumi, KUNITOMI Mie, TSUCHIYAMA Yoshinori, SHIKATA Kenichi

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    Grant amount:\2100000 ( Direct expense: \2100000 )

    We have investigated the possibility of application of anti-cell adhesion molecule therapies for renal diseases. In summary,
    1. We showed the up-regulated expression of ICAM-1, E-selectin and P-selectin in the glomeruli and interstitium of the kidney or the patients with glomerulonephritis and diabetic nephropathy.
    2. We calrified the mechanism that glomerular hyperfiltration induces intraglomerular expression of ICAM-1 and infiltration of macrophages.
    3. We showed that the ligands for L-selectin exist in the cytoplasm of tubular epithelial cells and re-distribute to the interstitium and peritubular capillaries after ureteral ligation in rat kidney. Furthermore, we showed that one of the ligands for L-selectin is sulfatide.
    4. We showed that administration of sulfatide which is a ligand for L- and P-selectin inhibits the infiltration of macrophage to renal interstitium in vivo.
    5. We showed that prostaglandin I_2 ameliorates renal injury by inhibition of ICAM-1 expression in rat crescentic glomerulonephritis model.
    These results showed the critical role of ICAM-1 and selectins for the infiltration of macrophege into renal tissues in various types of glomerular diseases. In conclusion, our results suggest the beneficial effects of anti-cell adhesion molecule therapy for glomerular diseases.

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  • Expression of interleukin-12 in synovial tissue from patients with rheumatoid arthritis.

    Grant number:08670518  1996 - 1997

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    YAMAMURA Masahiro, SHIKATA Ken-ichi

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    Grant amount:\2200000 ( Direct expense: \2200000 )

    The importance of interleukin-12 as a factor in the interferon-gamma (IFN-gamma) -dominant T cell cytokine response in the synovial tissue of patients with rheumatoid arthritis (RA) was examined. Synovial tissues from RA patients more strongly expressed IL-12 p40 mRNA than did osteorthritis (OA) tissues, as determined by RT-PCR.Dissociated tissue cells from RA patients sspontaneously released detectable amounts of IL-12 p70 in culture, whereas production of IL-12 by OA tissues was limited. By immunohistochemical analysis, IL-12-producing cells were localized mainly in the sublining layr of RA synovium, and mostly expressed the CD68 antigen. Levels of IFN-gamma production by RA synovial tissue cells were potently and selectively enhanced by IL-12. The ability of IL-2-expanding synovial T cells to produce IFN-gamma was augmented by costimulation with IL-12 and diminished by anti-IL-12, while it was not affected by IL-4. These dada suggest that IL-12, produced mainly by macrophage-lineage cells, may be involved in IFN-gamma dominant cytokine production by infiltrating T cells in joints with chronic RA.

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  • Role of advanced glycation end-product in the development and progression of diabetic nephropathy.

    Grant number:07671252  1995 - 1996

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    MAKINO Hirofumi, YAMAJI Hiroaki, HORIUCHI Masakimi, SHIKATA Kenichi

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    Grant amount:\2400000 ( Direct expense: \2400000 )

    In diabetic state, glycation reaction of the proteins (Maillard reaction) undergoes and advanced glycation endproduct (AGE) accumulates in varous tissues. AGEs bind to the their receptors on the macrophages, and are known to induce the production of cytokines and nitric oxide (NO). Extracellular matrix with AGE modification is resistant to the proteolytic degradation. To explore the role of AGEs in the progression of the diabetic nephropathy, immunohistochemical studies of AGE and extracellular matrix components were performed in the kidney biopsy specimens of diabetic nephropathy patients, streptozotocin-induced diabetic rat kidney, and OLETF rat. In the mesangial area and tubules, AGEs were accumulated in the diabetic kidney. Especially in the nodular lesions of the diabetic kidneys, AGE were noted. By ultra-high resolution scanning electron microscopy showed enlarged meshwork of mesangial matrix of nodular lesions. These results indicated that AGEs accumulated with the progression of the diabetic nephropathy. AGEs may bind to the receptor on the mesangial cells and thus stimulate the production and inhibit the proteolytic degradations. AGEs may play a pivotal role in the alterations of the structual architecture of the extracellular matrix and glomerulosclerosis of the diabetic nephropathy.

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  • 糖尿病性腎症における糸球体細胞外マトリックスの分子構築の変化

    Grant number:07671250  1995

    日本学術振興会  科学研究費助成事業  一般研究(C)

    太田 善介, 林 佳子, 四方 賢一, 槇野 博史

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    Grant amount:\2100000 ( Direct expense: \2100000 )

    1)糖尿病性腎症患者の腎生検組織を用いた、糸球体細胞外マトリックスの超微細構造の変化の検討
    糖尿病性腎症患者の腎生検組織を通常の方法で固定包理し超薄切片を作製し、ナトリウムエチラートによって脱包理し、リンタングステン酸によってネガティブ染色を行い、透過電子顕微鏡で観察した。その結果、糖尿病性腎症患者の糸球体基底膜では、主にtypeIVコラーゲンによって形成される微細な網目構造の拡大が認められた。また、網目構造の破綻により糸球体基底膜を貫通するトンネル構造が認められた。以上の結果から、糖尿病性腎症における蛋白尿の原因は、糸球体基底膜の網目構造の破綻であることが明らかになった。
    2)糖尿病モデルラットの腎組織を用いた、糸球体細胞外マトリックスの超微細構造の変化の検討
    streptozotocinを投与してインスリン依存性糖尿病を惹起したラット(STZ糖尿病ラット)とインスリン非依存性糖尿病のモデルであるOLETFラットの腎組織を用いて、1)と同様の方法で電顕により観察した。その結果、STZ糖尿病ラットとOLETFラットの糸球体基底膜には、経時的に網目構造の拡大が認められた。OLETFラットの糸球体細胞外マトリックスの変化を免疫組織学的に検討した結果、typeIV、V、VIコラーゲン、フィブロネクチンの増加が認められた。OLETFラットの糸球体基底膜は、経時的に肥厚し、網目構造の拡大とともにトンネル構造も認められた。以上の結果から、糖尿病性腎症における蛋白尿の原因は、糸球体基底膜の網目構造の破綻であることが明らかになった。

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  • Mechanism of inflammatory cell infiltration in the kidney tissue of glomerulonephritis and diabetic nephropathy. -Elucidation of the role of cell adhesion molecules and development of therapeutic drugs.-

    Grant number:06671141  1994 - 1995

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for General Scientific Research (C)

    SHIKATA Kenichi, MAKINO Hirofumi

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    Grant amount:\2000000 ( Direct expense: \2000000 )

    In STZ-induced diabetic rat, we investigated the macrophage infiltration into the glomeruli and expression of ICAM-1. After induction of the diabetes, ICAM-1 was upregulated in the glomeruli. In addition, intraglomerular macrophage infiltration was observed. By the normalization of the blood glucose levels by insulin injection, expression of ICAM-1 and macrophage infiltration were prevened. These results indicated that ICAM-1 may paly a pivotal role in the macrophage infiltration of the diabetic nephropathy.
    We examined the expression of P-and E-selectins in the kidney tissues by immunohistochemistry. Normal kidney specimens and kidney biopsy specimens of glomerulonephritis and diabetic nephropathy patients were used. In normal kidneys, P-and E-selections were not detected. In lupus nephritis and diabetic nephropathy, P- and E-selections were expressed in the glomeruli and the intertubular vessels. Selections may be involved in the leukocyte infiltration into the kidney tissues in lupus nephritis and diabetic nephropathy.
    By using the L-selectin-IgG chimeric molecule (LEC-IgG), the distribution of L-selectin ligands were investigated. L-selectin ligands were distributed on the distal tubular epithelium. After ligation of ureters of rats, L-selectin ligands were disappeared from the tubular cells and redistributed intertubular vessels. Tubular monocyte infiltraion was also observed. By th e injection of sulfatide and and anti-L-selectin antibody, monocyte infiltration was inhibited. Monocyte adhesive pathway via L-selectin may play a key role in the monocute infiltration into the kidney tissue in rat ureter ligation animal model.

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  • Expression of interleukin-19 in synovial tissue from patients with rheumatoid arthritis

    Grant number:06670485  1994 - 1995

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for General Scientific Research (C)

    YAMAMURA Masahiro, SHIKATA Ken-ichi, KASHIHARA Naoki

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    Grant amount:\2400000 ( Direct expense: \2400000 )

    The expression of interleukin-10 and its pathogenic role in rheumatoid arthritis (RA) was investigated. Concentrations of IL-10 in both serum and synovial fluid from RA patients were greater compared to those of osteoarthritis patients. Synovial tissues in RA more strongly expressed IL-10 mRNA than in OA, and spontaneously produced higher levels of IL-10. By Immunohistochemical staining and detection of IL-10 in isolated macrophages, fibroblasts, and T cells from RA synovium, macrophages in both the lining and sublining layer are major sources of this cytokine. IL-10 markedly inhibited the production of inflammatory cytokines such as IL-1 and TNF-α by RA synovium, but both cytokines were potent inducer of IL-10. On the other hand, T cell-derived anti-inflammatory cytokines, IL-4 and Il-13, are less efficient in inhibiting synovial inflammatory cytokines, 7but are able to inhibit proliferation of RA synovial fibroblasts. However, their expression in RA joint is extremely limited IL-10 expression was associated with levels of IgG-rheumatoid factor in RA. These results indicate that IL-10 may be mostly responsible for downregulation of chronic inflammation and rheumatoid factor production in RA, although its synoival expression if not sufficient to control the disease activity.
    Of IL-6-type cytokines, large amounts of IL-6, IL-11, and LIF were produced mainly by IL-1 or TNF-activated fibroblasts, whereas oncostatin M was exclusively by macrophages in RA joints. However, only IL-6 was circulating at significant levels in association with raised levels of serum CRP levels, indicating its contribution to systemic inflammatory reactions such as acute-pahse reactant production by liver.

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  • Molecular architecture and gene expression of glomerular extracellular matrix.

    Grant number:04404039  1992 - 1994

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for General Scientific Research (A)

    OTA Zensuke, SHIKATA Kenichi, KASHIHARA Naoki, IKEDA Shyuji, OGURA Toshio, MAKINO Hirofumi

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    Grant amount:\22000000 ( Direct expense: \22000000 )

    We observed the normal kidneys and kidneys of diabetic nephropathy and membranous nephropathy patients showing nephrotic syndrome by newly devised "tissue negative staining method" established by Z.Ota, principal investigator. In normal kidneys, glomerular basement membrane (GBM) showed fine meshwork structure consisted of fibrils, and pore size was 2-3nm. In nephrotic patients, pore size was increased and tunnel-like structures (named nephrotic tunnel) with 20-100 nm diameter, which penetrate GBMs from capillary lumen to urinaru lumen. The diameter of this nephrotic tunnel is larger than the albumin molecules, and thus this structure is tightly related to the etiology of the nephrotic syndrome.
    By ultra-high resolution scanning electron microscopy, we observed the isolated GBM and glomeruli treated with detergent. Furthermore, we investigated the components of the GBMs, by immunoelectron microscopy using the specific antibodies against type IV collagen, hepara sulfate proteoglycans and fibronectins. The GBM was mainly consisted of type IV collagens and three dimentional meshwork.
    In various forms of glomerulonephritis, the expression of integrins were investigated by immunohistochemistry. In IgA nephropathy, membranous proliferative glomerulonephritis, and lupus nephritis, beta1 integrins and alphav-related receptors were upregulated in the glomeruli. The ligands of integrins, i.e.finronectin, vitronectin and type IV collagens were also increased in the glomeurli. These results indicated that integrin may be involved in the progression of mesangial proliferative glomerulonephritis.

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  • Molecular biological approach to the abnormalities of extracelluar matrix of the diabetic nephropathy.

    Grant number:04671481  1992 - 1994

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for General Scientific Research (C)

    MAKINO Hirofumi, SHIKATA Kenichi, KASHIHARA Naoki, IKEDA Shyuji, NIMOMIYA Yoshifumi

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    Grant amount:\2200000 ( Direct expense: \2200000 )

    Extracellular matrix has been shown to be consisted of collagens, laminins and proteoglycans. In diabetic nephropathy, the altertions of biochemical properties of type IV collagen and the decreased expression of proteoglycans are considered to be major pathological changes of the disease and related to the phenotypic changes of glomerular cells. Immunoelectron microscopic studies of diabetic nepropathy patients with nephrotic syndrome showed the thicking of glomerular basement membranes (GBM), increased amount of type IV collagens with decreased density, and decreased heparan sulfate proteoglycan. These alterations of extracellular matrix components seems to contribute to the the impairment of size and charge barrier of the GBM and proteinuria. Furthermore, we cloned a novel chain of type IV collagen, i.e.alpha4 chain, which cDNA (NK4) included NC-1 domain and expands 1.9 Kb. Northern blot analyzes showed -9.5 Kb transcript. Immunofluorescence studies of alpha1, alpha2, alpha3, alpha4, and basement membrane associated-collagen (BAC) showed alpha1 and alpha2 localized to the glomerular mesangial area and glomerular capillary, while alpha3 and alpha4 localized mainly along the capillary wall. BAC immunoreactivity was observed in the mesangial area. In the kidney of diabetic patients, expanded mesangial matrix and thickened GBM showed increased expression of alpha1-alpha4 chains and BAC.Furthermore, we analyzed the expression of the interstitial collagens, such as III,V,VI collagens. Type III collagen exclusively expressed in the interstinum of the kidney and type V and VI collagens had mesangial expressions. In diabetic kidney, these collagens were increased in the mesangial area.

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  • Function of Cell Adhesion Molecule in Glomerulonephirtis

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    Grant type:Competitive

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  • Etiology and Therapy of Diabetic Nephropathy

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    Grant type:Competitive

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  • Therapeutic Strategies for Renal Diseases

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    Grant type:Competitive

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  • 腎疾患における細胞接着分子の機能

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  • 糖尿病性腎症の成因と治療

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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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  • 腎疾患に対する治療法の開発

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Media Coverage

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    Author:Myself 

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