start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=5 article-no= start-page=329 end-page=334 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Risk Factors for Infection in Patients with Remitted Rheumatic Diseases Treated with Glucocorticoids en-subtitle= kn-subtitle= en-abstract= kn-abstract=It is well known that infection is one of the major causes of morbidity and mortality in rheumatic disease patients treated with high-dose glucocorticoids, especially in the early phase after achievement of disease remission. The aim of this study was to identify the risk factors for infection, with a focus on the dose of glucocorticoids administered, following the achievement of disease remission in rheumatic diseases patients. We retrospectively analyzed the medical records of rheumatic disease patients who had been treated with glucocorticoids. The primary endpoint was the incidence rate of infection during a period from 1 to 2 months after the commencement of treatment. From April 2006 to March 2010, 19 of 92 patients suffered from infection during the observation period. Age≧65 yrs, presence of interstitial pneumonia, diagnosis of systemic vasculitis and serum creatinine level≧2.0mg/dl were found to be univariate predictors for infection. However, only the presence of interstitial pneumonia was an independent risk factor for infection (HR＝4.50, 95%CI＝1.65 to 14.44) by the Cox proportional hazard model. Even after achievement of clinical remission, careful observation is needed for patients with interstitial pneumonia, more so than for those receiving high-dose glucocorticoids. en-copyright= kn-copyright= en-aut-name=MatsumotoYoshinori en-aut-sei=Matsumoto en-aut-mei=Yoshinori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SadaKen-ei en-aut-sei=Sada en-aut-mei=Ken-ei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakanoMariko en-aut-sei=Takano en-aut-mei=Mariko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ToyotaNoriko en-aut-sei=Toyota en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamanakaRyutaro en-aut-sei=Yamanaka en-aut-mei=Ryutaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SugiyamaKoichi en-aut-sei=Sugiyama en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KawabataTomoko en-aut-sei=Kawabata en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OtsukaFumio en-aut-sei=Otsuka en-aut-mei=Fumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MakinoHirofumi en-aut-sei=Makino en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=infection kn-keyword=infection en-keyword=rheumatic disease kn-keyword=rheumatic disease en-keyword=glucocorticoids kn-keyword=glucocorticoids en-keyword=interstitial pneumonia kn-keyword=interstitial pneumonia en-keyword=risk factors kn-keyword=risk factors END start-ver=1.4 cd-journal=joma no-vol=144 cd-vols= no-issue=3 article-no= start-page=272 end-page=282 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201209 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Spred-2 deficiency exacerbates acetaminophen-induced hepatotoxicity in mice en-subtitle= kn-subtitle= en-abstract= kn-abstract=MAPKs are involved in acetaminophen (APAP)-hepatotoxicity, but the regulatory mechanism remains unknown. Here, we explored the role of Spred-2 that negatively regulates Ras/ERK pathway in APAP-hepatotoxicity. Spred-2 knockout (KO) mice demonstrated exacerbated liver injury, an event that was associated with increased numbers of CD4(+) T, CD8(+) T and NK cells in the liver compared to the control. Levels of CXCL9/CXCL10 that attract and activate these cells were increased in Spred-2 KO-liver. Kupffer cells isolated from Spred-2 KO mice after APAP challenge expressed higher levels of CXCL9/CXCL10 than those from the control. Upon stimulation with APAP or IFN gamma, naive Kupffer cells from Spred-2 KO mice expressed higher levels of CXCL9/CXCL10. NK cell-depletion attenuated APAP-hepatotoxicity with lowered hepatic IFN gamma and decreased numbers of not only NK cells but also CD4(+) T and CD8(+) T cells in the liver. These results suggest that Spred-2 negatively regulates APAP-hepatotoxicity under the control of Kupffer cells and NK cells. en-copyright= kn-copyright= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ItoToshihiro en-aut-sei=Ito en-aut-mei=Toshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FushimiSoichiro en-aut-sei=Fushimi en-aut-mei=Soichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NakashimaYuki en-aut-sei=Nakashima en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ItakuraJyunya en-aut-sei=Itakura en-aut-mei=Jyunya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=LiuQiuying en-aut-sei=Liu en-aut-mei=Qiuying kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=WinMin Min en-aut-sei=Win en-aut-mei=Min Min kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SunCuiming en-aut-sei=Sun en-aut-mei=Cuiming kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=ChenCao en-aut-sei=Chen en-aut-mei=Cao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=SatoMiwa en-aut-sei=Sato en-aut-mei=Miwa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MinoMegumi en-aut-sei=Mino en-aut-mei=Megumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=OginoTetsuya en-aut-sei=Ogino en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=MakinoHirofumi en-aut-sei=Makino en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=YoshimuraAkihiko en-aut-sei=Yoshimura en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=MatsukawaAkihiro en-aut-sei=Matsukawa en-aut-mei=Akihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=9 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=10 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=11 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=12 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=13 en-affil= kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci affil-num=14 en-affil= kn-affil=Keio Univ, Sch Med, Dept Microbiol & Immunol affil-num=15 en-affil= kn-affil=Okayama Univ, Dept Pathol & Expt Med, Grad Sch Med Dent & Pharmaceut Sci en-keyword=Acetaminophen kn-keyword=Acetaminophen en-keyword=Hepatotoxicity kn-keyword=Hepatotoxicity en-keyword=Liver immunology kn-keyword=Liver immunology en-keyword=Signaling pathway kn-keyword=Signaling pathway en-keyword=Toxicology kn-keyword=Toxicology END start-ver=1.4 cd-journal=joma no-vol=28 cd-vols= no-issue=5 article-no= start-page=299 end-page=310 dt-received= dt-revised= dt-accepted= dt-pub-year=1974 dt-pub=197410 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Studies on ferrous ion-induced lipid peroxidation of rat liver mitochondria. I. Effect of inorganic phosphate en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Effect of inorganic phosphate on ferrous ion- and ascorbate-induced lipid. peroxidations of isolated rat liver mitochondria was investigated. As a result it has been shown that phosphate accelerates the ferrous ion.induced lipid peroxidation; namely, phos. phate shortens the induction lag period of the lipid peroxidation reaction but the malondialdehyde after onset of its production is yielded at the same rate in various concentrations of phosphate. On the other hand, phosphate inhibits ascorbate.induced lipid peroxidation. There are stoichiometric interactions between the concentration of phos. phate and the induction period. Oxygen uptake by mitochondria was observed in the presence of both ferrous ion and phosphate at initial step of the reaction without being accompanied by malondialdehyde production, and afterwards there occurred malondialdehyde production with rapid rate of the oxygen uptake. Possible mechanisms and interactions among ferrous ion, ascorbate and phosphate were discussed.

en-copyright= kn-copyright= en-aut-name=YamamotoGoki en-aut-sei=Yamamoto en-aut-mei=Goki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TanabeMasatada en-aut-sei=Tanabe en-aut-mei=Masatada kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HashimotoGonosuke en-aut-sei=Hashimoto en-aut-mei=Gonosuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamamotoMichio en-aut-sei=Yamamoto en-aut-mei=Michio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University END start-ver=1.4 cd-journal=joma no-vol=88 cd-vols= no-issue=3-4 article-no= start-page=185 end-page=196 dt-received= dt-revised= dt-accepted= dt-pub-year=1976 dt-pub=1976 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the lipid peroxidation in mitochondria of x-ray whole body irradiated rat liver T. Change of Fe(++) -induced lipid peroxidation of mitochondria isolated from rat liver after irradiation kn-title=X線全身照射のラット肝ミトコンドリアにおける脂質過酸化反応に関する研究第一編 X線全身照射にともなうラット肝ミトコンドリアのFe++誘導脂質過酸化反応の変動について en-subtitle= kn-subtitle= en-abstract= kn-abstract=Lipid peroxidation of biomembrane is important in terms of the mechanism which are involved in the regulation and deterioration of their structure. To elucidate the behavior of lipid peroxidation in biomembrane after x-ray irradiation, the lipid peroxidation induced by Fe(++) in mitochondria after whole body irradiation was investigated, and the results are presented as follows. (1) Mitochondria were isolated from rat liver with the passage of day after 650 R irradiation, and the change of Fe(++) -induced lipid peroxidation was estimated by the TBA assay. Rates of the lipid peroxidation increased after irradiation and reached a maximum 3 days after irradiation, which was shown by shortening the lag of induction period and by the increase of TBA value per mg of protein. The increment of the activity was temporary and then the activity returned. (2) On the 3rd day after irradiation, the rat was more light in weight, and the wet weight of liver per body weight and the yield of mitochondria per tissue equivalent were increased transitorily in parallel with the change of the TBA value. (3) The shortening lag period and the high rate of TBA value depend on the dose of whole body irradiation. (4) The activity of oxidative phosphorylation of the mitochondria on the 3rd day after irradiation did not differ as compared with that of normal mitochondria. (5) These results suggest that the change of Fe(++) -induced lipid peroxidation of mitochondria after whole body irradiation is due to the irradiation. The factors in regulating the rate of lipid peroxidation were discussed. en-copyright= kn-copyright= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name=若林弘 kn-aut-sei=若林 kn-aut-mei=弘 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部放射線医学教室 END start-ver=1.4 cd-journal=joma no-vol=88 cd-vols= no-issue=3-4 article-no= start-page=197 end-page=207 dt-received= dt-revised= dt-accepted= dt-pub-year=1976 dt-pub=19760430 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the lipid peroxidation in mitochondria of x-ray whole-body irradiated rat liver U. Changes of fatty acid composition and ferrous ion-induced peroxidation of mitochondrial lipid after whole-body irradiation kn-title=X線全身照射のラット肝ミトコンドリアにおける脂質過酸化反応に関する研究 第二編 脂質ならびに脂肪酸組成の変動と抽出脂質のFe(++)誘導脂質過酸化反応について en-subtitle= kn-subtitle= en-abstract= kn-abstract=Ferrous ion-induced lipid peroxidation of the mitochondria isolated from rat liver on the 3rd day after x-ray whole-body irradiation at 650R showed shortening of the lag of induction period and more acceleration of the activity than those of normal mitochondria (Part 1). Further investigations were made on the mitochondria on the 3rd day after irradiation at 650R in regard to fatty acid compositions and Fe(++) -induced peroxidation of total or fractionated mitochondrial lipids. The results are represented as follows. 1) Fatty acid composition of the mitochondria after lipid peroxidation showed the decrease of polyenoic acids (C-20:4, C-22:6), suggesting the polyenoic acids are substrate of the reaction. 2) Changes of fatty acid composition of mitochondria after whole-body irradiation at 650R were shown decreasing of unsaturated fatty acid due to the decrement of C-18:1 and C-18:2, but the component of polyenoic acid increased relatively. These changes are transient, reaching a maximum on the 3rd day after irradiation, and this tendency is parallel to that of lipid peroxidation activity of the mitochondria whole-body irradiated. 3) No difference of the rate of peroxidation observed between total lipids extracted from normal and from whole-body irradiated mitochondria, and the lag of induction period was not seen in both reactions. 4) Peroxidation of the total lipid was seen markedly in the phospholipid fraction and slightly in the simple lipid fractions. Effect of whole-body irradiation on the peroxidation activities of the phospholipid was not observed significantly, despite of the difference seen in their fatty acid compositions. 5) Peroxidation of subfractionated phospholipid by a thin-layer chromatography showed marked activity in the fractions of lecithin and aminophosphatide containing large amounts of C-20:4 and C-22:6: Recovery of the activity of the subfractions increased markedly comparing to the total phospholipid, and effect of whole-body irradiation appeared significantly in these subfractions. However, relationship between activities of the peroxidation and fatty acid compositions of the subfractions cannot seen. It is suggested the mutual interaction of phopholipid subfractions on the peroxidation to decrease the activity, and some of lipid became more sensitive to peroxidation by irradiation. 6) Relative amount of phospholipid to total lipid increased in whole-body irradiated samples. 7) From these findings, it was discussed that the acceleration of Fe(++) -induced lipid peroxidation in mitochondrial level is due to the change of fatty acid composition and association of lipid in the membrane. en-copyright= kn-copyright= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name=若林弘 kn-aut-sei=若林 kn-aut-mei=弘 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部放射線医学教室 END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=3 article-no= start-page=227 end-page=230 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20141201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Molecular target therapies in rheumatic diseases kn-title=リウマチ性疾患における分子標的治療 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name=若林宏 kn-aut-sei=若林 kn-aut-mei=宏 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学 en-keyword=リウマチ性疾患 kn-keyword=リウマチ性疾患 en-keyword=自己免疫疾患 kn-keyword=自己免疫疾患 en-keyword=生物学的製剤 kn-keyword=生物学的製剤 en-keyword=分子標的薬 kn-keyword=分子標的薬 END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=3 article-no= start-page=209 end-page=215 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20141201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Hospital and clinic cooperation for the treatment of rheumatoid arthritis in Okayama Prefecture, Japan kn-title=岡山県下のクリニック・診療所におけるリウマチ診療・病診連携の実態に関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Objective: To survey the current status and problems of cooperation between clinics and hospitals in Okayama Prefecture, Japan for the treatment of rheumatoid arthritis (RA). 　Methods: We distributed a questionnaire to 300 of the 983 Okayama Prefecture clinics that had either an internal medicine or orthopedic surgery department, from December 2013 to February 2014. The questionnaire covered practice pattern for RA treatment in clinics, current status of the hospital and clinic cooperation, and acceptance of the biologic therapy. 　Results: One hundred clinics responded to the questionnaire. Seventy percent of the clinics reported making referrals to rheumatologists before the initiation of RA treatment, and half of the other 30% of the clinics administered methotrexate as the first-line treatment for RA by their own decision. Sixty-six clinics cooperated with flagship hospitals, conducting medical and laboratory examinations, providing prescriptions, and treating common diseases of patients. These clinics expected the cooperating rheumatologists to follow-up patients every 3 to 6 months and to make the diagnosis, make decisions regarding RA treatment changes, and perform surgery. Seventy-one percent of the clinics responded that cooperation with a hospital is possible even for patients who are administered biologics. As reasons for no cooperation with the flagship hospitals, clinics noted the lack of information about rheumatologists in the area and recent trends in the management of RA. 　Conclusion: The current study reported, for the first time, the actual conditions of management of RA in clinics, as well as future problems of hospital and clinic cooperation in Okayama Prefecture. en-copyright= kn-copyright= en-aut-name=SadaKen-ei en-aut-sei=Sada en-aut-mei=Ken-ei kn-aut-name=佐田憲映 kn-aut-sei=佐田 kn-aut-mei=憲映 aut-affil-num=1 ORCID= en-aut-name=NishidaKeiichiro en-aut-sei=Nishida en-aut-mei=Keiichiro kn-aut-name=西田圭一郎 kn-aut-sei=西田 kn-aut-mei=圭一郎 aut-affil-num=2 ORCID= en-aut-name=YamanakaTakao en-aut-sei=Yamanaka en-aut-mei=Takao kn-aut-name=山中隆夫 kn-aut-sei=山中 kn-aut-mei=隆夫 aut-affil-num=3 ORCID= en-aut-name=MisakiKenta en-aut-sei=Misaki en-aut-mei=Kenta kn-aut-name=三崎健太 kn-aut-sei=三崎 kn-aut-mei=健太 aut-affil-num=4 ORCID= en-aut-name=WakabayashiHiroshi en-aut-sei=Wakabayashi en-aut-mei=Hiroshi kn-aut-name=若林宏 kn-aut-sei=若林 kn-aut-mei=宏 aut-affil-num=5 ORCID= en-aut-name=ShinodaJunko en-aut-sei=Shinoda en-aut-mei=Junko kn-aut-name=篠田潤子 kn-aut-sei=篠田 kn-aut-mei=潤子 aut-affil-num=6 ORCID= en-aut-name=TakagiToru en-aut-sei=Takagi en-aut-mei=Toru kn-aut-name=木徹 kn-aut-sei=木 kn-aut-mei=徹 aut-affil-num=7 ORCID= en-aut-name=YanoRyusuke en-aut-sei=Yano en-aut-mei=Ryusuke kn-aut-name=矢野隆介 kn-aut-sei=矢野 kn-aut-mei=隆介 aut-affil-num=8 ORCID= en-aut-name=NakamuraAkihiko en-aut-sei=Nakamura en-aut-mei=Akihiko kn-aut-name=中村明彦 kn-aut-sei=中村 kn-aut-mei=明彦 aut-affil-num=9 ORCID= en-aut-name=NanbaYoshifumi en-aut-sei=Nanba en-aut-mei=Yoshifumi kn-aut-name=難波良文 kn-aut-sei=難波 kn-aut-mei=良文 aut-affil-num=10 ORCID= en-aut-name=MoritaYoshitaka en-aut-sei=Morita en-aut-mei=Yoshitaka kn-aut-name=守田吉孝 kn-aut-sei=守田 kn-aut-mei=吉孝 aut-affil-num=11 ORCID= en-aut-name=KoyamaYoshinobu en-aut-sei=Koyama en-aut-mei=Yoshinobu kn-aut-name=小山芳伸 kn-aut-sei=小山 kn-aut-mei=芳伸 aut-affil-num=12 ORCID= en-aut-name=YamamotoKeiji en-aut-sei=Yamamoto en-aut-mei=Keiji kn-aut-name=山本惠嗣 kn-aut-sei=山本 kn-aut-mei=惠嗣 aut-affil-num=13 ORCID= en-aut-name=EzawaKazuhiko en-aut-sei=Ezawa en-aut-mei=Kazuhiko kn-aut-name=江澤和彦 kn-aut-sei=江澤 kn-aut-mei=和彦 aut-affil-num=14 ORCID= en-aut-name=OtaYusuke en-aut-sei=Ota en-aut-mei=Yusuke kn-aut-name=太田裕介 kn-aut-sei=太田 kn-aut-mei=裕介 aut-affil-num=15 ORCID= en-aut-name=YoshiharaYoshiki en-aut-sei=Yoshihara en-aut-mei=Yoshiki kn-aut-name=吉原由樹 kn-aut-sei=吉原 kn-aut-mei=由樹 aut-affil-num=16 ORCID= en-aut-name=MiyoshiShinya en-aut-sei=Miyoshi en-aut-mei=Shinya kn-aut-name=三好信也 kn-aut-sei=三好 kn-aut-mei=信也 aut-affil-num=17 ORCID= en-aut-name=NatsumedaMasamitsu en-aut-sei=Natsumeda en-aut-mei=Masamitsu kn-aut-name=棗田将光 kn-aut-sei=棗田 kn-aut-mei=将光 aut-affil-num=18 ORCID= en-aut-name=UsuiMasaaki en-aut-sei=Usui en-aut-mei=Masaaki kn-aut-name=臼井正明 kn-aut-sei=臼井 kn-aut-mei=正明 aut-affil-num=19 ORCID= en-aut-name=YoshinagaYasuhiko en-aut-sei=Yoshinaga en-aut-mei=Yasuhiko kn-aut-name=吉永泰彦 kn-aut-sei=吉永 kn-aut-mei=泰彦 aut-affil-num=20 ORCID= en-aut-name=HayashiTakashi en-aut-sei=Hayashi en-aut-mei=Takashi kn-aut-name=林充 kn-aut-sei=林 kn-aut-mei=充 aut-affil-num=21 ORCID= en-aut-name=YamamuraMasahiro en-aut-sei=Yamamura en-aut-mei=Masahiro kn-aut-name=山村昌弘 kn-aut-sei=山村 kn-aut-mei=昌弘 aut-affil-num=22 ORCID= en-aut-name=HashizumeHiroyuki en-aut-sei=Hashizume en-aut-mei=Hiroyuki kn-aut-name=橋詰博行 kn-aut-sei=橋詰 kn-aut-mei=博行 aut-affil-num=23 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　人体構成学 affil-num=3 en-affil= kn-affil=南岡山医療センター　リウマチ科 affil-num=4 en-affil= kn-affil=倉敷中央病院　内分泌代謝・リウマチ内科 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=岡山労災病院　整形外科 affil-num=7 en-affil= kn-affil=岡山赤十字病院　整形外科 affil-num=8 en-affil= kn-affil=矢野内科医院 affil-num=9 en-affil= kn-affil=おさふねクリニック affil-num=10 en-affil= kn-affil=川崎医科大学附属病院　整形外科 affil-num=11 en-affil= kn-affil=川崎医科大学附属病院　リウマチ・膠原病科 affil-num=12 en-affil= kn-affil=岡山赤十字病院　膠原病リウマチ内科 affil-num=13 en-affil= kn-affil=山本整形外科医院 affil-num=14 en-affil= kn-affil=倉敷スイートホスピタル　内科 affil-num=15 en-affil= kn-affil=香川労災病院　整形外科 affil-num=16 en-affil= kn-affil=倉敷成人病センター　整形外科 affil-num=17 en-affil= kn-affil=倉敷成人病センター　整形外科 affil-num=18 en-affil= kn-affil=倉敷スイートホスピタル　内科 affil-num=19 en-affil= kn-affil=岡山市民病院　整形外科 affil-num=20 en-affil= kn-affil=倉敷成人病センター　リウマチ膠原病内科 affil-num=21 en-affil= kn-affil=佐用中央病院　整形外科 affil-num=22 en-affil= kn-affil=岡山済生会総合病院　内科 affil-num=23 en-affil= kn-affil=笠岡第一病院　整形外科 en-keyword=病診連携（hospital and clinic cooperation） kn-keyword=病診連携（hospital and clinic cooperation） en-keyword=関節リウマチ（rheumatoid arthritis） kn-keyword=関節リウマチ（rheumatoid arthritis） en-keyword=生物学的製剤（biologics） kn-keyword=生物学的製剤（biologics） en-keyword=メトトレキサート（methotrexate） kn-keyword=メトトレキサート（methotrexate） END