start-ver=1.4
cd-journal=joma
no-vol=27
cd-vols=
no-issue=1
article-no=
start-page=19
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250131
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Performance of the modified 2022 ACR/EULAR giant cell arteritis classification criteria without age restriction for discriminating from Takayasu arteritis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective To evaluate the ability to discriminate giant cell arteritis (GCA) from Takayasu arteritis (TAK) according to the modified 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology (ACR/EULAR) GCA classification criteria.<br>
Methods Patients enrolled in the Japanese nationwide retrospective registry were evaluated using the criteria with partial modification; wall thickening of descending thoracic-abdominal aorta were mainly diagnosed by contrast-enhanced computed tomography (CT) or magnetic resonance imaging instead of evaluating with positron emission tomography (PET)-CT. The discriminability of the criteria was evaluated using C-statistic (> 0.7: good ability).<br>
Results Newly diagnosed patients with GCA (n = 139) and TAK (n = 129) were assessed, and 23.3% of TAK were aged 50 years or older at onset. The sensitivity of the modified 2022 ACR/EULAR GCA classification criteria with a score ≥ 6 was 82.0%, 68.5%, and 32.1% in all GCA, GCA with large-vessel involvement, and GCA without cranial arteritis, respectively. The specificity of the modified criteria was 96.1% for the 129 TAK as controls. Five patients with late-onset TAK met the modified criteria, and four had cranial signs and symptoms, two had bilateral axillary artery involvement, and four had descending thoracic-abdominal aorta involvement. The discriminability of the criteria was good (C-statistic: 0.986, 95% confidence interval [CI]: 0.976–0.996) and remained good after excluding age (C-statistic: 0.927, 95% CI: 0.894–0.961). The discriminability of a set of large-vessel lesions (bilateral axillary artery and descending thoracic-abdominal aorta) and inflammatory markers was markedly decreased with poor C-statistic value (C-statistic: 0.598, 95% CI: 0.530–0.667). Discriminability was improved after adding polymyalgia rheumatica (PMR) (C-statistic: 0.757, 95% CI: 0.700–0.813) or age (C-statistic: 0.913, 95%CI: 0.874–0.951) to the set of large-vessel lesions. In GCA patients with a score ≤ 5, 52% had bilateral subclavian and/or axillary artery involvement.<br>
Conclusion The modified 2022 ACR/EULAR GCA classification criteria well performed in classifying GCA and TAK without PET-CT in routine clinical practice. A set of items included in the modified GCA classification criteria had good discriminative ability for GCA and TAK, even when age was excluded. However, age restriction or PMR was required to distinguish GCA without cranial lesions from TAK.
en-copyright=
kn-copyright=

en-aut-name=SugiharaTakahiko
en-aut-sei=Sugihara
en-aut-mei=Takahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HarigaiMasayoshi
en-aut-sei=Harigai
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshifujiHajime
en-aut-sei=Yoshifuji
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MaejimaYasuhiro
en-aut-sei=Maejima
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IshizakiJun
en-aut-sei=Ishizaki
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeYoshiko
en-aut-sei=Watanabe
en-aut-mei=Yoshiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=DobashiHiroaki
en-aut-sei=Dobashi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KomagataYoshinori
en-aut-sei=Komagata
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TamuraNaoto
en-aut-sei=Tamura
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NakaokaYoshikazu
en-aut-sei=Nakaoka
en-aut-mei=Yoshikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=Japan Research Committee of the Ministry of Health, Labour, and Welfare for Intractable Vasculitis (JPVAS)
en-aut-sei=Japan Research Committee of the Ministry of Health, Labour, and Welfare for Intractable Vasculitis (JPVAS)
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=2
en-affil=Division of Rheumatology, Department of Internal Medicine, Tokyo Women’s Medical University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=6
en-affil=Department of Hematology, Clinical Immunology and Infectious Diseases, Ehime University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Kawasaki Medical School
kn-affil=

affil-num=8
en-affil=Division of Hematology, Rheumatology and Respiratory Medicine, Department of Internal Medicine, Faculty of Medicine, Kagawa University
kn-affil=

affil-num=9
en-affil=Department of Nephrology and Rheumatology, Kyorin University School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Vascular Physiology, National Cerebral and Cardiovascular Center Research Institute
kn-affil=

affil-num=12
en-affil=
kn-affil=
en-keyword=GCA
kn-keyword=GCA
en-keyword=TAK
kn-keyword=TAK
en-keyword=Classification criteria
kn-keyword=Classification criteria
en-keyword=Bilateral axillary artery
kn-keyword=Bilateral axillary artery
en-keyword=Descending thoracic-abdominal aorta
kn-keyword=Descending thoracic-abdominal aorta
en-keyword=Bilateral subclavian artery
kn-keyword=Bilateral subclavian artery
END

start-ver=1.4
cd-journal=joma
no-vol=2021
cd-vols=
no-issue=
article-no=
start-page=1
end-page=8
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210413
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fisetin Attenuates Lipopolysaccharide-Induced Inflammatory Responses in Macrophage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Several studies have reported the efficacy and safety of polyphenols in human health; however, the verification of their efficacy remains insufficient. The aim of this study was to examine whether fisetin, one of flavonoids prevalently present in fruits and vegetables, could suppress lipopolysaccharide- (LPS-) induced inflammatory responses in macrophages. LPS increased proinflammatory mRNA abundance (MCP 1, IL-1 beta, and iNOS) but were suppressed by fisetin. The increment of nitric oxide by LPS, an oxidative stress factor, was attenuated by fisetin. In addition, LPS-enhanced phosphorylation of mitogen-activated protein kinase (ERK and JNK) was reduced. Finally, fisetin attenuated the expression or activity of uPA, uPAR, MMP-2, and MMP-9, which are known as associated factors of macrophage recruitment or infiltration. In conclusion, fisetin is a promising therapeutic agent for macrophage-related inflammation diseases, like sepsis and atherosclerosis.
en-copyright=
kn-copyright=

en-aut-name=HadaYoshiko
en-aut-sei=Hada
en-aut-mei=Yoshiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UchidaHaruhito
en-aut-sei=Uchida
en-aut-mei=Haruhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=134
cd-vols=
no-issue=20
article-no=
start-page=2771
end-page=2787
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201030
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibition of interleukin-6 signaling attenuates aortitis, left ventricular hypertrophy and arthritis in interleukin-1 receptor antagonist deficient mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of the present study was to examine whether inhibition of Interleukin (IL)-6 signaling by MR16-1, an IL-6 receptor antibody, attenuates aortitis, cardiac hypertrophy, and arthritis in IL-1 receptor antagonist deficient (IL-1RA KO) mice. Four weeks old mice were intraperitoneally administered with either MR16-1 or non-immune IgG at dosages that were adjusted over time for 5 weeks. These mice were stratified into four groups: MR16-1 treatment groups, KO/MR low group (first 2.0 mg, following 0.5 mg/week, n=14) and KO/MR high group (first 4.0 mg, following 2.0 mg/week, n=19) in IL-1RA KO mice, and IgG treatment groups, KO/IgG group (first 2.0 mg, following 1.0 mg/week, n=22) in IL-1RA KO mice, and wild/IgG group (first 2.0 mg, following 1.0 mg/week, n=17) in wild mice. Aortitis, cardiac hypertrophy and arthropathy were histologically analyzed. Sixty-eight percent of the KO/IgG group developed aortitis (53% developed severe aortitis). In contrast, only 21% of the KO/MR high group developed mild aortitis, without severe aortitis (P<0.01, vs KO/IgG group). Infiltration of inflammatory cells, such as neutrophils, T cells, and macrophages, was frequently observed around aortic sinus of the KO/IgG group. Left ventricle and cardiomyocyte hypertrophy were observed in IL-1RA KO mice. Administration of high dosage of MR16-1 significantly suppressed cardiomyocyte hypertrophy. MR16-1 attenuated the incidence and severity of arthritis in IL-1RA KO mice in a dose-dependent manner. In conclusion, blockade of IL-6 signaling may exert a beneficial effect to attenuate severe aortitis, left ventricle hypertrophy, and arthritis.
en-copyright=
kn-copyright=

en-aut-name=HadaYoshiko
en-aut-sei=Hada
en-aut-mei=Yoshiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MukaiTomoyuki
en-aut-sei=Mukai
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KojimaFumiaki
en-aut-sei=Kojima
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakeuchiHidemi
en-aut-sei=Takeuchi
en-aut-mei=Hidemi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KakioYuki
en-aut-sei=Kakio
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OtakaNozomu
en-aut-sei=Otaka
en-aut-mei=Nozomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoritaYoshitaka
en-aut-sei=Morita
en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

affil-num=3
en-affil=Department of Rheumatology, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Pharmacology, Kitasato University School of Allied Health Sciences
kn-affil=

affil-num=5
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science
kn-affil=

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

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

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

affil-num=9
en-affil=Department of Rheumatology, Kawasaki Medical School
kn-affil=

affil-num=10
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science
kn-affil=
en-keyword= MR16-1
kn-keyword= MR16-1
en-keyword=interleukin-1 receptor antagonist
kn-keyword=interleukin-1 receptor antagonist
en-keyword=aortitis
kn-keyword=aortitis
en-keyword=arthritis
kn-keyword=arthritis
en-keyword=LV hypertrophy
kn-keyword=LV hypertrophy
END

start-ver=1.4
cd-journal=joma
no-vol=132
cd-vols=
no-issue=2
article-no=
start-page=108
end-page=109
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Community-based medical collaboration
kn-title=地域医療連携
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=UchidaHaruhito  A.
en-aut-sei=Uchida
en-aut-mei=Haruhito  A.
kn-aut-name=内田治仁
kn-aut-sei=内田
kn-aut-mei=治仁
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences 
kn-affil=岡山大学大学院医歯薬学総合研究科　CKD・CVD 地域連携包括医療学
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=9
article-no=
start-page=1576
end-page=1580
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200618
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Tubulointerstitial Nephritis Cases With IgM-Positive Plasma Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=Matsuoka-UchiyamaNatsumi
en-aut-sei=Matsuoka-Uchiyama
en-aut-mei=Natsumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

en-aut-name=FukushimaKazuhiko
en-aut-sei=Fukushima
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitamuraShinji
en-aut-sei=Kitamura
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

en-aut-name=TakahashiNaoki
en-aut-sei=Takahashi
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IwanoMasayuki
en-aut-sei=Iwano
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Nephrology, Faculty of Medical Science, University of Fukui
kn-affil=

affil-num=8
en-affil=Department of Nephrology, Faculty of Medical Science, University of Fukui
kn-affil=

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

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=8
article-no=
start-page=e72214
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130819
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Calpain-2 Compensation Promotes Angiotensin II-Induced Ascending and Abdominal Aortic Aneurysms in Calpain-1 Deficient Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background and Objective

Recently, we demonstrated that angiotensin II (AngII)-infusion profoundly increased both aortic protein and activity of calpains, calcium-activated cysteine proteases, in mice. In addition, pharmacological inhibition of calpain attenuated AngII-induced abdominal aortic aneurysm (AA) in mice. Recent studies have shown that AngII infusion into mice leads to aneurysmal formation localized to the ascending aorta. However, the precise functional contribution of calpain isoforms (-1 or -2) in AngII-induced abdominal AA formation is not known. Similarly, a functional role of calpain in AngII-induced ascending AA remains to be defined. Using BDA-410, an inhibitor of calpains, and calpain-1 genetic deficient mice, we examined the relative contribution of calpain isoforms in AngII-induced ascending and abdominal AA development.

Methodology/Results

To investigate the relative contribution of calpain-1 and -2 in development of AngII-induced AAs, male LDLr −/− mice that were either calpain-1 +/+ or −/− were fed a saturated fat-enriched diet and infused with AngII (1,000 ng/kg/min) for 4 weeks. Calpain-1 deficiency had no significant effect on body weight or blood pressure during AngII infusion. Moreover, calpain-1 deficiency showed no discernible effects on AngII-induced ascending and abdominal AAs. Interestingly, AngII infusion induced increased expression of calpain-2 protein, thus compensating for total calpain activity in aortas of calpain-1 deficient mice. Oral administration of BDA-410, a calpain inhibitor, along with AngII-infusion significantly attenuated AngII-induced ascending and abdominal AA formation in both calpain-1 +/+ and −/− mice as compared to vehicle administered mice. Furthermore, BDA-410 administration attenuated AngII-induced aortic medial hypertrophy and macrophage accumulation. Western blot and immunostaining analyses revealed BDA-410 administration attenuated AngII-induced C-terminal fragmentation of filamin A, an actin binding cytoskeletal protein in aorta.

Conclusion

Calpain-2 compensates for loss of calpain-1, and both calpain isoforms are involved in AngII-induced aortic aneurysm formation in mice.
en-copyright=
kn-copyright=

en-aut-name=SubramanianVenkateswaran
en-aut-sei=Subramanian
en-aut-mei=Venkateswaran
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoorleghenJessica　J.
en-aut-sei=Moorleghen
en-aut-mei=Jessica　J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=BalakrishnanAnju
en-aut-sei=Balakrishnan
en-aut-mei=Anju
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HowattDeborah　A.
en-aut-sei=Howatt
en-aut-mei=Deborah　A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ChishtiAthar H.
en-aut-sei=Chishti
en-aut-mei=Athar H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Saha Cardiovascular Research Center, University of Kentucky

affil-num=2
en-affil=
kn-affil=Saha Cardiovascular Research Center, University of Kentucky

affil-num=3
en-affil=
kn-affil=Saha Cardiovascular Research Center, University of Kentucky

affil-num=4
en-affil=
kn-affil=Saha Cardiovascular Research Center, University of Kentucky

affil-num=5
en-affil=
kn-affil=Department of Molecular Physiology and Pharmacology, Sackler School Programs in Physiology, Pharmacology, and Microbiology, Tufts University School of Medicine

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

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=2
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130219
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Decreased Level of Serum Soluble Klotho Is an Independent Biomarker Associated with Arterial Stiffness in Patients with Chronic Kidney Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Klotho was originally identified in a mutant mouse strain unable to express the gene that consequently showed shortened life spans. In humans, low serum Klotho levels are related to the prevalence of cardiovascular diseases in community-dwelling adults. However, it is unclear whether the serum Klotho levels are associated with signs of vascular dysfunction such as arterial stiffness, a major determinant of prognosis, in human subjects with chronic kidney disease (CKD). 

Methods: We determined the levels of serum soluble Klotho in 114 patients with CKD using ELISA and investigated the relationship between the level of Klotho and markers of CKD-mineral and bone disorder (CKD-MBD) and various types of vascular dysfunction, including flow-mediated dilatation, a marker of endothelial dysfunction, ankle-brachial pulse wave velocity (baPWV), a marker of arterial stiffness, intima-media thickness (IMT), a marker of atherosclerosis, and the aortic calcification index (ACI), a marker of vascular calcification. 

Results: The serum Klotho level significantly correlated with the 1,25-dihydroxyvitamin D level and inversely correlated with the parathyroid hormone level and the fractional excretion of phosphate. There were significant decreases in serum Klotho in patients with arterial stiffness defined as baPWV >= 1400 cm/sec, atherosclerosis defined as maximum IMT >= 1.1 mm and vascular calcification scores of ACI>0%. The serum Klotho level was a significant determinant of arterial stiffness, but not endothelial dysfunction, atherosclerosis or vascular calcification, in the multivariate analysis in either metabolic model, the CKD model or the CKD-MBD model. The adjusted odds ratio of serum Klotho for the baPWV was 0.60 (p = 0.0075). 

Conclusions: Decreases in the serum soluble Klotho levels are independently associated with signs of vascular dysfunction such as arterial stiffness in patients with CKD. Further research exploring whether therapeutic approaches to maintain or elevate the Klotho level could improve arterial stiffness in CKD patients is warranted.
en-copyright=
kn-copyright=

en-aut-name=KitagawaMasashi
en-aut-sei=Kitagawa
en-aut-mei=Masashi
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SugiyamaHitoshi
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en-aut-mei=Hitoshi
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ORCID=

en-aut-name=MorinagaHiroshi
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kn-aut-mei=
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ORCID=

en-aut-name=InoueTatsuyuki
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en-aut-mei=Tatsuyuki
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kn-aut-mei=
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ORCID=

en-aut-name=TakiueKeiichi
en-aut-sei=Takiue
en-aut-mei=Keiichi
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kn-aut-mei=
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ORCID=

en-aut-name=OgawaAyu
en-aut-sei=Ogawa
en-aut-mei=Ayu
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kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamanariToshio
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en-aut-mei=Toshio
kn-aut-name=
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kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KikumotoYoko
en-aut-sei=Kikumoto
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UchidaHaruhito Adam
en-aut-sei=Uchida
en-aut-mei=Haruhito Adam
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KitamuraShinji
en-aut-sei=Kitamura
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MaeshimaYohei
en-aut-sei=Maeshima
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

en-aut-name=NishishitaShingo
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en-aut-mei=Shingo
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ORCID=

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=軽中等度高血圧患者における早朝家庭血圧と脈波伝播速度に対するテルミサルタンの臨床効果
kn-title=Practical Efficacy of Telmisartan for Decreasing Morning Home Blood Pressure and Pulse Wave Velocity in Patients with Mild-to-Moderate Hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=UchidaHaruhito
en-aut-sei=Uchida
en-aut-mei=Haruhito
kn-aut-name=内田治仁
kn-aut-sei=内田
kn-aut-mei=治仁
aut-affil-num=1
ORCID=

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